COLLEGE OF PHYSICAL AND RESPIRATORY THERAPY

Carlatan, City of San Fernando, La Union

SY 2016-2017

This Written Report on

Cerebrovascular Accident

Is Submitted to the
College of Physical and Respiratory Therapy

In Partial Fulfillment to the Requirements

On Subject
Seminar I

SUBMITTED TO:
Maverick Kaypee Colet, Ptrp
Bernardo Tayaban Jr. Ptrp
SUBMITTED BY:
Andrada, Dune Abraham
Carino Pauline Trisha
Estacio, Patricia Ashley
Gurtiza, Joanna Eden
Pioquinto, Renzdolf
Valite, Dale

December 2, 2016

I. DEFINITION OF TERMS
STROKE
is a sudden loss of neurological function caused by an interruption of the blood flow
to the brain
- (OSullivan, Susan B. & Schmitz, Thomas J. Physical Rehabilitation 5th Edition,
pp 706-761)
is a non-traumatic brain injury, caused by occlusion or rupture of cerebral blood
vessels, that results in sudden neurologic deficit characterized by loss of motor
control, altered sensation, cognitive or language impairment, disequilibrium, or
coma
- (Braddom, Randall L. Physical Medicine & Rehabilitation 3rd Edition, p. 1176)
sudden, focal neurological deficit resulting from ischemic or hemorrhagic lesions in
the brain
- (OSullivan & Siegelman National Physical Therapy Examination Review and
Study Guide 2014, p. 142)
CVA / Cerebrovascular accident
refer to the vascular conditions of the brain w/ variety of focal deficits including
changes in level of consciousness and impairments of sensory, motor, cognitive,
perceptual, and language functions
to be classified as stroke, neurological deficits must persists for at least 24 hours
- (OSullivan, Susan B. & Schmitz, Thomas J. Physical Rehabilitation 5th
Edition, p. 706)
CLASSIFICATION OF STROKE
A. TEMPORAL CLASSIFICATION

1. Transient Ischemic Attack (TIA)

Focal neurologic attack with complete recovery within 24 hrs
Temporary interruption of blood supply to the brain
No neurologic dysfunction
A TIA is characterized by a brief episode of neurologic dysfunction caused by
a focal disturbance of brain or retinal ischemia, with clinical symptoms
typically lasting less than 1 hour, and without evidence of infarction. TIA is
often a strong prognostic indicator of stroke and is commonly caused by
carotid or vertebrobasilar disease. About 10% to 15% of patients with TIA will
go on to have a stroke within 90 days; 5% will have a stroke within 2 days.53
The management of TIAs involves observation, treatment of causative factor
(if possible), anticoagulation, and carotid endarterectomy

2. Reversible Ischemic Neurologic Deficit (RIND)

Focal neurologic deficit that lasts longer than 24 hrs but still with reversible
signs and symptoms
usually is a result of small infarction with temporary impairment within a
week
3. Stroke in Evolution
A CVA in which the neurologic impairments continue to evolve or fluctuate
over hours or day
4. Complete Stroke

A CVA in which the neurologic impairments have fully evolved

Stable neurologic deficit
No reverse and with no progress

B. PATHOPHYSIOLOGIC CLASSIFICATION
1. Ischemic
Ischemic CVA is the result of cerebral hypoperfusion. An ischemic CVA due to
thrombotic disease, such as carotid artery stenosis or arteriosclerotic
intracranial arteries, usually has a slow onset. Symptoms of an ischemic
stroke caused by embolus from the heart in the setting of atrial fibrillation,
meningitis, prosthetic valves, patent foramen ovale, or endocarditis will have
a sudden onset.
a. Thrombosis
(atherothrombotic brain infarction [ABI]) Formation of a blood clot or
thrombus within the cerebral arteries or their branches or the internal
carotid or vertebral arteries, causing an occlusion and cerebral
infarction; large vessel thrombosis is the most common and is
associated with long-standing atherosclerosis.
40% of all stroke cases
Associated with atherosclerotic cerebrovascular disease
Atherosclerosis is the major risk factors which is secondary to Htn
Large vessels is most commonly affected
It is gradual in onset
Commonly occurs at night or during periods of inactivity
It has severe impairments
50% of TIAs
b. Embolic
Embolic stroke is caused by debris originating elsewhere that block
arterial access to a particular brain region. Since the process is not
localized as with thrombosis, local therapy only temporarily solves the
problem and further events may occur if the source of the emboli is not
identified and treated.
30% of all stroke cases
Usually of cardiac origin
Atrial Fibrillation is the major risk factor
Other risk factors: mural thrombos and paradoxical embolism
Involves small, distal cortical vessels
MCA most commonly affected
Abrupt in onset
Produces less severe damage
c. Lacunar
Blood flow is blocked in very small arterial vessels deep within the
cerebral white matter with involvement of the internal capsule;
characterized by contralateral pure motor or sensory deficits without
visual field, cognitive, or speech deficits.
20% of all stroke cases
Associated with poorly controlled Htn or DM
Small, deep perforating arteries (<1.5 cm in diameters) which
perfuse the subcortical structure including the internal capsule
Basal Ganglia, Thalamus, and brainstem
Gradual onset

Mild manifestation
Presents with contralateral pure motor or pure sensory deficit,
ipsilateral ataxia with crural paresis and dysarthria with clumsiness
of the hand.
Good prognosis with partial or complete resolution occurring over
the following 4-6 wks.
2. Hemorrhagic
Abnormal bleeding into the extravascular areas of the brain; usually
results from rupture of an aneurysm, extremely high blood pressure, brain
trauma, or brain tumors.

a. Intracranial
Small, deep, penetrating arteries
Abrupt onset
Causes more failures
Caused by compression of neural tissue, neural stretching and
ventricular compression
b. Subarachnoid
Ruptured berry aneurysm
Most headache
Causes, saccular aneurysm and AV malformation
C. NEUROLOGICAL CLASSIFICATION
1. MCA Syndrome
Most commonly seen within the inpatient rehabilitation setting
The MCA is particularly vulnerable to both cardioembolic and thrombotic
disease than can result in a variety of stroke syndromes
CHARACTERISTICS OF MCA

MAIN STEM
Contralateral Hemiplegia
Contralateral
Hemianesthesia
Contralateral
Hemianopsia
Hand/eye toward lesion
Uninhibited
Neurogenic
bladder
Dominant
Hemisphere:
global aphasia, apraxia

UPPER DIVISION
Contralateral Hemiplegia
Contralateral
Hemianesthesia
Contralateral
Hemianopsia
Hand/eye toward lesion
Uninhibited
Neurogenic
bladder
Dominant
Hemisphere:
Brocas aphasia, apraxia

LOWER DIVISION
Contralateral Hemiplegia

Dominant
Hemisphere:
Wernickes
aphasia,
apraxia
Non-dominant
Non-dominant
Non-dominant
hemisphere:
aprosody, hemisphere:
aprosody, hemisphere:
affective
affective agnosia, neglect affective agnosia, neglect agnosia
s/o, visiospatial deficit
s/o, visiospatial deficit
Dysphagia
Dysphagia
2. ACA SYNDROME
- Contralateral Hemiplegia
- Contralateral Hemianopsia
- Head/eye toward lesion

Grasp Reflex
Kinetic Mutism (Abulism)

3. PCA STROKE
- Hemisensory Deficit
- Visual Impairment
- Visual agnosia
Prosopagnosia

II. EPIDEMIOLOGY

Stroke is the third most leading causes of death and the most common cause of disability
among adults in United States.

Age
o Most common after 65 years of age
o 28% of stroke occur in individuals younger than 65 y/o
Sex
o About 1.25 times greater for males than females
o About 22% of men and 25% of women with an initial stroke will die within a
year
o 19% higher among adult men than in women of all races
Race
o Compared to whites, African-Americans have twice the risk of first-ever
stroke; rates are also higher in Mexican-Americans, American Indians, and
Alaska Natives
o Among black men less than 65 y/o, stroke incidence is two- to threefold
higher than among whites
Many important risk factors for stroke are found in higher frequency
among black people, including HTN, DM, heart disease, smoking,
excessive alcohol use, and sickle cell disease.
Incidence
Incidence of stroke increases dramatically with age, doubling in the decade
after 65 years of age
o White men
(65 to 75 y/o) - 14.4 per 1000 population
(75 to 84 y/o) - 24.6 per 1000 population
(85 & above) - 27.0 per 1000 population
Prevalence
o Stroke was the primary cause of death in 163, 538 persons in 2001, and it
remains the third leading cause of death in the USA; it is exceeded only by
cardiovascular disease and cancer.
o It affects approximately 700,000 individuals each year
500,000 are new strokes
200,000 are recurrent strokes
o The rate of stroke in Asian countries is higher than in the USA, with a greater
proportion of strokes caused by intracranial hemorrhage.
Mortality
The type of stroke is significant in determining survival
Hemorrhagic stroke
37 to 38% a month
Ischemic stroke
8 to 12% a month

Survival
lessened by age, HTN, heart disease and DM

III. ANATOMY, PHYSIOLOGY AND KINESIOLOGY

(OSullivan, Susan B. & Schmitz, Thomas J. Physical Rehabilitation 5th Edition, p.
706)
(Braddom, Randall L. Physical Medicine & Rehabilitation 3rd Edition, p. 1184)
NEUROANATOMY
- Is the study of the anatomy and stereotyped organization of nervous systems.
NEUROPHYSIOLOGY
- Is a branch of physiology and neuroscience that is concerned with the study of the
functioning of the nervous system.
NEUROLOGY
- Medical specialty dealing with disorders of the nervous system
- Diagnosis and treatment of all categories of disease involving the central, peripheral
and autonomic nervous systems, including their coverings, blood vessels, and all
effector tissue, such as muscle neurologists are physicians who have completed
post graduate training in neurology after graduation from medical school.
NERVOUS SYSTEM
Has 3 basic functions
1. Sensory function- senses certain changes (stimuli ), both within the body ( internal
environment ) and outside the body ( external environment )
2. Integrative function- analyzes the sensory information, stores and makes decisions
regarding appropriate behaviours.
3. Motor function- respond to stimuli by initiating muscular contractions or glandular
secretions.
ORGANIZATION OF THE NERVOUS SYSTEM
Central Nervous System
o Brain and Spinal Cord
Peripheral Nervous System
o Nervous tissue outside and spine
o Cranial nerves that arise from the brain
o Spinal nerves that emerge from the SC
o Sense organ
Somatic Nervous System
- Part of PNS that controls voluntary functions
- Consists of sensory neurons that convey information from cutaneous
and special sense receptors to the CNS and motor neurons from CNS
that conducts impulses to skeletal muscles only.
Autonomic Nervous System
- Parts of PNS that controls involuntary functions.
- Consists of sensory neurons that convey information from receptors primarily
in the viscera to the CNS and motor neurons from the CNS to conduct
impulses to smooth muscles, cardiac muscles and glands.
Parasympathetic division- rest and digest

Sympathetic division stimulatory stress responses flight or fight responses

Parasympathetic (Cervico-sacral)
Constricts eye pupils
Stimulate salivation
Slows heart rate
Constricts breathing
Dilates blood vessels
Stimulates digestion
Constricts bladder
Stimulates sex organs

Sympathetic (Thoracolumbar (T1L3))

Dilates eye pupils
Inhibits salivation
Accelerates heart rate
Facilitates breathing
Stimulates secretion of epinephrine
and norepinephrine
Stimulates release of free glucose
Inhibits digestion
Relaxes bladder
Inhibits sex organs

NEUROGLIA
NEUROGLIA (neuro-nerve; glia-glue )
Fill about half of the CNS
Generally smaller than neurons and are 5-50 times more numerous
Can multiply and divide in the mature nervous system.
BRAIN TUMORS COMMONLY DERIVE FROM GLIA=GLIOMA
Types of Neuroglia
Found in CNS
Astrocytes
o Star like cells
o Participate in the metabolism of neurotransmitters
o Maintain proper balance of potassium ions for generation of nerve impulses,
brain development, and help from blood brain barrier and provide link
between neurons and blood vessels.
Oligodendrocytes
o Most common glial cells in the CNS
o Have few processes and smaller than astrocytes
o Form a supporting network by twining around neurons and produce lipid and
protein wrapping called myelin sheath.

Microglia
o Small phagocytic neuroglia derived from monocytes
o Protect the CNS from dse by engulfing invading microbes and clearing away
debris from dead cells.
Ependymal
o Epithelial cells
o They range in shape from cuboidal to columnar and many are ciliated
o They line the fluid filled ventricles, cavities within the brain, and central
canal.

Found in PNS
Neurolemmocytes or Schwann cells- produce myelin sheath around PNS neurons
Satellite cells- supports neurons in ganglia
Myelination

Myelin Sheath
Multilayered lipid and protein covering the axons of most neurons.
Electrically insulates the axon of a neuron and increases the speed of nerve
impulse.
Neurolemma ( sheath of Schwann ) -outer nucleated sytoplasmic layer of the
neurolemmocyte
Neurofibral nodes or Nodes of Ranvier -intervals along an axon , gaps along myelin
sheath

The Neuron
An electrically excitable cell that processes and transmits information by electrical
and chemical signals that occurs via synapses.
Types of Neurons
1. Sensory neurons- touch, sound, light and numerous other stimuli affecting cells of
the sensory organs that then send signals to the spinal cord and brain.
2. Motor neurons- receive signals from the brain and spinal cord, cause muscle
contractions typical neuron possesses a cell body (soma). Dendrites and axon.
Parts of Neuron
Dendrites
- Thin structures that arise from the cell body, often extending for hundreds of
micrometers ; branching multiple times, giving rise to a complex ( dendritic
tree )
- Receiving or input portion of a neuron.
Axon
- Propagates nerve impulses toward another neuron, muscle fiber or gland cell
- Special cellular extension that arises from the cell body at a site called the
axon hillock, and travels for a distance , as far as 1m in humans or even more
in other species.
Cell body ( soma or perikaryon )
- Nucleus surrounded by cytoplasm that includes typical organelles.
- Gives rise to multiple dendrites , but never to more than one axon, although
the axon may branch hundreds of times before it terminates.
- At the majority of synapses, signals are sent from the axons of one neuron to
a dendrite of another.
- Most protein sysnthesis occurs exceptions to theses rules:
1. Neurons that lack dendrites
2. Neurons that have axon
3. Synapses that connect an axon to another axon or a dendrite to
another dendrite.
*insert axon diagram
NOTE: All neurons are electrically excitable, maintaining voltage gradients across
their membranes by means of metabolically driven ion pumps, which combine with
ion channels embedded in the membrane to generate intracellular versus
extracellular concentration differences of ions such as sodium, potassium, chloride
and calcium.

Axon Hillock- part of the neuron that has the greatest density of voltage
dependent sodium channels.
Axon Terminal- contains synapses, specialized structures where neurotransmitter
chemicals are released to communicate with target neurons.
Nerve fibers- general term for any neuronal process
Nerve- a bundle of many nerve fibers that course along the same path in the PNS
Ganglia- nerve cell bodies clustered together in the PNS.
Tract- a bundle of nerve fibers, without connective tissue elements in the CNS.

Structural Classification:
Polarity- most neurons can be anatomically characterized as:
Unipolar or pseudounipolar : dendrite and axon emerging from the same
process.
Bipolar: axon and single dendrite on opposite ends of the soma
Multipolar: more than two dendrites
o Golgi I: neurons with long projecting axonal processes, ex: pyramidal cells,
purkinje cells and anterior horn cells.
o Golgi II: neurons whose axonal process projects locally; ex: granule cell
Different kinds of neurons according to location in the nervous system and
distinct shape :

Purkinje cells- huge neurons in the cerebellum, a type of golgi 1 multipolar

neuron
Pyramidal cells- neurons with triangular soma, type golgi I
Basket cells- interneurons that form a dense plexus of terminal around to their
location in the nervous system and distinct shape.
Betz cells- large motor neurons
Medium spiny neurons- most neurons in the corpus striatum
Granule cells- type of golgi II neuron
Anterior horn cells- motorneurons located in the spinal cord
Renshaw cells- neurons with both ends linked to alpha motor neurons.

Functional Classification
Direction
o Afferent neurons convey information from tissues and organs into the CNS
and are called sensory neurons.
o Efferent neurons transmits signals from the CNS to the effector cells and are
called motor neurons.
o Interneurons connect neurons within specific regions of the CNS
Action on other neurons- a neuron affects other neuron by releasing a
neurotransmitter that binds to chemical receptors.
o Receptors can be excitatory ( causing an increase in firing rate ). Inhibitory
( causing a decrease in firing rate ), or modulatory ( causing long lasting
effects not directly related to firing rate)
o Two most common neurotransmitter in the brain: glutamate and GABA
REFLEX ARC
The pathway consisting of a sensory receptor, a sensory neuron, interneurons, a
motor neuron and an effector (muscle).

BRAIN
Adult brain is made up of about 100 billion neurons and 1000 billions neuroglia.
One of the largest organs of the body, averaging 1.3kg (3lbs)
CEREBRUM
o Gray matter: outer covering / external part of the brain containing nerve cells.
LAYERS:
I.
Molecules
II.
Outer Granular
III.
Outer Pyramidal
IV.
Inner Granular
V.
Inner Pyramidal
VI.
Multiform
Afferent fibers terminate in Layers II, III, and IV
Efferent fibers originate in layer V, where Betz cells (origin of corticospinal
fibers) are found
o

Outer layer of neurons (1mm thick)

Functional part contains about 100 billion neurons
Perception: hearing, visual, olfaction, muscle, and viscera
Reasoning, information integration
The cortex has 3 different types of cells:
Granular (stellate)- have short axons, transmit neurosignals only short
distance within the cortex
Fusiform and pyramidal cells- long, large nerve fibers that go all the way to
the spinal cord
White matter: internal part; consists of myelinated and unmyelinated axons

PROTECTION AND COVERING

o Brain is protected by the cranial bones and cranial meninges
Cranial meninges surround the brain
o Dura mater (pachymenix)
Avascular
2 layers: endosteal layer and meningeal layer
Folds
Falx cerebri- sickle shape fold of dura mater that lies in the
midline between the two cerebral hemisphere
Tentorium cerebelli- divides occipital lobes; roof of
cerebellum; crescent shape over the roof of the posterior cranial
fossa; separates cerebrum from cerebellum
Falx cerebella- divides 2 cerebelli
Diaphragmasellae- small circular/ fold; roof of sella turcic
o Arachnoid Mater
Thin delicate impermeable membrane between dura and pia mater.
Avascular
o Pia Mater
Adherent with the brain
Vascular
NOTE: Arachnoid Mater + Pia Mater = Leptomeninges
Superficial to Deep
Meningeal Artery
Epidural Space

Dura Mater
Superior Cerebral Veins
Arachnoid Mater
Subarachnoid Space ( contains CSF )
Subarachnoid Villi ( directs CSF )
Subarachnoid Granulations ( absorbs CSF )
Cerebrospinal Fluid (CSF)
Fluid that continuously circulates through the subarachnoid space around the brain
and the spinal cord.
The entire CNS contains between 80-150 ml (3-5 oz) of CSF
Pressure: 10 mmHg
Rate of production: 500 ml/day
Clear, colorless liquid that contains glucose, proteins, lactic acid, urea, cations (Na,
K, Ca, Mg) and anions (Cl, HCO3), and some WBC.
-

Main Functions that contributes to homeostasis:

Mechanical protection
Shock absorbing medium
Buoys the brain so that it floats in the cranial cavity.
Chemical protection
Produces optimal chemical environment for accurate neuronal
signaling.
Circulation
Medium for exchange of nutrients and waste products between the
blood and nervous tissue.

Note: Choroid Plexus- networks of capillaries in the walls of ventricles; mainly functions for
the production
CSF FLOW
Lateral Ventricles (1st and 2nd ventricles) (+) Choroid Plexus : located in Telencephalon
Interventricular foramina/ Foramen of Monroe/ (-) Choroid Plexus
Third Ventricle: located in Diencephalon
Cerebrala aqueduct (Aqueduct of Sylvius )/(-) Choroid Plexus: located in Mesencephalon
Fourth Ventricle( Midbrain )/ (+) Choroid Plexus: located in Rhombencephalon
Subarachnoid Space
Median Aperture of Magendie (1)
Lateral Aperture of Luschka (2)
Central canal of the spinal cord
Subarachnoid space around the
surface of the brain
Arachnoid Villi (CSF is gradually reabsorbed back into the blood)
Bloodstream
*Arachnoid Granulation/Pacchionis(where CSF is drained)
BLOOD BRAIN BARRIER
Glucose, oxygen, carbon dioxide, water and most lipid-soluble
substances , such as alcohol, caffeine, nicotine, heroin, and most
anesthetics -> pass rapidly from the circulation blood into brain cells.
Creatinine, urea and most ions such as Na, K, and Cl enter quite slowly
Protein, and most antibiotic drugs do not pass from blood into brain
cells.
*INSERT BRODMANNS AREA DIAGRAM
CEREBRUM
The Cerebrum

Superficial layer is gray matter CORTEX

Cortex is only 2-4 mm thick that contains billions of neurons
Seat of intelligence and provides us the ability to read, write, speak, make
calculations, and compose music, remember the past, plan of the future, and create
works that have never existed before.
MAJOR CEREBRAL LOBES

a. Cerebral Cortex
responsible for all conscious behavior by containing 3 kinds of
functional areas, which includes motor, sensory, and association
areas:
i.
Motor areas are located in the frontal cortex
ii.
Sensory areas are concerned with conscious awareness
of sensations and are located in the parietal, occipital,
and temporal cortex
iii.
Association areas include areas that are involved in
many traits like analyzing, interpreting sensory
experiences, memory, reasoning, verbalizing, judgment
and emotions
b. Hemisphere Dominance (Brain Lateralization)
Most basic functions (sensory & motor) are equally controlled by
both left & right hemisphere
communicating exits through corpus callosum
Gyrus
Aka convolutions/ folds/ bumps
Precentral Gyrus major gyrus, located immediately anterior to the central sulcus
Postcentral Gyrus major gyrus, located immediately posterior to the central
sulcus
Fissures
Deepest grooves between folds
Ex.
Median Longitudinal Fissure separates cerebral hemispheres
Transverse Fissure separates cerebrum from cerebellum
Sulcus
Shallower grooves between folds
Ex.
Central Sulcus of Rolando separates frontal lobe from parietal lobe;
separates precentral and postcental gyrus; landmark for motor and sensory
area.

Lateral cerebral sulcus/ Sylvian Sulcus separate the frontal lobe from
the temporal lobe.
Parieto-occipital sulcus separates parietal and temporal lobe from
occipital lobe.
Calcarine Sulcus media surface of the hemispheres; joined at an acute
angle by the parieto-occipital sulcus about halfway along the length.
Cingulate Sulcus separates the superior frontal gyrus and cingulated
gyrus.

Insula
Cannot be seen from the exterior surface of the brain; it lies deep within the lateral
cerebral fissure, deep to the parietal, frontal and temporal lobes.

White Matter; internal part; consists of myelinated and unmyelinated axons

extending in 3 principal directions.

Association Fibers transmit nerve impulses between gyri in the

same hemisphere.
Commissural Fibers transmit impulses from gyri in one cerebral
hemisphere to the corresponding gyri in the opposite cerebral
hemisphere.
Corpus Callosum connects right and left hemisphere to allow
for communication between the hemispheres. Forms roof of the
lateral and 3rd Ventricle.
Anterior Commissure
Posterior Commissure
Projection Fibers from descending and ascending tracts that
transmit impulses from the cerebrum and other parts of the brain to
the spinal cord or spinal cord to the brain.

Cortical Lobes
Anatomically
Frontal: Motor
Parietal: Sensory
Temporal: Memory and emotion; comprehending sounds
Occipital: Vision. Memories
Physiologically
Insular: Speech/ Planning/ Coordination; Island of Reil
Limbic: Emotion/ Memory
Concept of DOMINANT Hemisphere
In about 95% of all people, the left hemisphere in the dominant one
Theories:
At birth, the left posterior temporal lobe is slightly larger than the right the
left side normally begins to be used to a greater extent, therefore, learning is
gained much faster on the left side.
RIGHT Hemisphere VS LEFT Hemisphere

RIGHT
LEFT
Non-dominant
Dominant
Holistic Functioning:
Sequential Analysis:
Processing multi-sensory input
Systemic, logical interpretation of
simultaneously
to
provide
information.

Holistic
picture
of
ones
environment.
Holistic Functioning such as:
Dancing
Gymnastics
Singing
Arts
Visual Spatial Skills
Memory is stored in auditory, visual and
spatial modalities

Interpretation
and
production
symbolic information:
Language
Mathematics
Abstraction
Reasoning
Memory stored in language format

of

BRODMANNS AREA
Cytoarchitecture and organization of cells

The

cortex has been

divided
by
Korbinian
Brodmann
into
47
distinct

regions,
each
having a number.
BA

in the

Frontal Lobe

Area
4:
Primary
Motor Area

C
orrespon
ds
to
the
precentral gyrus

Contains large neurons (pyramidal cells)

Controls voluntary contractions of specific muscles
o Immediate paresis of contralateral musculature, hypotonia followed by spasticity
and (+) Babinski sign.
Area 6: Premotor Cortex
AKA motor association area
Immediately anterior to the primary cortex
Learned/ Past experience
Planning Movements
o Complex defects of movements in the absence of weakness
Area 8: Frontal Eyefield
For conjugate eye movements
Controls voluntary eye movements; voluntary scanning movements

o Defective scanning of opposite side

Area 9, 10, 11 and 12: Prefrontal Cortex
For judgment, insight, appropriate social behavior and emotional affect
o Disturbance in behavior, poor judgment, no insight, schizophrenia; Phineas Gage
Syndrome
Area 44, 45: Brocas Area
Primary motor area for speech
Muscles of tongue, lips and throat
Translation of speech or written words into thoughts
Speech production
Usually the left frontal lobe, just superior to the lateral cerebral sulcus
o Brocas Aphasia/ Motor Aphasia/ Anterior Expressive Aphasia/Non-Fluent Aphasia
o Capable of deciding what he wants but cannot make vocal system

BA in the Parietal Lobe

Area 3,1,2: Primary Sensory/ Somestheti Area

Post-Central gyrus
Receive information from sensory signals from the skin and proprioceptors
which monitors joint position from contralateral side of the body
o Impaired 2-point discrimination, touch, position sense and stereognosis.
Area 5, 7, 39, 40: Gnostic Area
Gnosis is the process of comprehension or knowing
Knowing area
Intelligence
Area 5, 7: Somatosensory Association
Just posterior to the primary sensory area
Receives input from the thalamus, other lower portions of the brain,
and primary sensory area
Integrates and interprets sensations
o Asteorognosis: Inability to identify an object by active touch.
Area 39: Angular Gyrus
Interpretation of visual information
Most inferior portion of the posterior parietal lobe; lies immediately
behind the Wernickes area.
o Angular Gyrus Syndrome: AKA Gertsmanns Syndrome.
o Combined acalculia, agraphia, finger agnosis, R-L disorientation, anomic
aphasia.
o Alexia, dyslexia, or word blindness
Area 40: Temporal Gyrus/ Supramarginal Gyrus
Ideomotor Apraxia
Area 43: Primary Gustatory Area
At the base of the post-central gyrus above the lateral cerebral sulcus in the
parietal cortex
For taste
BA in the Temporal Lobe
Area 41, 42: Auditory Area
Located on the superior part of the temporal lobe near the lateral cerebral
sulcus
Interprets sound, pitch, and rhythm
AKA Heschls Gyrus
Complete cortical deafness
Area 21, 22: Wernickes Area

Located inferior and posterior to the primary auditory area

Determines if a sound is speech, music, or noise
Language comprehension
Oral/ Written Words
AKA Sensory, posterior, receptive or fluent aphasia
Can understand either spoken word o written word but are unable to interpret
the thought
Area 28: Primary Olfactory Area
Located in the temporal lobe on the medial aspect
For smell

BA in Occipital Area

Area 17: Primary Visual Area

Striate cortex
AKA Calcarine Area
Located on the medial surface of the occipital lobe
o Visual Agnosia
Area 18, 19: Visual Association Area
Receives sensory impulses from the primary visual area and thalamus
Relates present to past visual experiences

DIENCEPHALON
- Paired structures between the brainstem and the cerebral hemispheres
- Continuous with the rostral part of midbrain
- Almost entirely surrounded by cerebral hemispheres
- These structures form the walls of the 3rd ventricle:
1. The roof of the 3rd ventricle: epithalamus which includes a single pineal gland in
the midline, paired right and left habenular nuclei, and choroid plexus of 3 rd
ventricle
2. Superior part of the lateral walls of the 3rd ventricle: two lobes of thalamus
3. Inferior part of lateral walls and floor of 3rd ventricle: paired right and left
subthalamus and hypothalamus
Superior to Inferior: (Paired Structures)
o Epithalamus
o Thalamus
o Subthalamus
o Hypothalamus
A. EPITHALAMUS
- Above the thalamus
- Contains pineal gland, which secretes melatonin (involved in sleep/wake cycle and
mood), habenular nuclei, and choroid plexus of 3 rd ventricle.
Pineal Gland
- About a size of a lentil or small pea and protrudes from dorsal midline of 3 rd
ventricle
- Secretes melatonin: liberated during darkness and it promotes sleepiness,
contributes to setting the timing of the bodys biological clock, which is controlled
from suprachiasmatic nucleus of hypothalamus

Habenula
- Habenular nucleus is involved in olfaction, especially emotional responses to smell
- Habenular nuclei receive input from several limbic structures (including the ventral
forebrain and septal nuclei) via the stria medullaris thalami.
B. THALAMUS
- 80% of diencephalon
- Measures about 3 cm (1.2 in)
- Consists of paired oval masses of gray matter organized into nuclei with
interspersed tracts of white matter
- Main sensory relay station where all sensory signals can be edited, sorted, and
routed except smell
- Receives afferent signal from cerevral cortex, basal ganglia, and cerebellum
- Profound input on motor (via Basal Ganglia and Cerebellum) and cognitive function
- Interthalamic Adhesion Mass Intermedia (intermediate mass): bridge of gray
matter that crosses the 3rd ventricle to join the right and left portions of thalamus
Areas of the thalamus
- Anterior Thalamic Nuclei found in the floor of the lateral ventricle, for emotional
tone; recent memory
- Ventral Anterior (VA) voluntary motoractivity; basal ganglia
- Ventral Lateral (VL) voluntary motor activity of motor cortex and cerebellum
- Ventral Posterior (VP) taste and somatic sensations (touch, pressure, vibration,
heat, cold, and pain)
- Ventral Posteriolateral (VPL) body sensation; important in spinothalamic tract
(somatosensory)
- Ventral Posteriomedial (VPM) sensations to consciousness, face, taste
sensation, CN 5,7,9; important in spinothalamic tract (somatosensory)
- Intralaminar Nuclei levels of consciousness and alertness
- Medial Geniculate hearing; CN VIII; previously considered as Metathalamus
- Lateral Geniculate vision; CN II; previously considered as Metathalamus
- Medial Dorsal olfactory and visceral and somatic sensation
- Pulvinar extends beyond the third ventricle and overhangs the superior colliculus
(Superior colliculus is a small elevation found on each side on the posterior aspect
of midbrain). Thus, pulvinar lies just above and lateral to superior colliculus.
*Thalamic
Lesions
- Cerebrovascular lesions of tumors of thalamus lead to: loss of sensation in
contralateral side of face and body followed by distressing discomfort and burning and
diffuse pain in anaesthetic areas (Thalamic pain)
*Thalamic
Syndrome
- Abnormal voluntary movements (chorea or hemiballismus with hemisensory
disturbance)
*Thalamic
Hand
- The contralateral hand is held in an abnormal posture in some patients
C. SUBTHALAMUS
- Communicates with BG to help motor control
- Contains the subthalamic nuclei and portions of the red nucleus and substantia
nigra
- Parts:
o Zona Incerta
o Forels Tegmentum Field
o Subthalamic Nucleus of Luy works with extrapyramidal tracts
*Subthalamic lesions

Should be regarded as one of the extrapyramidal motor nuclei and has a large
connection with globus pallidus
Lesion result in sudden forceful involuntary movements in a contralateral extremity,
movement may be jerky (Choreiform) or violent (Ballistic)

D. HYPOTHALAMUS
- Divided into a dozen or so nuclei in four major regions
1. Mammillary region/ bodies
o Adjacent to the midbrain
o Most posterior portion of hypothalamus
o Two, small, rounded projections that serve as relay stations in reflex
related to sense of smell
2. Tuberal Region
o Middle and wildest portion of hypothalamus
o Includes dorsomedial, ventromedial, and arcuate nuclei
o Tuber cinerium: on ventral surface; an elevated mass of gray matter
o Infundibulum: stalklike, attaches the pituitary gland to the hypothalamus
o Median Eminence of tuber cinerium: slightly raised region that encircles
the site where infundibulum becomes the stalk of the pituitary gland
3. Supraoptic Region
o Lies superior to the optic chiasm and contains paraventricular nucleus,
supraoptic nucleus, anterior hypothalamic nucleus, and suprachiasmatic
nucleus
4. Preoptic Region
o Anterior to the Supraoptic region
o Contains preoptic periventricular nucleus, medial preoptic nucleus, and
lateral preoptic nucleus
Functions:
- Autonomic regulatory center
o Anterior: Parasympathetic
o Posterior: Sympathetic
Intercourse
- Influences HR, BP, RR
- Emotional response
- Involved in fear, loathing, pleasure
- Drive center: sex
o Pineal gland: melatonin (activated in dark): gonadotrophic hormone
- Regulation of body temp.
o Posterior: production of heat
o Anterior: reduction of heat
- Food Intake
o Anteromedial: satiety (10 minutes)
o Lateral: hunger center; thirst center
- Water balance and thirst
- Sleep-wake cycle/ Circadian rhythm: suprachiasmatic
- Hormonal control
- Release hormones that influence hormonal secretion from the anterior pituitary
gland
- Paraventricular nuclei: vasopression (anti-diuretic)
- Preoptic nuclei: Oxytocin (contraction)
involved in emotional response: Limbic System
controls emotional experience and expression

can modify the way a person acts

produces a feeling of fear, anger, pleasure, and sorrow, etc.

THE LIMBIC SYSTEM

*Lesion of Hypothalamus
- Hormonal imbalances
- Malignant hypothermis
- Anorexia nervosa
- Inability to control hip
- Diabetes insipidus: inc urinatioin, inc fluid intake, diluted urine, polyurea
- Inappropriate ADH: inc vasopressin
- Diencephalic dysfunction: neurogenic storms; russel syndrome
BASAL GANGLIA
Aka basal nuclei
Have many connections with other parts of the brain. Thru these connections, they
help to program habitual or automatic movement sequences and set an appropriate
level of mucle tone.
Selectively inhibit other motor neuron circuits that are intrinsically active or
excitatory.
The forebrain structure include the caudate nucleus, the putamen, the nucleus
accumbens (or ventral stratum) and the globus pallidus.
Globus pallidus
Concerned with the regulation of muscle tone required for specific body movements
Divided into two segments: the internal (or medial) segment and the external (or
lateral) segment.
Caudate nucleus :
C-shape structure that is closely associated with the lateral wall of the lateral
ventricle.
Largest at its anterior pole (the head), and its size diminishes posteriorly as it
follows the course of the laterl ventricle (the body) all the way to the temporal lobe
(the tail) where it terminates at the amygdaloid nuclei.
Putamen
Large structure that is separated from the caudate nucleus by the anterior limb of
the internal capsule
Connected to the caudate head by bridges of cells that cut across the internal
capsule.
*caudate nucleus and putamen: controls large automatic movements of skeletal
muscles.
Nucleus accumbens
Often called the ventral stratum.

It receives signal from the prefrontal cortex (via the ventral tegmental area) and
sends other signal back there via the globus palilidus.

Corpus stratum (largest nucleus in BG): caudate nucleus + lenticular nucleus

Lenticular nucleus: putamen(lateral portion) + globus pallidus (medial portion)
Neostriatum: cauate nucleus + putamen
Other structure that are functionally linked to and sometimes considered part of
BG:
Substancia nigra("black substance"): axons from the substancia nigra
terminate in the caudate nucleus and putamen)
o The substantia nigra is a mesencephalic gray matter portion of the basal
ganglia that is divided into:
SNr (reticulata)
SNr often works in unison with GPi and the SNr-GPi complex
inhibits the thalamus.
Neurotransmitter: GABA
Its main known function is controlling eye movements.
SNc (compacta)
Substantia nigra pars compacta (SNc) however, produces the
neurotransmitter dopamine, which is very significant in
maintaining balance in the striatal pathway.
Red nuclei of the midbrain
Subthalamic nuclei of the diencephalon (connect with globus
pallidus)
o The subthalamic nucleus (STN) is a diencephalic gray
matter portion of the basal ganglia, and the only position
of
the
ganglia
that
produces
an
excitatory
neurotransmitter, glutamate.
The role of the subthalamic nucleus is to stimulate the SNr-GPi
complex and it is part of the indirect pathway. The subthalamic
nucleus receives inhibitory inpit from the external part of the
globus pallidus and sends excitatory input to the GPi.
The largest component, the striatum, receives input from many brain areas beyond
the basal ganglia, but only sends output to other components of the basal ganglia.
The pallidum receives input from the striatum, and sends inhibitory output to a
number of motor related areas.
The substantia nigra is the source of the striatal input of the neurotransmitter
dopamine, which plays an important role in basal ganglia function.
The subthalamic nucleus receives input mainly from the striatum and cerebral
cortex, and projects to the globus pallidus.
Two pathways process signals in the basal ganglia:
Direct pathway
Excitation of the direct pathway has the net effect of exciting thalamic
neurons (which in turn make excitatory connections onto cortical
neurons)/
Selectively facilitates certain motor (or cognitive) programs in the
cerebral cortex that are adaptive for the present task
1. The direct pathway starts with cells in the striatum that make inhibitory
connections with cells in the GPint.
2. The GPint cells in turn make inhibitory connections on cells in the thalamus.
Thus, the firing of GPint neurons inhibits the thalamus
3. Making the thalamus less likely to excite the neocortex.

4. When the direct pathway striatal neurons fire, however, they inhibit the
activity of the GPint neurons.
5. This inhibition releases the thalamic neurons from inhibition (I.e., it disinhibits
the thalamic neurons), allowing them to fire to excite the cortex.
6. Thus, because of the "double negative" in the pathway between the sriatum
and GPint and the GPint and thalamus, the pathway between the striatum
and net result of exciting the direct pathway striata neurons is to excite motor
cortex.
Cortex(stimulates) striatum (inhibits)"SNr-GPI"complex (less inhibition of thalamus)
thalamus (stimulates))cortex(stimulates) muscles, etc. (hyperkinetic state)

1.
2.
3.

4.
5.
6.
7.
8.
9.

Indirect pathway
Excitation of the pathway has the net effect of inhibiting thalamic
neurons (rendering them unable to excite motor cortex neurons).
Simultaneously inhibits the execution of competing motor programs.
The indirect pathway starts with a different set of cells in the striatum/
These neurons make inhibitory connections to the external segment of the
globus pallidus (GPext)
The GPext neurons make inhibitory connections to cells in the subthalamic
nucleus, which in turn make excitatory connections to cells in the
subthalamic nucleus, which in turn make excitatory connections to cells in
the GPint. (remember that the subthalamic- GPint pathway is the only purely
excitatory pathway within the intrinsic basal ganglia circuitry.)
The GPint neurons make inhibitory connections on the thalamic neurons.
When the GPint neurons make inhibitory connections on the thalamic
neurons.
When the subthalamic neurons are firing, they increase the firing rate of
GPint neurons, thus inccreasing the net inhibition on cortex.
Firing the GPet neurons inhibits the subthalamic neurons, thus making the
GPint neurons less active and disinhibiting the thalamus.
However, when the indirect pathway striatal neurons are active, they inhibit
the GPext neurons, thus dishibiting the subthalamic neurons.
With the subthalamic neurons free to fire, the GPint neurons inhibit the
thalamus, thereby producing a net inhibition on the motor cortex.

Cortex(stimulates) striatum (inhibits)GPe (less inhibition of STNSTN (stimulates)

"SNr-GPI" Complex(inhibits)thalamus (is stimulating less) cortex(Is stimulating less)
muscles, etc. (hyporkinetic state)
Thus , as a result of the complex sequences of excitation, ionhibition, and
disinhibition, the net effect of the cortex exciting the direct pathway is to further excite the
cortex (positive feedback loop), whereas the net effect of cortex exciting the indirect
pathway is to inhibit the cortex negative feedback loop).
Presumably, the function of the basal ganglia is related to a proper balance between
these two pathways. Motor cortex neurons have to excite the proper direct pathway
neurons to further increase their own firing, and they have to excite the proper indirect
pathways neurons that will inhibit other motor cortex neurons that are not adaptive for the
task at hand.
The nigrostriatal projection:
An important pathway in the modulation of the direct and indirect pathways is
dopaminergic, nigrostriatal projection from the substantia nigra pars compacta to
stratum.
Direct pathway striatal neurons have D1 dopamine receptors, which depolarize
cell in response to dopamine. In contrast, indirect pathway striatal neurons have
dopamine receptors, which hyperpolarize the cell in response to dopamine .

the
the
the
D2

The nigrostriatal pathway thus has the dual effect of exciting the direct pathway
while simultaneously inhibiting the indirect pathway. Because of this dual effect, excitation
of the nigrostriatal pathway has the net excitatory effect on the cortex) and inhibiting the
indirect pathway (thereby disinhibiting the net inhibitory effect of the indirect pathway on
the cortex).
The loss of these dopamine neurons in parkinson's disease causes the poverty of
movement that characterizes this disease of cortex, as the balance between direct
pathway excitation of cortex and indirect pathway inhibition of cortex is tipped in favor of
the indirect pathway with a subsequent pathological global inhibition of motor cortex
areas.
o

Affectation to subcortical nuclei for normal function and behavior is

emphasized by the numerous and diverse neurological conditions
associated with basal ganglia dysfunction, which include:
Tourette syndrome
Hemiballismus
Obsessive- compulsive disorder; dystonia
Psychostimulant addiction
Parkinson's disease (substantia nigra pars compacta)
Huntington's diseas(striatum)

Internal capsule
White matter structure situated in the inferomedial part of each cerebral
hemisphere of brain
Carries information past the basal ganglia, separating the caudate nucleus and the
thalamus from the putamen and the globus pallidus
Contains both ascending and descending axons
Contains to and coming from the cerebral cortex
The corticospinal tract constitutes a large part of the internal capsule, carrying
motor information from the primary motor cortex to the lower motor neurons in the spinal
cord.
The internal capsule is V-shaped when cut horizontally, in a transverse plane.
When cut horizontally:
The bend in the V is called the genu
The anterior limb or crus anterious is the part behind the genu, between the
thalamus and lenticular nucleus
The posterior limb or crus posterius is the part behind the genu, between the
thalamus and lenticular nucleus
The retrolenticular portion is caudal to the lenticular nucleus and carries the optic
radiation also known as the geniculocalcarine tract
The sublenticular portion is beneath the lenticular nucleus and are tracts involved in
the auditory pathway from the medial geniculate nucleus to the primary auditory
cortex (brodmann areas 41 and 42).
GENU
The genu of internal capsule is the flexure of the internal capsule
The fibers in the region of the genu are named the geniculate fibers; they originate in the
motor part of the cerebral cortex, and after passing downward through the base of the
cerebral peduncle with the cerebrospinal fibers, undergo decussation and end in the motor
nuclei of the cranial nerves of the opposite side.
It is formed by fibers from the corticonuclear tracts.
Anterior limb
The anterior limb of internal capsule (or fromtal part) contains:

(1) fibers running from the thalamus to the frontal lobe:

(2) fibers connecting the lentiform and caudate nuclei;
(3) fibers connecting the cortex with the corpus nuclei:
(4) fibers passing from the frontal lobe through the medial fifth of the base of the
cerebral peduncle to the nuclei pontis.

Posterior limb
The posterior limb of internal capsule (or occipital part) is the portion of the internal
capsule posterior the genu.
The anterior two-thirds of the occipital part of the internal capsule contains fibers of the
corticospinal tract, which arise in the motor area of the cerebral cortex and, passing
downward through the middle three-fifths of the base of the cerebral peduncle, are
continued into the pyramids of the medulla oblongata.
The posterior third of the occipital part contains:

(1) sensory fibers, largely derived from the thalamus, through some may be
continues upward from the medial lemniscus;
(2) the fibers of optic radiation, from the lower visual centers to the cortex of the
occipital lobe.
(3) acoustic fibers, from the lateral lemniscus to the temporal lobe; and
(4) fibers which pass from the occipital and temporal lobes to the nuclei pontis.
Blood supply
The superior parts of both the anterior and posterior limbs and the genu of the
internal capsule are supplied by the lenticulostriate arteries, which are branches of the M1
segment of the middle cerebral artery.
The inferior half of the anterior limb is supplied via the recurrent artery of heubner,
which is a branch of the anterior cerebral artery.
The inferior half of the posterior limb is supplied by the anterior choroidal artery,
which is a branch of the internal carotid artery.
Anterior limb: lenticulostriate branches of middle cerebral artery (superior half) and
recurrent artery of heubner off of the anterior cerebral artery (inferior half)
Genu: lenticulostriate branches of middle cerebral artery
Posterior limb: lenticulostriate branches of middle cerebral artery (superior half) and
anterior choroidal artery branch of the internal carotid artery (inferior half)
Limbic system
Encircling the brainstem is a ring of structures on the inner border of the cerebrum
and floor of the diencephalon
Governs emotional aspects of behavior
Hippocampus together with portions of the cerebrum also functions in memory
1. The limbic lobe consists of the parahippocampal cingulated gyri, both gyri of the
cerebral hemispheres, and hippocampus, a portion of the parahippocampal gyrus
that extends into the floor of the lateral ventricle.
2. The dentate gyrus is between the hippocampus and parahippocampla gyrus.
3. The amygdaloid body is several groups of neurons located at the tail end of the
caudate nucleus.
4. The septal nuclei are within the septal area, are formed by the region under the
corpus callosum and cerebral gyrus.
5. The mammillary nucleus of the hypothalamus are two round masses close to the
midline near the cerebral peduncles
6. The anterior nucleus f the thalamus is located in the floor of the lateral ventricle
7. The olfactory bulbs are flattened bodies of the olfactory pathway that rest on the
cribriform plate

8. Bundles of interconnecting myelinated axons link various components of limbic

system. They include the fornix, stria medullaris, medial forebrain bundle, and
mammilothalamic
tract.
CEREBELLUM
The cerebellum (little brain) is a structure that is located at the back of the brain,
underlying the occipital and temporal lobes of the cerebral cortex. Although the
cerebellum accounts for approximately 10% of the brains volume, it contains over 50% of
the total number of neurons in the brain. Historically the cerebellum has been considered
a motor structure, because cerebellar damage leads to impairments in motor control and
posture and because the majority of the cerebellums outputs are to parts of the motor
system. Motor commands of the descending pathways to make movements more adaptive
and accurate. The cerebellum is involved in the following functions:

Maintenance of balance and posture. The cerebellum is important for making

postural adjustments in order to maintain balance. Through its input from vestibular
receptors and proprioceptors, it modulates commands to motor neurons to compensate for
shifts in body position or changes in load upon muscles. Patients with cerebellar damage
suffer from balance disorders, and they often develop stereotyped postural strategies to
compensate for this problem (e.g., a wide-based stance).

Coordination of voluntary movements. Most movements are composed of a number

of different muscle groups acting together in a temporally coordinated fashion. One major
function of the cerebellum is to coordinate the timing and force of these different muscle
groups to produce fluid limb or body movements.

Motor learning. The cerebellum is important for motor learning. The cerebellum
plays a major role in adapting and fine-tuning motor programs to make accurate
movements through a trial-and-error process (e.g., learning to hit a baseball).

Cognitive functions. Although the cerebellum is most understood in terms of its

contributions to motor control, it is also involved in certain cognitive functions, such as
language. Thus, like the basal ganglia, the cerebellum is historically considered as part of
the motor system, but its functions extend beyond motor control in ways that are not yet
well understood.

Cerebellar Gross Anatomy

The cerebellum consists of two major parts.The cerebellar deep nuclei (or cerebellar
nuclei) are the sole output structures of the cerebellum. These nuclei are encased by a
highly convoluted sheet of tissue called the cerebellar cortex, which contains almost all of
the neurons in the cerebellum. A cross-section through the cerebellum reveals the intricate
pattern of folds and fissures that characterize the cerebellar cortex. Like the cerebral
cortex, cerebellar gyri are reproducible across individuals and have been identified and
named.
Divisions of the cerebellum: two major fissures running mediolaterally divide the cerebellar
cortex into three primary subdivisions:

Posterolateral fissure separates the flocculonodular lobe from the corpus

cerebella
Primary fissure separates the corpus cerebelli into a posterior lobe and
an anterior lobe.

The cerebellum is also divided sagittally into three zones that run from medial to lateral:

Vermis (from the Latin word for worm) is located along the midsagittal plane of the
cerebellum. Directly lateral to the vermis is the intermediate zone. Finally,
the lateral hemispheres are located lateral to the intermediate zone (there are no
clear morphological borders between the intermediate zone and the lateral
hemisphere that are visible from a gross specimen).

Cerebellar nuclei. All outputs from the cerebellum originate from the cerebellar deep
nuclei. Thus, a lesion to the cerebellar nuclei has the same effect as a complete lesion of
the entire cerebellum. It is important to know the inputs, outputs, and anatomical
relationships between the different cerebellar nuclei and the subdivisions of the
cerebellum.
1. The fastigial nucleus is the most medially located of the cerebellar nuclei. It receives
input from the vermis and from cerebellar afferents that carry vestibular, proximal
somatosensory, auditory, and visual information. It projects to the vestibular nuclei
and the reticular formation.
2. The interposed nuclei comprise the emboliform nucleus and the globose nucleus.
They are situated lateral to the fastigial nucleus. They receive input from the
intermediate zone and from cerebellar afferents that carry spinal, proximal
somatosensory, auditory, and visual information. They project to the
contralateral red nucleus (the origin of the rubrospinal tract).
3. The dentate nucleus is the largest of the cerebellar nuclei, located lateral to the
interposed nuclei. It receives input from the lateral hemisphere and from cerebellar
afferents that carry information from the cerebral cortex (via the pontine nuclei). It
projects to the contralateralred nucleus and the ventrolateral (VL) thalamic
nucleus.
4. The vestibular nuclei are located outside the cerebellum, in the medulla. Hence,
they are not strictly cerebellar nuclei, but they are considered to be functionally
equivalent to the cerebellar nuclei because their connectivity patterns are identical
to the cerebellar nuclei. The vestibular nuclei receive input from the flocculonodular
lobe and from the vestibular labyrinth. They project to various motor nuclei and
originate the vestibulospinal tracts.

It is convenient to remember that the anatomical locations of the cerebellar nuclei

correspond to the cerebellar cortex regions from which they receive input. Thus, the
medially located fastigial nucleus receives input from the medially located vermis; the
slightly lateral interposed nuclei receive input from the slightly lateral intermediate zone;
and the most lateral dentate nucleus receives input from the lateral hemispheres.
Cerebellar peduncles. Three fiber bundles carry the input and output of the cerebellum.
1. The inferior cerebellar peduncle (also called the restiform body) primarily contains
afferent fibers from the medulla, as well as efferents to the vestibular nuclei.
2. The middle cerebellar peduncle (also called the brachium pontis) primarily contains
afferents from the pontine nuclei.
3. The superior cerebellar peduncle (also called the brachium conjunctivum) primarily
contains efferent fibers from the cerebellar nuclei, as well as some afferents from
the spinocerebellar tract.
Thus, the inputs to the cerebellum are conveyed primarily through the inferior and middle
cerebellar peduncles, whereas the outputs are conveyed primarily through the superior
cerebellar peduncle. The inputs arise from the ipsilateral side of the body, and the outputs
also go to the ipsilateral side of the body. Note that this is true even for the outputs to the
contralateral red nucleus. Recall from the chapter on descending motor pathways that
the rubrospinal tract immediately crosses the midline after the fibers leave the red
nucleus. Thus, cerebellar output to the red nucleus affects the ipsilateral side of the body
by a double-crossed pathway. Unlike the cerebral cortex, the cerebellum receives input
from, and controls output to, the ipsilateral side of the body, and damage to the
cerebellum therefore results in deficits to the ipsilateral side of the body.

Functional Subdivisions of the Cerebellum

The anatomical subdivisions described above correspond to three major functional
subdivisions of the cerebellum.

Vestibulocerebellum. The
vestibulocerebellum
comprises
the flocculonodular
lobe and its connections with the lateral vestibular nuclei. Phylogenetically, the
vestibulocerebellum is the oldest part of the cerebellum. As its name implies, it is involved
in vestibular reflexes (such as the vestibuloocular reflex; see below) and in postural
maintenance.

Spinocerebellum. The spinocerebellum comprises the vermis and the intermediate

zones of the cerebellar cortex, as well as thefastigial and interposed nuclei. As its
name implies, it receives major inputs from the spinocerebellar tract. Its output projects to
rubrospinal, vestibulospinal, and reticulospinal tracts. It is involved in the integration of
sensory input with motor commands to produce adaptive motor coordination.

Cerebrocerebellum. The cerebrocerebellum is the largest functional subdivision of the

human cerebellum, comprising the lateralhemispheres and the dentate nuclei. Its
name derives from its extensive connections with the cerebral cortex, via the pontine
nuclei (afferents) and the VL thalamus (efferents). It is involved in the planning and timing
of movements. In addition, the cerebrocerebellum is involved in the cognitive functions of
the cerebellum.
Phylogenetic and functional divisions
The cerebellum can also be divided in three parts based on both phylogenetic criteria (the
evolutionary age of each part) and on functional criteria (the incoming and outgoing
connections each part has and the role played in normal cerebellar function). From the
phylogenetically oldest to the newest, the three parts are:

Functional
denomination
(phylogenetic
denomination)
Vestibulocerebellu
m
(Archicerebellum)

Spinocerebellum
(Paleocerebellum)

Cerebrocerebellu
m

Anatomical
parts
Flocculonod
ular
lobe
(and
immediately
adjacent
vermis)

Role

The vestibulocerebellum regulates balance

and eye movements.
It
receives vestibular
input from both the semicircular canals and
from the vestibular nuclei, and sends fibres
back to the medial and lateral vestibular nuclei.
It also receives visual input from the superior
colliculi and from the visual cortex (the latter
via the pontine nuclei, forming a cortico-pontocerebellar
pathway).
Lesions
of
the
vestibulocerebellum cause disturbances of
balance and gait.
Vermis and The spinocerebellum regulates body and limb
intermediate movements. It receives proprioception input
parts of the from the dorsal columns of thespinal cord
hemispheres (including the spinocerebellar tract) as well as
("paravermis from the trigeminal nerve, as well as from
")
visual and auditory systems. It sends fibres to
deep cerebellar nuclei which in turn project to
both the cerebral cortex and the brain stem,
thus providing modulation of descending motor
systems. The spinocerebellum contains sensory
maps as it receives data on the position of
various body parts in space: in particular, the
vermis receives fibres from the trunk and
proximal
portions
of
limbs,
while
the
intermediate parts of the hemispheres receive
fibres from the distal portions of limbs. The
spinocerebellum
is
able
to
elaborate
proprioceptive input in order to anticipate the
future position of a body part during the course
of a movement, in a "feed forward" manner.
Lateral parts The neocerebellum is involved in planning
of
movement and evaluating sensory information

(Neocerebellum,
Pontocerebellum)

thehemisphe for action. It receives input exclusively from the

res
cerebral cortex (especially the parietal lobe) via
the pontine nuclei (forming cortico-pontocerebellar pathways), and sends fibres mainly
to
the
ventrolateral thalamus
(in
turn
connected to motor areas of the premotor
cortex and primary motor area of the cerebral
cortex) and to the red nucleus (in turn
connected to the inferior olivary nucleus, which
links back to the cerebellar hemispheres). The
neocerebellum
is
involved
in
planning
movement that is about to occur and has
purely cognitive functions as well.

Three arteries supply blood to the cerebellum: the superior cerebellar

artery (SCA), anterior inferior cerebellar artery (AICA), andposterior inferior cerebellar
artery (PICA).
Superior cerebellar artery

The SCA branches off the lateral portion of the basilar artery, just inferior to its
bifurcation into the posterior cerebral artery. Here it wraps posteriorly around the
pons (to which it also supplies blood) before reaching the cerebellum. The SCA
supplies blood to most of the cerebellar cortex, the cerebellar nuclei, and the middle
and superior cerebellar peduncles.

Anterior inferior cerebellar artery

The AICA branches off the lateral portion of the basilar artery, just superior to the
junction of the vertebral arteries. From its origin, it branches along the inferior
portion of the pons at the cerebellopontine angle before reaching the cerebellum.
This artery supplies blood to the anterior portion of the inferior cerebellum, and to
the facial (CN VII) and vestibulocochlear nerves (CN VIII).

Obstruction of the AICA can cause paresis, paralysis, and loss of sensation in the
face; it can also cause hearing impairment. Moreover, it could cause an infarct of
the cerebellopontine angle. This could lead to hyperacusia (dysfunction of the
stapedius muscle, innervated by CN VII) and vertigo (wrong interpretation from the
vestibular semi-circular canal'sendolymph acceleration caused by alteration of CN
VIII).

Posterior inferior cerebellar artery

The PICA branches off the lateral portion of the vertebral arteries just inferior to
their junction with the basilar artery. Before reaching the inferior surface of the
cerebellum, the PICA sends branches into the medulla, supplying blood to
severalcranial nerve nuclei. In the cerebellum, the PICA supplies blood to the
posterior inferior portion of the cerebellum, the inferior cerebellar peduncle,
the nucleus ambiguus, the vagus motor nucleus, the spinal trigeminal nucleus,
the solitary nucleus, and the vestibulocochlear nuclei.

Disorders of the Cerebellum

Like the basal ganglia, the cerebellum has historically been considered part of the
motor system because damage to it produces motor disturbances. Unlike the basal
ganglia, damage to the cerebellum does not result in lack of movement or poverty
of movement. Instead, cerebellar dysfunction is characterized by a lack of
movement coordination. Also unlike basal ganglia (and motor cortex), damage to
the cerebellum causes impairments on the ipsilateral side of the body.

1. Ataxia is a general term used to describe the general impairments in movement

coordination and accuracy that accompany cerebellar damage. There are two major
forms of cerebellar ataxia.
a. Disturbances of posture or gait result from lesions to the vestibulocerebellum.
Patients have difficulty maintaining posture because of the loss of the finecontrol mechanisms programmed by cerebellar circuits that translate
vestibular signals into precise, well-timed muscle contractions to counter
small sways in the body. As a result, patients often develop abnormal gait and
stances to compensate. For example, the feet are often spaced widely apart
when the patient stands still, as this provides a more stable base to maintain
balance. In addition, patients display a staggering gait, with a tendency to fall
toward the side of the lesion. This gait resembles that of a drunken individual;
indeed, alcohol is known to affect the firing of Purkinje cells, which may
explain the loss of coordination that accompanies inebriation.
b. Decomposition of movement results from the loss of the cerebellums ability
to coordinate the activity and timing of many muscle groups to produce
smooth, fluid movements. Instead, cerebellar patient decompose each
movement into its component parts, performing them in serial, rather than all
at once in a coordinated fashion.
2. Dysmetria refers to the inappropriate force and distance that characterizes targetdirected movements of cerebellar patients. For example, in attempting to grab a
cup, they may move their hand outward with too much force or may move it too far,
with the result of knocking over the cup instead of grabbing it.
3. Dysdiadochokinesia refers to the inability of cerebellar patients to perform rapidly
alternating movements, such as rapidly pronating and supinating the hands and
forearms (Figure 6.6). This diagnostic sign results from the lack of the cerebellums
ability to coordinate the timing of muscle groups, alternately contracting and
inhibiting antagonistic muscles, to produce the rhythmic movements.
4. Scanning speech refers to the often staccato nature of speech of cerebellar
patients. The production of speech is a motor act, as muscles of the jaw, tongue,
and larynx need to work in unison to produce words and sounds. Cerebellar patients
have difficulty in coordinating these muscle groups appropriately, and therefore
their speech tends to be slow and disjointed.
5. Hypotonia is another symptom of cerebellar damage. There is a decreased,
pendulous myotatic reflex, as the decreased muscle resistance tends to cause the
limb to swing back and forth after the initial reflex contraction.
6. Intention tremor refers to the increasingly oscillatory trajectory of a cerebellar
patients limb in a target-directed movement (Figure 6.7). For example, the hand
will start out on a straight path toward the target, but as it gets closer, the hand
begins to move back and forth, and the patient must slow down the movement and

very carefully approach the target. Note that this tremor contrasts with the resting
tremor of Parkinsons disease, which disappears when the movement is made.
Intention tremor is absent when the hand is still, but appears toward the end of a
target-directed movement.
7. Nystagmus is an oscillatory movement of the eyes, resulting from damage to the
vestibulocerebellum. Recall that one function of the cerebellum is to fine-tune the
gain of the vestibuloocular response. Damage to the cerebellum can disrupt this
circuitry, resulting in a continuing oscillation of the eyes.
8. Delay in initiating movements. Cerebellar patients take longer to initiate
movements, often because they must actively plan sequences of movements that
are performed effortlessly by normal individuals.
9. In addition to movement disorders, cerebellar patients also demonstrate
subtle cognitive deficits, such as an impaired ability to estimate time intervals.
BRAINSTEM
- Brainstem occupies the posterior
cranial fossa of the skull
- Functions:
Serves as pathway for the
ascending and descending tracts
(Brain and Spinal cord)
Contains important reflex centers
Control of consciousness
Contains crania nerves nuclie
(CN3-CN12)
Parts of Brainstem
1. Medulla Oblongata
o Medulla oblongata is the
lower half of the brainstem,
which is continuous with the
spinal cord, the upper upper
half being the pons
o It is often referred to simply
as the medulla
External appearance
o It is conical shape
o Connects to the pons superiorly and to the spinal cord inferiorly
o The junction between the MO and the spinal cord is at the origin of the 1 st
cervical spinal nerve (at the level of foramen magnum)
o Central canal expands in the upper half of the MO to form the 4 th ventricle
Anterior surface
o On the anterior surface of the medulla is
(continuous with the anterior median fissure of
o On either side of the AMF, there
pyramids(corticobulbar, corticospinal)
Medullary Pyramids contain motor:
Corticobulbar and corticospinal tracts
The corticospinal tracts are on
pyramids

the anterior median fissure

the spinal cord)
swellings called medullary

the anterior surface of the

These tracts transport motor signals that originated in the

precentral gyrus and travelled through the internal capsule to
the medulla oblongata and pyramids
Extrapyramidal tracts are those motor tracts that do not
traverse the medullary pyramids

At the pyramids most caudal end, the corticospinal axons decussate (or
cross over) the midline and continue down the spinal cord on the
contralateral side.
o Fibers that decussated will go down the lateral corticospinal tract while the
fibers that did not decussate will travel down the anterior corticospinal tract
o Nearly 90% of the fibers decussate and travel down the lateral corticospinal
tract while the other 10% travels down the anterior corticospinal tract.
o Postero-lateral to the pyramids are the olives (inferior olivary nuclei leis
beneath them)
o Nerve roots of the hypoglossal nerve (XII) emerges from the groove between
the pyramids and olives)
o Posterior to the olives is the inferior cerebellar peduncle (connects MO to the
Oblangata)
o From the groove between the olives and the inferior cerebellar peduncle,
emrge the nerve roots of:
o Glossopharyngeal (IX)
o Vagus (X)
o Accessory nerve (XI)
Posterior surface
o Superior half: floor of the 4th ventricle (lower part)
o Inferior half: possess posterior median sulcus (PMS)
o On either of the PMS theres gracile tubercle (produced by underlying
gracile nucleus)
o Lateral to the gracile tubercle is the cuneate tubercle (produced by
underlying (cuneate nucleus)
Functions:
o The medulla contains the cardiac, respiratory, vomiting and vasomotor
centers and therefore deals with the autonomic (involuntary) functions of
breathing, heart rate, and BP
o The bulb is an archaic term for the medulla oblongata and in modern clinical
usage the word bulbar is retained for terms that relate to the medulla
oblongata, particularly in reference to medical conditions. Bulbar can refer to
the nerves and tracts connected to the medulla, and also by association to
the muscles thus innervated, such as those of the tongue, pharynx, and
larynx
o The medulla oblongata connects the higher levels of the brain to the spinal
cord, and is responsible for several functions of the autonomous nervous
system, include:
o Respiration-chemoreceptors
Chemoreceptors detect changes in acidity of the blood, thus if
the blood is considered too acidic by the medulla oblongata
electrical signals are sent to the muscle tissue in the lungs
increasing their contraction rate in order to reoxygenate the
blood
Dorsal: inspiration and rhythm
Ventral : respiration (controls inspiration and expiration)
o Cardiac center

o
o

Sympathetic, parasympathetic nervous system

Vasomotor center
baroreceptors
Reflex centers of vomiting, coughing, sneezing and swallowing. These
reflexes which include the pharyngeal reflex, the swallowing reflex
(also known as the palatal reflex) and the masseter reflex can be
termed, bulbar reflexes

Vascular Disorder of Medulla

Pathoge
nesis

Features

Medial
Medullary
Syndrome
Caused by the thrombosis
of the medullary branch
of the vertebral artery
(supply the medial part of
the medulla)
1. Contralateral
hemiparesis
(
damages
to
pyramidal tracts)
2. Loss of contralateral
dorsal
column
sensation (damage
to
medial
lemniscus)
3. Ipsilateral paralysis
of
tongue
and
deviates
to
the
paralyzed side when
protrudes (damages
to
hypoglossal
nerve)

Lateral
medullary
Syndrome
Caused by the thrombosis of
the
posterior
inferior
cerebellar artery, a branch of
the vertebral artery (supply
the lateral part of the
medulla)
1. Dysphagia
and
dysartria (damage to
nucleus
ambiguous
ipsilateral paralysis of
the
palate
and
laryngeal muscles)
2. Ipsilateral
analgesia
and thermo anesthesia
(damage
to
the
nucleus and the spinal
tract)
3. Nausea,
vomiting,
nystagmus and vertigo
(damage to vestibular
nucleus)
4. Ipsilateral
Horners
syndrome (damage to
descending
sympathetic fibers)
5. Contralateral loss of
sensation
pain,
temperature,
touch
and pressure (damage
to spinal lemniscus)

Wallenberg Syndrome
Posterior surface:
2. Pons
o The pons is also called the pons Varolii ("bridge of Varolius"), after the Italian
anatomist and surgeon Costanzo Varolio
o This white matter includes tracts that conducts signal from the cerebrum
down to the cerebellum and medulla, and tracts that carry the sensory
signals up into the thalamus
o Normal: measure about 2.5cm or 1 inch in length. Most of it appears as a
broad anterior bulge rostal to the medulla. Posteriorly, it consists mainly of

two pairs of thick stalks called cerebellar peduncles.

cerebellum to the pons and midbrain.

They connect the

Anterior surface:
o Middle cerebellar peduncles are located either side of the antero-lateral side
o Theres a shallow groove in the midline-Basilar groove (lodges the Basilar
artery)
o Trigeminal nerve (V) emerges from antero-lateral side
o Mid-pons : the motor nucleus for the trigeminal nerve (V) motor root
(small and medial)
o Mid-pons: the chief or pontine nucleus of the trigeminal nerve sensory
nucleus (V) (large and lateral)
o From the groove between the Medulla and Pons, emerge (medial to lateral)
o Lower down in the pons: abducens nucleus (VI)
o Lower down in the pons: facial nerve nucleus (VII)
o Lower down in the pons: Vestibulocochlear nuclei (vestibular nuclei and
cochlear nuclei (VII)
Posterior surface:
o Triangular in shape
o Forms the floor of the 4th ventricle (upper half)
o Median sulcus divides the posterior surface into symmetrical halves
o Medial eminence is lateral to the sulcus and its bounded laterally by the
Sulcus Limitans
o Inferior end of the medial eminence is expanded to form the facial colliculus
(produce by the root of facial nerve winding around the nucleus of the
abducent nerve)
o Superioer part of the sulcus liminats is called Substantia ferruginea (bluishgrey color)
o Vestibular area is lateral to the sulcus limitans (produced by the underlying
vestibular nucleus)
o Superior cerebellar peduncles are located most laterally
Functions:
o Assists medulla oblongata to control involuntary breathing
o Apneumotic (lower center)
Promote inspiration by stimulation of the neurons in the medulla
oblongata provudng a constant stimulus
The apneustic center of pons sends signals to the dorsal
respiratory center in the medulla to delay the switch off signal of
the inspiratory ramp provided by the pneumotaxic center of
pons.
It controls the intensity of breathing
o Pneumotaxic (upper center)
A.k.a. Pontine Respiratory Group (PRG)
Antagonizes the apneustic center, cyclining inhibiting inhalation
Limits the burst of action potentials in the phrenic nerve,
effectively decreasing the tidal volume and regulating the
respiratory rate.
Absence of the PRG results in an increase in depth of respiration
and decrease in respiratory rate
The PRG regulates the amount of air a person can take into body
in each breath

The dorsal respiratory group has rhythmic bursts of activity that

are constant in duration and interval.
If this was damage or uin any way harmed it would make
breathing on our own almost impossible.
Relayes messages between the spinal cord and the cerebrum, thalamus and
hypothalamus
The pons contains nuclei that relay signals from the forebrain to the brain to
the cerebellum, along with nuclei that deal primarily with sleep, respiration,
swallowing, bladder control breathing control, hearing, equilibrium, taste, eye
movement, facial expressions, facial sensation and posture
The pons is implicated in sleep paralysis and also plays a role in generating
dreams
4 nerves (CN5-8) functions including sensory roles in hearing , equilibrium
and taste and in facial sensation such as touch and pain, as well as motor
roles in eye movement, facial expressions, chewing, swallowing and the
secretions of saliva and tears

o
o

o
o

Millard-Gubler (lateral Pons)- weakness of facial muscles, nystagmus, weakness of

jaw
muscles
Locked-in Syndrome (Ventral Pons) - preserved upward gaze
3. Midbrain
2cm in length
- It connects to the pons and cerebellum with the forebrain
- It traversed by a narrow channel called cerebral aqueduct (filled with CSF)
- It is located below the cerebral cortex and above the hindbrain placing it near the
center of the brain
Midbrain Comprises of:
1. Tectum / corpora quadrigemina) (quadruplet bodies) are four solid lobes on the
dorsal side of the cerebral aqueduct
a. Inferior coliculli: a synapsing point for sound information, lower auditory
centers
b. Superior colliculli: involved with saccadic eye moevments, centers for
visual reflexes (head & neck)
i. 4 solid lobes help to decussate several fibers of the optic nerve ,
however some fibers also show ipsilateral arrangement
ii. The trochlear nerve comes out of the posterior surface of the
midbrain, below the inferior colliculus
2. Tegmentum
3. Cerebral aqueduct
o A narrow cavity in the midline
o Connects 3rd and 4th ventricles lined by ependymal
o Surrounded by the central grey matter
4. Cerebral peduncles
o Are paired structuires, present on the ventral side of the cerebral aqueduct
o Midbrain tegmentum
o Crus cerebri
o Substantia nigra
5. Several nuclei and fasciculi
Anterior surface
o There is a deep depression in the midline (inter peduncular fossa)
o Inner peduncular fossa is bounded on either side by the crus cerebri
o Many blood vessels perforate the floor of the IPF and its called the Posteior
Perforated substance

CN 3 (occulomotor nerve) emerges from the groove on the medial side of the
crus cerebri
Posterior surface
o Corpora Quadrigenina
4 colliculi (2 superior and 2 inferior)
o In midline below the inferior colliculli, the trochlear nerve emerges
o Lateral surface : superior and inferior brachia ascend an atero-lateral
direction
o Superior brachium:
o Inferior brachium : connects inferior colliculus to the medial medial geniculate
body 9nuclei of the thalamus)
Functions:
Important in voluntary muscle control
Relay station for auditory and visual information
Relays information between the cerebellum or spinal cord and
cerebrum
Controls eye movements
Parinuads Syndrome (superior colliculus)
o Impaired upward gaze
Benedicts syndrome ( Tegmentum)
o Damage on extrinsic muscle of eyes. Sensory loss on the contralateral side,
involuntary movements
o

BLOOD SUPPLY TO THE BRAIN

The brain is very sensitive to blood flow
o If blood flow is occluded only for 10 seconds it goes unconsciousness
o If blood flow is occluded for 20 seconds, it results in electrical activity
stopping
o If only 5 mins, irreversible brain damage occurs
Arterial systems supply the brain with blood: the internal carotid and
basilar arteries
I.

Internal Carotid System

a. Anterior Cerebral Arteries
- Surface branches supply cortex and white matter of:
o Inferior frontal lobe
o Medial surface of the frontal lobe and parietal lobe
o Anterior corpus callosum
Penetrating braches supply:
Deeper cerebrum
Diencephalon
Limbic structures
Head of caudate
Anterior limb of internal capsule
- Occlusion: Cause restricted contralateral motor and somatosensory
deficits primary lower limbs and perineum.
b. Middle Cerebral Arteries
- Surface branches supply the lateral aspect of the brain including the
frontal, parietal, and temporal lobes
Penetrating branches supply:
- Telencephalon
- Diencephalon

Including the entire internal capsuleOcclusion: Cause a

contralateral hemispheres and sensory loss but will spare
the lower body since that part is medial and supplied by
the anterior cerebral artery

c. Anterior Choroidal Arteries

- Supply the anterior hippocampus and posterior limb of the internal
capsule
II.
-

Basilar Artery System

It is formed by 2 arteries

a. Posterior Cerebral Arteries

- The posterior cerebral artery goes to supply the occipital lobe and lower temporal
lobes. The posterior perforated substance is from the penetrating branches of the
basilar artery.
- They also deliver blood to the thalamus and some other subcortical structures
- Occlusion:
o Visual field losses may cause other deficits referable to the midbrain and
diencephalon
o Thalamic pain syndrome when the posterior thalamic nucleus is disconnected
from the sensory cortex.
b. Pontine Arteries
- Are numerous and small vessels that enter the substance of the pons.
c. Labyrinthine Artery
- Long narrow artery that accompanies the facial and the vestibulocochlear nerves
into the internal acoustic meatus and supplies the inner ear
d. Anterior Inferior Cerebellar Artery
- Passes posteriorly and laterally
- Supplies the anterior and inferior parts of cerebellum
e.
-

Superior Cerebellar Artery

Arises from close to the termination of the basilar artery
Supplies the superior surface of the cerebellum
Also supplies the pons, and pineal gland

Circle of Willis
AKA Circulus Arteriosus
Main arterial anastomatic trunk of the brain

III.

Anastomosis occurs when

the vessels bring blood to
one
spot
and
then
redistribute it
The blood is the then
redistributed by the anterior,
middle and posterior cerebral
arteries.
Thus, the ends of the internal
carotids and the basilar
artery enter the circle while
three cerebral arteries arise
and exit from it
Two internal carotid are
joined
together
by
the
anterior
communicating
artery while the posterior
communicating artery links
the internal carotid system
with the basilar artery
These
connections
make
collateral circulation. This is
a
safety
mechanism,
allowing brain areas to
continue receiving adequate
blood supply even when
there is blockage somewhere
in an arterial system.
When
all
arteries
are
functioning normally, their blood supplies will not mix where they meet in the Circle
because the pressure of their streams will be equal.

IV. ETIOLOGY
Ischemic Stroke
Result of a thrombus, embolism, or conditions that produce low systemic perfusion
pressures
The resulting lack of cerebral blood flow (CBF) deprives the brain of the needed
oxygen and glucose, disrupts cellular metabolism, and leads to injury and death of
tissues
A thrombus results from platelet adhesion and aggregation on plaques
Cerebral Thrombosis
Formation or development of a blood clot within the cerebral arteries or their
branches
Thrombi lead to ischemia, or occlusion of an artery with resulting cerebral
infarction or tissue death (atherothrombotic brain infarction [ABI])
Thrombi can also become dislodged and travel to a more distal site in the form
of intra-artery embolus
Cerebral Embolus

Composed of bits of matter (blood clot, plaque, air) formed elsewhere and
released into the bloodstream, traveling to the cerebral arteries where they
lodge in a vessel, produce occlusion and infarction

Hemorrhagic Stroke
Result of rupture of a cerebral vessel or trauma
Results in increased ICP with injury to brain tissues and restriction of distal blood
flow
Intracerebral hemorrhage is caused by rupture of a cerebral vessel with
subsequent bleeding into the brain
Primary cerebral hemorrhage (non-traumatic spontaneous hemorrhage) typically
occurs in small blood vessels weakened by atherosclerosis producing an
aneurysm
Subarachnoid hemorrhage occurs from bleeding into the subarachnoid space
typically from saccular or berry aneurysm affecting primarily large blood vessels
Closely linked
RISK FACTORS (Stewart, 1999)
Nonmodifi able Risk Factors
Agethe single most important risk factor for stroke worldwide. After age 55,
incidence
increases for both males and females.
Risk more than doubles each decade after age 55.
Sex (male > female)
Race (African Americans 2> whites > Asians)
Family history of stroke
Modifi able (Treatable) Risk Factors
Hypertensionprobably the most important modifiable risk factor for both
ischemic and
hemorrhagic stroke. Subjects with blood pressure (BP) lower than 120/80 mm Hg
have
about half the lifetime risk of stroke compared to subjects with high BP (Seshadri,
1997).
History of TIA/prior stroke: ~ 5% of patients with TIA will develop a completed
stroke
within 1 month if untreated; ~ 14% within 1 year. After a TIA, the 90day risk of
stroke is
317.3% and is highest within the first 30 days.
Heart disease
Congestive heart failure (CHF) and coronary artery disease (CAD) increase
risk by
twofold.
Valvular heart disease and arrhythmias increase risk of embolic stroke:
n Atrial fibrillation: fivefold increased risk (Wolf, 1991)
Diabetes: twofold increase in risk. Unfortunately, good blood sugar control has not
been
shown to alter the risk of stroke.
Cigarette smoking: risk of ischemic stroke in smokers is about double that of
nonsmokers.
Carotid stenosis (and carotid bruit): risk of stroke decreases with carotid
endarterectomy
(CEA) on selected symptomatic patients (> 70% stenosis).
ETOH abuse/cocaine use: < 2 drinks/day relative risk 0.51; > 7 drinks/day relative
risk 2.96

(Sacco, 1999).
High-dose estrogens (birth control pills)considerable increased risk when linked
with
cigarette smoking
Systemic diseases associated with hypercoagulable states
Elevated RBC count, hematocrit, fibrinogen
Protein S and C deficiencies
Sickle-cell anemia
Cancer
Hyperlipidemiaseveral clinical trials have shown a reduction in stroke with use of
cholesterolreducing agents (~ 30% reduction risk of stroke with use of HMG-CoA reductase
inhibitors).
Migraine headaches
Sleep apnea
Patent foramen ovale (PFO)
[Obesity/sedentary life style (no clear relationship with increased risk of stroke)]
Other Risk Factors (Heart Disease and Stroke Statistics2008 Update)
Geographical location: higher risk of stroke in the southeastern United States than in
other areasthe so-called stroke belt states.
Socioeconomic factors: some evidence that strokes are more common in people with
lowincome
than among more affluent people.

V. PATHOPHYSIOLOGY
Hypertensio
n
Cerebrovasc
ular Disease

Blood
Pressure

Necrosi
s

Intimal
wall
damage

Ischemi
a

Platelet
aggregati
on

Occlusio
n

Embolu
s

Thrombus
formation

VI. SIGNS AND SYMPTOMS

MEDICAL RED FLAGS

Changes in Neurological Status

Symptoms
Possible
Causes
Decreased level of

Cerebral
arousal,
edema
enlargement of

Another
pupil on side of stroke
stroke,
sudden change in
muscle
tone and/or DTRs

Management

Cease
treatment and
seek
immediate
medical
attention

Deep Vein Thrombosis (DVT)

Occurs most often in legs
Symptoms

Possible Causes

Managemen
t

Swelling, heat,
and
erythema in the
affected
area
(especially
prevalent
on
the
affected
side)
Positive Homans
sign

Thrombus may
form in deep
veins in legs
due
to
immobilization

Cease
treatment
and
seek
immediate
medical
attention

Dysphagia
Symptoms

Possible Causes

Manageme
nt

Pain
on
Decreased For
swallowing
coordination
aspiration,
Choking
of swallowing
seek
Aspiration
muscles
immediate

Airway
Diminished medical
obstruction
swallow
attention
Pneumonia
reflex

Reduced Administer
lingual
the
and pharyngeal Heimlich
control
maneuver
Cranial nerve or CPR, if

deficits

warranted

Speechlanguage
feeding
program

Clinical Manifestations of Anterior Cerebral Artery Syndrome

Signs and Symptoms
Structures Involved
Contralateral hemiparesis involving Primary motor area, medial aspect of
mainly the LE (UE is more spared)
cortex,
internal capsule
Contralateral
hemisensory
loss Primary sensory area, medial aspect
involving mainly the LE (UE is more of cortex
spared)
Urinary incontinence
Posteromedial aspect of superior
frontal gyrus
Problems with imitation and bimanual Corpus callosum
tasks, apraxia
Abulia (akinetic mutism), slowness, Uncertain localization
delay, lack of spontaneity, motor
inaction
Contralateral grasp reflex, sucking Uncertain localization
reflex
Can be asymptomatic if circle of
Willis is competent.
Clinical Manifestations of Middle Cerebral Artery Syndrome
Signs and Symptoms
Structures Involved
Contralateral hemiparesis involving Primary motor cortex and internal
mainly the UE and face (LE is more capsule
spared)
Contralateral
hemisensory
loss Primary sensory cortex and internal
involving mainly the UE and face (LE capsule
is more spared)
Motor speech impairment: Brocas or Brocas cortical area (third frontal
nonfluent
aphasia
with
limited convolution)
vocabulary and slow, hesitant speech in
the
dominant
hemisphere,
typically the left
hemisphere
Receptive
speech
impairment: Wernickes cortical area (posterior
Wernickes or fluent aphasia with portion of the
impaired auditory comprehension temporal gyrus) in the dominant
and fluent speech with normal rate hemisphere,
and melody
typically the left
Global aphasia: nonfluent speech Both third frontal convolution and
with poor comprehension
posterior portion

Limb-kinetic apraxia

of the superior temporal gyrus

Parietal sensory association cortex in
the
nondominant
hemisphere,
typically the right
homonymous Optic radiation in internal capsule

Contralateral
hemianopsia
Loss of conjugate gaze to the Frontal eye fields or their descending
opposite side
tracts
Ataxia
of
contralateral
limb(s) Parietal lobe
(sensory ataxia)
Pure motor hemiplegia (lacunar Upper portion of posterior limb of
stroke)
internal capsule

Clinical Manifestations of Posterior Cerebral Artery Syndrome

Signs and Symptoms
Peripheral Territory
Contralateral
homonymous Primary visual cortex or optic
hemianopsia
radiation
Bilateral homonymous hemianopsia Calcarine cortex (macular sparing is
with some degree of macular sparing due to occipital pole
receiving collateral blood supply from
MCA)
Visual agnosia
Left occipital lobe
Prosopagnosia
(difficulty
naming Visual association cortex
people on sight)
Dyslexia (difficulty reading) without Dominant
calcarine
lesion
and
agraphia (difficulty writing), color posterior part of corpus
naming
(anomia),
and
color callosum
discrimination problems
Memory defect
Lesion of inferomedial portions of
temporal lobe bilaterally
or on the dominant side only
Topographic disorientation
Nondominant primary visual area,
usually bilaterally
Central Territory
Central post-stroke (thalamic) pain
Ventral posterolateral nucleus of
Spontaneous pain and dysesthesias; thalamus
sensory impairments (all modalities)
Involuntary
movements; Subthalamic nucleus or its pallidal
choreoathetosis, intention tremor, connections
hemiballismus
Contralateral hemiplegia
Cerebral peduncle of midbrain
Webers syndrome
Third nerve and cerebral peduncle of
Oculomotor
nerve
palsy
and midbrain
contralateral hemiplegia
Paresis of vertical eye movements, Supranuclear fibers to third cranial
slight miosis and ptosis,
nerve
and sluggish pupillary light response

Clinical Manifestations of Vertebrobasilar Artery Syndrome

Signs and Symptoms
Structures Involved
Medial medullary syndrome
Occlusion vertebral artery, medullary
branch
Ipsilateral to lesion
CN XII, hypoglossal, or nucleus
Paralysis with atrophy of half the
tongue with deviation to
the paralyzed side when tongue is
protruded
Contralateral to lesion
Corticospinal tract
Paralysis of UE and LE
Impaired tactile and proprioceptive Medial lemniscus
sense
Lateral medullary (Wallenburgs) Occlusion
of
posterior
inferior
syndrome
cerebellar artery or
vertebral artery
Ipsilateral to lesion
Descending tract and nucleus of CN
Decreased pain and temperature V, trigeminal
sensation in face
Cerebellum or inferior cerebellar Cerebellar ataxia: gait and limbs
peduncle
ataxia
Vertigo, nausea, vomiting
Vestibular nuclei and connections
Nystagmus
Vestibular nuclei and connections
Horners
syndrome:
miosis, Descending sympathetic tract
ptosis, decreased sweating
Dysphagia and dysphonia: paralysis CN IX, glossopharyngeal, and CN X,
of palatal and laryngeal
vagus, or nuclei
muscles, diminished gag reflex
Sensory impairment of ipsilateral UE, Cuneate and gracile nuclei
trunk, or LE
Contralateral to lesion
Spinal
lemniscusspinothalamic
Impaired pain and thermal sense tract
over 50% of body,
sometimes face
Complete
basilar
artery Basilar artery, ventral pons
syndrome (locked-in
syndrome)
Tetraplegia (quadriplegia)
Corticospinal tracts bilaterally
Bilateral cranial nerve palsy: upward Long tracts to cranial nerve nuclei
gaze is spared
bilaterally
Coma
Reticular activating system
Cognition is spared
Medial inferior pontine syndrome Occlusion of paramedian branch of
basilar artery
Ipsilateral to lesion
Pontine center for lateral gaze
Paralysis of conjugate gaze to side of paramedian pentine
lesion (preservation
reticular formation (PPRF)
of convergence)
Nystagmus
Vestibular nuclei and connections

Ataxia of limbs and gait

Diplopia on lateral gaze
Contralateral to lesion
Paresis of face, UE, and LE
Impaired tactile and proprioceptive
sense over 50% of the body
Lateral
inferior
pontine
syndrome

Middle cerebellar peduncle

CN VI, abducens, or nucleus
Corticobulbar and corticospinal tract
in lower pons
Medial lemniscus
Occlusion
of
anterior
inferior
cerebellar artery, a
branch of the basilar artery
CN VIII, vestibular, or nucleus

Ipsilateral to lesion
Horizontal and vertical nystagmus,
vertigo, nausea, vomiting
Facial paralysis
CN VII, facial, or nucleus
Paralysis of conjugate gaze to side of Pontine center for lateral gaze (PPRF)
lesion
Deafness, tinnitus
CN VIII, cochlear, or nucleus

Clinical Manifestations of Vertebrobasilar Artery Syndromecontd

Signs and Symptoms
Structures Involved
Ataxia
Middle cerebellar peduncle and
cerebellar
hemisphere
Impaired sensation over face
Main
sensory
nucleus
and
descending tract of fifth
nerve
Contralateral to lesion
Spinothalamic tract
Impaired pain and thermal sense
over half the body (may include face)
Medial midpontine syndrome
Occlusion of paramedian branch of
the mid-basilar artery
Ipsilateral to lesion
Middle cerebellar peduncle
Ataxia of limbs and gait (more
prominent in bilateral involvement)
Contralateral to lesion
Corticobulbar and corticospinal tract
Paralysis of face, UE, and LE
Deviation of eyes
Abducent nerve nucleus, medial
longitudinal fasciculus
Lateral midpontine syndrome
Occlusion of short circumferential
artery
Ipsilateral to lesion
Middle cerebellar peduncle
Ataxia of limbs
Paralysis of muscles of mastication
Motor fibers or nucleus of CN V,
trigeminal
Impaired sensation over side of face
Sensory fibers or nucleus of CN V,
trigeminal
Medial
superior
pontine Occlusion of paramedian branches of
syndrome
upper basilar
artery

Cerebellar ataxia

Superior
or
middle
cerebellar
peduncle
Medial longitudinal fasciculus
Corticobulbar and corticospinal tract

Internuclear ophthalmoplegia
Contralateral to lesion
Paralysis of face, UE, and LE
Lateral
superior
pontine
syndrome (occlusion of
superior cerebellar artery, a
branch of the basilar artery)
Ipsilateral to lesion
Middle
and
superior
cerebellar
Cerebellar ataxia of limbs and gait, peduncles, superior
falling to side of lesion
surface
of
cerebellum,
dentate
nucleus
Dizziness, nausea, vomiting
Vestibular nuclei
Horizontal nystagmus
Vestibular nuclei
Paresis of conjugate gaze (ipsilateral) Uncertain
Loss of optokinetic nystagmus
Uncertain
Horners syndrome: miosis, ptosis, Descending sympathetic fibers
decreased sweating on
opposite side face
Contralateral to lesion
Spinothalamic tract
Impaired pain and thermal sense of
face, limbs, and trunk
Impaired
touch,
vibration,
and Medial lemniscus (lateral portion)
position sense, more in LE than
UE (tendency to incongruity of pain
and touch deficits)
Hemispheric Differences Commonly Seen Following Stroke
Right Hemisphere Lesion
Left Hemisphere Lesion
Left-side hemiplegia/paresis
Right-side hemiplegia/paresis
Left-side sensory loss
Right-side sensory loss
Visualperceptual impairments:
Speech
and
language
Left-side unilateral neglect
impairments:
Agnosias
Dominant hemisphere:
Visuospatial disorders
Nonfluent (Brocas) aphasia
Disturbances of body image and Fluent (Wernickes) aphasia
body scheme
Global aphasia
Difficulty processing visual cues
Difficulty processing verbal cues,
verbal commands
Behavioral deficits:
Behavioral deficits:
Quick, impulsive behavioral style Slow, cautious behavioral style
Poor judgment, unrealistic
Disorganized
Inability to self-correct
Often very aware of impairments,
Poor
insight,
awareness
of extent of disability
impairments, denial of disability
Increased safety risk
Intellectual deficits:
Intellectual deficits:
Difficulty
with
abstract Disorganized problem solving

reasoning, problem solving

Difficulty
synthesizing
information and grasping whole
idea
of task
Rigidity of thought
Memory impairments, typically
related to spatial-perceptual
information
Emotional deficits:
Difficulty with ability to perceive
emotions
Difficulty with expression of negative
emotions
Task performance:
Fluctuations in performance

Difficulty initiating tasks, processing

delays
Highly distractible
Memory
impairments,
typically
related to language
Perseveration

Emotional deficits:
Difficulty with expression of positive
emotions

Task performance:
Apraxia common: difficulty planning
and sequencing
movements
Ideational
Ideomotor
Deficits of either hemisphere depending on lesion location:
Visual field defects: Homonymous hemianopsia
Emotional abnormalities: Lability, apathy, irritability, low frustration
levels, anxiety, depression
Cognitive deficits: Confusion, short attention span, loss of memory,
executive functions

BRAIN STEM STROKE

WEBER
Medial basal midbrain
SYNDROME

BENEDIKTS
SYNDROME

Tegmentum Syndrome

LOCK-IN
SYNDROME

Bilateral basal pons

MILLARD-GUBLER
SYNDROME

Lateral Pons

Ipsilateral
3rd
nerve palsy
Contralateral
hemiplegia
Ipsilateral
3rd
nerve palsy
Contralateral loss
of
pain
and
temperature
Contralateral loss
of joint position
Bilateral
hemiplegia
Bilateral on palsy
(upward
gaze
spared)
Ipsilateral
6th
nerve palsy
Ipsilateral
7th

WALLENBURGS
SYNDROME

Lateral Medulla

nerve palsy
Contralateral
hemiplegia
Ipsilateral
Hemiataxia
Ipsilateral loss of
facial pain and
temperature
Contralateral loss
of body pain and
temperature
sense
Nystagmus
Ipsilateral
Horners
Syndrome
Dysphagia
Dysphonia

1. Anterior Cerebral Artery Syndrome

The anterior cerebral artery (ACA) is the first and smaller of the two terminal
branches of the internal carotid artery.
It supplies the medial aspect of the cerebral hemisphere (frontal and parietal
lobes) and subcortical structures, including the basal ganglia, anterior fornix,
and anterior four fifths of the corpus callosum.
Because of the anterior communicating artery allows perfusion of the
proximal anterior cerebral artery from either side, occlusion proximal to this
point results in minimal deficit.
Most common characteristics of ACA syndrome: contralateral
hemiparesis and sensory loss with greater involvement of the LE.
Middle Cerebral Artery Syndrome
The middle cerebral artery (MCA) is the second of the two main branches of
the internal carotid artery.
It supplies the entire lateral aspect of the cerebral hemisphere (frontal,
temporal, and parietal lobes) and subcortical structures, including the internal
capsule, corona radiate, globus pallidus, most of caudate nucleus, and the
putamen.
Occlusion of the proximal MCA produces extensive neurological damage with
significant cerebral edema.
Most common characteristics of MCA syndrome: contralateral spastic
hemiparesis and sensory loss of the face, UE and LE, with face and UE more
involved than LE.
2. Posterior Cerebral Artery Syndrome
The 2 posterior cerebral arteries (PCAs) arise as terminal branches of the
basilar artery and each supplies the corresponding occipital lobe and
medial and inferior temporal lobe
Occlusion proximal to the posterior communicating artery typically results
in minimal deficits owing to the collateral blood supply from the posterior
communicating artery.

Occlusion of thalamic branches may produce hemianesthesia

(contralateral sensory loss) or central post-stroke (thalamic) pain.

3. Internal Carotid Artery Syndrome

The internal carotid artery (ICA) supplies both the MCA and the ACA.
Occlusion of the ICA typically produces massive infarction in the region of
the brain supplied by the MCA
Significant edema is common with possible uncal herniation, coma, and
death (mass effect)
4. Lacunar Syndromes
Lacunar syndromes are caused by small vessel disease deep in the
cerebral white mater (penetrating artery disease)
They are strongly associated with hypertensive hemorrhage and diabetic
microvascular disease.
Lacunar syndromes are consistent with specific anatomic sites
5. Vertrobasilar Artery Syndrome
The vertebral arteries arise from the subclavian arteries and travel into
the brain along the medulla where they merge at the inferior border of the
pons to form the basilar artery.
The vertebral arteries supply the cerebellum (via posterior inferior
cerebellar arteries) and the medulla (via the medullary arteries).
The basilar artery supplies the pons (via pontine arteries), the internal ear
(via labyrinthine arteries), and the cerebellum (via the anterior inferior
and superior cerebellar arteries.
Occlusions of the vertebrobasilar system can produce a wide variety of
symptoms with both ipsilateral and contralateral signs, because some of
the tracts in the brainstem will have crossed and others will not.

(OSullivan, Susan B. & Schmitz, Thomas J. Physical Rehabilitation 5th Edition,

pp. 710-712)

CLINICAL MANEFESTATIONS

1. Sensation
Loss of sensation after stroke can have a significant effect on joint and skin
protection, balance, coordination and motor control
Loss of proprioception, superficial touch, pain and temperature, 2-point
discrimination, homonymous hemianopsia
Forced gait deviation
2.
3. Motor function
4. Sequential Recovery Stage
During the early stage of stroke, flaccidity with no voluntary movements is
common
Usually replaced by the development of spasticity, hyperreflexia and mass
patterns of movement, termed as Synergy.
5.
3. Alteration in tone
Flaccidity is usually present immediately after the stroke and is generally
short lived, lasting hours, days or weeks
Spasticity emerges in about 90% of cases and tends to occur in predictable
muscle groups, commonly the antigravity muscles
6.
4. Synergy pattern
Synergy patterns of the extremities are stereotyped, primitive movement
patterns associated with the presence of spasticity
Muscles that are not usually involved in either synergy are the ff;
7. (FLATS)
8. F- fingers extensors
9. L- latissimus dorsi
A- Ankle evertors
10.T- teres major
11.S- Serratus anterior
12.
5. Reflexes
Altered and vary according to the stages of recovery
Initially: hypotonia and areflexia
Middle stage of recovery; hyperreflexia emerges
Clonus and clasp- knife reflex
(+) babinski
TNR: STNR, ATNR (Fencers Raimistes)
TLR
(+) supporting reaction
Associated reactions: Souquess Raimistes Phenomenon

6. Paresis
Muscle weakness is a common finding, not all muscles affected equally
13.
7. Incoordination
Ataxia of the extremities or trunk is common in patient with cerebellar lesion
14.
8. Motor programming deficit
Apraxia
o Defined as an inability to perform purposive movements although
there is no sensory impairment
Ideomotor
o Movement is not possible upon command but may occur automatically

Ideational
o Purposeful movement is not possible, either automatically or on
command
15.
9. Functional abilities
Functional mobility skills following stroke are typically impaired or absent
Motor and perceptual impairments have the greatest impact on functional
performance
Other limiting factors include disorientation, communication disorder, sensory
loss and cardiorespiratory disorder endurance
16.
10.Speech and language disorder
Dysarthia
o Refers to a category of motor speech disorders caused by impairment
in parts of the CNS or PNS that mediate the speech production
Aphasia
o Is a general term used to describe an acquired communication disorder
caused by brain damage
o Characterized by an impairment of language comprehension,
formulation and use

17.
Types of Aphasia
18.
a. Fluent Aphasia
o Speech flows smoothly with a variety of grammatical constructions and
preserved melody of speech
b. Non-fluent Aphasia
o The flow of speech is slow and hesitant, vocabulary is limited and
syntax is impaired
c. Global Aphasia
o Severe aphasia characterized by marked impairments of the
production and comprehension of language
19.
11.Perceptual deficits
Visuospatial distortions
Disturbance in body image
Unilateral neglect
Topographical disorientation
Body scheme (a postural model of the body scheme and the relip of its
parts)
Body image of ones body that influence feelings about ones body
20.
12.Cognitive and behavioral changes
Emotional liability
Dementia
21.
13.Bladder and bowel dysfunction
Urinary Incontinence
Generally this problem improves quickly early removal of catheter is describe
to prevent the development of inspection of is patients stool softeners and
low redisue and may require stool out get prevent the development of
infection
Patients are frequently impacted and may require stool softeners and low
residue diets to resolve this problem
22.

14.Orofacial dysfunction
Dysphagia
o Is a common complication after stroke.
o It occurs in lesions affecting the medullary brainstem (CN IX & X) as
well as in acute hemispheric lesions
23.
Secondary Impairments
1. Psychological problem
Anxiety, depression or denial
24.
2. LOM, Contracture and Deformity
Result from loss of voluntary movement and immobilization
25.
3. DVT
DVT and pulmonary embolism are potential complication for all immobilized
patient
Sx: calf pain or tenderness, swelling and discoloration of the leg
26.
4. Pain
Lesion in thalamus ( posterolateral ventral nuclei)
May initailly experience a contralateral sensory loss; Sequel of pain are
reduced function, impaired concentration, depression and rehab potential
27.
5. Shoulder dysfunction
Shoulder subluxation and pain
Reflex sympathetic dystrophy (RSD or Sh. Hand Syndrome)
28.
29.
Potential Complications and Problems Following a Stroke
1 Falls
- More frequent in right hemisphere stroke patients
- Requires balance training , cognitive training, use of special devices and
environmental modification to ensure safety
30.
2 Musculoskeletal Problems
- Usually includes shoulder pain and contracture d/t subluxations, impingement
syndrome, rotator cuff tears, frozen shoulder, brachial plexopathy, RSD, bursitis,
tendinitis, and central pain
- Shoulder problems noted in 70-80% of patients
- Treatment: ROM exercises, arm troughs, laptrays, shoulder slings, medications,
physical modalities
31.
3 Bowel and bladder incontinence
- present in 1/3 to 2/3 of all stroke survivors but with good potential for recovery
- if problem persist may suggest poor functional & neurologic prognosis
32.
4 Physiologic deconditioning
33.
5 Common associated medical problems
- HPN
- Diabetes
- Ischemic heart dse., angina
- Congestive heart failure, cardiac arrhythmia
34.
6 Common secondary post-stroke problems (early and late)

Urinary Tract Infection

Pressure Sore
Dehydration
Malnutrition
Dysphagia
Shoulder dysfunction; RSD
Depression
Sexual dysfunction
Seizure

Spasticity
Contracture
Central
post-stroke
pain
syndrome
Falls and injuries
Medication overuse
Deconditioning and endurance
limitations
Fatigue
Insomnia

35.
36.
Typical Post-Stroke Problems
1 Absent or weak muscle strength
2 Joint contracture
- Management: ROM exercises, proper positioning, stretching, and splinting,
antispasticity meds if with spasticity
3 Incoordination
- Etiology: weakness; poor proprioception; neglect
- Management: specific training techniques
4 Abnormal muscle tone (hypertonicity)
- Management: conservative avoid/ remove noxious stimuli, positioning, ROM
exercises
37.Pharmacologic dantrolene sodium
38.Nerve block with phenol
39.Surgical tendon release transfer
40.
41.
42.
43.

VII. DIFFERENTIAL DIAGNOSIS

44.

1.

2. Ischemic (85%)

4.

5. Thro
mbot
ic

6. Emb
olic

7. Lacu
nar

15.
Frequen
cy
(%)
21.
Factors
22.
associat
ed
23.
with
onse
t

16.
35

17.
30

18.
30

24.
Occurs
durin
g
25.
sleep

26.
Occurs
while
27.
awake

28.

40.
Major
caus
es/
41.
etiology

42.
Perfusio
n
failur
e
43.
distal to
site
of
44.
severe
sten
osis
45.
or

47.
Due
main
ly
48.
to
cardi
ac
49.
source

50.
Small
lesio
ns
51.
seen
main
ly
52.
in:
53.

puta
men
54.

3. Hemorrhagic
(15%)
8. Intra
11.
cere
Subarac
bral
hnoi
9. (hyp
d
erten
12.
sive)
hemorrh
10.
age
hemorr
13.
hage
(rupture
d
14.
aneurys
m)
19.
20.
10
5
29.
In 90%
of
case
s
30.
occurs
when
31.
patient
is
32.
calm
and
33.
unstress
ed
34.
Blacks
>
Whit
es
60.
Hyperte
nsion

35.
Occurs
durin
g
36.
activity
37.
(often
38.
strenuo
us
39.
activity)

61.
From
ruptu
red
62.
aneurys
ms
63.
and
64.
vascular
65.
malform
ation
s

45.
45.
45.
45.
45.
45.
45.
45.
45.
45.
45.
45.
45.
45.
45.
45.
45.
45.
45.
45.
45.
45.
45.
45.
45.
45.
45.
45.
45.
45.
45.
45.
45.
45.
45.
45.
45.
45.
45.
45.
45.
45.
45.
45.
45.
45.
45.
45.
45.
45.
45.
45.
45.
45.
45.
45.

45.
46.
47.
48.
49.
50.ISCHEMIC STROKE

51. Condition
54.
Intracerebr
al hemorrhage

52.

53.

CT or MRI
demonstrates
hemorrhage
(hyperattenuatio
n)

CT or MRI may be
normal or may
reveal evidence
of older infarcts

Cerebral edema
on CT or MRI

55.
Transient
ischemic attack

56.
Hypertensiv
e encephalopathy

Differentiati
ng
signs/symptoms
No symptoms or
signs reliably
distinguish
hemorrhagic
stroke from
ischemic stroke
Hemorrhagic
stroke is more
often associated
with reduced
level of
consciousness
and signs of
increased
intracranial
pressure than
ischemic stroke
Transient
neurological last
less than 24
hours, with no
evidence of acute
infarct
The combination
of headache.
Cognitive
abnormalities or
decreased level
of consciousness,
and HTN
significantly
above patients
baseline BP
indicates
hypertensive
encephalopathy.
Other possible
signs/symptoms
include visual
changes or loss,
or signs of
increased

Differentiati
ng investigations

57.
mia

Hypoglyce

58.
Complicate
d Migraine

59.
Seizure and
Postictal deficits

intracranial
pressure
There may be a
history of
diabetes with use
of insulin or
insulin
secretagogues
Decreased level
of consciousness
Repetitive history
of similar events;
preceding aura,
headache in a
marching
patterns
differentiates
complicated
migraine
Stroke often
presents with
negative
symptoms (e.g.,
visual loss,
numbness, or
weakness.)
Positive
symptoms (e.g.,
marching
paresthesia,
visual
hallucinations,
and abnormal
motor
manifestations)
are more likely
with complicated
migraine
Hx seizures;
witnessed seizure
followed by
postictal deficits;
for example,
drowsiness and
tongue biting
Wrong-way eye
deviation should
prompt
consideration of
seizures but can
also occur with

Low serum
glucose at time of
symptoms

MRI shows no
evidence of
infarction

EEG confirms
evidence of
seizure.
MRI shows no
evidence of
infarction.

60.
Conversion
and somatisation
disorders

strokes affecting
the pons or
thalamus
Neurological
signs and
symptoms do not
fit a vascular
territory.
No cranial nerve
deficits.
Additionally,
conversion
disorder displays
multiple signs
that are
neurologically
inconsistent.
Hx alcohol abuse.

61.
Wernicke'
s
encephalopathy

Irritability,
confusion, and
delirium common
presenting
features

62.

Symptoms and
signs more likely
to have been on
going
May be hx cancer
of metastatic
lesion causing
symptoms

Brain Tumor

MRI shows no
evidence of
infarction

Decreased blood
thiamine level
and successful
therapeutic trial
of thiamine

CT head
demonstrates
lesion or lesions

63.
64.Hemorrhagic Stroke

65.

Condition

68.
Ischemic
Stroke

66.
Differentiati
ng
signs/symptoms
- Symptoms occur
suddenly
- In ischemic
stroke, patients
do not exhibit GI
symptoms (N/V)
or headache
typically

67.
Differentiati
ng investigations
-

Acute
hemorrhage
appears bright
due to hyper
attenuation of the
x-ray beams in
CT scan. In
contrast,
ischemic infarct
appears as hypo
attenuation,
although may not
appear for many

69.
Hypertensiv
e Encephalopathy

70.
mia

Hypoglyce

71.
Complicate
d Migraine

72.
Seizure
disorder

73.
Conversion
s and
somatization
disorders

HTN significantly
above patients
baseline BP
associated with
headache,
decreased
consciousness or
cognitive
abnormalities,
visual changes or
loss, and signs of
increased
intracranial
pressure. Less
frequently these
patients present
with focal
abnormalities in
the neurological
examination
Sweating, tremor,
hunger,
confusion, and
ultimately a
decreased level
of consciousness
May have known
history of DM and
insulin use or
medical
conditions
associated with
hypoglycemia
Repetitive history
of similar events
preceding aura;
headache in a
marching pattern
A history of
seizures and/or
witnessed seizure
followed by
postictal deficits

Neurological
signs and
symptoms do not
fit a vascular
territory. No

hours after stroke

onset
Cerebral edema
on CT or MRI.
Certain patients
present
characteristic
changes in the
posterior aspect
of the brain

Low serum
glucose on blood
chemistry

MRI shows no
evidence of
infarction

ECG results may

identify seizure
activity.
MRI shows no
evidence of
infarction
CT and MRI
shows no
evidence of
infarction or
hemorrhage in

cranial nerve
deficits
Additionally,
conversion
disorder displays
multiple signs
that are
neurologically
inconsistent

conversion
disorder.

74.
75.
76.

Parkinsons disease is a chronic, progressive disease of nervous system

characterized by the cardinal features of rigidity, akinesia, bradykinesia, tremor and
postural instability. May cause a variety of indirect impairments and complications,
some of which are produced by various combinations of cardinal signs, including
movement and gait disturbances, masked face, cognitive and perceptual disturbances,
communication and swallowing dysfunction, autonomic dysfunction and so forth.
Multiple Sclerosis is a chronic, often disabling, demyelinating disease of the CNS.
Has clinical and pathological findings like paralysis, and the cardinal symptoms of
intention tremor, scanning speech, and nystagmus and later termed Charcots Triad.
Cardiovascular collapse is a general term connoting loss of effective blood flow due
to acute dysfunction of the heart and/or peripheral vasculature. Cardiovascular collapse
may be caused by vasodepressor syncope (vasovagal syncope, postural hypotension
with syncope, neurocardiogenic syncope), a transient severe bradycardia, or cardiac
arrest.
Bells palsy disease of the 7th cranial nerve that produces unilateral or bilateral
facial weakness or paralysis.
Intracranial aneurysm - is a weakness of the wall of an intracranial artery that
causes localized dilation. Its most common form is the berry aneurysm, a saclike
outpouching in a cerebral artery.
SCI include fractures, contusions, & compressions of the vertebral column, usually as
a result of trauma to the head or neck.
77.
78.
79.
80.National Institutes of Health Stroke Scale, or NIH Stroke Scale (NIHSS)

VIII. DIAGNOSTIC TESTS/TOOLS

81.
82.
Poi
n
t
s
84.
85.
0-3
86.
0-2
87.
0-2
88.

NIH Stroke Scale

83.
Description

1. Level of
consciousness
a. Alertness
b. Orientation
c. Follows command
2. Best gaze
3. Visual fields
4. Facial Palsy

0-2
5. Motor Function (arm)
89.
a. Right
0-3
b. Left
90.
6. Motor Function (leg)
0-3
a. Right
91.
b. Left
92.
7. Limb Ataxia
0-4
8. Sensory
93.
9. Language (aphasia)
0-4
10.
Dysarthria
94.
(articulation)
95.
11.
Neglect
0-4
96.
0-4
97.
0-2
98.
0-2
99.
0-3
100.
0-2
101.
0-2
102. NIH: National Institutes of
Health
103. Level of stroke severity:
104. 0 = no stroke
105. 0-4 = minor stroke
106. 5-15 = moderate stroke
107. 15-20 = moderate/ severe
stroke
108. 21-42 = severe stroke
109.
110.
PROCEDURE:
111.
112.
NOTE:
While administering the NIHSS it is important that the examiner does not coach or
help with the assigned task.
The examiner may demonstrate the commands to patients that are unable to
comprehend verbal instructions, however the score should reflect the patient's own
ability.
It is acceptable for the examiner to physically help the patient get into position to
begin the test, but the examiner must not provide further assistance while the
patient is attempting to complete the task.
For each item the examiner should score the patient's first effort, and repeated
attempts should not affect the patient's score.
An exception to this rule exist in the language assessment (Item 9) in which the
patient's best effort should be scored. Some of the items contain "Default Coma

Scores", these scores are automatically assigned to patients that scored a 3 in item
1a.
113.
114.
1. Level of Consciousness
Level of consciousness testing is divided into three sections. The first LOC items test
for the patient's responsiveness. The second LOC item is based on the patient's
ability to answer questions that are verbally presented by the examiner. The final
LOC sub-section is based on the patient's ability to follow verbal commands to
perform simple task.
Although this item is broken into three parts, each sub-section is added to the final
score as if it is its own item.
115.
116.
A) LOC Responsiveness
117.
Scores for this item are assigned by a medical practitioner based on the
stimuli required to arouse patient. The examiner should first assess if the patient is
fully alert to his or her surroundings. If the patient is not completely alert, the
examiner should attempt a verbal stimulus to arouse the patient. Failure of verbal
stimuli indicates an attempt to arouse the patient via repeated physical stimuli. If
none of these stimuli are successful in eliciting a response, the patient can be
considered totally unresponsive.
118.
119.
S
120.
Test results

121.
0

122.

123.
1

124.
Not alert; Verbally arousable or aroused by minor stimulation to
obey, answer, or respond.

125.
2

126.

Alert; Responsive

Not alert; Only responsive to repeated or strong and painful stimuli

127.
128.
Totally unresponsive; Responds only with reflexes or is areflexic
3
129.
130.
Notes
If patients scores a 3 in this factor, the default coma scores should be used when
applicable
131.
132.
B) LOC Questions
133.
Patient is verbally asked his or her age and for the name of the current
month.
134.
135.
136.
Test results
Score
137.
0

138.

Correctly answers both questions

139.
1

140.

Correctly answers one question

142.

Does not correctly answer either question

141.
2
143.
144.

Notes

Default Coma Score: 2

The patient must answer each question 100% correct without help to get credit
Patients unable to speak are allowed to write the answer
Aphasic patients or patients in a stuporous state who are unable to understand the
commands receive a score of 2
Patients that are unable to talk due to trauma, dysarthria, language barrier,
or intubation are given a score of 1
145.
C) LOC Commands
146.
The patient is instructed to first open and close his or her eyes and then grip
and release his or her hand.
147.
148.
149.
Test results
Score
150.
0

151.

Correctly performs both tasks

152.
1

153.

Correctly performs 1 task

154.
155.
Does not correctly perform either task
2
156.
157.
Notes
Commands can only be repeated once.
The hand grip command can be replaced with any other simple one step command
if the patient cannot use his or her hands.
A patient's attempt is regarded as successful if an attempt is made but is
incomplete due to weakness
If the patient does not understand the command, the command can be visually
demonstrated to him or her without an impact on his or her score
Patients with trauma, amputations, or other physical impediments can be given
other simple one-step commands if these commands are not appropriate
158.
159.
2. Horizontal Eye Movement
Assesses ability for patient to track a pen or finger from side to side only using his
or her eyes.
This is designed to assess motor ability to gaze towards the hemisphere opposite of
injury.
This item is tested because Conjugated eye deviation is present in approximately
20% of stroke cases. CED is more common in right hemispheric strokes and typically
in lesions affecting the basal ganglia and temporoparietal cortex. Damage to these
areas can result in decreased spatial attention and reduced control of eye
movements.
160.
161.
S
162.
Test results
163.
164.
0
165.
1

Normal; Able to follow pen or finger to both sides

166.
Partial gaze palsy; gaze is abnormal in one or both eyes, but gaze is
not totally paralyzed. Patient can gaze towards hemisphere of infarct, but
can't go past midline

167. 168.

Total gaze paresis; gaze is fixed to one side

2
169.
170.
Notes
If patient is unable to follow the command to track an object, the investigator can
make eye contact with the patient and then move side to side. The patient's gaze palsy
can then be assessed by his or her ability to maintain eye contact.
If patient is unable to follow any commands, assess the horizontal eye movement
via the oculocephalic maneuver. This is done by manually turning the patient's head
from midline to one side and assessing the eye's reflex to return to a midline position.
If the patient has isolated peripheral nerve paresis assign a score of 1
171.
172.
3. Visual field test
Assess the patient's vision in each visual fields. Each eye is tested individually, by
covering one eye and then the other. Each upper and lower quadrant is tested by
asking the patient to indicate how many fingers the investigator is presenting in
each quadrant. The investigator should instruct the patient to maintain eye contact
throughout this test, and not allow the patient to realign focus towards each
stimulus. With the first eye covered, place a random number of fingers in each
quadrant and ask the patient how many fingers are being presented. Repeat this
testing for the opposite eye.
173.
174.
S
175.
Test results
176.
177.
0

No vision loss

178. 179.
Partial hemianopia or complete quadrantanopia; patient recognizes
1
no visual stimulus in one specific quadrant
180. 181.
Complete hemianopia; patient recognizes no visual stimulus in one
2
half of the visual field

182.
183.
Bilateral Blindness, including blindness from any cause
3
184.
185.
Notes
If patient is non-verbal, he or she can be allowed to respond by holding up the
number of fingers the investigator is presenting
If patient is not responsive the visual fields can be tested by visual threat, this
involves the investigator moving an object towards the eye and observing the patient's
response.
186.
187.
4. Facial Palsy
Facial palsy is partial or complete paralysis of portions of the face.
Typically this paralysis is most pronounced in the lower half of one facial side.
However, depending on lesion location the paralysis may be present in other facial
regions.
While inspecting the symmetry of each facial expression:
a. First, the examiner should instruct patient to show his or her teeth (or gums).
b. Second, the patient should be asked to squeeze his or her eyes closed as
hard as possible.
c. After reopening his or her eyes, the patient is then instructed to raise his or
her eyebrows.
188.

189.
S

190.

191.
192.
0

Test results

Normal and symmetrical movement

193. 194.
Minor paralysis; function is less than clearly normal, such as
1
flattened nasolabial fold or minor asymmetry in smile
195.
196.
2

Partial paralysis; particularly paralysis in lower face

197. 198.
Complete facial Hemiparesis, total paralysis in upper and lower
3
portions of one face side
199.
200.
Notes
If the patient is unable to understand verbal commands, the instructions should be
demonstrated to the patient.
Patients incapable of comprehending an commands may be tested by applying
a noxious stimulus and observing for any paralysis in the resulting grimace.
201.
202.
5. Motor Arm
With palm facing downwards, have the patient extend one arm 90 degrees out in
front if the patient is sitting, and 45 degrees out in front if the patient is lying down.
If necessary, help the patient get into the correct position.
As soon as the patient's arm is in position the investigator should begin verbally
counting down from 10 while simultaneously counting down on his or her fingers in
full view of the patient.
Observe to detect any downward arm drift prior to the end of the 10 seconds.
Downward movement that occurs directly after the investigator places the patient's
arm in position should not be considered downward drift. Repeat this test for the
opposite arm. This item should be scored for the right and left arm individually,
denoted as item 5a and 5b.
203.
204.
S
205.
Test results
206. 207.
No arm drift; the arm remains in the initial position for the full 10
0
seconds
208. 209.
Drift; the arm drifts to an intermediate position prior to the end of the
1
full 10 seconds, but not at any point relies on a support

210.
2

211.
Limited effort against gravity; the arm is able to obtain the starting
position, but drifts down from the initial position to a physical support prior
to the end of the 10 seconds

212.
3

213.
No effort against gravity; the arm falls immediately after being helped
to the initial position, however the patient is able to move the arm in some
form (e.g. shoulder shrug)

214. 215.
No movement; patient has no ability to enact voluntary movement in
4
this arm
216.
217.
Notes
Default Coma Score: 8
Test the non paralyzed arm first if applicable

Score should be recorded for each arm separately, resulting in a maximum potential
score of 8.
Motor Arm assessment should be skipped in the case of an amputee, however a
note should be made in the scoring of the amputation.
If patient is unable to understand commands, the investigator should deliver the
instructions via demonstration
218.
219.
6. Motor Leg
With the patient in the supine position, one leg is placed 30 degrees above
horizontal.
As soon as the patient's leg is in position the investigator should begin verbally
counting down from 5 while simultaneously counting down on his or her fingers in
full view of the patient. Observe any downward leg drift prior to the end of the 5
seconds.
Downward movement that occurs directly after the investigator places the patient's
leg in position should not be considered downward drift.
Repeat this test for the opposite leg. Scores for this section should be recorded
separately as 6a and 6b for the left and right legs respectively.
220.
221.
S
222.
Test results
223. 224.
No leg drift; the leg remains in the initial position for the full 5
0
seconds
225. 226.
Drift; the leg drifts to an intermediate position prior to the end of the
1
full 5 seconds, but at no point touches the bed for support

227.
2

228.
Limited effort against gravity; the leg is able to obtain the starting
position, but drifts down from the initial position to a physical support prior
to the end of the 5 seconds

229.
3

230.
No effort against gravity; the leg falls immediately after being helped
to the initial position, however the patient is able to move the leg in some
form (e.g. hip flex)

231. 232.
No movement; patient has no ability to enact voluntary movement in
4
this leg
233.
234.
Notes
Default Coma Score: 8
This is performed for each leg, indicating a maximum possible score of 8
Test the non paralyzed leg first if applicable
Motor leg assessment should be skipped in the case of an amputee, however a note
should be made in the score records
If patient is unable to understand commands, the investigator should deliver the
instructions via demonstration
235.
236.
7. Limb Ataxia
This test for the presence of a unilateral cerebellar lesion, and distinguishes a
difference between general weakness and incoordination.
The patient should be instructed to first touch his or her finger to the examiner's
finger then move that finger back to his or her nose, repeat this movement 3-4
times for each hand.

Next the patient should be instructed to move his or her heel up and down the shin
of his or her opposite leg. This test should be repeated for the other leg as well.
237.
238.
S
239.
Test results

240.
0

241.

Normal coordination; smooth and accurate movement

242.
1

243.

Ataxia present in 1 limb; rigid and inaccurate movement in one limb

244. 245.
Ataxia present in 2 or more limbs: rigid and inaccurate movement in
2
both limbs on one side
246.
247.
Notes
If significant weakness is present, score 0
If patient is unable to understand commands or move limbs, score is 0
Patient's eyes should remain open throughout this section
If applicable, test the un-paretic side first
248.
249.
8. Sensory
Sensory testing is performed via pinpricks in the proximal portion of all four limbs.
While applying pinpricks, the investigator should ask whether or not the patient
feels the pricks, and if he or she feels the pricks differently on one side when
compared to the other side.
250.
251.
S
252.
Test results
253.
254.
0

No evidence of sensory loss

255. 256.
Mild-to-Moderate sensory loss; patient feels the pinprick, however he
1
or she feels as if it is duller on one side

257. 258.
Severe to total sensory loss on one side; patient is not aware he or
2
she is being touched in all unilateral extremities
259.
260.
Notes
Default Coma Score: 2
The investigator should insure that the sensory loss being detected is a result of the
stroke, and should therefore test multiple spots on the body.
For patients unable to understand the instructions, the pinprick can be replaced by
a noxious stimulus and the grimace can be judged to determine sensory score.
261.
262.
9. Language
This item measures the patient's language skills.
After completing items 1-8 it is likely the investigator has gained an approximation
of the patient's language skills; however it is important to confirm this measurement
at this time.
The stroke scale includes a picture of a picture of a scenario, a list of simple
sentences, a figure of assorted random objects, and a list of words.
The patient should be asked to explain the scenario depicted in the first figure.

Next, he or she should read the list of sentences and name each of the objects
depicted in the next figure.
The scoring for this item should be based on both the results from the test
performed in this item in addition to the language skills demonstrated up to this
point in the stroke scale.
263.
264.
S
265.
Test results
266.
267.
0

Normal; no obvious speech deficit

268. 269.
Mild-to-moderate aphasia; detectable loss in fluency, however, the
1
examiner should still be able to extract information from patient's speech
270. 271.
Severe aphasia; all speech is fragmented, and examiner is unable to
2
extract the figure's content from the patients speech.

272.
273.
Unable to speak or understand speech
3
274.
275.
Notes
Default Coma Score: 3
Patients with visual loss should be asked to identify objects placed in his or her
hands
This is an exception to recording only the patients first attempt. In this item, the
patients best language skills should be recorded
276.
277.
10. Speech
Dysarthria is the lack of motor skills required to produce understandable speech. It
is strictly a motor problem, and is not related to the patient's ability to comprehend
speech.
Strokes that cause dysarthria typically affect areas such as the anterior opercular,
medial prefrontal and premotor, and anterior cingulate regions.
These brain regions are vital in coordinating motor control of the tongue, throat,
lips, and lungs.
To perform this item the patient is be asked to read from the list of words provided
with the stroke scale while the examiner observes the patients articulation and
clarity of speech.
278.
279.
S
280.
Test results
281.
282.
0

Normal; clear and smooth speech

283. 284.
Mild-to-moderate dysarthria; some slurring of speech, however the
1
patient can be understood

285. 286.
Severe dysarthria; speech is so slurred that he or she cannot be
2
understood, or patients that cannot produce any speech
287.
288.
Notes
Default Coma Score:2
An intubated patient should not be rated on this item, instead make note of the
situation in the scoring documents.

289.
290.
11. Extinction and Inattention
Sufficient information regarding this item may have been obtained by the examiner
in items 1-10 to properly score the patient.
However, if any ambiguity exist the examiner should test this item via a technique
referred to as "double simultaneous stimulation".
This is performed by having the patient close his or her eyes and asking him or her
to identify the side on which they are being touched by the examiner.
During this time the examiner is alternating between touching the patient on the
right and left side. Next, the examiner touches the patient on both sides at the
same time.
This should be repeated on the patients face, arms, and legs.
To test extinction in vision, the examiner should hold up one finger in front of each
of the patient's eyes and ask the patient to determine which finger is wiggling or if
both are wiggling.
The examiner should then alternate between wiggling each finger and wiggling both
fingers at the same time.
291.
292.
S
293.
Test results

294.
0

295.

296.
1

297.
Inattention on one side in one modality; visual, tactile, auditory, or
spatial

Normal; patient correctly answers all questions

298. 299.
Hemi-inattention; does not recognize stimuli in more than one
2
modality on the same side.
300.
301.
Notes
Default Coma Score: 2
Patient with severe vision loss that correctly identifies all other stimulations scores a
0
302.
303.
304.

Board Review: Sarah J. Currorullo

DIAGNOSTIC TOOLS

305.
308.

CT SCAN

306.
INFARCTIO
N
- Focally decrease
density
(hypodense)
=
darker
than
normal
309.
Black
- Not
seen
immediately
(unless there is a
mass effect)
- May be seen after
24 hrs. (due to
increase edema);

307.
HEMORRH
AGE
- Blood
- Hyperdense
(radio-opaque
310.
White
- Seen immediately

311.

MRI

seen best 3-4

days
- Edema
- Fluid: high signal
density
312.
White
- Can
be
seen
immediately
as
bright area on T2
= edema = water

Blood
Low
signal
density
313.
Black (on
either T1-T2)

314.
315.
1. Head CT Scan
316. Major role in evaluating presence of blood (cerebral hemorrhage or
hemorrhagic infarction), especially when thrombolysis is being considered.
If an intracranial hemorrhage (ICH) is suspected, a head CT without contrast is the
study of choice. This avoids confusing blood with contrast, as both appear white
on CT scan.
317. Cerebral Infarction:
Regardless of stroke location or size, head CT studies are often normal during the
first few hours after brain infarction.
The infarcted area appears as a hypodense (black) lesion usually after 2448
hours after the stroke (occasionally positive scans at 36 hours l subtle CT changes
may be seen early with large infarcts, such as obscuration of gray-white matter
junction, sulcal effacement, or early hypodensity).
Hypodensity initially mild and poorly defined; edema better seen on third or fourth
day as a well-defined hypodense area.
Head CT with contrast: IV contrast provides no brain enhancement in day 1 or 2,
as it must wait for enough damage to the blood brain barrier; more evident in 12
weeks. Changes disappear 2 to 3 months later.
Some studies suggest worse prognosis for patients receiving IV contrast early.
Hemorrhage can occur within an infarcted area where it will appear as a
hyperdense mass within the hypodense edema of the infarct.
318. Hemorrhagic Infarct:
High density (white) lesion seen immediately in ~ 100% of cases. Proven to be
totally reliable in hemorrhages 1 cm or larger in diameter. Demonstration of clot
rupture into the ventricular system (32% in one series) not as ominous as once
thought.
319. Subarachnoid Hemorrhage:
Positive scan in 90% when CT performed within 45 days (may be demonstrated
for only 810 days). SAH can really be visualized only in the acute stage, when
blood is denser (whiter) than the cerebrospinal fluid (CSF).
Appears as a hyperdense (or isodense) area on CT scanlook for blood in the
basal cisterns or increased density in the region around the brainstem. May
sometimes localize aneurysm based upon hematoma or uneven distribution of
blood in cisterns.
Once diagnosis of SAH has been established, angiography is generally performed
to localize and define the anatomic details of the aneurysm and determine if other
aneurysms exist.
320.
2. Brain MRI Scan
321. More sensitive than CT scan in detecting ischemic infarcts (including small
lacunes) and posterior cranial fossa infarcts (images are not degraded by bone
artifacts) Edema due to ischemia detected earlier than with CTwithin a few
hours of onset of infarct.
322. Cerebral Infarction:
Early, increased (white) signal intensity on T2-weighted images, more pronounced

at 24 hours to 7 days. Tl-weighted images may show mildly decreased signal.

Chronic (21 days or more)decreased Tl- and T2-weighted signals
323. Intracerebral Hemorrhage:
Acute hemorrhage: decreased (black) signal or isointense on Tl- and T2-weighted
images
Edema surrounding hemorrhage appears as decreased intensity on Tl-weighted
image; increased (white) signal on T2 images.
As hemorrhage ages, it develops increased signal on Tl and T2 images
324. Subarachnoid or Intraventricular Hemorrhage:
Acutely low signal (black) on Tl and T2 images
325. Lacunes:
CT scan documents most supratentorial lacunar infarctions, and MRI successfully
documents both supratentorial and infratentorial infarctions when lacunes are 0.5
cm or greater
326.
3. Carotid Ultrasound
327. Real time B-mode imaging; direct Doppler examination. Screening test for
carotid stenosis; identification of ulcerative plaques less certain. Useful in following
patients for progression of stenosis.
328.
4. Transcranial Doppler
329. Low-frequency Doppler sound wave used to insonate basal cranial vessels
through temporal bone, orbit, foramen magnum.
Velocity and direction of blood flow in all vessels of Circle of Willis may be
identified.
Detects vasospasm and intracranial collateral pathways.
330.
5. Angiography
331. Includes conventional angiography, magnetic resonance angiography
(MRA), and intraarterial digital subtraction angiography (DSA). These studies
evaluate extracranial and intracranial circulation.
Valuable tools for diagnosing aneurysms, vascular malformations, arterial
dissections, narrowed or occluded vessels, and angiitis.
Complications occur in 212%. Include aortic or carotid artery dissection,
embolic stroke, vascular spasm, and vascular occlusion.
Morbidity associated with procedure: 2.5%.
Carotid and vertebral angiography are the only certain means of demonstrating
an aneurysm.
Positive in 85% of patients with clinical SAH
DSA studies safer; may be performed as outpatient.
332. MRA:
Can reliably detect extracranial carotid artery stenosis.
May be useful in evaluating patency of large cervical and basal vessels.
Detects most aneurysms on the basal vessels; insufficient sensitivity to replace
conventional angiography.
333.
6. Transthoracic Echocardiography (TTE)/Transesophageal
Echocardiography (TEE)
334. TTE can quickly assess heart valves and ejection fraction.
TEE superior for evaluating aorta, pulmonary artery, heart valves, atria, atrial
septum, left atrial appendage, and coronary arteries; TEE also used for detection of
patent foramen ovale.
Using cardiac catheterization and/or operation as a gold standard, contrast TEE
was found to be more sensitive (100% vs 63%, p < 0.005) and accurate (97% vs
78%, p < 0.05) than contrast TTE in the detection of PFO (Chen, 1992).
335.
7. Lumbar Puncture (LP)
336. Can detect blood in the CSF.
Primarily in subarachnoid hemorrhage when head CT is not available or,
occasionally, when CT is negative and there is high clinical suspicion.

337.
338.
339.
340.
341.
PHARMACOLOGICAL MANAGEMENT
342.

VIII MANAGEMENT

343.
Medications Commonly Used to Treat Patients with Stroke
344.
Thrombolytics (Alteplase [Activase or tPA]): Converts
plasminogen to plasmin, degrades fibrin present in clots,
dissolves clots and reestablishes blood flow (e.g., lysis of
thrombi causing ischemic stroke; also to dissolve clots in
coronary arteries, pulmonary emboli, deep vein thrombosis).
345.
Possible adverse effects: The most common complication
is bleeding and brain hemorrhage.
346.
347.
Anticoagulants (e.g., warfarin [Coumadin], heparin,
dabigatran etexilate [Pradaxa]): Used to reduce the risk of
blood clots and prevent existing clots from getting bigger by
thinning the blood; indications include DVT prophylaxis, stroke
prevention, peripheral vascular disease. With Coumadin,
clotting times are closely monitored. Heparin is given
intravenously and is faster acting.
348.
Possible adverse effects: Increased risk of bleeding and
hemorrhage, hematomas.
349.
350.
Antiplatelet therapy (e.g., acetylsalicylic acid [aspirin];
clopidogrel bisulfate [Plavix]; dabigatran etexilate [Pradaxa];
ticlopidine hydrochloride [Ticlid]): Prevent platelets (blood
cells) from sticking together; long-term, low-dose is used to
decrease the risk of thrombosis and recurrent stroke; higher
doses may be used in place of anticoagulants and may be
recommended for patients with atrial fibrillation.
351.
Possible adverse effects: Increased risk of gastric ulcers
and bleeding.
352.
353.
Antihypertensive agents (e.g., ACE inhibitors, alphablockers [Minipress], beta-blockers, calcium channel blockers,
direct
vasodilators,
diuretics,
postganglionic
neuron
inhibitors): Used to control hypertension.
354.
Possible adverse effects: Dizziness, hypotension, among
other symptoms.
355.
356.
Angiotensin II receptor antagonists (telmisartan
[Micardis], losartan potassium [Cozaar]): Block angiotensin II,
a chemical that triggers muscle contraction around blood
vessels, narrowing them; enlarges blood vessels and reduces
blood pressure.
357.
Possible adverse effects: Dizziness, hypotension, among
other symptoms.
358.

359.
Anticholesterol agents/statins (atorvastatin calcium
[Lipitor], rosuvastatin calcium [Crestor], Zocor, Mevacor,
Lescol): Lower cholesterol by inhibiting the enzyme in the
blood that produces cholesterol in the liver; for management
of hypercholesterolemia and mixed dyslipidemias.
360.
Possible adverse effects: Dizziness, headache, insomnia,
weakness.
361.
362.

Antispasmodics/spasmolytics
(e.g.,
carisoprodol
[Soma], chlorzoaxazone [Parafon Forte], cyclobenzaprine
[Flexeril],
diazepam
[Valiu],
methocarbamol
[Robaxin],
orphenadrine [Norflex/Norgesic]): Used to relax skeletal
muscle and decrease muscle spasm.
363.
Possible adverse effects: May cause drowsiness,
dizziness, dry mouth, among other symptoms.
364.
365.
Antispastics (e.g., baclofen [Lioresal], dantrolene
sodium [Dantrium], diazepam [Valium], tizanidine [Zanaflex]):
Used to relax skeletal muscle and decrease muscle spasm.
366.
Possible adverse effects: May cause drowsiness,
dizziness, confusion, weakness, among other symptoms.
367.
368.
Anticonvulsants (e.g., carbamazepine [Tegretol],
clonazepam [Klonopin], diazepam [Valium], phenobarbital
[Luminal], phenytoin [Dilantin]): Used to control seizures; act
as a generalized CNS depressant.
369.
Possible adverse effects: May cause drowsiness, ataxia,
sedation, among other symptoms.
370.
371.
Antidepressants (e.g., fluoxetine [Prozac], monoamine
oxidase
inhibitors,
sertraline
[Zoloft],
tricyclics
[Amitriptyline]):
372.
Used to control depression. Possible adverse effects: May
cause anxiety, tremor, insomnia, nausea.

373.
374.
375.
MEDICAL MANAGEMENT
376.
377.
Medical management of completed stroke includes strategies to achieve the
following:
378. Improve cerebral perfusion by reestablishing circulation and oxygenation
and assist in stopping progression of the lesion to limit deficits. Oxygen is delivered
via mask or nasal cannula. Patients in a coma may require intubation or assisted
ventilation and suctioning.
379. Maintain adequate blood pressure. Hypotension or extreme hypertension is
treated; antihypertension agents have the added risk of inducing hypotension and
decreasing cerebral perfusion.
380. Maintain sufficient cardiac output. If the causes of stroke are cardiac in
origin, medical management focuses on control of arrhythmias and cardiac
decompensation.
381. Restore/maintain fluid and electrolyte balance.

382. Maintain blood glucose levels within the normal range.

383. Control seizures and infections.
384. Control edema, intracranial pressure, and herniation using antiedema
agents. Ventriculostomy may be indicated to monitor and drain cerebrospinal fluid.
385. Maintain bowel and bladder function, which may include urinary catheter.
Catheterization is typically short-term but may be long-term with the patient in
coma.
386. Maintain integrity of skin and joints by instituting protective positioning, a
turning schedule every 2 hours, and early physical and occupational therapy.
387. Decrease the risk of complications such as DVT, aspiration, decubitus
ulcers, and so forth.
388.
SURGICAL MANAGEMENT
389.
390.
Emergency procedures. Doctors sometimes treat ischemic strokes with
procedures that must be performed as soon as possible, depending on features of
the blood clot:
Medications delivered directly to the brain. Doctors may insert a long, thin
tube (catheter) through an artery in your groin and thread it to your brain to deliver
TPA directly into the area where the stroke is occurring. The time window for this
treatment is somewhat longer than for intravenous TPA but is still limited.
Mechanical clot removal. Doctors may use a catheter to maneuver a tiny device
into your brain to physically break up or grab and remove the clot.
391.
Other procedures. To decrease your risk of having another stroke or
transient ischemic attack, your doctor may recommend a procedure to open up an
artery that's narrowed by fatty deposits (plaques). Doctors sometimes recommend
the following procedures to prevent a stroke. Options will vary depending on your
situation:
Carotid endarterectomy. In a carotid endarterectomy, a surgeon removes
plaques from arteries that run along each side of your neck to your brain (carotid
arteries). In this procedure, your surgeon makes an incision along the front of your
neck, opens your carotid artery and removes plaques that block the carotid artery.
392.
Your surgeon then repairs the artery with stitches or a patch made from a
vein or artificial material (graft). The procedure may reduce your risk of ischemic
stroke. However, a carotid endarterectomy also involves risks, especially for people
with heart disease or other medical conditions.
Angioplasty and stents. In an angioplasty, a surgeon gains access to your carotid
arteries most often through an artery in your groin. Here, he or she can gently and
safely navigate to the carotid arteries in your neck. A balloon is then used to expand
the narrowed artery. Then a stent can be inserted to support the opened artery.

393.
Hemorrhagic Stroke
394.
Surgical blood vessel repair. Surgery may be used to repair blood vessel
abnormalities associated with hemorrhagic strokes. Your doctor may recommend
one of these procedures after a stroke or if an aneurysm or arteriovenous
malformation (AVM) or other type of vascular malformation caused your
hemorrhagic stroke:

Surgical clipping. A surgeon places a tiny clamp at the base of the aneurysm, to
stop blood flow to it. This clamp can keep the aneurysm from bursting, or it can
prevent re-bleeding of an aneurysm that has recently hemorrhaged.

Coiling (endovascular embolization). In this procedure, a surgeon inserts a

catheter into an artery in your groin and guides it to your brain using X-ray imaging.
Your surgeon then guides tiny detachable coils into the aneurysm (aneurysm coiling).
The coils fill the aneurysm, which blocks blood flow into the aneurysm and causes the
blood to clot.

Surgical AVM removal. Surgeons may remove a smaller AVM if it's located in an
accessible area of your brain, to eliminate the risk of rupture and lower the risk of
hemorrhagic stroke. However, it's not always possible to remove an AVM if its removal
would cause too large a reduction in brain function, or if it's large or located deep
within your brain.
Intracranial bypass. In some unique circumstances, surgical bypass of intracranial
blood vessels may be an option to treat poor blood flow to a region of the brain or
complex vascular lesions, such as aneurysm repair.
Stereotactic radiosurgery. Using multiple beams of highly focused radiation,
stereotactic radiosurgery is an advanced minimally invasive treatment used to repair
vascular malformations.
395.
PHYSICAL THERAPY MANAGEMENT
396.
397.
Techniques of Treatment: Approximately 48 hours after stroke, i.e., after
ensuring completion o stroke, if patients is medically stable and alert, bedside
physical therapy may be started.
398.
The techniques employed depend on the stage of recovery the patient has
reached, or at which the process of recovery has become arrested.
399.
The Stages are:
400.
1. Acute/ initial flaccid stage: Lasts from a few days to several weeks and
may be longer.
401.
2. Stage of spasticity
402.
3. Stage of relative recovery
403.
Dos:
Position the patient to avoid pressure sore, contracture and over stretching of joint
structures.
Change the position once in two hours from affected side to unaffected and to
supine.
Have a firm mattress and height adjustable to enable easy transfer.
404.
Donts
No foot boards, due to danger of increased spasticity and equinus
Position the bed, is such a way that the patient will neglect his affected side

Speech language therapy for patient with problems on understanding speech or

written word, difficulty on formulation words and problems in eating.
Assistive technology (wheel chair)
Electrical stimulation prevent muscle atrophy
TENS decrease muscle pain
FES to facilitate gains in voluntary motor control, muscle strength and reduction of
spasticity.
Electromyographic Biofeedback (EMG-BFB) used to improve motor function in
patients with hemiplegia.
Stretching stretch contracted muscles.
ROM Exercise maintains joint integrity.
Roods technique for modification of muscle tone and voluntary motor activity
through use of cutaneous sensory stimulation.
Bobath technique postures appropriate for task. Suppress synergies with sensory
input and motor feedback.
Ankle foot orthosis to control deficient knee and ankle/foot function.
405.

406.
Exercises: These includes:
407. 1. PROM to the involved extremities, active resisted exercises to the
unaffected extremities
2. Bed mobility turning in bed on his own, assisted or bridging
3. Progressive mobilization include head and trunk control, sitting balance.
Involvement of family members can assist in feeding and other ADLs
Foley catheter removed as soon as possible. Constipation avoided through
hydration, diet, activity.
Transfer bed to chair/wheelchair (in the initial stage)
Standing balance>
408.
Lower Extremity Management
409. The ultimate goal is to make the patient ambulant and as independent as
possible. Due to the dominant extensor synergy in the lower limb. The patient
stands on his/her spasticity and ultimately walks independently in most occasions.
410. 1. Goof dynamic sitting and standing balance, return of adequate voluntary
control of the lower limb and absence of contracture of hip/knee and ankle are
pre0requisites for ambulation. Walking too early may increase spasticity.
2. Weight bearing in the upright position is preceded by activity designed to
promote good sitting balance and ability to transfer from sitting to standing without
stimulation abnormal spastic reactions.
3. The ankle dorsiflexors and evertors are the last to show improvement in function.
Assistive devices like AFO, quadripod canes with rubber tips may help improve the
gait.
4. Gait training should be provided on a variety of surfaces, and stairs. Patients
should be taught safety skills for falling and getting up from the floor.
5. Newer techniques Boifeedback FES
411.
Upper Extremity Management
412. In moat strokes the upper limb is the hardest hit. Lack of movement and
sensation especially in the dominant arm is frightening and frustrating for the
patient.
413. 1. Formal evaluation by the OT must be made as early as possible and
repeated at intervals. The OT also employs and teaches PROM exercise for the
affected upper lim. Active ROM exercise, co-ordination, gaining voluntary control
and dexterity exercises are added as motor function improves. Muscle re-education,
including PNF, Bio feed EMG back and FES may be employed.
2. Training and modifications in ADL using custom made devices to assist in various
activities.
3. A resting hand splint may be used to prevent joint contracture secondary to
abnormal posturing or to decrease tone in the spastic hand. However these are
contraindicated in patients with significant voluntary movement or in a flaccid hand.
4. Specific problems related to the upper limb like shoulder sublaxtion, shoulder
hand syndrome, brachial plexus and other peripheral nerve injuries are treated.
5. A recent hypothesis is that final recovery in the involved upper limb may be
inhibited by learned non-user substitution by the involved limb. Forced used of
the involved upper limb, is advocated thus retraining the involved arm and creating
the need for function.
414.
Sitting in Bed
415. 1. The patient should be as upright as possible with the head and trunk in line
and his weight evenly distributed on both buttocks.
2. The affected arm is protracted at the shoulder, both hands are clasped together
and placed forward on a bed table.
416.
Activities in Sitting
417. The patient should be moved into sitting as soon as possible to stimulate
balance reactions and proprioception.
418. 1. Weight transference from side to side, feet unsupported.
2 Standing from a chair.

419.
Activities in Standing
420. Correct weight bearing at early stage provides good afferent stimulation and
is most effective way for normalizing tone.
421. 1. Weight Bearing on the affected leg.
2. Releasing the knee and moving the hemiplegic leg (preparation for the swing
phase of gait)
3. Stairs climbing stairs at an early stage, even before independent gait is
achieved, is both therapeutic and functional.
4. Activities on the balance board the tilt board is essential when re-educating
correct transference of weight.
422.
Activities for the Recovering Arm
423.
In Lying
424. 1. Elevation of arm fully and asking the patient to let it stay there.
2. Ask patient to touch head and place his hand on the opposite shoulders.
3. Elbow flexion, extension.
425.
In Sitting
426. 1. protective extension sideways.
2. Holding a towel and swinging it freely.
3. Drawing a figure with help of therapists hand.
427.
Stage of Spasticity
428. When spasticity has developed, the process of recovery is often arrested. It is
at this stage that most patients with residual hemiplegia come for rehabilitation.
The gradual development of spasticity occurs during the first stage, i.e. the
mainly flaccid stage. The treatment during the first and second stages, therefore,
overlaps, and some treatment done in supine, for instance, will have to be
continued, but progressed towards sitting and standing.
Spasticity usually develops slowly with a predilection for the flexors muscles
of the upper, and the extensors muscles of the lower limbs. It usually increases with
the patients activities and use effort throughout the first 18 months.
429.
Treatment at the Spastic Stage
430. Breaking up of the total patterns.
431.
Ice to reduce spasticity
Crushed or shaved ice should be mixed with just sufficient water to allow the
hand to be easily submerged
Stroking or teasing the hand or foot with a piece of ice.
432.
Pressure Tapping
433. With fingers pressed together, tapping firmly over the dorsum and lateral
aspect of the patients foot encourages dorsiflexion. Elbow and hip extension can
also be facilitated by tapping
434.
Stage of Relative Recovery
435. These patients should now be able to walk unaided, i.e. without using a stick
to walk or without the need to use the affected arm for support and to hold an
object in the hand if it placed into it.
436.
Treatment for Standing up
437. 1. When practicing to stand-up, the patient should be made to carry as much
of his weight as possible on the affected leg.
2. The therapist can put her foot lightly on the patients foot. The patient is then
encouraged to lean well forward at the hips, so that he starts putting weight on both
his legs before he actually stands-up
438.
Treatment for Walking
439. 1 When walking with the patient, the therapist, nurse or relatives should
never be on his sound side as the patient himself can balance and control his
movements on that side.
2. The patient should be able to manage with an ordinary walking stick.
3. Bracing may be used

440.
Treatment to Improved the Patients Gait
441. 1. Full dorsiflexion of ankle and toes is essential for normal walking and for
heel to strike.
2. He should keel the heel of the affected leg down on the floor.
3. Walking backwards and forwards should be practiced alternately.
442.
Outcome
443. Out of those inpatients who survive longer than one month after stroke, 10%
experience an almost complete spontaneous recovery. Another 10% do not benefit
from any form of treatment because of the severity of disability; it is the remaining
80% with significant neurological deficits, who will benefit from rehabilitation.
444.
Support and Braces
445. 1. The subluxation of the scapulohumeral joint, common in hemiplegia, can
be prevented by the use of an appropriate sling as soon as the patient begins to sit
up, proper positioning while lying.
2. A drop foot or unstable knee should be supported with suitable bracing.
3. FES/AFO and shoe modifications.
446.
Speech
447. Spontaneous recovery is known to occur up to 2 weeks following the stroke.
However, early and accurate diagnosis of the communication disability is essential.
448.
Cognitive Aspects
449. There are significant differences in cognitive abilities between patients with
(L) hemiplegia and those with (R) hemiplegia. The (L) hemiplegic patient lack insight
and judgement. Learning is impaired and neglect is more common, hence cognitive
retraining is difficult. The (R) hemiplegic patient may be unable to communicate
effectively but retains the ability to learn from mistakes and from observing others.
The (R) hemiplegic exhibits more unilateral neglect. Cognitive retraining is with
team approach includes OT speech therapists and psychologist.
450.
Language
451. A speech pathologists should be consulted to evaluate the extent of the
individuals speech problems and then recommended therapy.
1. All persons in contact with the aphasic stroke patient should contribute to his
language redevelopment by speaking to him frequently in slow, precise and quiet
tones.
2. One concept sentences are more likely to be understood.
452.
Mobility aids: One arm propelled wheelchair.
453.
Home Modifications
454. The social worker may also make inquiries into physical layout of the house,
family members living at home, and availability of local assistance
455.
Precautions during Bathing
456. 1. Should test the bating water with his unaffected arm.
2. Bath oils and salts should be avoided as they make the floor slippery.
3. Non-slip rubber mat is a wise safety measure.
4. Grab rail along the bath wall.
5. Non-slip toweling mat on the floor.
6. Items should be within reach.
457.
Toilet
458. 1. Recommending suitable methods for managing hygiene one handed.
2. By ensuring that the tap is within easy reach
459.
Undressing and Dressing
460. Ideally clothing should be loose fitting, easy to take off and put on but
not so large that they hamper activity.
461.
Vocational Rehabilitation
462. Stroke outcome studies vary on the reports of successful return to work.
Routine sexual counselling and professional advice regarding sexual activities must
be included in the rehabilitation program. This depends on the age, inhibitions and
mental makeup of patient.

The role of the rehabilitation social worker is crucial and he should be

involved as aresources and support person.
Poststroke depression and anxiety are very real problems and should be dealt
with aggressively
463.
464.
Sequential Recovery Stages in Hemiplegia
Stage 1 recovery from hemiplegia occurs in stereotyped sequence of events that begins
with a period of flaccidity immediately following the acute episode. No movement of the
limbs can be elicited.
Stage 2 as recovery begins, the basic limb synergies or some of their components may
appear as associated reactions, or minimal voluntary movement responses may be
present. At this time, spasticity begins to develop.
Stage 3 thereafter, the patient gains voluntary control of movements synergies,
although full range of all synergy components does not necessarily develop. Spasticity
has further increased and may become severe.
Stage 4 some movements combinations that do not follow the path of either synergy
are mastered, first with difficulty, then with more ease, and spasticity begins to decline.
Stage 5 if progress continues more difficult movement combinations are learned as the
basic limb synergies lose their dominance over motor acts.
Stage 6 with the disappearance of spasticity, individual joint movements become
possible and coordination approaches normal. From here on, as the last recovery step,
normal motor function is restored, but this last stage is not achieved by all, for the
recovery process can plateau at any stage.
Main Recovery Stages (Bobath)
Initial Flaccid stage
Stage of Spasticity
Stage of Relative Recovery
465.
466.

IX. REFERENCES

467.

o Books
Acute Care Handbook for Physical Therapists 2E Jaime C. Paz,

468.

Michele P. West
Adams and Victor's Principles of Neurology, 10th Edition Allan

H. Ropper, Martin A. Samuels, Joshua P. Klein

Braddom's Physical Medicine & Rehabilitation 5th E
DeLisa's Physical Medicine & Rehabilitation, 5E
Physical Rehabilitation - Schmitz, Thomas, O'Sullivan, Susan,

Fulk, George
Marieb Human Anatomy & Physiology 9th Edition Elaine N.

Marieb, and Katja Hoehn

Handbook of Pathophysiology - Joan P. Frizzell
PT-OT Reviewer Ramona Luisa Pablo-Santos
Physical Medicine and Rehabilitation Board Review 2E Sara J.

Cuccurullo
o Website
o
http://emedicine.medscape.com/article/2172609-overview