Neuro: Lesions

PRINCIPLES SPINAL CORD LESIONS: Can be contralateral, ipsilateral, or bilateral. See figure below. o Total transection Loss of ALL sensation and motor control bilaterally at all levels below the lesion. o Loss of central portion Loss of ALL sensation and motor control bilaterally at every level below the lesion EXCEPT the sacral dermatomes (sacral sparing). o Hemisection Loss of fine touch/propriocep/vibration (DC/ML) ipsilaterally Loss of crude touch/pain/temp (STT) contralaterally at all levels below the lesion. o Loss of white commissure Loss of crude touch, pain, and temp (STT) bilaterally at the level of the lesion but NOT below the lesion. o Loss of dorsal columns Loss of fine touch, proprioception and vibration (DC/ML) bilaterally o Loss of anterolateral system Loss of crude touch, pain, and temp (STT) bilaterally o Loss of spinocerebellar tracts Ataxia BRAIN STEM LESIONS: Can be contralateral or ipsilateral. o Medial Lesions Loss of contralateral motor control (pyramidal tracts). o Lateral Lesions Loss of crude touch, pain, and temp (TTT) in ipsilateral face Loss of fine touch, proprioception, and vibration (DC/ML) in contralateral half of entire body This occurs because the spinothalamic and spinal trigeminal tracts are adjacent in the lateral part of the brainstem. o Vertebrobasiliar Stroke Lesions Three Ds: Contralateral Dysarthria (DC/ML), Ipsilateral Diplopia (CN6), Ipsilateral Dysphagia (CN9 & 10) CEREBRAL LESIONS: Always contralateral. o Internal Capsule Lesion

Loss of ALL sensation and motor control on contralateral half of body (pyramidal and thalamic somatosensory tracts) Muscle weakness on lower quarter of face (corticobulbar tracts) Ventral lesions present with contralateral homonymous hemianopsia IN ADDITION to these sx if optic radiations are affected Trunk ataxia, abnormal eye movements (diplopia) Ipsilateral limb ataxia, intention tremor, fall toward the side of the lesion

CEREBELLAR LESIONS o Vermis o Hemispheres

UMN vs. LMN LESIONS: Everything is lowered in LMN lesion and ramped up in UMN lesions. Note that fasciculations occur with LMN lesions, NOT UMN!

CENTRAL NERVOUS SYSTEM CEREBRUM

Location of Lesion Non-dominant Parietal Lobe Brocas area BROCAS APHASIA Stroke in MCA. Name of Disease SPATIAL NEGLECT SYNDROME Disease Mechanism

Aphasia, Agnosia, Apraxia

Effects (Relative to Location of Lesion) Cognition: Agnosia of the contralateral side of the world.

Cognition: Influent speech with intact understanding.

Brocas area WERNICKES APHASIA Stroke in MCA. Cognition: Fluent speech with impaired understanding.

Thalamus, Caudate, Occipital Lobe

WEBERS SYNDROME

Stroke in PCA.

Contralateral Body: Loss of pain and temperature sensation due to loss of STT, deficits of CN7, CN9 & CN10, hemiparesis and UMN lesion sx, Parkinsonism due to loss of substantia nigra Contralateral Face: Lower face weakness due to loss of corticobulbar tract. Contralateral Eye: Contralateral hemianopia with macular sparing, Ipsilateral Eye: Horners syndrome due to CN3 deficit (ptosis, fixed pupil, down & out gaze).

CENTRAL NERVOUS SYSTEM CEREBELLUM, LIMBIC SYSTEM, DIENCEPHALON, BASAL GANGLIA

Location of Lesion Vermis Hemisphere Cerebellopontine Angle CEREBELLUM Ataxia ACOUSTIC NEURINOMA Tumor spreads from inner ear to the cerebellopontine angle, where CN7 and CN8 exit the brainstem. Tumor compresses CN7 & CN8. Can also compress CN9, CN10 and corticospinal tracts. Name of Disease Disease Mechanism Effects (Relative to Location of Lesion) Axial Muscles: Truncal ataxia, dysarthria. Appendicular Muscles: Body falls toward ipsilateral side. Ipsilateral Ear: Dizziness, pulsating tinnitus deafness. Loss of higher frequencies first. Contrast with Mienieres disease, which loses lower frequencies first. Ipsilateral Face: Paralysis of facial muscles and loss of corneal reflex (efferent arm) due to loss of CN7. Ipsilateral Body: Ataxia due to loss of CN8 and corticospinal tracts. Throat: Hoarseness and trouble swallowing due to loss of CN9 & 10. Tongue: Loss of taste due to loss of CN7. Behavior: Hyperorality, hypersexuality, disinhibited behavior. Memory: Unable to make NEW memories. Old memories are intact. Cognition: Confusion, ophthalmoplegia, ataxia with memory loss, confabulation, personality changes. Arousal: Reduced arousal and wakefulness. Disinhibition of basal ganglia output. Disinhibition of basal ganglia output. Inhibition of basal ganglia output due to destruction of dopaminergic neurons. Contralateral Limb: Wild, flailing involuntary movements. Chorea (sudden, jerky, dancing movements), athetosis (slow, writing, snake-like movements), aggression, depression, dementia. Often initially mistaken for substance abuse. Muscle rigidity (cogwheel rigidity), bradykinesia, resting tremor (pillrolling between thumb and index finger), expressionless face, stooped posture, shuffling gait, postural instability, dementia.

LIMBIC SYSTEM Anterograde Amnesia & Inappropriate Behavior DIENCEPHALON Vegetative States & Endocrine Imbalance BASAL GANGLIA Dyskinesia

Amygdala (Bilat) Hippocampus Mammillary Bodies (Bilat) Reticular Activating System Subthalamic Nucleus Striatum

KLUVER-BUCY SYNDROME ANTEROGRADE AMNESIA WERNICKE-KORSAKOFF SYNDROME COMA HEMIBALLISMUS HUNTINGTONS DISEASE

Associated with HSV-1.

Substantia Nigra

PARKINSONS DISEASE

** Chorea: Sudden, jerky, dancing movements of limbs. ** Athetosis: Slow, writing, snake-like movements of fingers. ** Myoclonus: Sudden, brief muscle contraction (jerk or hiccup). ** Dystonia: Sustained involuntary muscle contraction (writers cramp, blepharospasm). ** Tremor: Rhythmic contraction and relaxation of muscles in one or more body parts (most often the hands).

CENTRAL NERVOUS SYSTEM - BRAINSTEM

Location of Lesion Midbrain (Level of Superior Colliculi) Name of Disease Disease Mechanism Pinealoma impinges on the midbrain. Effects (Relative to Location of Lesion) Eyes: Paralysis of conjugate vertical gaze.

PARINAUD SYNDROME

pg 387 Midbrain (Level of Inferior Colliculi)

Demyelination of superior cerebellar peduncle, CN4, and MLF. Lesions are random and asymmetric. Note that MS can also affect the cervical spinal cord. MULTIPLE SCLEROSIS

Contralateral Limbs: Intention tremor, dysmetria, dysdiadochokinesia due to loss of superior cerebellar peduncle. Contralateral Eye: Unable to depress while adducted due to loss of CN4 nucleus. Ipsilateral Eye: Internuclear ophthalmoplegia (unable to adduct while gazing away from lesion) due to loss of MLF. Both Eyes: Nystagmus and optic neuritis (sudden loss of vision). Can also have scanning speech due to cerebral lesions. Contralateral Limbs: Upper and lower limbs both have weakness, hyperreflexia, positive Babinski sign due to loss of CST, plus loss of fine touch, vibration, and proprioception due to loss of ML. Contralateral Face: Loss of pain sensation due to loss of TTT. Ipsilateral Face: Paralysis of facial muscles due to loss of CN7. Ipsilateral Eye: Esotropia and inability to abduct due to loss of CN6. Inability to adduct during contralateral gaze due to loss of MLF. Both Eyes: Paralysis of ipsilateral gaze (unable to look toward lesion). Ipsilateral Face: No pain due to loss of spinal trigeminal tract. Ipsilateral Pharynx: No gag reflex due to loss of CN10. Ipsilateral Eye: Horner syndrome due to loss of reticular formation. Contralateral Body: No pain due to loss of STT, plus ataxia and dysmetria due to loss of inferior cerebellar peduncle.

pg 387 Caudal Pons Stroke in basilar artery. Affects the brainstem, cerebellum, thalamus, and occipital cortex. Lesions of the corticospinal tract, medial lemniscus, trigeminothalamic tract, parapontine reticular formation, medial longitudinal fasciculus, CN7, and CN6. Symptoms Include the 3 Ds: Dysarthria, Diplopia, Dysphagia.

VERTEBROBASILAR INSUFFICIENCY

pg 384 Stroke in vertebral artery or PICA. Affects the spinal trigeminal tract, the spinothalamic tract, the inferior cerebellar peduncle, reticular formation, and CN10. LATERAL MEDULLARY (WALLENBERG) SYNDROME

Rostral Medulla

pg 383

** Page numbers refer to Basic Clinical Neuroscience, Young & Tolbert, 2 Edition

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PERIPHERAL NERVOUS SYSTEM CRANIAL NERVES

Location of Lesion CN12 CN11 CN10 Weakening of muscles from lack of innervation. Bells Palsy is a LMN lesion of the facial nucleus or nerve. Remember that each quadrant of the face has its own LMN. LMNs of the upper half of the face have bilateral UMNs, whereas LMNs of the lower half have only one contralateral UMN. Weakening of muscles from lack of innervation. Name of Disease Disease Mechanism Weakening of muscles from lack of innervation. Weakening of muscles from lack of innervation. Effects Ipsilateral Side of Tongue: Tongue deviates toward the side of the lesion (due to unopposed force from the opposite side of the tongue). Ipsilateral SCM and Trapezius Muscles: Unable to turn head to contralateral side of lesion (SCM). Should droop on ipsilateral side of lesion (trapezius). Ipsilateral Pharynx: Uvula deviates away from side of lesion (since the pharynx muscles on that side collapse). Face: UMN lesion results in paralysis of the contralateral lower quarter of the face. LMN lesion (Bells Palsy) results in paralysis of the ipsilateral half of the face.

CN7

BELLS PALSY

CN5 CN3, CN4, CN6

Ipsilateral Pterygoid Muscle: Jaw deviates toward the side of the lesion (due to unopposed force from the opposite pterygoid muscle).

PERIPHERAL NERVOUS SYSTEM SPINAL CORD

Location of Lesion Any Level of the Cord Name of Disease

LMNs = Flaccid Paralysis (HYPOreflexia & Atrophy), UMNs = Spastic Paralysis (HYPERreflexia w/o Atrophy)
Disease Mechanism nd Damage to white commissure (location of the 2 order neurons of the spinothalamic tract). Caused by syringomyelia (which is associated with type 1 and 2 Chiari malformations) or spinal cord cavitation. Effects are isolated to the same dermatome as the lesion; however, the lesion can expand to affect other tracts. Effects SENSORY - Bilateral Body at Level of Lesion: Loss of pain, temp, and crude touch due to loss of STT. Figure shows effects of commissural syndrome at C5-C7.

COMMISSURAL SYNDROME

FRIEDREICHS ATAXIA

Congenital impairment of mitochondrial functioning due to recessive trinucleotide (GAA) repeat mutation in gene coding for frataxin. Demyelination and degeneration of dorsal columns, lateral corticospinal tracts, and spinocerebellar tracts.

Any Level of the Cord

Hemisection of the spinal cord. Affects anterior horn, lateral corticospinal tract, dorsal column, spinothalamic tract, intermediolateral cell column (sym). If the hemisection occurs ABOVE T1 (in the cervical spinal cord), the patient will present with Horners Syndrome IN ADDITION to all the deficits listed in the next column.

*Remember that STT crosses and exits at TWO LEVELS below its origin in the spinal cord.

BROWN-SEQUARD SYNDROME

SENSORY - Bilateral Body at and Below Lesion: Loss of proprioception, DTRs, and vibration due to loss of DC. MOTOR (UMN) Bilateral Body at and Below Lesion: Ataxia due to loss of spinocerebellar tracts and lateral CST. Also associated with nystagmus, dysarthria, pes cavus (high arch of foot), hypertrophic cardiomyopathy, hammer toes, and kyphoscoliosis (in childhood). MOTOR (UMN+LMN) - Ipsilat Body at 2 Levels* Below Lesion: Loss of all sensation due to loss of DC, uncrossed STT, and crossed STT, plus flaccid paralysis (LMN lesion) due to loss of ventral horn. MOTOR (UMN+LMN) - Ipsilat Body 2+ Levels Below Lesion: Loss of fine touch, proprioception, and vibration due to loss of DC, plus loss of pain, temp, and crude touch due to loss of STT, plus spastic paralysis (UMN lesion) due to loss of CST. MOTOR (LMN) Contralateral Body Below Lesion: Loss of pain, temp, crude touch due to loss of crossed STT.

PERIPHERAL NERVOUS SYSTEM SPINAL CORD

Location of Lesion Anterior Horn Name of Disease POLIOMYELITIS OR SPINAL MUSCULAR DYSTROPHY Cervical & Thoracic Cord

LMNs = Flaccid Paralysis (HYPOreflexia & Atrophy), UMNs = Spastic Paralysis (HYPERreflexia w/o Atrophy)
Disease Mechanism Degeneration of LMNs in anterior horn. Poliomyelitis is acquired (from polio infection) whereas spinal muscular dystrophy (aka Werdnig-Hoffmann Disease) is congenital (SMN1 gene mutation). Infants with spinal muscular dystrophy are known as floppy baby and only survive for 7 months. Demyelination of white matter tracts. Affects posterior and lateral columns of the upper thoracic and cervical spinal cord, plus the peripheral nerves and cerebrum. Impairs the DC/ML and lateral corticospinal tracts. Effects MOTOR (LMN) - Fasciculations, atrophy, weakness, fibrillation, hyporeflexia.

Hyporeflexia

B12 DEFICIENCY

AMYOTROPHIC LATERAL SCLEROSIS (ALS) Lou-Gehrigs Disease Dorsal Columns TABES DORSALIS

Defect in superoxide dismutase I (SODI) causes both LMN and UMN lesions with NO SENSORY DEFICITS. Retrograde degeneration of motor neurons (replaced by gliosis).

MOTOR (LMN & UMN): Fasciculations and atrophy. Progressive and fatal with no sensory, cognitive, or occulomotor deficits.

Tertiary neurosyphilis causes degeneration of dorsal columns and dorsal roots.

SENSORY - Bilateral Body at and Below Lesion: Loss of proprioception and loss of DTRs due to loss of DC, locomotor ataxia due to loss of sensory outflow (dorsal roots). Also associated with Charcots joints, shooting pain, Argyll Robertson pupils (accommodate but do not react), positive Romberg sign, and sensory ataxia at night.

PERIPHERAL NERVOUS SYSTEM SPINAL CORD

Location of Lesion Anywhere along the 3-neuron oculosympathetic pathway between the hypothalamus and the eyes & face (see figures below). Name of Disease

LMNs = Flaccid Paralysis (HYPOreflexia & Atrophy), UMNs = Spastic Paralysis (HYPERreflexia w/o Atrophy)
Disease Mechanism Can be caused by anything that damages the sym pathway to the face, including the hypothalamus, intermediolateral cell column, cervical sym chain, internal carotid, ciliary ganglion, or short ciliary nerve. Diseases that can cause this damage include lateral medullary syndrome, otitis media, Pancoast tumor, MS, thyroid cancer, cavernous sinus thrombosis, syringomyelia, or trauma (brachial plexus injury). Effects Ipsilateral Face: Ptosis due to weakening of superior tarsal muscle, plus anhidrosis, flushing, and miosis (constricted and fixed pupil) due to loss of sympathetic innervation.

HORNERS SYNDROME