Chapter 14

Level of Consciousness
the

most critical clinical index of nervous system function, with changes indicating either improvement or deterioration of the individuals condition

Table 14-3 Levels of Altered Consciousness

Alterations in Cognitive Networks

Full consciousness: awareness of self and the
environment

Arousal: state of awakeness

Mediated by the reticular activating system Content of Thought: all cognitive functions Awareness of self, environment and affective states (moods)

Alterations in Arousal
Causes Table 14-1 & 14-2

Structural

Divided by location above or below tentorial plate Metabolic Psychogenic

Alterations in Arousal
Pathological processes
Infectious, vascular, neoplastic,

traumatic, congenital, degenerative, polygenic

Metabolic

Hypoxia, electrolyte disturbances, hypoglycemia, drugs and toxins

Alterations in Arousal
range from slight drowsiness to coma

Coma produced by either

Bilateral cerebral hemisphere damage or

suppression Brain stem* lesions or metabolic derangement that damages and suppresses the reticular activating system

*midbrain, medulla, pons (Figure 12-5)

Alterations in Arousal
Clinical manifestations : critical for evaluation

extent of brain dysfunction index for identifying or CNS function 1) Level of consciousness 2) Pattern of breathing - Post hyperventilation apnea (PHVA) - CheyneStokes respiration (CSR) 3) Pupillary changes (size and reactivity) 4) Oculomotor response (position and reflexes) 5) Motor response (skeletal muscle)

President Lincoln April 14, 1865

Pathway of the bullet

Clinical Manifestations

Clinical Manifestations

Clinical Manifestations

Decorticate & Decerebrate

Brain Death
never recover nor maintain internal homeostasis

Total Brain Death criteria (5):

(cerebrum, brain stem & cerebellum)
Completion of all appropriate and

therapeutic procedures Unresponsive coma (absence of motor and reflex responses) No spontaneous respirations (apnea)

Brain death criteria

No ocular responses Isoelectric EEG: 6 to 12 hours without

hypothermia/depressant drugs

Cerebral Death
death exclusive of brain stem and

cerebellum
No behavioral or environmental responses

Brain continues to maintain internal homeostasis

Survivors
Coma
Vegetative state (wakeful unconscious state) Minimal conscious state

Locked-in syndrome

Seizures
Sudden, transient alteration of brain function

caused by an abrupt explosive disorderly discharge of cerebral neurons

Alteration in brain function (transient)
Altered level of arousal Convulsion seizure with tonic-clonic movement Epilepsy seizures recur without treatment (5 to

10/1000)

Conditions - Seizures
Cerebral lesions Biochemical disorders

Cerebral trauma
Epilepsy

Seizures
Partial (focal/local)

Simple, complex, secondary, generalized

Generalized (bilateral/symmetric) Unclassified

Seizures
Epileptogenic focus Group of neurons that appear to be

hypersensitive to sudden depolarization

Hyperthermia, hypoxia, hypoglycemia,

hyponatremia, sensory stimulation and certain sleep phases

Aura partial seizure precedes generalized

Prodroma early manifestation hours to days

before

Seizures
Tonic contraction Excitation spreads to subcortical, thalamic and brain stem areas Loss of consciousness

Clonic relaxation Inhibitory neurons of cortex, anterior thalamus and basal ganglia

Alterations in Awareness
Memory
Retrograde amnesia past memories Antegrade amnesia new memories Temporary or permanent (severe head injury or

Alzheimer disease)
Executive attention deficits

Inability to maintain sustained attention Inability to set goals Working memory deficit Table 14-6 Clinical manifestations

Memories:amygdala
thalamus

hippocampus prefrontal cortex

Data Processing Deficits

Agnosia failure to recognize the form and
nature of an object: CVA
Tactile, visual, auditory

Dysphasia inability to arrange words in

logical order: CVA (middle cerebral artery-L cerebral hemisphere)
Expressive cannot find words, difficulty writing

(Brocas area) Receptive language is meaningless (inappropriate words, neologisms) Wernicke

Data Processing Deficits

Dementia*
Progressive failure of cerebral functions that is not

caused by an impaired level of consciousness orienting, memory language and executive attention networks
Table 14-13 Comparison of Delirium & Dementia

Dementia
Degeneration of neurons Compression-space occupying lesion Atherosclerosis Genes-Alzheimer & Huntington diseases

CNS infection HIV, Creutzfeldt-Jakob

nerve cell

damage and brain atrophy

Alzheimer Disease (AD)

Familial onset Early-onset-chromo mutations # 21 (very rare) Late onset-90% cases ? Chromo #19*

Theories
Mutation for encoding amyloid precursor protein Alteration in apolipoprotein E* Loss of neurotransmitter of choline

Alzheimer Disease (AD)

Neurofibrillary tangles Senile plaques Clinical manifestations Forgetfulness, emotional upset, disorientation, confusion, lack of concentration, decline in abstraction, problem solving and judgment Diagnosis R/O other causes

Burden of Alzheimers Disease

5.4 million Americans

16 million by 2050 6th leading cause of death:#prevented, cured, slowed >/= 65y/o average survival: 4-8 yrs, may up to 20yrs

Caregivers burden: 60% emotional stress : 30%depressed Cost 2011: $183 billion $1 trillion by 2050

J.Alzheimers Assoc. March 2011

Know the Signs

Memory loss that disrupts daily life
Trouble planning or solving problems Difficulty completing tasks Confusion with time or place Trouble understanding images and spatial

relationships New problems with speaking or writing words Misplacing things and inability to retrace steps Decreased or poor judgment

Know the Signs

Social withdrawal
Change in mood or personality

Review Table 14-14

Cerebral Hemodynamics
CBF blood flow CPP perfusion pressure CBV blood volume

Cerebral oxygenation

critical factor

Injury States
cerebral perfusion Normal perfusion but intracranial pressure

(ICP)
cerebral blood volume

SO: must maintain CPP and control ICP

Increased Intracranial Pressure (IICP)

intracranial content, edema, excess CSF or

hemorrhage

Normal 5 to 15 mmHg Stages 1-4 (Figure 14-10)

Stage 1 vasoconstriction and external compression

of venous system - ICP (autoregulation) Stage 2

General

Autoregulation -

blood vessel diameter to maintain a constant blood flow is lost with ICP vasoconstriction to elevate BP > ICP
a) O2 CO2 deterioration b) small pupils, neurologic hyperventilation, widened pulse pressure and HR

Local vasodilation 2 to CO2 BV ICP

approaches SBP - perfusion with severe hypoxia/acidosis IICP not evenly distributed throughout the cranial vault

Cerebral Edema
Increase in the fluid (intracellular or extracellular)

within the brain ( volume)

Results: trauma, infection,

hemorrhage, tumor, ischemia, infarct or hypoxia

1) Vasogenic: BBB is disrupted - plasma protein to extracellular space - ICP 2) Cytotoxic: toxic factors failure NA-K+ transport system: K+ out, H2O in 3) Ischemic (infarction): vasogenic and cytotoxic cell necrosis lysosomes BBB 4) Interstitial (hydrocephalus): volume about ventricles

Hydrocephalus (Types Table 14-16)

Excess fluid within the cranial vault,

subarachnoid space or both

Caused by interference in CSF flow

reaborption fluid production

Obstruction
Infancy through adulthood

Spinal Shock
complete cessation of spinal cord function below the lesion
Complete flaccid paralysis

Absence of reflexes
Marked disturbance of bowel and bladder function Days to weeks Return of spinal reflexes

hyperactive spasticity, rigidity

Michael J Fox

Parkinson Disease
After age 40 peak onset 58 62 years 107 to 187 per 100,000 Severe degeneration of the basal ganglia involving

dopaminergic nigrostriatal pathway

Dopamine: inhibitory neurotransmitter Acetylcholine: stimulatory neurotransmitter

IMBALANCE of neurotransmitters motor modulation Ach________________Dopamine

Parkinson Disease

Parkinson Disease
Clinical manifestations Tremor at rest Rigidity (muscle stiffness) Bradykinesia (poverty of movement) Postural disturbance Dysarthria (uttering of words) Dysphagia (difficulty swallowing) Progressive dementia

Parkinson Disease