Chapter 14. Level of Consciousness “ the most critical clinical index of nervous system function,...

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Transcript of Chapter 14. Level of Consciousness “ the most critical clinical index of nervous system function,...

Chapter 14

Level of Consciousness“ the most critical clinical index of nervous system function, with changes indicating either improvement or deterioration of the individual’s condition”

Table 14-3 Levels of Altered Consciousness

Alterations in Cognitive NetworksFull consciousness: awareness of self and

the environment

Arousal: state of awakenessMediated by the reticular activating system

Content of Thought: all cognitive functionsAwareness of self, environment and affective states (moods)

Alterations in ArousalCauses Table 14-1 & 14-2

StructuralDivided by location above or below tentorial plate

MetabolicPsychogenic

Alterations in ArousalPathological processes

Infectious, vascular, neoplastic, traumatic, congenital, degenerative, polygenic

MetabolicHypoxia, electrolyte disturbances, hypoglycemia, drugs and toxins

Alterations in Arousal“range from slight drowsiness to coma”

Coma – produced by eitherBilateral cerebral hemisphere damage or

suppressionBrain 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 consciousness2) Pattern of breathing

- Post hyperventilation apnea (PHVA) - Cheyne–Stokes 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 responsesIsoelectric EEG: 6 to 12 hours without hypothermia/depressant drugs

Cerebral Death “death exclusive of brain stem and

cerebellum”

No behavioral or environmental responsesBrain continues to maintain internal

homeostasisSurvivors

ComaVegetative 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 depolarizationHyperthermia, 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 – relaxationInhibitory neurons of cortex, anterior

thalamus and basal ganglia

Alterations in Awareness

MemoryRetrograde amnesia – past memoriesAntegrade amnesia – new memoriesTemporary or permanent (severe head injury or

Alzheimer disease)

Executive attention deficits Inability to maintain sustained attention Inability to set goals Working memory deficitTable 14-6 Clinical manifestations

Memories:amygdala hippocampus thalamus prefrontal cortex

Data Processing Deficits Agnosia – failure to recognize the form

and nature of an object: CVATactile, visual, auditory

Dysphasia – inability to arrange words in logical order: CVA (middle cerebral artery-L cerebral hemisphere)

Expressive – cannot find words, difficulty writing (Broca’s 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

DementiaDegeneration 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*

TheoriesMutation for encoding amyloid precursor proteinAlteration in apolipoprotein E*Loss of neurotransmitter of choline

acetyltransferase

Alzheimer Disease (AD)Neurofibrillary tangles

Senile plaques

Clinical manifestationsForgetfulness, emotional upset, disorientation,

confusion, lack of concentration, decline in abstraction, problem solving and judgment

Diagnosis – R/O other causes

Burden of Alzheimer’s Disease5.4 million Americans 16 million by 20506th leading cause of death:#prevented, cured, slowed>/= 65y/o average survival: 4-8 yrs, may up to 20yrsCaregivers burden: 60% emotional stress

: 30%depressedCost 2011: $183 billion $1 trillion by 2050

J.Alzheimer’s Assoc. March 2011

Know the SignsMemory loss that disrupts daily lifeTrouble planning or solving problemsDifficulty completing tasksConfusion with time or placeTrouble understanding images and spatial

relationshipsNew problems with speaking or writing wordsMisplacing things and inability to retrace

stepsDecreased or poor judgment

Know the SignsSocial 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

GeneralAutoregulation - blood vessel

diameter to maintain a constant blood flow is lost with ↑ ICP

↑ vasoconstriction to elevate BP > ICPa) ↓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 productionObstruction

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 pathwayDopamine: inhibitory neurotransmitterAcetylcholine: stimulatory neurotransmitter

IMBALANCE of” neurotransmitters motor modulation”

Ach________________Dopamine

Parkinson Disease

Parkinson Disease Clinical manifestations

Tremor at restRigidity (muscle stiffness)Bradykinesia (poverty of movement)Postural disturbanceDysarthria (uttering of words)Dysphagia (difficulty swallowing)Progressive dementia

Parkinson Disease