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Alterations in Cognitive Systems, Cerebral Hemodynamics , and Motor 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”
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Alterations in Cognitive Systems, Cerebral Hemodynamics, and Motor 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 Networks • Full consciousness: awareness of self and the environment • Arousal: state of awakeness • Mediated by the reticularactivatingsystem • 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) - Cheyne–Stokes respiration (CSR) 3) Pupillary changes (size and reactivity) 4) Oculomotor response (position and reflexes) 5) Motor response (skeletal muscle)
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 exclusiveof 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 • Antegradeamnesia – 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
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 (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
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 acetyltransferase
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 Alzheimer’s 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.Alzheimer’s 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 • Cytotoxic: toxic factors → failure NA-K+ transport system: K+ out, H2O in • Ischemic (infarction): vasogenic and cytotoxic → cell necrosis → lysosomes → BBB↑ • 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
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 • Clinical manifestations • Tremor at rest • Rigidity (muscle stiffness) • Bradykinesia (poverty of movement) • Postural disturbance • Dysarthria (uttering of words) • Dysphagia (difficulty swallowing) • Progressive dementia