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Alterations in Cognitive Systems, Cerebral Hemodynamics , and Motor Function

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

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  1. Alterations in Cognitive Systems, Cerebral Hemodynamics, and Motor Function Chapter 14

  2. 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

  3. 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)

  4. Alterations in Arousal • Causes Table 14-1 & 14-2 • Structural • Divided by location above or below tentorial plate • Metabolic • Psychogenic

  5. Alterations in Arousal • Pathological processes • Infectious, vascular, neoplastic, traumatic, congenital, degenerative, polygenic • Metabolic • Hypoxia, electrolyte disturbances, hypoglycemia, drugs and toxins

  6. 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)

  7. 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)

  8. President Lincoln April 14, 1865

  9. Pathway of the bullet

  10. Clinical Manifestations

  11. Clinical Manifestations

  12. Clinical Manifestations

  13. Decorticate & Decerebrate

  14. 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)

  15. Brain death– criteria • No ocular responses • Isoelectric EEG: 6 to 12 hours without hypothermia/depressant drugs

  16. 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

  17. 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)

  18. Conditions - Seizures • Cerebral lesions • Biochemical disorders • Cerebral trauma • Epilepsy

  19. Seizures • Partial (focal/local) • Simple, complex, secondary, generalized • Generalized (bilateral/symmetric) • Unclassified

  20. 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

  21. 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

  22. 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

  23. Memories:amygdalahippocampus thalamusprefrontal cortex

  24. 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

  25. 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

  26. Dementia • Degeneration of neurons • Compression-space occupying lesion • Atherosclerosis • Genes-Alzheimer & Huntington diseases • CNS infection –HIV, Creutzfeldt-Jakob “nerve cell damage and brain atrophy”

  27. 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

  28. 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

  29. 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

  30. 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

  31. Know the Signs • Social withdrawal • Change in mood or personality • Review Table 14-14

  32. Cerebral Hemodynamics • CBF – blood flow • CPP – perfusion pressure • CBV – blood volume • Cerebral oxygenation – “critical factor”

  33. Injury States • ↓ cerebral perfusion • Normal perfusion but ↑ intracranial pressure (ICP) • ↑ cerebral blood volume SO: “must maintain CPP and control ICP”

  34. 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

  35. 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

  36. 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

  37. 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

  38. 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

  39. Michael J Fox

  40. 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

  41. Parkinson Disease

  42. 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

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