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RHS 332: Clinical Neurology

RHS 332: Clinical Neurology. Ahmad Alghadir, M.S. Ph.D. P.T. Room: 2071 aalghadir@hotmail.com alghadir@ksu.edu.sa. Recommended texts. S.B. O’sullivan, T.J. Schmitz, Physical Rehabilitation: Assessment and Treatment , F.A. Davis Company. 3 rd ed. 1994.

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RHS 332: Clinical Neurology

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  1. RHS 332: Clinical Neurology Ahmad Alghadir, M.S. Ph.D. P.T. Room: 2071 aalghadir@hotmail.com alghadir@ksu.edu.sa Ahmad Alghadir M.S. Ph.D. P.T.

  2. Recommended texts • S.B. O’sullivan, T.J. Schmitz, Physical Rehabilitation: Assessment and Treatment, F.A. Davis Company. 3rd ed. 1994. • R.L. Braddom, Physical Medicine & Rehabilitation, W.B. Saunders Company. 1st ed. 1996. Ahmad Alghadir M.S. Ph.D. P.T.

  3. Stroke Ahmad Alghadir M.S. Ph.D. P.T.

  4. Introduction • Cerebrovascular accident (CVA): “sudden, focal neurologic deficit resulting from ischemic or hemorrhagic lesions in the brain.” • Deficits: sensory, motor (hemiplegia or hemiparesis), functional, coordination, mental, and language impairments. Ahmad Alghadir M.S. Ph.D. P.T.

  5. “ The location and extent of the lesion and the amount of collateral blood flow determine the severity of neurologic deficits.” Ahmad Alghadir M.S. Ph.D. P.T.

  6. Epidemiology (US) • “The most common cause of adult disability.” • “500,000 new victims each year.” • 30% die during the acute phase. • Of the survivors, 35% have severe disability. • 20% of strokes occur in persons under the age of 65. Ahmad Alghadir M.S. Ph.D. P.T.

  7. Males have a 30% greater incidence of stroke than females. Ahmad Alghadir M.S. Ph.D. P.T.

  8. Etiology • Cerebral thrombosis (blood clot):  occlusion  ischemia  infarction. • Cerebral embolism (foreign body):  occlusion  ischemia  infarction. • Hemorrhage:  ischemia and mechanical injury  infarction. Ahmad Alghadir M.S. Ph.D. P.T.

  9. Risk factors • Hypertension:  rupture  hemorrhage. • Atherosclerosis:  slow blood stream  thrombosis  occlusion  ischemia  atherothrombotic brain infarction (ABI, 57%). • Atherosclerosis:  stenosis  hypertension  rupture  hemorrhage. • Atherosclerosis:  weakness  rupture  hemorrhage. Ahmad Alghadir M.S. Ph.D. P.T.

  10. Elevated blood cholesterol and lipids. • Excessive alcohol consumption. • Transient ischemic attacks. • Physical inactivity. • Heart diseases. • Prior stroke. • Diabetes. • Smoking. • Obesity. Ahmad Alghadir M.S. Ph.D. P.T.

  11. Pathophysiology • Core (focal infarction)  irreversible neuronal death. • Penumbra (surrounding ischemic area) reversible metabolic changes. Ahmad Alghadir M.S. Ph.D. P.T.

  12. Cerebral edema: begins within hours of the insult  reaches a maximum by about 4 days  subsides gradually  disappears by 3 weeks. • Cerebral edema  elevation of intracranial pressure  caudal shift of brain  death (most common cause of death in acute stroke). Ahmad Alghadir M.S. Ph.D. P.T.

  13. Symptoms of stroke result from a restriction of cerebral blood flow (CBF) greater than 80%. Ahmad Alghadir M.S. Ph.D. P.T.

  14. Factors influencing symptoms of stroke include: • “The location of the ischemic process.” • “The size of the ischemic area.” • “The nature and functions of the structures involved.” • “The availability of collateral blood flow” (rapidity of the occlusion). Ahmad Alghadir M.S. Ph.D. P.T.

  15. CBF • CCA  ICA ACA  medial aspect of frontal and parietal lobes. • CCA  ICA MCA  lateral aspect of frontal, parietal, temporal, and occipital lobes. • SA  VA  BA  PCA  medial aspect of temporal and occipital lobes. Ahmad Alghadir M.S. Ph.D. P.T.

  16. Autoregulatory mechanisms • Modulate a constant rate of CBF through the brain (50-60 ml / 100 g of brain tissue / m) (17% of cardiac output). • Blood concentration of O2 and CO2: increase in CO2 or decrease in O2 vasodilation  increase CBF / decrease in CO2 or increase in O2 vasoconstriction  decrease CBF. Ahmad Alghadir M.S. Ph.D. P.T.

  17. Blood pH: fall in pH (increased acidity)  vasodilation  increase CBF / rise in pH (increased alkalinity)  vasoconstriction  decrease CBF. • Blood pressure: fall in pressure  vasodilation  increase CBF / rise in pressure  vasoconstriction  decrease CBF. Ahmad Alghadir M.S. Ph.D. P.T.

  18. Blood viscosity: increase in viscosity  vasodilation  increase CBF / decrease in viscosity  vasoconstriction  decrease CBF. • Local function of brain tissue: increase in function  vasodilation  increase CBF / decrease in function  vasoconstriction  decrease CBF. Ahmad Alghadir M.S. Ph.D. P.T.

  19. Vascular syndromes • ACA stroke: • Occlusion proximal to anterior communicating artery  minimal deficits. • Occlusion distal to anterior communicating artery  • “Contralateral hemiparesis and cortical sensory loss with greater involvement of the lower extremity than upper extremity.” Ahmad Alghadir M.S. Ph.D. P.T.

  20. Memory and behavioral impairments. • Unilateral neglect. • Incontinence. • Apraxia: “inability to perform purposeful movements” (corpus callosum). • Agraphia: “loss of the ability to write” (corpus callosum). Ahmad Alghadir M.S. Ph.D. P.T.

  21. MCA stroke: • “Contralateral hemiparesis or hemiplegia and sensory deficit of the face, arm, and leg, with the face and arm more involved than the leg.” • Loss of conjugate gaze to the opposite side. • Contralateral homonymous hemianopsia. Ahmad Alghadir M.S. Ph.D. P.T.

  22. Unilateral neglect. • Aphasia. Ahmad Alghadir M.S. Ph.D. P.T.

  23. Ahmad Alghadir M.S. Ph.D. P.T.

  24. Ahmad Alghadir M.S. Ph.D. P.T.

  25. PCA stroke: • Visual agnosia: inability to recognize familiar objects visually. • Prosopagnosia: inability to recognize faces. • Contralateral homonymous hemianopsia. • Cortical blindness (bilateral infarction). • Loss of memory. Ahmad Alghadir M.S. Ph.D. P.T.

  26. Hemianesthesia: contralateral sensory loss (thalamus). • Thalamic sensory syndrome: contralateral unpleasant hemibody sensation (thalamus). • Resting tremor (basal ganglia). • Athetosis (basal ganglia). • Hemiballismus (subthalamic nucleus). • Contralateral hemiplegia (cerebral peduncle). Ahmad Alghadir M.S. Ph.D. P.T.

  27. ICA stroke: • Complete occlusion  massive infarction  coma  death. • Incomplete occlusion  mixture of ACA and MCA stroke. Ahmad Alghadir M.S. Ph.D. P.T.

  28. VBA stroke: • Complete occlusion  progressive occipital headache  coma  death. • Incomplete occlusion  all of the above + cerebellar symptoms + cranial nerve abnormalities. Ahmad Alghadir M.S. Ph.D. P.T.

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