Ahmad Alghadir M.S. Ph.D. P.T. RHS 332: Clinical Neurology Ahmad Alghadir, M.S. Ph.D. P.T. Room: 2071

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Presentation transcript:

Ahmad Alghadir M.S. Ph.D. P.T. RHS 332: Clinical Neurology Ahmad Alghadir, M.S. Ph.D. P.T. Room: 2071

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

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

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

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

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

Ahmad Alghadir M.S. Ph.D. P.T. Factors influencing symptoms of stroke include: 1.“The location of the ischemic process.” 2.“The size of the ischemic area.” 3.“The nature and functions of the structures involved.” 4.“The availability of collateral blood flow” (rapidity of the occlusion).

Ahmad Alghadir M.S. Ph.D. P.T. 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. Autoregulatory mechanisms Modulate a constant rate of CBF through the brain (50-60 ml / 100 g of brain tissue / m) (17% of cardiac output). 1.Blood concentration of O 2 and CO 2 : increase in CO 2 or decrease in O 2  vasodilation  increase CBF / decrease in CO 2 or increase in O 2  vasoconstriction  decrease CBF.

Ahmad Alghadir M.S. Ph.D. P.T. 2.Blood pH: fall in pH (increased acidity)  vasodilation  increase CBF / rise in pH (increased alkalinity)  vasoconstriction  decrease CBF. 3.Blood pressure: fall in pressure  vasodilation  increase CBF / rise in pressure  vasoconstriction  decrease CBF.

Ahmad Alghadir M.S. Ph.D. P.T. 4.Blood viscosity: increase in viscosity  vasodilation  increase CBF / decrease in viscosity  vasoconstriction  decrease CBF. 5.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. Vascular syndromes 1.ACA stroke: Occlusion proximal to anterior communicating artery  minimal deficits. Occlusion distal to anterior communicating artery  a)“Contralateral hemiparesis and cortical sensory loss with greater involvement of the lower extremity than upper extremity.”

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

Ahmad Alghadir M.S. Ph.D. P.T. 2.MCA stroke: a)“Contralateral hemiparesis or hemiplegia and sensory deficit of the face, arm, and leg, with the face and arm more involved than the leg.” b)Loss of conjugate gaze to the opposite side. c)Contralateral homonymous hemianopsia.

Ahmad Alghadir M.S. Ph.D. P.T. d)Unilateral neglect. e)Aphasia.

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

3.PCA stroke: a)Visual agnosia: inability to recognize familiar objects visually. b)Prosopagnosia: inability to recognize faces. c)Contralateral homonymous hemianopsia. d)Cortical blindness (bilateral infarction). e)Loss of memory.

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

Ahmad Alghadir M.S. Ph.D. P.T. 4.ICA stroke: Complete occlusion  massive infarction  coma  death. Incomplete occlusion  mixture of ACA and MCA stroke.

Ahmad Alghadir M.S. Ph.D. P.T. 5.VBA stroke: Complete occlusion  progressive occipital headache  coma  death. Incomplete occlusion  all of the above + cerebellar symptoms + cranial nerve abnormalities.