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Neuroscience Exam 2

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Department
Exercise Science
Course
ES 342
Professor
Wilson
Semester
Fall

Description
Neuroscience Exam 2 Myasthenia Gravis Lambert-Eaton “Myasthenic” Syndrome LEMS Post-synaptic abnormalities Pre-synaptic abnorm.Ca++ Pathology channels Decreased nACh Receptors Decreased release of Ach at NMJ Etiology Autoimmune Autoimmune Antibodies to nACh receptors Antibodies to presynaptic Ca++ channels at terminal region of motor neuron. Calcium entry problem. Associated Tumor Thymoma 15% Oat- cell carcinoma of lung 70% Speed of Onset Chronic Consciousness Normal Normal C.L.M Normal Normal Sensory Normal Normal Autonomic Normal Abnormal (dry mouth) Weakness that progressively Weakness- muscle strength Motor worsens with muscle use improve with activity. Cranial Nerves Normal cranial nerves Normal Muscles innervated by cranial nerves (bulbar m.) show Proximal and distal limb muscles appear to be affected more than weakness -ptosis: droop upper eye bulbar muscles. - diplopia: double vision -dysphagia: difficulty swallowing - dysarthria: difficulty speaking Region affected Peripheral Peripheral Demographics All age groups (mean age 20) Affects older individuals (mean Male female ratio (a:2) 55) Male female ratio (10:1) Stable of slowly progressive Prognosis >90% survival rate Response to Anti Yes Minimal Cholinesterases Reduction of receptors Increase in m strength after activity Widening of synaptic cleft Permeability increases after Enzyme degrading Ach activity Less depolarization Handout 10 Cerebral blood flow: increase activation of brain= increase blood flow to area of increase neural activity Cortical gray matter: BF 4-6 times more blood flow than cortical white mater Gray matter cell bodies (metabolic center)= higher energy requirements -Blood flow from (L and R carotid arteries) and (vertebral basilar system) -> connect at circle of willis Cerebral blood flow= 750- 1000 cc/ min = 50cc / gm of tissue CO= 20% of resting valu In any hemodynamic system, blood flow is directly proportional to the perfusion pressures and inversely proportional to the total resistance of the system. -CBF= (mean arterial pressure – central venous P) / (cerebral vascular Resistance -decrease BF= lower that 60 -increase BF= higher than 150 i) Extracerebral Factors: Factors outside the cranial cavity that modify or regulate the cerebral blood flow are primarily related to the cardiovascular system. - Systemic BP Pv= low and Pa= large fluxation major impact - Efficiency of CO – indirect impact - Viscosity of blood. Increase RBC = increase thickness -Anemia (loss of RBC) BF increase 30% - Polycythemia (increase RBC) BF decrease BF 50% ii)Intracerebral Factors: The state of the cerebral vasculature also can influence cerebral blood flow. - Intracranial arterial disease: artherscleoris =inc. R and dec. vessels = dec. BF - Changes in intracranial pressure= 5-15mmHg normal. Inc= impingement BV venous Inc Venous P= dec BF Regulation of Cerebral Blood Flow i) Neurogenic Control: -least important factor - Sympathetic= vasoconstriction with norepinephrine protects capillaries from high BP - parasympathetic control= release of Nitric Oxide vasodilation ii) Chemical Factors: - Strong influence - CO2= most potent physio and pharmalogical agent affecting CBF o Inc brain activity, CO2, cerebral BF,  Increase PaCO2= vasodilation  Decrease PaCO2= vasoconstriction - Oxygen: decrease PaO2= vasodilation Increase PaO2= vasoconstriction o FIO2= 100%- CBF dec 13% o FIO2= 13%- CBF inc. 35% o FI02= 20.9% normally iii) Metabolic Regulation: LOCAL ONLY. REGIIONAL EFFECT-CBF coupled to activity. Brain metabolites. Local vasodilation: adenosine, K, H, oxygen free radicals iv) Autoregulation: Ability of an organ to maintain BF constant despite change P Accomplished through –neurologic control, chemical factors, metabolic regulation In certain ischemic situations, autoregulation is sufficient to increase cerebral blood flow and to prevent infarction; in other situations, it may reduce the size of the resultant infarct. CEREBRAL METABOLISM: High metabolic activity and high oxygen consumption characterize cerebral metabolism. A constant supply of energy is necessary for: - establishment of membrane potentials 70% energy goes to pumps - maintenance of RMP transmembrane - axonal membrane transport fast antero/retro - synthesis of various components- neurotransmitters - Glucose main substance brain delivered through BF glycogen not used by brain Aerobic conditions= 38mmoles ATP/ g of glucose Anaerobic conditions= 2mmoles of ATP/ g of glucose STROKE : or cerebrovascular accident, refers to the neurological symptoms and signs, usually focal and acute, that result from diseases involving blood vessels. Diseases of the blood vessels ranking third (heart, cancer, BV, accidents) first of chronic functional incapacity. 2,000,000 people impaired by the neurological consequences of cerebrovascular disease. 25-64 age of many a) Occlusive: closing of BV thrombosis or atherosclerosis b) Hemorrhagic: bleed of vessels hypertension or aneurysm (1/3 of all stroke) Ischemic Cascade leading ultimately to neuronal dysfunction and death 1) CBF dec= dec O2 and glucose 2) Local Auto regulation impaired 3) Local metabolites try to restore BF – Anaerobic glycolysis= inc LA and dec Ph 4) failure of mitocondial function= no ATP -> leakage of K from cells and NA and Cl in cell depolarize -increase tissure water, impair neurotransmitter reuptake 5) Relase of excitatory neurotransmitter (glutamate) - increase permiablity to Na going in cell. Ca in terminal. – cellualar lysis -increase neuronal necrosis -nuerotoxic at high levels 6) Activation of phospholipases and Proteases – enzymes break down phospolipic membrane and protiens 7) membrane damage: mitochondrial damage – irreversible 8) CELL DEATH If the period of ischemia is short and the supply of high-energy phosphate bonds can be reestablished, neuronal function can resume. The local accumulation of adenosine, potassium, and hydrogen, which occurs in response to the production of lactic acid, produces local vasodilatation in an attempt to restore an adequate blood supply. if the cell continues to be deprived of its nourishment, catabolic and morphologic changes occur in the neuron. Initially, the cell begins to swell (acute cell change); if its metabolic needs are not met, the cell becomes irreversibly damaged (infarction). Lesions involving: a) The internal carotid artery may alter function in the distribution of any or all of its three clinically l) The ophthalmic artery, producing ipsilateral monocular loss of vision 2) The anterior cerebral artery, contralateral weakness and sensory loss primarily in the leg. 3) The middle
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