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Cerebrovascular Disorders

Circle of Willis 4 main blood vessels: 2 internal carotids from front, 2 veterbral arteries and enter along brain stem Once veterbral arteries enter brain stem, they fuse to form basilar artery, basilar plus internals join to form circle of willis. provides interconnect
Cerebral sinus Where venous blood collects and eventually drains into jugular veins. They do not have valves, just passive flow back to heart.
Autoregulation Ability of the brain to maintain constant cerebral blood flow despite changes in systemic arterial pressure (MABP between 60-140 mmHg) Also-ability to adjust flow to meet localized metabolic needs
Carbon Dioxide and blood flow Carbon dioxide: increased CO2 causes increased blood flow. Co2: increase = increase in localized blood flow, because co2 comes from cellular respiration– if cells are working harder then they need more 02
Hydrogen and blood flow Hydrogen ion concentration: increased [H+] causes increased blood flow. H+: are result of anaerobic metabolism– lactic acid and H+ so they are working hard and need more 02
Oxygen and blood flow Oxygen concentration: decreased [O2] increases blood flow. O2: decrease means it needs more
Stroke Often seen as CVA (cerebrovascular accident) in medical charting Brain damage causing neurologic deficit due to disruption in blood flow ~600,000 Americans afflicted each year Two types: Ischemic and Hemorrhagic
Stroke Risk Factors Age: increase; Sex:19% greater incidence in men; Race: African Americans 60% greater risk of death or disability; Heart disase: cardioembolic stroke; Cocaine; HYPERTENSION/atherosclerosis; Polycythemia, sickle cell disease (during crisis), other blood
Transient Ischemic Attack (TIA) Neurologic deficits that last for less than 24 hours “Brain angina” Temporary decrease in blood flow to an area that reverses before infarction takes place (zone of penumbra without central infarction) Often ignored symptoms
Thrombotic Stroke Cerebral thrombosis is a narrowing of an artery by fatty deposits called plaque. Plaque can cause a clot to form, which blocks the passage of blood through the artery.
Embolic Stroke An embolus is a blood clot or other debris circulating in the blood. When it reaches an artery in the brain that is too narrow to pass through, it lodges there and blocks the flow of blood.
Hemorrhagic Stroke A burst blood vessel may allow blood to seep into and damage brain tissues until clotting shuts off the leak. Much higher morbidity and mortality 15-20%
Bruits Plaque along the artery, if it breaks off, it'll clog a smaller artery
Ischemic Stroke Due to thrombotic:atherosclerotic plaques, hypercoagulation disorders (sickle cell, polycythemia); HTN or embolic: Usually cardiac source-mural thrombi, valve vegetations, atrial fibrillation; HTN
Ischemic penumbra Surrounding the infarct is a much larger area of ischemic, but viable cells. Receives some partial or collateral flow and may recover if ischemia is mild or perfusion is restored.
Anterior Cerebral Artery Area of perfusion: Medial aspect of frontal lobe CM: contralateral hemiparesis and sensory loss of lower extremity, impaired cognition and decision making
Middle Cerebral Artery Most commons site for CVA Area of perfusion: Lateral cerebral hemispheres, basal ganglia Symptoms: Contralateral hemiplegia, contralateral sensory loss, aphasia (L side), neglect syndrome
Posterior Cerebral Artery Area of perfusion: Occipital lobe, medial aspect of temporal lobe Symptoms: Visual defects, memory impairment, cranial nerve deficits
Small Vessel Stroke (lacunar infarcts) Small penetrating arterioles, affects basal ganglia, pons, cerebellum, internal capsule. In healing process, leave small cavities (lacunae) See motor and sensory deficits, very focal, good prognosis
Pharmacologic Treatment Thrombolytic Agents: streptokinase, uronkinase, tPA Risks:intracranial hemorrhage
Guidelines and contraindications for pharm treatment of stroke hemorrhagic stroke ruled out by CT, must be administered within 3 hours of symptom onset. CI: Use of oral anticoagulants, history of GI bleed, previous stroke or head injury in last 3 months, surgery within the past 14 days, BP > 200/120 mmHg
Aneurysm Bulge at the site of a localized weakness in muscle of vessel wall, usually at bifurcations Congenital defects Cigarette smoking and HTN are greatest risks If larger than 10mm, 50% chance of rupture per year.
Ruptured aneurysm Bleeding into the subarachnoid space. Most frequently between 30-60 years of age Mortality and morbidity high-only 1/3 recover without major deficiencies All ruptured aneurysms are hemorrhagic stroke, but not all hem. strokes are ruptured aneurysms.
Ruptured aneurysm symptoms Intense headache Meningeal irritation: nuchal rigidity (stiff neck from CSF), photophbia Cranial nerve deficits (diplopia, blurred vision) Loss of consciousness, increased ICP, LOC 50% with rupture have history of headaches in weeks leading up ruptur
Ruptured Aneurysm: Vasospasm Difficult to treat, high M & M 3-10 days after initial bleed Narrowing of vessels to supplying area of bleed Neurologic status gradually deteriorates Pharm: nimodipine (calcium channel blocker) can be used to prevent or treat
Arteriovenous Malformation (AVM) Abnormal arteries and veins linked by fistulas No capillary bed, little muscle Defect in embryonic development Worsens with age 70% with AVMs have learning disabilities Potential cause of hemorrhagic stroke Venous pressure very low– and eventually r
AVM: Hemodynamic Effects Blood shunted from high pressure arterial system to low pressure venous system wihtout capillary buffering-high pressure, rupture Impaired perfusion in area due to oxygenated blood being shunted away-slowly progressing neurologic defects (vascular steal)
Disabilites r/t Alterations in Blood Flow: Motor Motor cortex damage: weakness on contralateral side, clumsiness, loss of fine motor skills. Tendency toward foot drop, edema in limbs affected Corticospinal tract: initial flaccidity then spasticity-contractures
Disabilities: Dysarthria Imapired articulation when speaking Content of speech, understanding, ability to read not affected Due to impaired motor control to facial muscles
Disabilities: Aphasia (language) Wernicke's, anomic Wernicke's aphasia: inability to comprehend speech of others and of self, inability to read (Wernicke's area in temporal lobe) Anomic aphasia: nearly normal, problems finding individual words
Disabilities: Aphasia Conduction Conduction aphasia: inappropriate word use (impaired repetition, word substitutions). Good fluency and comprehension. Destruction of fibers between Wernicke's and Broca's areas.
Disabilities: Aphasia Expression Expressive aphasia: Damage to Broca's area. Speech very limited, single words only, limited writing ability. Comprehension normal, person aware of deficit-depression
Disabilities: Denial or Hemiattention Injury in areas of the brain that interpret incoming sensory information Denial of one half of body or environment Unaware of deficit More common in strokes or injuries in the nondominant hemisphere (usually right)
Created by: Marissagostanian