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  1. 2. Cerebrovascular Diseases Alina Valdes, M.D.
  2. 3. Stroke - Background <ul><li>Symptoms begin abruptly </li></ul><ul><ul><li>Inadequate blood flow </li></ul></ul><ul><ul><ul><li>Ischemic stroke </li></ul></ul></ul><ul><ul><ul><ul><li>Focal – thrombotic or embolic occlusion of major artery </li></ul></ul></ul></ul><ul><ul><ul><ul><li>Global – inadequate cerebral perfusion </li></ul></ul></ul></ul><ul><ul><li>Hemorrhage </li></ul></ul><ul><ul><ul><li>Parenchymal – into brain tissue </li></ul></ul></ul><ul><ul><ul><li>Subarachnoid – surrounding subarachnoid space </li></ul></ul></ul><ul><li>Approximately 80% are ischemic in origin </li></ul>
  3. 4. <ul><li>Third leading medical cause of death and second most frequent cause of morbidity in developed countries </li></ul><ul><li>Rates similar among men and women </li></ul><ul><li>Incidence and rate of mortality higher in blacks than whites </li></ul><ul><li>Since 1990, incidence in U.S. has declined about 1.5%, probably as result of improvements in general public health and decline of cardiovascular deaths and better control of risk factors </li></ul>
  4. 5. Risk Factors for Ischemic Strokes <ul><li>Diabetes </li></ul><ul><li>Hypertension </li></ul><ul><li>Smoking </li></ul><ul><li>Family history of premature vascular disease </li></ul><ul><li>Hyperlipidemia </li></ul><ul><li>Atrial fibrillation </li></ul><ul><li>History of transient ischemic attack (TIA) </li></ul><ul><li>History of recent myocardial infarction </li></ul><ul><li>History of congestive heart failure (LV ejection fraction < 25%) </li></ul><ul><li>Drugs (sympathomimetics, oral contraceptive pill, cocaine ) </li></ul>
  5. 6. Cerebral Circulation <ul><li>Anterior Circulation </li></ul><ul><ul><li>Common carotid artery bifurcates into: </li></ul></ul><ul><ul><ul><li>External </li></ul></ul></ul><ul><ul><ul><li>Internal </li></ul></ul></ul><ul><ul><ul><ul><li>Enters skull through carotid canal and passes through cavernous sinus </li></ul></ul></ul></ul><ul><ul><ul><ul><li>Gives off ophthalmic , anterior choroidal , and posterior communicating arteries </li></ul></ul></ul></ul>
  6. 7. <ul><ul><ul><ul><li>Bifurcates into anterior cerebral artery and middle cerebral artery </li></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>Anterior cerebral artery supplies medial surfaces of cerebral hemispheres </li></ul></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>Middle cerebral artery supplies lateral surface, basal ganglia, and subcortical white matter </li></ul></ul></ul></ul></ul>
  7. 8. <ul><li>Posterior Circulation </li></ul><ul><ul><li>Vertebral arteries go up within transverse processes of cervical vertebrae </li></ul></ul><ul><ul><ul><li>Intracranial vertebral artery gives off: </li></ul></ul></ul><ul><ul><ul><ul><li>Anterior spinal artery </li></ul></ul></ul></ul><ul><ul><ul><ul><li>Posterior inferior cerebellar artery </li></ul></ul></ul></ul><ul><ul><li>Both Vertebral arteries then join to form: </li></ul></ul><ul><ul><ul><li>Basilar artery at pontomedullary junction </li></ul></ul></ul><ul><ul><ul><ul><li>Supplies cerebellum via anterior inferior cerebellar artery and superior cerebellar artery </li></ul></ul></ul></ul><ul><ul><ul><ul><li>Bifurcates into posterior cerebral arteries at level of pontomesencephalic junction </li></ul></ul></ul></ul>
  8. 9. <ul><li>Circle of Willis </li></ul><ul><ul><li>Formed at base of brain by: </li></ul></ul><ul><ul><ul><li>Union of both anterior cerebral arteries via the anterior communicating artery and </li></ul></ul></ul><ul><ul><ul><li>Union of the middle cerebral artery with the posterior cerebral artery via the posterior communicating artery </li></ul></ul></ul><ul><ul><li>Allows communication between both anterior circulations as well as between posterior and anterior circulations on each side </li></ul></ul><ul><ul><li>Congenital anomalies frequent so may have reduction of collateral blood supply if adjacent vessel becomes occluded </li></ul></ul>
  9. 10. Physiology <ul><li>Brain has few energy stores </li></ul><ul><li>Relies on extensive and reliable cerebral blood flow </li></ul><ul><li>Autoregulation: maintains cerebral blood flow at constant level despite wide variation in cerebral perfusion pressure </li></ul><ul><li>Cerebral blood flow remains relatively constant when mean arterial pressure between 50 and 150 mm Hg </li></ul><ul><li>In chronic systemic hypertension, upper and lower levels of autoregulation raised, so have higher tolerance of hypertension but less to effects of hypotension </li></ul>
  10. 11. Ischemic Stroke <ul><li>May result from: </li></ul><ul><ul><li>Thrombotic or embolic occlusion of major vessel causing decreased blood blow to supplied area </li></ul></ul><ul><ul><li>Decreased systemic perfusion </li></ul></ul><ul><li>If ischemia prolonged, results in infarction (necrosis) </li></ul><ul><ul><li>“ pale” infarct – anemic </li></ul></ul><ul><ul><li>“ hemorrhagic” infarct – in areas of endothelial necrosis </li></ul></ul>
  11. 12. <ul><li>Ischemic penumbra </li></ul><ul><ul><li>Transition zone between normal and infarcted central core </li></ul></ul><ul><ul><li>Moderately ischemic tissue </li></ul></ul><ul><ul><li>Target area for salvage </li></ul></ul><ul><li>Global cerebral ischemia </li></ul><ul><ul><li>Usually results from cardiac arrest or ventricular fibrillation </li></ul></ul><ul><ul><li>Susceptible populations of neurons: </li></ul></ul><ul><ul><ul><li>Hippocampus </li></ul></ul></ul><ul><ul><ul><li>Cerebellar Purkinje cells </li></ul></ul></ul><ul><ul><ul><li>Deeper layers of cerebral cortex (causing laminar necrosis ) </li></ul></ul></ul>
  12. 13. <ul><li>Pure hypoxia </li></ul><ul><ul><li>Causes cerebral dysfunction </li></ul></ul><ul><ul><ul><li>Lethargy and confusion </li></ul></ul></ul><ul><ul><li>Rarely causes irreversible brain injury </li></ul></ul><ul><ul><ul><li>Hypoglycemia – exacerbates </li></ul></ul></ul><ul><ul><li>May be reversible if blood flow restored within 15 minutes </li></ul></ul>
  13. 14. <ul><li>Cerebral edema </li></ul><ul><ul><li>Cytotoxic – intracellular </li></ul></ul><ul><ul><ul><li>Develops rapidly in ischemic neurons as ion pumps fail </li></ul></ul></ul><ul><ul><li>Vasogenic – interstitial </li></ul></ul><ul><ul><ul><li>Occurs as damage to endothelial cells disrupts blood-brain barrier and allows macromolecules to enter interstitial space </li></ul></ul></ul><ul><ul><li>Can cause transtentorial herniation and death due to increase brain fluid content (as much as 10%) in 3 to 5 days </li></ul></ul>
  14. 15. Causes of Acute Cerebral Ischemia <ul><li>Focal </li></ul><ul><ul><li>Mural abnormalities </li></ul></ul><ul><ul><ul><li>Atherosclerosis – approximately 2/3 of strokes </li></ul></ul></ul><ul><ul><ul><ul><li>Embolization of plaque to distal vessels (artery-to-artery) </li></ul></ul></ul></ul><ul><ul><ul><ul><li>In situ thrombosis </li></ul></ul></ul></ul><ul><ul><ul><li>Vasculitis </li></ul></ul></ul><ul><ul><ul><li>Vasospasm (migraine, subarachnoid hemorrhage) </li></ul></ul></ul><ul><ul><ul><li>Compression (by tumor, aneurysm) </li></ul></ul></ul><ul><ul><ul><li>Fibromuscular dysplasia/Moyamoya </li></ul></ul></ul><ul><ul><ul><li>Dissection (spontaneous, traumatic) </li></ul></ul></ul>
  15. 16. <ul><ul><li>Embolism </li></ul></ul><ul><ul><ul><li>Cardiogenic (atrial fibrillation, mural thrombus, myxoma, valvular vegetations) – majority of remaining 1/3 </li></ul></ul></ul><ul><ul><ul><li>Artery-to-artery </li></ul></ul></ul><ul><ul><ul><li>Fat </li></ul></ul></ul><ul><ul><ul><li>Air </li></ul></ul></ul><ul><ul><ul><li>Paradoxical (emboli of venous origin passing through a patent foramen ovale) </li></ul></ul></ul>
  16. 17. <ul><ul><li>Hematologic </li></ul></ul><ul><ul><ul><li>Hypercoagulable state </li></ul></ul></ul><ul><ul><ul><li>Sickle cell disease </li></ul></ul></ul><ul><ul><ul><li>Homocystinuria </li></ul></ul></ul><ul><ul><ul><li>Antiphospholipid antibodies (lupus anticoagulant, anticardiolipin antibodies) </li></ul></ul></ul><ul><ul><ul><li>Protein C or protein S deficiency </li></ul></ul></ul>
  17. 18. <ul><li>Global </li></ul><ul><ul><li>Hypoperfusion </li></ul></ul><ul><ul><ul><li>Cardiac arrest </li></ul></ul></ul><ul><ul><ul><li>Ventricular fibrillation </li></ul></ul></ul>
  18. 19. Transient Ischemic Attack (TIA) <ul><li>Transient neurologic deficit due to reduced blood flow </li></ul><ul><li>Lasting less than 24 hours – most resolve within 1 hour </li></ul><ul><li>Full functional recovery </li></ul>
  19. 20. Stroke - Classes <ul><li>Completed stroke </li></ul><ul><ul><li>Infarction has happened </li></ul></ul><ul><ul><li>Usually have maximal clinical deficit at time of symptoms </li></ul></ul><ul><ul><li>Variable recovery over time </li></ul></ul><ul><li>Stroke in evolution </li></ul><ul><ul><li>Symptom progression </li></ul></ul><ul><ul><li>Propagation of thrombus or worsening cerebral edema or hemorrhage into infarcted area </li></ul></ul><ul><ul><li>Coexistent medical conditions may adversely affect outcome </li></ul></ul>
  20. 21. <ul><li>Lacunar stroke </li></ul><ul><ul><li>Small, deep infarction involving penetrating branch of large cerebral artery </li></ul></ul><ul><ul><li>Usually associated with chronic hypertension </li></ul></ul><ul><ul><li>In normotensive patients, probably result of microatheroma of penetrating arteries, especially of basal ganglia, thalamus, and white matter of internal capsule and pons </li></ul></ul><ul><li>RIND </li></ul><ul><ul><li>Neuro deficit > 24 hours but reverses within 3 weeks </li></ul></ul>
  21. 22. Clinical Presentations of Acute Stroke <ul><li>Alteration in Consciousness </li></ul><ul><ul><li>Stupor or Coma </li></ul></ul><ul><ul><li>Confusion or agitation/memory loss </li></ul></ul><ul><ul><li>Seizures </li></ul></ul><ul><ul><li>Delirium    </li></ul></ul><ul><li>Headache </li></ul><ul><ul><li>Intense or unusually severe </li></ul></ul><ul><ul><li>Associated with decreased level of consciousness/neurological deficit </li></ul></ul><ul><ul><li>Unusual/severe neck or facial pain </li></ul></ul>
  22. 23. <ul><li>Aphasia (incoherent speech or difficulty understanding speech) </li></ul><ul><li>Facial weakness or asymmetry </li></ul><ul><ul><li>Paralysis of facial muscles (e.g., when patients speaks or smiles) </li></ul></ul><ul><ul><li>May be on same side (ipsilateral) or opposite side contralateral to limb paralysis </li></ul></ul><ul><li>Incoordination, weakness, paralysis, or sensory loss of one or more limbs (usually one half of the body and in particular the hand) </li></ul>
  23. 24. <ul><li>Ataxia (poor balance, clumsiness, or difficulty walking) </li></ul><ul><li>Visual loss </li></ul><ul><ul><li>Monocular or binocular </li></ul></ul><ul><ul><li>May be partial loss of the field   </li></ul></ul><ul><li>Intensive vertigo, double vision, unilateral hearing loss, nausea, vomiting, photophobia, or phonophobia </li></ul>
  24. 25. Left (Dominant) Hemisphere Stroke: Common Pattern <ul><li>Aphasia </li></ul><ul><li>Right hemiparesis </li></ul><ul><li>Right-sided sensory loss </li></ul><ul><li>Right visual field defect </li></ul><ul><li>Poor right conjugate gaze </li></ul><ul><li>Dysarthria </li></ul><ul><li>Difficulty reading, writing, or calculating </li></ul>
  25. 26. Right (Non-dominant) Hemisphere Stroke: Common Pattern <ul><li>Neglect of left visual field </li></ul><ul><li>Extinction of left-sided stimuli </li></ul><ul><li>Left hemiparesis </li></ul><ul><li>Left-sided sensory loss </li></ul><ul><li>Left visual field defect </li></ul><ul><li>Poor left conjugate gaze </li></ul><ul><li>Dysarthria </li></ul><ul><li>Spatial disorientation </li></ul>
  26. 27. Brain Stem / Cerebellum / Posterior Hemisphere Stroke: Common Pattern <ul><li>Motor or sensory loss in all four limbs </li></ul><ul><li>Crossed signs </li></ul><ul><li>Limb or gait ataxia </li></ul><ul><li>Dysarthria </li></ul><ul><li>Dysconjugate gaze </li></ul><ul><li>Nystagmus </li></ul><ul><li>Amnesia </li></ul><ul><li>Bilateral visual field defects </li></ul>
  27. 28. Small Subcortical Hemisphere or Brain Stem Stroke: Common Pattern <ul><li>Pure Motor </li></ul><ul><ul><li>Weakness of face and limbs on one side of the body without abnormalities of higher brain function, sensation, or vision    </li></ul></ul><ul><li>Pure Sensory </li></ul><ul><ul><li>Decreased sensation of face and limbs on one side of the body without abnormalities of higher brain function, motor function, or vision </li></ul></ul>
  28. 29. Differential Diagnosis of Stroke <ul><li>Ischemic stroke/ Hemorrhagic stroke </li></ul><ul><li>TIA </li></ul><ul><li>RIND </li></ul><ul><li>Craniocerebral / cervical trauma </li></ul><ul><li>Meningitis/encephalitis </li></ul><ul><li>Intracranial mass </li></ul><ul><ul><li>Tumor </li></ul></ul><ul><ul><li>Subdural hematoma   </li></ul></ul><ul><li>Seizure with persistent neurological signs </li></ul><ul><ul><li>Vs. Todd’s paralysis – transient hemiparesis </li></ul></ul>
  29. 30. <ul><li>Migraine with persistent neurological signs </li></ul><ul><ul><li>Vs. hemiplegic migraine – weakness contralateral to side of headache </li></ul></ul><ul><li>Metabolic </li></ul><ul><ul><li>Hyperglycemia (nonketotic hyperosmolar coma) </li></ul></ul><ul><ul><li>Hypoglycemia </li></ul></ul><ul><ul><li>Post-cardiac arrest ischemia </li></ul></ul><ul><ul><li>Drug/narcotic overdose </li></ul></ul>
  30. 31. Tests for the Emergent Evaluation of the Patient With Acute Ischemic Stroke <ul><li>CT of the brain without contrast </li></ul><ul><ul><li>Only 5% of acute ischemic strokes readily visible in first 24 hours </li></ul></ul><ul><li>Electrocardiogram </li></ul><ul><li>Chest x-ray </li></ul>
  31. 32. <ul><li>Hematologic studies (complete blood count, platelet count, prothrombin time, partial thromboplastin time) </li></ul><ul><ul><ul><li>Lipid profile </li></ul></ul></ul><ul><ul><ul><li>Sed rate </li></ul></ul></ul><ul><li>Serum electrolytes </li></ul><ul><li>Blood glucose </li></ul><ul><li>Renal and hepatic chemical analyses </li></ul><ul><li>National Institutes of Health Scale (NIHSS) score </li></ul>
  32. 33. The NIH Stroke Scale <ul><li>Administer stroke scale items in the order listed. Record performance in each category after each subscale exam. Do not go back and change scores. Follow directions provided for each exam technique. Scores should reflect what the patient does, not what the clinician thinks the patient can do. The clinician should record answers while administering the exam and work quickly. Except where indicated, the patient should not be coached (i.e., repeated requests to patient to make a special effort). </li></ul>
  33. 34. IF ANY ITEM IS LEFT UNTESTED, A DETAILED EXPLANATION MUST BE CLEARLY WRITTEN ON THE FORM. ALL UNTESTED ITEMS WILL BE REVIEWED BY THE MEDICAL MONITOR, AND DISCUSSED WITH THE EXAMINER BY TELEPHONE.   Instructions Scale Definition Score 1a. Level of Consciousness: The investigator must choose a response, even if a full evaluation is prevented by such obstacles as an endotracheal tube, language barrier, orotracheal trauma/bandages. A 3 is scored only if the patient makes no movement (other than reflexive posturing) in response to noxious stimulation . <ul><ul><li>0 = Alert; keenly responsive. </li></ul></ul><ul><ul><li>1 = Not alert, but arousable by minor stimulation to obey, answer, or respond. </li></ul></ul><ul><ul><li>2 = Not alert, requires repeated stimulation to attend, or is obtunded and requires strong or painful stimulation to make movements (not stereotyped). </li></ul></ul><ul><ul><li>3 = Responds only with reflex motor or autonomic effects or totally unresponsive, flaccid, areflexic. </li></ul></ul>        ____
  34. 35. 1b. LOC Questions: The patient is asked the month and his/her age. The answer must be correct - there is no partial credit for being close. Aphasic and stuporous patients who do not comprehend the questions will score 2. Patients unable to speak because of endotracheal intubation, orotracheal trauma, severe dysarthria from any cause, language barrier or any other problem not secondary to aphasia are given a 1. It is important that only the initial answer be graded and that the examiner not &quot;help&quot; the patient with verbal or non-verbal cues. <ul><ul><li>  0 = Answers both questions correctly. </li></ul></ul><ul><ul><li>1 = Answers one question correctly. </li></ul></ul><ul><ul><li>  </li></ul></ul><ul><ul><li>2 = Answers neither question correctly. </li></ul></ul>    ____ 1c. LOC Commands: The patient is asked to open and close the eyes and then to grip and release the non-paretic hand. Substitute another one step command if the hands cannot be used. Credit is given if an unequivocal attempt is made but not completed due to weakness. If the patient does not respond to command, the task should be demonstrated to them (pantomime) and score the result (i.e., follows none, one or two commands). Patients with trauma, amputation, or other physical impediments should be given suitable one-step commands. Only the first attempt is scored. <ul><ul><li>0 = Performs both tasks correctly </li></ul></ul><ul><ul><li>  </li></ul></ul><ul><ul><li>1 = Performs one task correctly </li></ul></ul><ul><ul><li>  </li></ul></ul><ul><ul><li>2 = Performs neither task correctly </li></ul></ul>      ____
  35. 36. 2. Best Gaze: Only horizontal eye movements will be tested. Voluntary or reflexive (oculocephalic) eye movements will be scored but caloric testing is not done. If the patient has a conjugate deviation of the eyes that can be overcome by voluntary or reflexive activity, the score will be 1. If a patient has an isolated peripheral nerve paresis (CN III, IV or VI) score a 1. Gaze is testable in all aphasic patients. Patients with ocular trauma, bandages, pre-existing blindness or other disorder of visual acuity or fields should be tested with reflexive movements and a choice made by the investigator. Establishing eye contact and then moving about the patient from side to side will occasionally clarify the presence of a partial gaze palsy. <ul><ul><li>0 = Normal </li></ul></ul><ul><ul><li>  </li></ul></ul><ul><ul><li>1 = Partial gaze palsy. This score is given when gaze is abnormal in one or both eyes, but where forced deviation or total gaze paresis are not present. </li></ul></ul><ul><ul><li>  </li></ul></ul><ul><ul><li>2 = Forced deviation, or total gaze paresis not overcome by the oculocephalic maneuver. </li></ul></ul>      ____
  36. 37. 3. Visual: Visual fields (upper and lower quadrants) are tested by confrontation, using finger counting or visual threat as appropriate. Patient must be encouraged, but if they look at the side of the moving fingers appropriately, this can be scored as normal. If there is unilateral blindness or enucleation, visual fields in the remaining eye are scored. Score 1 only if a clear-cut asymmetry, including quadrantanopia is found. If patient is blind from any cause score 3. Double simultaneous stimulation is performed at this point. If there is extinction patient receives a 1 and the results are used to answer question 11. <ul><ul><li>0 = No visual loss </li></ul></ul><ul><ul><li>  </li></ul></ul><ul><ul><li>1 = Partial hemianopia </li></ul></ul><ul><ul><li>  </li></ul></ul><ul><ul><li>2 = Complete hemianopia </li></ul></ul><ul><ul><li>  </li></ul></ul><ul><ul><li>3 = Bilateral hemianopia (blind including cortical blindness) </li></ul></ul>      ____ 4. Facial Palsy: Ask, or use pantomime to encourage the patient to show teeth or raise eyebrows and close eyes. Score symmetry of grimace in response to noxious stimuli in the poorly responsive or non-comprehending patient. If facial trauma/bandages, orotracheal tube, tape or other physical barrier obscures the face, these should be removed to the extent possible. <ul><ul><li>0 = Normal symmetrical movement </li></ul></ul><ul><ul><li>1 = Minor paralysis (flattened nasolabial fold, asymmetry on smiling) </li></ul></ul><ul><ul><li>2 = Partial paralysis (total or near total paralysis of lower face) </li></ul></ul><ul><ul><li>3 = Complete paralysis of one or both sides (absence of facial movement in the upper and lower face) </li></ul></ul>      ____
  37. 38. 5 & 6. Motor Arm and Leg: The limb is placed in the appropriate position: extend the arms (palms down) 90 degrees (if sitting) or 45 degrees (if supine) and the leg 30 degrees (always tested supine). Drift is scored if the arm falls before 10 seconds or the leg before 5 seconds. The aphasic patient is encouraged using urgency in the voice and pantomime but not noxious stimulation. Each limb is tested in turn, beginning with the non-paretic arm. Only in the case of amputation or joint fusion at the shoulder or hip may the score be &quot;9&quot; and the examiner must clearly write the explanation for scoring as a &quot;9&quot;. <ul><ul><li>0 = No drift, limb holds 90 (or 45) degrees for full 10 seconds. </li></ul></ul><ul><ul><li>1 = Drift, Limb holds 90 (or 45) degrees, but drifts down before full 10 seconds; does not hit bed or other support. </li></ul></ul><ul><ul><li>2 = Some effort against gravity, limb cannot get to or maintain (if cued) 90 (or 45) degrees, drifts down to bed, but has some effort against gravity. </li></ul></ul><ul><ul><li>3 = No effort against gravity, limb falls. </li></ul></ul><ul><ul><li>4 = No movement </li></ul></ul><ul><ul><li>9 = Amputation, joint fusion explain: ______________________ </li></ul></ul><ul><ul><li>  </li></ul></ul><ul><ul><ul><ul><ul><li>5a. Left Arm </li></ul></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>5b. Right Arm </li></ul></ul></ul></ul></ul>    ____ ____   <ul><ul><li>0 = No drift, leg holds 30 degrees position for full 5 seconds. </li></ul></ul><ul><ul><li>1 = Drift, leg falls by the end of the 5 second period but does not hit bed. </li></ul></ul><ul><ul><li>2 = Some effort against gravity; leg falls to bed by 5 seconds, but has some effort against gravity. </li></ul></ul><ul><ul><li>3 = No effort against gravity, leg falls to bed immediately. </li></ul></ul><ul><ul><li>4 = No movement </li></ul></ul><ul><ul><li>9 = Amputation, joint fusion explain:_________________ </li></ul></ul><ul><ul><li>6a. Left Leg </li></ul></ul><ul><ul><li>6b. Right Leg </li></ul></ul>                      ____ ____  
  38. 39. 7. Limb Ataxia: This item is aimed at finding evidence of a unilateral cerebellar lesion. Test with eyes open. In case of visual defect, insure testing is done in intact visual field. The finger-nose-finger and heel-shin tests are performed on both sides, and ataxia is scored only if present out of proportion to weakness. Ataxia is absent in the patient who cannot understand or is paralyzed. Only in the case of amputation or joint fusion may the item be scored &quot;9&quot;, and the examiner must clearly write the explanation for not scoring. In case of blindness test by touching nose from extended arm position. <ul><ul><li>0 = Absent </li></ul></ul><ul><ul><li>1 = Present in one limb </li></ul></ul><ul><ul><li>2 = Present in two limbs </li></ul></ul><ul><ul><li>If present, is ataxia in </li></ul></ul><ul><ul><li>Right arm 1 = Yes 2 = No </li></ul></ul><ul><ul><li>9 = amputation or joint fusion, explain ___________________ </li></ul></ul><ul><ul><li>Left arm 1 = Yes 2 = No </li></ul></ul><ul><ul><li>9 = amputation or joint fusion, explain ___________________ </li></ul></ul><ul><ul><li>Right leg 1 = Yes 2 = No </li></ul></ul><ul><ul><li>9 = amputation or joint fusion, explain ___________________ </li></ul></ul><ul><ul><li>Left leg 1 = Yes 2 = No </li></ul></ul><ul><ul><li>9 = amputation or joint fusion, explain ___________________ </li></ul></ul>    ____   ____ ____ ____
  39. 40. 8. Sensory: Sensation or grimace to pin prick when tested, or withdrawal from noxious stimulus in the obtunded or aphasic patient. Only sensory loss attributed to stroke is scored as abnormal and the examiner should test as many body areas [arms (not hands), legs, trunk, face] as needed to accurately check for hemisensory loss. A score of 2, &quot;severe or total,&quot; should only be given when a severe or total loss of sensation can be clearly demonstrated. Stuporous and aphasic patients will therefore probably score 1 or 0. The patient with brain stem stroke who has bilateral loss of sensation is scored 2. If the patient does not respond and is quadriplegic score 2. Patients in coma (item 1a=3) are arbitrarily given a 2 on this item. <ul><ul><li>0 = Normal; no sensory loss. </li></ul></ul><ul><ul><li>  </li></ul></ul><ul><ul><li>1 = Mild to moderate sensory loss; patient feels pinprick is less sharp or is dull on the affected side; or there is a loss of superficial pain with pinprick but patient is aware he/she is being touched. </li></ul></ul><ul><ul><li>  </li></ul></ul><ul><ul><li>2 = Severe to total sensory loss; patient is not aware of being touched in the face, arm, and leg. </li></ul></ul>          ____
  40. 41. 9. Best Language: A great deal of information about comprehension will be obtained during the preceding sections of the examination. The patient is asked to describe what is happening in the attached picture, to name the items on the attached naming sheet, and to read from the attached list of sentences. Comprehension is judged from responses here as well as to all of the commands in the preceding general neurological exam. If visual loss interferes with the tests, ask the patient to identify objects placed in the hand, repeat, and produce speech. The intubated patient should be asked to write. The patient in coma (question 1a=3) will arbitrarily score 3 on this item. The examiner must choose a score in the patient with stupor or limited cooperation but a score of 3 should be used only if the patient is mute and follows no one step commands . <ul><ul><li>0 = No aphasia, normal </li></ul></ul><ul><ul><li>  </li></ul></ul><ul><ul><li>1 = Mild to moderate aphasia; some obvious loss of fluency or facility of comprehension, without significant limitation on ideas expressed or form of expression. Reduction of speech and/or comprehension, however, makes conversation about provided material difficult or impossible. For example in conversation about provided materials examiner can identify picture or naming card from patient's response. </li></ul></ul><ul><ul><li>  </li></ul></ul><ul><ul><li>2 = Severe aphasia; all communication is through fragmentary expression; great need for inference, questioning, and guessing by the listener. Range of information that can be exchanged is limited; listener carries burden of communication. Examiner cannot identify materials provided from patient response. </li></ul></ul><ul><ul><li>  </li></ul></ul><ul><ul><li>3 = Mute, global aphasia; no usable speech or auditory comprehension. </li></ul></ul>                  ____
  41. 42.   10. Dysarthria: If patient is thought to be normal an adequate sample of speech must be obtained by asking patient to read or repeat words from the attached list. If the patient has severe aphasia, the clarity of articulation of spontaneous speech can be rated. Only if the patient is intubated or has other physical barrier to producing speech, may the item be scored &quot;9&quot;, and the examiner must clearly write an explanation for not scoring. Do not tell the patient why he/she is being tested. <ul><ul><li>0 = Normal </li></ul></ul><ul><ul><li>1 = Mild to moderate; patient slurs at least some words and, at worst, can be understood with some difficulty. </li></ul></ul><ul><ul><li>2 = Severe; patient's speech is so slurred as to be unintelligible in the absence of or out of proportion to any dysphasia, or is mute/anarthric. </li></ul></ul><ul><ul><li>9 = Intubated or other physical barrier, explain____________________ </li></ul></ul>      ____ 11. Extinction and Inattention (formerly Neglect): Sufficient information to identify neglect may be obtained during the prior testing. If the patient has a severe visual loss preventing visual double simultaneous stimulation, and the cutaneous stimuli are normal, the score is normal. If the patient has aphasia but does appear to attend to both sides, the score is normal. The presence of visual spatial neglect or anosagnosia may also be taken as evidence of abnormality. Since the abnormality is scored only if present, the item is never untestable. <ul><ul><li>0 = No abnormality. </li></ul></ul><ul><ul><li>  </li></ul></ul><ul><ul><li>1 = Visual, tactile, auditory, spatial, or personal inattention or extinction to bilateral simultaneous stimulation in one of the sensory modalities. </li></ul></ul><ul><ul><li>  </li></ul></ul><ul><ul><li>2 = Profound hemi-inattention or hemi-inattention to more than one modality. Does not recognize own hand or orients to only one side of space. </li></ul></ul>      ____
  42. 43. Additional item, not a part of the NIH Stroke Scale score. A. Distal Motor Function: The patient's hand is held up at the forearm by the examiner and patient is asked to extend his/her fingers as much as possible. If the patient can't or doesn't extend the fingers the examiner places the fingers in full extension and observes for any flexion movement for 5 seconds. The patient's first attempts only are graded. Repetition of the instructions or of the testing is prohibited. <ul><ul><li>0 = Normal (No flexion after 5 seconds) </li></ul></ul><ul><ul><li>  </li></ul></ul><ul><ul><li>1 = At least some extension after 5 seconds, but not fully extended. Any movement of the fingers which is not command is not scored. </li></ul></ul><ul><ul><li>  </li></ul></ul><ul><ul><li>2 = No voluntary extension after 5 seconds. Movements of the fingers at another time are not scored. </li></ul></ul><ul><ul><li>a. Left Arm </li></ul></ul><ul><ul><li>  </li></ul></ul><ul><ul><li>b. Right Arm </li></ul></ul>                  ____   ____
  43. 44. Primary Stroke Prevention <ul><li>Reduction of risk factors </li></ul><ul><ul><li>Treat hypertension </li></ul></ul><ul><ul><li>Stop smoking </li></ul></ul><ul><ul><li>Treat diabetes </li></ul></ul><ul><ul><li>Treat hyperlipidemia </li></ul></ul>
  44. 45. <ul><li>Atrial fibrillation </li></ul><ul><ul><li>Increases yearly risk of stroke 17-fold in setting of valvular heart disease </li></ul></ul><ul><ul><li>Anticoagulation with warfarin to INR of 2 to 3 </li></ul></ul><ul><ul><li>Treat with aspirin, 325 mg/day if nonvalvular or no other risk factors </li></ul></ul><ul><ul><li>Long-term anticoagulation if prosthetic heart valve </li></ul></ul><ul><ul><li>No warfarin if bacterial endocarditis due to risk of cerebral hemorrhage from septic embolization </li></ul></ul>
  45. 46. <ul><li>Transient ischemic attack </li></ul><ul><ul><li>Significant risk factor for recurrent stroke, with average 5% risk per year </li></ul></ul><ul><ul><li>Prophylactic antiplatelet therapy shown to prevent secondary effects </li></ul></ul><ul><ul><ul><li>Aspirin </li></ul></ul></ul><ul><ul><ul><li>Ticlopidine – Ticlid: thrombotic stroke reduction </li></ul></ul></ul><ul><ul><ul><li>Clopidogrel – Plavix: reduce events associated with atherosclerosis that include strokes, MI, PVD </li></ul></ul></ul><ul><ul><li>Treat with warfarin if significant risk for cardiogenic thromboembolism </li></ul></ul><ul><ul><li>Hospital admission for new-onset and recurrent TIA’s unless confident in diagnosis of etiology </li></ul></ul><ul><ul><li>Angiography – treat medically or surgically </li></ul></ul>
  46. 47. <ul><li>Carotid stenosis </li></ul><ul><ul><li>Asymptomatic bruit or extracranial stenosis less than 60% </li></ul></ul><ul><ul><ul><li>Treat with antiplatelet drugs </li></ul></ul></ul><ul><ul><li>Extracranial stenosis more than 70% (with or without symptoms) </li></ul></ul><ul><ul><ul><li>Carotid endarterectomy </li></ul></ul></ul><ul><ul><li>Moderate asymptomatic stenosis (60%-70%) </li></ul></ul><ul><ul><ul><li>Medical versus surgical therapy </li></ul></ul></ul><ul><li>Aortic arch thrombi </li></ul><ul><ul><li>Detectable with transesophageal echocardiography </li></ul></ul><ul><ul><li>Potential sources of emboli, especially if > 4 mm in thickness </li></ul></ul><ul><ul><li>Thick plaque independent predictor of recurrent stroke </li></ul></ul><ul><ul><li>Thrombectomy option for refractory disease </li></ul></ul>
  47. 48. Management of Acute Stroke <ul><li>General measures </li></ul><ul><ul><li>Reduce risk of complications from immobility </li></ul></ul><ul><ul><ul><li>Pneumonia </li></ul></ul></ul><ul><ul><ul><li>DVT </li></ul></ul></ul><ul><ul><ul><li>UTI </li></ul></ul></ul><ul><ul><li>Physical, occupational, and speech therapy </li></ul></ul><ul><ul><li>Evaluation of swallowing </li></ul></ul><ul><ul><li>Treatment of HTN and DM </li></ul></ul><ul><ul><li>Correction of dehydration </li></ul></ul><ul><ul><li>Prevention and treatment of fever </li></ul></ul><ul><ul><li>Poststroke depression </li></ul></ul>
  48. 49. <ul><li>Use of anticoagulants </li></ul><ul><ul><li>Antiplatelet therapy remains treatment of choice to prevent recurrent thromboembolism in majority of patients </li></ul></ul><ul><ul><li>Anticoagulation may be appropriate </li></ul></ul><ul><ul><ul><li>Atrial fibrillation </li></ul></ul></ul><ul><ul><ul><li>Recent MI </li></ul></ul></ul><ul><ul><ul><li>Suspected propagation of thrombus or stroke in evolution </li></ul></ul></ul><ul><ul><li>Cranial CT needed to rule out intracerebral or subarachnoid hemorrhage </li></ul></ul><ul><ul><li>Baseline PT, PTT, platelet count, tests for hypercoagulable states </li></ul></ul><ul><ul><li>History of active peptic ulceration or uncontrolled hypertension </li></ul></ul>
  49. 50. <ul><li>Thrombolysis – t-PA </li></ul><ul><ul><li>Guidelines for treatment: </li></ul></ul><ul><ul><ul><li>Present within 3 hours of onset of clearly defined stroke – frequency of symptomatic hemorrhage most likely increases after this time </li></ul></ul></ul><ul><ul><ul><li>CT scan shows no evidence of intracranial hemorrhage </li></ul></ul></ul><ul><ul><li>No anticoagulants or antiplatelet agents given for 24 hours </li></ul></ul><ul><ul><li>Avoid BP values > defined above </li></ul></ul>
  50. 51. <ul><ul><li>Guidelines not to treat: </li></ul></ul><ul><ul><ul><li>Previous stroke or serious head trauma in preceding 3 months </li></ul></ul></ul><ul><ul><ul><li>History of intracranial hemorrhage </li></ul></ul></ul><ul><ul><ul><li>Repeated systolic BP’s > 185 mm Hg or diastolic BP’s > 110 mm Hg </li></ul></ul></ul><ul><ul><ul><li>Requires aggressive treatment to reduce BP to specified limits </li></ul></ul></ul><ul><ul><ul><li>Taking anticoagulants or propensity to hemorrhage </li></ul></ul></ul><ul><ul><ul><li>Recent invasive surgical procedure </li></ul></ul></ul><ul><ul><ul><li>Rapidly improving neurological deficit or minor symptoms </li></ul></ul></ul>
  51. 52. <ul><ul><li>Statistically significant improvement in stroke scale scores at 24 hours </li></ul></ul><ul><ul><li>At 3 months following stroke, proportion of patients with minimal or no disability was higher in treated patients </li></ul></ul><ul><ul><li>No significant differences in mortality between treated and untreated </li></ul></ul><ul><ul><li>No increase in number of patients given t-PA and left with severe disability </li></ul></ul><ul><ul><li>Treated patients more likely to sustain symptomatic intracerebral hemorrhage within first 36 hours </li></ul></ul><ul><ul><ul><li>Tended to have severe neurologic deficits and cerebral edema on CT </li></ul></ul></ul><ul><ul><li>Rate of asymptomatic intracerebral hemorrhage similar among treated (8%) and control (6%) </li></ul></ul>
  52. 53. <ul><li>Cerebral edema </li></ul><ul><ul><li>Large hemispheric infarctions can cause brain shift and transtentorial herniation </li></ul></ul><ul><ul><li>Intubation and hyperventilation produce transient cerebral vasoconstriction and may reduce intracranial pressure </li></ul></ul><ul><ul><li>Mannitol reduces volume surrounding unaffected brain but also transient </li></ul></ul><ul><ul><li>Corticosteroids no benefit in cytotoxic edema </li></ul></ul>
  53. 54. <ul><li>Hypertensive encephalopathy </li></ul><ul><ul><li>Diffuse cerebral effects of HTN not caused by infarction or hemorrhage </li></ul></ul><ul><ul><li>Potentially reversible with control of BP </li></ul></ul><ul><ul><li>Headache, visual blurring, confusion, and drowsiness </li></ul></ul><ul><ul><li>May have seizures </li></ul></ul><ul><ul><li>BP usually very high (250/150) </li></ul></ul><ul><ul><li>Papilledema and retinal hemorrhages usually seen on fundoscopy </li></ul></ul><ul><ul><li>CT and MRI show diffuse cerebral edema, especially in occipital lobes </li></ul></ul><ul><ul><li>Medical emergency </li></ul></ul><ul><ul><li>Prompt but controlled lowering of BP avoiding hypotension </li></ul></ul>
  54. 55. Extensive right-sided cerebral infarction (left side of picture) demonstrated by unenhanced CT scan, performed 4 days after the onset of stroke. There is no evidence of hemorrhage. High-quality CT scanners allow diagnosis of cerebral infarction within 6-8 hours of onset.
  55. 56. Cerebral embolism in a patient following cardiac surgery, demonstrated by unenhanced CT scan. The open arrowhead points to a high-density embolus within the distal right internal carotid artery; the filled arrowhead points to a similar embolus in the right middle cerebral artery. There is extensive hypodensity in the right middle cerebral artery distribution, reflecting an extensive area of infarction.
  56. 57. Right-sided facial palsy resulting from stroke. The patient also had right hemiplegia and complete aphasia. The signs are those of upper motor neuron lesion. The limbs are at first flaccid and areflexic, but after a variable period the reflexes recover and become exaggerated, and an extensor plantar response appears. Weakness in the face and elsewhere may recover gradually over a variable period of time.
  57. 58. Loss of postural stability is common following stroke. When the non-dominant hemisphere is involved, walking apraxia and loss of postural control are usually apparent. The patient is unable to sit upright and tends to fall sideways. Appropriate support with pillows or cushions should be provided.
  58. 59. Intracerebral Hemorrhage <ul><li>Diffuse – subarachnoid hemorrhage </li></ul><ul><li>Focal – intraparenchymal </li></ul><ul><li>Accounts for 20% of all strokes </li></ul><ul><li>Acute rise in intracranial pressure from arterial rupture frequently results in LOC at outset </li></ul><ul><li>Some patients die from herniation </li></ul>
  59. 60. Causes of Spontaneous Intracerebral Hemorrhage (ICH) <ul><li>Intraparenchymal hemorrhage </li></ul><ul><ul><li>Trauma </li></ul></ul><ul><ul><li>Hypertension </li></ul></ul><ul><ul><li>Amyloid (congophilic) angiopathy </li></ul></ul><ul><ul><li>Arteriovenous malformation </li></ul></ul><ul><ul><li>Bleeding diathesis (anticoagulants, thrombolytics) </li></ul></ul><ul><ul><li>Drugs (amphetamines, cocaine) </li></ul></ul><ul><li>Subarachnoid hemorrhage </li></ul><ul><ul><li>Congenital saccular aneurysm (85%) </li></ul></ul><ul><ul><li>Unknown (15%) </li></ul></ul>
  60. 61. <ul><ul><li>Hypertensive intracerebral hemorrhage </li></ul></ul><ul><ul><ul><li>Often occurs at same sites affected by lacunar infarctions </li></ul></ul></ul><ul><ul><ul><li>Charcot-Bouchard aneurysms: microaneurysms identified pathologically in some cases </li></ul></ul></ul><ul><ul><ul><li>Commonest sites: </li></ul></ul></ul><ul><ul><ul><ul><li>Putamen – 40% </li></ul></ul></ul></ul><ul><ul><ul><ul><li>Thalamus – 12% </li></ul></ul></ul></ul><ul><ul><ul><ul><li>Lobar white matter – 15% to 20% </li></ul></ul></ul></ul><ul><ul><ul><ul><li>Caudate – 8% </li></ul></ul></ul></ul><ul><ul><ul><ul><li>Pons – 8% </li></ul></ul></ul></ul><ul><ul><ul><ul><li>Cerebellum – 8% </li></ul></ul></ul></ul><ul><ul><ul><li>CT readily identifies </li></ul></ul></ul><ul><ul><ul><li>Severity of headache generally correlates with size </li></ul></ul></ul>
  61. 62. <ul><ul><ul><li>Decreased level of alertness caused by: </li></ul></ul></ul><ul><ul><ul><ul><li>Mass effect </li></ul></ul></ul></ul><ul><ul><ul><ul><li>Increased intracranial pressure </li></ul></ul></ul></ul><ul><ul><ul><ul><li>Direct involvement of brain stem reticular activating system </li></ul></ul></ul></ul><ul><ul><ul><li>Seizures more frequent during acute phase than in ischemic stroke </li></ul></ul></ul><ul><ul><ul><li>Both basal ganglia and thalamic hemorrhages may rupture into adjacent ventricle and cause secondary hydrocephalus </li></ul></ul></ul><ul><ul><ul><li>Cerebellar hemorrhage may cause obstructive hydrocephalus from compression of fourth ventricle </li></ul></ul></ul>
  62. 63. <ul><ul><ul><li>With hematoma, level of consciousness often worsens first 24 to 48 hours after initial symptoms due to edema around lesion </li></ul></ul></ul><ul><ul><ul><li>Herniation if edema causes enough brain shift </li></ul></ul></ul><ul><ul><ul><ul><li>Direct pressure on vital brain stem structures </li></ul></ul></ul></ul><ul><ul><ul><ul><li>Infarction of adjacent blood vessels due to compression </li></ul></ul></ul></ul>
  63. 64. <ul><ul><li>Lobar hemorrhage </li></ul></ul><ul><ul><ul><li>Occur in peripheral distribution of cerebral white matter </li></ul></ul></ul><ul><ul><ul><li>More benign prognosis since usually smaller than hypertensive bleeds </li></ul></ul></ul><ul><ul><ul><li>Young persons: </li></ul></ul></ul><ul><ul><ul><ul><li>Arteriovenous malformations </li></ul></ul></ul></ul><ul><ul><ul><ul><li>Ingestion of sympathomimetic drugs </li></ul></ul></ul></ul><ul><ul><ul><li>Elderly persons: </li></ul></ul></ul><ul><ul><ul><ul><li>Congophilic amyloid angiopathy – signs develop insidiously as in anticoagulant-associated hemorrhage </li></ul></ul></ul></ul>
  64. 65. Diagnosis, Management, and Prognosis of ICH <ul><li>CT diagnostic test of choice </li></ul><ul><ul><li>hyperintense area with mass effect and later hypointense surrounding edema </li></ul></ul><ul><li>MRI less sensitive in early stages </li></ul><ul><li>Management depends on size and location </li></ul><ul><ul><li>In acute phase, mass effect far greater than in large cerebral infarction, so greater risk of herniation and death </li></ul></ul><ul><ul><li>In chronic phase, prognosis for surviving patients much better than with ischemic stroke </li></ul></ul>
  65. 66. <ul><li>Therapy directed at reducing mass effect </li></ul><ul><ul><li>Medical: controlled hyperventilation or mannitol </li></ul></ul><ul><ul><li>Surgical: rare </li></ul></ul><ul><ul><ul><li>Saved for cerebellar hemorrhages where at risk for acute obstructive hydrocephalus by compression of fourth ventricle or direct pressure on caudal brain stem </li></ul></ul></ul>
  66. 67. Hemorrhagic cerebral infarction demonstrated by unenhanced CT scan one day after the onset of stroke. Note the high-density hemorrhage within the low density of the edematous, infarcted region in the right hemisphere. Hemorrhage is evident from its onset on CT scanning.
  67. 68. Intracranial Aneurysms <ul><li>Three forms: </li></ul><ul><ul><li>Fusiform </li></ul></ul><ul><ul><ul><li>Represent ectatic dilatations of large arteries, usually basilar or intracranial carotid </li></ul></ul></ul><ul><ul><ul><li>Rarely rupture but may compress adjacent brain tissue or cranial nerves and cause local neurologic dysfunction </li></ul></ul></ul><ul><ul><ul><li>Rarely surgically accessible </li></ul></ul></ul><ul><ul><li>Mycotic </li></ul></ul><ul><ul><ul><li>Occur with bacterial endocardits from septic emboli </li></ul></ul></ul><ul><ul><ul><li>Often multiple </li></ul></ul></ul><ul><ul><ul><li>Located distally in arterial tree </li></ul></ul></ul><ul><ul><ul><li>Accessible to surgical repair if not respond to antibiotics </li></ul></ul></ul>
  68. 69. <ul><ul><li>Saccular </li></ul></ul><ul><ul><ul><li>Form at arterial bifurcations </li></ul></ul></ul><ul><ul><ul><li>80% located in anterior circulation </li></ul></ul></ul><ul><ul><ul><li>Congenital defect in artery with gradual deterioration from hemodynamic stress </li></ul></ul></ul><ul><ul><ul><li>Higher incidence in patients with polycystic kidney disease and Marfan’s syndrome </li></ul></ul></ul><ul><ul><ul><li>Present in approximately 6% of population </li></ul></ul></ul><ul><ul><ul><li>Multiple in 25% of cases </li></ul></ul></ul><ul><ul><ul><li>Annual incidence of rupture only 10 per 100,000 </li></ul></ul></ul><ul><ul><ul><li>If rupture, 33% die before reach hospital; another 20% die in hospital </li></ul></ul></ul><ul><ul><ul><li>Only 30% recover without significant disability </li></ul></ul></ul>
  69. 70. Right cavernous carotid aneurysm (arrowed), shown on coronal MRI. The signal void at the periphery of the aneurysm represents flowing blood, while the intensity in the central portion may represent either a clot or slowly flowing blood. MRI may demonstrate aneurysms clearly, but is much less successful than CT at demonstrating the presence or absence of blood in the subarachnoid space.
  70. 71. Berry aneurysm on the anterior communicating artery (a). The angiogram also shows that the anterior cerebral artery (b) is in spasm.
  71. 72. Subarachnoid Hemorrhage <ul><li>Aneurysms can rupture any time but more common during strenuous activity </li></ul><ul><li>Most common manifestation is headache </li></ul><ul><ul><li>“ worst headache of my life” </li></ul></ul><ul><li>Neck pain and rigidity </li></ul><ul><li>Loss of consciousness and vomiting common </li></ul><ul><li>Seen on CT in 95% of cases – location may suggest site of rupture </li></ul><ul><li>Normal CT not rule out so do lumbar puncture – xanthochromia (develops after 6 hours) </li></ul>
  72. 73. <ul><li>Contrast CT or MRI can show aneurysms > 5 mm as well as arteriovenous malformations </li></ul><ul><li>Gold standard – cerebral angiography </li></ul><ul><ul><li>Intracranial aneurysms </li></ul></ul><ul><ul><li>Performed when considering surgery </li></ul></ul><ul><li>Complications </li></ul><ul><ul><li>Hypertension (systemic and intracranial) </li></ul></ul><ul><ul><li>Vasospasm – peak timing is between 5 and 9 days after bleed and may cause change in neuro status </li></ul></ul><ul><ul><li>Hemorrhage (rebleeding) </li></ul></ul><ul><ul><li>Hydrocephalus </li></ul></ul><ul><ul><li>Hyponatremia (SIADH; cerebral salt wasting) </li></ul></ul>
  73. 74. Hunt and Hess Classification of Subarachnoid Hemorrhage <ul><li>Classification Symptoms </li></ul><ul><ul><li>Grade I </li></ul></ul><ul><ul><ul><li>Asymptomatic of minimal headache and slight nuchal rigidity. </li></ul></ul></ul><ul><ul><li>Grade II </li></ul></ul><ul><ul><ul><li>Moderate to severe headache, nuchal rigidity, no neurological deficit other than cranial nerve palsy. </li></ul></ul></ul><ul><ul><li>Grade III </li></ul></ul><ul><ul><ul><li>Drowsiness, confusion, or mild focal deficit . </li></ul></ul></ul><ul><ul><li>Grade IV </li></ul></ul><ul><ul><ul><li>Stupor, moderate to severe hemiparesis, possible early decerebrate ridigity and vegetative disturbance. </li></ul></ul></ul><ul><ul><li>Grade V </li></ul></ul><ul><ul><ul><li>Deep coma, decerebrate ridigity, moribund appearance. </li></ul></ul></ul>
  74. 75. Subarachnoid hemorrhage from an anterior communicating artery aneurysm. This uncontrasted CT scan shows areas of increased density representing blood in the interhemispheric fissure (arrows) and the septum pellucidum (arrowheads). A lesser amount of blood is present in the sylvan fissures and the perimesencephalic cistern.
  75. 76. Vascular Malformations <ul><li>Venous angiomas </li></ul><ul><ul><li>Most common </li></ul></ul><ul><ul><li>Tend to lie close to brain surface </li></ul></ul><ul><li>Capillary telangiectases </li></ul><ul><ul><li>Composed of capillaries </li></ul></ul><ul><ul><li>Typically located within brain stem </li></ul></ul><ul><li>Cavernous angiomas </li></ul><ul><ul><li>Composed of dilated sinusoidal channels </li></ul></ul><ul><ul><li>Readily seen on CT </li></ul></ul><ul><ul><li>Rarely bleed </li></ul></ul>
  76. 77. <ul><li>Arteriovenous malformations </li></ul><ul><ul><li>Composed of tangles of arteries connected directly to veins </li></ul></ul><ul><ul><li>May produce headache, seizures, or hemorrhage </li></ul></ul><ul><ul><li>Account for 1% of all strokes </li></ul></ul><ul><ul><li>Initial bleed before fourth decade – 7% rebleed in first year after </li></ul></ul><ul><ul><li>Hemorrhage into brain parenchyma, subarachnoid space, or intraventricular space </li></ul></ul><ul><ul><li>In older patients (> 55 years), treated conservatively </li></ul></ul><ul><ul><li>In younger patients, mostly treated with surgical removal but also by irradiation with embolization of artery </li></ul></ul>
  77. 78. Left parietal arteriovenous malformation, shown in an anteroposterior view of an internal carotid angiogram. Bleeding from AVM is usually less severe than that from aneurysms, but their size may lead to other symptoms including epilepsy.
  78. 79. Glasgow Outcome Scale (GOS) <ul><li>1) Good recovery - patient can lead a full and independent life with or without minimal neurological deficit. </li></ul><ul><li>2) Moderately disabled - patient has neurological or intellectual impairment but is independent. </li></ul><ul><li>3) Severely disabled - Patient conscious but totally dependent on others to get through daily activities. </li></ul><ul><li>4) Vegetative survival </li></ul><ul><li>5) Dead </li></ul>
  79. 80. Infarction in CT Imaging of the Brain in Acute Stroke <ul><li>Infarction: focal hypodense area, in cortical, subcortical, or deep gray or white matter, following vascular territory, or watershed distribution. Early subtle findings include obscuration of gray/white matter contrast and effacement of sulci, or &quot;insular ribbon.&quot; </li></ul>
  80. 81. <ul><li>Hemorrhage: hyperdense image in white or deep gray matter, with or without involvement of cortical surface (40 to 90 HU). Petechial refers to scattered hyperdense points, coalescing to form irregularly hyperdense areas with hypodense interruptions. Hematoma refers to a solid, homogeneously hyperdense image. </li></ul>
  81. 82. <ul><li>Hyperdense image in major intracranial artery: suggestive of vascular embolic material.    </li></ul><ul><li>Calcification: hyperdense image within or attached to vessel wall (>120 HU).    </li></ul><ul><li>Incidental: silent infarct, subdural collection, tumor, giant aneurysm, arteriovenous malformation. </li></ul>
  82. 83. Infarction in MRI of the Brain in Acute Stroke <ul><li>Acute: Subtle low signal (hypointense) on T1, often difficult to see at this stage, and high signal (hyperintense) on spin density and/or T2-weighted and proton density-weighted images starting 8 h after onset; should follow vascular distribution. Mass effect maximal at 24 h, sometimes starting 2 h after onset, even in the absence of parenchymal signal changes. No parenchymal enhancement with paramagnetic contrast agent. Territorial intravascular paramagnetic contrast enhancement of &quot;slow-flow&quot; arteries in hyperacute infarcts; at 48 h, parenchymal and meningeal enhancement can be expected. </li></ul>
  83. 84. <ul><li>Subacute (1 wk or older): Low signal on T1, high signal on T2-weighted images. Follows vascular distribution. Revascularization and blood-brain barrier breakdown may cause parenchymal enhancement with contrast agents.    </li></ul><ul><li>Old (several weeks to years): Low signal on T1, high signal on T2. Mass effect disappears after 1 mo. Loss of tissue with large infarcts. Parenchymal enhancement fades after several months. </li></ul>
  84. 85. Hemorrhage in MRI of the Brain <ul><li>Hyperacute </li></ul><ul><ul><li>Hours old, mainly oxyhemoglobin with surrounding edema </li></ul></ul><ul><ul><li>T1 Weighted: Hypointense </li></ul></ul><ul><ul><li>T2 Weighted: Hyperintense </li></ul></ul><ul><li>Acute </li></ul><ul><ul><li>Days old, mainly deoxyhemoglobin with surrounding edema </li></ul></ul><ul><ul><li>T1 Weighted: Hypointense </li></ul></ul><ul><ul><li>T2 Weighted: Hypointense, surrounded by hyperintense margin </li></ul></ul>
  85. 86. <ul><li>Subacute </li></ul><ul><ul><li>Weeks old, mainly methemoglobin </li></ul></ul><ul><ul><li>T1 Weighted: Hyperintense </li></ul></ul><ul><ul><li>T2 Weighted: Hypointense, early subacute with predominantly intracellular methemoglobin. Hyperintense, late subacute with predominantly extracellular methemoglobin </li></ul></ul><ul><li>Chronic </li></ul><ul><ul><li>Years old, hemosiderin slit or hemosiderin margin surrounding fluid cavity </li></ul></ul><ul><ul><li>T1 Weighted: Hypointense </li></ul></ul><ul><ul><li>T2 Weighted: Hypointense slit, or hypointense margin surrounding hyperintense fluid cavity </li></ul></ul>