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This document discusses various types of cerebrovascular diseases including stroke, TIA, and aneurysms. It defines stroke as a focal neurological disturbance lasting over 24 hours caused by a blood vessel problem in the brain. TIA is similar but symptoms resolve within 24 hours. The document outlines risk factors for stroke including hypertension, atrial fibrillation, and diabetes. It describes clinical manifestations of strokes in different brain arteries and associated neurological deficits.

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Introduction • Include ; – TIA – Stroke – cerebrovascular anomalies such as intracranial aneurysms – arteriovenous malformations (AVMs). 8/7/2023 Dr.Tamiru S. 2
– Stroke; rapidly developed clinical sign of focal disturbance of cerebral function of presumed vascular origin and of more than 24 hours – Cerebral ischemia is caused by a reduction in blood flow that lasts longer than several seconds. – Infarction – absence of blood flow more than a few minutes 8/7/2023 3 Dr.Tamiru S.
– TIA; all neurologic signs and symptoms resolve within 24 hours regardless of whether there is imaging evidence of new permanent brain injury – TIA recovery is complete within 24 hours. • 10% of patients will go on to have a stroke. 8/7/2023 4 Dr.Tamiru S.
– Neurologic symptoms are manifest within seconds because neurons lack glycogen, so energy failure is rapid – When blood flow is quickly restored, brain tissue can recover fully and the patient's symptoms are only transient 8/7/2023 5 Dr.Tamiru S.
– Focal ischemia or infarction is caused by thrombosis of the cerebral vessels or by emboli from a proximal arterial source or the heart. – Intracranial hemorrhage is caused by bleeding directly into or around the brain; it produces neurologic symptoms; • by producing a mass effect on neural structures • from the toxic effects of blood itself • increasing intracranial pressure. 8/7/2023 6 Dr.Tamiru S.
Stroke – is the third largest killer in the Western World. – is one of the major causes of disability, particularly in the elderly. – patients may present with a variety of physical, cognitive and psychosocial problems. – Most patients show signs of recovery over time. 8/7/2023 7 Dr.Tamiru S.
8 Epidemiology Ethiopia – Important cause of hospital morbidity & mortality – 6.5% of admissions were due to stroke – Study in Tikur Anbessa hospital ( Sept. 2000 - Aug.2001) • Hemorrhagic stroke – the most common  57% (of all patients)  59.2% (of those with CT)
• Peak incidence  55-64yrs • HTN the most frequent risk factor (65.6%) followed by cardiac disease (22.7%) • The overall mortality 44.5% Ethiop Med J. 2005 Oct;43(4):251-9 8/7/2023 Dr.Tamiru S. 9
Sub-types Of Stroke • Ischemic - 85% Thrombotic 25% -lacunar 20-25% -large vessel 1-5% Embolic 75% -cardioembolic 20% -artery to artery 15% -cryptogenic 30% -others 10% 8/7/2023 10 Dr.Tamiru S.
• Hemorrhagic -15% – ICH- 10% – SAH- 5% 8/7/2023 11 Dr.Tamiru S.
Embolic – The occlusion is caused by an embolus (solid, liquid, or gaseous mass) carried to a blood vessel from another area – Most common emboli are blood clots – Risk factors for blood clots include Atrial Fibrillation and diseased or damaged carotid or vertebral arteries 8/7/2023 12 Dr.Tamiru S.
– Rare causes of emboli include air, tumor tissue, and fat – Occurs suddenly & may rarely be accompanied by headache – Sudden, maximum deficit at the onset – Common sites »MCA or one of the branches »PCA »ACA( infrequently) 8/7/2023 Dr.Tamiru S. 13
Thrombotic – The occlusion is caused by a cerebral thrombus; a blood clot which develops gradually in a previously diseased artery and obstructs it – Caused by atherosclerosis: • platelets adhere to the roughened surface of the plaque deposit and a blood clot is created • atheromatous plaque results in narrowing and reduction of blood flow 8/7/2023 14 Dr.Tamiru S.
Ischemic Stroke CBF & Ischemic Thresholds – Normal CBF 50-60 ml/100 g/minute • Varies in different regions of the brain – CBF 20-30ml/100g/min Loss of electrical activity – CBF 10 ml/100g/min Neuronal death 8/7/2023 15 Dr.Tamiru S.
Brain can’t tolerate decrease in blood flow for a long time - 0ml/100 g tissue per minute ---4-10min - 16-18ml/100 g tissue per minute---hours - <20ml/100 g tissue per minute---ischemia unless prolonged for hours or days 8/7/2023 16 Dr.Tamiru S.
– Acute occlusion of an intracranial vessel causes reduction in blood flow to the brain region it supplies. – The magnitude of flow reduction is a function of collateral blood flow and this depends on individual vascular anatomy, the site of occlusion, and likely systemic blood pressure. 8/7/2023 17 Dr.Tamiru S.
– Tissue surrounding the core region of infarction is ischemic but reversibly dysfunctional and is referred to as the ischemic penumbra. – The ischemic penumbra will eventually infarct if no change in flow occurs, and hence saving the ischemic penumbra is the goal of revascularization therapies. 8/7/2023 18 Dr.Tamiru S.
Focal cerebral infarction occurs via two distinct pathways (1)a necrotic pathway; cellular cytoskeletal breakdown due to energy failure of the cell (2)apoptotic pathway; cells become programmed to die. 8/7/2023 19 Dr.Tamiru S.
– Ischemia produces necrosis by starving neurons of glucose and oxygen, which in turn results in failure of mitochondria to produce ATP. – Without ATP, membrane ion pumps stop functioning and neurons depolarize, allowing intracellular calcium to rise. 8/7/2023 20 Dr.Tamiru S.
– Cellular depolarization also causes glutamate release from synaptic terminals; excess extracellular glutamate produces neurotoxicity by activating postsynaptic glutamate receptors that increase neuronal calcium influx. 8/7/2023 21 Dr.Tamiru S.
– Free radicals are produced by membrane lipid degradation and mitochondrial dysfunction. – Fever dramatically worsens brain injury during ischemia, as does hyperglycemia [ 200 mg/dl]. 8/7/2023 Dr.Tamiru S. 22
Causes of Ischemic Stroke Common Causes • Thrombosis  Lacunar stroke (small vessel)  Large vessel thrombosis  Dehydration • Embolic occlusion 1. Artery-to-artery Carotid bifurcation Aortic arch Arterial dissection 8/7/2023 23 Dr.Tamiru S.
2. Cardioembolic Atrial fibrillation Mural thrombus Myocardial infarction Dilated cardiomyopathy Valvular lesions  Mitral stenosis  Mechanical valve  Bacterial endocarditis 8/7/2023 24 Dr.Tamiru S.
• Paradoxical embolus  Atrial septal defect  Patent foramen ovale Atrial septal aneurysm Spontaneous echo contrast 8/7/2023 25 Dr.Tamiru S.
Uncommon Causes – Hypercoagulable disorders – Venous sinous thrombosis – Fibromuscular dysplasia – Vasculitis – Subarachnoid hemorrhage vasospasm – Drugs: cocaine, amphetamine – Moyamoya disease – Eclampsia • Cardiogenic  Mitral valve calcification  Atrial myxoma  Intracardiac tumor  Marantic endocarditis  Libman-Sacks endocarditis 8/7/2023 26 Dr.Tamiru S.
Risk Factors Ethiopia Established hypertension- 65.6% Cardiac disease - 22.7% Established diabetes -11.7% TIA Previous stroke Atrial fibrillation *most patient were not on treatment for hypertension *majority of cardiac pts have VHD *AF was found in most of the cardiac patients but treatment was not started for most of them 8/7/2023 27 Dr.Tamiru S.
Risk Factors for Stroke 8/7/2023 28 Dr.Tamiru S.
• Nonmodifiable – Age – Gender – Race/ethnicity – Family history – Genetics 8/7/2023 29 Dr.Tamiru S.
• Patients at risk should be brought to ER if they develop –Loss of sensory/motor function –Change in vision, gait, ability to speak or understand –Severe headache 8/7/2023 30 Dr.Tamiru S.
Clinical Manifestations Internal Carotid Artery – often clinically silent if the circle of Willis is complete. – transient monocular blindness (also called amaurosis fugax). 8/7/2023 31 Dr.Tamiru S.
– Severe stenosis if bilateral, can cause hypoperfusion of the cerebral hemispheres and symptoms in border zones between the MCA and other major vascular territories (watershed areas), especially if superimposed on generalized hypoperfusion secondary to severe hypotension. 8/7/2023 32 Dr.Tamiru S.
Anterior Cerebral Artery – is relatively rare in comparison to strokes in other major branches of the circle of Willis – account for 2% of all cerebral infarcts. – upper motor neuron weakness and cortical sensory deficits (neglect) in contralateral leg. – leg weakness > arm weakness 8/7/2023 33 Dr.Tamiru S.
– urinary incontinence, generalized depression of psychomotor activity (abulia), and transcortical motor aphasia manifested as loss of verbal fluency with preserved ability to repeat. – bilateral damage usually causes a patient to be mute, with severe mood disturbances and long- lasting incontinence. 8/7/2023 34 Dr.Tamiru S.
Middle Cerebral Artery – are the most common site of stroke 2/3 of all infarcts. – edema during the first 3 to 4 days may lead to severely increased intracranial pressure and herniation. 8/7/2023 35 Dr.Tamiru S.
– Contralateral weakness – Face & arm > leg – Aphasia – dominant hemisphere – Neglect – non-dominant hemisphere – Neglect may be motor, verbal or visual – Head & eye deviation toward side of infarct. – hemianopia common in large MCA infarcts 8/7/2023 36 Dr.Tamiru S.
– Strokes of the inferior division in the dominant hemisphere characteristically produce receptive aphasia of the Wernicke type (severe loss of speech comprehension with preserved spoken and written language). – Occlusion of more distal branches causes less clinical damage. 8/7/2023 37 Dr.Tamiru S.
Posterior Cerebral Artery – In about 3/4, both posterior cerebral arteries (PCAs) arise from the basilar artery; in most others, one PCA arises from the basilar artery and the other arises from the ICA. – In a few individuals, both PCAs originate from the ICAs – As a consequence, the syndromes associated with occlusion of the PCA are highly variable. 8/7/2023 38 Dr.Tamiru S.
Posterior Cerebral Artery Infarction Thalamic lesions: – Sensory symptoms: loss of tactile, temperature & pain sensation – Typically complain of numbness & tingling on one side of the body – Hypoesthesia and dysesthesia common 8/7/2023 39 Dr.Tamiru S.
Occipital Lesions: – Homonymous visual field defect – May cause midbrain lesions leading to oculomotor palsy or internuclear ophthalmoplegia 8/7/2023 40 Dr.Tamiru S.
Cerebellar Infarction – May cause a pure vestibular syndrome leading to misdiagnosis of labyrinthitis – Increased ICP 6-12 h secondary to edema may require emergent surgical decompression – Vertigo, headache, Nystagmus 8/7/2023 41 Dr.Tamiru S.
– Strokes of the perforating branches cause complete contralateral hemianesthesia with loss of all sensation because of collateral blood supply from the MCA. 8/7/2023 42 Dr.Tamiru S.
– Difficulty reading (dyslexia) and performing calculations (dyscalculia) may occur. – Recovery is often good, but the initial numbness may be replaced by paresthesias or excruciating pain; this Dejerine-Roussy syndrome is caused by damage to the thalamus. 8/7/2023 43 Dr.Tamiru S.
– Involvement of the subthalamic nucleus may produce hemiballismus, with wild flinging movements of the limbs on one side of the body. – Distal branch occlusions of the PCA cause partial syndromes; occlusion of the terminal branch can produce a variety of incomplete visual field deficits. 8/7/2023 44 Dr.Tamiru S.
Vertebral and Basilar Arteries – Characteristic of occlusion of the blood supply to the brain stem are “crossed syndromes” (i.e., contralateral loss of strength and selected contralateral and ipsilateral sensory symptoms below the level of the lesion, in addition to ipsilateral motor and sensory deficits localized to the level of the lesion). 8/7/2023 45 Dr.Tamiru S.
– Severe vertigo, nausea, vomiting, nystagmus, ipsilateral ataxia (of the cerebellar type), and ipsilateral Horner's syndrome (ptosis, myosis, and decreased sweating). 8/7/2023 46 Dr.Tamiru S.
Diagnosis • History • Time of onset of symptoms • Did the patient wake up with symptoms? 8/7/2023 47 Dr.Tamiru S.
Physical Examination – Helps localize the site of the lesion – Arterial blood pressure, including measurement in both arms to evaluate the possibility of aortic dissection or vascular abnormalities that result in reduced blood flow to the brain when the arms are exercised (subclavian steal). – The pulse may reveal arrhythmias 8/7/2023 48 Dr.Tamiru S.
– Cardiac murmurs may suggest valvular lesions – Bruits of the carotid arteries – Ophthalmoscopic visualization of retinal cholesterol or platelet-fibrin emboli suggests more proximal atherosclerotic disease 8/7/2023 49 Dr.Tamiru S.
Laboratory Examination – CBC – ESR – RBS/FBS – A prothrombin time and partial thromboplastin time – Lipid profile – VDRL 8/7/2023 50 Dr.Tamiru S.
– Tests for homocysteinuria, collagen vascular diseases, amyloidosis – Antiphospholipid antibodies are elevated in some patients with immune-related diseases. – Measurement of protein C, protein S, antithrombin III, blood viscosity, and platelet function 8/7/2023 51 Dr.Tamiru S.
• Cardiovascular Testing – Echocardiography – ECG 8/7/2023 52 Dr.Tamiru S.
Noninvasive Brain Imaging – Which is essential to verify causes of focal neurologic dysfunction, can generally distinguish ischemic stroke from other diseases. 8/7/2023 53 Dr.Tamiru S.
Imaging Studies in Stroke CT SCAN – Preferred standard initial modality in all acute strokes – Better than MRI for detection of Acute blood – Can identify other ICSOL mimickers of stroke 8/7/2023 54 Dr.Tamiru S.
• Pitfalls –Infarcts missed / not reliably seen in the first 24-48 hrs –Misses small cortical infarcts –Misses posterior fossa infarcts b/c of bone artifact 8/7/2023 Dr.Tamiru S. 55
MRI – Shows location and extent of infarction in all areas – Less sensitive for acute blood – More expensive, time consuming, not readily available – cannot be used in patients who have ferromagnetic materials within their bodies, is often impossible to use in critically ill patients – Outside the acute period – more useful – MRI perfusion studies, Diffusion weighted image – MR angiography 8/7/2023 56 Dr.Tamiru S.
Cerebral Angiography – is reserved for patients who are suspected to have a surgically correctable lesion 8/7/2023 57 Dr.Tamiru S.
Cerebral Angiography • “Gold- Standard” for stenosis, aneurysm, vasospasm, thrombi,vasculitis,FMD,AVF • Therapeutic –Stents –Balloon angioplasty –Embolization –Intra- Arterial thrombolytics • Invasive, not widely available, risky 8/7/2023 58 Dr.Tamiru S.
Ultrasound • “Duplex U/Sound”– can identify stenosis at the origin of internal carotid artery • TCD of MCA, ACA, PCA ,Vertebro-basilar flow Perfusion Techniques • CT , MRI perfusion scans • SPECT 8/7/2023 59 Dr.Tamiru S.
Treatment • After the clinical diagnosis of stroke is made, an orderly process of evaluation and treatment should follow • The first goal is to prevent or reverse brain injury. 8/7/2023 60 Dr.Tamiru S.
• ABC • Immediate Imaging • Ischemic Stroke diagnosed………….. 1. Medical Support 2. Thrombolysis 3. Anticoagulation 4. Antiplatelet agents 5. Neuroprotection 6. Stroke centers and rehabilitation. 8/7/2023 61 Dr.Tamiru S.
Medical Support • Optimize cerebral perfusion to the penumbra • Prevent/Treat complications of bedridden pts • Infections, DVT, PE Blood Pressure Mx • BP Should be lowered only if »Malignant HTN »>185/110 »Thrombolytic planned • B blockers ( esmolol, labetolol) 8/7/2023 62 Dr.Tamiru S.
• Treat fever • Maintain serum glucose < 200 mg/dl Raised ICP – 5-10% have significant edema---Peak at 2-3 day – Standard treatment – Craniotomy, hemicraniectomy 8/7/2023 63 Dr.Tamiru S.
Thrombolysis 8/7/2023 64 Dr.Tamiru S.
8/7/2023 65 Dr.Tamiru S.
HEMORRHAGIC CEREBROVASCULAR DISEASE – Can be diffuse (i.e., bleeding into the subarachnoid or intraventricular spaces) or focal (intraparenchymal hemorrhage). – About 2/3 of intracranial bleeding are predominantly subarachnoid hemorrhages, whereas about a third are intracerebral hemorrhages. 8/7/2023 66 Dr.Tamiru S.
SUBARACHNOID HEMORRHAGE Causes • Saccular aneurysm • Trauma • AVM • Extension from an intraparenchymal hge • Neoplasms • Vasculitis 8/7/2023 67 Dr.Tamiru S.
Saccular (“Berry”) Aneurysm – About 2% of adults harbor intracranial aneurysms – For patients who arrive alive at hospital, the mortality rate over the next month is about 45%. – From survivors, >50% left with major neurologic deficits as a result of the initial hemorrhage, cerebral vasospasm with infarction, or hydrocephalus. 8/7/2023 68 Dr.Tamiru S.
– If the patient survives but the aneurysm is not obliterated, the rate of rebleeding is about 20% in the first 2 weeks and about 3% per year afterwards. – Unruptured, asymptomatic aneurysms are much less dangerous than a recently ruptured aneurysm. – The annual risk of rupture for aneurysms <10 mm in size is ~0.1%, and for aneurysms ≥10 mm in size is ~0.5 to 1%; 8/7/2023 69 Dr.Tamiru S.
– The three most common locations are the terminal internal carotid artery, MCA bifurcation, and top of the basilar artery. – They often cause symptoms by compressing the adjacent brain or cranial nerves 8/7/2023 70 Dr.Tamiru S.
– Approximately 85% of aneurysms occur in the anterior circulation, mostly on the circle of Willis. – About 20% of patients have multiple aneurysms, many at mirror sites bilaterally. 8/7/2023 71 Dr.Tamiru S.
Clinical Manifestations – Most unruptured are completely asymptomatic. – The classic symptom of a subarachnoid hemorrhage is a very rapidly developing, severe headache, typically called the “worst headache of my life,” that is sometimes accompanied by a stiff neck. – The headache is usually generalized, often with neck stiffness, and vomiting is common. 8/7/2023 72 Dr.Tamiru S.
– sudden transient loss of consciousness that occurs in nearly half of patients- 10 % prolonged – most patients first complain of headache upon regaining consciousness. 8/7/2023 73 Dr.Tamiru S.
Delayed Complications Rerupture • At 2wks-20% • At 4 wks-30% • Peak 7 days • Mortality – 60% • Early treatment eliminates this risk. 8/7/2023 74 Dr.Tamiru S.
Hydrocephalus – Acute hydrocephalus can cause stupor and coma. – Subacute hydrocephalus develops over a few days or weeks and causes progressive drowsiness or slowed mentation (abulia) with incontinence. – Chronic hydrocephalus may develop weeks to months after SAH and manifest as gait difficulty, incontinence, or impaired mentation. 8/7/2023 75 Dr.Tamiru S.
Vasospasm – Narrowing of the arteries at the base of the brain following SAH causes symptomatic ischemia and infarction in ~30% – Major cause of delayed morbidity and death. – Appear 4 to 14 days after the hemorrhage, most often at 7 days. – The severity and distribution of vasospasm determine whether infarction will occur. 8/7/2023 76 Dr.Tamiru S.
Hyponatremia – In the first 2 weeks following SAH – It usually results from inappropriate secretion of vasopressin and secretion of atrial and brain natriuretic factors, which produce a natriuresis. – clears over the course of 1 to 2 wks – should not be treated with free-water restriction as this may increase the risk of stroke. 8/7/2023 77 Dr.Tamiru S.
Laboratory Findings – CBC – Clotting times should be determined to assess whether the patient has an infection or clotting abnormalities. – Blood should also be sent for electrolyte analysis to serve as a baseline for detecting later complications. 8/7/2023 78 Dr.Tamiru S.
Imaging 95 % - detected by CT Scan within 72 hrs LP  spinal fluid yellow (xanthochromic) within 6 to 12 h of SAH.  Peaks at 48 h  lasts for 1 to 4 weeks, depending on the amount of subarachnoid blood. 8/7/2023 79 Dr.Tamiru S.
– Conventional x-ray angiography (both carotids and both vertebrals) to localize and define the anatomic details of the aneurysm and to determine if other unruptured aneurysms exist – CT angiography is an alternative method for locating the aneurysm 8/7/2023 80 Dr.Tamiru S.
• ECG – ST-segment and T-wave changes – Prolonged QRS complex, increased QT interval, and prominent “peaked” or deeply inverted symmetric T waves are usually secondary to the intracranial hemorrhage 8/7/2023 81 Dr.Tamiru S.
TREATMENT • Medical – ABC – BP control, maintain adequate cerebral perfusion – Raised ICP (e.g., mild hyperventilation, mannitol, and sedation) – bed rest in a quiet room and stool softeners – mild sedation and analgesia – hydration is necessary to avoid a decrease in blood volume predisposing to brain ischemia. 8/7/2023 82 Dr.Tamiru S.
– phenytoin is often given as prophylactic therapy since a seizure may promote rebleeding. – Glucocorticoids routine use is not recommended. 8/7/2023 83 Dr.Tamiru S.
• Antifibrinolytic agents are not routinely prescribed but may be considered in patients in whom aneurysm treatment cannot proceed immediately. – associated with a reduced incidence of aneurysmal rerupture but associated with an increased incidence of delayed cerebral infarction and DVT. 8/7/2023 84 Dr.Tamiru S.
• Vasospasm – remains the leading cause of morbidity and mortality – Treatment with the calcium channel antagonist nimodipine (60 mg orally every 4 h) improves outcome 8/7/2023 85 Dr.Tamiru S.
– Free-water restriction is contraindicated – supplemental oral salt coupled with normal saline will mitigate hyponatremia, but often patients also require hypertonic saline. 8/7/2023 86 Dr.Tamiru S.
– Pneumatic compression stockings applied to prevent pulmonary embolism – Systemic heparin is contraindicated in patients with ruptured and untreated aneurysms 8/7/2023 Dr.Tamiru S. 87
– ventricular drainage- raised ICP – An aneurysm can be “clipped” by a neurosurgeon or “coiled” by a neurointerventional radiologist. – Surgical repair involves placing a metal clip across the aneurysm neck, thereby immediately eliminating the risk of rebleeding. 8/7/2023 88 Dr.Tamiru S.
INTRAPARENCHYMAL HEMORRHAGE – is the most common type of intracranial hemorrhage. – It accounts for about 10% of all strokes and is associated with a 50% case fatality rate. 8/7/2023 89 Dr.Tamiru S.
– Hypertension, trauma, and cerebral amyloid angiopathy cause the majority of these hemorrhages. – Advanced age and heavy alcohol consumption increase the risk – cocaine use is one of the most important causes in the young. 8/7/2023 90 Dr.Tamiru S.
Hypertensive Intraparenchymal Hemorrhage – Usually results from spontaneous rupture of a small penetrating artery deep in the brain. – The most common sites are the basal ganglia (especially the putamen), thalamus, cerebellum, and pons. 8/7/2023 91 Dr.Tamiru S.
– When occur in other brain areas or in nonhypertensive patients, greater consideration should be given to hemorrhagic disorders, neoplasms, vascular malformations, and other causes. 8/7/2023 92 Dr.Tamiru S.
– Most develop over 30–90 minutes, whereas those associated with anticoagulant therapy may evolve for as long as 24–48 hours. – Within 48 hours macrophages begin to phagocytize the hemorrhage at its outer surface. – After 1–6 months, the hemorrhage is generally resolved to a slitlike orange cavity lined with glial scar and hemosiderin-laden macrophages. 8/7/2023 93 Dr.Tamiru S.
Clinical Manifestations – almost always occur while the patient is awake and sometimes when stressed. – presents as the abrupt onset of focal neurologic deficit- worsens steadily over 30–90 minutes . – Seizures are uncommon. – associated with a diminishing level of consciousness and signs of increased ICP such as headache and vomiting. 8/7/2023 94 Dr.Tamiru S.
Putamen – Most common site – Adjacent internal capsule is invariably involved – hemiparesis – Facial palsy – Slurred speech – Eyes- away from hemiparesis – If large—raised ICP and Brainstem compression 8/7/2023 95 Dr.Tamiru S.
Thalamus – hemiparesis/ hemiplegia – Prominent sensory deficit – Dejerine-Roussy Syndrome – Aphasia, mutism ,apractognosia – Visual field defect – Typical occular disturbances – Downward and inward looking eyes – Unequal pupils – Skew deviation – nystagmus 8/7/2023 96 Dr.Tamiru S.
Pons – Deep coma, quadriplegia – Decerebrate rigidity – Pin-point pupils, reacting to light – Absent Doll’s eye, occulovestibular reflex – Hyperpnea, hypertension, hyperhidrosis – Death in few hrs , small bleed can survive 8/7/2023 97 Dr.Tamiru S.
Cerebellum – Develop over several hrs – Occipital headache, repeated vomiting, ataxia – Dizziness, vertigo – Dysarthria and dysphagia may occur. – Brainstem compression, hydrocephalus – High index of suspicion 8/7/2023 98 Dr.Tamiru S.
Treatment – ABC – Nearly 50% of patients with a hypertensive ICH die – coagulopathy should be reversed as soon as possible – Treat severe hypertension to prevent hematoma progression 8/7/2023 99 Dr.Tamiru S.
Evacuation of hematoma – Evacuation of supratentorial hematomas does not appear to improve outcome. – Beneficial for Cerebellar • >3 cm –evacuate • 1-3 cm –monitor for raised ICP • <1 cm – if pt is alert and without brainstem signs, evacuation is unnecessary 8/7/2023 100 Dr.Tamiru S.

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Stroke.pptx

  • 2.
    Introduction • Include ; –TIA – Stroke – cerebrovascular anomalies such as intracranial aneurysms – arteriovenous malformations (AVMs). 8/7/2023 Dr.Tamiru S. 2
  • 3.
    – Stroke; rapidlydeveloped clinical sign of focal disturbance of cerebral function of presumed vascular origin and of more than 24 hours – Cerebral ischemia is caused by a reduction in blood flow that lasts longer than several seconds. – Infarction – absence of blood flow more than a few minutes 8/7/2023 3 Dr.Tamiru S.
  • 4.
    – TIA; allneurologic signs and symptoms resolve within 24 hours regardless of whether there is imaging evidence of new permanent brain injury – TIA recovery is complete within 24 hours. • 10% of patients will go on to have a stroke. 8/7/2023 4 Dr.Tamiru S.
  • 5.
    – Neurologic symptomsare manifest within seconds because neurons lack glycogen, so energy failure is rapid – When blood flow is quickly restored, brain tissue can recover fully and the patient's symptoms are only transient 8/7/2023 5 Dr.Tamiru S.
  • 6.
    – Focal ischemiaor infarction is caused by thrombosis of the cerebral vessels or by emboli from a proximal arterial source or the heart. – Intracranial hemorrhage is caused by bleeding directly into or around the brain; it produces neurologic symptoms; • by producing a mass effect on neural structures • from the toxic effects of blood itself • increasing intracranial pressure. 8/7/2023 6 Dr.Tamiru S.
  • 7.
    Stroke – is thethird largest killer in the Western World. – is one of the major causes of disability, particularly in the elderly. – patients may present with a variety of physical, cognitive and psychosocial problems. – Most patients show signs of recovery over time. 8/7/2023 7 Dr.Tamiru S.
  • 8.
    8 Epidemiology Ethiopia – Important causeof hospital morbidity & mortality – 6.5% of admissions were due to stroke – Study in Tikur Anbessa hospital ( Sept. 2000 - Aug.2001) • Hemorrhagic stroke – the most common  57% (of all patients)  59.2% (of those with CT)
  • 9.
    • Peak incidence 55-64yrs • HTN the most frequent risk factor (65.6%) followed by cardiac disease (22.7%) • The overall mortality 44.5% Ethiop Med J. 2005 Oct;43(4):251-9 8/7/2023 Dr.Tamiru S. 9
  • 10.
    Sub-types Of Stroke •Ischemic - 85% Thrombotic 25% -lacunar 20-25% -large vessel 1-5% Embolic 75% -cardioembolic 20% -artery to artery 15% -cryptogenic 30% -others 10% 8/7/2023 10 Dr.Tamiru S.
  • 11.
    • Hemorrhagic -15% –ICH- 10% – SAH- 5% 8/7/2023 11 Dr.Tamiru S.
  • 12.
    Embolic – The occlusionis caused by an embolus (solid, liquid, or gaseous mass) carried to a blood vessel from another area – Most common emboli are blood clots – Risk factors for blood clots include Atrial Fibrillation and diseased or damaged carotid or vertebral arteries 8/7/2023 12 Dr.Tamiru S.
  • 13.
    – Rare causesof emboli include air, tumor tissue, and fat – Occurs suddenly & may rarely be accompanied by headache – Sudden, maximum deficit at the onset – Common sites »MCA or one of the branches »PCA »ACA( infrequently) 8/7/2023 Dr.Tamiru S. 13
  • 14.
    Thrombotic – The occlusionis caused by a cerebral thrombus; a blood clot which develops gradually in a previously diseased artery and obstructs it – Caused by atherosclerosis: • platelets adhere to the roughened surface of the plaque deposit and a blood clot is created • atheromatous plaque results in narrowing and reduction of blood flow 8/7/2023 14 Dr.Tamiru S.
  • 15.
    Ischemic Stroke CBF &Ischemic Thresholds – Normal CBF 50-60 ml/100 g/minute • Varies in different regions of the brain – CBF 20-30ml/100g/min Loss of electrical activity – CBF 10 ml/100g/min Neuronal death 8/7/2023 15 Dr.Tamiru S.
  • 16.
    Brain can’t toleratedecrease in blood flow for a long time - 0ml/100 g tissue per minute ---4-10min - 16-18ml/100 g tissue per minute---hours - <20ml/100 g tissue per minute---ischemia unless prolonged for hours or days 8/7/2023 16 Dr.Tamiru S.
  • 17.
    – Acute occlusionof an intracranial vessel causes reduction in blood flow to the brain region it supplies. – The magnitude of flow reduction is a function of collateral blood flow and this depends on individual vascular anatomy, the site of occlusion, and likely systemic blood pressure. 8/7/2023 17 Dr.Tamiru S.
  • 18.
    – Tissue surroundingthe core region of infarction is ischemic but reversibly dysfunctional and is referred to as the ischemic penumbra. – The ischemic penumbra will eventually infarct if no change in flow occurs, and hence saving the ischemic penumbra is the goal of revascularization therapies. 8/7/2023 18 Dr.Tamiru S.
  • 19.
    Focal cerebral infarctionoccurs via two distinct pathways (1)a necrotic pathway; cellular cytoskeletal breakdown due to energy failure of the cell (2)apoptotic pathway; cells become programmed to die. 8/7/2023 19 Dr.Tamiru S.
  • 20.
    – Ischemia producesnecrosis by starving neurons of glucose and oxygen, which in turn results in failure of mitochondria to produce ATP. – Without ATP, membrane ion pumps stop functioning and neurons depolarize, allowing intracellular calcium to rise. 8/7/2023 20 Dr.Tamiru S.
  • 21.
    – Cellular depolarizationalso causes glutamate release from synaptic terminals; excess extracellular glutamate produces neurotoxicity by activating postsynaptic glutamate receptors that increase neuronal calcium influx. 8/7/2023 21 Dr.Tamiru S.
  • 22.
    – Free radicalsare produced by membrane lipid degradation and mitochondrial dysfunction. – Fever dramatically worsens brain injury during ischemia, as does hyperglycemia [ 200 mg/dl]. 8/7/2023 Dr.Tamiru S. 22
  • 23.
    Causes of IschemicStroke Common Causes • Thrombosis  Lacunar stroke (small vessel)  Large vessel thrombosis  Dehydration • Embolic occlusion 1. Artery-to-artery Carotid bifurcation Aortic arch Arterial dissection 8/7/2023 23 Dr.Tamiru S.
  • 24.
    2. Cardioembolic Atrial fibrillation Muralthrombus Myocardial infarction Dilated cardiomyopathy Valvular lesions  Mitral stenosis  Mechanical valve  Bacterial endocarditis 8/7/2023 24 Dr.Tamiru S.
  • 25.
    • Paradoxical embolus Atrial septal defect  Patent foramen ovale Atrial septal aneurysm Spontaneous echo contrast 8/7/2023 25 Dr.Tamiru S.
  • 26.
    Uncommon Causes – Hypercoagulabledisorders – Venous sinous thrombosis – Fibromuscular dysplasia – Vasculitis – Subarachnoid hemorrhage vasospasm – Drugs: cocaine, amphetamine – Moyamoya disease – Eclampsia • Cardiogenic  Mitral valve calcification  Atrial myxoma  Intracardiac tumor  Marantic endocarditis  Libman-Sacks endocarditis 8/7/2023 26 Dr.Tamiru S.
  • 27.
    Risk Factors Ethiopia Established hypertension-65.6% Cardiac disease - 22.7% Established diabetes -11.7% TIA Previous stroke Atrial fibrillation *most patient were not on treatment for hypertension *majority of cardiac pts have VHD *AF was found in most of the cardiac patients but treatment was not started for most of them 8/7/2023 27 Dr.Tamiru S.
  • 28.
    Risk Factors forStroke 8/7/2023 28 Dr.Tamiru S.
  • 29.
    • Nonmodifiable – Age –Gender – Race/ethnicity – Family history – Genetics 8/7/2023 29 Dr.Tamiru S.
  • 30.
    • Patients atrisk should be brought to ER if they develop –Loss of sensory/motor function –Change in vision, gait, ability to speak or understand –Severe headache 8/7/2023 30 Dr.Tamiru S.
  • 31.
    Clinical Manifestations Internal CarotidArtery – often clinically silent if the circle of Willis is complete. – transient monocular blindness (also called amaurosis fugax). 8/7/2023 31 Dr.Tamiru S.
  • 32.
    – Severe stenosisif bilateral, can cause hypoperfusion of the cerebral hemispheres and symptoms in border zones between the MCA and other major vascular territories (watershed areas), especially if superimposed on generalized hypoperfusion secondary to severe hypotension. 8/7/2023 32 Dr.Tamiru S.
  • 33.
    Anterior Cerebral Artery –is relatively rare in comparison to strokes in other major branches of the circle of Willis – account for 2% of all cerebral infarcts. – upper motor neuron weakness and cortical sensory deficits (neglect) in contralateral leg. – leg weakness > arm weakness 8/7/2023 33 Dr.Tamiru S.
  • 34.
    – urinary incontinence,generalized depression of psychomotor activity (abulia), and transcortical motor aphasia manifested as loss of verbal fluency with preserved ability to repeat. – bilateral damage usually causes a patient to be mute, with severe mood disturbances and long- lasting incontinence. 8/7/2023 34 Dr.Tamiru S.
  • 35.
    Middle Cerebral Artery –are the most common site of stroke 2/3 of all infarcts. – edema during the first 3 to 4 days may lead to severely increased intracranial pressure and herniation. 8/7/2023 35 Dr.Tamiru S.
  • 36.
    – Contralateral weakness –Face & arm > leg – Aphasia – dominant hemisphere – Neglect – non-dominant hemisphere – Neglect may be motor, verbal or visual – Head & eye deviation toward side of infarct. – hemianopia common in large MCA infarcts 8/7/2023 36 Dr.Tamiru S.
  • 37.
    – Strokes ofthe inferior division in the dominant hemisphere characteristically produce receptive aphasia of the Wernicke type (severe loss of speech comprehension with preserved spoken and written language). – Occlusion of more distal branches causes less clinical damage. 8/7/2023 37 Dr.Tamiru S.
  • 38.
    Posterior Cerebral Artery –In about 3/4, both posterior cerebral arteries (PCAs) arise from the basilar artery; in most others, one PCA arises from the basilar artery and the other arises from the ICA. – In a few individuals, both PCAs originate from the ICAs – As a consequence, the syndromes associated with occlusion of the PCA are highly variable. 8/7/2023 38 Dr.Tamiru S.
  • 39.
    Posterior Cerebral ArteryInfarction Thalamic lesions: – Sensory symptoms: loss of tactile, temperature & pain sensation – Typically complain of numbness & tingling on one side of the body – Hypoesthesia and dysesthesia common 8/7/2023 39 Dr.Tamiru S.
  • 40.
    Occipital Lesions: – Homonymousvisual field defect – May cause midbrain lesions leading to oculomotor palsy or internuclear ophthalmoplegia 8/7/2023 40 Dr.Tamiru S.
  • 41.
    Cerebellar Infarction – Maycause a pure vestibular syndrome leading to misdiagnosis of labyrinthitis – Increased ICP 6-12 h secondary to edema may require emergent surgical decompression – Vertigo, headache, Nystagmus 8/7/2023 41 Dr.Tamiru S.
  • 42.
    – Strokes ofthe perforating branches cause complete contralateral hemianesthesia with loss of all sensation because of collateral blood supply from the MCA. 8/7/2023 42 Dr.Tamiru S.
  • 43.
    – Difficulty reading(dyslexia) and performing calculations (dyscalculia) may occur. – Recovery is often good, but the initial numbness may be replaced by paresthesias or excruciating pain; this Dejerine-Roussy syndrome is caused by damage to the thalamus. 8/7/2023 43 Dr.Tamiru S.
  • 44.
    – Involvement ofthe subthalamic nucleus may produce hemiballismus, with wild flinging movements of the limbs on one side of the body. – Distal branch occlusions of the PCA cause partial syndromes; occlusion of the terminal branch can produce a variety of incomplete visual field deficits. 8/7/2023 44 Dr.Tamiru S.
  • 45.
    Vertebral and BasilarArteries – Characteristic of occlusion of the blood supply to the brain stem are “crossed syndromes” (i.e., contralateral loss of strength and selected contralateral and ipsilateral sensory symptoms below the level of the lesion, in addition to ipsilateral motor and sensory deficits localized to the level of the lesion). 8/7/2023 45 Dr.Tamiru S.
  • 46.
    – Severe vertigo,nausea, vomiting, nystagmus, ipsilateral ataxia (of the cerebellar type), and ipsilateral Horner's syndrome (ptosis, myosis, and decreased sweating). 8/7/2023 46 Dr.Tamiru S.
  • 47.
    Diagnosis • History • Timeof onset of symptoms • Did the patient wake up with symptoms? 8/7/2023 47 Dr.Tamiru S.
  • 48.
    Physical Examination – Helpslocalize the site of the lesion – Arterial blood pressure, including measurement in both arms to evaluate the possibility of aortic dissection or vascular abnormalities that result in reduced blood flow to the brain when the arms are exercised (subclavian steal). – The pulse may reveal arrhythmias 8/7/2023 48 Dr.Tamiru S.
  • 49.
    – Cardiac murmursmay suggest valvular lesions – Bruits of the carotid arteries – Ophthalmoscopic visualization of retinal cholesterol or platelet-fibrin emboli suggests more proximal atherosclerotic disease 8/7/2023 49 Dr.Tamiru S.
  • 50.
    Laboratory Examination – CBC –ESR – RBS/FBS – A prothrombin time and partial thromboplastin time – Lipid profile – VDRL 8/7/2023 50 Dr.Tamiru S.
  • 51.
    – Tests forhomocysteinuria, collagen vascular diseases, amyloidosis – Antiphospholipid antibodies are elevated in some patients with immune-related diseases. – Measurement of protein C, protein S, antithrombin III, blood viscosity, and platelet function 8/7/2023 51 Dr.Tamiru S.
  • 52.
    • Cardiovascular Testing –Echocardiography – ECG 8/7/2023 52 Dr.Tamiru S.
  • 53.
    Noninvasive Brain Imaging –Which is essential to verify causes of focal neurologic dysfunction, can generally distinguish ischemic stroke from other diseases. 8/7/2023 53 Dr.Tamiru S.
  • 54.
    Imaging Studies inStroke CT SCAN – Preferred standard initial modality in all acute strokes – Better than MRI for detection of Acute blood – Can identify other ICSOL mimickers of stroke 8/7/2023 54 Dr.Tamiru S.
  • 55.
    • Pitfalls –Infarcts missed/ not reliably seen in the first 24-48 hrs –Misses small cortical infarcts –Misses posterior fossa infarcts b/c of bone artifact 8/7/2023 Dr.Tamiru S. 55
  • 56.
    MRI – Shows locationand extent of infarction in all areas – Less sensitive for acute blood – More expensive, time consuming, not readily available – cannot be used in patients who have ferromagnetic materials within their bodies, is often impossible to use in critically ill patients – Outside the acute period – more useful – MRI perfusion studies, Diffusion weighted image – MR angiography 8/7/2023 56 Dr.Tamiru S.
  • 57.
    Cerebral Angiography – isreserved for patients who are suspected to have a surgically correctable lesion 8/7/2023 57 Dr.Tamiru S.
  • 58.
    Cerebral Angiography • “Gold-Standard” for stenosis, aneurysm, vasospasm, thrombi,vasculitis,FMD,AVF • Therapeutic –Stents –Balloon angioplasty –Embolization –Intra- Arterial thrombolytics • Invasive, not widely available, risky 8/7/2023 58 Dr.Tamiru S.
  • 59.
    Ultrasound • “Duplex U/Sound”–can identify stenosis at the origin of internal carotid artery • TCD of MCA, ACA, PCA ,Vertebro-basilar flow Perfusion Techniques • CT , MRI perfusion scans • SPECT 8/7/2023 59 Dr.Tamiru S.
  • 60.
    Treatment • After theclinical diagnosis of stroke is made, an orderly process of evaluation and treatment should follow • The first goal is to prevent or reverse brain injury. 8/7/2023 60 Dr.Tamiru S.
  • 61.
    • ABC • ImmediateImaging • Ischemic Stroke diagnosed………….. 1. Medical Support 2. Thrombolysis 3. Anticoagulation 4. Antiplatelet agents 5. Neuroprotection 6. Stroke centers and rehabilitation. 8/7/2023 61 Dr.Tamiru S.
  • 62.
    Medical Support • Optimizecerebral perfusion to the penumbra • Prevent/Treat complications of bedridden pts • Infections, DVT, PE Blood Pressure Mx • BP Should be lowered only if »Malignant HTN »>185/110 »Thrombolytic planned • B blockers ( esmolol, labetolol) 8/7/2023 62 Dr.Tamiru S.
  • 63.
    • Treat fever •Maintain serum glucose < 200 mg/dl Raised ICP – 5-10% have significant edema---Peak at 2-3 day – Standard treatment – Craniotomy, hemicraniectomy 8/7/2023 63 Dr.Tamiru S.
  • 64.
  • 65.
  • 66.
    HEMORRHAGIC CEREBROVASCULAR DISEASE –Can be diffuse (i.e., bleeding into the subarachnoid or intraventricular spaces) or focal (intraparenchymal hemorrhage). – About 2/3 of intracranial bleeding are predominantly subarachnoid hemorrhages, whereas about a third are intracerebral hemorrhages. 8/7/2023 66 Dr.Tamiru S.
  • 67.
    SUBARACHNOID HEMORRHAGE Causes • Saccularaneurysm • Trauma • AVM • Extension from an intraparenchymal hge • Neoplasms • Vasculitis 8/7/2023 67 Dr.Tamiru S.
  • 68.
    Saccular (“Berry”) Aneurysm –About 2% of adults harbor intracranial aneurysms – For patients who arrive alive at hospital, the mortality rate over the next month is about 45%. – From survivors, >50% left with major neurologic deficits as a result of the initial hemorrhage, cerebral vasospasm with infarction, or hydrocephalus. 8/7/2023 68 Dr.Tamiru S.
  • 69.
    – If thepatient survives but the aneurysm is not obliterated, the rate of rebleeding is about 20% in the first 2 weeks and about 3% per year afterwards. – Unruptured, asymptomatic aneurysms are much less dangerous than a recently ruptured aneurysm. – The annual risk of rupture for aneurysms <10 mm in size is ~0.1%, and for aneurysms ≥10 mm in size is ~0.5 to 1%; 8/7/2023 69 Dr.Tamiru S.
  • 70.
    – The threemost common locations are the terminal internal carotid artery, MCA bifurcation, and top of the basilar artery. – They often cause symptoms by compressing the adjacent brain or cranial nerves 8/7/2023 70 Dr.Tamiru S.
  • 71.
    – Approximately 85%of aneurysms occur in the anterior circulation, mostly on the circle of Willis. – About 20% of patients have multiple aneurysms, many at mirror sites bilaterally. 8/7/2023 71 Dr.Tamiru S.
  • 72.
    Clinical Manifestations – Mostunruptured are completely asymptomatic. – The classic symptom of a subarachnoid hemorrhage is a very rapidly developing, severe headache, typically called the “worst headache of my life,” that is sometimes accompanied by a stiff neck. – The headache is usually generalized, often with neck stiffness, and vomiting is common. 8/7/2023 72 Dr.Tamiru S.
  • 73.
    – sudden transientloss of consciousness that occurs in nearly half of patients- 10 % prolonged – most patients first complain of headache upon regaining consciousness. 8/7/2023 73 Dr.Tamiru S.
  • 74.
    Delayed Complications Rerupture • At2wks-20% • At 4 wks-30% • Peak 7 days • Mortality – 60% • Early treatment eliminates this risk. 8/7/2023 74 Dr.Tamiru S.
  • 75.
    Hydrocephalus – Acute hydrocephaluscan cause stupor and coma. – Subacute hydrocephalus develops over a few days or weeks and causes progressive drowsiness or slowed mentation (abulia) with incontinence. – Chronic hydrocephalus may develop weeks to months after SAH and manifest as gait difficulty, incontinence, or impaired mentation. 8/7/2023 75 Dr.Tamiru S.
  • 76.
    Vasospasm – Narrowing ofthe arteries at the base of the brain following SAH causes symptomatic ischemia and infarction in ~30% – Major cause of delayed morbidity and death. – Appear 4 to 14 days after the hemorrhage, most often at 7 days. – The severity and distribution of vasospasm determine whether infarction will occur. 8/7/2023 76 Dr.Tamiru S.
  • 77.
    Hyponatremia – In thefirst 2 weeks following SAH – It usually results from inappropriate secretion of vasopressin and secretion of atrial and brain natriuretic factors, which produce a natriuresis. – clears over the course of 1 to 2 wks – should not be treated with free-water restriction as this may increase the risk of stroke. 8/7/2023 77 Dr.Tamiru S.
  • 78.
    Laboratory Findings – CBC –Clotting times should be determined to assess whether the patient has an infection or clotting abnormalities. – Blood should also be sent for electrolyte analysis to serve as a baseline for detecting later complications. 8/7/2023 78 Dr.Tamiru S.
  • 79.
    Imaging 95 % -detected by CT Scan within 72 hrs LP  spinal fluid yellow (xanthochromic) within 6 to 12 h of SAH.  Peaks at 48 h  lasts for 1 to 4 weeks, depending on the amount of subarachnoid blood. 8/7/2023 79 Dr.Tamiru S.
  • 80.
    – Conventional x-rayangiography (both carotids and both vertebrals) to localize and define the anatomic details of the aneurysm and to determine if other unruptured aneurysms exist – CT angiography is an alternative method for locating the aneurysm 8/7/2023 80 Dr.Tamiru S.
  • 81.
    • ECG – ST-segmentand T-wave changes – Prolonged QRS complex, increased QT interval, and prominent “peaked” or deeply inverted symmetric T waves are usually secondary to the intracranial hemorrhage 8/7/2023 81 Dr.Tamiru S.
  • 82.
    TREATMENT • Medical – ABC –BP control, maintain adequate cerebral perfusion – Raised ICP (e.g., mild hyperventilation, mannitol, and sedation) – bed rest in a quiet room and stool softeners – mild sedation and analgesia – hydration is necessary to avoid a decrease in blood volume predisposing to brain ischemia. 8/7/2023 82 Dr.Tamiru S.
  • 83.
    – phenytoin isoften given as prophylactic therapy since a seizure may promote rebleeding. – Glucocorticoids routine use is not recommended. 8/7/2023 83 Dr.Tamiru S.
  • 84.
    • Antifibrinolytic agentsare not routinely prescribed but may be considered in patients in whom aneurysm treatment cannot proceed immediately. – associated with a reduced incidence of aneurysmal rerupture but associated with an increased incidence of delayed cerebral infarction and DVT. 8/7/2023 84 Dr.Tamiru S.
  • 85.
    • Vasospasm – remainsthe leading cause of morbidity and mortality – Treatment with the calcium channel antagonist nimodipine (60 mg orally every 4 h) improves outcome 8/7/2023 85 Dr.Tamiru S.
  • 86.
    – Free-water restrictionis contraindicated – supplemental oral salt coupled with normal saline will mitigate hyponatremia, but often patients also require hypertonic saline. 8/7/2023 86 Dr.Tamiru S.
  • 87.
    – Pneumatic compressionstockings applied to prevent pulmonary embolism – Systemic heparin is contraindicated in patients with ruptured and untreated aneurysms 8/7/2023 Dr.Tamiru S. 87
  • 88.
    – ventricular drainage-raised ICP – An aneurysm can be “clipped” by a neurosurgeon or “coiled” by a neurointerventional radiologist. – Surgical repair involves placing a metal clip across the aneurysm neck, thereby immediately eliminating the risk of rebleeding. 8/7/2023 88 Dr.Tamiru S.
  • 89.
    INTRAPARENCHYMAL HEMORRHAGE – isthe most common type of intracranial hemorrhage. – It accounts for about 10% of all strokes and is associated with a 50% case fatality rate. 8/7/2023 89 Dr.Tamiru S.
  • 90.
    – Hypertension, trauma,and cerebral amyloid angiopathy cause the majority of these hemorrhages. – Advanced age and heavy alcohol consumption increase the risk – cocaine use is one of the most important causes in the young. 8/7/2023 90 Dr.Tamiru S.
  • 91.
    Hypertensive Intraparenchymal Hemorrhage –Usually results from spontaneous rupture of a small penetrating artery deep in the brain. – The most common sites are the basal ganglia (especially the putamen), thalamus, cerebellum, and pons. 8/7/2023 91 Dr.Tamiru S.
  • 92.
    – When occurin other brain areas or in nonhypertensive patients, greater consideration should be given to hemorrhagic disorders, neoplasms, vascular malformations, and other causes. 8/7/2023 92 Dr.Tamiru S.
  • 93.
    – Most developover 30–90 minutes, whereas those associated with anticoagulant therapy may evolve for as long as 24–48 hours. – Within 48 hours macrophages begin to phagocytize the hemorrhage at its outer surface. – After 1–6 months, the hemorrhage is generally resolved to a slitlike orange cavity lined with glial scar and hemosiderin-laden macrophages. 8/7/2023 93 Dr.Tamiru S.
  • 94.
    Clinical Manifestations – almostalways occur while the patient is awake and sometimes when stressed. – presents as the abrupt onset of focal neurologic deficit- worsens steadily over 30–90 minutes . – Seizures are uncommon. – associated with a diminishing level of consciousness and signs of increased ICP such as headache and vomiting. 8/7/2023 94 Dr.Tamiru S.
  • 95.
    Putamen – Most commonsite – Adjacent internal capsule is invariably involved – hemiparesis – Facial palsy – Slurred speech – Eyes- away from hemiparesis – If large—raised ICP and Brainstem compression 8/7/2023 95 Dr.Tamiru S.
  • 96.
    Thalamus – hemiparesis/ hemiplegia –Prominent sensory deficit – Dejerine-Roussy Syndrome – Aphasia, mutism ,apractognosia – Visual field defect – Typical occular disturbances – Downward and inward looking eyes – Unequal pupils – Skew deviation – nystagmus 8/7/2023 96 Dr.Tamiru S.
  • 97.
    Pons – Deep coma,quadriplegia – Decerebrate rigidity – Pin-point pupils, reacting to light – Absent Doll’s eye, occulovestibular reflex – Hyperpnea, hypertension, hyperhidrosis – Death in few hrs , small bleed can survive 8/7/2023 97 Dr.Tamiru S.
  • 98.
    Cerebellum – Develop overseveral hrs – Occipital headache, repeated vomiting, ataxia – Dizziness, vertigo – Dysarthria and dysphagia may occur. – Brainstem compression, hydrocephalus – High index of suspicion 8/7/2023 98 Dr.Tamiru S.
  • 99.
    Treatment – ABC – Nearly50% of patients with a hypertensive ICH die – coagulopathy should be reversed as soon as possible – Treat severe hypertension to prevent hematoma progression 8/7/2023 99 Dr.Tamiru S.
  • 100.
    Evacuation of hematoma –Evacuation of supratentorial hematomas does not appear to improve outcome. – Beneficial for Cerebellar • >3 cm –evacuate • 1-3 cm –monitor for raised ICP • <1 cm – if pt is alert and without brainstem signs, evacuation is unnecessary 8/7/2023 100 Dr.Tamiru S.