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![Uncommon
Causes
Hypercoagulable disorders
Protein C deficiency
Protein S deficiency
Antithrombin III deficiency
Antiphospholipid syndrome
Factor V Leiden mutationa
Prothrombin G20210 mutationa
Systemic malignancy
Sickle cell anemia
Systemic lupus erythematosu
DIC
Nephrotic syndrome
Inflammatory bowel disease
Oral contraceptives
Venous sinus thrombosisb
Vasculitis
Systemic vasculitis [PAN,
granulomatosis with polyangiitis
(Wegener's), Takayasu's, & giant
cell arteritis]
Primary CNS vasculitis
Meningitis (syphilis, tuberculosis,
fungal, bacterial, zoster)
Cardiogenic
Mitral valve calcification
Atrial myxoma
Intracardiac tumor
Libman-Sacks endocarditis
Subarachnoid hemorrhage
vasospasm
Drugs: cocaine, amphetamin
Eclampsia](https://image.slidesharecdn.com/2-190511144646/85/2-stroke-10-320.jpg)
Uploaded byAmanuel Dole
2. stroke
This document outlines a presentation on stroke. It begins with an introduction and classification of stroke, followed by sections on risk factors, pathophysiology, signs and symptoms, differential diagnosis, and approach to patients. It discusses that stroke is caused by a lack of blood flow to the brain and defines different types of stroke, including ischemic and hemorrhagic. Risk factors highlighted include age, hypertension, cardiac issues, and genetic factors. Signs and symptoms vary depending on the location and type of stroke.
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2. stroke
- 2. Outline of presentation Introduction Classification Risk Factors Phatophysiology of stroke Signs and Symptoms of stroke Differential Diagnosis Approach to the Patient
- 3. Stroke A stroke,or cerebrovascular accident Thus, the definition of stroke is clinical, and brain imaging are used to support the diagnosis
- 4. Stroke/CVA includesome of the most common and devastating disorders There are approximately 785,000 new or recurrent strokes annually in the United States; Incidence increases with age Worldwide, stroke is also a leading cause of death, with stroke mortality being particularly high in Eastern Europe and Asia. 200,000 deaths /year in the US By 2020, 19 out of 25 million annual stroke deaths will be in developing countries .
- 5. Stroke isalso the leading cause of disability in adults. Of the hundreds of thousands of stroke survivors each year, approximately 30% require assistance with activities of daily living, 20% require assistance with ambulation, and
- 6.
- 8. Causes of IschemicStroke - Common Causes Thrombosis (60%) Lacunar stroke (small vessel)-20% of all stroke Large vessel thrombosis Dehydration Embolic occlusion (40%) Artery-to-artery Carotid bifurcation Aortic arch Arterial dissection Cardioembolic (20%) Atrial fibrillation Mural thrombus Myocardial infarction Dilated cardiomyopathy Valvular lesions Mitral stenosis Mechanical valve Bacterial endocarditis Paradoxical embolus Atrial septal defect
- 10. Uncommon Causes Hypercoagulable disorders ProteinC deficiency Protein S deficiency Antithrombin III deficiency Antiphospholipid syndrome Factor V Leiden mutationa Prothrombin G20210 mutationa Systemic malignancy Sickle cell anemia Systemic lupus erythematosu DIC Nephrotic syndrome Inflammatory bowel disease Oral contraceptives Venous sinus thrombosisb Vasculitis Systemic vasculitis [PAN, granulomatosis with polyangiitis (Wegener's), Takayasu's, & giant cell arteritis] Primary CNS vasculitis Meningitis (syphilis, tuberculosis, fungal, bacterial, zoster) Cardiogenic Mitral valve calcification Atrial myxoma Intracardiac tumor Libman-Sacks endocarditis Subarachnoid hemorrhage vasospasm Drugs: cocaine, amphetamin Eclampsia
- 11.
- 12. Cerebral Blood Flowand Pathophysiology Cerebral blood flow is normally maintained at a relatively constant rate of approximately 50 to 70 mL/100 g brain tissue per minute. A process called autoregulation helps maintain perfusion pressure despite fluctuations in blood pressure and cerebrovascular resistance A decrease in blood flow below a critical threshold level results in ischemia and infarction.
- 13. CBF & IschemicThresholds 13 Normal CBF 50-60 cc/100 g/minute Varies in different regions of the brain CBF 20-30cc/100g/min Loss of electrical activity CBF </= 10 cc/100g/min Neuronal death
- 14. Occlusive-Ischemic Vascular Disease When a portion of neural tissue is deprived of its blood supply, ischemia develops. If the normal protective mechanisms are insufficient to compensate for this deprivation, death of tissue, or infarction, results. The process of metabolic failure leading to cell death involves the cessation of blood flow, loss of energy, and neuronal depolarization. The resultant release of glutamate, entry of calcium ions into the cell, generation of oxygen free radicals and nitric oxide, and the activation of proteases and lipases o all contribute to cell breakdown and infarction.
- 15. Microcellular Mechanisms ofNeuronal Injury: Excitotoxicity
- 16. Acute Ischemic Injury 16 The occlusion of a large vessel (such as MCA) is rarely complete and cerebral blood flow (CBF) depends on the degree of obstruction, and collateral circulation Many factors influence progression and extent of ischemic injury
- 17. Conditions influencing progressionand extent of ischemic injury 17 Rate & duration of the ischemic event Collateral circulation in the involved area of the brain Systemic circulation & arterial blood pressure Temperature Glucose
- 18. Major arteries supplyingthe supratentorial and posterior fossa levels.
- 19. Arterial supply ofthe brain
- 20. Blood Supply tothe Cerebral Hemispheres
- 21. Ischemic Stroke –Signs and Symptoms… Carotid Circulation Unilateral paralysis (opposite side) Numbness (opposite side) Language disturbance Aphasia – difficult comprehension, nonsense, difficult reading/writing Dysarthria – slurred speech, abnormal pronunciation. Visual disturbance (opposite side)
- 22. Ischemic Stroke –Signs and Symptoms… • Vertebrobasilar Circulation Vertigo & Hearing loss Visual disturbance Diplopia Ocular palsy – inability to move to one side Paralysis Numbness Dysarthria Ataxia
- 23. Transient Ischemic Attacks A transient episode of neurological dysfunction caused by focal brain, spinal cord, or retinal ischemia, without acute infarction. Most last < 30 mins 24 hour cut off not clinically useful A newly proposed definition classifies those with new brain infarction as ischemic strokes regardless of whether symptoms persist. With a TIA, the occluded blood vessel reopens and neurologic function is restored.
- 24. Transient Ischemic Attacks… The causes of TIA are similar to the causes of ischemic stroke, but because TIAs may herald stroke they are an important risk factor that should be considered separately. Early risk of stroke is very high 11.5% after 1 week 15% after 1 month 18.5% after 3 months
- 25. Intracranial Hemorrhage Hemorrhagesare classified by their location and the underlying vascular pathology. Intracerebral (10%) Hypertension (most common) Amyloid angiopathy in elderly Trauma Subarachnoid (5%) Aneurysm (most common) Arteriovenous malformation
- 26.
- 27. Intracerebral Hemorrhage Themost common type ; ~10% of all strokes and is associated with a 50% case fatality rate Hypertension, trauma, and cerebral amyloid angiopathy cause the majority of these hemorrhages A growing body of evidence suggests that genetic factors such as possessing the E2 and E4 alleles of the apolipoprotein E gene play an important
- 28. EPIDEMIOLOGY Nontraumatic intracerebralhemorrhage (ICH) causes 8 - 15% (10%) of all first-ever strokes in Australia, England, and the United States ; it accounts for 25 % of strokes in Japan . The overall incidence of ICH ranges from 12 to 31 per 100,000 people, and it varies by race . The rate of occurrence is highest in Asians, intermediate in blacks, and lowest in whites. The higher rate of ICH in black compared with white Americans is predominately attributable to excess ICH in deep cerebral and brainstem locations where hypertension is the major risk factor .
- 29. EPIDEMIOLOGY … Theincidence of ICH increases with age, doubling every 10 years after age 35 . As the population ages, the incidence of ICH may rise in the future due to amyloid angiopathy. Gender does not appear to have a significant impact on risk
- 30. Hypertensive Intraparenchymal Hemorrhage Pathophysiology Results from spontaneous rupture of a small penetrating artery deep in the brain that branch off major intracerebral arteries, often at 90º angles with the parent vessel; These small(100micro m) penetrating arteries may be particularly susceptible to the effects of hypertension, as they are directly exposed to the pressure of the much larger parent vessel, without the protection of a preceding gradual decrease in vessel caliber Site : Putamen, Globus pallidus, Thalamus, Cerebellar hemisphere, Pons In both hypertensive and nonhypertensive patients, the circadian rhythm of ICH onset, with peaks at 8 am and 8 pm
- 31. Risk factors Hypertensionis the most important risk factor for the development of ICH , hypertension more than doubled the risk of ICH Hypertension has also been shown to be a risk factor for ICH in the setting of other underlying etiologies for ICH (eg, cerebral amyloid angiopathy, antithrombotic-associated ICH) . In addition to hypertension, a systematic review and a large population-based study identified the following risk factors for ICH: Older age High alcohol intake Black ethnicity Lower cholesterol and lower LDL cholesterol Lower triglycerides
- 32. Clinical Manifestations Thehemorrhage generally presents as the abrupt onset of focal neurologic deficit The neurologic symptoms usually increase gradually over minutes or a few hours (30–90 min). Some hypertensive hemorrhages occur with exertion or intense emotional activity. However, most cases take place during routine
- 33. Clinical Manifestations… Signsof increased ICP, such as headache , vomiting and a decreased level of consciousness – is more common in hemorrhagic stroke than ischemic stroke .
- 34. Neurologic signs Neurologicsigns vary depending upon the location of the hemorrhage. Bleeding into Basal ganglia; putamen occurs in approximately 35 percent of cases, subcortex in 30 percent, cerebellum in 16 percent, thalamus in 15 percent, and pons in 5 to 12 percent .
- 35. Putamenal hemorrhage Spreadof hemorrhage into the putamen most commonly occurs along white matter fiber tracts, causing hemiplegia, hemisensory loss, homonymous hemianopsia, gaze palsy, stupor, and coma.
- 36. Cerebellar hemorrhage Cerebellarhemorrhages usually originate in the dentate nucleus, extend into the hemisphere and fourth ventricle, and possibly into the pon. These bleeds cause an inability to walk due to ataxia, vomiting, headache (which may be referred to the neck or shoulder, usually occipital), and facial weakness. There is notably no weakness. The patient may become stuporous due to brainstem compression Cerebellar hemorrhage is a crucial diagnosis to make since these patients frequently deteriorate and require surgery.
- 37. Thalamic hemorrhage Athalamic hemorrhage may extend in a transverse direction to the posterior limb of the internal capsule, downward to put pressure on the midbrain, or may rupture into the third ventricle. Symptoms include hemiparesis, hemisensory loss, and occasionally transient homonymous hemianopsia. There may also be an upgaze palsy with miotic pupils that are unreactive. Aphasia may occur if the bleed affects the dominant hemisphere or neglect in the nondominant hemisphere.
- 38. Lobar hemorrhage Lobarhemorrhages vary in their neurologic signs depending upon location. They most often affect the parietal and occipital lobes. These bleeds are associated with a higher incidence of seizures. Occipital hemorrhages frequently present with a very dense contralateral homonymous hemianopsia. Hemorrhages in the frontal region will bring about a contralateral weakness.
- 39. Pontine hemorrhage Pontinehemorrhage lead to deep coma over the first few minutes following the hemorrhage, probably due to disruption of the reticular activating system. The motor examination is marked by total paralysis. The pupils are pinpoint and react to a strong light source. Horizontal eye movements are absent, and there may be, facial palsy, deafness, and dysarthria when the patient is awake. Locked in syndrome
- 40.
- 41. Saccular (Berry) Aneurysm Annualrisk of rupture of ASxic Aneurysm o<1 cm -0.1 % , o >1 cm 0.5-1 % o>2.5 cm (Giant )--6% risk factors for rupture : smoking , HTN , Alcohol.. C/F : Sign & symptoms of raised ICP “The worst headache of my life” is described by ~80% of patients , high index of suspicion 41
- 42. Delayed Complications Rerupture-highest in the 1st 72hrs Hydrocephalus : Acute, Subacute , Chronic Vasospasm : ischemia , @ 4- 14 days usually @ 7 days Hyponatremia : “Cerebral Salt Wasting Syndrome” Dx : Hallmark– Blood in the CSF
- 43.
- 44. (White areas indicate hyperdensity= blood) Large left frontal intracerebral hemorrhage. Intraventricular bleeding is also present
- 45. Hypodense area: • Ischemicarea • Indicates >24 hours old • No fibrinolytics!
- 46. Acute subarachnoid hemorrhage Diffuse areasof white (hyperdense) images Blood visible in ventricles and multiple areas on surface of brain
- 47. Investigations … Establishinga cause is essential in reducing the risk of recurrence A chest x-ray Electrocardiogram (ECG) & Echocardiography Carotid dopler Urinalysis Complete blood count Erythrocyte sedimentation rate Serum electrolytes Blood urea nitrogen Creatinine Blood sugar Serologic test for syphilis Serum lipid profile Prothrombin time, and partial thromboplastin time (PTT)
- 48. Differential Diagnosis ofStroke Head/Cervical trauma Meningitis/encephalitis Hypertensive encephalopathy Intracranial mass Tumor Sub/epi dural hematoma Todd’s paralysis Migraine Metabolic Hyper/hypo glycemia Electrolyte disterbances Hepatic / Uremic encephalopathy Post arrest ischemia Drug OD
- 50.
Editor's Notes
- #4 Thus, the definition of stroke is clinical, and laboratory studies including brain imaging are used to support the diagnosis
- #5 Despite any decrease in mortality in developed countries, stroke mortality and incidence are increasing in the rapidly industrializing developing nations.Socioeconomic factors, dietary and lifestyle behaviors, different patterns of risk factors, and environmental conditions may explain the different incidences of stroke observed in different parts of The world. There are approximately 785,000 new or recurrent strokes annually in the United States (600,000 being first events and 185,000 being recurrent events).
- #7 The incidence of cerebrovascular diseases increases with age, and the number of strokes is projected to increase as the elderly population grows
- #8 Modifiable risk factors may be subdivided into lifestyle and behavioral risk factors and non-lifestyle factors, although these two subgroups are interrelated. Presumed modifiable lifestyle risk factors include cigarette consumption and illicit drug use. Non-lifestyle risk factors include low socioeconomic status, arterial hypertension, dyslipidemia, heart disease, and asymptomatic carotid artery disease. Stroke secondary to sickle cell disease is also a modifiable non-lifestyle risk factor. Potentially modifiable risk factors (that have yet to be shown to decrease risk when modified, however) include diabetes mellitus (DM), hyperhomocysteinemia, and left ventricular hypertrophy. Less well-documented risk factors include blood markers (i.e., C-reactive protein), ankle-brachial blood pressure ratios, silent cerebral infarcts, white-matter hyperintensities on magnetic resonance imaging (MRI), and degree of carotid artery intima-media thickness.
- #10 (1) occlusion of an intracranial vessel by an embolus that arises at a distant site (e.g., cardiogenic sources such as atrial fibrillation or artery-to-artery emboli from carotid atherosclerotic plaque), often affecting the large intracranial vessels; (2) in situ thrombosis of an intracranial vessel, typically affecting the small penetrating arteries that arise from the major intracranial arteries; (3) hypoperfusion caused by flow-limiting stenosis of a major extracranial (e.g., internal carotid) or intracranial vessel, often producing "watershed" ischemia
- #11 Polyarterites nodusa (PAN)
- #12 In an ischemic stroke lack of circulating blood …. And in a hemorrhagic stroke extravasculaar release of blood Hemorrhage: Extravascular release of blood causes damage by cutting off connecting pathways, resulting in local or generalized pressure injury
- #15 Atherosclerosis is the most important disease process responsible for thromboembolic disease;
- #16 PARP, poly-A ribose polymerase; iNOS, inducible nitric oxide synthase
- #18 Coagulation abnormalities
- #19 All the arteries that supply the supratentorial and posterior fossa levels arise from the aortic arch . The innominate (brachiocephalic) artery divides into the right common carotid and right subclavian arteries. The left common carotid artery arises directly from the apex of the aortic arch. The right and left common carotid arteries ascend in the neck lateral to the trachea. Slightly below the angle of the jaw, the common carotid artery bifurcates into the internal and external carotid arteries.
- #21 The anterior cerebral artery (Fig. 12.6) supplies the medial surface of the cerebral hemisphere and the superior Border of the frontal and parietal lobes. The middle cerebral artery (Fig. 12.7) supplies most of the lateral surface of the cerebral hemisphere, including the lateral portions of the frontal lobe, the superior and lateral portions of the temporal lobe, and the deep structures of the frontal and parietal lobes. The posterior cerebral artery supplies the entire occipital lobe and the inferior and medial portions of the temporal lobe
- #22 Monocular blindness (same side)
- #24 The standard definition of TIA requires that all neurologic signs and symptoms resolve within 24 h …
- #26 Clinical diagnosis of hemorrhagic stroke and ischemic stroke accounted for 57% and 43% respectively. hemorrhagic stroke 80.8 % intraparenchymal and 19.2% subarachioid
- #28 Care of ICH patients in a dedicated neuroscience intensive care unit is associated with a lower mortality rate
- #31 Hypertensive hemorrhages occur in the territory of penetrator arteries. When hemorrhages occur in other brain areas or in nonhypertensive patients, greater consideration should be given to hemorrhagic disorders, neoplasms, vascular malformations, and other causes Hemorrhage enlargement — Serial CT scans in patients with hypertensive hemorrhage have shown that the hemorrhage enlarges in the first six hours after presentation in a subset of patients
- #32 A number of additional studies have found an inverse relationship between total and LDL-cholesterol and the risk of ICH [74-81]. At least one study suggested that the association is stronger for subcortical or hypertensive ICH than lobar hemorrhage [78]. However, treatment with statins does not appear to increase the risk of primary ICH or to negatively impact prognosis Most cases of ICH are not believed to have a genetic component. One exception is cerebral amyloid angiopathy-related ICH which has been shown to have an association with APOE genotype. However, a large-scale genetic association study of 2189 ICH cases and 4041 controls revealed that APOE allele ε4 was also associated with deep ICH (OR = 1.21), a location not typical for cerebral amyloid angiopathy
- #33 Most hypertensive intraparenchymal hemorrhages develop over 30–90 min In contrast to brain embolism and subarachnoid hemorrhage, the neurologic symptoms do not begin abruptly and are not maximal at onset.
- #34 Signs of increased ICP, such as headache , vomiting and a decreased level of consciousness develop if the hematoma becomes sufficiently large. Headache may be due to traction on meningeal pain fibers, increased intracranial pressure (ICP), or blood in the cerebrospinal fluid (CSF); it is most common with cerebellar and lobar hemorrhages.
- #39 Hemorrhages in the frontal region will bring about a contralateral plegia or paresis of the leg with relative sparing of the arm.
- #43 95 % - Detected by CT Scan within 72 hrs -ve CT scan – LP Yellow (xanthochromic CSF)- within 6-12 hrs Peak @ 48 hrs Stays for 1-4 wks X-ray, CT angiography EKG Electrolytes
- #48 …prothrombin time, and partial thromboplastin time (PTT) are often useful and should be considered in all patients
- #49 Stroke mimics : There are several common causes of sudden-onset neurologic symptoms that may mimic stroke, including seizure, intracranial tumor, migraine, and metabolic encephalopathy
- #50 Intravenous Recombinant Tissue Plasminogen Activator (rtPA)