# Stroke ## Aphasia ### Broca's Broca’s aphasia is an **expressive aphasia**, which is a loss of the ability to produce language. Broca aphasia results from damage to Broca’s area (language motor area), which includes the following areas of the dominant hemisphere: * **Inferior frontal gyrus** * **Dorsolateral frontal cortex** * **Anterior parietal cortex** Patients with **Broca aphasia** show the following symptoms: * Nonfluent - Production of few words or difficulty producing words * Good comprehension * Loss of oral coordination * Possible face and arm hemiparesis (from damage to the adjacent motor cortex) ### Wernicke Wernicke’s aphasia is a **receptive aphasia**, which is a loss of the ability to understand language. Wernicke’s aphasia results from damage to Wernicke’s area (language understanding area), which includes the following areas of the brain: * **Posterior superior temporal gyrus** * **Inferior parietal lobe** Patients with **Wernicke’s aphasia** show the following symptoms: * **Fluent speech** * **Poor comprehension**, which presents as word substitutions, meaningless words, or meaningless phrases. ### Conductive Conduction aphasia, also known as **associative aphasia**, is a **loss of the ability to tie in language production and language understanding.** Conduction aphasia is the result of damage to the **arcuate fasciculus**, which connects Broca’s and Wernicke’s areas of the brain. This includes: * **Supramarginal gyrus** * **Angular Gyrus** Symptoms of patients with **conduction aphasia** include: * Fluent speech * **Difficulty in Repetition** * Frequent word correction attempts * Word substitutions * Word-finding pauses ### Global Global aphasia is a **complete loss of language expression, understanding, and association**. Global aphasia results from **decreased blood flow through the middle cerebral artery** (MCA), leading to massive **infarcts of the left cerebral hemisphere**, thereby damaging: * Broca’s area * Wernicke’s area * Arcuate fasciculus Symptoms of patients with global aphasia include: * **Nonfluent speech** * **Poor comprehension** * **Difficulty producing words** * **Limb ataxia, which is a result of damage to adjacent motor cortex** ![](https://f001.backblazeb2.com/file/wikiFiles/L12233.jpg) ## Stroke * 2 types of strokes in general: ischemic, hemorrhagic ![](https://f001.backblazeb2.com/file/wikiFiles/A4D8C40A-91F3-4FDA-971E-0834D5435140.jpg) ### Ischemic Ischemic stroke results when **blood flow to the brain is limited, resulting in decreased oxygenation of brain parenchyma.** **Ischemic stroke or cerebrovascular accident** (CVA) is the leading cause of neurologic disability and third leading cause of death. **Thrombosis** and **emboli** are the two mechanisms by which an ischemic stroke can occur. Can also be **lacunar.** #### Embolic Embolic stroke is the most common etiology of CVA, most commonly originating from: * **Heart** * **Internal carotid artery** * **Aorta** * **Emboli that arise from blood clots in the peripheral veins.**These patients will also likely have a patent foramen ovale. #### Thrombotic Thrombotic strokes occur due to **atherosclerotic lesions** within the carotid artery or the arteries of the brain. #### Lacunar Another form of ischemic stroke is a Lacunar stroke. Lacunar stroke is a **small vessel thrombotic disease with narrowing of the arterial lumen due to thickening of the vessel wall.** Lacunar strokes are the cause of **20%** of all strokes. Lacunar infarcts affect the **subcortical structures** supplied by small branches of the Middle Cerebral Artery (MCA), circle of Willis, basilar and vertebral arteries. Patients who have lacunar strokes typically have a **history of hypertension**. #### Risks Risk Factors for ischemic stroke include both lifestyle risk factors and comorbidities of the patient. Life style risk factors: * **Smoking** * **Diet** * **Vasoconstrictive drug use** * **Oral contraceptive use** Comorbidities associated with stroke: * **Previous stroke or family history of stroke** * **Hypercoagulability** * **Hypertension** * **Diabetes** * **Atrial Fibrillation** #### Symptoms Clinical features of CVA depend on the **type of ischemic stroke** and the **location of the occlusion**. Embolic strokes are **very rapid in onset** and **present with maximal deficits.** Thrombotic strokes can be **rapid or stepwise** in onset and the **patient typically awakens from sleep with the deficits**. Complications of ischemic stroke include: * **Progression of the neurologic deficits** * **Cerebral edema leading to mass effects** * **Hemorrhage** * **Seizures** Strokes that occur in the **anterior cerebral artery (ACA)** present with contralateral lower extremity motor and sensory deficiencies. Strokes that occur in the **middle cerebral artery** present with contralateral hemiparesis (if proximal to small branch), hemisensory loss, aphasia, and apraxia. Symptoms are more common in the upper extremities than the lower extremities. Strokes that occur in the posterior cerebral artery (PCA) most commonly present with **hemianopia**. In addition, infarction of the left PCA may present with: * **Alexia without agraphia**: can write, can't read * **Anomic aphasia**: word finding difficulty * **Gerstmann syndrome**: agraphia, acalculia, finger agnosia And infarction of the right PCA may present with: * **Prosopagnosia**: can't recognize face * **Spatial disorientation** * **Visual neglect** Strokes that occur within the **vertebral or basilar arteries** present with: * Ipsilateral ataxia * Ipsilateral diplopia * Ipsilateral dysphagia * Ipsilateral dysarthria * Vertigo Lacunar strokes typically present as **pure motor or pure sensory deficits.** #### Management Careful observation for stroke progression and cerebral edema in patients with acute stroke is indicated for **24-36 hours.** Patients should be monitored on a **telemetry floor**, and neurologic checks should be performed every 4 hours. When diagnosing a CVA, a **noncontrast CT** scan is the **first line imaging** test to be ordered. **An infarct will not appear on CT scan for 24-48 hours**, but this test is important to rule out intracranial hemorrhage and to identify patients who will benefit from thrombolytic therapy. **MRI** of the brain is the **most sensitive** test to identify all early ischemic changes but is time consuming and should not be used in the acute setting. Other important tests include * **Labs** to assess CBC, cardiac enzymes, electrolytes, BUN, creatinine, lipid profile, PTT, PT and INR. * **Carotid duplex** to assess for stenosis * **ECG and echocardiogram** to assess for atrial fibrillation or acute MI that may be a source of emboli * **Magnetic Resonance Arteriogram (MRA)** to identify stenosis of vessels within the head and neck. * **Assessment of hypercoagulable states** in those with a history of thombotic events Treatment of ischemic stroke typically includes the use of intravenous recombinant **tissue plasminogen activator** (tPA, also called **alteplase**) if the drug can be administered **within 3-4.5 hours** of the onset of symptoms, and there are no contraindications to its use. Exclusion criteria for tPA include * **Significant head trauma or intracranial surgery** * **Previous intracranial hemorrhage** * **Intracranial neoplasm or arterial malformation** * **Current anticoagulant use** * **Platelet count less than 100,000** * **Uncontrolled hypertension** * **Age >80** * **Do not give tPA if the time of the stroke is unknown** If the patient cannot receive tPA, **aspirin (160-325 mg/day) is best given within 24 hours**. If a patient cannot take aspirin, clopidogrel should be used. If the patient has received tPA, **wait 24 hours** before beginning an aspirin regimen. In an ischemic stroke patient, it is important to allow for **permissive hypertension**. The increased blood pressure will help maintain perfusion of the ischemic tissue. However, if the patient has systolic BP >220 mmHg or diastolic >120 mmHg they should be treated with IV labetalol or nicardipine. Carotid endarterectomy is indicated in **symptomatic patients with ≥70% carotid artery stenosis** or **asymptomatic patients with ≥80% stenosis**. Other long term preventative measures for future ischemic stroke include: * Aspirin or clopidogrel use if stroke is secondary to small vessel disease or thrombosis * Anticoagulation in patients with atrial fibrillation or hypercoagulable disorders * Management of comorbidities (e.g. hypercholesterolemia, diabetes, hypertension) ### Parenchymal Hemorrhage #### Pathogenesis Parenchymal hemorrhage, also known as intracerebral hemorrhage, is **bleeding within the brain tissue**. Parenchymal hemorrhage has multiple mechanisms that lead to brain injury, including: * **Direct injury** due to an expanding blood clot * **Mass effect** leading to increased intracranial pressure * **Ischemic injury** **Parenchymal hemorrhage** is the second most common cause of stroke, second only to ischemic stroke in frequency. **Small vessel vasculopathy secondary to chronic hypertension** is the most common cause of parenchymal hemorrhage. The underlying pathology is a combination of **microatheroma** formation and **lipohyalinosis** that ultimately leads to thrombotic small-vessel occlusion. **Cerebral amyloid angiopathy** is the most common cause of nontraumatic **lobar** parenchymal hemorrhage in elderly patients. **Intracranial vascular anomalies** (e.g. **arteriovenous malformations**) are the most common cause of parenchymal hemorrhage in children. Exposure to vascular perfusion injuries have also been associated with IVH. Examples of such events are: (1) hypoxic or ischemic episodes, (2) hypotension, (3) reperfusion of damaged vessels, (4) increased venous pressure, and (5) abrupt changes in cerebral flow. Parenchymal hemorrhages due to *hypertension* most commonly occur in the **basal ganglia** (especially the **putamen**), **thalamus**, and **pons**. In contrast, parenchymal hemorrhages due to *cerebral amyloid angiopathy* most commonly occur in the **parietal** and **occipital lobes**. #### Symptoms Patients with **parenchymal hemorrhage** present with focal neurologic symptoms (e.g. hemiplegia, homonymous hemianopsia) that are followed by manifestations of increased intracranial pressure (e.g. headache, vomiting). These manifestations intensify *gradually* over time. In contrast, patients with subarachnoid hemorrhage present *abruptly* with an *intense* headache *without* focal neurologic symptoms. **Seizures** can occur in the days following a parenchymal hemorrhage; this is especially common in patients with superficial (e.g. lobar) hemorrhages. ![](https://f001.backblazeb2.com/file/wikiFiles/L8773.jpg) #### Cerebellar Symptoms Typical features of cerebellar hemorrhage include **occipital headache** (may radiate to neck/shoulders), **neck stiffness** (due to extension of blood into the 4th ventricle), nausea/vomiting, and nystagmus. Patients may also have **ipsilateral hemiataxia** of the trunk (cerebellar vermis) and/or limbs (cerebellar hemispheres) as the corticopontocerebellar fibers decussate twice. Hemiparesis and sensory loss are usually absent, but extension of the bleed to the brainstem can cause cranial neuropathies (eg, **ipsilateral facial nerve palsy**). Further hematoma expansion may lead to brainstem compression resulting in stupor, coma, and ultimately death. Early diagnosis with **noncontrast head CT scan** is crucial as emergency decompression may be life-saving, especially if the hemorrhage is >3 cm. #### Diagnosis and Management **Noncontrast head CT scan** is most widely used to diagnose parenchymal hemorrhage. **Magnetic resonance angiography** or **CT angiography** can be used to localize the site of bleeding. MRI may be more useful in diagnosing **micro hemorrhages** within the brain parenchyma. Treatment of parenchymal hemorrhage is supportive care. Focus is made on: * **Maintaining normal intracranial pressure** * **Maintaining normal blood pressure** * **Using anticonvulsants to control seizure activity** * **Surgical decompression for large hemorrhages** Surgical repair of any **arteriovenous malformations or aneurysms** may be required. ### Subarachnoid Hemorrhage **Subarachnoid Hemorrhage** is a **brain bleed that occurs below the arachnoid layer** of the meninges and is most commonly due to the **rupture of a berry aneurysm**. Other causes include **trauma to the circle of Willis, or an arteriovenous malformation.** Risk factors for subarachnoid hemorrhage include: * **Hypertension** (most common) * **Autosomal dominant polycystic kidney disease** (ADPKD) * **Bleeding disorders or use of a blood thinner** * **Ehlers-Danlos syndrome** * **Smoking** (most important preventable risk factor) Common sites for the occurrence of a subarachnoid hemorrhage include: * **Junction of the anterior communicating artery and anterior cerebral artery** * **Junction of the posterior communicating artery and the internal carotid artery** * **Bifurcation of the middle cerebral artery** #### Symptoms Many patients who have a **subarachnoid hemorrhage** will present with the sudden onset of a severely painful headache (“worst headache of my life”). **Thunderclap headache** The onset of the headache may or may not be associated with a **brief loss of consciousness, nausea or vomiting, and meningismus.** #### Diagnosis Diagnosis of a subarachnoid hemorrhage is made by a **noncontrast CT scan**. A lumbar puncture is performed to diagnose subarachnoid hemorrhage (SAH) if there is a **strong suspicion of SAH and the CT scan is negative**. The **presence of blood in the cerebrospinal fluid** or **xanthochromia** (yellow tint of the cerebrospinal fluid) is indicative of SAH. The patient must be assessed for **papilledema** before performing the lumbar puncture so as not to cause herniation. If papilledema is present, repeat the CT scan first. Treatment of a subarachnoid hemorrhage is **surgical clipping and coiling**. **Cerebral angiogram** is the gold standard test for determining the location of bleeding in patients with a SAH. The patient must be medically managed to reduce the risk of rebleeding. This includes **managing blood pressure, using anti-seizure medications to prevent seizures, and stool softeners or laxatives** to prevent straining during bowel movement Symptomatic vasospasm and cerebral infarction are important contributors to unfavorable outcomes after SAH. It typically begins after day three post hemorrhage, reaching a peak at days seven to eight. **Nimodipine** may mitigate this complication. **Hyponatremia** is a potential complication due to "cerebral salt-wasting syndrome" or SIADH., ![](https://f001.backblazeb2.com/file/wikiFiles/L13726.jpg) ## Transient Ischemic Attack **Transient ischemic attack** (TIA) is defined as an **acute episode of neurologic dysfunction** caused by focal brain, spinal cord, or retinal **ischemia, without acute infarction**. A TIA becomes an ischemic stroke only when infarction of CNS tissue occurs, and not necessarily a time course of greater than 24 hours. Transient ischemic attack is caused by a **temporary disruption of blood supply to the brain** from underlying conditions such as aortic stenosis, vascular spasm, atherosclerosis, and emboli (the same conditions that cause strokes). Risk factors for a TIA include: * **Age over 55 years** * **Hypertension** * **Diabetes mellitus** * **Coronary artery disease** * **Smoking** * **Hyperlipidemia** * **Hypercoagulable states** Having a TIA puts a patient at risk for **experiencing a stroke in the future.** Symptoms of a TIA present very much like that of a stroke, with a **patient experiencing weakness, paralysis, numbness, loss of coordination, vision abnormalities, slurred speech, and mental confusion.** The symptoms appear suddenly, but **typically abate within one day**, with many cases resolving within an hour. Physical exam may reveal **carotid bruits or harsh systolic murmurs** indicative of carotid atherosclerosis and aortic stenosis respectively. Physical exam may also reveal an **irregularly irregular rhythm** that is indicative of atrial fibrillation. ### Diagnosis Diagnosis can be based on a thorough **history and physical exam accompanied by CT or MRI findings.** MRI is more likely to identify infarction of tissue. Ultrasound can be useful for determining **possible sources of atherosclerosis.** Echocardiography can be useful to determine **heart defects as an underlying cause of emboli**. **Magnetic resonance angiography (MRA), computed tomography angiography (CTA), carotid duplex ultrasonography (CDUS), and transcranial doppler ultrasonography (TCD)** can be used to identify if there is an obstructive lesion in a larger artery supplying the CNS. Treatment consists of **addressing the underlying conditions** leading to ischemia**.** Patients with TIA due to atherosclerosis should be given **antiplatelet** (e.g. **aspirin** or **clopidogrel**) and**statin therapy.** Patients with TIA due to severe carotid stenosis (i.e. 70 to 99% occlusion, symptomatic disease) should undergo **carotid endarterectomy** to increase blood flow to the brain. Patients with TIA due to aortic stenosis should be offered **beta blockers, valvuloplasty or valve replacement**. ![](https://f001.backblazeb2.com/file/wikiFiles/L13667.jpg) * if resolve or outside 4 hour window: use aspirin --- # Agent Instructions: Querying This Documentation If you need additional information that is not directly available in this page, you can query the documentation dynamically by asking a question. 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