A stroke is an acute compromise of the cerebral perfusion or vasculature or cerebrovascular accident (CVA). Approximately 85% strokes are ischemic and rest are hemorrhagic.  In this discussion we mainly confine to ischemic strokes. Over the past several decades, the incidence of stroke and mortality are decreasing.  Stroke is the leading cause of adult disability worldwide. It is thus critical to recognize stroke early and treat it rapidly to prevent or minimize morbidity and mortality. There are many causes of stroke. Hypertension is the leading cause of ischemic stroke. In the younger population, there are numerous causes of stroke including clotting disorders, carotid dissection, and illicit drug abuse. In the acute setting, a quick history and examination to be performed. As time is brain it is very important not to waste any time. As acute stroke management is evolving rapidly we have to consider patients for IV tPA up to 4.5 hours and mechanical thrombectomy up to 6 hours. Recent DAWN trial showed that we can extend the window for mechanical thrombectomy up to 24 hours in selected cases of large vessel occlusion. 
Ischemic etiologies can further be divided into embolic, thrombotic, and lacunar. In general, the common risk factors for stroke include hypertension, diabetes, smoking, obesity, atrial fibrillation, and drug use. Of all the risk factors, Hypertension is the most common modifiable risk factor for stroke. Hypertension is most prevalent in blacks and also occur earlier in life.  According to JNC8, the recommended blood pressure targets in patients with stroke should be less than 140/90mm Hg.  Chronic uncontrolled hypertension causes small vessel strokes mainly in the internal capsule, thalamus, pons, and cerebellum. Lifestyle measures such as weight loss, salt restriction, taking more fruits and vegetables (Such as Mediterranean diet) are helpful in decreasing the blood pressure. Every 10 mm Hg reduction in blood pressure is associated with a 1/3rd reduction in stroke risk in primary prevention.  One-third of the adults in the USA have elevated LDL, leading to plaque formation in the intracerebral vasculature. Eventually, due to the excessive plaque build up thrombotic strokes occur. In the older population, the risk of cardioembolic stroke increases mainly due to atrial fibrillation. The rest 20% of strokes are due to hemorrhagic in nature. Hemorraghic etiologies can be from hypertension, aneurysm rupture, arteriovenous malformations, venous angiomas, bleeding due to illicit drugs like cocaine, hemorrhagic metastasis, amyloid angiopathy, and other obscure etiologies.
Stroke is the fifth leading cause of death in the US. The incidence of stroke is around 800,000 people annually. Stroke is the leading cause of disability.  The incidence of stroke has declined, but the morbidity has increased. Due to longer life expectancy, the lifetime risk of stroke is higher in women.
Stroke is the result of ischemia to an area of the brain. The Na+/K+ ATPase pumps fail mainly because of poor production of ATP and failure of the aerobic mechanism. Ischemia leads to depolarization of cells which results in calcium influx into cells, elevated lactic acid, acidosis, and free radicals. Cell death increases glutamate and leads to a cascade of chemicals (excitotoxicity). 
The most important piece of historical information that the physician should obtain is the time of symptoms onset or time last seen normal. This is critical because it determines the eligibility to receive rtPA or endovascular intervention for stroke.  Other important information to obtain is risk factors for arteriosclerosis and cardiovascular disease, diabetes, smoking, atrial fibrillations drug abuse, migraine, seizures, infection trauma or pregnancy.
The stroke exam is a multi-person coordinated rapid exam. While staff obtain vitals, attach telemetry, and obtain IV access, the physician performs rapid neurological evaluation. National Institutes of Health Stroke Scale (NIHSS) is routinely used to get the baseline evaluation. The exam has to be rapid as “time is brain.” One must examine the following items:
With a good history and physical exam, we can localize the stroke. There are various stroke syndromes.
Anterior Cerebral Artery (ACA) Infarction
There is significant collateral blood supply in the anterior circulating artery territory. So, pure ACA strokes are rare. The ACA distribution involves mainly Broca’s area, primary motor, primary sensory and pre-frontal cortex. So patients present with motor aphasia, personality issues, and contralateral leg weakness and numbness. Hand and face are usually spared.
Middle Cerebral Artery (MCA) Infarction
Middle cerebral artery has the main trunk (M1) and it divides into two M2 Branches. The M1 (horizontal branch) supplies the basal ganglia and M2 (Sylvian branches) supplies part of the parietal, frontal and temporal lobes. As MCA supplies a wide territory it is extremely important to rule out MCA occlusion. The MCA syndrome causes contralateral arm and face numbness and weakness, gaze deviation towards the affected side. Aphasia in the left-sided lesions and neglect in the right-sided lesions.
Posterior Cerebral Artery (PCA) Infarction
The posterior cerebral artery mainly supplies occipital lobe, thalamus and some portion of the temporal lobe. The classic presentation of posterior cerebral artery stroke is homonymous hemianopsia. Apart from this hypersomnolence, cognitive issues, the hemisensory loss can be seen when the deep PCA is involved. Some times there is bilateral infarction of distal PCAs producing cortical blindness and the patient is unaware of the blindness and deny it. This is called Anton-Babinski syndrome.
The patients with cerebellar strokes present with ataxia, dysarthria, nausea, vomiting and vertigo.
The initial workup of a stroke patient involves stabilizing the Airway, Breathing, and Circulation (ABC). This is followed by a rapid, concise, history and exam such as the NIHSS which is administered simultaneously as the patient gets IV access, telemetry, and labs were drawn. The patient should then get a stat non-contrasted head CT or a combination of Head CT, CT Angiography, and perfusion imaging. "Time is brain," and so we should not waste any time at all. Ideally, rtPA should be prepared as imaging is occurring, and as soon as the non-contrasted head CT can be visualized, and a bleed is excluded, rtPA should be administered after discussing the risks and benefits, and excluding rtPA contraindications. Time is critical, as only patients who get all the required studies within 4.5 hours qualify for potentially lifesaving thrombolysis. After IV rtPA, the CT angiography should be reviewed to determine if the patient qualifies for endovascular therapy as well.
In recent years there are significant advancements in acute stroke care. Multiple stroke trials in 2015 showed that Endovascular thrombectomy in the first six hours is much better than standard medical care in patients with large vessel occlusion in the arteries of the proximal anterior circulation. These benefits sustained irrespective of geographical location and patient characteristics.
Again in 2018, a significant paradigm shift happened in stroke care. DAWN trial showed significant benefits of Endovascular thrombectomy in patients with large vessel occlusion in the arteries of the proximal anterior circulation. This trial extended stroke window up to 24 hours in selected patients using perfusion imaging. Due to this, we can treat more patients even up to 24 hours. 
All patients should be treated with an antiplatelet agent and a statin, and be admitted for a full stroke evaluation. Hypertension is often seen in the acute stroke. This should not be aggressively treated. A baseline electrocardiogram is recommended. The following labs would be indicated when a diagnosis of stroke is entertained:
A transthoracic echocardiogram, telemetry monitoring, and neck vessel imaging are necessary to elucidate the etiology of stroke.
Acute ischemic stroke patients who meet the criteria for rtPA and do not have any contraindications should receive IV rtPA. Patients who have large vessel occlusions should be evaluated for possible endovascular intervention. All patients suspected of having acute ischemic stroke should be admitted for a full neurological work up. Neurology consultation should be obtained. The workup of acute ischemic stroke includes a search for a source of thrombus, which includes carotid evaluation by ultrasound, CTA, MRA, or conventional angiography. A Transthoracic echocardiogram is obtained to ascertain for low ejection fraction, the cardiac source of the clot, or patent foramen ovale. EKG and telemetry are obtained to ascertain for rhythms predisposing to stroke such as atrial fibrillation. Labs such as a fasting lipid panel, and hemoglobin A1C, are obtained to ascertain for modifiable risk factors for stroke. Other labs such as a hypercoagulable panel in young patients or B12 and syphilis testing in selected patients is also obtained. Antiplatelet and statins remain the mainstay of medical management of stroke.
A notable potential complication after fibrinolytic therapy is hemorrhagic transformation. Hemorrhagic transformation is classified as hemorrhagic infarction and parenchymal hematoma, each with 2 subsets. Predictive factors for the occurrence of this complication include increased infarction area, gray matter location, atrial fibrillation, and cerebral embolism, acute hyperglycemia, low platelet count, and poor collateral circulation. 
When to start anticoagulation in patients with atrial fibrillation after acute stroke is always a dilemma. Usually, it depends on various factors like the size of the stroke and other comorbidities. Usually, if the size of the stroke is smaller to moderate and no hemorrhage, we start anticoagulation in 7-14 days. 
Some times there are patients with small hemorrhagic transformation after acute stroke, and in this scenario, it is better to wait for anticoagulation for a couple of weeks. This delay is not associated with excessive stroke recurrence. 
For patients with significant disabilities, physical therapy and occupational therapy consults should be obtained. Similarly, if swallowing and speech are of concern, then speech/swallow consults should be obtained. All patients should have follow-ups arranged with their primary care providers, and with neurology at appropriate times post discharge. For symptomatic and significant carotid artery stenosis, referrals to vascular or neurological surgery should be sought.
The differential diagnosis is broad and can include stroke mimics such as TIA, metabolic derangement (in other words, hypoglycemia, hyponatremia), hemiplegic migraine, infection, brain tumor, syncope, and conversion disorder. 
Other issues to remember:
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