Stroke no short forms

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"stroke"[MeSH Terms] AND "ischemic stroke"

Stroke is a large topic, so here is a map and a short overview. The overview spells out every term in full, as you asked. Please pick one area to go into in depth.

Topic map

Definition and types: ischemic stroke, intracerebral hemorrhage, subarachnoid hemorrhage, transient ischemic attack
Causes and risk factors: atherosclerosis, cardioembolism, small vessel disease, atrial fibrillation, hypertension, diabetes, smoking
Vascular anatomy and syndromes: the middle cerebral artery, anterior cerebral artery, posterior circulation, and lacunar syndromes
Recognition and emergency assessment: symptoms, scoring scales, time windows
Imaging and diagnostic workup: non-contrast computed tomography, magnetic resonance imaging, vessel imaging, cardiac evaluation
Acute treatment: intravenous thrombolysis, mechanical thrombectomy, blood pressure management, hemorrhage management
Secondary prevention: antiplatelet drugs, anticoagulants, statins, carotid revascularization
Rehabilitation and complications

Brief overview A stroke is a sudden loss of brain function caused by a disturbance of blood supply. About 85 percent of strokes are ischemic, caused by a blocked artery. The rest are hemorrhagic, caused by bleeding inside the brain tissue or around it. A transient ischemic attack has the same symptoms but resolves completely, and it is a strong warning sign of a later stroke.

Typical features are sudden weakness or numbness of the face, arm, or leg on one side, trouble speaking or understanding speech, loss of vision, loss of balance, and a sudden severe headache. Because brain tissue dies quickly, rapid recognition and a brain imaging scan to separate ischemic from hemorrhagic stroke come first. The two types are treated very differently.

Eligible patients with ischemic stroke can receive clot-dissolving medicine given into a vein, and those with a blocked large artery can have the clot removed with a catheter. Prevention depends on the cause. It includes blood pressure control, cholesterol-lowering therapy, antiplatelet or anticoagulant medicine, and stopping smoking.

The library has dedicated ischemic stroke chapters in Bradley and Daroff's Neurology in Clinical Practice and in Rosen's Emergency Medicine. A search of recent systematic reviews turned up three. One covers telling ischemic from hemorrhagic stroke by presenting symptoms (PubMed identifier 40759192). One covers stroke despite oral anticoagulation in atrial fibrillation (41427999). One covers prognosis of ischemic stroke with a negative diffusion-weighted scan (38737347). None of them contradicts the standard textbook framework above.

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Which part of stroke should I cover in detail (all terms written out in full)?

Stroke is a large topic, so here is a map and a short overview. The overview spells out every term in full, as you asked. Please pick one area to go into in depth.

Topic map

Definition and types: ischemic stroke, intracerebral hemorrhage, subarachnoid hemorrhage, transient ischemic attack
Causes and risk factors: atherosclerosis, cardioembolism, small vessel disease, atrial fibrillation, hypertension, diabetes, smoking
Vascular anatomy and syndromes: the middle cerebral artery, anterior cerebral artery, posterior circulation, and lacunar syndromes
Recognition and emergency assessment: symptoms, scoring scales, time windows
Imaging and diagnostic workup: non-contrast computed tomography, magnetic resonance imaging, vessel imaging, cardiac evaluation
Acute treatment: intravenous thrombolysis, mechanical thrombectomy, blood pressure management, hemorrhage management
Secondary prevention: antiplatelet drugs, anticoagulants, statins, carotid revascularization
Rehabilitation and complications

Brief overview A stroke is a sudden loss of brain function caused by a disturbance of blood supply. About 85 percent of strokes are ischemic, caused by a blocked artery. The rest are hemorrhagic, caused by bleeding inside the brain tissue or around it. A transient ischemic attack has the same symptoms but resolves completely, and it is a strong warning sign of a later stroke.

Typical features are sudden weakness or numbness of the face, arm, or leg on one side, trouble speaking or understanding speech, loss of vision, loss of balance, and a sudden severe headache. Because brain tissue dies quickly, rapid recognition and a brain imaging scan to separate ischemic from hemorrhagic stroke come first. The two types are treated very differently.

Eligible patients with ischemic stroke can receive clot-dissolving medicine given into a vein, and those with a blocked large artery can have the clot removed with a catheter. Prevention depends on the cause. It includes blood pressure control, cholesterol-lowering therapy, antiplatelet or anticoagulant medicine, and stopping smoking.

The library has dedicated ischemic stroke chapters in Bradley and Daroff's Neurology in Clinical Practice and in Rosen's Emergency Medicine. A search of recent systematic reviews turned up three. One covers telling ischemic from hemorrhagic stroke by presenting symptoms (PubMed identifier 40759192). One covers stroke despite oral anticoagulation in atrial fibrillation (41427999). One covers prognosis of ischemic stroke with a negative diffusion-weighted scan (38737347). None of them contradicts the standard textbook framework above.

Stroke

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ischemic stroke brain imaging infarct diffusion-weighted

A multi-modal comparison of brain imaging from a patient with an acute ischemic stroke, featuring four axial views: Non-Contrast Computed Tomography (NCCT) with skull removal, Diffusion-Weighted Imaging (DWI), Fluid-Attenuated Inversion Recovery (FLAIR), and a labeled NCCT. The image demonstrates a clear clinicoradiological mismatch. The DWI modality reveals a distinct area of hyperintensity in the left hemisphere, signifying cytotoxic edema and the restricted diffusion characteristic of an acute infarct. In contrast, the FLAIR sequence shows minimal signal changes in the corresponding area, suggesting a 'DWI-FLAIR mismatch' indicative of hyperacute stroke within the thrombolysis window. The final panel displays the NCCT with manual segmentations: the 'Infarct Core' (IC) is highlighted in green, while the surrounding 'Infarct Penumbra' (IP) is highlighted in red. This comparison highlights the difficulty of visualizing early ischemic changes on NCCT compared to the sensitivity of MRI sequences, emphasizing the role of automated segmentation in identifying salvageable brain tissue.

**Imaging Modality:** Magnetic Resonance Imaging (MRI); Diffusion-Weighted Imaging (DWI).

This composite image illustrates diagnostic findings and biomarker data from ischemic stroke (IS) patients. (a, b) Axial brain MRI scans showing a subcortical lacunar infarct in the right hemisphere. Panel (a) is a Diffusion-Weighted Imaging (DWI) sequence where the acute infarct appears as a bright hyperintense lesion (white arrow). Panel (b) is the corresponding Apparent Diffusion Coefficient (ADC) map, showing the same lesion as a dark hypointense area (white arrow), confirming restricted diffusion. (c) A box plot representing the infarct volume distribution (mm³) among IS patients. (d, e) Comparative box plots showing significantly elevated serum levels of Neurofilament light chain (NF-L) and Glial Fibrillary Acidic Protein (GFAP) in IS patients versus healthy controls (Ctl), indicating neuro-axonal and glial damage. (f) A correlation plot with linear regression and 95% confidence intervals demonstrating positive associations between serum NF-L and plasma TNFR1 and TNFR2 levels. These data illustrate the relationship between structural brain injury, inflammatory signaling, and biomarker release post-ischemic stroke.

This composite diagnostic image illustrates the process of defining a Volume of Interest (VOI) for an acute ischemic stroke using neuroimaging. Panel A shows an axial slice of a diffusion-weighted MRI (DWI) displaying a hyperintense lesion in the region of the basal ganglia, consistent with an acute infarct. Panel B demonstrates the manual segmentation of this infarct, highlighted as a red Region of Interest (ROI). Panel C presents a 3D reconstruction of the segmented infarct volume, providing a volumetric representation of the lesion. Panel D shows an axial map (likely an Apparent Diffusion Coefficient or Fractional Anisotropy map) with two mirrored ROIs: the primary infarct site in the left hemisphere (red) and its anatomically mirrored counterpart in the unaffected right hemisphere (green). This methodology is used in neuroradiology research to compare diffusion parameters between ischemic and healthy brain tissue, excluding cerebrospinal fluid (CSF) to ensure data accuracy. The image is intended for advanced medical education regarding stroke imaging analysis and neuroimaging post-processing techniques.

Stroke

A stroke is a sudden loss of brain function caused by a disturbance of blood supply. It is the fourth leading cause of death and the most common reason for long-term disability worldwide. Timely restoration of blood flow to threatened brain tissue is the most effective treatment (Bradley and Daroff's Neurology in Clinical Practice, p. 1131).

1. Types

Type	Mechanism	Approximate share
Ischemic stroke	Blocked artery	About 85 percent
Intracerebral hemorrhage	Bleeding into brain tissue, usually from hypertension	About 10 percent
Subarachnoid hemorrhage	Bleeding around the brain, often from a ruptured aneurysm	About 5 percent
Transient ischemic attack	Temporary blockage with full recovery and no dead tissue on imaging	Warning event

The shares are from my own background knowledge, not the retrieved textbook passages.

2. Causes of ischemic stroke

According to Rosen's Emergency Medicine (section on ischemic stroke):

Large artery thrombosis accounts for about one third of ischemic strokes. A clot forms on an ulcerated atherosclerotic plaque, typically where an artery branches, such as the internal carotid artery.
Small vessel (lacunar) stroke produces infarcts from a few millimetres to 2 centimetres. It affects the basal ganglia, thalamus, pons, and internal capsule. About 80 to 90 percent of these patients have hypertension, and diabetes is also common.
Cardioembolic stroke accounts for about one quarter. Atrial fibrillation is the most common source and raises stroke risk about fivefold.
Artery-to-artery embolism comes from a carotid plaque. One example is amaurosis fugax, which is temporary loss of vision in one eye.
In the young (3 to 4 percent of strokes occur at ages 15 to 45), carotid or vertebral artery dissection is the leading identified cause. Other causes are pregnancy, oral contraceptives, antiphospholipid antibodies, protein C or S deficiency, sickle cell anemia, polycythemia, and cocaine or amphetamine use.
More than one third of first strokes have no clear cause identified.

Modifiable risk factors: hypertension, diabetes, smoking, high cholesterol, atrial fibrillation, obesity, physical inactivity, and heavy alcohol use.

3. Recognition

Typical sudden features are:

facial droop
weakness or numbness of one arm or leg, usually on one side
slurred or lost speech, or trouble understanding speech
loss of vision in one eye or half of the visual field
loss of balance, vertigo, or double vision (suggesting the back of the brain)
a sudden severe headache (suggesting hemorrhage)

The key action is to record the time the patient was last known to be well and call emergency services at once. The time of onset decides which treatments are possible.

4. Emergency assessment and imaging

Check airway, breathing, circulation, and blood glucose. Low blood sugar can mimic stroke.
Perform urgent non-contrast computed tomography of the head to exclude hemorrhage. It is often normal in the first hours of an ischemic stroke.
Image the blood vessels (computed tomography angiography or magnetic resonance angiography) to find a large vessel occlusion.
Use magnetic resonance imaging with diffusion-weighted sequences or perfusion imaging to show the dead core and the salvageable surrounding tissue, called the penumbra.
Later workup includes a heart rhythm recording, an echocardiogram, a lipid profile, and glycated hemoglobin.

Multi-modal brain imaging of acute ischemic stroke showing diffusion restriction and infarct core versus penumbra

The figure shows a bright diffusion-weighted lesion in the left hemisphere. The matching fluid-attenuated inversion recovery sequence shows little change. This "mismatch" suggests a hyperacute stroke that is still within the window for clot-dissolving treatment.

5. Acute treatment of ischemic stroke

Intravenous thrombolysis with recombinant tissue plasminogen activator (alteplase):

It was first approved for a 3-hour window, then extended to 3 to 4.5 hours after onset.
Selected patients can benefit up to 9 hours from last seen well when advanced imaging shows salvageable tissue.
Its limits are the narrow time window, a weak effect on large proximal occlusions, and the need for advanced imaging at later times.
Fewer than 5 percent of eligible patients received it in the textbook's cited data (Bradley and Daroff's Neurology in Clinical Practice, p. 1131).
Blood pressure must be below about 185 over 110 millimetres of mercury before treatment, and there must be no hemorrhage on imaging.
Tenecteplase is used as an alternative in many centres. I did not verify current local guidance, so check it for your setting.

Mechanical thrombectomy (catheter removal of the clot):

Five randomized trials in 2015 showed benefit for large vessel occlusion in the early window.
The DAWN and DEFUSE 3 trials extended benefit to as late as 24 hours from last seen well in patients selected by imaging (Bradley and Daroff's Neurology in Clinical Practice, p. 1131).
Patient selection matters to avoid both overtreatment and undertreatment.

General care:

Admit to a dedicated stroke unit.
Correct low oxygen levels.
Avoid aggressive blood pressure lowering unless the patient is receiving thrombolysis or has very high pressure.
Treat fever and high or low glucose.
Screen swallowing before giving food or drink.
Give aspirin within 24 to 48 hours if thrombolysis was not given.

Hemorrhagic stroke:

Lower the blood pressure.
Reverse any anticoagulant medicine.
Involve neurosurgery for large cerebellar bleeds, hydrocephalus, or ruptured aneurysm.
For subarachnoid hemorrhage, secure the aneurysm by clipping or coiling and give nimodipine to reduce delayed ischemia.

6. Secondary prevention

Antiplatelet therapy: aspirin or clopidogrel. After a minor stroke or high-risk transient ischemic attack, short-term (about 21 days) combined aspirin and clopidogrel is used.
Anticoagulation for atrial fibrillation, with a direct oral anticoagulant preferred over warfarin in most patients.
Blood pressure control, a high-intensity statin, and diabetes control.
Carotid endarterectomy or stenting for symptomatic narrowing of the carotid artery, mainly 70 to 99 percent.
Lifestyle: stop smoking, exercise, adopt a Mediterranean-style diet, limit alcohol, and manage weight.

7. Recovery and complications

Start rehabilitation early, with physical, occupational, and speech therapy.
Watch for aspiration pneumonia, deep vein thrombosis, pressure sores, depression, seizures, spasticity, shoulder pain, and swelling of the brain after a large infarct.

Recent evidence check

I found no recent systematic review that contradicts the textbook framework above. Three from 2024 and 2025:

a review of telling ischemic from hemorrhagic stroke by presenting symptoms (PubMed identifier 40759192)
a review of stroke despite oral anticoagulation in atrial fibrillation (41427999)
a review of prognosis in ischemic stroke with a negative diffusion-weighted scan (38737347)

Some details above (blood pressure thresholds, short-term dual antiplatelet therapy, tenecteplase, and the carotid narrowing ranges for surgery) come from my own knowledge, not the retrieved textbook passages. Check them against current guidelines before clinical use.

Tell me which part you want in more depth and I will go further. Examples are the artery-by-artery syndromes, the thrombolysis eligibility checklist, hemorrhage management, or rehabilitation.