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Neurology

Stroke: Ischemic and Hemorrhagic — Diagnosis, NIHSS Scale, and Treatment

WhiteCoat Pro Editorial BoardApril 11, 2026Updated April 19, 20264 min read
Table of contents · 10 sections
  1. 1. Classification
  2. 2. Risk factors
  3. 3. Clinical presentation
  4. 4. FAST screening
  5. 5. NIHSS scale
  6. 6. Diagnostics
  7. 7. Ischemic stroke management
  8. 8. Hemorrhagic stroke
  9. 9. Secondary prevention
  10. 10. FAQ

In a nutshell. Stroke is sudden neurological deficit of vascular origin. 85% are ischemic, 15% are hemorrhagic. The key to diagnosis is assessment using the NIHSS scale and non-contrast CT (to rule out hemorrhage). The time window for thrombolysis is 4.5 h, and for thrombectomy it is up to 24 h in patients with perfusion mismatch.

1. Classification

  • Ischemic stroke (85%) is acute arterial occlusion resulting in cerebral infarction. TOAST subtypes: cardioembolic, atherothrombotic, lacunar, of rare etiology, of undetermined etiology.
  • Hemorrhagic stroke (15%): intracerebral hemorrhage (10%), subarachnoid hemorrhage (5%).
  • Transient ischemic attack (TIA) — neurological deficit < 24 h with no CT/MRI evidence of an acute lesion.

2. Risk factors

  • Non-modifiable: age, male sex, family history.
  • Modifiable: arterial hypertension (the main factor!), atrial fibrillation, diabetes mellitus, smoking, dyslipidemia, obesity, physical inactivity, alcohol abuse, sleep apnea.

3. Clinical presentation

Stroke symptoms correspond to the vascular territory of the affected artery.

Carotid territory (middle cerebral artery — MCA)

  • Contralateral hemiparesis / hemiplegia (arm affected more than the leg).
  • Contralateral hemianesthesia.
  • Motor or sensory aphasia (dominant hemisphere).
  • Hemianopia.
  • Neglect (nondominant hemisphere).

Vertebrobasilar territory

  • Dizziness, ataxia, nystagmus.
  • Diplopia, dysarthria, dysphagia.
  • Alternating syndromes (contralateral paresis + ipsilateral cranial nerve palsy).
  • Homonymous hemianopia (PCA).

Lacunar syndromes

  • Pure motor hemiparesis, pure sensory stroke, ataxic hemiparesis, clumsy hand-dysarthria, sensorimotor stroke.

4. FAST screening

  • Face — drooping of the face when smiling.
  • Arms — inability to hold up both arms.
  • Speech — slurred or strange speech.
  • Time — time to call emergency services.

5. NIHSS scale

NIH Stroke Scale — 15 items: level of consciousness, orientation, commands, gaze, visual fields, facial palsy, limb motor function, ataxia, sensory, aphasia, dysarthria, neglect. Maximum score is 42.

  • 0 — no stroke.
  • 1–4 — mild.
  • 5–15 — moderate.
  • 16–20 — moderate-to-severe.
  • 21–42 — severe.

NIHSS ≥ 6 + proximal occlusion — candidate for thrombectomy.

6. Diagnostics

MethodRole
Non-contrast CTFirst-line method: ruling out hemorrhage. Early signs of ischemia: sulcal effacement, hypoattenuation in the arterial territory
CT angiographyDetection of occlusion, indication for thrombectomy
CT perfusion or MRI-DWI/PWIAssessment of the penumbra — the salvageable tissue zone; the basis for decision-making regarding thrombectomy in the extended time window (up to 24 h)
MRIMore sensitive for small lesions and in the posterior fossa
Carotid duplex ultrasonographyStenosis screening, risk stratification
EchocardiographyRuling out cardioembolism
Holter ECG monitoringDetection of paroxysmal atrial fibrillation

7. Ischemic stroke management

Intravenous thrombolysis

  • Drug: alteplase 0.9 mg/kg (max 90 mg): 10% as a bolus, the rest as a 60-minute infusion.
  • Window: up to 4.5 h from symptom onset.
  • Contraindications: intracranial hemorrhage, major trauma / surgery within 14 days, gastrointestinal bleeding within 3 weeks, BP > 185/110 (refractory), INR > 1.7, platelets < 100 × 10⁹/L, DOACs within the last 48 h (unless specific reversal agents are used).
  • Risk: symptomatic intracranial hemorrhage 6%.

Thrombectomy

  • Endovascular clot removal using a stent retriever.
  • Window: ≤ 6 h standard; 6–24 h if mismatch present per DAWN/DEFUSE-3 (pronounced penumbra).
  • Indication: proximal occlusion (ICA, M1 MCA), NIHSS ≥ 6, pre-stroke mRS ≤ 1.

General management

  • BP control: with thrombolysis < 180/105; without thrombolysis, "permissive" hypertension up to 220/110 is acceptable for the first 24 h.
  • Glycemic control: 7.8–10 mmol/L.
  • Oxygenation: SpO₂ > 94 %.
  • DVT prophylaxis: LMWH after 24 h if no hemorrhagic transformation is present.
  • Aspirin 325 mg in the first 48 h (except post-thrombolysis — after 24 h).

8. Hemorrhagic stroke

Intracerebral haemorrhage

  • Rapid clinical presentation: headache, vomiting, altered mental status, focal symptoms.
  • Diagnosis — CT (hyperdense lesion).
  • Treatment: strict BP control (target SBP 130–140 mm Hg in the first 24 h), discontinuation and reversal of anticoagulants, seizure prophylaxis for cortical localization.
  • Surgery (hematoma evacuation) — for cerebellar hemorrhage > 3 cm or progressive midline shift.

Subarachnoid haemorrhage

  • "Thunderclap" onset — sudden, severe headache.
  • Meningeal signs, photophobia, possible loss of consciousness, focal symptoms.
  • CT is positive in 98 % of cases within the first 6 h; if negative — lumbar puncture (xanthochromia).
  • Cause in 85 % — rupture of a Willis circle aneurysm.
  • Hunt–Hess scale assesses severity.
  • Treatment: endovascular embolization or aneurysm clipping, nimodipine for vasospasm prophylaxis, strict BP control.

9. Secondary prevention

  • Atherothrombotic stroke: antiplatelets (ASA 75–100 mg or clopidogrel 75 mg), high-intensity statins, BP and DM control.
  • Cardioembolic (AF): anticoagulation — DOACs preferred over warfarin; CHA₂DS₂-VASc and HAS-BLED scoring.
  • Symptomatic carotid stenosis > 70 %: endarterectomy within 14 days.
  • Non-pharmacological: smoking cessation, moderate physical activity, weight control, Mediterranean diet.

10. FAQ

How does a TIA differ from a stroke?
TIA — complete recovery < 24 h without a lesion on MRI-DWI. By modern definition, the key criterion is the absence of infarction, not just duration.

Can thrombolysis and thrombectomy be performed simultaneously?
Yes. The EXTEND-IA and DAWN trials demonstrated the superiority of a combined strategy ("bridging" in large vessel occlusion).

Why shouldn't BP be aggressively lowered in the acute period?
High BP maintains penumbral perfusion. A sharp drop enlarges the infarction zone.

When is decompressive hemicraniectomy indicated?
For malignant edema in the MCA territory (within 48 h of onset), in patients < 60 years; reduces mortality from 80 % to 30 %.

How to clinically distinguish ischemic from hemorrhagic stroke?
Reliably — only by CT. Clinical signs (rapid mental status depression, vomiting, severe headache) are more characteristic of hemorrhage, but are nonspecific.

See also: Cranial nerves · Multiple sclerosis · Myocardial infarction · Anticoagulants · NIHSS · CHA₂DS₂-VASc · Neurology Directory

This material is educational in nature and does not replace a doctor's consultation. Verify treatment regimens and dosages with current clinical guidelines.

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