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Thalamic Stroke
π§ Introduction
A thalamic stroke occurs when blood flow to the thalamus is interrupted.
This deep brain structure is a relay hub for sensory, motor, visual, and cognitive signals.
Although relatively rare, thalamic strokes cause a wide spectrum of clinical deficits β from hemianesthesia to cognitive and behavioural syndromes.
They can be either ischaemic (most often small vessel disease) or haemorrhagic.
π©Έ Anatomy & Vascular Supply
The thalamus is supplied by small perforating arteries from the PCA & PComA:
- Paramedian Arteries: P1 PCA, sometimes via Artery of Percheron β bilateral infarcts.
- Thalamogeniculate Arteries: From PCA β lateral thalamus.
- Posterior Choroidal Arteries: Posterior thalamus & choroid plexus.
- Tuberothalamic (Polar) Artery: From PComA β anterior thalamus.
β οΈ Etiology
- Ischaemic: Small vessel lipohyalinosis (HTN/DM), artery-to-artery or cardioembolism, artery of Percheron occlusion.
- Haemorrhagic: Hypertensive bleed, amyloid angiopathy, AVMs, cavernomas, haemorrhagic transformation.
- Other: Deep venous thrombosis, neoplasm infiltration.
π©Ί Clinical Features
Depends on arterial territory β think βthalamic strokes = sensory + extrasβ:
- π Sensory loss: Contralateral hemianesthesia of all modalities.
- πͺ Motor weakness: If internal capsule fibres are compressed.
- π₯ Thalamic pain (DejerineβRoussy): Neuropathic pain weeks later.
- π Visual field loss: Contralateral hemianopia/quadrantanopia.
- βοΈ Ataxia & tremor: Limb incoordination, intention tremor.
- π Oculomotor signs: Vertical gaze palsy, pupillary changes.
- π Consciousness changes: Drowsiness, coma (bilateral lesions).
- π§© Cognitive/behavioural: Memory loss, apathy, language disturbance (anterior thalamus).
π· Imaging
- π₯ Non-contrast CT: Exclude bleed; hyperdense thalamus = ICH.
- π§² MRI (DWI): Most sensitive for small infarcts, artery of Percheron lesions.
- π©» CTA / MRA: Vessel anatomy & occlusion detection.
- π‘ DSA: For suspected AVM/cavernoma.
π Investigations
- π§ͺ Bloods: CBC, U&E, glucose, lipid, coagulation.
- β€οΈ Cardiac work-up: ECG (AF), echo (thrombus, PFO).
- π©Ί Vascular studies: Carotid Doppler if extracranial source suspected.
- π Risk profiling: BP, HbA1c, cholesterol.
π Management
Acute
- π©Ή Ischaemic: IV tPA (β€4.5 h), thrombectomy if large vessel, aspirin if no bleed.
- π©Έ Haemorrhagic: BP control, ICP management, ICU monitoring, rare surgical evacuation.
Secondary Prevention
- π Antithrombotics: Antiplatelets or anticoagulants (if AF).
- π Statins: LDL lowering, plaque stabilisation.
- π©Ί Risk factor control: HTN, DM, smoking, lifestyle change.
Rehabilitation
- π Physio: Motor retraining, gait recovery.
- π OT: ADL independence, adaptation.
- π£ Speech & swallow therapy when indicated.
- π₯ Pain management: TCAs, gabapentinoids for central pain.
- π§βπ€βπ§ Psych support: Depression, anxiety screening.
π Prognosis
- β
Many unilateral strokes recover well with rehab.
- β οΈ Persistent sensory loss, pain, cognitive change common.
- β οΈ Mortality higher in haemorrhagic forms or large bilateral infarcts.
π References
- Schmahmann JD. Vascular syndromes of the thalamus. Stroke. 2003.
- Kumral E, et al. Thalamic infarcts: findings, etiology, prognosis. Neurology. 1995.
- Guenego A, et al. Artery of Percheron infarct patterns. Neuroradiology. 2015.
- AHA/ASA Acute Stroke Guidelines. Stroke. 2019.