Thalamic Stroke

Thalamic stroke is ischaemic or haemorrhagic stroke of the thalamus. It causes sensory loss, cognitive and behavioural change, disturbed consciousness and, later, central post-stroke pain.

Thalamic infarcts account for about 11% of ischaemic strokes, and thalamic haemorrhage for about 10 to 15% of intracerebral haemorrhages. Posterior cerebral artery disease, small vessel disease and cardioembolism are the main causes of infarction, and hypertension causes most haemorrhages.

Vascular territories. Tuberothalamic (polar), paramedian, inferolateral and posterior choroidal territories. The artery of Percheron is a single trunk that supplies both paramedian thalami, and its occlusion causes bilateral infarction.

Prognosis. Most recover well from sensory deficit, but amnesia, apathy and chronic pain persist in many.

Pathophysiology.

Occlusion of the small perforators from the posterior communicating and posterior cerebral arteries infarcts relay nuclei. Disruption of sensory relay, limbic and reticular connections produces the sensory, memory and arousal syndromes.

Central post-stroke pain follows damage to the spinothalamic and thalamocortical tracts, with hyperexcitability in surviving neurons.

• Inferolateral infarct: contralateral hemisensory loss, sometimes with ataxia (Déjerine-Roussy syndrome) and later burning pain and allodynia.
• Paramedian and tuberothalamic infarct: amnesia, apathy, aphasia with left sided lesions, neglect with right sided lesions, vertical gaze palsy and hypersomnolence.
• Artery of Percheron infarct: reduced consciousness, vertical gaze palsy and memory loss.
• Haemorrhage: sudden headache, sensory deficit, reduced consciousness and eye deviation.
• Central post-stroke pain: persistent burning or lancinating pain in the affected body half, developing weeks to months after the event.

Red flags.

• Fluctuating or reduced consciousness (bilateral lesion, artery of Percheron occlusion, hydrocephalus).
• Large haemorrhage with intraventricular extension.
• Sudden deterioration after a stroke.

• Non-contrast CT to exclude haemorrhage, then MRI with diffusion weighted imaging; the bilateral paramedian pattern or midbrain V sign suggests Percheron occlusion.
• CT angiography or MR angiography of the posterior circulation; ECG, rhythm monitoring and echocardiography.
• Neuropsychological assessment for memory and executive deficits; sleep assessment.
• Pain history with a neuropathic pain tool.

Differential diagnosis. Deep venous thrombosis with bilateral thalamic oedema, top of the basilar syndrome, Wernicke encephalopathy, tumour, infection, demyelination, Creutzfeldt-Jakob disease and extrapontine myelinolysis.

• Acute: reperfusion with thrombolysis when eligible, supportive care and early rehabilitation.
• Alteplase 0.9 mg/kg intravenously (maximum 90 mg), 10% as a bolus over 1 minute and the rest as an infusion over 60 minutes, within 4.5 hours of onset or last known well. Monitor neurological observations and blood pressure every 15 minutes for 2 hours, every 30 minutes for the next 6 hours, then hourly to 24 hours; keep blood pressure under 185/110 mmHg before and under 180/105 mmHg after treatment; repeat imaging at 24 hours or with deterioration. Contraindicated with previous intracranial haemorrhage, INR over 1.7, platelets under 100 x 10^9/L, glucose under 2.7 mmol/L, anticoagulant use within 48 hours or major surgery within 14 days; no renal adjustment.
• Aspirin 300 mg orally once as a loading dose (300 mg rectally if swallowing is impaired), starting 24 hours after thrombolysis, then 75 mg orally once daily with food. Maximum 300 mg daily. Monitor bleeding, dyspepsia and full blood count. Avoid in active peptic ulcer, bleeding disorders and in children under 16 years; use caution when eGFR is under 10.
• Atorvastatin 80 mg orally once daily, long term. Maximum 80 mg daily. Monitor lipids at 4 to 12 weeks and ALT at baseline and if symptoms occur. No dose change in renal impairment; avoid in active liver disease; limit to 20 mg daily with clarithromycin; contraindicated in pregnancy and breastfeeding. Aim for LDL cholesterol under 1.8 mmol/L.
• Haemorrhage: blood pressure lowering, haematoma and hydrocephalus monitoring, and neurosurgical review for intraventricular extension with hydrocephalus.
• Central post-stroke pain: amitriptyline 10 mg orally at night, increased by 10 mg every 1 to 2 weeks as tolerated to 30 to 50 mg at night. Maximum 75 mg at night. Review at 6 to 8 weeks and stop if there is no benefit. Monitor sedation, anticholinergic effects, postural hypotension and mood; baseline ECG when over 40 years or with cardiac risk. Avoid after recent myocardial infarction, with arrhythmia, in angle closure glaucoma or urinary retention, and with other serotonergic drugs. Start at 10 mg and cap at 50 mg in older adults; reduce dose in hepatic impairment; no renal adjustment.
• Alternative or add on for central post-stroke pain: pregabalin 75 mg orally twice daily, increased after 3 to 7 days to 300 mg daily and, if needed after a further 7 days, to a maximum of 600 mg daily. Review at 4 weeks and stop if there is no meaningful benefit; withdraw over at least 1 week. Monitor sedation, dizziness, peripheral oedema, weight gain, mood and misuse. Adjust for renal function: creatinine clearance 30 to 60 mL/min, 75 to 300 mg daily in 2 or 3 divided doses; 15 to 30 mL/min, 25 to 150 mg daily; under 15 mL/min, 25 to 75 mg daily. Avoid in pregnancy unless benefit outweighs risk.
• Cognitive rehabilitation, sleep and mood treatment; avoid sedatives when consciousness is impaired.

Monitoring. Review pain and function at 4 to 6 weeks and every 3 months; reassess cognition and mood at 3 and 12 months.

Referral and escalation. Stroke service for all patients; pain clinic for refractory central pain; neuropsychology for cognitive deficits.

Special groups. Older adults: use lower antidepressant and pregabalin doses with slow titration and falls precautions.