Makindo Medical Notes

Related Subjects: |Subarachnoid Haemorrhage |Perimesencephalic Subarachnoid haemorrhage |Haemorrhagic stroke |Cerebellar Haemorrhage |Putaminal Haemorrhage |Thalamic Haemorrhage |ICH Classification and Severity Scores

Patients with a thalamic stroke can sometimes appear as if they are sleeping, rather than in a comatose state.

Introduction

Thalamic strokes involve an interruption of blood flow to the thalamus, a deep-seated structure in the brain that acts as a relay center for motor and sensory signals to the cerebral cortex. Thalamic strokes can be either ischaemic or haemorrhagic and account for a small percentage of all strokes. Due to the thalamus's role in various neurological functions, thalamic strokes can lead to a wide range of clinical manifestations, including sensory deficits, motor weakness, visual disturbances, and cognitive impairments.

Anatomy and Vascular Supply

• The thalamus is supplied by small penetrating arteries originating from the posterior cerebral artery (PCA) and the posterior communicating artery (PComA). Key arterial branches include:
• Paramedian Thalamic Arteries: Arise from the P1 segment of the PCA or from the artery of Percheron (a single arterial trunk supplying bilateral paramedian thalami).
• Thalamogeniculate Arteries: Branches of the PCA supplying the lateral thalamus.
• Posterior Choroidal Arteries: Supply the posterior thalamus and adjacent structures.
• Tuberothalamic (Polar) Artery: Branches from the posterior communicating artery, supplying the anterior thalamus.

Etiology

• Ischaemic Infarction:
  • Small vessel disease (lipohyalinosis) due to hypertension and diabetes.
  • Embolic occlusion from cardiac sources or large artery atherosclerosis.
  • Artery of Percheron occlusion leading to bilateral thalamic infarcts.
• Intracerebral Hemorrhage:
  • Hypertensive hemorrhage affecting small penetrating arteries.
  • Cerebral amyloid angiopathy in the elderly.
  • Vascular malformations (e.g., arteriovenous malformations, cavernous angiomas).
  • Haemorrhagic transformation of an ischemic stroke.
• Other Causes:
  • Venous infarction due to deep cerebral vein thrombosis.
  • Neoplasms or infiltrative diseases affecting the thalamus.

Clinical Features

• Sensory Deficits: Contralateral hemianesthesia affecting all modalities (touch, pain, temperature, proprioception).
• Motor Deficits: Contralateral hemiparesis due to involvement of adjacent internal capsule fibers.
• Thalamic Pain Syndrome (Dejerine–Roussy Syndrome): Persistent, often severe, neuropathic pain developing weeks to months after the initial stroke.
• Visual Field Defects: Contralateral homonymous hemianopia or quadrantanopia due to optic tract involvement.
• Ataxia and Movement Disorders: Contralateral cerebellar ataxia, intention tremor, or choreiform movements.
• Oculomotor Disturbances:
  • Vertical gaze palsy, especially with paramedian thalamic infarcts.
  • Pupillary abnormalities (e.g., mid-position pupils, light-near dissociation).
• Altered Consciousness: Drowsiness, confusion, or coma, particularly with bilateral thalamic involvement (e.g., artery of Percheron infarct).
• Cognitive and Behavioral Changes: Memory impairment, language difficulties, apathy, or disorientation when the anterior thalamus is involved.

Diagnostic Imaging

• Non-Contrast Computed Tomography (CT) Scan:
  • First-line imaging to exclude hemorrhage.
  • May reveal hyperdense area in hemorrhagic stroke or hypodense area in established infarction.
• Magnetic Resonance Imaging (MRI):
  • Diffusion-weighted imaging (DWI) is sensitive for detecting acute ischaemia.
  • Better visualization of small infarcts or hemorrhages in the thalamus.
  • MRI angiography (MRA) can assess vessel occlusions.
• Computed Tomography Angiography (CTA):
  • Useful for evaluating vascular anatomy and identifying arterial occlusions or anomalies.
• Digital Subtraction Angiography (DSA):
  • Considered when vascular malformations are suspected.

Investigations

• Laboratory Tests:
  • Complete blood count (CBC), electrolytes, glucose, lipid profile.
  • Coagulation profile to assess for coagulopathies.
• Cardiac Evaluation:
  • Electrocardiogram (ECG) to detect arrhythmias like atrial fibrillation.
  • Echocardiography to assess for cardiac sources of emboli.
• Vascular Imaging:
  • Carotid Doppler ultrasound to evaluate extracranial carotid arteries.
• Risk Factor Assessment:
  • Blood pressure monitoring for hypertension.
  • Hemoglobin A1c for diabetes control.

Acute Management

• Ischaemic Stroke:
  • Intravenous Thrombolysis: Administration of tissue plasminogen activator (tPA) within the therapeutic window (generally within 4.5 hours of symptom onset).
  • Mechanical Thrombectomy: May be considered if a proximal arterial occlusion is identified and the patient meets criteria.
  • Antiplatelet Therapy: Aspirin is initiated if thrombolysis is not administered or after exclusion of hemorrhage.
• Hemorrhagic Stroke:
  • Blood Pressure Control: Careful management to prevent hematoma expansion.
  • Management of Increased Intracranial Pressure: Elevate head of bed, osmotherapy, monitoring in intensive care if necessary.
  • Surgical Intervention: Rare for deep thalamic hemorrhages due to inaccessibility; reserved for select cases.

Secondary Prevention

• Risk Factor Modification:
  • Control hypertension, diabetes, and hyperlipidemia.
  • Lifestyle changes: smoking cessation, diet, and exercise.
• Antithrombotic Therapy:
  • Long-term antiplatelet agents for ischemic strokes.
  • Anticoagulation if atrial fibrillation or other cardiac embolic sources are identified.
• Statin Therapy: To reduce cholesterol levels and stabilize atherosclerotic plaques.

Rehabilitation and Supportive Care

• Physical Therapy: To improve motor function and mobility.
• Occupational Therapy: Assistance with activities of daily living.
• Speech and Language Therapy: If language or swallowing deficits are present.
• Pain Management: For thalamic pain syndrome, using medications such as antidepressants and anticonvulsants.
• Psychological Support: Address cognitive and emotional challenges, including depression and anxiety.

Prognosis

The outcome of thalamic strokes varies:

• Functional Recovery: Many patients experience significant recovery with rehabilitation, especially if the stroke is unilateral and limited in size.
• Persistent Deficits: Sensory disturbances, pain syndromes, or cognitive impairments may persist.
• Mortality: Higher in hemorrhagic strokes, especially with large hematomas or ventricular extension.

References

• Schmahmann JD. Vascular syndromes of the thalamus. Stroke. 2003;34(9):2264-2278.
• Caplan LR, DeWitt LD, Pessin MS, et al. Caudolateral thalamic infarcts. Arch Neurol. 1988;45(4):434-440.
• Kumral E, Evyapan D, Balkir K, Kutluhan S. Thalamic infarcts: clinical findings, etiology, and prognosis in 47 patients. Neurology. 1995;45(3):462-468.
• Guenego A, Sabben C, Naggara O, et al. Artery of Percheron infarct: imaging patterns and clinical spectrum. Neuroradiology. 2015;57(6):589-596.
• Adams HP Jr, del Zoppo G, Alberts MJ, et al. Guidelines for the early management of adults with ischemic stroke. Stroke. 2007;38(5):1655-1711.

Images

• Figure 1: Thalamic Stroke Illustration.
• Figure 2: Thalamic Hemorrhage Location.
• Figure 3: Detailed Thalamic Stroke Image.