Makindo Medical Notes

Related Subjects: |Acute Stroke Assessment (ROSIER&NIHSS) |Atrial Fibrillation |Atrial Myxoma |Causes of Stroke |Ischaemic Stroke |Cancer and Stroke |Cardioembolic stroke |CT Basics for Stroke |Endocarditis and Stroke |Haemorrhagic Stroke |Stroke Thrombolysis |Hyperacute Stroke Care

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 ischemic or hemorrhagic 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

Thalamic strokes can result from:

• Ischemic 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).
  • Hemorrhagic transformation of an ischemic stroke.
• Other Causes:
  • Venous infarction due to deep cerebral vein thrombosis.
  • Neoplasms or infiltrative diseases affecting the thalamus.

Clinical Features

The clinical presentation varies depending on the affected thalamic region and the extent of the lesion:

• 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

Imaging studies are crucial for diagnosis and determining the type of stroke:

• 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

Additional investigations are conducted to identify risk factors and guide management:

• 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.

Management

Management of thalamic strokes follows standard stroke protocols, with specific considerations:

Acute Management

• Ischemic 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.