What are the symptoms of a thalamic and midbrain infarct?

Symptoms of Thalamic and Midbrain Infarction

Thalamic and midbrain infarcts present with a constellation of symptoms including altered consciousness (ranging from somnolence to coma), vertical gaze abnormalities, oculomotor deficits, sensory loss, ataxia, and memory impairment, with the specific presentation depending on whether the infarct is paramedian, lateral, or bilateral.

Altered Level of Consciousness

• Profound somnolence or coma is the hallmark of bilateral paramedian thalamic infarction, particularly when the artery of Percheron (a single arterial trunk supplying both thalami and midbrain) is occluded 1, 2.
• Patients may be profoundly somnolent but easily rousable, or may present in a comatose state that gradually improves over days 2, 3.
• Altered consciousness occurs due to involvement of the reticular activating system and arousal pathways in the paramedian thalamus and rostral midbrain 1.
• The level of consciousness is the most reliable indicator of impending deterioration in brainstem stroke 4.

Oculomotor and Pupillary Abnormalities

• Vertical gaze palsy is the most common oculomotor finding, occurring in paramedian thalamic infarcts that involve the rostral midbrain tegmentum 5.
• Combined upgaze and downgaze palsy suggests involvement of the paramedian tegmentum of the rostral midbrain and predicts permanent oculomotor deficits 5.
• Third nerve palsy occurs in approximately 28% of patients with neuro-ophthalmologic manifestations of thalamic infarction 5.
• Skew deviation with invariable hypotropia of the contralesional eye is seen in 45% of patients with oculomotor features 5.
• Pseudoabducens palsy (mimicking sixth nerve palsy) occurs in approximately 23% of cases 5.
• Isolated ptosis and miosis may occur due to involvement of sympathetic pathways 5.
• Pupillary changes, including anisocoria or pinpoint pupils, may indicate brainstem compression 4.

Sensory Deficits

• Hemisensory loss is characteristic of lateral thalamic infarction, affecting the posterolateral and posteromedial ventral nuclei 6.
• Pure sensory stroke syndrome can result from smaller lateral thalamic infarcts in the posterolateral-posteromedial ventral complex 6.
• Sensory-motor stroke occurs when the infarct extends to involve the adjacent internal capsule 6.

Motor Deficits and Movement Disorders

• Hemiataxia (cerebellar-type ataxia on one side) occurs with lateral thalamic infarction involving the lateral and posterolateral ventral nuclei 6.
• Bilateral cerebellar ataxia is seen with paramedian thalamic and midbrain infarcts 3.
• Involuntary movements (choreoathetosis, tremor) can develop with lateral thalamic lesions 6.
• Hemiparesis may occur when the infarct extends to involve the midbrain or internal capsule 6.
• Decreased muscle tone is common in the acute phase 3.

Cognitive and Behavioral Abnormalities

• Amnesia and lack of spontaneity are prominent features of paramedian thalamic infarction 3.
• Palilalia (compulsive repetition of syllables, words, or phrases) can occur with bilateral paramedian thalamic and midbrain lesions, with speech rate increasing and volume decreasing until the patient whispers 3.
• Executive dysfunction and behavioral changes occur with thalamic involvement 7.

Visual Deficits

• Visual field defects (typically homonymous hemianopia) occur in approximately 18% of patients with neuro-ophthalmologic manifestations, due to involvement of the optic radiations or occipital lobe when the posterior cerebral artery is occluded proximally 5, 6.
• Hemianopia may develop later when extensive posterior cerebral artery territory infarction occurs 6.

Location-Specific Patterns

• Paramedian infarcts (84.8% of neuro-ophthalmologic cases) cause vertical gaze palsy, altered consciousness, memory impairment, and behavioral changes 5.
• Lateral thalamic infarcts cause three distinct syndromes: (1) hemisensory loss with hemiataxia and involuntary movements, (2) pure sensory stroke, or (3) sensory-motor stroke 6.
• Bilateral thalamic infarcts from artery of Percheron occlusion cause profound somnolence with severely dysregulated consciousness and alertness 1, 2.

Prognostic Indicators

• Most oculomotor abnormalities resolve spontaneously within a few months, but 18% of patients show permanent deficits 5.
• Permanent oculomotor deficits are predicted by: no improvement within 3 months, combined upgaze and downgaze palsy, and involvement of the paramedian tegmentum of the rostral midbrain 5.
• Patients with artery of Percheron infarcts can show rapid remarkable recovery over 48 hours with appropriate treatment 2.

Critical Diagnostic Pitfalls

• Early CT scans can be normal or non-revealing in thalamic and midbrain infarcts, making MRI essential when clinical suspicion is high 8, 1, 2.
• CT is relatively insensitive for detecting acute and small subcortical infarctions, especially in the posterior fossa 8.
• In patients presenting with drowsiness or somnolence without focal deficits, posterior circulation stroke should be considered and CT must be followed by MRI to confirm the diagnosis 2.
• The thalamus accounts for only 4.6% of stroke locations, making it an uncommon but important diagnosis to consider 8.