Right Thalamocapsular Infarct: Expected Clinical Findings
A right thalamocapsular infarct produces a characteristic triad of left-sided motor weakness, left-sided sensory loss (often severe and involving all modalities), and frequently left-sided neglect or visuospatial deficits. 1
Core Motor Deficits
- Left hemiparesis affecting the face, arm, and leg is the hallmark motor finding, resulting from involvement of the posterior limb of the internal capsule adjacent to the thalamic lesion 1
- The motor weakness can range from mild (barely able to move against gravity) to dense hemiplegia, with progression possible over 24-48 hours 1
- Extensor plantar response (Babinski sign) on the left side is typically present 1
- Dysarthria may occur, particularly if the infarct extends into the capsular genu 2
Sensory Manifestations
The sensory deficit is often the most prominent and persistent feature of thalamocapsular infarction:
- Dense left hemisensory syndrome involving the head, face, trunk, arm, and leg in a faciobrachiocrural distribution is characteristic 3, 1
- Loss of all sensory modalities (pain, temperature, touch, proprioception, vibration) is common when the ventral posterior nucleus is involved 3
- Patients frequently describe the affected limb as feeling "numb" or "heavy" 1
- Sensory deficits typically improve more slowly than motor deficits—motor recovery may begin within 24 hours, while sensory improvement may not start until 8+ days post-stroke 1
Pain and Dysesthesias
- Acute pain and/or dysesthesias occur in approximately 24% of patients at stroke onset, particularly when the ventrocaudalis nucleus is damaged 3
- Paresthesias in the contralateral body are reported by approximately 72% of patients with ventrocaudalis involvement 3
- Delayed thalamic pain syndrome (central post-stroke pain) can develop 2-15 days after stroke onset (mean 10.5 days) in patients with ventrocaudalis nucleus involvement 3
Cognitive and Behavioral Features
Right hemisphere thalamocapsular infarcts produce distinct cognitive deficits:
- Left-sided neglect is common with right thalamic lesions, though the evidence base is stronger for left hemisphere cognitive deficits 4, 2
- Visuospatial processing deficits may occur with right-sided lesions 5
- Fluctuating alertness, inattention, apathy, and abulia can occur if the capsular genu is involved, suggesting thalamocortical disconnection 2
- Functional imaging may show reduced perfusion in the ipsilateral frontal cortex due to interrupted thalamic peduncles 2
Visual Deficits
- Left homonymous hemianopia can occur if the infarct extends posteriorly to involve the optic radiations, though this is less common in pure thalamocapsular lesions 6, 7
- Visual field defects were present in only 7 of 342 thalamic infarcts (2%) in one large series 7
Oculomotor Abnormalities
When the infarct extends to involve paramedian structures, neuro-ophthalmologic findings may include:
- Vertical gaze palsy (most common oculomotor finding in thalamic infarcts overall) 7
- Skew deviation with hypotropia of the left (contralesional) eye 7
- Third nerve palsy or pseudoabducens palsy 7
- These features are more typical of paramedian thalamic territory involvement rather than pure thalamocapsular infarcts 7
Temporal Evolution and Prognosis
Motor recovery typically precedes sensory recovery:
- Motor improvement usually begins within 24 hours and progresses to ambulatory status within 2-3 weeks 1
- Sensory deficits are more persistent, often remaining prominent at hospital discharge 1
- Most patients achieve functional independence, though residual sensory deficits are common 1
Critical Pitfall to Avoid
Do not mistake the initial presentation for a pure sensory stroke—while sensory symptoms may be the presenting complaint, careful examination will reveal motor weakness that may be subtle initially but can progress over the first 24-30 hours. 1 The combination of thalamic (sensory) and capsular (motor) involvement distinguishes thalamocapsular infarcts from pure thalamic sensory strokes. 3, 1