How can basal ganglia lesions cause hemisensory loss, hemiparesis, and unsteady gait, and how can the lesion be localized based on clinical features and examination?

Localizing Basal Ganglia Lesions Based on Clinical Features

Basal ganglia lesions cause hemisensory loss, hemiparesis, and unsteady gait primarily through involvement of adjacent white matter structures—particularly the internal capsule, corona radiata, and periventricular pathways—rather than through isolated basal ganglia damage alone. 1, 2

Why Basal Ganglia Lesions Produce These "Non-Typical" Features

The Critical Role of Adjacent White Matter

• Pure basal ganglia lesions (confined to putamen, caudate, or globus pallidus) rarely cause hemiparesis or hemisensory loss 1
• Hemiparesis occurs when lesions extend into the internal capsule or corona radiata, which carry the pyramidal tract fibers running adjacent to the basal ganglia 2, 3
• Hemisensory changes require involvement of thalamocortical pathways or the posterior limb of the internal capsule, where sensory fibers travel 3
• Unsteady gait results from disruption of motor control pathways when lesions affect periventricular or peristriatal white matter, particularly the superior longitudinal fasciculus and frontostriatal connections 1

Anatomical Vulnerability

• The lenticular nucleus (putamen and globus pallidus) sits immediately adjacent to the internal capsule, making combined involvement common in vascular or other pathologic processes 1, 2
• Lesions appearing to involve "basal ganglia" on imaging frequently extend into lateral periventricular white matter, even when this is not immediately obvious on initial review 1

Clinical Localization Algorithm

Step 1: Assess the Pattern of Motor Deficit

If hemiparesis is present:

• Look for upper motor neuron signs (hyperreflexia, spasticity, Babinski sign) indicating pyramidal tract involvement in the internal capsule or corona radiata 2, 3
• Pure basal ganglia lesions without capsular involvement typically produce movement disorders (dystonia, chorea, bradykinesia) rather than frank weakness 1, 4
• The presence of hemiparesis strongly suggests the lesion extends beyond the basal ganglia proper into adjacent white matter 1, 2

Step 2: Evaluate Sensory Involvement

If hemisensory loss is present:

• This indicates involvement of the posterior limb of the internal capsule or thalamus, as pure basal ganglia lesions do not produce sensory deficits 3
• Combined motor and sensory deficits suggest a lesion affecting both the anterior and posterior limbs of the internal capsule (lenticulocapsular region) 2, 3
• Thalamic involvement should be suspected if sensory loss is disproportionate to motor weakness 3

Step 3: Characterize Gait Abnormality

Distinguish between different gait patterns:

• Hemiplegic gait (circumduction) indicates pyramidal tract involvement in the internal capsule 2
• Ataxic or unsteady gait without clear hemiparesis may suggest cerebellar pathway involvement or bilateral lesions 5
• Parkinsonian gait (shuffling, reduced arm swing) suggests true basal ganglia pathology affecting the extrapyramidal system 4

Step 4: Assess for Additional Localizing Features

Key examination findings that refine localization:

• Altered mental status or aphasia: Suggests extension into periventricular white matter affecting association fibers, or bilateral lesions 3
• Dystonia or chorea: Indicates true basal ganglia involvement (putamen, caudate) 3, 4
• Seizures at presentation: May occur with cortical or subcortical involvement but does not localize specifically 3
• Bilateral presentation: Consider metabolic, toxic, or infectious etiologies affecting central grey matter symmetrically 6, 4

Critical Pitfalls to Avoid

Common Mislocalization Errors

• Do not assume isolated basal ganglia involvement based on imaging alone—carefully assess for subtle extension into the internal capsule or periventricular white matter 1, 2
• Hemiparesis with a "basal ganglia lesion" almost always means capsular involvement, even if the capsule appears relatively spared on initial imaging 1, 2
• MRI is superior to CT for detecting white matter extension and should be obtained when clinical features don't match apparent imaging localization 2, 3

Lateralization Considerations

• Left hemisphere lesions are more likely to produce apraxia in addition to motor and sensory deficits 1
• The side of the lesion does not predict the specific clinical presentation within the basal ganglia/thalamic region, but bilateral lesions more commonly present with altered consciousness 3

Practical Clinical Approach

When examining a patient with suspected basal ganglia pathology:

1. Test for pyramidal tract signs systematically: Tone, reflexes, Babinski, pronator drift 2, 3
2. Assess all sensory modalities: Light touch, pinprick, proprioception, vibration 3
3. Observe gait carefully: Note whether it is hemiplegic, parkinsonian, ataxic, or mixed 5, 4
4. Look for movement disorders: Dystonia, chorea, tremor, bradykinesia 4
5. Assess higher cortical functions: Language, praxis, attention 1, 3

The presence of hemiparesis and hemisensory loss with a "basal ganglia lesion" should prompt careful review of imaging for internal capsule involvement, as this combination is the hallmark of lenticulocapsular stroke rather than isolated basal ganglia pathology 2, 3.