What are the clinical features of a basal ganglia stroke?

Clinical Features of Basal Ganglia Stroke

Basal ganglia strokes present with a characteristic triad of motor, cognitive, and neuropsychological deficits that are often more persistent and treatment-resistant than cortical strokes, with distinctive patterns including flaccid paralysis, widespread cognitive impairment affecting multiple domains, and altered functional brain connectivity.

Motor Manifestations

Basal ganglia strokes produce distinctive motor features that differ from cortical presentations:

• Flaccid paralysis and hypotonia are characteristic findings, contrasting with the spastic hemiparesis typically seen in cortical strokes 1
• Hemiparesis affecting the contralateral side is common, often accompanied by hemisensory loss 1
• Persistently impaired balance and ambulation occur more frequently than with cortical lesions, with patients showing diminished response to rehabilitation efforts compared to those with cortical or combined lesions 1
• Motor deficits may be isolated in some cases, presenting as pure motor weakness without sensory signs 1

A critical pitfall: Patients with stroke confined to the basal ganglia and internal capsule demonstrate significantly worse functional outcomes despite similar rehabilitation intensity compared to cortical stroke patients, likely due to disrupted corticothalamic-basal ganglia interactions 1.

Cognitive and Neuropsychological Impairment

Basal ganglia strokes cause widespread cognitive dysfunction across multiple domains:

• Visuospatial dysfunction and memory impairment are the most prominent deficits and best predictors of basal ganglia stroke, with discriminant analysis showing 95.5% classification accuracy 2
• 96.7% of patients display defective performance on at least three neuropsychological tests, indicating pervasive cognitive involvement 2
• Executive function, attention, and language deficits occur across different cognitive domains, reflecting the basal ganglia's role in multiple neuronal pathways connecting cortical and subcortical areas 2
• Lower Mini-Mental State Examination (MMSE) and Montreal Cognitive Assessment (MoCA) scores are consistently observed compared to healthy controls 3, 4

Language Dysfunction (Post-Stroke Basal Ganglia Aphasia)

Basal ganglia aphasia presents with atypical features distinct from cortical aphasia:

• Significantly impaired word fluency and naming are the primary language deficits, while repetition abilities remain relatively preserved 3, 5
• Reduced fluency, comprehension (auditory word recognition and sequential commands), and reading comprehension occur within the first week after stroke onset 3
• Aphasia is often transient and atypical, with prevalence as high as 22% in basal ganglia strokes 5
• Damaged white matter tracts including the left inferior fronto-occipital fasciculus (IFOF), corpus callosum forceps minor, arcuate fasciculus, and uncinate fasciculus correlate with specific language impairments 3

The mechanism involves disruption of limbic pathways, dorsally located tracts in the left hemisphere, and left basal ganglia pathways rather than direct damage to classical language areas 3.

Neuropsychiatric Features

• Increased anxiety and depression scores (Hamilton Anxiety Scale-17 and Hamilton Depression Scale-17) are significantly elevated within 7 days of stroke onset 3
• Emotional dysfunction accompanies the cognitive and language deficits 3

Visual Field Defects

• Homonymous hemianopia commonly occurs alongside motor and sensory deficits 1

Functional Connectivity Alterations

Advanced imaging reveals specific network disruptions:

• Increased degree centrality in the left inferior temporal gyrus (ITG) and hippocampus head indicates compensatory reorganization 4
• Reduced effective connectivity from the left ITG to precentral and postcentral gyri, with paradoxically increased reverse connectivity 4
• Impairment of multifunctional networks throughout the whole brain, not just localized to the lesion site 4

Clinical Predictors of Outcome

• Side of stroke and admission Glasgow Coma Scale (GCS) score correlate significantly with cognitive outcomes 2
• Lesions confined to basal ganglia/internal capsule predict worse rehabilitation outcomes compared to cortical or combined lesions, despite similar initial impairment severity 1

Key Clinical Pitfall

The most important caveat is that isolated basal ganglia strokes may appear less severe on initial imaging but result in more persistent functional disability due to disruption of critical subcortical-cortical circuits. These patients require more intensive and prolonged rehabilitation despite appearing to have "smaller" strokes than cortical lesions 1.