Can Basal Ganglia Stroke Cause Extrapyramidal Symptoms?
Yes, basal ganglia strokes can absolutely cause extrapyramidal symptoms (EPS), including parkinsonism, dystonia, chorea, and tremor, because these structures are the anatomical substrate for normal movement control.
Anatomical Basis for Stroke-Induced EPS
The basal ganglia are critical components of the extrapyramidal motor system, and their disruption through stroke produces movement disorders through the same pathways affected by dopamine-blocking medications 1. Lesions within and adjacent to the basal ganglia pathways can produce both parkinsonian features and tremor syndromes 2.
Specific Stroke Locations That Cause EPS
- Putamen and caudate nucleus: These are the most common sites where vascular lesions produce hemichorea and other movement disorders 3
- Lenticular nucleus, globus pallidus, and internal capsule: Demyelinating or ischemic lesions in these regions produce extrapyramidal symptoms 1
- Thalamus: Lesions here disrupt the basal ganglia-thalamo-cortical circuit, which is the pathophysiological basis for movement disorders 1
Clinical Presentations of Stroke-Related EPS
Contralateral Hemiparkinsonism
Stroke patients can develop tremor, rigidity, and bradykinesia on the side opposite the lesion, appearing months to years after the initial event 2. One documented case showed a patient developing these symptoms 2 years post-stroke, with tremors ranging from 4Hz (resting) to 7Hz (postural/kinetic/intentional) 2.
Hemichorea
Acute hemichorea can result from transient ischemic attacks in the basal ganglia, even when diffusion-weighted imaging (DWI) is negative in these structures 3. The basal ganglia are particularly sensitive to ischemia, hypoxia, and reperfusion injury, which explains why even brief periods of hypoperfusion (such as a 5.6-second cardiac arrest) can trigger these symptoms 3.
Key Distinguishing Features from Medication-Induced EPS
Timing and Laterality
- Stroke-related EPS are typically unilateral (contralateral to the lesion), whereas medication-induced EPS are usually bilateral 2, 3
- Stroke-related symptoms may have delayed onset (weeks to years after the event) 2
- Medication-induced EPS typically occur within days to weeks of drug initiation or dose increase 4
Imaging Findings
MRI or CT will show structural abnormalities in the basal ganglia region with stroke-related EPS 1. Specifically:
- Increased density on CT or hyperintensity on T2 MRI in the basal ganglia 1
- Restricted diffusion on DWI at the lesion site (though negative DWI doesn't exclude transient ischemic attacks) 3
Clinical Pitfalls to Avoid
Do not assume all EPS are medication-related, especially in patients with vascular risk factors or known cerebrovascular disease 1. Secondary causes of movement disorders include:
- Cerebrovascular diseases 1
- Traumatic brain injury 1
- Demyelinating diseases (particularly multiple sclerosis involving thalamus, lenticular nucleus, globus pallidus, or internal capsule) 1
- Metabolic abnormalities and basal ganglia calcification 1
In patients presenting with acute hemichorea and negative basal ganglia DWI, consider transient ischemic attack from cardiac causes 3. Obtain dynamic electrocardiogram monitoring to identify brief cardiac arrest or arrhythmias 3.
Diagnostic Approach
When evaluating a patient with new-onset EPS:
Obtain detailed medication history focusing on antipsychotics, antiemetics (metoclopramide, prochlorperazine), and other dopamine-blocking agents 4, 5
Perform brain imaging (MRI preferred over CT) to evaluate for structural lesions in the basal ganglia, thalamus, and adjacent white matter tracts 1
Assess for vascular risk factors including atrial fibrillation, cardiac arrhythmias, and atherosclerotic disease 3
Consider the temporal relationship: Medication-induced EPS typically occur within days of drug exposure, while stroke-related symptoms may be delayed 4, 2