Correct Answer: A. Subthalamic nuclei
The clinical presentation of involuntary, violent, flinging movements of the limbs on one side following a stroke is pathognomonic for hemiballismus, a hyperkinetic movement disorder. This occurs due to a lesion in the subthalamic nucleus (STN), which is part of the indirect motor pathway of the basal ganglia. The STN normally exerts inhibitory control over the globus pallidus interna (GPi) via GABAergic neurons. When the STN is damaged (typically by lacunar infarction in the territory of the penetrating branches of the middle cerebral artery), loss of this inhibitory drive leads to unopposed activity of the GPi, resulting in excessive, uncontrolled motor output. The flinging, ballistic nature of the movements—often described as "throwing" movements—is characteristic and unilateral because the STN lesion affects contralateral limb control. This is a classic stroke syndrome in Indian neurology practice, particularly in elderly hypertensive patients. The acute onset (2 days post-stroke) and the specific motor phenomenology (violent, involuntary flinging) are the key discriminators pointing to STN pathology rather than other basal ganglia structures.
Why the other options are wrong
B. Globus pallidus — Globus pallidus lesions cause hypokinetic disorders (bradykinesia, rigidity, akinesia), not hyperkinetic movements. The globus pallidus is the output nucleus of the basal ganglia; its damage reduces motor output rather than causing violent flinging movements. This is an NBE trap pairing basal ganglia with movement disorders without distinguishing between hypo- and hyperkinetic syndromes. C. Caudate nucleus — Caudate nucleus lesions are rare in acute stroke and do not produce hemiballismus. Caudate pathology is more associated with behavioral changes, cognitive dysfunction, and rarely chorea in specific conditions (e.g., Huntington's disease). The caudate is part of the indirect pathway but is not the critical node for hemiballismus pathogenesis. D. Putamen — Putamen lesions cause contralateral hemiparesis and sensory loss (lacunar stroke syndrome), not hemiballismus. While the putamen is part of the basal ganglia, its damage results in motor weakness and loss of motor control, not involuntary flinging movements. This option exploits confusion between different basal ganglia stroke syndromes.
High-Yield Facts
- Hemiballismus = involuntary, violent, flinging movements of contralateral limbs; pathognomonic for subthalamic nucleus lesion.
- STN lesion mechanism: Loss of GABAergic inhibition on globus pallidus interna → unopposed motor output → hyperkinetic movement.
- Lacunar infarction in the territory of penetrating branches of MCA (lenticulostriate arteries) is the most common cause of STN stroke in India.
- Hypokinetic vs. hyperkinetic: Globus pallidus/putamen lesions → hypokinetic (bradykinesia, rigidity); STN lesion → hyperkinetic (ballismus, chorea).
- Acute onset (hours to days) of unilateral flinging movements in a stroke patient = STN syndrome until proven otherwise.
Mnemonics
STN = Violent Flinging (Ballismus) Subthalamic Throws Nuts — Remember: STN lesion → loss of inhibition → violent, uncontrolled throwing-like movements (ballismus). Use when you see 'flinging' or 'ballistic' in the stem. Basal Ganglia Movement Disorders HYPOkinetic (Globus Pallidus/Putamen) = Bradykinesia, Rigidity, Akinesia. HYPERkinetic (STN) = Ballismus, Chorea, Tremor. The prefix tells you the direction of motor dysfunction.
NBE Trap
NBE pairs "basal ganglia lesion" with "movement disorder" to lure students into choosing any basal ganglia structure without distinguishing between hypokinetic syndromes (globus pallidus, putamen) and hyperkinetic syndromes (STN). The specific descriptor "violent, flinging movements" is the key discriminator that must be recognized as hemiballismus.
Clinical Pearl
In Indian stroke units, hemiballismus is an underrecognized but classic presentation of lacunar infarction in hypertensive elderly patients. The violent, flinging movements often alarm family members and may be mistaken for seizures; recognizing the STN syndrome allows for appropriate imaging (MRI with DWI) and stroke management rather than unnecessary antiepileptic therapy.
_Reference: Guyton & Hall Textbook of Medical Physiology (Basal Ganglia and Movement Control); Harrison's Principles of Internal Medicine Ch. 442 (Movement Disorders)_