Case Report: Ischaemic Stroke Presented with Hemichorea-Hemiballism

ABSTRACT

A stroke can cause a variety of movement abnormalities, each with a unique natural history, prognosis, and course of therapy from its idiopathic counterpart (Tater & Sanjay, 2021).One of the most striking diseases in neurology is hemichorea-hemiballismus.
In the emergency room, it is not usually observed (Alonso et al., 2015;Carbayo et al., 2020).
Because it is clinically uncommon, poststroke hyperkinetic movement disorder can sometimes develop gradually over time rather than immediately after an acute stroke, which makes diagnosis more challenging and prone to mistake (Chen & Xu, 2020).This is an uncommon case of an ischemic stroke patient who had an abrupt involuntary movement.

Case
A 56-year-old man presented to the emergency room with sudden involuntary movement in the right upper and lower limbs for 5 hours before he came to hospital.
This movement disappeared only during sleep, and it was impairing his basic activities of daily living.There was no headache, language difficulty, visual disturbance, paraesthesia, or sign of infection.He had no family history of such disorders.There was no history of diabetes mellitus, hypertension, epilepsy, trauma and no prior exposure to neuroleptics.
Patient is an active smoker.
On initial exam, patient is obese the blood pressure was 119/81 mmHg, the temperature was 36,5°C, the pulse was 98 beats per minute, the respiratory rate was 22 breaths per minute, and the oxygen saturation was 99% while breathing room air.He was alert and cooperative.The patient had no carotid bruits and no significant jugular venous distention.
Cardiovascular exam revealed a regular rate and rhythm with no murmurs.A complete neurological evaluation revealed an uncontrolled, nonrhythmic, nonpatterned, aimless, and frequently jerky movement of the right upper and lower limbs with a ballistic component that varies in amplitude Ariobimo, B.N., Puspamaniar, V.A., Nujum, N., Puspitorini, L. IIMJ Volume 5 No. 1, December 2023 (24-35) and frequency.(Carrion & Carrion, 2013).Hyperkinetic movement disorders are a rare presentation of stroke.The pathophysiology of these abnormal movements remains uncertain (Carbayo et Ariobimo, B.N., Puspamaniar, V.A., Nujum, N., Puspitorini, L. al., 2020).The prevalence of hyperkinetic diseases tends to exceed that of hypokinetic syndromes (Caproni & Colosimo, 2017).A range of hyperkinetic movement disorders called hemichorea-hemiballismus include choreic and/or ballistic motions of variable intensity (Alonso et al., 2015;Wei & Zhang, 2021).Hemichorea describes motions that impact both the proximal and distal limbs and are similar in nature but less in amplitude.Early in the presentation, there is a pronounced hemiballism, and as the condition resolves, a lesser amplitude hemichorea emerges (Alonso et al., 2015).
Movement disorders share common etiologies, prognoses, and treatments, hence there is probably little pathophysiologic variation between them.In actuality, they frequently coexist in the same patient (Alonso et al., 2015;Tater & Sanjay, 2021).
A their distribution zone lacks a collateral blood supply and is functionally characterized as "terminal" (Guida et al., 2013).The regular basal ganglia circuitry transmission pattern would be interrupted by increased dopamine release brought on by ischemia.Acute circuitry dysfunction would cause excessive motor facilitation and a lack of thalamic movement control (Guida et al., 2013;Laganiere et al., 2016).
Less frequently, the cortex in the superficial area of the middle cerebral artery may also be affected by the stroke lesion (parietal, insular and temporal cortex) (Laganiere et al., 2016).The motor circuitry transmits information from the brain to the thalamus and back through its primary subcortical component, the basal ganglia.Two circuits make up the Hemichorea typically appears within a few hours of the start of the stroke (as in our patient's case), although delays of up to five days have also been documented.The idea of pathogenesis mediated by restorative neuroplasticity has been brought forward as a result of this delay (Guida et al., 2013;Ueta et al., 2021).Hemichorea appears to happen a few days after stroke, whereas hemiballism is typically seen to happen promptly with the onset of stroke.However, there have been cases where a delay of up to five months was reported (Tater & Sanjay, 2021).
Some treatment options are shared by vascular movement disorders and idiopathic variants of these illnesses (Caproni & Colosimo, 2017;Carbayo et al., 2020).All patients with acute ischemic stroke who meet the requirements for this treatment within 4.5 hours of stroke start are advised to receive thrombolytic therapy (Bembenek et al., 2015).In rats with ischemic stroke, penetration and drastically reduce infarct volume (Paliwal et al., 2018).Animal experiments showed that piracetam could help humans who are suffering from an acute stroke (Tortiglione et al., 2002).A meta-analysis of research using rat models of cerebral ischemia and stroke provided more evidence for piracetam's potential value (Wheble et al., 2008).
Hemichorea/hemiballism following a stroke frequently goes away on its own, thus a wait-and-see approach is recommended.
The majority of instances resolve on their own, but when movement is and harmful enough to cause injury, pharmaceutical therapy is required (Tater & Sanjay, 2021).A symptomatic approach may be helpful for some individuals with hemichorea/ hemiballism whose involuntary movements have a major impact on their quality of life, increase their risk of falling, and reduce their independence in daily tasks (Caproni & Colosimo, 2017;Tater & Sanjay, 2021).Immediately after a stroke, abnormal involuntary motions start to appear and may eventually go away on their own.This usually happens within a few hours or days (Siniscalchi et al., 2012).In six months, up to 90% of these movement abnormalities with abrupt onset may go away (Caproni & Colosimo, 2017).Minimal functional impairment may linger in post-ischemic hemichorea-hemiballismus.The prognosis for syndromes connected to cortical ischemia localizations is believed to be (Guida et al., 2013).

Conclusion
Even Gamma-aminobutyric acid (GABA) transmission disruption from the striatum to the external globus pallidus (GPE) may be the pathogenesis of hemichorea caused by contralateral lesions of the striatal neurons of the indirect striato-thalamocortical pathways, which can then increase GPE neuronal activity and inhibit the subthalamic nucleus (Cincotta & Walker, 2022; Defebvre & Krystkowiak, 2016).Such inhibition would cause the internal globus pallidus (GPI) neurons to lose control, which could ultimately result in the motor thalamus's ability to inhibit movement.The same dysfunction, with a lack of motor thalamic inhibition, may be brought on by lesions of the subthalamic nucleus.An excitatory neural circuit from a portion of the frontal or parietal cortex (the somatosensory cortex projecting into the caudate nucleus and putamen) must be disrupted in order to create AIMs in cases of hemichorea-hemiballism brought on by a cortical injury.Patients with cortical strokes have a functional prognosis that is significantly better than patients with subthalamic lesions; in the former group of patients, AIMs are likely brought on by transient hypoperfusion or a functional "disconnection" rather than by the breakdown of basal ganglia circuitry (Defebvre & Krystkowiak, 2016).There have been numerous theories put forth: Although the indirect pathway only accounts for one-third of the overall population of motor striatal neurons, specific disruption of the indirect pathway is required to cause AIM.The striatal infarct is very large and also involves the pyramidal tract, which causes a motor deficit.Alternatively, the transient nature of these AIMs may be caused by regulation of the accessory striato-nigro-striatal, corticocerebral cortex and not the basal ganglia, leading to aberrant movements like chorea or ballism (Carbayo et al., 2020).
cerebellar circuitry: the GMT (Guillain-Mollaret triangle), also known as the dentate-rubro-olivary pathway, and the cortico-cerebello-cortical, also known as the dentate-rubro-thalamic pathway.Strokes that impact the subcortical regions are known to be more likely than cortical strokes to cause aberrant motions(Tater &   Sanjay, 2021).Movement abnormalities are three times more common after subcortical strokes than after cortical strokes, with the basal ganglia (44%) and thalamus (33%) being most frequently affected.Movement difficulties following a stroke are uncommonly associated with cerebellar abnormalities that affect it alone (Hao et al., 2015; Tater & Sanjay, 2021).Ischemic stroke diagnosis relied on skilled clinical assessment without explicit neuroimaging (Chen & Xu, 2020).While hemiballismus is characterized by violent irregular flinging movements of the limbs brought on by contractions of the proximal muscles, hemichorea consists of continuous random, anarchic, and jerking movements involving both the distal and proximal muscles (though it is occasionally localized more distally) (Defebvre & Krystkowiak, 2016).Chorea is a symptom that is distinguished by sudden, uncontrollable movements brought on by an ongoing stream of erratically contracted muscles (Ueta et al., 2021).Ballism is a type of highamplitude flinging chorea, which is characterized by short, arrhythmic movements that seem to flow from one muscle to the next (Caproni & Colosimo, 2017).While chorea frequently affects the entire body and is widespread, it can also be noticeably asymmetrical or even unilateral in a considerable number of circumstances.While stroke is the most prevalent cause of unilateral involvement and is traditionally associated with a contralateral anatomical lesion, such as one of the putamen or the subthalamic nucleus, systemic disease can also result in unilateral or noticeably asymmetric presentations (Chen & Xu, 2020).The involvement of several extra-striatal cortical areas and subcortical regions in movement disorders has been demonstrated by a number of functional neuroimaging studies based on positron emission tomography and resting state functional magnetic resonance imaging, emphasizing Ariobimo, B.N., Puspamaniar, V.A., Nujum, N., Puspitorini, L. a role of network dysfunction and abnormal functional connectivity in these conditions (Caproni & Colosimo, 2017).The mean age of onset was lower (35 years) in cases of other major causes of hemichoreahemiballism (abscesses, metastatic lesions, AIDS, levodopa medication, Sydenham's chorea, neonatal anoxic brain injury, multiple sclerosis, and central nervous system lupus) than in the stroke subgroup (61 years) (Defebvre & Krystkowiak, 2016).This type of AIM should be treated as a neurological emergency and treated as soon as feasible in a stroke center because any delay in diagnosis may have detrimental effects on the patient's clinical and therapeutic management.Patients with ischemic or hemorrhagic stroke, as well as those with cerebrovascular abnormalities and dural arteriovenous fistulas, can exhibit AIMs (Defebvre & Krystkowiak, 2016).Any anatomo clinical correlations will be easier to make if the vascular lesion is confined and has clearly defined limits.cases, AIM started immediately the day of the stroke, but they can sometimes deteriorate progressively over many weeks or come back after a latent period of several months.They are noticed on the side opposite the stroke; only when bilateral basal ganglia lesions are seen on brain MRI do bilateral symptoms become apparent.Usually, both the upper and lower limbs are affected, but occasionally, only one body portion is (neck, arm or leg)