Secondary Movement Disorders: Drug‑Related, Systemic, and Neurological Etiologies Across Clinical Spectra

1. Introduction

Movement disorders encompass a heterogeneous group of neurological conditions characterized by abnormal voluntary or involuntary movements, including hypokinetic syndromes such as parkinsonism and hyperkinetic manifestations such as tremor, dystonia, chorea, myoclonus, and tics [1]. Traditionally, movement disorders have been conceptualized as primary neurodegenerative or genetic diseases; however, it is now increasingly recognized that a substantial proportion arise secondary to medications, systemic illnesses, metabolic disturbances, vascular insults, infections, autoimmune processes, and toxic exposures [2]. These secondary movement disorders are of particular clinical importance because many are potentially reversible if the underlying cause is promptly identified and appropriately managed [3,4].

The pathophysiological basis of movement disorders lies in dysfunction of complex motor networks involving the basal ganglia, cerebellum, thalamus, brainstem, and their cortical connections [5]. Disruption of dopaminergic, GABAergic, glutamatergic, cholinergic, and monoaminergic neurotransmission—whether through structural lesions, metabolic imbalance, immune-mediated injury, or pharmacologic interference—can result in a wide spectrum of phenomenology [6]. Importantly, similar clinical phenotypes may emerge from distinct mechanisms, while a single etiologic factor may produce diverse motor manifestations, contributing to diagnostic uncertainty and frequent misclassification as primary movement disorders [7].

Medication-induced movement disorders represent one of the most common and underrecognized categories of secondary movement disorders [8]. Antiseizure medications, antipsychotics, antidepressants, mood stabilizers, headache therapies, and other centrally acting agents may induce or exacerbate tremor, parkinsonism, dystonia, dyskinesia, myoclonus, and ataxia [9]. These adverse effects may occur acutely or insidiously, may be dose-dependent or idiosyncratic, and often resemble idiopathic neurodegenerative syndromes [10]. Failure to recognize drug-related etiologies may result in unnecessary diagnostic testing, inappropriate escalation of therapy, and avoidable morbidity [11].

Beyond pharmacologic causes, systemic neurological and medical conditions are increasingly implicated in the development of movement disorders. Cerebrovascular disease, particularly lesions involving the basal ganglia, thalamus, cerebellum, or brainstem, can lead to acute or delayed-onset movement disorders, including hemichorea, dystonia, tremor, and vascular parkinsonism [12]. Infections—through direct neurotropism, immune-mediated mechanisms, or post-infectious inflammation—remain important and often treatable causes worldwide [13]. Autoimmune and demyelinating diseases, metabolic abnormalities, hepatic and renal dysfunction, and endocrine disorders further expand the differential diagnosis, emphasizing the need for a broad, systematic approach [14].

Neuroimaging has become indispensable in the evaluation of suspected secondary movement disorders, aiding in lesion localization, etiologic clarification, and differentiation from primary neurodegenerative processes [15]. Advances in structural, functional, and molecular imaging have reinforced the concept of movement disorders as network diseases rather than isolated basal ganglia dysfunction [16]. Similarly, growing interest in biomarkers and pathogenetic pathways—including neuroinflammation, mitochondrial dysfunction, proteostasis failure, and α-synuclein aggregation—has begun to bridge the gap between secondary and primary movement disorder mechanisms [17].

The aim of this review is to provide a comprehensive, clinically oriented overview of secondary movement disorders across a wide range of etiologies, with particular emphasis on drug-induced syndromes, systemic diseases, and structural brain disorders. By integrating clinical phenomenology, pathophysiology, neuroimaging, and management principles, this article seeks to improve recognition of secondary causes, facilitate timely diagnosis, and promote targeted, potentially reversible interventions in patients presenting with movement disorders.

2. Methodology

This work was conducted as a comprehensive narrative review of the literature addressing secondary movement disorders arising from medications, systemic diseases, metabolic abnormalities, vascular disorders, infections, autoimmune conditions, and structural brain lesions. A structured search of the PubMed/MEDLINE, Scopus, and Web of Science databases was performed, including articles published up to December 2025. Search terms combined keywords and Medical Subject Headings related to movement disorders and secondary etiologies, including “movement disorders,” “parkinsonism,” “tremor,” “dystonia,” “chorea,” “myoclonus,” “drug-induced movement disorders,” “secondary parkinsonism,” “stroke,” “infection,” “autoimmune encephalitis,” “metabolic disease,” and “neuroimaging.” Peer-reviewed original studies, systematic and narrative reviews, observational studies, clinical trials, case series, and selected case reports were included when they provided clinically or mechanistically relevant information. Articles were screened by title and abstract, followed by full-text review for relevance, with additional studies identified through reference list screening. Data extraction focused on clinical phenomenology, underlying etiologies, proposed pathophysiological mechanisms, neuroimaging findings, management strategies, and clinical outcomes. Given the heterogeneity of study designs and etiologic factors, findings were synthesized qualitatively and organized thematically by causative category to highlight shared mechanisms, diagnostic challenges, and therapeutic implications across secondary movement disorders.

3. Antiseizure Medications and Movement Disorders

Antiseizure medications (ASMs) are widely used in the management of epilepsy, neuropathic pain, and psychiatric disorders [18], yet several agents have been implicated in the development or exacerbation of movement disorders [19]. These adverse effects reflect the broad influence of ASMs on GABAergic, glutamatergic, and ion channel–mediated neurotransmission within basal ganglia–thalamo–cortical circuits [20]. Moreover, patients with drug-resistant epilepsy are more likely to develop abnormal movements [21], and somatosensory symptoms can lead to further challenging in diagnosis [22,23]. Also, some epileptic encephalopathies can have abnormal involuntary movements like Rasmussen encephalitis [24]. Another confounder can be reflexive epilepsy syndromes [25] and even functional seizures [26].

Valproate is the most consistently associated ASM, linked to reversible parkinsonism, postural tremor, and, less commonly, chorea and dystonia [27]. Valproate-induced parkinsonism typically occurs in older adults and may unmask subclinical nigrostriatal dysfunction, with symptoms improving after drug discontinuation [28,29]. Hyperammonemia and mitochondrial toxicity have also been proposed as contributory mechanisms [30,31].

Phenytoin has been associated with cerebellar ataxia [32], tremor [33], choreoathetosis [34], and orofacial dyskinesias [35], particularly in the setting of chronic exposure [36] or supratherapeutic levels [37]. Structural cerebellar changes may persist despite withdrawal [38], highlighting the potential for long-term neurotoxicity [39].

Pregabalin and gabapentin [40], α2δ subunit calcium channel ligands [41], are widely used for neuropathic pain [42], epilepsy, and anxiety disorders and are generally considered safe from a movement disorder standpoint [43,44]. However, both agents have been reported to induce or exacerbate abnormal movements, most commonly postural tremor and myoclonus, particularly at higher doses or in patients with renal impairment [45]. Less frequently, cases of ataxia [46], parkinsonism [47], and dyskinesia have been described, likely reflecting dose-dependent modulation of excitatory neurotransmission within cerebellothalamic and basal ganglia circuits [48]. Symptoms are typically reversible with dose reduction or drug discontinuation [49], underscoring the importance of medication review in patients presenting with new or worsening movement disorders.

Newer ASMs are not exempt from motor adverse effects. Levetiracetam has been reported to induce tremor, tics, and rare cases of dyskinesia, likely reflecting altered synaptic vesicle protein 2A–mediated neurotransmission [50]. Topiramate may cause tremor, myoclonus, or, infrequently, dystonia, possibly related to enhanced GABAergic tone and inhibition of glutamatergic pathways [51]. Lamotrigine has been infrequently associated with tremor, myoclonus, and, rarely, exacerbation of parkinsonism [52,53]. Belly dancer dyskinesia is a rare hyperkinetic movement disorder characterized by involuntary [54], rhythmic contractions of the abdominal wall muscles [55]. Baclofen, a GABA receptor agonist [56], is commonly used to treat spasticity and may improve dystonia or painful muscle spasms, but in toxic levels can cause catatonia [57].

Cenobamate, a newer antiseizure medication approved for focal-onset seizures, exerts its effects through dual modulation of voltage-gated sodium channels and positive allosteric modulation of GABA receptors [58]. While clinical trials have primarily reported central nervous system adverse effects such as somnolence, dizziness, and ataxia, postmarketing experience suggests that movement disorders are uncommon but may include tremor and gait instability, particularly during rapid titration or in combination with other sodium channel–blocking agents [59]. Given its potent pharmacodynamic profile and potential for drug–drug interactions, careful dose escalation and monitoring are warranted, especially in patients with preexisting movement disorders or cerebellar dysfunction [60].

In contrast, some ASMs may exert therapeutic effects on movement disorders. Clonazepam is commonly used in myoclonus and tics, while carbamazepine may benefit certain paroxysmal dyskinesias [61]. Recognition of ASM-induced movement disorders is critical, as symptoms may mimic primary neurodegenerative or functional syndromes [62]. Also, adverse effect to ASMs is the most common cause of withdrawal of ASMs [63].

4. Depression and Movement Disorders

Depression is highly prevalent across movement disorders and represents both a non-motor manifestation of neurodegenerative disease and a contributor to disability and reduced quality of life [64]. In Parkinson’s disease (PD), depression affects up to 40–50% of patients and may precede motor symptom onset, supporting its role as a prodromal feature [65,66]. Similar associations are observed in Huntington’s disease, dystonia, and atypical parkinsonian syndromes, where mood disturbances often correlate poorly with motor severity, suggesting partially independent neurobiological mechanisms [67].

The pathophysiology linking depression and movement disorders involves shared dysfunction within frontostriatal, limbic, and monoaminergic networks [68]. Degeneration or dysregulation of dopaminergic, serotonergic, and noradrenergic pathways contributes to both impaired motor control and altered emotional processing [69]. Neuroimaging studies further demonstrate abnormalities in the prefrontal cortex, amygdala, and basal ganglia, reinforcing the concept of movement disorders as network diseases extending beyond motor circuits [70].

Pharmacologic treatment introduces additional complexity. Dopaminergic therapies, including levodopa and dopamine agonists, may improve depressive symptoms through enhancement of mesolimbic dopamine signaling, though fluctuations can contribute to mood instability, apathy, or impulse control disorders [71]. Conversely, antidepressant medications may influence motor function [72]. Selective serotonin reuptake inhibitors (SSRIs) are generally well tolerated but have been associated with tremor, akathisia, or, rarely, parkinsonism. Tricyclic antidepressants and serotonin–norepinephrine reuptake inhibitors may worsen orthostatic hypotension [73] or cognitive impairment [74], particularly in PD [75]. Mirtazapine has been infrequently associated with extrapyramidal symptoms, including tremor, akathisia, dystonia [76], and rare cases of parkinsonism [77], likely reflecting complex serotonergic–noradrenergic modulation of dopaminergic pathways [78]. Buspirone is generally considered motor-neutral but has been infrequently associated with tremor [79] and dystonia [80], rarely, akathisia [81]. Bupropion, a norepinephrine–dopamine reuptake inhibitor used to treat depression [82], has been associated with tremor and, less commonly, myoclonus [83], tics, dystonia, or exacerbation of underlying movement disorders [84].

Trazodone acts as a serotonin 5-HT₂A antagonist and weak serotonin reuptake inhibitor, with secondary α-adrenergic antagonism [85]; altered serotonergic–dopaminergic balance may rarely provoke or worsen extrapyramidal symptoms, including tremor, dystonia, parkinsonism [86], or myoclonus [87].

In hyperkinetic disorders, such as dystonia or tardive syndromes, antidepressants may unmask or exacerbate abnormal movements through serotonergic–dopaminergic interactions [88]. Careful medication selection, individualized risk–benefit assessment, and collaboration between neurology and psychiatry are therefore essential.

5. Headache and Movement Disorders

Headache disorders and movement disorders frequently coexist, suggesting shared neurobiological mechanisms rather than a purely coincidental relationship [89]. Migraine is the most commonly reported headache phenotype among patients with movement disorders, particularly Parkinson’s disease (PD), dystonia, and essential tremor [90]. Epidemiologic studies indicate that migraine prevalence may be higher in PD patients prior to motor symptom onset, raising the possibility that headache represents an early, non-motor manifestation of neurodegenerative disease [91]. Noteworthy, headache can also be a post-ictal phenomena [92].

The pathophysiological overlap between headache and movement disorders centers on dysfunction within dopaminergic, serotonergic, and trigeminovascular pathways [93]. Dopamine plays a critical modulatory role in migraine biology [94], as evidenced by dopaminergic hypersensitivity during migraine attacks and the frequent occurrence of migraine-associated symptoms such as nausea, yawning [95], and hypotension [96]. This dopaminergic involvement may also explain the association between headache and hyperkinetic disorders, including dystonia and tic disorders, where altered basal ganglia–thalamo–cortical circuits are central [97].

Dystonia-related headache, particularly in cervical dystonia, illustrates a direct structural and functional link between abnormal motor activity and head pain [98]. Sustained muscle contractions, impaired sensorimotor integration, and altered proprioceptive feedback are thought to contribute to secondary headache syndromes in this population [99]. Importantly, treatment of the underlying movement disorder—such as botulinum toxin injections—often leads to significant improvement in headache burden, supporting a causal relationship.

In PD, headache phenotype may evolve over the disease course and be influenced by dopaminergic therapy [100]. Fluctuation-related headache and early-morning headache have been described, reflecting complex interactions between central pain processing and dopamine depletion.

Several medications commonly used in the acute and preventive treatment of headache disorders have been implicated in the development or exacerbation of movement disorders [101]. These adverse effects are typically mediated through dopaminergic antagonism, serotonergic modulation, or maladaptive neuroplastic changes within basal ganglia–thalamo–cortical circuits.

Dopamine receptor antagonists, frequently prescribed for acute migraine-associated nausea, are the most well-recognized offenders. Agents such as metoclopramide and prochlorperazine can induce acute dystonia, akathisia, parkinsonism, and, with repeated exposure, tardive dyskinesia [102]. These risks are heightened in younger patients and with parenteral administration. Although often reversible, tardive syndromes may persist despite drug discontinuation, underscoring the importance of judicious use.

Triptans, while generally considered safe from a motor standpoint, have been rarely associated with tremor, myoclonus, and serotonin toxicity—particularly when combined with selective serotonin reuptake inhibitors or monoamine oxidase inhibitors [103]. In such cases, neuromuscular hyperactivity rather than basal ganglia dysfunction is the predominant mechanism.

Valproate, widely used for migraine prophylaxis [104], has been linked to reversible parkinsonism, particularly in older adults or those with underlying nigrostriatal vulnerability [105]; also, dose-dependent pancytopenia was already observed [106]. Similarly, topiramate may precipitate tremor and, less commonly, myoclonus or dystonia, likely related to altered GABAergic and glutamatergic neurotransmission [107,108].

Emerging migraine therapies are not exempt from neurologic adverse effects. Rare cases of tremor and dyskinesia have been reported with calcitonin gene-related peptide (CGRP) receptor antagonists [109,110], although a direct causal relationship remains uncertain [111]. Flunarizine, used in migraine prophylaxis [112], has been associated with drug-induced parkinsonism and other extrapyramidal symptoms due to dopamine receptor blockade [113].

Opioids can be associated with both headache disorders and movement abnormalities through their effects on central pain and motor pathways [114]. Chronic opioid use is a well-recognized cause of medication-overuse headache, driven by altered nociceptive processing and opioid-induced hyperalgesia [115]. In parallel, opioids may precipitate movement disorders such as myoclonus, tremor, dystonia, or, rarely, parkinsonism, particularly at high doses or in the setting of renal dysfunction and metabolite accumulation [116]. These complications are thought to arise from opioid effects on μ-receptor–mediated neurotransmission, including dysregulation of dopaminergic and inhibitory pathways [117]. Recognition is important, as dose reduction or opioid discontinuation often leads to improvement in both headache and movement symptoms.

6. Antipsychotics, Mood Stabilizers, and Movement Disorders

Antipsychotics and mood stabilizers are widely prescribed for psychotic, bipolar, and affective disorders, yet their use is closely linked to the development or exacerbation of movement disorders [118]. These adverse effects arise primarily from disruption of dopaminergic signaling within basal ganglia–thalamo–cortical circuits, as well as broader modulation of serotonergic, GABAergic, and glutamatergic pathways [119].

Antipsychotics, particularly dopamine D₂ receptor antagonists, are the most common cause of drug-induced movement disorders. First-generation antipsychotics are strongly associated with acute dystonia, akathisia, drug-induced parkinsonism, and tardive syndromes [120]. Second-generation antipsychotics demonstrate a lower but variable risk, depending on dopaminergic affinity and serotonergic modulation [121]. Agents such as risperidone and paliperidone retain relatively high extrapyramidal risk, whereas quetiapine and clozapine are considered motor-sparing and are preferred in patients with Parkinson’s disease psychosis [122]. Tardive dyskinesia, characterized by involuntary choreiform or dystonic movements, remains a major long-term complication and may persist despite antipsychotic discontinuation [123].

Mood stabilizers also exert clinically relevant motor effects. Valproate is associated with postural tremor and reversible parkinsonism, particularly in older adults or with prolonged exposure [124]. Lithium commonly causes fine tremor and [125], at toxic levels, may provoke ataxia, myoclonus [126], or choreiform movements; chronic use has also been linked to irreversible cerebellar dysfunction in rare cases [127]. Carbamazepine and oxcarbazepine may induce ataxia, tremor, or nystagmus, reflecting sodium channel blockade and cerebellar involvement [128]. Lamotrigine is generally well tolerated but has been rarely associated with tremor or myoclonus [52].

Methylphenidate may induce or exacerbate tics, chorea, dystonia, or stereotypies through dopaminergic overstimulation, particularly in susceptible individuals [129].

7. Stroke and Movement Disorders

Stroke is an important but underrecognized cause of secondary movement disorders [130], resulting from disruption of motor control networks involving the basal ganglia, thalamus [131], cerebellum [132], and their cortical connections [133]. Cerebrovascular disorders are among the most common causes of neurological disorders [134]. Although relatively uncommon, post-stroke movement disorders provide key insights into human motor circuit function and often pose diagnostic and therapeutic challenges [135]. Atrial fibrillation increases the risk of cardioembolic stroke involving basal ganglia and thalamic circuits [136,137,138], thereby serving as an important vascular contributor to secondary movement disorders [139]. A study from Brazil revealed significant increase of cardiovascular risk factors related to the development of stroke and movement disorders [140]. But, not only ischemic also hemorrhagic strokes were already described with movement disorders [141,142].

The most frequently observed post-stroke movement disorders are hemichorea and hemiballismus [143], typically arising from lesions affecting the subthalamic nucleus, caudate nucleus, putamen, or thalamus [144]. These hyperkinetic syndromes usually present acutely or subacutely following ischemic stroke and are contralateral to the lesion [145]. Pathophysiologically, loss of inhibitory basal ganglia output leads to excessive thalamocortical excitation and involuntary movements [146]. While often self-limited, symptoms may persist and require pharmacologic intervention.

Sleep disorders, movement disorders, and stroke are tightly interconnected through shared neuroanatomical and vascular mechanisms [147]. Conditions such as REM sleep behavior disorder and restless legs syndrome frequently coexist with Parkinsonian syndromes and may precede clinical onset [148]. Disordered sleep also increases vascular risk via hypertension and inflammation [149], while stroke can disrupt motor and sleep-regulatory circuits, leading to secondary parkinsonism, insomnia, hypersomnia, and worsened functional recovery, with important implications for prognosis, prevention, and multidisciplinary neurological care strategies [150].

Other movement disorders associated with stroke include dystonia, tremor, myoclonus, and parkinsonism, which may present weeks to months after the vascular insult [151]. Delayed onset is thought to reflect maladaptive plasticity and reorganization within motor circuits rather than direct tissue injury alone [152]. Vascular parkinsonism, classically associated with bilateral subcortical ischemic changes [153], manifests with predominant lower-body bradykinesia, gait disturbance [154], and postural instability, often with poor levodopa responsiveness [155]. Other possible clinical manifestations involve the development of abnormal eye movements [156]. Limb-shaking TIA is a rare manifestation of cerebral hypoperfusion [157], characterized by transient, involuntary limb movements that can mimic focal seizures and abnormal movements [158]. Seizures may occur in IPAH secondary to cerebral hypoperfusion [159], hypoxemia, syncope-related anoxic injury, or complications of severe right-sided heart failure and elevated pulmonary pressures [160]. Basal ganglia involvement in artery of Heubner stroke leading to movement disorder [161].

Lesion location plays a major role in phenotypic expression [162]. Thalamic and brainstem strokes are commonly linked to tremor and Holmes tremor [163], whereas cerebellar infarcts may result in ataxia and action tremor [164]. Noteworthy, significant dysphagia can be observed [165]. Corpus callosum infarcts can lead to astasia [166]. Neuroimaging is essential for diagnosis, aiding lesion localization and exclusion of neurodegenerative or functional etiologies [167]. Stroke involving the precentral ‘hand knob’ region can result in focal hand weakness and secondary movement disorders due to disruption of primary motor cortex output [168]. On the other side, there is also the cortical (spastic) foot drop [169,170]. A rare clinical presentation in which venous outflow obstruction leads to elevated intracranial pressure or focal brainstem/temporal involvement, resulting in an ipsilateral peripheral facial nerve palsy [171]. More common clinical manifestations include seizures, occurring in more than half of the individuals affected by cerebral venous sinus thrombosis [172].

8. Infections and Movement Disorders

Infections represent an important and potentially reversible cause of secondary movement disorders, arising through direct neurotropism, immune-mediated mechanisms, vascular injury, or post-infectious neuroinflammation [173]. Both acute and delayed movement abnormalities have been described across bacterial, viral, and parasitic infections, often reflecting involvement of the basal ganglia, thalamus, cerebellum, or brainstem [174]. Noteworthy, aspiration pneumonia is a leading cause of morbidity and mortality in Parkinson’s disease [175].

Viral infections are among the most commonly implicated. Human immunodeficiency virus (HIV) can produce a wide spectrum of movement disorders [176], including chorea, dystonia, tremor, and parkinsonism, through direct central nervous system involvement or opportunistic infections [177]. Post-encephalitic parkinsonism, historically associated with encephalitis lethargica [178], has also been reported following infections with influenza [179,180,181], Japanese encephalitis virus [182], measles [183,184], dengue virus [185,186,187], West Nile virus [188], and more recently SARS-CoV-2 [189,190]. These syndromes may emerge weeks to months after infection, suggesting immune-mediated or neurodegenerative mechanisms [191].

Herpesvirus infections, particularly HSV and VZV, can involve basal ganglia and thalamic structures [192], resulting in acute or post-infectious movement disorders such as chorea, tremor, parkinsonism, and others abnormal eye movements [193].

Bacterial infections can similarly affect motor circuits [194]. Sydenham chorea, a post-streptococcal autoimmune disorder, is characterized by involuntary choreiform movements and remains a prototypical example of infection-induced movement disorder [195]. Tuberculosis and neurosyphilis may present with tremor, dystonia [196], or parkinsonism [197] due to meningoencephalitis [198], vasculitis [199], or intracranial granulomas involving deep gray matter structures [200,201]. In neurosyphilis, the Jarisch–Herxheimer reaction may transiently worsen or unmask movement disorders [202] due to acute inflammatory responses following antibiotic initiation [203]. Bartonella henselae infection can cause central nervous system involvement with rare secondary movement disorders, including chorea, tremor, GBS [204], or parkinsonism [205].

A chronic infection caused by Mycobacterium leprae that can produce peripheral neuropathy and immune-mediated complications [206], occasionally manifesting with tremor, neuropathic pain, or secondary movement abnormalities due to nerve damage [207]. An aggressive angioinvasive fungal infection that may cause cranial neuropathies [208], cavernous sinus thrombosis, cerebral infarction or hemorrhage, seizures [209], altered mental status, and focal neurological deficits due to vascular invasion and rapid tissue necrosis is zygomycosis [210].

Parasitic infections, particularly toxoplasmosis [211] in immunocompromised individuals, frequently involve the basal ganglia and are associated with hemichorea [212], dystonia, and tremor [213], especially in cases of rhombencephalitis [214]. Neurocysticercosis may also produce a range of hyperkinetic [215] and hypokinetic movement disorders depending on lesion location and inflammatory burden [216,217]. African trypanosomiasis may cause extrapyramidal movement disorders due to basal ganglia involvement [218]. Neuroschistosomiasis can produce movement disorders through inflammatory involvement of the brain and spinal cord [219].

Antibiotics have been implicated in a range of secondary movement disorders through mechanisms that include neurotoxicity, metabolic disturbance, and immune-mediated effects [220]. β-lactams (particularly high-dose penicillins and cephalosporins) and fluoroquinolones can precipitate tremor [221], myoclonus [222,223], chorea [224], idiopathic intracranial hypertension [225], and seizures, especially in older adults or patients with renal impairment, likely due to GABAergic inhibition and excitatory neurotransmission imbalance [226,227]. Metronidazole is classically associated with reversible cerebellar ataxia, dysarthria, and tremor, often accompanied by characteristic dentate nucleus hyperintensities on MRI [228]. Macrolides and sulfonamides have rarely been linked to extrapyramidal symptoms, including dystonia and parkinsonism, potentially via drug–drug interactions or metabolic toxicity [229]. Additionally, antibiotic exposure may unmask underlying movement disorders or contribute indirectly through antibiotic-associated encephalopathy leading to asterixis [230].

9. Demyelinating Disease and Movement Disorders

Demyelinating diseases, particularly multiple sclerosis (MS), are increasingly recognized as causes of secondary movement disorders [231]. Tremor is the most common manifestation in MS [232], frequently presenting as postural or intention tremor due to cerebellar and cerebellothalamic pathway involvement. Other reported movement disorders include dystonia, chorea, myoclonus, parkinsonism, and ataxia, reflecting demyelinating lesions affecting the basal ganglia, thalamus, brainstem, or spinal cord [233]; which can especially be seen in recurrent cases [234]. Movement symptoms may fluctuate with disease activity and often correlate with lesion location on neuroimaging. Recognition of demyelination-related movement disorders is important, as targeted immunomodulatory therapy and symptomatic treatment may lead to clinical improvement [235].

Autoimmune diseases are an increasingly recognized and potentially treatable cause of movement disorders [236]. Immune-mediated inflammation or antibody-driven disruption of basal ganglia, cerebellar, or cortical networks can produce a wide spectrum of phenotypes, including chorea, dystonia, tremor, myoclonus, ataxia, and parkinsonism [237,238]. Classic examples include Sydenham chorea [239], anti–NMDA receptor encephalitis, GAD-65 [240], MOG [241], anti–LGI1–associated faciobrachial dystonic seizures [242], and movement disorders linked to lupus [243], antiphospholipid syndrome, Sjögren syndrome [244], and paraneoplastic syndromes [245]. Symptoms may be acute or subacute, fluctuate over time, and coexist with cognitive, psychiatric, or systemic features [246]. Prompt recognition is critical, as immunotherapy—including corticosteroids, intravenous immunoglobulin, plasma exchange, or targeted biologics—can lead to significant neurological improvement and prevention of long-term disability.