Movement Disorders in Psychiatric Practice

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CATEGORY 1 CME

Premiere Date: September 20, 2025

Expiration Date: March 20, 2027

This activity offers CE credits for:

1. Physicians (CME)

2. Other

All other clinicians either will receive a CME Attendance Certificate or may choose any of the types of CE credit being offered.

ACTIVITY GOAL

To understand movement disorders and the best way to address them in psychiatric practice.

LEARNING OBJECTIVES

1. Discuss neurological conditions marked by movement disorders, such as Parkinson and Huntington diseases, and their significant psychiatric manifestations.

2. Describe treatment of movement disorders, which requires a comprehensive approach to address both motor and behavioral symptoms.

TARGET AUDIENCE

This accredited continuing education (CE) activity is intended for psychiatrists, psychologists, primary care physicians, physician assistants, nurse practitioners, and other health care professionals who seek to improve their care for patients with mental health disorders.

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This activity has been planned and implemented in accordance with the accreditation requirements and policies of the Accreditation Council for Continuing Medical Education (ACCME) through the joint providership of Physicians’ Education Resource,® LLC, and Psychiatric Times®. Physicians’ Education Resource, LLC, is accredited by the ACCME to provide continuing medical education for physicians.

Physicians’ Education Resource, LLC, designates this enduring material for a maximum of 1.5 AMA PRA Category 1 Credits.™ Physicians should claim only the credit commensurate with the extent of their participation in the activity.

This activity is funded entirely by Physicians’ Education Resource, LLC. No commercial support was received.

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This accredited CE activity may or may not discuss investigational, unapproved, or off-label use of drugs. Participants are advised to consult prescribing information for any products discussed. The information provided in this accredited CE activity is for continuing medical education purposes only and is not meant to substitute for the independent clinical judgment of a physician relative to diagnostic or treatment options for a specific patient’s medical condition. The opinions expressed in the content are solely those of the individual faculty members and do not reflect those of Physicians’ Education Resource, LLC.

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Movement disorders comprise a heterogeneous group of neurological conditions affecting the basal ganglia function, thus causing abnormal involuntary movements. Historically, movement disorders have been referred to as extrapyramidal symptoms. As research advances proved that the basal ganglia have connections with corticomedullar tracts (ie, the pyramidal tract), the term extrapyramidal has been abandoned.¹

TABLE 1. Clinical Features of Hyperkinetic and Bradykinetic Syndromes

Movement disorders are categorized into hyperkinetic and bradykinetic based on their clinical presentation,² but distinct clinical entities often have features of both. Table 1 presents an overview of the clinical features of hyperkinetic and bradykinetic syndromes. Table 2 presents more information on hyperkinetic disorders secondary to antipsychotics. Although neurologists are usually the primary clinicians dealing with movement disorders, they are very common in psychiatric practice. For instance, movement disorders are often an intrinsic feature of severe psychiatric disorders or may arise in the context of antipsychotic therapy. In this CME article, we will briefly review the different scenarios in which psychiatrists can encounter movement disorders.

TABLE 2. Hyperkinetic Disorders Secondary to Antipsychotics

Movement Disorders Secondary to Antipsychotics

Movement disorders can develop within hours to days of starting an antipsychotic with potent antidopaminergic D2 action. They comprise different types of hyperkinesia (dystonia, akathisia, tardive dyskinesia) and a bradykinetic presentation (parkinsonism).

Regarding hyperkinetic syndromes, dystonia and akathisia are the main acute presentations, affecting approximately 10% to 20% and 10% to 40%, respectively, of patients.³ Chronic hyperkinetic symptoms can develop after prolonged exposure to antipsychotics, are usually chorea-like, and are called tardive dyskinesias. The prevalence of tardive dyskinesias in long-term antipsychotic users is estimated to be approximately 20% to 30%, although it can be higher in those treated with first-generation antipsychotics (FGAs) or with high doses for extended periods of time.⁴ VMAT2 inhibitors (eg, deutetrabenazine, valbenazine) have been approved by the US Food and Drug Administration for the management of tardive dyskinesias. Parkinsonism due to antipsychotic use is a common syndrome observed in patients treated with dopamine antagonists, particularly high-potency FGAs like haloperidol. It manifests as motor symptoms similar to those seen in patients with Parkinson disease, including bradykinesia (slowness of movements with difficulty initiating voluntary movements), rigidity, resting tremor, and postural instability. Signs like poker (or mask) face, cogwheel rigidity, and hypophonia are prototypical parkinsonian signs.

The prevalence of parkinsonism in patients using antipsychotics varies depending on several factors, such as the class of antipsychotic used (first generation vs second generation), dosage, duration of treatment, and individual patient characteristics (older age, being female, and comorbid neurodegenerative conditions are related to higher risk).⁵ Parkinsonism occurs in approximately 30% to 40% of patients treated with FGAs, with higher-potency agents such as haloperidol, fluphenazine, and perphenazine having a higher incidence. Second-generation antipsychotics (SGAs) generally have a lower incidence of parkinsonism compared with FGAs, with rates ranging from 10% to 20%. However, certain SGAs such as risperidone, olanzapine, and aripiprazole may still cause parkinsonism, particularly at higher doses or with prolonged use.⁶

The pathophysiology of antipsychotic-induced parkinsonism mainly involves D2 antagonism that has been implicated in both the development of this motor syndrome (effect on nigrostriatal pathway) and the treatment of positive symptoms (effect on mesolimbic and mesocortical pathways). Other mechanisms are related to cholinergic imbalance and neuroplastic modifications. Accordingly, its treatment involves minimizing D2 antagonism through reducing the dose of current antipsychotic, switching to SGA with lower D2 antagonism (eg, quetiapine, clozapine) and/or adding an anticholinergic (eg, benztropine, trihexyphenidyl) or amantadine.⁷

Movement Disorders Secondary to Mood Stabilizers

Lithium-induced movement disorders. Lithium can induce various movement disorders, with tremors being the most common (4%-65%). In general, tremors associated with lithium use are often fine, rhythmic shaking, predominantly affecting the hands and sometimes the head. It can be difficult to distinguish from mild essential tremor. Symptoms are worse with stress, anxiety, or caffeine intake and may become more pronounced at higher lithium doses.⁸ Tremors can also manifest in the form of postural and kinetic tremors, the latter typically occurring in the early phase of voluntary movements, such as writing or holding objects. Lithium-induced parkinsonism, dystonia, and dyskinesia are rare and usually occur with chronic use.

Their pathophysiology is associated with lithium influence on neurotransmitter systems, especially serotonin and dopamine, leading to increased neuronal excitability, influencing motor control pathways.⁹ Lithium also influences electrolyte levels, including calcium and sodium, which may contribute to tremor development.

Lithium-induced tremors are generally reversible upon dose reduction or discontinuation of the medication. However, in some cases, tremors may persist even after stopping lithium.¹⁰ Medications such as propranolol may help in their management.⁹ Occupational therapy can also help patients adapt to tremors in daily activities.

Valproate-induced movement disorders. As with lithium, tremor is the most frequent movement disorder associated with valproate. The prevalence of tremors is reported to be between 6% and 45%, with 25% of patients developing tremors within 3 to 12 months of treatment. Tremors usually resemble essential tremors, manifesting as kinetic and postural. Interestingly, the tremorgenic effect of valproate seems to depend on the formulation. Tremors are less prominent with controlled-release formulations compared with others, mostly due to less peak-trough variation. Its pathophysiology is linked to the disruption of neurotransmitter balance, particularly through affecting γ-aminobutyric acid (GABA), sodium channel suppression, and possibly serotonin pathways, leading to increased motor activity.¹¹ Management entails reduction of valproate dose, addition of β-blockers (like propranolol), or switching to other antiepileptic or mood-stabilizing medications. Prognosis is generally good; symptoms may improve with dose adjustment or discontinuation of the medication.

Valproate can also induce akathisia, dystonia, and parkinsonism. Valproate-induced parkinsonism is uncommon but a well-recognized adverse effect, typically presenting with bradykinesia, rigidity, and tremor, which may resolve after dose reduction or discontinuation.¹²

Movement Disorders Secondary to Drugs of Abuse

Drugs of abuse can induce a variety of movement disorders, either through direct neurotoxic effects on the brain or by altering neurotransmitter systems that regulate motor function. The severity and nature of these movement disorders depend on the specific substance involved, the dose, and the duration of use. The most frequent movement disorders associated with drug abuse are hyperkinesias, such as tics and chorea. These movement abnormalities can either appear acutely during intoxication or persist as long-term effects after prolonged drug use or withdrawal.¹³

Amphetamines and cocaine can increase the release and inhibit the reuptake of dopamine and norepinephrine in the brain, particularly in the basal ganglia. Therefore, movement disorders can be a consequence of their use/abuse. They are most frequently associated with tics, chorea, and stereotypies (repetitive movements such as scratching or pacing). Long-term use can lead to parkinsonism, especially in cases of high-dose or chronic abuse. Their prevalence is not well documented but is thought to be relatively high among individuals who abuse these substances over long periods. Treatment of movement disorders induced by amphetamines and cocaine typically involves the discontinuation of the offending drug and symptom management—for example, antipsychotics for troublesome or severe tics. For long-term management, especially in cases of induced parkinsonism, dopaminergic agents or anticholinergic drugs may be prescribed, though these should be used with caution due to the risk of dependence.

Cannabis abuse is associated with a range of movement disorders, including tremors, dystonia, atypical gait, and motor incoordination. Cannabis primarily acts on the endocannabinoidsystem, which plays a significant role in motor control by modulating dopamine and GABA signaling in the basal ganglia and other regions of the brain. The prevalence of movement disorders in cannabis users is not as high as with stimulants but can be common in long-term or heavy users.¹⁴ Treatment typically focuses on cessation of cannabis use and symptom management.

Bath salts, a synthetic cathinone, are amphetamine-like substances that increase the release of dopamine, norepinephrine, and serotonin in the brain. They are known to cause severe agitation, paranoia, and aggressive behavior, along with a variety of movement disorders, including tremors, myoclonus, dystonia, and tics.¹⁵ In some cases, bath salts abuse can lead to severe, persistent symptoms that resemble those seen in neuroleptic-induced parkinsonism or neuroleptic malignant syndrome. Prevalence data on bath salts–induced movement disorders are scarce, but related cases are seen mostly in emergency or acute psychiatric settings due to extreme behavioral disorders. Management of movement disorders related to bath salts typically involves supportive care (hydration, cooling), sedation with benzodiazepines, and antipsychotics. For more severe symptoms, dopamine antagonists may be used, but the focus should remain on cessation of drug use and addressing the acute psychiatric symptoms, as the movement disorders often resolve with the elimination of the drug from the system.

Opioid use and abuse are associated with hypokinetic movement disorders. Opioids act primarily on μ-opioid receptors and can modulate dopaminergic pathways involved in motor function. Long-term opioid abuse can lead to the development of opioid-induced parkinsonism that closely resembles idiopathic Parkinson disease with resting tremor, bradykinesia, and postural instability. Although this condition is reversible upon opioid cessation, some patients may continue to experience motor symptoms for a prolonged period. The treatment of opioid- induced movement disorders primarily involves opioid cessation, with the use of dopaminergic drugs (eg, levodopa) to alleviate symptoms of parkinsonism. In opioid withdrawal, movement disorders may worsen temporarily.

Spontaneous Movement Disorders in Psychosis

In individuals with schizophrenia, movement disorders are often seen as antipsychotic-induced syndromes. However, they may spontaneously occur in the context of unmedicated patients with chronic schizophrenia. Indeed, over 20% of patients with schizophrenia never exposed to neuroleptic medication have hyperkinetic signs,¹⁶ and even a higher proportion show evidence of parkinsonism.¹⁷ Thus, drug-induced movement disorders in patients with chronic nonaffective psychoses can be an expression of underlying liabilities to such pathologies. Also reflecting the latter, neurological soft signs (NSS) have been recognized and considered trait markers of schizophrenia.

NSS are subtle, nonspecific neurological signs that indicate dysfunction in the central nervous system. NSS are considered soft because they are less definitive and harder to pinpoint than typical (or hard) neurological signs, such as a focal weakness. In the context of schizophrenia, NSS can be present in the absence of overt neurological condition and correlate with the severity of cognitive and psychotic symptoms. They manifest in the form of motor (eg, coordination problems, postural instability, clumsiness, or dysdiadochokinesia); sensory/perceptual (eg, tactile and proprioceptive abnormalities, sensory integration difficulties); gait (unusual gait patterns); or eye movement (saccadic eye movement) abnormalities.^18,19 Overall, their presence is associated with worse cognitive and functional outcomes.^19,20

Diseases With Concurrent Behavioral and Movement Disorders

Another context where psychiatrists can encounter movement disorders is when dealing with patients with neurodegenerative diseases, such as Huntington disease and Parkinson disease. Although their discussion is beyond the scope of this review, it is worth highlighting these diseases are quintessential neuropsychiatric conditions defined by characteristic movement disorders and frequently associated with a myriad of behavioral/psychiatric symptoms.²¹ These disorders are caused by neurodegeneration of the basal ganglia and other brain areasregulating cognition, mood, and behavior.^22,23

Huntington disease is a genetic neurodegenerative disease caused by a mutation in the HTT gene leading to the pathological accumulation of the protein huntingtin and subsequent neurodegeneration. The clinical hallmarks include chorea and cognitive decline. Irritability, impulsivity, and depression are very common, often antedating the onset of motor symptoms. Obsessive-compulsive behaviors and psychosis can also occur, making Huntington disease a challenging condition for both patients and caregivers. Treatment focuses on symptom management, such as using VMAT2 inhibitors for chorea and antipsychotics and/or antidepressants for behavioral symptoms.²⁴

Parkinson disease is pathologically defined by the loss of dopaminergic neurons in the substantia nigra leading to bradykinesia, rigidity, resting tremor, and later postural instability. Many individuals experience depression, anxiety, cognitive decline, and psychosis (including complex visual hallucinations and delusions) requiring psychiatric assessment and treatment. Impulse control disorders (gambling, hypersexuality) may also occur, especially with the use of dopaminergic agonists (eg, ropinirole). Treatment focuses on dopaminergic therapy for motor symptoms (eg, levodopa) and antidepressants and/or antipsychotics for psychiatric symptoms. Given the high vulnerability of this population to antipsychotic-induced parkinsonism, quetiapine and clozapine are preferred, with pimavanserin being another pharmacological alternative for psychosis.²⁵

Future Perspectives

Movement disorders in psychiatric practice represent a complex and often overlooked group of symptoms that can significantly influence the clinical course and treatment outcomes of patients. The development of antipsychotics with novel mechanisms of action (ie, nondopaminergic), potentially causing less impact on basal ganglia function, alongside the emergence of neuromodulation methods is reshaping how clinicians approach movement-related symptoms in psychiatric practice.

Despite these advancements, treatment and management of movement disorders in psychiatric patients remain challenging. Early detection and prevention are pivotal for better clinical outcomes, especially a more judicious use of antipsychotics given their potential for acute and long-term motor consequences. There is also a need for clinical guidelines that can assist in the management of the diverse types of movement disorders in the psychiatric context.

In conclusion, while movement disorders in psychiatry present ongoing challenges, they also offer exciting opportunities for scientific exploration and clinical innovation. As the field moves forward, greater focus on personalized care, early intervention, and multimodal treatment strategies will be critical in improving both the quality of life and the overall prognosis for individuals affected by these complex disorders.

Dr Salem is an assistant professor in the Department of Psychiatry and Human Behavior at the Warren Alpert Medical School of Brown University in Providence, Rhode Island. Dr de Erausquin is distinguished professor of neurology and radiological sciences at the Glenn Biggs Institute for Alzheimer’s and Neurodegenerative Diseases at the University of Texas Health Science Center in San Antonio, Texas. Dr Teixeira is professor of psychiatry and neurology at the Glenn Biggs Institute for Alzheimer’s and Neurodegenerative Diseases at the University of Texas Health Science Center in San Antonio, Texas.

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