Movement and psychiatric disorders are frequently comorbid. When they are, movement abnormalities and psychiatric symptoms often overlap and exacerbate one another. For example, in depressed patients with Parkinson disease (PD), bradykinesia and psychomotor slowing can present similarly and tremor and motor “freezing” can be worsened by anxiety. In some cases, the disorders are thought to share a biological origin (eg, tic disorders). In other cases, the treatment of one condition may evoke the other—for example, treating psychosis with neuroleptics may result in tardive dyskinesia. Clinically, the combined presentation of symptoms often confounds diagnosis and complicates treatment.
The overall prevalence of movement disorders associated with psychiatric disorders is unknown and difficult to estimate because comorbidity occurs across a broad range of conditions and in a wide variety of circumstances. A general estimate, in patients with movement symptoms severe enough to seek neurological treatment, is that 40% of neurology outpatients and 34% of neurology inpatients have psychiatric disorders.1 Comorbidity between movement and psychiatric disorders typically occurs in one or more of the following scenarios:
• Two discrete conditions co-occur (eg, major depression develops in a patient with PD)
• A movement disorder is an adverse effect of treatment (eg, drug-induced parkinsonism)
• The movement disorder is a direct result of the psychiatric condition (eg, conversion disorder)
Discrete comorbid conditions
Movement disorders that have a prominent tremor component can be worsened by pharmacological treatment of psychiatric conditions. For instance, essential tremor and ataxias have an action-type tremor. Action tremor is any tremor that occurs with voluntary activation of muscles and includes postural, kinetic, and intention tremors.2 Many antidepressants, mood stabilizers, and antipsychotics can worsen action-type tremors and should be used cautiously in patients with tremor.
A 39-year-old woman with a history of essential tremor and bipolar disorder is hospitalized for mania. She takes primidone(Drug information on primidone), quetiapine(Drug information on quetiapine), and bupropion. She has been largely nonadherent with quetiapine, so the decision is made to start lithium(Drug information on lithium), which can be monitored in the blood. After restarting quetiapine, lithium is introduced and increased to a total dose of 900 mg daily on the day before discharge. On the day of discharge, all signs of mania have resolved and her lithium level is 0.7 mEq/L.
Three days after discharge, she presents to the emergency department (ED) with a high-amplitude action tremor that prevents her from eating, drinking, or writing. There has been no change in her essential tremor therapy, and she has been adherent to her medication regimen. What happened?
On the day before her discharge, the lithium dose was increased from 600 mg to 900 mg. Although her blood level was only 0.7 mEq/L on the day of discharge, the half-life of lithium averages 20 to 24 hours. Therefore, her lithium level was still rising and had not yet reached steady-state in her blood by discharge. In the ED, she was found to be within the therapeutic range (0.8 to 1.2 mEq/L) for lithium. However, patients with essential tremor and other disorders with prominent tremor often experience exacerbation of the preexisting tremor, even at therapeutic doses. The tremor returned to baseline after the lithium dose was reduced and the primidone dose was increased.
A 58-year-old woman with a 6-year history of PD has been having 1 to 3 panic attacks daily for the past 3 months. Panic disorder was diagnosed when she was 24 and had been well controlled with sertraline(Drug information on sertraline), with fewer than 2 panic attacks per year. Her medical history is significant for gastroesophageal reflux disorder and osteoporosis. Her medications include carbidopa/levodopa 25/100 mg, 2 tablets 4 times daily and 1 tablet at bedtime, calcium and vitamin D supplements, and sertraline 100 mg daily. She has had no medication changes in the past year.
The panic attack episodes last for 30 to 60 minutes; typically come on gradually over the course of 15 to 20 minutes; and include sweating, flushing, palpitations, increased tremor, difficulty in drawing a full breath, intense anxiety, and a fear that “something bad is happing.” Episodes seem to occur most often in the late morning, mid-afternoon, and just after dinner. She finds that she cannot concentrate or function well during these episodes and, as a result, has been refusing activities outside of the house between 10am and 7pm.
Medical examination and relevant laboratory studies revealed no acute health issues. Her blood pressure is 130/80 mm Hg while sitting and 119/76 mm Hg while standing; pulse is 65 beats per minute while sitting and 68 while standing. Several treatment trials, including increased dosages of sertraline, a cross-taper first to escitalopram(Drug information on escitalopram) then to duloxetine(Drug information on duloxetine), and the addition of clonazepam(Drug information on clonazepam) up to 1 mg bid, have been unsuccessful.
Anxiety occurs with wearing-off in up to 88% of patients with PD.3 Wearing-off is the predictable emergence of motor or nonmotor PD symptoms before the next scheduled antiparkinsonian medication dose.4 Wearing-off develops in up to 80% of PD patients within 5 to 10 years of starting levodopa(Drug information on levodopa) therapy. Therefore, the most likely cause of the daily panic attacks, in the absence of medication changes or medical issues, is the progression of the disease causing wearing-off of the previously adequate antiparkinsonian therapy.
This vignette illustrates some of the challenges in assessing and treating psychiatric disorders that are comorbid with a movement disorder. In this case, the nonmotor symptoms of PD associated with wearing-off include anxiety, return of tremor, and other autonomic symptoms that closely mimic the symptoms of a classic psychiatric panic attack. Distinguishing features include the gradual onset of symptoms and cyclical occurrence toward the end of each carbidopa/levodopa dosing interval.
Patients and doctors often fail to recognize the relationship between the timing of PD medications and anxiety episodes. Several issues can confound detection, including variability in patient adherence to a strict medication schedule and wearing-off episodes that may be better tolerated and therefore unreported during a particular interval because of reduced activity or napping. To improve detection, have the patient or caregiver keep a journal of the anxiety symptoms in relation to the time of actual antiparkinsonian medication administration. Clinicians can use scales such as the Wearing-off Questionnaire, which has been designed to help identify nonmotor symptoms of wearing-off in PD and distinguish them from other disorders.5
When movement and psychiatric disorders present concurrently, multidisciplinary cooperation between the neurologist and psychiatrist is essential. Neurological and psychiatric symptoms often overlap and exacerbate one another. When this happens, optimal treatment response cannot be achieved unless both conditions are recognized and addressed. In this case, while antidepressants and benzodiazepines may help reduce wearing-off related anxiety, they usually do not produce significant or long-lasting relief.
Definitive treatment of wearing-off related anxiety is best achieved through adjustment of antiparkinsonian therapy. Common strategies to prevent or decrease wearing-off are to decrease the interval between levodopa doses (eg, from every 4 hours to every 3 hours); add a catechol O-methyltransferase inhibitor; start adjunctive therapy with a dopamine(Drug information on dopamine) agonist; or use a monoamine oxidase B inhibitor. Cognitive-behavioral therapy (CBT) is also effective for anxiety and should be used in conjunction with these strategies.
Movement disorders with associated dementia syndromes. Cognitive impairment and dementia occur in a wide range of movement disorders. The time of onset, quality, and prominence of cognitive symptoms vary between movement disorders, which may complicate recognition. In Lewy body dementia for instance, cognitive impairment affects cortical and subcortical processes and is often the first and most clinically apparent symptom. However, in Huntington disease, the course of decline is more insidious because factual information and overall intelligence quotient scores remain stable until relatively late in the disease, despite significant executive dysfunction and procedural learning deficits.
Psychiatrists who treat patients with movement disorders should remain vigilant for cognitive changes, such as executive dysfunction in essential tremor and primary dystonia; frontal-subcortical dementia syndromes in progressive supranuclear palsy, corticobasal syndrome, and multisystem atrophy; and sporadic and progressive cognitive impairment in multiple sclerosis and certain cerebellar ataxias. Consider formal neuropsychological testing to establish a cognitive baseline and to detect more subtle cognitive impairments.
Movement disorders as a consequence of psychiatric treatment
Akathisia. In ancient Greek, akathisia means “not to sit.” Patients with this condition present with complaints of inner tension, restlessness, anxiety, and the urge to move. Observable motor features are complex, semi-purposeful, and repetitive (eg, foot shuffling or tapping, pacing, shifting of weight, rocking).
Psychopharmacological agents that induce this movement disorder include typical and atypical antipsychotics, antidepressants, dopamine blocking antiemetics, reserpine, α-methyldopa, lithium, calcium channel blockers, and tetrabenazine(Drug information on tetrabenazine). Onset is variable but is often associated with dose escalations. Treatment includes lowering or stopping associated medication or switching to an antipsychotic with lower risk of extrapyramidal symptoms (EPS). In addition, iron levels need to be checked. In order of best evidence, the following agents are safer, with a smaller risk of inducing akathisia: ß-blockers, benzodiazepines, anticholinergics, clonidine(Drug information on clonidine), amantadine(Drug information on amantadine). Mirtazapine(Drug information on mirtazapine) and serotonin antagonists (cyproheptadine, mianserin(Drug information on mianserin)) may also be safer to use.6
Tardive dyskinesia. This movement disorder most often affects the orofacial and lingual musculature (eg, lip smacking, chewing, protrusion, curling or twisting of the tongue, puckering, bulging of the cheeks). Choreoathetoid movements of the fingers, hands, and upper and lower extremities are also common. Dyskinesias increase with emotional arousal or distraction, and diminish with sleep, relaxation, or volitional effort.
Associated with prolonged exposure to antipsychotic medications, the onset of tardive dyskinesia is typically after longer than 3 months of exposure. Reducing or stopping the current antipsychotic or switching to a lower-potency antipsychotic may temporarily worsen tardive dyskinesia, but will ultimately help in most cases. Treatment with anticholinergic medications or tetrabenazine may also be indicated.6
Acute dystonia. This disorder presents as a syndrome of sustained muscle contractions, frequently causing twisting and repetitive movements or abnormal postures, such as blepharospasm, forced jaw opening, grimacing, laryngospasm, oculogyric crisis, spasmodic torticollis, and tongue protrusion or twisting. In 95% of cases, dystonia appears within 5 days of starting or increasing a dose of antipsychotic medication. First-line treatment includes anticholinergics (oral or intramuscular) or antihistamines; benzodiazepines can be used as second-line treatment. If the patient is unresponsive, check for hypocalcemia.6
Neuroleptic malignant syndrome. This is a life-threatening syndrome characterized by autonomic and mental status changes, fever, and severe muscular rigidity. The first symptom to emerge in 82% of patients is change in mental status. Supporting, but nonspecific, laboratory findings include elevated serum creatine kinase level, leukocytosis, elevated liver function tests, hypocalcemia, hypomagnesemia, hyperkalemia, and metabolic acidosis.
More than half of cases (66%) occur within the first 1 to 2 weeks after initiation of antipsychotic medications. Higher doses and rapid dose escalation are risk factors. Treatment includes removal of the causative agent and supportive care (intravenous fluids, metabolites). Some patients will need to be admitted to an ICU. Benzodiazepines can be used for agitation, and electroconvulsive therapy is an option. Controversial treatments include dantrolene(Drug information on dantrolene), bromocriptine(Drug information on bromocriptine), and amantadine.6
Drug-induced parkinsonism. This syndrome mimics PD, with symptoms of bradykinesia, rest or postural tremor, and rigidity. Onset is subacute and bilateral, with early presence of postural tremor and concurrent oral-buccal dyskinesias, which are usually not responsive to levodopa. Antipsychotics, lithium, antiemetics (prochlorperazine, metoclopromide), calcium channel blockers, reserpine, α-methyldopa, tetrabenazine, and some antidepressants are responsible for the disorder.
Lowering the dosage of or stopping the responsible medication or switching to an antipsychotic with lower EPS liability will usually remit symptoms within days or weeks; in the elderly, it may take longer—sometimes several months. Up to 15% of cases may persist.6
Punding. From the Swedish slang for “block-head,” punding was first described in amphetamine addicts. Patients with this movement disorder present with complex stereotyped behavior, with repetitive examining, handling, or manipulation of objects usually without clear purpose. Stimulants and dopamine agonists are the responsible agents, and treatment consists of lowering the dosage of or stopping the medication.7
Serotonin syndrome. This adverse drug reaction stems from an excess of serotonin. It presents as a triad of autonomic hyperactivity, mental status change, and neuromuscular symptoms. Akathisia, clonus, diaphoresis, hyperreflexia, muscular rigidity, and tremor may also be seen. Antidepressants, valproate(Drug information on valproate), fentanyl(Drug information on fentanyl), tramadol(Drug information on tramadol), metoclopramide(Drug information on metoclopramide), sumatriptan(Drug information on sumatriptan), lithium, and MAOIs are responsible for this disorder. Up to 60% of patients present within 6 hours of initiation of medication, a dosage change, or an overdose. Treatment involves stopping the medication and providing supportive care to control autonomic instability and hyperthermia. Serotonin 2A antagonists may also be used.8
Tremor. Postural tremor is most common and usually presents bilaterally as unintentional, rhythmic, muscle movement involving oscillations of one or more parts of the body. Responsible agents include antidepressants, antipsychotics, lamotrigine(Drug information on lamotrigine), lithium, and valproic acid; treatment consists of lowering the dosage of or stopping the associated medication.2
Movement disorder as the result of a psychiatric condition
Psychogenic movement disorders are “disorders that cannot be attributed to any known structural or neurochemical disease but result from an underlying psychiatric illness or malingering.”9 Patients who have these problems often meet diagnostic criteria for a somatoform disorder; conversion disorder is the most common. Symptoms include a variety of abnormal movements, and gait is often affected. The disorders can present as entire movement disorder syndromes (eg, psychogenic parkinsonism).
Psychogenic movement disorders are thought to account for up to 9% of all neurological diagnoses and represent 2% to 3% of cases seen in movement disorder specialty practices.10 Women are more often affected than men, and the typical age at onset is between 37 and 50 years. Organic neurological disorders are present in 10% to 15% of patients and often have overlapping symptoms, making it difficult to distinguish between the two conditions. The Table lists clinical features that are characteristic of psychogenic movement disorders. Ancillary tests that can help clarify the diagnosis in some cases are electromyography; evoked potentials; and functional imaging, such as dopamine transporter imaging.
Untreated psychogenic movement disorders become chronic in 65% to 95% of patients and produce significant disability and increased health care costs.10 The first goal of treatment is accurate diagnosis to prevent iatrogenic harm by avoiding unnecessary invasive tests or medications.
A therapeutic approach outlined by Williams and colleagues11 asserts that gaining the patient’s acceptance of the psychogenic origin of the diagnosis is fundamental to treatment success. They recommend a multidisciplinary diagnostic debriefing that involves the neurologist, psychiatrist, and patient, delivered in a way that is sensitive to the patient’s conception of the disease. Although no single treatment approach has yet been shown to be superior to others, a limited number of clinical trials have found antidepressants, psychotherapy (particularly CBT, which has a positive treatment effect in up to 71% of patients), and referrals to occupational and physical therapy to be helpful.
Model for multidisciplinary management
Multidisciplinary treatment for patients with comorbid movement and psychiatric disorders should be established as soon as comorbidity is identified. The team typically includes a psychiatrist/therapist, neurologist, and physical and occupational therapists. Formal neuro-psychological testing and speech/language pathology are often helpful when cognitive impairment, dysphagia, and speech problems are present. Communication is the most important aspect of the team-based approach. Good communication ensures that overlapping treatments do not unnecessarily exacerbate comorbid symptoms and helps clarify the overall goal of treatment, which should be to improve the quality of life and functioning of the patient rather than to serve as a checklist for alleviating individual symptoms.
1. Nicholson TR, Stone J, Kanaan RA. Conversion disorder: a problematic diagnosis. J Neurol Neurosurg Psychiatry. 2011;82:1267-1273.
2. Arbaizar B, Gómez-Acebo I, Llorca J. Postural induced-tremor in psychiatry. Psychiatry Clin Neurosci. 2008;62:638-645.
3. Witjas T, Kaphan E, Azulay JP, et al. Nonmotor fluctuations in Parkinson’s disease: frequent and disabling. Neurology. 2002;59:408-413.
4. Stacy M, Bowron A, Guttman M, et al. Identification of motor and nonmotor wearing-off in Parkinson’s disease: comparison of a patient questionnaire versus a clinician assessment. Mov Disord. 2005;20:726-733.
5. Stacy M. The wearing-off phenomenon and the use of questionnaires to facilitate its recognition in Parkinson’s disease. J Neural Transm. 2010;117:837-846.
6. Caroff SN, Hurford I, Lybrand J, Campbell EC. Movement disorders induced by antipsychotic drugs: implications of the CATIE schizophrenia trial. Neurol Clin. 2011;29:127-148.
7. O’Sullivan SS, Evans AH, Lees AJ. Punding in Parkinson’s disease. Pract Neurol. 2007;7:397-399.
8. Boyer EW, Shannon M. The serotonin syndrome [published corrections appear in N Engl J Med. 2007;256:2437; N Engl J Med. 2009;361:1714]. N Engl J Med. 2005;352:1112-1120.
9. Hallett M, Weiner WJ, Kompoliti K. Psychogenic movement disorders. Parkinsonism Relat Disord. 2012;18(suppl 1):S155-S157.
10. Hinson VK, Haren WB. Psychogenic movement disorders. Lancet Neurol. 2006;5:695-700.
11. Williams DT, Ford B, Fahn S. Treatment issues in psychogenic-neuropsychiatric movement disorders. Adv Neurol. 2005;96:350-363.
Martin, L. (2013). Comorbid Movement and Psychiatric Disorders. Psych Central. Retrieved on March 9, 2014, from http://pro.psychcentral.com/2013/comorbid-movement-and-psychiatric-disorders/001257.html
Last reviewed: By John M. Grohol, Psy.D. on 5 Mar 2013