Tremor is the most common movement disorder in adults. Due to the visibility, feelings of shame are often present. Many (psycho)pharmacological drugs can induce tremor or increase its severity as a side effect. Sometimes the burden of this side effect is greater than the burden of the psychiatric problem.

Knowledge of the different kinds of tremor in psychiatry, and the drugs that may be responsible. Differential diagnosis Treatment of tremor in psychiatry.

A literature search on the most recent insights into classification, diagnosis, differentiation and treatment was carried out with emphasis on drug-induced tremor and its treatment.

The basic classification is resting, action and intention tremor. Tremors may be due to neurological and metabolic syndromes. Differentiation can often be made according to the time of onset, relation with starting or increasing the dosage of the medication and the course. Rest tremor is often related to antipsychotics and antiemetics and action tremor to lithium, antidepressants, valproic acid, and other anticonvulsants, but also to many drugs used in somatic conditions. The development of intention tremor should alarm the doctor because it could be an intoxication. Treatment of drug-induced tremor consists of reducing the dose or discontinuing the drug in question or switching to another drug with less risk of tremor. If this is not effective, adding a tremor suppressant may help (propranolol, primidone in action tremor and anticholinergics or amantadine in resting tremor.

Tremor is a common side effect of many (psycho)pharmacological agents and treatment is often possible.

No significant relationships.

Akathisia is a relatively common adverse effect of antipsychotics although some second-generation antipsychotics are known to have a lower liability for the condition. The core feature of akathisia is mental unease characterized by a sense of agitation, usually accompanied by motor restlessness, which can cause patients to pace up and down and be unable to stay seated for more than a short time. An association between this discomfiting subjective experience and suicidal ideation has been postulated but remains uncertain.

Our aim is to perform a non-systematic review of the literature regarding the current understanding of antipsychotic-induced akathisia and its management.

A semi-structured review was conducted on Pubmed concerning the relationship between akathisia and antipsychotics.

All antipsychotics drugs can cause akathisia. The management of antipsychotic-induced akathisia should include a dose reduction of the antipsychotic treatment or a switch to quetiapine or olanzapine. If ineffective, a trial with propranolol may be useful as well as the addition of a 5-HT2A antagonist like mirtazapine or mianserine. At last the inclusion of a benzodiazepine may be helpful albeit the risk of dependence and anticholinergics mainly when other extrapyramidal symptoms are present.

High‐dose antipsychotic medication, antipsychotic polypharmacy and rapid increase in antipsychotic dosage should be avoided to prevent akathisia. There is limited evidence for any pharmacological treatment for akathisia such as switching to an antipsychotic medication with a lower liability for the condition, or adding a beta‐adrenergic blocker, a 5‐HT2A antagonist or an anticholinergic agent although some patients may benefit from such interventions.

Subjective reports of dysphoric responses to neuroleptic medication are common in clinical practice. However, cognitive and affective side effects of neuroleptic medications are difficult to differentiate from the symptoms of schizophrenia. We sought to elucidate the relative contribution of extrapyramidal side effects and symptomatology to dysphoric response.

Fifty clinically stable outpatients with schizophrenia attending a rehabilitation centre were assessed for extrapyramidal side effects and symptomatology before completing the drug attitude inventory (DAI).

Presence of extrapyramidal side effects, found in 28 patients (Z = −1.99, p = 0.05), and severity of negative symptoms (r = −0.47, p = 0.001) were independently associated with dysphoric response, explaining a significant proportion of the variance (R = 0.53, R2 = 25.2%, F = 9.27, df = 2, p = 0.0004).

Patients who report a dysphoric response which they associate with neuroleptic medications have more extrapyramidal side effects and more severe negative symptoms. While these responses may be part of the negative symptoms of the illness or due to other factors such as depression, we raise the possibility that they may be clinically indistinguishable from, and be a subjective measure of, the so-called ‘neuroleptic-induced deficit syndrome’.

Wilson's disease commonly presents with neurological or hepatic manifestations. When it presents with only psychiatric symptoms, or with extrapyramidal symptoms secondary to neuroleptic exposure, the diagnosis of underlying Wilson's disease may be missed.

An 18-year-old boy presented to the psychiatric clinic with a manic syndrome and high propensity for extrapyramidal symptoms to neuroleptic. Initial examination revealed splenomegaly and pancytopenia. Subsequent detection of Kayser–Fleischer ring and typical biochemical findings confirmed the diagnosis of Wilson's disease.

While the psychiatric symptoms came under control with lithium carbonate, extrapyramidal symptoms continue to persist even after neuroleptic withdrawal. Pancytopenia thought to be due to hypersplenism persists, and patient has developed features of liver cirrhosis. Treatment with zinc and folic acid has been started, and the patient is under evaluation for treatment with penicillamine.

The psychiatrist needs to recognize that Wilson's disease can uncommonly present with isolated psychiatric symptoms, including mania. Early and severe extrapyramidal symptoms secondary to neuroleptic exposure in an adolescent age group warrants a detailed evaluation to rule out underlying neuropsychiatric conditions.