Neuroleptics dystonias

Acute dystonias occur immediately after neuroleptization and are manifested by motor impairments, particularly in the head, neck, and shoulder region. After several days to months, a parkinsonian syndrome (pseudoparkinsonism) or akathisia (motor restlessness) may develop. All these disturbances can be treated by administration of antiparkin-son drugs of the anticholinergic type, such as biperiden (i.e., in acute dystonia). As a rule, these disturbances disappear after withdrawal of neuroleptic medication. Tardive dyskinesia may become evident after chronic neuroleptization for several years, particularly when the drug is discontinued. It is due to hypersensitivity of the dopamine receptor system and can be exacerbated by administration of anticholinergics. 

Extrapyramidal reactions include parkinsonism, acute muscular dystonias, akathisia, tardive dyskinesia and malignant neuroleptic syndrome. They can also cause hypersensitivity reaction including cholestatic jaundice, skin rash, urticaria, photosensitivity and contact dermatitis. There is also blue pigmentation of skin, lenticular opacities on prolonged use of drug. 

Late-onset or tardive dystonia, akathisia, and possibly other types of EPS have also been described as separate disorders from classic TD. Tardive dystonia is characterized by the late appearance of dystonias that persist even though neuroleptics are discontinued. It is rare, with a prevalence of about 1.5%. It is probably a separate diagnostic entity inasmuch as anticholinergics benefit tardive dystonia, whereas these drugs can worsen TD. The onset of tardive dystonia occurs after a shorter total drug exposure time than generally seen with TD. 

Neuroleptics may also cause blepharospasm, which is a forcible closure of the eyelids and when severe can interfere with activities such as driving this condition can also be socially disabling and disfiguring. In addition, there are a few cases indistinguishable from idiopathic Meighs syndrome, which presents with blepharospasm and oromandibular dystonia (470). Of interest, clozapine has been reported to be beneficial for these symptoms. 

Gagrat D, Hamilton J, Belmaker RH. Intravenous diazepam in the treatment of neuroleptic-induced acute dystonia and akathisia. Am J Psychiatry 1978 135 1232-1233. 

Ballerini M, Bellini S, Niccolai C, et al. Neuroleptic-induced dystonia incidence and risk factors. Eur Psychiatry. 2002 17 366-368. 

Parkinsonism, dystonias, akathisia Dopamine blockade of basal ganglia All potent typical neuroleptics... 

The most common symptomatic dystonias result from the administration of neuroleptics and occur as acute dystonic reactions or as tardive dyskinesia. 

Acute dystonic reactions occurring following the administration of potent neuroleptics are reported primarily in young men and usually develop shortly after the start of therapy. By contrast, tardive dystonia occurs following chronic neuroleptic treatments as with tardive dyskinesia, symptoms often begin after the abrupt withdrawal of the neuroleptic. Although less severe than acute dystonic reactions, tardive dystonia is frequently permanent and difficult to treat. 

Regarding neuroleptic-induced dystonias, it is well known that typical neuroleptics cause catalepsy in rats and movement disorders in man. By contrast, the atypical neuroleptics clozapine and sulpiride have a low propensity to cause movement disorders in man even though they have established antipsychotic effects. These atypical neuroleptics, unlike many of the typical neuroleptics, have a low affinity for sigma receptors which lends support to the hypothesis that the dystonias produced by typical... 

A report found that even small doses of Risperdal (average dose of 1.7 mg/day) produced or worsened acute extrapyramidal reactions in one-third of an elderly population suffering from dementia (Baker, 1996). Among 41 patients, 6 developed new parkinsonism, 5 had a worsening of previous parkinsonism, one developed cervical dystonia, and one developed neuroleptic malignant syndrome while also taking Tegretol and Mellaril. 

These acute EPS reactions often resemble TD, and indeed, the dystonias and akathisia can become tardive (persistent) disorders. All of them, including parkinsonism, result from neuroleptic effects on the dopaminergic neurotransmitter system in the basal ganglia. 

In a 1988 review of tardive dystonia, Burke and Kang found 21 reports describing 131 patients (for reviews, see also Greenberg et al., 1985 Kane et al., 1992). As already emphasized, because all the atypical neuroleptics are potent dopamine blockers (except clozapine), it should have been assumed that all of them could cause TD and tardive dystonia. Case reports confirm that risperidone (Vercueil et al., 1999 Narendran et al., 2000) and olanzapine (Gunal et al., 2001 Dunayevich et al., 1999) can cause tardive dystonia. 

Kiriakakis et al. (1988) concluded, Tardive dystonia can develop at any time between 4 days and 23 years after exposure to [neuroleptics] and there is no safe period. It can afflict anyone independently of their psychiatric diagnosis, and patients with schizophrenia have accounted for only half of reported TD cases. From assorted studies, they estimate the prevalence at 2.8% among neuroleptic-treated patients. 

In my clinical and forensic experience, the emphasis on muscle rigidity is much too narrow. NMS can be accompanied by any kind of severe extrapyramidal reaction. Especially early in NMS, patients can display any of the wide array of neuroleptic-induced abnormal movements, including choreoathetoid movements, dystonia, and akinesia. Some cases look very much like severe TD, and often, the patients are left with persistent symptoms of TD. 

Prozac s pharmacological mechanism for suppressing dopamine is more indirect than that of the neuroleptics. However, the clinical result can be very similar. Prozac can cause akathisia (agitation with hyperactivity), parkinsonism ( Fluoxetine, 1990), and dystonia (muscle spasms) (Meltzer et al., 1979 Reccoppa et al., 1990). 

Extrapyramidal symptoms (including akathisia, dystonia, dyskinesia, tardive dyskinesia, parkinsonism, and brux-ism) have been reported in association with SSRIs, especially in the presence of predisposing factors (SEDA-14, 14 12). Current data suggest that SSRIs should be used with caution in patients with parkinsonism (see the monograph on fluoxetine). Concomitant treatment with neuroleptic drugs and high concentrations of SSRIs seems to predispose to extrapyramidal symptoms. Elderly patients and women are also at increased risk. 

Aspiration asphyxia in patients treated with neuroleptic drugs has been described (SEDA-4,40 SEDA-5, 51), and it has been suggested that this could have been due to laryngeal-pharyngeal dystonia (158). Patients with asthma treated with neuroleptic drugs may be at increased risk of serious complications of asthma (159). 

Acute laryngeal dystonia is probably under-reported but it is potentially lethal and can mimic anaphylaxis (204). It can occur within hours to days of starting therapy with neuroleptic drugs and is characterized by sudden onset of difficulty in breathing and swallowing (SEDA-22, 51). 

A 35-year-old woman with schizophrenia developed acute respiratory distress and laryngeal stridor (196). Neuroleptic drug-induced laryngeal dystonia was diagnosed. She was given biperiden lactate 10 mg intramuscularly and her symptoms resolved fully within 30 minutes. On the advice of a psychiatrist, and to sedate her for admission to a psychiatric hospital, her mother had secretly put 50 drops of haloperidol (10 mg/ml) in her food 1 hour before the symptoms appeared. 

In addition, the authors reviewed 26 previously published cases of neuroleptic drug-induced laryngeal dystonia. They suggested that this condition could be the cause of... 

Tardive dystonia is a rare, late-onset, persistent dystonia associated with neuroleptic drugs, which usually affects young men. It tends to affect the muscles of the neck, shoulder girdle, and trunk, causing opisthotonos. Sometimes, patients can become incapacitated (325,226). The incidence is 1-2% (327). Once developed, it is a very persistent disorder, with a low remission rate of only 14% withdrawal of neuroleptic drugs increases the chances of remission. 

Tardive dystonia has sometimes been thought to be a subtype of tardive dyskinesia (SED-13, 123). However, some features of this condition are clearly different from those of tardive dyskinesia (SEDA-20, 41). The diagnosis of tardive dystonia should meet the following criteria (a) the presence of chronic dystonia (b) a history of neuroleptic drug treatment preceding (less than 2 months) or... 

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