Tardive dystonia

There are at least two relatively common variants of TD tardive dystonia and tardive akathisia. According to Burke et al. (1982), tardive dystonia involves sustained involuntary twisting movements, generally slow, which may affect the limbs, trunk, neck, or face (p. 1335). The face and neck are by far the most frequently affected areas of the body. Severe deformities of the neck (torticollis) can cause extreme pain and disability. I have seen several cases affecting the orbital muscles of the eyes (blepharospasm) to the degree that the individual s vision was impaired, requiring botulinum (Botox) injections to paralyze the muscles. I have also seen respiratory and abdominal muscles affected in a painful and debilitating manner. 

Tardive dystonia can produce cramplike, painful spasms that temporarily prevent the individual from carrying out normal activities. Sometimes the spasms are so continuous that the individual is largely disabled. Damage to the joint and skeleton system, including fractures, can occur (Burke et al., 1988). The pain and muscle tension as well as the effort to compensate for the spasms can be exhausting and demoralizing. 

The torsions (twisting movements, often involving the neck) can be worsened by activity such as attempts to write or walk. Sometimes they can be relieved by particular movements such as touching the chin to relieve torticollis or touching the brow to relieve blepharospasm. 

As Burke and Kang (1988) pointed out, tardive dystonia can be mistakenly dismissed as a manifestation of hysteria or some other psychological problem In this regard it is important to realize that dystonia, like many other neurological disorders, can be influenced transiently by suggestion, placebo, or sedation (e.g., during an amobarbital interview) and such maneuvers cannot exclude a true dystonia. Also, like many other neurological disorders, it can sometimes be partially controlled by extreme exertions of will. 

Tardive dystonia can make an individual appear unsympathetic or bizarre, especially to the uninformed observer, who equates the facial grimaces or neck distortions with being crazy. As in all the drug-induced dyskinesias, the individual may try to cover up the disorder with additional movements that make the disorder seem voluntary and therefore not a product of mental illness. The result can be very confusing and even distressing to the observer. I have read several medical records in which 

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In 1985, 1 finally took the county public health psychiatrist s recommendation to try Desipramine, an ostensibly mild tricyclic antidepressant. I took tiny dot doses, and for a month or so I felt encouraged except for intense muscle tension and clenching. The psychiatrist said it was not remotely possible that this response was related to the medication. I took a low dose for four more months before throwing them out. The side effects had escalated horribly, and become what I later learned are called tardive dyskinesia and tardive dystonia. Subsequently, chemical and electromagnetic field exposures, feeling compromised or ashamed, or stress can trigger uncontrollable movement, hyperactivity, rigid posture and then, frequently, paralysis. 

CA/S-Agitation, akathesia, akinesia, anxiety, asthenia, confusion, convulsions, dizziness, drowsiness, dystonia, extrapyramidal symptoms, gait abnormal, headache, hypokinesia, insomnia, libido decreased, light-headedness, restlessness, somnolence, syncope, tardive dystonia, tremor, vertigo. 

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. 

Friedman J. Clozapine treatment of psychosis in patients with tardive dystonia. Movement Disord 1994 9 321-324. 

Adityanjee AM, Estrera AB. Successful treatment of tardive dystonia with clozapine. Bioi Psychiatry 1996 39 1064-1066. 

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. 

Patients who have suffered these experiences may remember them with pain, fear, and resentment for the rest of their lives. Needless to say, if their doctors originally blamed the reactions on the patient s psychiatric problems, the patient can feel enormously betrayed. Often the attacks can be aborted with proper medical intervention, but they can go on endlessly if untreated or if they develop into an irreversible tardive dystonia (chapter 4). 

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 practice, I have consulted with and evaluated many cases of tardive dystonia, mostly involving the face, neck, and shoulders, but sometimes the torso. I see a disproportionate number of... 

Fatigue to the point of exhaustion almost always accompanies tardive disorders of any severity. Patients often become exhausted by the movements, by the effort to hide them, and by increased difficulty associated with carrying out daily activities. The primary impact on the brain itself may also produce fatigue. Although the disorders tend to disappear in sleep, they can make it difficult to fall asleep, adding to the exhaustion. Having to contend with the physical pain associated with tardive akathisia (inner torment) and with tardive dystonia (muscle spasms) can also wear a person down. 

The risk of causing EPS, another SSRI-induced neurologist disorder, was apparent from early on. The FDA s Kapit (1986) warned, It is possible that a tardive syndrome related to fluoxetine may exist. It will be necessary to be on the lookout for such events (p. 32). By January 1993, more than two dozen reports of Prozac-induced tardive dyskinesia had reached the FDA (1993), but the profession has not taken much notice. Numerous case reports confirm that the SSRIs can produce persistent extrapyramidal reactions, including tardive dystonia with painful and disabling spasms of the neck and shoulder musculature. 

Burke, R., Fahn, S., Jankovic, J., Marsden, C. D., Lang, A. E., Gollomp, S., et al. (1982). Tardive dystonia Late-onset and persistent dystonia caused by antipsychotic drugs. 

Burke, R., 6c Kang, U. J. (1988). Tardive dystonia Clinical aspects and treatment. In J. Jankovic 6c E. Tolosa (Eds.), Facial dyskinesias Advances in neurology (Vol. 49,... 

Chakrabarti, S., Chand, P. (2002). Lithium-induced tardive dystonia. Neurology India, 50, 473-475. 

Dunayevich, E., Strakowski, S. (1999). Olanzapine-induced tardive dystonia. American... 

Friedman, J., Kucharski, L., 8c Wagner, R. L. (1987). Tardive dystonia in a psychiatric hospital. Journal of Neurology, Neurosurgery and Psychiatry, 50, 801-803. 

Gunal, D., Onultan, O., Afsar, N., Aktan, S. (2001). Tardive dystonia associated with olanzapine therapy. Neurological Science, 22, 331-332. 

Kiriakakis, V., Bhatia, K., Quinn, N., Marsden, C. (1998). The natural history of tardive dystonia A long-term follow-up study of 107 cases. Brain, 121, 2053-2066. 

Narendran, R., Young, C., 6c Pato, M. (2000). Possible risperidone-induced tardive dystonia. Annals of Pharmacotherapy, 34, 1487-1488. 

Vercueil, L., Foucher, I. (1999). Risperidone-induced tardive dystonia and psychosis. The Lancet, 353, 981. 

Reversible tardive dystonia has been attributed to lithium (192). 

Chakrabarti S, Chand PK. Lithium-induced tardive dystonia. Neurol India 2002 50(4) 473-5. 

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