Reply from the authors

In his letter commenting on our case report [1], Prof. Dose raises the important problem of differentiating between catatonia and neuroleptic-induced pseudocatatonia. We agree that mental side effects of anti-psychotic treatment tend to be neglected in clinical psychiatry. The fact that the use of typical neuroleptic drugs is still much more widespread in Germany than in the US and other European countries highlights this problem. However, we strongly believe that the patient we referred to in our case report suffered from catatonia rather than from the adverse side effects of the antipsychotic medication.

The clinical presentation of the 56-year-old patient changed from paranoid-hallucinatory to catatonic after suffering from Lyme encephalitis. Catatonia, as a result of organic medical conditions, has been described before [2]. Between 1986 and 1994, he was admitted to hospital several times presenting with catatonic symptoms. Most of these times, he was not taking any premedication on admission due to non-compliance. In the typical hospital course, he slowly recovered, but terminated treatment when extrapyramidal symptoms evolved. Despite the difficult differential diagnosis, the initial presentation seemed to be catatonic in nature (mutism, bizarre posturing with waxy flexibility, verbal stereotypes) rather than extrapyramidal (rigor, tremor, bradykinesia). Beyond that, a “residual extrapyramidal symptomatology” would have been hard to explain. When he was treated in our hospital in 1994, he received a maximum of 16 mg of benperidol per day (not 60 mg, as mentioned by Prof. Dose) and improved dramatically when the treatment was changed to risperidone. In our paper, we have discussed the possibility that the relief from extrapyramidal side effects could have been partially responsible for this clinical improvement.

In the following years, the patient remained stable when taking risperidone and relapsed with catatonia when he decreased or stopped medication. His clinical improvement after restarting risperidone was impressive. In the most recent years, the patient has never again been exposed to typical neuroleptics.

Taken together, we postulate that the different time courses of catatonic and extrapyramidal symptomatology allows differentiation between these two disorders in a patient, and that the continuity of symptoms in the absence of any exposure to typical neuroleptic indicates catatonia. Despite being a rare disorder, catatonia might still be recognized in some patients and should be treated adequately.

References

• 11 Hesslinger B, Walden J, Normann C. acute and treatment of Catatonia with risperidone.  Pharmacopsychiatry. 2001;  34 25-26
• 12 Peralta V, Cuesta M J, Serrano J F, Mata I. The Kahlbaum syndrome.  Comprehensive Psychiatry. 1997;  38 61-67