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Donald F. Klein, Max Fink, Edward Shorter and Thomas A. Ban: Comment exchange on Flagrant Catatonic Behavior

Hector Warnes’ general comment on the catatonic type of schizophrenia

 

                Since the first publication on  this disorder Karl Kahlbaum (1874) considered it to have multiple possible causes including neurological ones. Later on Stauder (1934) described the lethal type of this disorder. Oliver Sacks (1973) in his book Awakenings described 20 patients who were survivors of  the influenza pandemic which started in 1918 and caused in many of them encephalitis lethargica (sleeping  sickness). Most of these patients showed symptoms akin to catatonic behavior which responded to L-dopa and from the immobility, rigidity, mutism and negativism they shifted to mobility and the ability to walk and talk. Unfortunately, the treatment was effective for only a short period of time and most relapsed later on or further deteriorated; this was attributed to Parkinson's disease.

            The decline of the classical type of catatonic schizophrenia is not accepted by everyone (Wilcox and Duffy 2015).  It reminds me of the decline of classical hysterical disorders  or conversion hysteria or hysterical dissociation which still prevail in developing countries. Donald Klein and Max Fink attributed this decline  to a neurotropic virus that had mutated and had lost its malignancy, probably like the influenza pandemic virus of 1918. 

            The validity of psychiatric diagnosis has been questioned particularly on long-term follow up studies. Prototypical cases of a disorder 20 years or so ago started to show dimensional and categorical changes that led to the concept of "spectrum disorders" in view of many comparable genetic polymorphism.

            A still good diagnostic tool in classical catatonia would be to inject IV Amytal or 4 mg of Lorazepam which reverses the symptoms of rigidity, mutism and stupor; the patient becomes lucid, while often delusional and the muscular tonus decrease markedly. If we were dealing with a depressive psychomotor retardation in this case, the content of the delusions and affect would be quite different. Tom Ban reminds us that the depressive retardation is not the same as the akinetic and negativistic posturing catatonic behavior. 

            We must remember that the bizarre grimacing, echolalia, stereotypy, mannerism, posturing, verbigeration, automatic obedience, repetitive movements, staring, waxy flexibility and stupor alternating at times with excitement are the text book cases rarely seen since the introduction of the neuroleptics and good nursing care.  Unfortunately, the test with Amytal or Lorazepam lasts only about 30 minutes before the patient regresses to his former state.

            The differential diagnosis is paramount and well described in the paper of Wilcox and Duffy (2015). The DSM 5 largely follows the diagnostic criteria of Kahlbaum. We must keep in mind, of course, a Neuroleptic Malignant syndrome may mimic a catatonic behavior,  a Gilles de la Tourette,  a glioma of the third ventricle, an akinetic mutism, a stiff man syndrome, severe extrapyramidalism, encephalitis, parathyroid adenoma and so on. 

            The lethal form of the disorder, possibly due to refusal of food, dehydration, protracted rigidity and immobility, may lead to pulmonary emboli, edema and even rhabdomyolysis with kidney failure.

 

References:

 

Kahlbaum K. Die Katatonie oder das Spannungsirresein. Klinische Abhandlungen über psychische Krankheiter. Berlin: Hirschwald; 1874.  

Stauder KH.  Die Todliche Katatonie. Arch. Psychiatr Nervenkr. 1934; 102:614-34.

Sacks O. Awakenings. New York: Vintage Press; 1990.

Wilcox JA, Duffy PR. The Syndrome of catatonia. Behav Sci. Basel. 2015; 5: 576-88.

 

May 23, 2019