Tuesday, 21.09.2021

Edward Shorter`s comment on Jack R. Foucher et al. Wernicke-Kleist-Leonhard phenotypes of endogenous psychoses : a review of their validity

 

Hector Warnes’ additional comment on Edward Shorter’s comment

 

        I agree that “catatonic states” is a group apart and a differential diagnosis is required (Rasmussen, Mazurek and Rosebush 2016; Stoudemire 1982; Peralta, Cuesta, Serrano et al. 1997).  As such, it may be part of a severe affective disorder but also of a schizophrenia. Originally, the Kahlbaum syndrome was described as a catatonic primary affective disorder with motor manifestations (Kahlbaum 1874). In this form of catatonia, the patient is in a state of psychomotor retardation, mutism, withdrawal, negativism, expresses mostly nihilistic delusions should he/she be able to utter a few words and refuses to eat. One feels that the patient has given up all hopes and wants to die.

        In the latter the patient shows a bizarre conduct, rigidity (Spannungsirresein) with posturing, mannerisms, stereotypies, echolalia, echopraxia, waxy flexibility, staring, negativism and at times stupor. An intravenous injection of sodium amytal or lorazepam may transiently improve the patient who then may express delusional ideas of the type described by Kurt Schneider (1966).

        Should the patient switch to a state of excitement or agitation with hyperkinesis, the diagnosis of motility psychosis (one of three clinical manifestations of cycloid psychosis, the other two being anxiety and/or ecstasy psychosis and confusional psychosis) may apply. Leonhard (1999), using brain imaging techniques and event related potentials in addition to variability in symptomatology (he developed a 22-symptom check list), favorable course and good prognosis, distinguished this group as distinct from schizophrenia and bipolar affective disorders. Franzek and Beckmann (1998), in a systematic twin study in cycloid psychosis, found that monozygotic pairs of twins had similar concordance rates to dizygotic pairs pointing to low heritability. Another excellent paper was published by Brockington, Perris, Kendell et al. (1982) on the course and outcome of cycloid psychosis.

        Eugen Bleuler, in his classical 1911 Dementia Praecox or the Group of Schizophrenias, has a chapter on catatonic states associating them with the motility psychosis of Wernicke. In the akinetic group he described stupor, melancholia attonita and flexibilitas cerea. In the same chapter he described catatonic symptoms associated with melancholic or manic states. With little semiological expertise Bleuler was able to observe changes to catatonic raptus in hyperkinetic states (flight of activities without any purpose). I was very impressed by Bleuler’s clinical acumen.

        Many catatonic states have medical complications because of negativism, refusal to eat or drink, immobility, deep vein thrombosis, pulmonary embolism, pneumonia, muscle contractions, pressure ulcers with infection and so on.

        Fink, Shorter and Taylor (2010) considered catatonia not to be part of the Dementia Praecox group of Kraepelin but an independent syndrome in medical nomenclature.

        Catatonic or stuporous syndromes were noted in herpes encephalitis, in Parkinson's disease, in the neuroleptic malignant syndrome (with a 10% mortality rate), in the stiff person syndrome (considered to be an autoimmune disorder), severe cerebral non-convulsive status epilepticus, akinetic mutism, malignant hyperthermia, the locked-in syndrome (due to a ventral pontine lesion) and severe autistic spectrum disorder.

        I would like to pay tribute to Oliver Sacks (1973) for having researched the survivors of the epidemic of encephalitis lethargica of 1924. These patients still had preserved cognition but remained in severe apathy with catatonic immobility and rigidity (frozen and mute), a total lack of interest, initiative and concentration. The treatment with L-dopa led to an "awakening" or recovery which, however, was not permanent.

        Craddock, O'Donovan and Owen (2005), in concordance with other studies, found that genetically there appear to be differences and common genomic regions implicated in schizophrenia and bipolar disorders or, as they call it, "a gradient of polygenic liability across both disorders." More data point as well to an inflammatory process in acute cases of both disorders, particularly high levels of IL-6-TNF and other cytokine receptors.

        Between the spectrum disorders, the overlapping of many discreet psychiatric syndromes and even by studying genomes, I am confused about the multiplicity of psychiatric illnesses with the implication that certain functions which we have already thoroughly researched (which is true for speech, memory, REM sleep, right and left hemispheric functions, limbic system functions, frontal lobe response to hyper and hypo-perfusion and so on). I raise the point whether lesions found in anatomo-pathological specimens in specific localized brain regions are really hard-wired forever. We presume that there are psychiatric illnesses which are immune to change, that neural connections are permanent and that patients suffering from stroke on the dominant side are not likely to recover their speech which contradicts the evidence that neurogenesis and neuroplasticity has amply shown, even in mice or other animals.

        I am aware that some severe refractory endogenous depressions have a smaller volume of the hippocampus which may in the course of decades lead to dementia.  Neuroplasticity is the capacity of neural networks in the brain to change and kindle their connections in response to sensory stimulation, enriched information load and development which in many cases would repair the damage or dysfunction (just as occurs with the patient with aphasia following a stroke). There are countless neurotransmitters being discovered which inhibit or facilitate neural connectivity and which stimulate myelination, signaling transcription factors, growth factors, metabolism, neural growth, neurogenesis, etc.

 

References:

 

Bleuler E. Dementia praecox oder Gruppe der Schizophrenien. Deuticke Verlag, 1911.

Brockington IF, Perris C, Kendell RE, Hillier VE, Wainwright S. The Course and outcome of Cycloid Psychosis. Psychol. Med.  1982; 12(1): 97-105. 

Craddock N, O´Donovan MC, Owen M J. The genetics of schizophrenia and Bipolar Disorders. J. Med. Genetic. 2005; 42(3):193-204.  

Fink M, Shorter E, Taylor MA. Catatonia is not schizophrenia: Kraepelin's error and the need to recognize catatonia as an independent syndrome in medical nomenclature. Schizophr. Bull. 2010; 36:314-20. 

Franzek E, Beckmann H. Different genetic background of schizophrenia spectrum psychosis: a twin study. Am. J. Psychiatry. 1998; 155;76-83.

Kahlbaum K. Die Katatonie oder das Spannungsirresein, Berlin, Hirschwald, 1874.

Leonhard K. Classification of Endogenous Psychoses and their Differentiated Etiology, 2nd edition. Beckmann H, editor. New York/Wien: Springer Verlag. 1999.

Peralta V, Cuesta MJ, Serrano JF, Mata I. The Kahlbaum syndrome: a study of its clinical validity, nosological status, and relationship with schizophrenia and mood disorder. Compr. Psychiatry. 1997; 38(1):61-7. 

Rasmussen SA, Mazurek MF, Rosebush PI. Catatonia: our current understanding of its diagnosis treatment and pathophysiology World J. Psychiatry. 2016; 6(4):391-8. 

Sacks OW Awakenings. Picador, London. 1973. 

Schneider K. Klinische Psychopathologie (Siebente verbesserte Auflage). Stuttgart, Thieme, 1966. 

Stoudemire A. The differential diagnosis of catatonic states. Psychosomatics. 1982; 23(3):245-52.

 

November 12, 2020