Table 2 - Karl Leonhard's classification of the nonaffective endogenous psychoses68.

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Table 2. Karl Leonhard's classification of the nonaffective endogenous psychoses⁶⁸

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I. Group of systematic schizophrenias

(Insidious onset, auditory and somatic hallucinations, delusions, early blunting of affect, continuous unremitting course, personality deterioration)

Paraphrenias

(Auditory hallucinosis, audible thoughts, thought broadcast, passivity experiences, delusional misidentifications, falsifications of memory)

Hebephrenias

(Extreme autistic withdrawal, flat affect, impoverished or disorganized speech and behaviour)

Catatonias

(Excessive parakinesias, mannerisms, verbigeration, posturing, stereotypies, mutism, auditory hallucinations)

II. Group of unsystematic (atypical) schizophrenias

(Rapid onset, relatively preserved affect, remitting course, mild personality deterioration)

Affect-laden paraphrenia

(Paranoid delusions with affective loading)

Cataphasia (schizophasia)

(Incoherent, pressured speech but well-organized behaviour)

Periodic catatonia

(Episodic hyper- or hypokinesia, mixed excitatory and hallucinatory symptoms)

III. Group of cycloid psychoses

(Sudden onset, pervasive delusional mood, multimodal hallucinations, labile affect, polarity of manifestations, typically complete recovery from episode)

Anxiety-happiness psychosis

(Extreme shifts of affect, polarity e.g. intense fear – ecstatic elation)

Motility psychosis

(Impulsive hypermotility – psychomotor inhibition)

Confusion psychosis

(Incoherent pressure of speech – mutism)

Leonhard's family studies, although richly descriptive, may be methodologically outdated by present-day criteria. However, his conjectures have found support in a twin study,⁷⁰ in which the highest MZ/DZ concordance rate differential was obtained with 'unsystematic' schizophrenia (88.9% MZ, 25.0% DZ) and the lowest with cycloid psychoses (38.5% MZ, 36.4% DZ), consistent with the prediction about the role of genetic factors in the aetiology of the different psychoses. A genome scan of 12 German multiplex pedigrees with periodic catatonia (one of the 'unsystematic' schizophrenias with a 26.9% recurrence risk⁷¹), revealed significant linkage on chromosome 15q15, and suggestive evidence on 22q13.⁷²^,⁷³ The follow-up of the 15q finding has so far excluded the nicotinic acetylcholine receptor alpha7 subunit gene, the zinc transporter SLC30A4, and the NOTCH4 gene.⁷⁴^,⁷⁵^,⁷⁶ The putative 22q13 locus contains the MLC1 (WKL1) gene, coding for a cation channel expressed exclusively in the brain and causing, in its mutated form, a severe neurodegenerative disorder (megaencephalic leukoencephalopathy). A rare missense mutation in this gene, cosegregating with periodic catatonia in a single pedigree was detected, but not confirmed in an independent sample.⁷⁷^,⁷⁸ Although the jury is still out, the apparent clinical homogeneity of the syndrome of periodic catatonia may not be underpinned by genetic homogeneity.

Date: 2016-04-22; view: 796

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