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Query: UMLS:C0004352 (autism)
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Folk concepts for mental disorder were studied among rural Lao people. While predominatly inferring etiology (e.g. spirit-caused disorder), certain terms also emphasized particular descriptive psychopathology or behavioral abnormality. Preventive strategies were stressed for insanity due to "excessive worry' or "broken taboo'. These broad folk categories of disorder bore considerable similarity to some psychiatric and neurologic categories within medicine. These includes psychosis, mania, neurosis, organic brain syndrome, mental retardation, cerebral palsy, epilepsy, and childhood autism. Lao folk terms for mental disorder also closely resembled those of other southern Asian cultures, although illiterate tribal peoples appeared to have fewer terms than literate peasant peoples. Folk terms from more distant regions had broad similarity to those of southeast Asia, but lacked the specificity found within the region.
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PMID:Folk concepts of mental disorder among the Lao: continuities with similar concepts in other cultures and in psychiatry. 52 21

Despite its chequered history, Kahlbaum's 1874 description of catatonia (tension insanity) and its categorization as a clinical illness is in outline still valid. Kahlbaum also acknowledged the existence of catatonia in children. Corresponding case studies have also been analyzed. The originators and disciples of the Wernicke-Kleist-Leonhard school proved catatonia in early childhood as a discrete entity with specific psychopathology. This does not mean that catatonic symptoms do not occur in other illnesses and in particular in organic psychoses. These are, however, of a totally different nature. Autism, as first described in connection with schizophrenic negativism by Bleuler in 1910, is one of the key symptoms of schizophrenia. As identified by Kanner in 1943, abnormal social interaction and communication, together with retarded development, are the main characteristics of autism in early childhood. Asperger's concept of autistic disorder (1944), although based on psychopathological theory, did not include retardation in development as an aspect. Consequently, autistic behavior can occur in a variety of mental disorders. Research into possible etiological and pathogenetic factors has been undertaken, but no clear link found as yet.
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PMID:Classification matters for catatonia and autism in children. 1669 88

Kraepelin's dichotomy, manic-depressive insanity and dementia praecox, are contrasting and true endogenous disease entities which affect excitability, the fundamental property of the CNS. Kraepelin wanted to establish a valid classification and hit the extremes in brain structure and function at a time when we had no knowledge of brain dysfunction in "functional" psychoses. The aetiology is now known: the psychoses are part of human growth and maturation and might be classified according to their brain dysfunction, which is exactly what Kraepelin wanted. However, presumably to reduce the stigma attached to the word "psychosis", there is currently a strong initiative to eliminate the concept. But knowledge of what is happening in the brain in a psychosis might be more helpful in reducing stigma. It is suggested that psychosis is due to an affection of the supplementary motor area (SMA), located at the centre of the Medial Frontal Lobe network. The SMA is one of the rare universally connected areas of the brain, as should be the case for such a key structure that makes decisions as to the right moment for action. This important network, which partly has continuous neurogenesis, has sufficiently widespread connections. The SMA, a premotor area located on the medial side of the frontal lobes, is one of the last regions to reach a concurrence of synaptogenesis. An affection of the SMA, a deficient or abolished Delayed Response Task, seriously disturbs our relation and adaptation to the surroundings. We usually master the Delayed Response Task around the age of 7 months, a time at which the second CNS regressive event takes place, which proceeds from the posterior to the anterior of the brain. In very late maturation, a persistent affection of the SMA might occur. We experience a chronic psychosis: infantile autism (IA), a chronic inability to act consciously, which contrasts with the episodic SMA affection post-puberty, when excitation is reduced due to excessive pruning of excitatory synapses. Silent spots are the result of insufficient fill-in mechanisms following a breakdown of circuitry. They may affect the SMA in the case of very late puberty. An acute reduction in excitation and concomitantly a marked increase in silent spots might lead to an acute psychosis. A frontal preference is likely, given that a reduction might occur anywhere in the cortex, but particularly in the areas maturing latest. The varying localisations probably explain the difficulty in accepting schizophrenia as a disease entity. The multifactorial inheritance of the dichotomy implies that the genetics are not fate, a psychotic development might be prevented given enough epigenetic factors: brain food (omega 3). Might the present dietary adversity, with its lack of brain food, be responsible for a rising incidence in psychosis? A psychosis is an understandable and preventable dysfunction of the brain, and its mechanisms are known. Primarily a disorder of reduced excitation in an attenuated CNS, this explains why all the neuroleptics are convulsants, raising excitation, in contrast to all antidepressives, which are anti-epileptic.
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PMID:What is a psychosis and where is it located? 1851 23

MODERN PSYCHIATRIC NOSOLOGIES SEPARATE CATATONIA ALONG THE LINES OF PRESUMED ETIOLOGY: bipolar, major depression, schizophrenia, and/or due to a general medical condition. Catatonic signs have always possessed significant diagnostic, therapeutic, and prognostic value. Kahlbaum's description of this syndrome in his monograph "Katatonia" included careful documentation of phenomenology. Kahlbaum selected the term katatonia to describe "tension insanity." He felt that the neuromotor signs were more important than the content of delusions (e.g. megalomania). While he felt that he was describing a unitary illness, he did identify mood disturbance, psychosis, and medical factors in this new illness.(1) In modern times, the term catatonia has become limited to describe a specifier of neuropsychiatric illnesses.The authors of this article feel that the term katatonia should be used to describe a group of neuropsychiatric illnesses presenting with catatonic signs. This may prevent the misconception that "catatonia is schizophrenia" and improve the detection of katatonia in patients. Specifically, katatonia is also observed in mood disorders, general medical conditions, and pervasive developmental disorders. The literature also supports the view of Dr. Leo Kanner and his description for neuromotor and neuropsychiatric signs in autistic disorder. This scale is named in honor of Dr. Kanner. It was developed by the authors and includes some of Dr. Kanner's core concepts. This paper will identify the clinical features of katatonia and introduce the KANNER scale (see Appendix 1) to improve conceptualization, detection, and measurement of this important clinical syndrome.
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PMID:Katatonia: a new conceptual understanding of catatonia and a new rating scale. 1972 75

Epidemiologic studies, including prospective birth cohort investigations, have implicated maternal immune activation in the etiology of neuropsychiatric disorders. Maternal infectious pathogens and inflammation are plausible risk factors for these outcomes and have been associated with schizophrenia, autism spectrum disorder, and bipolar disorder. Concurrent with epidemiologic research are animal models of prenatal immune activation, which have documented behavioral, neurochemical, neuroanatomic, and neurophysiologic disruptions that mirror phenotypes observed in these neuropsychiatric disorders. Epidemiologic studies of maternal immune activation offer the advantage of directly evaluating human populations but are limited in their ability to uncover pathogenic mechanisms. Animal models, on the other hand, are limited in their generalizability to psychiatric disorders but have made significant strides toward discovering causal relationships and biological pathways between maternal immune activation and neuropsychiatric phenotypes. Incorporating these risk factors in reverse translational animal models of maternal immune activation has yielded a wealth of data supporting the predictive potential of epidemiologic studies. To further enhance the translatability between epidemiology and basic science, the authors propose a complementary approach that includes deconstructing neuropsychiatric outcomes of maternal immune activation into key pathophysiologically defined phenotypes that are identifiable in humans and animals and that evaluate the interspecies concordance regarding interactions between maternal immune activation and genetic and epigenetic factors, including processes involving intergenerational disease transmission. [AJP AT 175: Remembering Our Past As We Envision Our Future October 1857: The Pathology of Insanity J.C. Bucknill: "In the brain the state of inflammation itself either very quickly ceases or very soon causes death; but when it does cease it leaves behind it consequences which are frequently the causes of insanity, and the conditions of cerebral atrophy." (Am J Psychiatry 1857; 14:172-193 )].
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PMID:Maternal Immune Activation and Neuropsychiatric Illness: A Translational Research Perspective. 3022 Feb 21