Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036341 (schizophrenia)
 60,220 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We studied 55 patients admitted during 14 months to two inpatient psychiatric units of a municipal hospital who exhibited one or more of the catatonic signs of mutism, stereotypy, posturing, catalepsy, automatic obedience, negativism, echolalia/echopraxia, or stupor. Only four of the 55 patients satisfied our research criteria for schizophrenia, whereas over two thirds had diagnosable affective disorders, usually mania. The eight catatonic motor signs were nonspecific and homogeneously distributed among the various research diagnostic groups, with the number and type of individual signs unrelated to short-term treatment outcome. A favorable treatment response was shown for the entire catatonic sample, with two thirds markedly improved or in remission at the time of discharge. These findings are consistent with those of other investigators of the catatonic syndrome for the past 100 years.
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PMID:Catatonia. A prospective clinical study. 126 74

Catatonia, once solely attributed to schizophrenia, is now thought to be associated with many disorders. Autistic disorder shares some symptoms with catatonia, namely, mutism, echopraxia/echolalia, and sterotypes. Catatonia in autism may therefore be a variant of the autistic condition. However, organic deficits and psychiatric disorders, such as bipolar disorder, have also been deficits and psychiatric disorders, such as bipolar disorder, have also been linked with the manifestation of catatonia. Individuals with autism presenting with these comorbid conditions may therefore be at increased risk for catatonia. Little is written of the association of autism and catatonia to clarify the possibility of catatonia as a variant or a sign of a comorbid condition. The authors discuss three autistic patients and suggest specific etiologies for the symptoms of catatonia which presented in these cases. The therapeutic and diagnostic importance of comorbid disorders in autism is stressed.
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PMID:Catatonia in autistic disorder: a sign of comorbidity or variable expression? 177 64

The hypothesis that some symptoms of schizophrenia only manifest in the early stages whereas others only appear later is tested with 33 inpatients in 'terminal states'. It is found that while the onset shows no specificity, the outcome is very typical. The initial symptoms are polymorphous; thought disorders can be found in less than one third of the patients and frank incoherence approaching the severity of schizophasia not at all. Many years later appear symptoms registered as paralogism, echolalia, verbigeration, stilted speech, neologism, hypotonic thinking, retardation, derailment, and incongruous answers. Only then, sometimes 25 years after the onset of the illness, the peculiar and highly specific picture of the schizophasic disorder becomes established.
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PMID:Long-term study of schizophasic patients. 408 22

Language and behavioral deviance in early childhood in preschizophrenia individuals suggests that the pathologic processes predisposing to schizophrenia are present from early in life. However, the etiologic antecedents of such impairments, and the degree to which they predict adult schizophrenia, have not been conclusively demonstrated. To address this, we examined language and behavioral predictors of adult psychiatric outcome in a population cohort (72 individuals with schizophrenia or schizoaffective disorder, 63 of their unaffected siblings, and 7,941 with no diagnosis) evaluated prospectively with behavioral examinations and a speech and language evaluation at 8 months, 4 years, and 7 years of age. Psychiatric outcome was ascertained via adult treatment contacts, and diagnoses were made by chart review according to DSM-IV criteria. Social maladjustment at age 7 was found to predict adult schizophrenia, and focal deviant behaviors (e.g., echolalia, meaningless laughter) at ages 4 and 7 were significantly associated with both schizophrenia and sibling status. Unintelligible speech at age 7 was a highly significant predictor of adult schizophrenia (odds ratio = 12.7), and poor expressive language ability predicted both schizophrenia and unaffected sibling outcome. Early behavioral and language dysfunction did not differentially characterize preschizophrenia subjects with a history of fetal hypoxia or an early age of first treatment contact. Given that unaffected siblings show similar signs of deviance, such problems may indicate genotypic susceptibility to the disorder, or shared environmental influences, or both.
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PMID:A prospective cohort study of childhood behavioral deviance and language abnormalities as predictors of adult schizophrenia. 1088 39

The authors report on five patients who first developed Tourette's syndrome (TS) and later schizophrenia with the typical positive and negative symptoms; all five had an unfavorable course of schizophrenia. These observations as well as other reported cases raise the question of whether both disorders may share a common background. This is discussed under the aspects of similar symptomatology (echolalia, motor symptoms, cognitive deficits, obsessive-compulsive symptoms), similar pathophysiological signs, genetics and signs of an underlying inflammatory process in subgroups of cases, as well as common therapeutic strategies. A genetically determined susceptibility could possibly underlie both disorders, e.g., an autoimmunologically triggered inflammation or a common pathophysiology of certain symptoms. Both disorders show disturbances of the multiple functional pathways, which seem to be involved in the pathophysiology of both. The clinical overlap of TS and of schizophrenia may be due to a final common pathophysiological pathway.
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PMID:Comorbidity of Tourette's syndrome and schizophrenia--biological and physiological parallels. 1250 10

This study examines in detail - i) the magnitude, nature and severity of thought disorder in schizophrenia, ii) the correlations between type and severity of thought disorder with socio-demographic and clinical variables, and iii) differences between different subtypes of schizophrenia. Forty five schizophrenics (Research Diagnostic Criteria) were assessed by 'live' interview as well as tape recorded interviews. Instruments used for assessment were (a) Scale for assessment of Thought, Language and Communication (Andreasen 1978), (b) Brief Psychiatric Rating Scale (Overall & Gorham 1962), (c) Mini Mental State (Folstein 1975), and (d) Clinical and demographic data recording proforma. The Schizophrenic patients were subdivided as (i) Acute and chronic (R.D.C.), (ii) Paranoid and non-paranoid; and (iii) Negative, positive, mixed (Andreasen's criteria) and intragroup and intergroup differences were computed.Poverty of speech, tangentiality, derailment, loss of goal, perseveration were found to be the commonest thought disorders. Positive and negative thought disorders were seen in equiproportion in both positive and negative schizophrenics. Significant differences were noted between thought disorders and education as well as habitat. Rural patients more often had negative formal thought disorders. Literates had more often clanging, neologism, circumstantiality and echolalia. This study provides ample information on the nature of thought disorder in Indian schizophrenic subjects.
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PMID:A study of thought, language and communication (T.L.C) disorders in schizophrnia. 2192 21

Catatonia, originally described by Karl Kahlbaum in 1874, may be regarded as a set of clinical features found in a subtype of schizophrenia, but the syndrome may also stem from organic causes including vascular parkinsonism, brain masses, globus pallidus lesions, metabolic derangements, and pharmacologic agents, especially first generation antipsychotics. Catatonia may include paratonia, waxy flexibility (cerea flexibilitas), stupor, mutism, echolalia, and catalepsy (abnormal posturing). A case of catatonia as a result of acute renal failure in a patient with dementia with Lewy bodies is described. This patient recovered after intravenous fluid administration and reinstitution of the atypical dopamine receptor blocking agent quetiapine, but benzodiazepines and amantadine are additional possible treatments. Recognition of organic causes of catatonia leads to timely treatment and resolution of the syndrome.
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PMID:Renal failure in dementia with lewy bodies presenting as catatonia. 2346 22

Associations between large cavum septum pellucidum and functional psychosis disorders, especially schizophrenia, have been reported. We report a case of late-onset catatonia associated with enlarged CSP and cavum vergae. A 66-year-old woman was presented with altered mental status and stereotypic movement. She was initially treated with aripiprazole and lorazepam. After 4 weeks, she was treated with electroconvulsive therapy. By 10 treatments, echolalia vanished, and catatonic behavior was alleviated. Developmental anomalies in the midline structure may increase susceptibility to psychosis, even in the elderly.
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PMID:Cavum septum pellucidum and cavum vergae with late-onset catatonia. 2367 24

In the new classification of the DSM-V, catatonia is individualized as a disease of its own. It is defined by presence of at least two out of five criteria: motor immobility, negativism, echolalia or echopraxia, sterile motor activity, atypical movements. The priority is to look first for organic causes: the main ones are neurologic disorders. Intoxication may also be found (illegal drugs or medication), and the role of neuroleptic malignant syndrome in catatonia remains unclear. Among the psychiatric causes, first come bipolar disorders, especially mania; then schizophrenia. Idiopathic forms can also be observed. Epidemiological work on catatonia show highly variable results, highlighting a possible underestimation of the diagnosis. Among the differential diagnoses, which are rare motor syndromes, neuroleptic malignant syndrome and serotonin syndrome are also discussed. The diagnosis of catatonia is clinical and can be obtained using standardized diagnostic scales. The use of zolpidem provides both a diagnostic and therapeutic guidance for the degree of response to drug treatment. The physiopathological hypotheses describe an intracerebral GABAergic, dopaminergic and glutamatergic dysfunction in catatonic patients. The complete mechanisms are still partly unknown. Benzodiazepines are the first treatment of choice. Electroconvulsive therapy is used secondarily or in severe cases. First-generation antipsychotics are prohibited, at the risk of worsening the catatonia in becoming malignant and lethal. The renewed interest in the catatonic syndrome during the past recent years has expanded research on the mechanisms of this syndrome and opened the way to new therapeutic options. The latest works tend to modulate the strict prohibition of antipsychotic in a catatonic patient.
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PMID:[Catatonia]. 2585 94

Background: Catatonic phenomena such as stupor, mutism, stereotypy, echolalia, echopraxia, affective flattening, psychomotor deficits, and social withdrawal are characteristic symptoms of both schizophrenia and autism spectrum disorders (ASD), suggesting overlapping pathophysiological similarities such as altered glutamatergic and dopaminergic synaptic transmission and common genetic mutations. In daily clinical practice, ASD can be masked by manifest catatonic or psychotic symptoms and represent a diagnostic challenge, especially in patients with unknown or empty medical history. Unclear diagnosis is one of the main factors for delayed treatment. However, we are still missing diagnostic recommendations when dealing with ASD patients suffering from catatonic syndrome. Case presentation: A 31-year-old male patient without history of psychiatric disease presented with a severe catatonic syndrome and was admitted to our closed psychiatric ward. After the treatment with high-dose lorazepam and intramuscular olanzapine, catatonic symptoms largely remitted, but autistic traits persisted. Following a detailed anamnesis and a thorough neuropsychological testing, we diagnosed the patient with high-functioning autism and catatonic schizophrenia. The patient was discharged in a remitted state with long-acting injectable olanzapine. Conclusion: This case represents an example of diagnostic and therapeutic challenges of catatonic schizophrenia in high-functioning autism due to clinical and neurobiological overlaps of these conditions. We discuss clinical features together with pathophysiological concepts of both conditions. Furthermore, we tackle social and legal hurdles in Germany that naturally arise in these patients. Finally, we present diagnostic "red flags" that can be used to rationally select and conduct current recommended diagnostic assessments if there is a suspicion of ASD in patients with catatonic syndrome in order to provide them with the most appropriate treatment.
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PMID:Two Sides of the Same Coin: A Case Report of First-Episode Catatonic Syndrome in a High-Functioning Autism Patient. 3103 60


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