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)

Although psychiatric symptoms are not rare in Wilson's disease (WD), their association with epileptic seizures has not been reported. We describe three patients with such clinical manifestations who had predominantly cerebral white matter lesions in the frontal lobe. There were two men and one woman with ages ranging from 20 to 26 yr. The early presentations were psychiatric symptoms and epileptic seizures with or without secondary generalization. The psychiatric features were usually misinterpreted as schizophrenia-like disease and the diagnosis was delayed. The cerebral white matter lesions on magnetic resonance imaging (MRI) were usually asymmetric and mainly restricted to the frontal lobes. The present observation suggests that early onset of psychiatric manifestations and seizures commonly occur in WD with frontal white matter lesions.
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PMID:Psychosis and epileptic seizures in Wilson's disease with predominantly white matter lesions in the frontal lobe. 1859 Oct 1

Drug-induced parkinsonism (DIP) is condition that mimics Parkinson's disease. Characterized mainly by rigidity and bradykinesia, it has less prominent tremor and gait instability. DIP is generally caused by lipophilic drugs that "block" dopamine D2 receptors in the brain, although presynaptic dopamine depletion, false transmitters, mitochondrial respiratory chain dysfunction, and overactivity in the gamma-aminobutyric acid (GABA)ergic system or cholinomimetic action have also been postulated as possible mechanisms. The onset of DIP is acute to subacute. It is more common in women and has a bimodal age distribution. Other diseases that can resemble DIP include neuropsychiatric conditions (eg, depression, negative symptoms of schizophrenia) and Wilson's disease. Physicians may be able to prevent DIP by prescribing neuroleptic agents appropriately and with caution. The risk of DIP is presumably lower with the use of "atypical" antipsychotic agents but it is not eliminated, especially in those most vulnerable to parkinsonism (eg, the elderly or cognitively impaired). The best treatment is discontinuation of the provoking medication. Prospective studies are needed to further define the mechanism of DIP, identify individual susceptibility, determine the impact of atypical antipsychotic agents, and develop further treatment options for those unable to stop the offending agent.
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PMID:Drug-induced parkinsonism. 1936 50

Sydenham's chorea is the most frequently acquired movement disorder in childhood and is characterized by involuntary and abrupt movement patterns. Some patients also show neuropsychiatric dysfunctions and psychiatric disorders, including anxiety, obsessive-compulsive disorders and tic disorders. In contrast, the association with psychotic symptoms has been reported very rarely up to now (n=4, two case reports, one prospective and one retrospective study). We report on a 12-year-old girl with acute paranoid hallucinatory symptoms and choreiform movements. Whereas her paranoid-hallucinatory symptoms responded to antipsychotic therapy, the negative symptoms and choreiform movement patterns only disappeared during additional prednisolone treatment. After tapering prednisolone, her negative symptoms and the choreiform movements reappeared. Dysfunctions of the corpus striatum have been linked to the pathogenesis of schizophrenia. This striatal dysfunction may secondarily affect working memory and the prefrontal cortex, resulting in impaired cognitive flexibility. Choreiform movements in chorea minor are attributed to dysfunction of the basal ganglia based on post-streptococcal autoimmune-mediated mechanisms. Huntington's disease and Wilson's disease are movement disorders caused by basal-ganglia dysfunction and are also associated with psychotic symptoms. In the present case, the association of psychotic and choreiform symptoms might be caused by dysfunction of the basal ganglia. The negative symptoms may result from disturbances of the prefrontal cortex impaired by basal-ganglia dysfunction.
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PMID:[Schizophreniform symptoms in Chorea Minor--case report and literature review]. 2046 57

Transcranial sonography, which displays tissue echogenicity of the brain through the intact skull, reveals reduced echogenicity of the brainstem raphe (BR) as a characteristic finding in unipolar depression and in depression associated with Parkinson's or Wilson's disease, but in general not in healthy adults, bipolar affective disorders, schizophrenia, multiple sclerosis with depression, or Parkinson's disease without concomitant depression. The reason for the reduced echogenicity of the BR is not entirely clear. Magnetic resonance imaging investigations, however, provide evidence that the signal alteration may be caused by a modification of tissue cell density, the interstitial matrix composition, or an alteration of fiber tracts integrity. An involvement of the basal limbic system in the pathogenesis of unipolar depression and depression associated with certain neurodegenerative diseases is assumed.
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PMID:Transcranial sonography in depression. 2069 7

The blue copper protein ceruloplasmin has been of interest to psychiatrists for decades following Heilmeyer's observation of elevated serum copper levels in schizophrenic patients. Immunoturbidimetry, however, does not yield elevated serum ceruloplasmin concentrations in schizophrenia while ceruloplasmin-related oxidase activity appears to be elevated in patients with schizophrenia and reduced in patients with Alzheimer's disease. Low serum concentrations of immuno-turbidimetrically measured ceruloplasmin, and of oxidase activity, are typical of Wilson's disease, Menkes' disease, and aceruloplasminemia, three familial neurodegenerative disorders of pronounced variability, with regard to both genotype and phenotype. Especially patients with Wilson's disease may exhibit behavioural symptoms only over a long period. Heterozygous carriers of Wilson's disease and aceruloplasminaemia may have low serum ceruloplasmin concentrations; they will not develop somatic symptoms, but the significance of these carrier states, or of "hypoceruloplasminaemia", with regard to mental disorders is unknown.
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PMID:[The role of ceruloplasmin in the differential diagnosis of neuropsychiatric disorders]. 2081 66

A series of 31 cases of Wilson's disease (WD) were assessed retrospectively on a range of variables including psychiatric, neurologic and biochemical data recorded at index admission over a period of 7 years. 18 patients (58%) showed psychopathological features. 5 patients (16.1%) were reported to have poor scholastic performance at the onset of illness and 1 patient (3.2%) had abnormal behaviour (mania like) many years prior to the appearance of neurological symptoms. The most common psychiatric features were cognitive impairment (45.2%), affective symptomatology (41.9%) and behavioural abnormalities (29%). Only one patient had a schizophrenia like psychosis. The psychiatric manifestation of Wilson's disease as they present in our setting and their clinical relevance are discussed.
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PMID:The psychiatric aspects of wilson's disease-a study from a neurology unit. 2158 32

Homeostasis of metal ions such as Zn(2+) is essential for proper brain function. Moreover, the list of psychiatric and neurodegenerative disorders involving a dysregulation of brain Zn(2+)-levels is long and steadily growing, including Parkinson's and Alzheimer's disease as well as schizophrenia, attention deficit and hyperactivity disorder, depression, amyotrophic lateral sclerosis, Down's syndrome, multiple sclerosis, Wilson's disease and Pick's disease. Furthermore, alterations in Zn(2+)-levels are seen in transient forebrain ischemia, seizures, traumatic brain injury and alcoholism. Thus, the possibility of altering Zn(2+)-levels within the brain is emerging as a new target for the prevention and treatment of psychiatric and neurological diseases. Although the role of Zn(2+) in the brain has been extensively studied over the past decades, methods for controlled regulation and manipulation of Zn(2+) concentrations within the brain are still in their infancy. Since the use of dietary Zn(2+) supplementation and restriction has major limitations, new methods and alternative approaches are currently under investigation, such as the use of intracranial infusion of Zn(2+) chelators or nanoparticle technologies to elevate or decrease intracellular Zn(2+) levels. Therefore, this review briefly summarizes the role of Zn(2+) in psychiatric and neurodegenerative diseases and highlights key findings and impediments of brain Zn(2+)-level manipulation. Furthermore, some methods and compounds, such as metal ion chelation, redistribution and supplementation that are used to control brain Zn(2+)-levels in order to treat brain disorders are evaluated.
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PMID:Brain-Delivery of Zinc-Ions as Potential Treatment for Neurological Diseases: Mini Review. 2210 82

Wilson's disease (WD) or hepatolenticular degeneration is an inherited neurodegenerative disorder of copper metabolism (autosomal recessive, chromosome13). Psychiatric disorders in WD include dementia, characterized by mental slowness, poor concentration, and memory impairment. Symptoms may progress rapidly, especially in younger patients, but are more often gradual in development with periods of remission and exacerbation. Delusional disorder and schizophrenia-like psychosis are rare forms of psychiatric presentation. In this report, the patient with WD presented by psychosis symptoms and treated mistaken as schizophrenia for almost ten years. Although he has treated with antipsychotics, he had periods of remissions and relapses and never was symptoms free. Since psychosis can be the manifestation of medical diseases such as WD, overall view of these patients is necessary and medical diseases should be considered as a differential diagnosis.
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PMID:Mismanagement of Wilson's disease as psychotic disorder. 2332 92

Possible underlying organic causes of psychiatric symptoms can be overlooked in the clinical setting. It is important to increase awareness amongst psychiatric and neurological professionals with regard to certain inborn errors of metabolism as, in some cases, disease-specific therapies are available that can, for instance, treat underlying metabolic causes. The following article describes the basic pathophysiology, clinical and neurological features, and available diagnostic procedures of six treatable metabolic diseases that are associated with neuropsychiatric symptoms: Wilson's disease, cerebrotendinous xanthomatosis, porphyrias, homocysteinemia, urea cycle disorders, and Niemann-Pick disease type C (NP-C). NP-C is taken as a particularly relevant example because, while it is traditionally considered to be a condition that presents with severe neurological and systemic manifestations in children, an increasing number of patients are being detected who have the adolescent- or adult-onset form, which is frequently associated with neuropsychiatric signs. A notable proportion of adult-onset cases have been reported where NP-C has mistakenly been diagnosed and treated as a psychiatric condition, usually based on patients' initial presentation with psychotic or schizophrenia-like symptoms. Underlying organic causes of psychiatric disorders such as psychosis should be considered among patients with atypical symptoms and/or resistance to standard therapy. Alongside improved frameworks for additional multidisciplinary diagnostic work in patients with suspected organic disease, the development of convenient and affordable biochemical screening and/or diagnostic methods has enabled new ways to narrow down differential diagnoses.
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PMID:Psychiatric signs and symptoms in treatable inborn errors of metabolism. 2514 92

Movement disorders are common in psychiatry. The movement disorder can either be the symptom of a psychiatric disorder, can share a common aetiological factor with it, or can be the consequence of psychopharmacological therapy. Most common features include tic, stereotypy, compulsion, akathisia, dyskinesias, tremor, hypokinesia and disturbances of posture and gait. We discuss characteristics and clinical importance of these features. Movement disorders are frequently present in mood disorders, anxiety disorders, schizophrenia, catatonia, Tourette-disorder and psychogenic movement disorder, leading to differential-diagnostic and therapeutical difficulties in everyday practice. Movement disorders due to psychopharmacotherapy can be classified as early-onset, late-onset and tardive. Frequent psychiatric comorbidity is found in primary movement disorders, such as Parkinson's disease, Wilson's disease, Huntington's disease, diffuse Lewy-body disorder. Complex neuropsychiatric approach is effective concerning overlapping clinical features and spectrums of disorders in terms of movement disorders and psychiatric diseases.
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PMID:[Movement disorders is psychiatric diseases]. 2557 84


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