Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P50583 (asymmetrical)
 12,197 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Reversal or reduction of normal structural cerebral asymmetries may be related to the pathogenesis of schizophrenia, but this relationship remains controversial. We review the literature and describe a further study designed to detect whether anomalous asymmetries are present early in the illness (at the first episode), whether they predict deficits in language processing, and whether they may be related to a genetic predisposition for schizophrenia. Asymmetries of brain widths and segments of the sylvian fissure were assessed in a magnetic resonance imaging study of 87 patients with a first episode of schizophrenia and 52 normal controls. These asymmetries were correlated with specific measures of language processing, memory, and hand skill. An independent group of 14 pairs of siblings with schizophrenia were also evaluated for evidence of heritability to cerebral asymmetries. Width asymmetries were reduced in patients compared with controls in the posterior (p = 0.02) and occipital (p = 0.05) regions. Brain horizontal length, on the other hand, was significantly more asymmetrical in patients (left > right; p = 0.04). For sylvian fissure measurements, asymmetries in controls (left > right) were greatest for the horizontal component; this asymmetry tended to detect differences in patients by comparison with controls (p < 0.06). In a range of tests of language and memory, few significant correlations between performance and cerebral asymmetries were detected either in patients or controls, although patients consistently scored poorer than controls in the majority of tests. In 14 pairs of psychotic siblings, within-pair correlations for the horizontal sylvian fissure asymmetry were significantly greater than between-pair correlations. These findings are consistent with the early presence (possibly genetic) of anomalous cerebral asymmetry. However, the functional correlates of reduced asymmetry remain obscure.
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PMID:Anomalous cerebral asymmetry and language processing in schizophrenia. 916 36

Pathologically asymmetrical P300 fields with right lateralized peaks were described in core schizophrenia as an expression of left-temporal functional deficits, while higher than normal amplitudes were found in cycloid psychosis. This latter finding appeared to be specific for cycloid psychosis and was explained by a generalized cerebral hyperarousal. Based on some psychopathological analogies with cycloid psychosis, and on the comparable pharmacological treatment of the acute episodes, a group of 19 manic patients was investigated immediately after remission and clinical stabilization of an episode. Patients with psychotic features were excluded to avoid overlaps with cycloid psychosis. Patients showed normal P300 amplitudes and no pathological asymmetries of the field, but more posterior positive areas compared to age- and sex-matched controls. This indicates that the neurophysiological changes underlying mania are different from both core schizophrenia and cycloid psychosis. Based on previous three-dimensional source location studies, this finding indicates that disinhibition due to reduced frontal lobe activity, and not hyperarousal, is the basic functional mechanism of manic disorders.
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PMID:Distinct neurophysiological mechanisms for manic and cycloid psychoses: evidence from a P300 study on manic patients. 987 88

A 43-year-old, right-handed woman experienced right hand paresthesias and a visual field abnormality. We attributed her symptoms to psychiatric abnormalities, due to the presence of delusions and auditory hallucinations. Upon photostimulation, she experienced left visual field hallucinations and demonstrated slow waves on the right parieto-occipital regions. The clinical and electro-encephalographic findings suggested that these episodes were epileptic seizures originating from the right occipital region. Ictal fear appeared at the end of the seizure, reflecting the spread of seizure activity to the mesial temporal region. Ictal SPECT images showed hyper-perfusion in the right occipital region and left cerebellar cortex. rCBF in the occipital lobe was significantly asymmetrical. When we encounter an epileptic patient with psychosis who has a visual hallucination, we should consider the possibility of epileptic seizure originating from the occipital lobe.
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PMID:[Ictal visual hallucination intermittent photic stimulation: using evaluation of the clinical findings, ictal EEG, ictal SPECT, and rCBF]. 1051 57

There is evidence that brain lateralization underlying hemispheric specialization can be observed also at biochemical level. However, hemispheric differences in nitric oxide mediator system have not yet been evaluated. The hippocampus and planum temporale are highly asymmetrical regions but the degree of their laterality is altered in demented or psychotic people. In the study, l-glutamate/l-arginine/l-citrulline concentrations, nitric oxide synthase activities/expressions and nitrites/nitrates levels were estimated in autoptic hippocampi. Right/left laterality in endothelial synthase activity and in nitrites/nitrates was observed in controls. Lateral changes were estimated in patients with Alzheimer disease (a marked increase in activities of constitutive synthases and in expression of inducible enzyme in the left side) and schizophrenia (an increase in activities of all enzymes especially in the right side). Significant shifts from positive to negative correlations were found between laterality of some components of nitric oxide pathway and of planum temporale volumetry under pathological conditions. The hippocampal nitric oxide system appears to be globally right/left lateralized, especially via actions of highly asymmetrical endothelial synthase. The results suggest a specific involvement of all synthases in the development of selected diseases and show that lateral analyses are of sufficient sensitivity to reveal subtle links. The volumetric asymmetry of the planum temporale as a marker of handedness is not probably simply linked to brain laterality at biochemical level but reflects alterations due to pathological processes.
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PMID:Lateralization of hippocampal nitric oxide mediator system in people with Alzheimer disease, multi-infarct dementia and schizophrenia. 1864 32

The cardinal symptoms of Parkinson disease (PD) are asymmetrical bradykinesia, rigidity, resting tremor and postural instability. However, the presence and spectrum of, and disability caused by, nonmotor symptoms (NMS) are being increasingly recognized. NMS include dementia, psychosis, depression and apathy, and are a major source of disability in later stages of PD, in association with axial symptoms that are resistant to levodopa therapy. The model of clinical progression of PD should, therefore, incorporate NMS, instead of being restricted to motor signs and levodopa-induced motor complications. Patients with disabling motor complications are classified as having advanced PD, which has been thought to represent the ultimate stage of disease. However, deep brain stimulation to treat motor complications has dramatically changed this scenario, with implications for the definition of advanced-stage disease. As treatment improves and survival times increase, patients are increasingly progressing to a later phase of disease in which they are highly dependent on caregivers, and disability is dominated by motor symptoms and NMS that are resistant to levodopa. In this article, we review the changing landscape of the later stages of PD, and propose a definition of late-stage PD to designate patients who have progressed beyond the advanced stage.
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PMID:Late-stage Parkinson disease. 2277 51

Review of the first comprehensive meta-analysis of VBM (voxel-based morphometry) studies in schizophrenia indicates asymmetrical reductions of anterior cingulate gyrus to the right, and medial temporal lobe (including the uncus) and para-hippocampal gyrus to the left. In subsequent meta-analyses of schizophrenia and bipolar disorder change in these limbic structures is systematically related to change in the insula. Deficits in insula (and para-hippocampal gyrus) to the left, and dorsal anterior cingulate gyrus to the right are greater in schizophrenic psychoses whereas deficits in anterior cingulate to the left and insula to the right are greater in bipolar illness. Thus (1) brain structures implicated in schizophrenia include those implicated in bipolar disorder, (2) the variation that separates the prototypical psychoses may be a subset of that relating to the structural asymmetry (the "torque") characteristic of the human brain, and (3) the meta-analysis of Bora et al. (2012) indicates that laterality of involvement of the insula and cingulate gyrus across the spectrum of bipolar and schizophrenic psychoses is critically dependent upon the sex ratio. Thus structural change underlying the continuum of psychosis relates to the interaction of laterality and sex.
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PMID:Laterality interacts with sex across the schizophrenia/bipolarity continuum: an interpretation of meta-analyses of structural MRI. 2401 47

A man presenting in his 50s, following conviction for a non-violent crime, to forensic psychiatric services, and then to a neuropsychiatry service with an unusual presentation of psychosis: second person auditory hallucinations, grandiose delusions and somatic delusions. Detailed collateral and family history revealed a background of progressive cognitive deficit and a family history of motor neuron disease. MRI of the brain revealed asymmetrical parieto-occipital volume loss and genetic testing demonstrated a pathogenic expansion of the chromosome 9 open reading frame 72 (C9ORF72) gene consistent with familial frontotemporal dementia caused by a hexanucleotide repeat expansion at C9ORF72, a recently discovered cause of familial frontotemporal dementia/motor neuron disease. This form of frontotemporal dementia should be considered as an important potential differential diagnosis for patients presenting with psychotic symptoms in later life, in whom a detailed family history and thorough cognitive assessment is essential.
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PMID:Neurodegenerative disorder masquerading as psychosis in a forensic psychiatry setting. 2492 30

Clinical indications of amyloid imaging in atypical dementia remain unclear. We report a 68-year-old female without past psychiatric history who was hospitalized for auditory hallucinations and persecutory delusions associated with cognitive and motor deficits. Although psychotic symptoms resolved with antipsychotic treatment, cognitive and motor impairments remained. She further showed severe visuoconstructive and executive deficits, ideomotor apraxia, elements of Gerstmann's syndrome, bilateral agraphesthesia and discrete asymmetric motor deficits. Blood tests were unremarkable. Structural brain imaging revealed diffuse fronto-temporo-parietal atrophy, which was most severe in the parietal regions. Meanwhile, FDG-PET suggested asymmetrical fronto-temporo-parietal hypometabolism, with sparing of the posterior cingulate gyrus. A diagnosis of possible corticobasal syndrome (CBS) was made. Amyloid-PET using the novel tracer NAV4694 was ordered, and revealed significant deposition of fibrillar amyloid (SUVR 2.05). The primary diagnosis was CBS with underlying Alzheimer pathology and treatment with a cholinesterase inhibitor was initiated. Determination of underlying pathological CBS subtype is not simple even when based on extensive investigation including clinical presentation, atrophy patterns on MRI, and regional hypometabolism on FDG-PET. By contrast, amyloid imaging quickly confirmed Alzheimer pathology, and allowed rapid initiation of treatment in this complex case with early psychiatric symptoms. This case study illustrates the clinical utility of amyloid imaging in the setting of atypical cases seen in a tertiary memory clinic.
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PMID:Clinical Utility of Amyloid Imaging in a Complex Case of Corticobasal Syndrome Presenting with Psychiatric Symptoms. 2622 55

Ignacio Matte Blanco (1908-1995) left very few specific indications about the applications of his theoretical notions to his interpretative style. The author shows how he uses Matte Blanco to formulate some of his own interpretations. The first part of the paper uses clinical vignettes to illustrate some of Matte-Blanco's concepts. Their theoretical vocabulary is thus made explicit. Then two psychoanalytic sessions are discussed at greater length, together with one from a therapy, so that the use of Matte-Blanco's notions can be seen clearly, allowing for a fresh perspective on areas of psychoanalytic theory, particularly dreams, psychopathology viewed according to the proportions of asymmetrical and symmetrical functioning in the patient's bi-logical mental system, the multidimensionality of the unconscious, the structural unconscious, the emotion-thought relationship, projective identification, resistance, and negative therapeutic reaction. The practical consequences of all this are elaborated, particularly the ensuing possibility of 'thinking with the patient' in the session. This enables the patient to introject a form of mental functioning in which the asymmetrical mode is not invaded by the symmetric mode (a parallel can be seen here with the Bionian concept of dialogue between the psychotic and non-psychotic parts of the mind).
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PMID:Clinical applications of Matte Blanco's thinking. 2733 15

SLE (systemic lupus erythematosus) is a multisystem autoimmune disorder of unknown aetiology which can present with myriad clinical presentation. The neurological manifestations of SLE consist of central nervous system (CNS) and peripheral nervous system manifestations (PNS). The CNS manifestations are aseptic meningitis, cerebrovascular accidents (stroke), demyelinating disorders, headache, involuntary movements like chorea, myelopathy, acute confusional states, cognitive dysfunction, mood disorder, seizures, psychosis and cranial nerve palsies.1 The PNS manifestations are Guillain Barre syndrome (GBS), autonomic disorder, mononeuropathy, polyneuropathy and plexopathy.1 Neuropathy in SLE can be clinically classified as mononeuritis multiplex and symmetrical and asymmetrical polyneuropathy. Symmetrical polyneuropathy being the most commonly seen clinical entity amongst the neuropathies in SLE. The neuropathy can be slowly progressive or acute in onset. Electrophysiologically, neuropathy is classified as axonal neuropathy, small fibre neuropathy, demyelinating neuropathy, mixed axonal-demyelinating sensorimotor polyneuropathy and plexopathy. Axonal neuropathy is further divided into sensory, sensorimotor and mononeuritis multiplex. Demyelinating neuropathy can be of two types: acute inflammatory demyelinating polyneuropathy (AIDP) and sensory demyelinating polyneuropathy. Anecdotal case reports also suggest that CIDP can occur as part of SLE neuropathy.2.
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PMID:SLE Neuropathy-Anything New? 2766 98


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