Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UMLS:C0036341 (
schizophrenia
)
60,220
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Some systems ideas applied to individual persons are used to try to explain symptoms of
schizophrenia
and a syndrome of uncontrolled fragments of movement which sometimes occurs as a side effect of chronic, antipsychotic drug therapy. The behavior of normal organisms may be conceptualized in three echelons of control, with each successively higher echelon organizing, by selective
disinhibition
, semiautonomous, spontaneous fragments of activity which comprise the next lower echelon. It is hypothesized that
schizophrenia
involves a deficiency of inhibition by the frontal cortex, first echelon, on the corpus striatum, second echelon. This results first in insufficiently integrated fragments of behavior, and second in premature associative linkages among active elements. First echelon control develops as a normal person matures and gradually loses some of the playful activities of childhood. It is hypothesized that by disrupting certain aspects of activity in the corpus striatum, neuroleptic drugs reduce schizophrenic symptoms but also reduce the capacity of the second echelon to inhibit and integrate the smaller behavioral fragments wired into lower parts of the brain, third echelon. This results in uncontrolled movements. Though many researchers already favor the hypothesis that neuroleptic drugs act on the corpus striatum, the broader theory presented here is new and depends in large part on general living systems considerations. Emphasis is on conceptual decomposition of the integrated behavior of a whole organism into less complex subsystems. Individually, these have neither too much nor too little complexity to yield a plausible model. Some experimental predictions and predictions about possible therapies are made from the theory.
...
PMID:A neural systems theory of schizophrenia and tardive dyskinesia. 99 93
Regional cerebral blood flow (rCBF) was measured in 30 schizophrenic patients with severe, persistent and stable symptoms using positron emission tomography (PET). Directed and non-directed correlational analysis of the relationship between psychopathology and rCBF was used to identify brain structures implicated in three behavioural subsyndromes of
schizophrenia
. Psychopathology and neurophysiology (rCBF) exhibited high correlations in the left medial temporal region, mesencephalic, thalamic and left striatal structures. The highest correlation was in the left parahippocampal region. A canonical analysis of the same data highlighted the left parahippocampal region and left striatum (globus pallidus) as sites which linked the behavioural subsyndromes in terms of shared rCBF correlates. Increasing severity of psychopathology was associated with increased rCBF in these regions.
Disinhibition
of left medial temporal lobe activity mediated by fronto-limbic connections is a possible explanation for these findings; however, the prefrontal component appears to be critically dependent on the behavioural subsyndrome.
...
PMID:The left medial temporal region and schizophrenia. A PET study. 160 74
This is a case of Ramsay Hunt syndrome with mental disorder. The patient had action myoclonus, grand mal seizure and severe cerebellar ataxia.
Schizophrenia
-like symptoms including delusion of persecution and self-reference, auditory hallucination and incoherence were characteristically observed before the neurological disturbance became manifest. Subsequently, euphoria,
disinhibition
, moria and mild dementia appeared with neurological symptoms. The possibility of Ramsay Hunt syndrome to accompany organic mental syndromes and the relationship between cerebellar dysfunction and psychiatric symptoms are discussed.
...
PMID:Ramsay Hunt syndrome with mental disorder. 181 81
Two cases of electroconvulsive therapy (ECT) in adolescence are presented and the literature on the use of ECT in childhood and adolescence is reviewed. ECT was effective in children and adolescents with bipolar disorder and depression. Inadequate information exists to make a judgment regarding
schizophrenia
, delirium, and anorexia nervosa. ECT is not effective in autism and chronic organic brain syndromes. Complications cited include organicity and seizures in the period immediately after ECT, anxiety reactions, and
disinhibition
. Long-term memory deficit or cognitive impairment has not been found, although further research to rule out residual impairment is needed.
...
PMID:A review of ECT for children and adolescents. 222 48
The dopamine hypothesis still provides a valuable approach to the study of
schizophrenia
and its treatment by drugs. Although the neuroleptic drugs appear to act via an inhibition of dopamine receptors, measurements of dopamine metabolites in vivo, or of the transmitter and its receptors in post-mortem brain tissue, do not provide unequivocal evidence of a hyperactivity of dopaminergic neurotransmission in the disease. Nevertheless, increased dopamine function might be a consequence of a primary neuronal abnormality in another system. Recent imaging studies and neuropathological reports suggest that, in some patients, there may be a deficit and/or disturbance of neurons in certain temporal limbic regions, and this is supported by some neurochemical investigations, particularly of neuropeptide and amino-acid transmitter systems. A loss of such neurons could conceivably lead to a
disinhibition
of limbic dopamine neurons, providing the means whereby neuroleptic drug treatment might ameliorate the effects of a neuronal deficit in
schizophrenia
.
...
PMID:Beyond the dopamine hypothesis. The neurochemical pathology of schizophrenia. 269 61
Previous electrophysiological studies have demonstrated that non-dopaminergic (non-DA) neurons within the substantia nigra pars reticulata (SNR) are extremely sensitive to the inhibitory effects of GABA and GABA-mimetic drugs, including benzodiazepines, whereas dopaminergic (DA) neurons in the substantia nigra pars compacta (SNC) are less sensitive to these compounds and may be influenced indirectly by SNR neurons. The interactions between A10 DA and non-DA neurons within the adjacent ventral tegmental area (VTA) are not as well characterized. In the present experiments, single unit recording and microiontophoretic techniques were used to determine the effects of benzodiazepines on DA and non-DA neurons in the VTA of chloral hydrate anesthetized rats. Diazepam, administered intravenously (i.v.), potently inhibited non-DA, SNR-like cells within the VTA. The effects of diazepam on A10 DA cells were more variable than those observed on non-DA, SNR-like cells in this region, but 77% of such cells showed moderate to marked excitation. Both of these effects were reversed by the benzodiazepine antagonist Ro 15-1788; on many cells, this agent produced marked rebound effects beyond the original basal firing rates. However, when administered alone, Ro 15-1788 exerted no effect on either cell population. Microiontophoretic administration of the benzodiazepines chlordiazepoxide and flurazepam resulted in marked inhibition of non-DA SNR-like cells, but produced either mild inhibition or no effect on A10 DA cells; excitation of DA cells was never observed even though the same neuron was excited by i.v. diazepam. These findings suggest that benzodiazepines act directly upon non-DA, SNR-like cells in the VTA to produce inhibition of activity and a
disinhibition
of A10 DA cells. This relationship makes it unlikely that benzodiazepines would enhance feedback inhibition of DA cells following neuroleptic administration. In fact, when administered following haloperidol, i.v. diazepam failed to reverse haloperidol-induced increases of A10 DA cell firing; if anything, diazepam further depolarized the cell. If antipsychotic drugs produce their clinical effects, in part, by inducing depolarization inactivation of DA cells, then benzodiazepines might be a useful adjunctive therapy in the treatment of
schizophrenia
.
...
PMID:Inhibition of non-dopamine cells in the ventral tegmental area by benzodiazepines: relationship to A10 dopamine cell activity. 289 84
Diazepam-binding inhibitor is a novel peptide purified to homogeneity from rat and human brain. Diazepam-binding inhibitor is present, though not exclusively, in gamma-aminobutyric acid (GABA)-containing neurons where it is believed to inhibit GABAergic neurotransmission mediated by GABA by binding to the benzodiazepine-GABA receptor complex. Since an impairment of central GABAergic tone has been postulated to be associated with a number of neuropsychiatric disorders, we measured human diazepam-binding inhibitor immunoreactivity in the cerebrospinal fluid (CSF) of patients suffering from endogenous depression,
schizophrenia
, and dementia of the Alzheimer's type. Patients with major depression had significantly higher concentrations of human diazepam-binding inhibitor immunoreactivity in CSF when compared with age- and sex-matched normal volunteers, while no difference in CSF diazepam-binding inhibitor immunoreactivity was found in schizophrenics or patients with dementia of the Alzheimer's type when compared with controls. The possibility is discussed that the increased CSF human diazepam-binding inhibitor immunoreactivity observed in depressed patients may represent a functional
disinhibition
of GABAergic neurotransmission associated with depression.
...
PMID:Diazepam-binding inhibitor. A brain neuropeptide present in human spinal fluid: studies in depression, schizophrenia, and Alzheimer's disease. 302 63
Auditory event-related potentials (ERPs) to pure tones and performance on a measure of item recognition were compared in 20 controls, 14 alcoholics, 20 depressed and 21 schizophrenic patients. Compared with normal controls, P2 and N2 were delayed and of diminished amplitude in the psychopathological groups. Increased amplitude of P1 in alcoholics, diminished N1 in depressed patients, increased latencies of N1 in schizophrenics and N2 in alcoholics were pathology-specific. Unusual patterns of response in the item recognition test (elevated intercept and flattened slope) and its relationship with ERPs distinguished the diagnostic groups from the controls. Support for the preferential involvement of the left hemisphere in
schizophrenia
and of the right hemisphere in depression was found.
Disinhibition
of CNS activity in the response of alcoholics (increased P1 and delayed P3) was indicated. The findings suggested that discriminant analysis of auditory ERPs to simple, pure tones, in conjunction with psychometric data significantly differentiated pathologic groups from each other and from controls.
...
PMID:Event-related potentials and item recognition in depressed, schizophrenic and alcoholic patients. 367 47
A clinico-psychological study covered 28 children aged 4-13 years with protracted hypomanic states (2-8 years) in 3-10-year-long
schizophrenia
. The authors investigated peculiarities of the development of cognitive activity (thought and perception). Comparison was made between groups of schizophrenics and control groups (the syndrome of motor
disinhibition
, schizoid psychopathy). The findings of a clinico-psychological examination have helped to elucidate differences in the development of cognitive activity in the above groups of children which may be used for the differential diagnosis and prognosis of the disease course.
...
PMID:[Clinico-psychological examination of children with protracted hypomanic conditions in schizophrenia]. 381 14
The phenomena of eye movement impairments in
schizophrenia
are interpreted in this paper, Part I of a two-paper series, in the context of neural mechanisms of attention and eye movement control. The predominant pattern of attention and eye movement impairment in
schizophrenia
--a disruption of smooth pursuit by saccadic intrusions--is consistent with a
disinhibition
of saccades. This
disinhibition
may be related to a dysfunction of frontal eye field mechanisms involved in feedback regulation of saccades and smooth pursuit during visual tracking. A second, less specific type of smooth pursuit impairment consists of saccadic substitution, and may be interpreted in terms of a dysfunction of temporo-parietal mechanisms of task-engagement.
...
PMID:Frontal lobe dysfunctions in schizophrenia--I. Eye movement impairments. 637 Dec 23
1
2
3
4
5
6
7
8
9
10
Next >>