FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W1994573280> ?p ?o ?g. }

• W1994573280 endingPage "323" @default.
• W1994573280 startingPage "321" @default.
• W1994573280 abstract "More than 25 years have passed since the first computer assisted tomography study (1) demonstrated increased cerebral ventricular size in 17 institutionalized schizophrenic patients compared with age-matched controls. With the application of magnetic resonance imaging (MRI), it became clear that many brain structures were involved. In addition to the lateral and third ventricles, the overwhelming majority of studies demonstrated involvement of medial temporal lobe structures such as the amygdala, hippocampus and parahippocampal gyrus as well as the superior temporal gyrus. Many studies also found evidence for involvement of the prefrontal and orbitofrontal, parietal and some subcortical regions including the basal ganglia and thalamus (2). However, effect size of these differences appeared to be only moderate (3, 4) suggesting that there is considerable overlap between schizophrenic patients and controls. There is a consensus from both computerized tomographic and MRI studies that ventricular enlargement is present in the first episode patients prior to treatment with medication. Findings in other structures in first episode patients, never treated patients have been much less consistent (5). In fact, one recent study had gone as far as to suggest that abnormalities other than ventricular enlargement in chronic schizophrenic patients may be a later stage development of the disease and/or medication induced (6). The study by Yoneyama et al. in this issue reminds us that structural abnormalities can be seen in other conditions. Using a morphometric MRI voxel-based methodology, Yoneyama et al. (7) demonstrated that patients meeting ICD-10 diagnostic criteria for schizotypal disorder and schizophrenia-related codes of the Minnesota Multiphasic Personality Inventory show significantly decreased gray matter volumes in the bilateral insular regions in the left enthorinal cortex compared with controls. These findings are in keeping with several other studies which have demonstrated temporal and subcortical but not ventricular changes in schizotypal patients (8). Structure abnormalities are also found in relatives of schizophrenic patients. However lateral ventricular enlargement is not found consistently or only in subgroups of relatives such as those with multiple affected relatives or relatives with a schizotypal personality disorder (8,9). Ventricular enlargement and increased sulcal prominence can be demonstrated in mood disorders as well although these changes are less striking than in schizophrenia (10). The overlap between morphometric changes in schizophrenic patients, other conditions and even healthy individuals precludes the use of these measurements in diagnosis. However, several longitudinal MRI studies suggest that they could be potentially useful in defining progression to schizophrenia in a group of prodromal patients. For example, Pantelis et al. (11) studied 75 patients with prodromal symptoms of psychosis. Twenty-one of these patients were scanned again at 12 months by which time 10 had developed psychosis and 11 had not. Individuals who developed psychosis showed reduced gray matter in the left parahippocampal, fusiform, orbitofrontal and cerebellar cortices and the cingulate gyri. With the exception of the cerebellar changes, these deficits were not seen in individuals who did not become psychotic. Another longitudinal study of early onset schizophrenia showed that hippocampal changes seemed to be associated with the development of schizophrenia compared with patients with psychosis, not otherwise specified (12). Many schizophrenic patients have no measurable structural abnormalities. In those who do have abnormalities, the structures involved often varies from patient to patient. This may not be unexpected as there are likely many genes which contribute to the risk of schizophrenia (13). The examination of structural changes related to a particular genetic marker in patients and their families could suggest how a particular gene leads to illness vulnerability. While brain structural changes could be useful in defining an endophenotype, it must be remembered that the most striking anatomical abnormalities have been described in the brains of monozygotic twins discordant for schizophrenia. Suddath et al. (14) found the hippocampus to be smaller on the left in 14 of 15 affected twins compared with their normal twins indicating that more than genetic factors are involved. While some may be discouraged by inconsistent structural findings in schizophrenic patients, there is no doubt that these studies have helped us understand brain mechanisms in schizophrenia. What they seem to suggest is that each patient follows a unique pathway to his or her illness which may be influenced by a variety of genetic, obstetrical and/or viral factors. Each of these factors affects a part of one or more functional neuronal circuits leading to dysfunction of the whole circuit which might explain why patients with different volumetric deficits show the same symptoms. Almost all of the volumetric studies point towards the basal ganglia-thalamocortical cortical neuronal circuit and related structures. It is of interest that activity within this neuronal circuit is regulated by dopamine while cortical/subcortical connections are glutamatergic as both of these neurotransmitters have been implicated in the pathophysiology of schizophrenia. While further advances in structural imaging technology and molecular genetics will undoubtedly lead to further cross-sectional studies, what is really needed at this point is more longitudinal studies. In fact, many of the patients in the Yoneyama et al. (7) study may go on to develop schizophrenia as patients were followed up for only 2 years. Such studies could help define a disease process which may be unleashed by pre-existing neurodevelopemental deficits. A more complete knowledge of this disease process could lead to new treatments if progressive volumetric deficits reflect glutamate-induced neurodegeneration (15). If we are to understand the disease process related to longitudinal volumetric changes, it is essential that more than structural changes be examined. Weinburger and McClure (16) point out that many of the longitudinal changes could be explained by the effects of medication or reduced neuronal information-processing load. Longitudinal studies with magnetic resonance spectroscopy which allows the measurement of membrane phosolipids, markers of neuronal integrity and glutamate could help sort out whether these changes are related to neurodegeneration or other factors." @default.
• W1994573280 created "2016-06-24" @default.
• W1994573280 creator A5049858309 @default.
• W1994573280 creator A5051368688 @default.
• W1994573280 date "2003-10-06" @default.
• W1994573280 modified "2023-10-16" @default.
• W1994573280 title "Structural neuroimaging in schizophrenia" @default.
• W1994573280 cites W1502336554 @default.
• W1994573280 cites W1965924747 @default.
• W1994573280 cites W1968986034 @default.
• W1994573280 cites W1979315240 @default.
• W1994573280 cites W1985994929 @default.
• W1994573280 cites W2003759197 @default.
• W1994573280 cites W2014243309 @default.
• W1994573280 cites W2026334669 @default.
• W1994573280 cites W2057074067 @default.
• W1994573280 cites W2062648684 @default.
• W1994573280 cites W2083645773 @default.
• W1994573280 cites W2093625493 @default.
• W1994573280 cites W2127679160 @default.
• W1994573280 cites W2152247222 @default.
• W1994573280 cites W2154280785 @default.
• W1994573280 cites W2156123885 @default.
• W1994573280 doi "https://doi.org/10.1034/j.1600-0447.2003.00211.x" @default.
• W1994573280 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/14531751" @default.
• W1994573280 hasPublicationYear "2003" @default.
• W1994573280 type Work @default.
• W1994573280 sameAs 1994573280 @default.
• W1994573280 citedByCount "4" @default.
• W1994573280 countsByYear W19945732802022 @default.
• W1994573280 countsByYear W19945732802023 @default.
• W1994573280 crossrefType "journal-article" @default.
• W1994573280 hasAuthorship W1994573280A5049858309 @default.
• W1994573280 hasAuthorship W1994573280A5051368688 @default.
• W1994573280 hasBestOaLocation W19945732801 @default.
• W1994573280 hasConcept C118552586 @default.
• W1994573280 hasConcept C126838900 @default.
• W1994573280 hasConcept C143409427 @default.
• W1994573280 hasConcept C15744967 @default.
• W1994573280 hasConcept C169760540 @default.
• W1994573280 hasConcept C2776412080 @default.
• W1994573280 hasConcept C2778048536 @default.
• W1994573280 hasConcept C2778186239 @default.
• W1994573280 hasConcept C2780744974 @default.
• W1994573280 hasConcept C2781099131 @default.
• W1994573280 hasConcept C2781161787 @default.
• W1994573280 hasConcept C58693492 @default.
• W1994573280 hasConcept C71924100 @default.
• W1994573280 hasConceptScore W1994573280C118552586 @default.
• W1994573280 hasConceptScore W1994573280C126838900 @default.
• W1994573280 hasConceptScore W1994573280C143409427 @default.
• W1994573280 hasConceptScore W1994573280C15744967 @default.
• W1994573280 hasConceptScore W1994573280C169760540 @default.
• W1994573280 hasConceptScore W1994573280C2776412080 @default.
• W1994573280 hasConceptScore W1994573280C2778048536 @default.
• W1994573280 hasConceptScore W1994573280C2778186239 @default.
• W1994573280 hasConceptScore W1994573280C2780744974 @default.
• W1994573280 hasConceptScore W1994573280C2781099131 @default.
• W1994573280 hasConceptScore W1994573280C2781161787 @default.
• W1994573280 hasConceptScore W1994573280C58693492 @default.
• W1994573280 hasConceptScore W1994573280C71924100 @default.
• W1994573280 hasIssue "5" @default.
• W1994573280 hasLocation W19945732801 @default.
• W1994573280 hasLocation W19945732802 @default.
• W1994573280 hasOpenAccess W1994573280 @default.
• W1994573280 hasPrimaryLocation W19945732801 @default.
• W1994573280 hasRelatedWork W1994579977 @default.
• W1994573280 hasRelatedWork W2053384222 @default.
• W1994573280 hasRelatedWork W2060790609 @default.
• W1994573280 hasRelatedWork W2063609102 @default.
• W1994573280 hasRelatedWork W2065159577 @default.
• W1994573280 hasRelatedWork W2094176512 @default.
• W1994573280 hasRelatedWork W2102101945 @default.
• W1994573280 hasRelatedWork W2364563968 @default.
• W1994573280 hasRelatedWork W2809240167 @default.
• W1994573280 hasRelatedWork W3032082508 @default.
• W1994573280 hasVolume "108" @default.
• W1994573280 isParatext "false" @default.
• W1994573280 isRetracted "false" @default.
• W1994573280 magId "1994573280" @default.
• W1994573280 workType "article" @default.