Brain dysmorphology in adults with congenital rubella plus schizophrenialike symptoms

Lim, Kelvin O.; Beal, D.M.; Harvey, Robert L.; Myers, Tim; Lane, Barton; Sullivan, Edith V.; Faustman, William O.; Pfefferbaum, Adolf

doi:10.1016/0006-3223(94)00219-s

Cited by 37 publications

(15 citation statements)

References 65 publications

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“…This is consistent with recent post mortem studies indicating that brain volume reduction in schizophrenia is due to increased neuronal density and not to neuronal loss (Selemon, Rajkowska, & Goldman-Rakic, 1995). Interestingly, the same pattern of gray matter reduction with white matter sparing has been observed in a sample of patients with congenital rubella and schizophrenia-like symptoms, suggesting that this pattern of brain dysmorphology can result from a viral disturbance of early neurodevelopment (Lim et al, 1995).…”

Section: Brain Morphologysupporting

confidence: 59%

Research Update: Childhood‐onset Schizophrenia: Implications of Clinical and Neurobiological Research

Jacobsen

Rapoport²

1998

Child Psychology Psychiatry

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Childhood-onset schizophrenia is a rare, clinically severe form of schizophrenia, which is associated with disrupted cognitive, linguistic, and social development well before the appearance of frank psychotic symptoms. This disruption of multiple developmental domains signals the important opportunity these patients present for examining neurodevelopmental and other etiologic hypotheses of schizophrenia. The present research update reviews studies of the phenomenology and neurobiology of childhood-onset schizophrenia conducted since 1994. Findings from these studies indicate that children can be diagnosed with schizophrenia using unmodified DSM-III, -IIIR, and -IV criteria, and that the atypical neuroleptic clozapine is an effective medication for this treatment refractory group. Neuropsychologic and neurobiologic studies generally support continuity with adult-onset schizophrenia, with evidence of more severe premorbid impairment. Longitudinal studies show preliminary evidence of progressive ventricular enlargement and more prolonged deterioration in intellectual function than is seen in the adult-onset disorder. If replicated, these observations, together with the insidious onset of this disorder, would suggest that the pathologic underpinning of childhood-onset schizophrenia is not a single static lesion or event but may be a continuous or multi-event process.

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Section: Brain Morphologysupporting

confidence: 59%

Research Update: Childhood‐onset Schizophrenia: Implications of Clinical and Neurobiological Research

Jacobsen

Rapoport²

1998

Child Psychology Psychiatry

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“…Interestingly, inflammatory changes are generally not apparent. Recently, magnetic resonance imaging was used to study a group of 11 CRS adults with schizophrenia-like symptoms [16]. The study confirmed reduced cranial volume, but surprisingly found specifical ly reduced cortical gray matter and enlargement of the ventricles, which had not previously been observed as an aspect of CRS-induced pathology.…”

Section: Congenital Rubella Syndrom Ementioning

confidence: 67%

Neurological Aspects of Rubella Virus Infection

Frey

1997

Intervirology

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Rubella virus is a single-stranded, plus-sense RNA virus belonging to the Togaviridae family. Rubella virus infection causes a benign disease known as rubella or German measles, however infection during early pregnancy can lead to severe birth defects known as congenital rubella syndrome (CRS). Sequelae of rubella virus infection include three distinct neurological syndromes: a postinfectious encephalitis following acute infection, a spectrum of neurological manifestations following congenital infection, and an extremely rare neuodegenerative disorder, progressive rubella panencephalitis (PRP), that can follow either congenital or postnatal infection. The pathogenesis of all three of these syndromes is incompletely understood. Virus invasion and replication in the brain has only been definitively demonstrated in CRS and appears to account for the majority of neurological lesions observed in this disease. Immune-mediated pathology is particularly evident in PRP and may be autoimmune in nature, possibly triggered by molecular mimicry between viral and host epitopes, considering the apparent lack of virus in the brain. The pathogenesis of rubella encephalitis following acute infection has not been determined.

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“…In schizophrenia, rates of BF were reported to be 5% to 10% of patients (Brown et al , 1995, and were comparable to rates in control subjects (7% to 14% (Brown et al , 1995). An increased prevalence of BF reported in congenital rubella patients with schizophrenia (Lane et al 1996;Lim et al 1995) was felt to be related to ischemic changes associated with congenital rubella but not with schizophrenia (Lane et al 1996). Ischemic changes may be responsible for the increased BF in 22qDS.…”

Section: Discussionmentioning

confidence: 99%

Qualitative MRI findings in adults with 22q11 deletion syndrome and schizophrenia

Chow¹,

Mikulis²,

Zipursky³

et al. 1999

Biological Psychiatry

112

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Background-A genetic syndrome associated with schizophrenia, 22q11 deletion syndrome (22qDS), may represent a genetic subtype of schizophrenia (22qDS-Sz). Structural brain changes are common in schizophrenia and may involve developmental anomalies, but there are no data yet for 22qDS-Sz. The objective of this study was to assess brain structure in adults with 22qDS-Sz using magnetic resonance imaging (MRI).

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Brain dysmorphology in adults with congenital rubella plus schizophrenialike symptoms

Cited by 37 publications

References 65 publications

Research Update: Childhood‐onset Schizophrenia: Implications of Clinical and Neurobiological Research

Research Update: Childhood‐onset Schizophrenia: Implications of Clinical and Neurobiological Research

Neurological Aspects of Rubella Virus Infection

Qualitative MRI findings in adults with 22q11 deletion syndrome and schizophrenia

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