Biomedical subjects

Tiia Pirkola

Publications and source records attributed to Tiia Pirkola.

4 recordsLinked to original sources

PubMed2005

Spatial working memory function in twins with schizophrenia and bipolar disorder.

BACKGROUND: Family studies are in conflict as to whether schizophrenia and bipolar disorder have independent genetic etiologies. Given the relatively low prevalence (approximately 1%) of these disorders, the use of quantitative endophenotypic markers of genetic liability might provide a more sensitive strategy for evaluating their genetic overlap. We have previously demonstrated that spatial working memory deficits increase in a dose-dependent fashion with increasing genetic proximity to a proband among the unaffected co-twins of schizophrenic patients. Here, we evaluated whether such deficits might also mark genetic susceptibility to bipolar disorder. METHODS: The Wechsler Memory Scale-Revised Visual Memory Span and Digit Span subtests were administered to 46 schizophrenic patients, 32 of their unaffected co-twins, 22 bipolar patients, 16 of their unaffected co-twins, and 100 control twins, representing unselectively nationwide twin samples. RESULTS: Schizophrenic patients and their unaffected co-twins performed significantly worse than control subjects on the spatial working memory task, whereas only the schizophrenic patients performed significantly below the control subjects on the verbal working memory task. Neither bipolar patients nor their unaffected co-twins differed from control subjects on these measures. CONCLUSIONS: Our findings support the hypothesis that impairment in spatial working memory might effectively reflect an expression of genetic liability to schizophrenia but less clearly to bipolar disorder.

Aged↗

PubMed2003

Do schizotypal symptoms mediate the relationship between genetic risk for schizophrenia and impaired neuropsychological performance in co-twins of schizophrenic patients?

BACKGROUND: Neurocognitive deficits and symptoms of schizotypal personality disorder are both elevated in the first-degree relatives of schizophrenic patients, but their relationship to each other and their potential common genetic source remain unclear. METHODS: Fifty unaffected co-twins of schizophrenic patients and 123 control twins were assessed with a neuropsychological battery and structured clinical interviews. RESULTS: Working memory was influenced by genetic risk for schizophrenia but not schizotypal symptoms. Nearly all other domains were influenced by schizotypy symptoms but only in the co-twins of schizophrenic patients. Schizotypy symptoms in the absence of a family history did not seem to be related to impaired neurocognitive functioning. CONCLUSIONS: Schizotypy symptoms in those with genetic risk for schizophrenia are associated with increased risk for cognitive deficits. Some neurocognitive deficits might covary with subpsychotic symptoms due to a shared genetic factor. Community-ascertained schizotypal individuals might not be appropriate for modeling underlying genetic risk for schizophrenia.

Female↗

PubMed2002

Fetal hypoxia and structural brain abnormalities in schizophrenic patients, their siblings, and controls.

BACKGROUND: Cortical gray matter reductions and cerebrospinal fluid (CSF) increases are robust correlates of schizophrenia, but their relationships to obstetric and other etiologic risk factors remain to be established. METHODS: Structured diagnostic interviews, obstetric hospital records, and magnetic resonance imaging scans of the brain were obtained for 64 schizophrenic or schizoaffective patients (representative of all such probands in a Helsinki, Finland, birth cohort), along with 51 of their nonpsychotic full siblings and 54 demographically similar controls without family histories of psychosis. RESULTS: Fetal hypoxia predicted reduced gray matter and increased CSF bilaterally throughout the cortex in patients (gray matter effect sizes, -0.31 to -0.56; CSF effect sizes, 0.25 to 0.47) and siblings (gray matter effect sizes, 0.33 to 0.47; CSF effect sizes, 0.17 to 0.33), most strongly in the temporal lobe. Effect sizes were 2 to 3 times greater among cases born small for their gestational age. Hypoxia also correlated significantly with ventricular enlargement, but only among patients (effect size, 0.31). In contrast, fetal hypoxia was not related to white matter among patients and siblings, nor to any tissue type in any region among controls. The associations were independent of family membership, overall brain volume, age, sex, substance abuse, and prenatal infection. CONCLUSIONS: Fetal hypoxia is associated with greater structural brain abnormalities among schizophrenic patients and their nonschizophrenic siblings than among controls at low genetic risk for schizophrenia. This pattern of results points to a gene-environment interaction account of the disorder's neurodevelopmental pathogenesis.

Adult↗

PubMed2002

Contributions of genetic risk and fetal hypoxia to hippocampal volume in patients with schizophrenia or schizoaffective disorder, their unaffected siblings, and healthy unrelated volunteers.

OBJECTIVE: The authors examined in an epidemiologic sample the contributions of genetic predisposition and history of fetal hypoxia to hippocampal volume in patients with psychosis. METHOD: High-resolution magnetic resonance imaging was used to measure hippocampal volumes in 72 psychotic probands (60 with schizophrenia and 12 with schizoaffective disorder, ascertained so as to be representative of all such probands in a Helsinki birth cohort), 58 nonpsychotic full siblings of the probands, and 53 demographically similar healthy comparison subjects with no family history of psychosis. RESULTS: Hippocampal volume differences occurred in a stepwise fashion with each increase in genetic load for schizophrenia. The probands had smaller hippocampal volumes than did their full siblings, who in turn had smaller hippocampal volumes than did the healthy comparison subjects. Among the probands, smaller hippocampal volumes were seen in those who experienced fetal hypoxia than in those who did not, a difference not noted within the other two groups. Finally, within the schizophrenic/schizoaffective disorder patients, smaller hippocampal volumes correlated positively with age at onset independent of duration of illness. CONCLUSIONS: These findings suggest that in patients with schizophrenia spectrum disorders, hippocampal volume is influenced in part by schizophrenia susceptibility genes and an interaction of these genes with fetal hypoxia. They further suggest that hippocampal volume in schizophrenia or schizoaffective disorder may be linked to time of disease onset.

Adult↗