Grey and white matter abnormalities are associated with impaired spatial working memory ability in first-episode schizophrenia

BackgroundStudies of chronic schizophrenia suggest that there are subgroups with different profiles of cognitive impairment.AimsTo determine whether such heterogeneity is present at illness onset and any relationship to clinical variables.MethodNinety-three community patients with first-episode schizophrenia and 50 healthy volunteers were assessed for premorbid (Revised National Adult Reading Test) and current IQ, memory and executive function.ResultsHalf of those with schizophrenia had preserved IQ in the normal range but there was evidence of a specific impairment in spatial working memory even in those with high/average IQ; 37 out of 93 (40%) had generalised cognitive decline. Those with low premorbid IQ were significantly younger at illness onset. For the entire group, age at onset correlated positively with premorbid but not current IQ.ConclusionsAt illness onset, cognitive heterogeneity is present in people with schizophrenia, with a high proportion having undergone general cognitive decline. However, working memory impairment may be a common feature. Lower premorbid IQ is a risk factor for an earlier onset.

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Gradual cerebral hypoperfusion in spontaneously hypertensive rats induces slowly evolving white matter abnormalities and impairs working memory

Journal of Cerebral Blood Flow & Metabolism ◽

10.1177/0271678x15606717 ◽

2016 ◽

Vol 36 (9) ◽

pp. 1592-1602 ◽

Cited By ~ 19

Author(s):

Akihiro Kitamura ◽

Satoshi Saito ◽

Takakuni Maki ◽

Naoya Oishi ◽

Takashi Ayaki ◽

...

Keyword(s):

Working Memory ◽

White Matter ◽

Mortality Rate ◽

Baseline Level ◽

Spontaneously Hypertensive Rats ◽

Spatial Working Memory ◽

Small Vessel ◽

Hypertensive Rats ◽

Spontaneously Hypertensive ◽

White Matter Abnormalities

Rats subjected to bilateral common carotid arteries (CCAs) occlusion or 2-vessel occlusion (2VO) have been used as animal models of subcortical ischemic vascular dementia (SIVD). However, these models possess an inherent limitation in that cerebral blood flow (CBF) drops sharply and substantially after ligation of CCAs without vascular risk factors and causative small vessel changes. We previously reported a novel rat model of 2-vessel gradual occlusion (2VGO) in which ameroid constrictors (ACs) were placed bilaterally in the CCAs of Wistar-Kyoto rats. To simulate SIVD pathology more closely, we applied ACs in spontaneously hypertensive rats (SHRs), which naturally develop small vessel pathology, and compared their phenotypes with SHR-2VO and sham-operated rats. The mortality rate of the SHR-2VGO was 0% while that of the SHR-2VO was 56.5%. The CBF of the SHR-2VO dropped to 50% of the baseline level at 3 h, whereas the SHR-2VGO showed a gradual CBF reduction reaching only 68% of the baseline level at seven days. The SHR-2VGO showed slowly evolving white matter abnormalities and subsequent spatial working memory impairments of a similar magnitude to the remaining SHR-2VO at 28 days. We suggest the SHR-2VGO robustly replicates selective aspects of the pathophysiology of SIVD with low mortality rate.

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