Stable Cognitive Deficits Research Articles

Wernicke–Korsakov Syndrome

Objective. To study the characteristics of the diagnosis and treatment of non-alcoholic-related Wernicke–Korsakov syndrome (WKS). Materials and methods. Eight patients (five men and three women) with mean age 38.9 ± 1.4 years with WKS were observed; WKS in three patients developed on the background of acute and two on the background of exacerbations of chronic gastrointestinal tract diseases with malabsorption, and in three after surgery to the upper segments of the gastrointestinal tract Results. Illness debuted with impaired consciousness. Symptoms of ataxia, oculomotor disorders, and bulbar syndrome started after 24–48 h. One patient developed a treatment-resistant state of tonic-clonic seizures. The brain MRI picture was characterized by the presence of hyperintense foci on T2-weighted images in the areas of the hypothalamus, mammillary bodies, brainstem, and cerebellum, with accumulation of contrast in the mammillary bodies. Patients received treatment with a complex of group B vitamins (Neurobion) and thiamine, with positive results Conclusions. Patients with gastrointestinal tract diseases accompanied by malabsorption are at risk of developing WKS. The appearance of changes in consciousness, ataxia, and oculomotor disorders in these patients is an indication to start thiamine therapy, thus preventing the development of stable cognitive deficit.

The Barrier to Informed Choice in Cancer Screening: Statistical Illiteracy in Physicians and Patients.

An efficient health care requires both informed doctors and patients. Our current healthcare system falls short on both counts. Most doctors and patients do not understand the available medical evidence. To illustrate the extent of the problem in the setting of cancer screening: In a representative sample of some 5000 women in nine European countries, 92% overestimated the reduction of breast cancer mortality by mammography by a factor of 10-200, or did not know. For a similar sample of about 5000 men with respect to PSA screening, this number was 89%. Of more than 300 US citizens who regularly attended one or more cancer screening test, more than 90% had never been informed about the biggest harms of screening-overdiagnosis and overtreatment-by their physicians. Among 160 German gynecologists, some 80% did not understand the positive predictive value of a positive mammogram, with estimates varying between 1 and 90%. In a national sample of 412 US primary care physicians, 47% mistakenly believed that if more cancers are detected by a screening test, this proves that the test saves lives, and 76% wrongly thought that if screen-detected cancers have better 5-year survival rates than cancers detected by symptoms, this would prove that the screening test saves lives. And of 20 German gynecologists, not a single one provided a woman with all information on the benefits and harms of cancer screening required in order to make an informed choice. Why is risk literacy so scarce in health care? One frequently discussed explanation assumes that people suffer from cognitive deficits that make them predictably irrational and basically hopeless at dealing with risks, so that they need to be "nudged" into healthy behavior. Yet research has demonstrated that the problem lies less in stable cognitive deficits than in how information is presented to physicians and patients. This includes biased reporting in medical journals, brochures, and the media that uses relative risks and other misleading statistics, motivated by conflicts of interest and defensive medicine that do not promote informed physicians and patients. What can be done? Every medical school should teach its students how to understand evidence in general and health statistics in particular. To cultivate informed patients, elementary and high schools should start teaching the mathematics of uncertainty-statistical thinking. Guidelines about complete and transparent reporting in journals, brochures, and the media need to be better enforced, and laws need to be changed in order to protect patients and doctors alike against the practice of defensive medicine instead of encouraging it. A critical mass of informed citizens will not resolve all healthcare problems, but it can constitute a major triggering factor for better care.

Risk factors and prevention of recurrent dynamics of depression

The existing literature in the field demonstrates that in the majority of cases depressive disorder has a recurrent course that resulted in negative consequences: an increase in a number of chronic and marked episodes, a higher risk of suicide and stable cognitive deficit. An analysis of predictors promoting the formation of recurrent depressive disorder allows an identification of a constellation of biological, psychological, therapeutic, social factors which should be taken into account in the choice of methods of prevention of the next episode of depression. Currently, the prolonged supporting psychopharmacotherapy, including antidepressant therapy, is a main tactics in the prevention of recurrent dynamics of depressive disorder though its efficacy is understudied.

Expression of the FGF2 and TIMP1 Genes in the Adult Rat Brain after Administration of Interleukin-1β during Early Postnatal Ontogeny

Hypotheses relating to the developmental nature of cognitive impairments in schizophrenia and other neuropathologies propose that the development of stable cognitive deficit involves important roles for hypoxia, trauma, and infections operating during the prenatal and early postnatal periods. These pathological states are accompanied by increases in the production of proinflammatory cytokine interleukin-1β (IL-1β) in cells of the nervous and immune systems. We report here studies of the characteristics of the expression of the Fgf1 and Timp1 genes, which are involved in regulating the cerebral mechanisms of neuroplasticity, in cells of the medial prefrontal cortex and the dorsal and ventral areas of the hippocampus in adult rats given IL-1β during early postnatal ontogeny. Experiments were performed in standard conditions and on acquisition of a conditioned active avoidance reflex. Learning impairments in experimental animals were accompanied by decreased production of FGF-2 mRNA in cells of the medial prefrontal cortex and ventral hippocampus. There were no differences between groups in conditions without cognitive loading.

Wernicke-Korsakoff syndrome

To study the diagnosis and treatment of non-alcoholic Wernicke-Korsakoff syndrome (WKS). Eight patients (5 men and 3 women), mean age 38,9±1,4 years, with WKS developed due to acute gastrointestinal tract (GIT) disease (3 patients), the exacerbation of chronic GIT disease with malabsorption (2 patients) and after surgery on the upper GIT (3 patients) were included in the study. The disease manifested with consciousness disturbance, symptoms of ataxia, eye movement disorders and bulbar syndrome that developed after 24-48 h. Treatment resistant tonic-clonic seizures were developed in 1 patient. MRI revealed hyper intensive signals on T2-weighted images in the hypothalamus, mamillar bodies, brain stem, hippocampus as well as contrast accumulation in the mamillar bodies. Treatment with vitamin B complex (neurobion) and thiamine exerted a positive effect. Patients with GIT disease with malabsorption are at risk of WKS. Consciousness disturbance, symptoms of ataxia, eye movement disorders indicate the necessity of treatment with thiamine that allows to prevent the development of stable cognitive deficit.

The Cannabis Pathway to Non-Affective Psychosis may Reflect Less Neurobiological Vulnerability.

There is a high prevalence of cannabis use reported in non-affective psychosis. Early prospective longitudinal studies conclude that cannabis use is a risk factor for psychosis, and neurochemical studies on cannabis have suggested potential mechanisms for this effect. Recent advances in the field of neuroscience and genetics may have important implications for our understanding of this relationship. Importantly, we need to better understand the vulnerability × cannabis interaction to shed light on the mediators of cannabis as a risk factor for psychosis. Thus, the present study reviews recent literature on several variables relevant for understanding the relationship between cannabis and psychosis, including age of onset, cognition, brain functioning, family history, genetics, and neurological soft signs (NSS) in non-affective psychosis. Compared with non-using non-affective psychosis, the present review shows that there seem to be fewer stable cognitive deficits in patients with cannabis use and psychosis, in addition to fewer NSS and possibly more normalized brain functioning, indicating less neurobiological vulnerability for psychosis. There are, however, some familiar and genetic vulnerabilities present in the cannabis psychosis group, which may influence the cannabis pathway to psychosis by increasing sensitivity to cannabis. Furthermore, an earlier age of onset suggests a different pathway to psychosis in the cannabis-using patients. Two alternative vulnerability models are presented to integrate these seemingly paradoxical findings

Normalisation of frontal theta activity following methylphenidate treatment in adult attention-deficit/hyperactivity disorder

Attention-deficit/hyperactivity disorder (ADHD) is associated with cognitive performance and functional brain changes that are sensitive to task conditions, indicating a role for dynamic impairments rather than stable cognitive deficits. Prominent hypotheses consistent with this observation are a failure to optimise brain arousal or activation states. Here we investigate cortical activation during different conditions. Using a sample of 41 non-comorbid adults with ADHD and 48 controls, we examine quantitative EEG activity during a resting state, a cued continuous performance test with flankers (CPT-OX) and the sustained attention to response task (SART). We further investigate the effects of methylphenidate in a subsample of 21 ADHD cases. Control participants showed a task-related increase in theta activity when engaged in cognitive tasks, primarily in frontal and parietal regions, which was absent in participants with ADHD. Treatment with methylphenidate resulted in normalisation of the resting state to task activation pattern. These findings suggest that ADHD in adults is associated with insufficient allocation of neuronal resources required for normal cortical activation commensurate with task demands. Further work is required to clarify the causal role of the deficit in cortical activation and provide a clearer understanding of the mechanisms involved.

Cognitive changes in patients with acute phase psychosis—Effects of illicit drug use

Illicit drug use may influence cognition in non-affective psychosis. Previous studies have shown better cognition in psychosis with illicit drug use as compared to psychosis only. Possibly, illicit drug using patients have more transient drug-related cognitive deficits. Thus, the aim of the present study was to examine cognitive change the first weeks after admission to a psychiatric emergency ward, expecting more cognitive improvement at follow-up in the illicit drug group as compared to psychosis only. Patients with acute non-affective psychosis with (26%) and without illicit drug use were examined at baseline (n=123) and follow-up (n=67), with alternative forms of the Repeatable Battery for the Assessment of Neuropsychological Status. Latent Growth Curve models, controlling for cognition at baseline and age differences between the groups, were used to analyze cognitive change. The illicit drug using patients showed the largest improvement in cognition, especially among the youngest patients. Younger patients with non-affective psychosis and illicit drug use showed more cognitive improvement the first weeks after acute psychosis as compared to psychosis only. This suggests that the illicit drug users constitute a sub-group with less stable cognitive deficits and less cognitive vulnerability.

Developmental Lag and Course of Cognitive Deficits From the Premorbid to Postonset Period in Schizophrenia

Developmental Lag and Course of Cognitive Deficits From the Premorbid to Postonset Period in Schizophrenia

Stable Cognitive Deficits in Schizophrenia Patients With Comorbid Obsessive-Compulsive Symptoms: A 12-Month Longitudinal Study

Amongst schizophrenia patients, a large subgroup of up to 25% also suffers from comorbid obsessive-compulsive symptoms (OCSs). The association between comorbid OCSs in these patients and neuropsychological impairment remains unclear and somewhat contradictory. Longitudinal approaches investigating the stability of OCS-associated cognitive deficits are missing. Thirty-seven patients with schizophrenia and comorbid OCSs and 43 schizophrenia patients without OCS were assessed with a comprehensive cognitive test battery and compared at baseline and, again, 12 months later. Schizophrenia patients with comorbid OCSs showed significant pronounced deficits, with increasing effect sizes over the 12-month assessment period in specific cognitive areas such as visuospatial perception and visual memory (WAIS-R block design, Rey-Osterrieth Complex Figure Test), executive functioning (perseveration in the Wisconsin Card Sorting test), and cognitive flexibility (Trail Making test B). These cognitive domains are correlated with OCS severity and are known to be candidate cognitive domains in obsessive-compulsive disorder (OCD). OCSs in schizophrenia is associated with specific and longitudinally stable cognitive deficits, strongly arguing for at least partially overlapping neurobiological mechanisms with OCD. Prospective studies involving patients with at-risk mental states for psychosis are necessary to decipher the interaction of cognitive impairment and the clinical manifestations of schizophrenia and OCSs. This might facilitate the definition of patients at high risk for OCSs, an early detection of subclinical levels, therapeutic interventions, and clinical monitoring.

Mentalizing under influence: abnormal dependence on prior expectations in patients with schizophrenia

An impaired ability to appreciate other people's mental states is a well-established and stable cognitive deficit in schizophrenia, which might explain some aspects of patients' social dysfunction. Yet, despite a wealth of literature on this topic, the basic mechanisms underlying these impairments are still poorly understood, and their links with the clinical dimensions of schizophrenia remain unclear. The present study aimed to investigate the extent to which patients' impaired ability to appreciate other people's intentions (known as mentalizing) may be accounted for by abnormal interaction between the two types of information that contribute to this ability: (i) the sensory evidence conveyed by movement kinematics; and (ii) the observer's prior expectations. We hypothesized that this is not a generalized impairment, but one confined to certain types of intentions. To test this assumption, we designed four tasks in which participants were required to infer either: (i) basic intentions (i.e. the simple goal of a motor act); (ii) superordinate intentions (i.e. the general goal of a sequence of motor acts); (iii) social basic; or (iv) social superordinate intentions (i.e. simple or general goals achieved within the context of a reciprocal interaction). In each of these tasks, both prior expectations and sensory information were manipulated. We found that patients correctly inferred non-social, basic intentions, but experienced difficulties when inferring non-social superordinate intentions and both basic and superordinate social intentions. These poor performances were associated with two abnormal patterns of interaction between prior expectations and sensory evidence. In the non-social superordinate condition, patients relied heavily on their prior expectations, while disregarding sensory evidence. This pattern of interaction predicted the severity of 'positive' symptoms. Social conditions prompted exactly the opposite pattern of interaction: patients exhibited weaker dependence on prior expectations while relying strongly on sensory evidence, and this predicted the severity of 'negative' symptoms. We suggest both these patterns can be accounted for by a disturbance in the Bayesian inferential mechanism that integrates sensory evidence (conveyed by movement kinematics) into prior beliefs (about others' mental states and attitudes) to produce accurate inferences about other people's intentions.

Deficient maturation of aspects of attention and executive functions in early onset schizophrenia

The few existing long-term, neuropsychological follow-up studies of early onset schizophrenia (EOS) patients have reported relative stability in some cognitive functions but abnormal developmental trajectories in verbal memory, set shifting, aspects of attention, and speed of information processing throughout late adolescence into early adulthood. The current 5-year follow-up study compared the development of specific cognitive functions in EOS patients (N = 17) from the time of first-episode to chronic phase with that of healthy controls (N = 38) and secondarily to patients with other early onset, non-organic, non-affective psychoses (EOP) (N = 11). Speed of processing of executive functions, set shifting, and attention improved significantly in the healthy controls and reflected continuous functional maturation during late adolescence and early adulthood. The developmental progression of attention and set shifting but not speed of processing of executive functions was significantly subnormal in EOS patients. Other specific cognitive functions that had attained functional maturity in the healthy controls before or around the time of the baseline assessment showed normal development in EOS patients during the follow-up period, indicating stable cognitive deficits. These results suggest post-onset developmental deficits in two out of the three aspects of attention and executive functions that have protracted maturational trajectories and that overlap the age of onset of EOS. No significant difference in the development of any specific cognitive function was found between the EOS and EOP group.

Motor speed predicts stability of cognitive deficits in both schizophrenic and bipolar I patients at one-year follow-up

Background We examined whether motor speed assessed by the finger tapping test predicts generalized and specific stable deficits because of a common patho-genic process in bipolar and schizophrenic patients. Methods: One hundred and two patients underwent a battery of neuropsychological tests. Patients with a score of less than one standard deviation from their siblings' sample in two assessments with an interval of one year were defined as suffering from stable deficits because of a common pathogenic process. In addition to univariate analyses, factor analyses, ordinal logistic regression, and multiple linear regressions were used. A general score was also calculated. Results: No differences were found between schizophrenic and bipolar patients in the deficits of verbal fluency, shift reasoning ability and executive attention. Schizophrenic patients had greater persistent cognitive deficit because of a common pathogenic factor in the verbal memory dimension than bipolar patients. Motor speed predicted the specific deficits of verbal fluency, shift reasoning, executive attention and the general deficit of both bipolar I and schizophrenic patients. Bipolar patients suffered a lesser specific deficit in the verbal memory dimension than schizophrenic patients did, this domain not being predicted by motor speed. Motor speed predicted the generalized deficit and the specific dimensions in which schizophrenic and bipolar patients showed no differences. Conclusions: These results suggest the presence of general and specific stable cognitive deficits because of a common pathogenic factor related to psychomotor slowness. Motor speed seems to be suitable endophenocognitype for schizophrenia and bipolar disorder.

Why cognitive performance in ADHD may not reveal true potential: Findings from a large population-based sample

Focusing on symptoms of attention deficit hyperactivity disorder (ADHD) in a sample obtained from the general population, we aimed to investigate the effects of incentives and event rate on reaction time (RT) performance and response inhibition. We assessed 1156 children, at a mean age of 8 years, on their performance on an inhibition task and a RT task under different experimental conditions that manipulated event rate and incentives. Children with high ADHD (ADHD-H) symptoms showed cognitive performance deficits only under some of the experimental conditions compared to a control group. The fast-incentive condition of the RT task succeeded in normalizing the RT variability, as well as the slow overall speed, in the ADHD-H group. Analyses of ADHD symptom scores as a quantitative trait in the total sample were overall consistent with these findings. The findings suggest that at least some cognitive performance deficits in children with high ADHD symptoms do not reflect stable cognitive deficits. The degree to which cognitive impairments in ADHD can be modulated by energetic or motivational factors has important implications for clinical and educational interventions.

387 – Largely stable cognitive deficits across first-episode and chronic schizophrenia

387 – Largely stable cognitive deficits across first-episode and chronic schizophrenia

Reaction time performance in ADHD: improvement under fast-incentive condition and familial effects

Reaction time (RT) variability is one of the strongest findings to emerge in cognitive-experimental research of attention deficit hyperactivity disorder (ADHD). We set out to confirm the association between ADHD and slow and variable RTs and investigate the degree to which RT performance improves under fast event rate and incentives. Using a group familial correlation approach, we tested the hypothesis that there are shared familial effects on RT performance and ADHD. A total of 144 ADHD combined-type probands, 125 siblings of the ADHD probands and 60 control participants, ages 6-18, performed a four-choice RT task with baseline and fast-incentive conditions. ADHD was associated with slow and variable RTs, and with greater improvement in speed and RT variability from baseline to fast-incentive condition. RT performance showed shared familial influences with ADHD. Under the assumption that the familial effects represent genetic influences, the proportion of the phenotypic correlation due to shared familial influences was estimated as 60-70%. The data are inconsistent with models that consider RT variability as reflecting a stable cognitive deficit in ADHD, but instead emphasize the extent to which energetic or motivational factors can have a greater effect on RT performance in ADHD. The findings support the role of RT variability as an endophenotype mediating the link between genes and ADHD.

Effects of nicotinic therapies on attention and executive functions in chronic low‐dose MPTP‐treated monkeys

Chronic administration of low doses of the neurotoxin MPTP to nonhuman primates induces cognitive deficits similar to those seen in early Parkinson's disease (PD) patients, without the confounding effect of significant motor impairment. The present study assessed the extent to which specific attentional and central executive deficits in chronic low dose (CLD) MPTP-treated monkeys could be modified by nicotinic therapies. Four adult male rhesus monkeys were trained to perform attention and executive function tasks and were then administered low doses of MPTP (dose range: 0.025-0.1 mg/kg, i.v.) over 98-158 days until stable cognitive deficits appeared. Results showed that both nicotine and the alpha4beta4 subtype-selective nAChR agonist SIB-1553A could improve certain aspects of attentional and central executive functioning in this model of early Parkinsonism. Nicotine failed to improve performance of CLD-MPTP-treated animals on an attention set-shifting task while SIB-1553A significantly improved at least some aspects of performance, suggesting that the compound increased the animals' ability to maintain a previously formed response set and restored cognitive flexibility. Both nicotine and SIB-1553A caused a dose-dependent enhancement of performance on the focused attention (cued reaction time) task, decreasing reaction times on both cued and noncued trials. Nicotine caused a significant reduction in reaction times but did not alter the error profile on an impulse (motor readiness) task. SIB-1553A reduced reaction times but caused an increase in bar release (i.e. impulsivity) errors. These data suggest that nicotinic drugs may have therapeutic potential for treating cognitive dysfunction in PD.

Donepezil for mild cognitive impairment

Problems with memory which do not meet the diagnostic criteria for dementia, usually called mild cognitive impairment (MCI), can be the first sign of an impending dementia, particularly Alzheimer's disease (AD). There is no consensus on a definition or diagnostic criteria for MCI, and MCI remains a vague term and those so described are a heterogeneous population, consisting of people who may rapidly progress to dementia but also of people with stable cognitive deficits and some who may actually improve. Treatment in the very earliest stages of AD may delay progression to AD. Donepezil (Aricept, E2020), a cholinesterase inhibitor, has been shown to benefit all severities of AD including mild and it would be reasonable to investigate its efficacy for those with MCI. To assess the effects of donepezil in people with mild cognitive impairment but no diagnosis of dementia. The trials were identified from a search of the Specialized Register of the Cochrane Dementia and Cognitive Improvement Group on 6 January 2006. This register contains records from major health care databases like CENTRAL, MEDLINE, EMBASE, CINAHL and PsycINFO and many ongoing trial databases and is updated regularly. All double blind, randomized trials in which treatment with donepezil was compared with placebo for patients with mild cognitive impairment. Data were extracted from the published reports of the included studies, pooled where appropriate and the treatment effects or the risks and benefits estimated. The two included studies, with a total of 782 patients, all with a MMSE greater than 23 points, identified similar patients for inclusion, but were quite different with respect to design and objective. Pooling results in a meta-analysis was not possible. In the first study the 13-item ADAS-Cog showed benefit associated with 10 mg/day donepezil compared with placebo at 24 weeks (MD 1.90, 95% CI 0.51 to 3.29, p=0.007), but four other measures of cognitive function did not. The analysis of withdrawals before the end of treatment at 24 weeks, withdrawals due to an adverse event, and numbers experiencing an adverse event, showed a significant difference between the donepezil group and the placebo group in favour of placebo, (43/133 donepezil 23/137 placebo, OR 2.37, 95% CI 1.33 to 4.22, p=0.003), (29/133 donepezil 10/137 placebo, OR 3.54, 95% CI 1.65 to 7.60, p=0.001), (116/133 donepezil, 100/137 placebo, OR 2.52 95% CI 1.34 to 4.76, p=0.004). Various adverse effects were recorded, and several types of event, diarrhoea, nausea, vomiting, leg cramps and abnormal dreams, were reported more frequently in the donepezil group compared with the placebo. In the second study there was a significant difference between the number of patients diagnosed with AD or another dementia between the donepezil group and the placebo group in favour of donepezil after one year of treatment (16/253 donepezil 38/259 placebo) (OR 0.39, 95% CI 0.21 to 0.72, p=0.003), but no difference after 3 years of treatment (63/253 donepezil 73/259 placebo) (OR 0.84, 95% CI 0.57 to 1.25, p=0.4). There are two included studies. One study demonstrated a modest treatment effect in cognitive function as assessed by ADAS-Cog13 but not for other outcomes assessing different domains of cognitive function. Donepezil was associated with significantly more adverse effects compared with placebo, mostly gastrointestinal. From the second study, there is no evidence that donepezil delays the onset of AD. There is no evidence to support the use of donepezil for patients with MCI. The putative benefits are minor, short lived and associated with significant side effects.

Differences in α7 nicotinic acetylcholine receptor binding in motor symptomatic and asymptomatic MPTP-treated monkeys

We studied [ 125I]α-bungarotoxin (btx) binding to α7 nicotinic acetylcholine receptors in normal and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) exposed macaque monkeys. [ 125I]α-Btx binds throughout the normal monkey brain, with the greatest density in the thalamic nuclei and with moderate to low binding in the hippocampus, prefrontal cortex, caudate, putamen, and substantia nigra. Chronic adminstration of low doses of MPTP resulted in animals with stable cognitive deficits without overt parkinsonian motor symptoms. [ 125I]α-Btx binding in the brains of these animals was significantly increased in the outermost layers of the supplementary motor cortex (area 6M, ~50%), primary motor cortex (area 4, ~112%) and throughout the putamen (~50–72%). In contrast, there was no change in [ 125I]α-btx binding in the brain regions thought to be involved in mediating the cognitive functions impaired in these monkeys (e.g., the hippocampus, areas 9/46D and 46D of the principal sulcus, and area 24c of the cingulate sulcus). Animals with cognitive dysfunction that received escalating doses of MPTP for >6 months developed motor signs of parkinsonism which were indistinguishable from those seen in animals rendered acutely parkinsonian with short term administration of large doses of MPTP. These two “motor symptomatic” groups had significantly increased [ 125I]α-btx binding only in the dorsolateral putamen. Immunohistochemical studies showed that the increased [ 125I]α-btx binding, when observed, was associated with enhanced immunohistochemical staining localized to neurons and was not a result of an astrocytic response to MPTP. These results suggest that the increase in α7 nicotinic acetylcholine receptor expression in the chronic low-dose MPTP treated, motor asymptomatic monkeys may be a part of compensatory processes contributing to the maintained motor functioning in these animals.

Subcortical hypoperfusion following surgery for aneurysmal subarachnoid haemorrhage: implications for cognitive performance?

The incidence and severity of cognitive deficits after surgery for aneurysmal subarachnoid haemorrhage and their relationship to aneurysm site remains controversial. The aim of this study was to investigate the pattern of regional cerebral blood flow which exists in patients one year post-surgery and to identify whether different patterns exist which may be related to the type of cognitive deficit or the location of the aneurysm. 62 patients underwent cognitive assessment and HMPAO SPECT imaging at a mean time of 12 months following surgery. Results were compared to those from healthy control subjects (n = 55 for neuropsychological testing; n = 14 for SPECT imaging). In the patient group, significant stable cognitive deficits occurred in all cognitive domains but no cognitive measure differentiated aneurysm site. On SPECT images, statistical parametric mapping identified a large common area of subcortical hypoperfusion in the patient group as a whole. The findings of this study suggest a possible link between reduced subcortical function and the extent and severity of cognitive deficits.