Coiling versus clipping for the treatment of aneurysmal subarachnoid hemorrhage: a longitudinal investigation into cognitive outcome.

OBJECTIVE: Endovascular coiling has been used increasingly as an alternative to neurosurgical clipping for treating subarachnoid hemorrhage secondary to aneurysm rupture. The aim of the present study was to provide a prospective, longitudinal investigation into cognitive function in patients with aneurysmal subarachnoid hemorrhage treated with either neurosurgical clipping or endovascular coiling. METHODS: Twenty-three patients who were treated for aneurysmal subarachnoid hemorrhage at the National Hospital for Neurology and Neurosurgery in London, England, were recruited prospectively. Twelve patients who underwent surgical clipping were compared with a group of 11 patients who underwent endovascular coiling. All patients underwent a comprehensive, standardized neuropsychological assessment using the same battery of tests at the acute stage (within 2 wk after treatment). All patients who underwent coiling and 11 of the 12 patients who underwent clipping were reassessed at the post-acute long-term follow-up (6 mo) stage. RESULTS: Group comparisons at the acute assessment revealed a significant difference favoring coiling patients on only one measure of verbal recall. However, there were no other significant differences between the groups at this stage. At the post-acute assessment, the clipped group performed better than the coiled group on measures of intellectual functioning (P < 0.05), although no other differences were found on a range of cognitive tests. Intragroup comparisons between the acute and post-acute assessments found equivocal, significant improvements in measures of intellectual functioning, memory, executive functions, and speed of information processing in both groups of patients. CONCLUSION: We argue that there are minimal differences in the long-term cognitive outcome between endovascular coiling and surgical clipping. In the acute phase after treatment, we suggest that coiled patients, having been spared neurosurgical intervention, may have a slightly better cognitive outcome than clipped patients. However, these differences level off and both groups of patients ultimately experience widespread improvement in cognitive functioning by the post-acute stage of recovery.

Psychosocial adjustment following relief of chronic narcolepsy.

BACKGROUND AND PURPOSE: No previous research has examined the psychosocial adjustment of chronic narcolepsy patients following efficacious pharmacotherapy. In contrast, considerable research has examined the process of psychosocial adjustment following surgical relief of chronic epilepsy. This process can manifest as a clinical syndrome, the 'burden of normality', comprising psychological, behavioural, affective and sociological features. The aim of the present study was to characterise the process of psychosocial adjustment of patients with successfully treated narcolepsy and to explore the applicability of the burden of normality. PATIENTS AND METHODS: Thirty-three narcolepsy patients and 31 epilepsy surgery patients were recruited through routine outpatient follow-up at the Austin Hospital in Melbourne. All patients underwent in-depth, qualitative psychosocial assessment using a well-validated semi-structured interview, the Austin CEP Interview. They were also administered quantitative measures of anxiety (State Trait Anxiety Inventory) and depression (Beck Depression Inventory-II). RESULTS: Narcolepsy patients spontaneously reported similar themes of post-treatment adjustment to successfully treated epilepsy patients, including symptoms of the burden of normality. Chi-squared analyses revealed that the two groups differed only on disease-specific factors, reflecting the later diagnosis and treatment of narcolepsy (P<0.05). CONCLUSION: The results support a general model of adjustment following successful treatment of chronic neurological illness, as the patient discards perceptions of illness and behaviours associated with being 'sick' and learns to become 'well'. Recognition of the burden of normality has important clinical implications for maximising the post-treatment care and outcome of narcolepsy patients.

Cognitive dysfunction in patients with cerebral microbleeds on T2*-weighted gradient-echo MRI.

Gradient echo T2*-weighted MRI has high sensitivity in detecting cerebral microbleeds, which appear as small dot-like hypointense lesions. Microbleeds are strongly associated with intracerebral haemorrhage, hypertension, lacunar stroke and ischaemic small vessel disease, and have generated interest as a marker of bleeding-prone microangiopathy. Microbleeds have generally been considered to be clinically silent; however, since they are located in widespread cortical and basal ganglia regions and are histologically characterized by tissue damage, we hypothesized that they would cause cognitive dysfunction. We therefore studied patients with microbleeds (n = 25) and a non-microbleed control group (n = 30) matched for age, gender and intelligence quotient. To avoid the confounding effects of coexisting cerebrovascular disease, the groups were also matched for the extent of MRI-visible white matter changes of presumed ischaemic origin, location of cortical strokes, and for the proportion of patients with different stroke subtypes (including lacunar stroke). A battery of neuropsychological tests was used to assess current intellectual function, verbal and visual memory, naming and perceptual skills, speed and attention and executive function. Microbleeds were most common in the basal ganglia but were also found in frontal, parieto-occipital, temporal and infratentorial regions. There was a striking difference between the groups in the prevalence of executive dysfunction, which was present in 60% of microbleed patients compared with 30% of non-microbleed patients (P = 0.03). Logistic regression confirmed that microbleeds (but not white matter changes) were an independent predictor of executive impairment (adjusted odds ratio = 1.32, 95% confidence interval 1.01-1.70, P = 0.04). Patients with executive dysfunction had more microbleeds in the frontal region (mean count 1.54 versus 0.03; P = 0.002) and in the basal ganglia (mean 1.17 versus 0.32; P = 0.048). There was a modest correlation between the number of microbleeds and the number of cognitive domains impaired (r = 0.44, P = 0.03). This study provides novel evidence that microbleeds are associated with cognitive dysfunction, independent of the extent of white matter changes of presumed ischaemic origin, or the presence of ischaemic stroke. The striking effect of microbleeds on executive dysfunction is likely to result from associated tissue damage in the frontal lobes and basal ganglia. These findings have implications for the diagnosis of stroke patients with cognitive impairment, and for the appropriate use of antihypertensive and antiplatelet treatments in these patients.