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BACKGROUND: The subacute phase after aSAH carries the risk of delayed neurological deterioration due to cerebral vasospasm (CVS) and delayed cerebral ischemia (DCI). CVS is the delayed narrowing of one or more basal arteries of the brain after aSAH, which may go in line with radiographic evidence of diminished cerebral perfusion distal of the affected arteries. DCI is the clinical manifestation of CVS and may present as focal neurological deficit and/or as worsening on the GCS scale. Both CVS and DCI are associated with the presence of infarcts and worse neurological outcome. The association of DCI and neuropsychological deficits (NPD) in patients surviving aSAH is less studied.

OBJECTIVE:
It was our aim to test the hypothesis that DCI has a negative impact on the neuropsychological outcome in aSAH patients.

METHODS:
2-center study on surviving aSAH patients btw. 01-2009 and 08-2012, clinical data derived from Swiss SOS database, consent from both ethics committees. CVS was defined as mean blood flow velocity (Vmean) > 140 cm/sec or increase in Vmean > 50cm/sec/24h or as a Lindegaard-Index > 3 in transcranial Doppler sonography or confirmation by CT-angiography or digital subtraction angiography. DCI was defined as occurrence of focal neurological impairment and/or decrease of at least 2 points on the GCS after ruling out of other causes (hydrocephalus, electrolyte disturbance, epilepsy, infection). Occurrence of new cerebral infarctions on imaging at discharge (as surrogate marker) was also regarded as DCI.
Included were surviving patients with available full neuropsychological assessment (face-to-face interview, 2-2.5 hours) by an independent neuropsychologist (median: 45 days after aneurysm occlusion). Cognitive domains tested: (A) Memory, (B) Attention, (C) Executive Function, (D) Visual and spatial perception, (E) Language/Calculation, (F) Behaviour. Grading of patient’s cognitive status according to normative population data as no (regular), or as minimal, moderate or severe disability. Logistic regression was used to assess the effect size of the relationship between DCI and NPD using a univariable- and a multivariable model (forced-entry methodology).

RESULTS:
226 aSAH patients were treated, of which 39 died (17.2%). 187 surviving patients were identified for possible enrollment. Full neuropsychological assessment was available in 92 patients (40.7%; 35 male and 57 female; mean age 51.4 ± 11.6 years (± SD)), which thus served as study population. Higher neurological morbidity was associated with DCI as demonstrated by worse modified Rankin scores at discharge lower proportion of patients with good outcome and higher rates of neurological deficits (p<0.0001). NPD were significantly more frequent, more severe and included more neuropsychological domains in patients with DCI (p=0.001), even though time from occlusion therapy to neuropsychological evaluation was significantly longer in patients suffering from DCI (p=0.027). On univariate analysis, patients suffering from DCI were 6.38 (OR; 95% CI: 1.98, 20.50) times as likely to have moderate to severe NPD as patients without DCI (p=0.002). On multivariate analysis, patients suffering from DCI were 4.9 (OR; 95% CI: 1.26, 19.58) times as likely to have moderate to severe NPD as patients who do not suffer from DCI (p=0.022). DCI was the strongest predictor of moderate to severe NPD in our cohort.

CONCLUSION:
Our results indicate that patients experiencing DCI following aSAH have a five-fold risk of suffering from moderate to severe NPD compared to patients without DCI. In our cohort, 86% of patients with DCI revealed moderate to severe NPD after a mean of three months following aneurysm rupture and subsequent treatment. Overall, three factors emerged as independent predictors of moderate to severe NPD: DCI, Age, Chronic hydrocephalus.