Erja Poutiainen

Cognitive and Neurophysiological Outcome of Cardiac Arrest Survivors Treated With Therapeutic Hypothermia

Background and Purpose— Cognitive deficits are common in survivors of cardiac arrest (CA). The aim of this study was to examine the effect of therapeutic hypothermia after CA on cognitive functioning and neurophysiological outcome. Methods— A cohort of 70 consecutive adult patients resuscitated from out-of-hospital ventricular fibrillation CA were randomly assigned to therapeutic hypothermia of 33°C for 24 hours accomplished by external cooling or normothermia. Neuropsychological examination was performed to 45 of the 47 conscious survivors of CA (27 in hypothermia and 18 in normothermia group) 3 months after the incident. Quantitative electroencephalography (Q-EEG) and auditory P300 event-related potentials were studied on 42 patients at the same time point. Results— There were no differences between the 2 treatment groups in demographic variables, depression, or delays related to the resuscitation. No differences were found in any of the cognitive functions between the 2 groups. 67% of patients in hypothermia and 44% patients in normothermia group were cognitively intact or had only very mild impairment. Severe cognitive deficits were found in 15% and 28% of patients, respectively. All Q-EEG parameters were better in the hypothermia-treated group, but the differences did not reach statistical significance. The amplitude of P300 potential was significantly higher in hypothermia-reated group. Conclusions— The use of therapeutic hypothermia was not associated with cognitive decline or neurophysiological deficits after out-of-hospital CA.

Cognitive changes as early signs of HIV infection

ABSTRACT‐ Neuropsychological examination was performed on 13 patients and 10 matched controls to assess the brain involvement of patients with human immunodeficiency virus (HIV) infection. HIV‐infected patients showed a significant decline in visuomotor, visuoconstructive and practical abilities as well as in motorfree visuospatial performance and repeating a long sentence. These findings could not be explained by the concomitant mental depression of these patients. Neither were they associated with any particular stage of HIV infection. The results suggest that mild cognitive changes may be detected even in the early stages of HIV infection, when examined by appropriate neuropsychological methods.

Microangiopathy with encephalopathy, hearing loss and retinal arteriolar occlusions: Two new cases

Two young women developed encephalopathy, hearing loss and retinal arteriolar occlusions. Their behaviour became immature and cognitive functions were severely impaired. One of the patients underwent brain biopsy, which showed several microinfarcts in both white and grey matter and microangiopathic changes, with thickened arteriolar segments staining intensely for laminin and fibronectin. These findings support the concept of a new type of microangiopathy involving the brain, inner ear and retina.

Cognitive performance in HIV‐1 infection: relationship to severity of disease and brain atrophy

We examined cognitive performance in 72 HIV‐1 infected patients and 34 controls. None of the patients had opportunistic infections or unusual neoplasms of the central nervous system (CNS). Factors other than HIV‐1 known to cause cognitive decline were excluded from both groups. Cognitive functioning analysed with special emphasis on the severity of HIV infection was related to neuroradiological and immunological findings. In patients with AIDS‐related complex (CDC IVa) or AIDS (CDC IVc,d), a deterioration of memory as well as cognitive speed and flexibility was detected. Furthermore, memory deficits were associated with central cerebral and infratentorial atrophy in those patients, while no association was found between cognitive deficits and immunological abnormalities. Patients at CDC stages II or III showed slight association between altered cognitive speed and flexibility and elevated leukocyte count, suggesting a subclinical CNS disease already at early stages of HIV infection.

Cognitive impairment after acute encephalitis: comparison of herpes simplex and other aetiologies.

OBJECTIVE: To compare the cognitive defects after acute acyclovir treated herpes simplex encephalitis with those after other types of acute encephalitis. METHODS: Seventy seven consecutive patients between 1985 and 1995 and 29 normal controls were studied. Of the 77 patients without concomitant neurological conditions, 17 had herpes simplex, one virus encephalitis (HSVE group), 27 had some other identified aetiology (non-HSVE group), and in 33 patients the cause was unknown. Acyclovir treatment was started less than four days after the first mental symptoms in 12 of 17 patients with HSVE. A thorough neuropsychological assessment was carried out about one month after the onset. RESULTS: The HSVE group had deficits in verbal memory, verbal-semantic functions, and visuoperceptual functions more often than the non-HSVE group. The risk for cognitive defects was twofold to four-fold in the patients with HSVE compared with the non-HSVE patients. Two (12%) of the patients with HSVE and 12 (44%) of the non-HSVE patients were cognitively intact. Six patients with HSVE (46%) and 17 (89%) non-HSVE patients later returned to work. The lesions on CT or MRI were bilateral only in one patient with HSVE. The defects in the three patients with adenovirus infection were severe and resembled the amnesia after HSVE. Cognitive impairment, not previously reported, was found in encephalitis after rotavirus infection and epidemic nephropathy. CONCLUSION: The recovery in the HSVE group was better than expected based on the medical literature. On the other hand there were surprisingly severe cognitive defects in encephalitis after other viruses. With early acyclovir treatment patients with the least severe HSVE were equivalent to those with non-HSV encephalitis with good outcome whereas those with the most severe non-HSV encephalitis were equivalent to those with HSVE with poor outcome.

The severity of cognitive deficits predicts return to work after a first-ever ischaemic stroke

Background The inability of stroke patients to return to work contributes disproportionately to the socioeconomic impact of stroke and is best predicted by the severity of stroke. However, the role of cognitive deficits in stroke severity has not been scrutinised. We studied whether the initial cognitive severity of stroke, compared with other influential factors, predicts the inability to return to work after stroke. Methods Consecutive patients aged 18–65 with a first-ever ischaemic stroke, working full time previously, were assessed neuropsychologically within the first weeks after stroke and at the 6-month follow-up. Similarly, 50 healthy demographic controls were assessed twice. The cognitive severity of stroke was operationalised as the number of initial cognitive deficits. Cognitive severity as a predictor of the inability to return to work was compared with demographic, occupational, neurological, radiological and functional data, vascular risk factors and mood state. Results The mean age of the 140 patients assessed both initially and at follow-up was 52 years. They had a mean of 13 years of education and 59% were men. At 6 months, only 41% of the patients had returned to work despite the relatively minor neurological and functional impairments of the cohort. In our model, the number of early cognitive deficits (OR=2.252, CI 1.294 to 3.918) was the only significant predictor of the inability to return to work. Conclusions The initial cognitive severity of stroke predicts the later inability to return to work. The benefits of neuropsychological assessments within the first weeks after stroke are emphasised.

CSF and serum β‐2‐microglobulin in HIV infection related to neurological dysfunction

ABSTRACT— Elevated (< 2.2 mg/l) CSF β‐2‐microglobulin (β2m) level was found in 9 of 16 neurologically symptomatic patients but in only 4 of 21 who were neurologically symptom‐free (P < 0.01). Serum β2m concentration was elevated (<2.5 mg/l) in 12 of 16 neurologically symptomatic patients but in only 8 of 21 symptom‐free patients (P < 0.01). When the CSF and serum β2m levels were related to various stages of HIV infection, the highest mean values for both CSF and serum were found in patients with acquired immunodeficiency syndrome (AIDS), followed by lower values in AIDS‐related complex (ARC), lymphadenopathy syndrome (LAS), and asymptomatic seropositive individuals (ASX), in decreasing order of preference. Our results suggest that elevated β2m in CSF and serum is related to the stage of general HIV infection and that elevated CSF β2m in the presence of intact BBB may be useful in evaluating CNS involvement in HIV‐infected patients.

Subcortical type cognitive impairment in herpes zoster encephalitis.

Nine immunocompetent patients with acute herpes zoster encephalitis (HZE) were studied with the help of neurological, neuroradiological and neuropsychological investigations. All patients were treated with acyclovir. Neuropsychological performance was compared with that of a group of 16 healthy controls. Computed tomography of the head showed infarct-like hypodense lesions in two patients, involving the internal capsule in one case and the temporoparietal cortex and white matter in another. Hypoperfusion shown by single photon emission computed tomography, mostly involving the frontal areas bilaterally, was seen in six of the seven patients examined. Hyperperfusion as seen in herpes simplex encephalitis was not encountered. One patient remained mildly demented, but all the other patients recovered relatively well. Neuropsychological examination after acyclovir treatment showed a decline in memory and speed of cognitive processes, without circumscribed neuropsychological deficits. Six of the nine patients showed behavioural disinhibition, and mood changes were also observed. Memory impairment in HZE was not as global or as severe as is described after encephalitis due to herpes simplex virus. In HZE both the brain perfusion pattern and the neuropsychological test profile showed features compatible with subcortical dysfunction.

Dementia associated with human immunodeficiency virus: subcortical or cortical?

Two different types of dementia and corresponding neuropathological findings of patients with human immunodeficiency virus (HIV) infection are presented. In one case, “subcortical” dementia with slow movements and mental processes as well as problems in active recall but without focal defects corresponded to diffuse leukoencephalopathy. In another case, “cortical” dementia with impaired abstraction and memory as well as several focal defects corresponded to microglial nodules in cortical and in deep grey matter, with only a mild diffuse leukoencephalopathy. Thus, in contrast to earlier interpretations, subcortical dementia does not appear to be the only form of dementia in HIV‐infected patients, and cortical dysfunction may also occur.

The cognitive burden of stroke emerges even with an intact NIH Stroke Scale Score: a cohort study

Background We aim to facilitate recognition of the cognitive burden of stroke by describing the parallels between cognitive deficits and the National Institutes of Health Stroke Scale (NIHSS), a widely used measure of stroke severity. Methods A consecutive cohort of 223 working-age patients with an acute first-ever ischaemic stroke was assessed neuropsychologically within the first weeks after stroke and at a 6-months follow-up visit and compared with 50 healthy demographic controls. The NIHSS was administered at the time of hospital admittance and upon discharge from the acute care unit. The associations between total NIHSS scores and domain-specific cognitive deficits were analysed correlatively and with a binary logistic regression. Results Of the NIHSS measurements (admittance median=3, range 0–24; discharge median=1, range 0–13), the total score at the time of discharge had systematically stronger correlations with cognitive impairment. Adjusted for demographics, the NIHSS discharge score stably predicted every cognitive deficit with ORs ranging from 1.4 (95% CI 1.2 to 1.6) for episodic memory to 1.9 (95% CI 1.5 to 2.3) for motor skills. The specificities of the models ranged from 89.5–97.7%, but the sensitivities were as low as 11.6–47.9%. Cognitive deficits were found in 41% of patients with intact NIHSS scores and in all patients with NIHSS scores ≥4, a finding that could not be accounted for by confounding factors. Conclusions Cognitive deficits were common even in patients with the lowest NIHSS scores. Thus, low NIHSS scores are not effective indicators of good cognitive outcomes after stroke.