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H B Van der Worp

Publications and source records attributed to H B Van der Worp.

5 recordsLinked to original sources
PubMed2005

Domain-specific cognitive recovery after first-ever stroke: a follow-up study of 111 cases.

The objective of this study is to examine the prognosis of acute cognitive disorders post-stroke, and to evaluate which clinical factors predict domain-specific cognitive recovery. We followed the course of cognitive functioning in 111 stroke patients and 77 healthy controls by administering two neuropsychological examinations with a 6 to 10 month interval (mean interval, 7.5 +/- 1.3 months). The baseline examination was administered within three weeks post-stroke (mean interval, 7.9 +/- 4.2 days). To examine determinants of domain-specific cognitive recovery, we recorded vascular risk factors, clinical variables, and lesion characteristics. Recovery in visual perception/construction (83%) and visual memory (78%) was the most common. An acute cognitive disorder predicted a long-term disorder in the same domain (all p < .05), except for visual perception/construction. Factors associated with poor cognitive recovery were age (all p < .01), preexistent verbal ability (all p < .005), lesion locations involving the temporal (all p < .05), frontal (p < .05) and occipital lobe (allp < .05), lesion volume (p < or = .001), and diabetes mellitus (p < .01). An early neuropsychological examination provides valuable information on long-term cognitive performance. The prognosis of higher-level visual disorders is the most favorable. Cognitive recovery is associated with age, preexistent ability, lesion volume, lesion location, and diabetes mellitus.

Aged↗
PubMed1992

Quantitative EEG changes due to cerebral vasoconstriction. Indomethacin versus hyperventilation-induced reduction in cerebral blood flow in normal subjects.

Hyperventilation leads to an increase in slow EEG activity as well as to a decrease in alpha activity. These effects may be considered a result of reduction in cerebral blood flow due to vasoconstriction, but metabolic factors, such as alkalosis and the increased formation of cerebral lactate, may also have to be taken into account. As indomethacin decreases cerebral blood flow it is possible to study cerebral vasoconstriction, without concomitant metabolic alkalosis or cerebral lactate formation. Two parallel groups of 12 healthy male subjects (age 20-25) were studied with quantitative EEG (qEEG) and cerebral blood flow velocity as parameters. In the first group the effect of 100 mg indomethacin was studied. In the parallel group a standardized hyperventilation procedure was performed. In the indomethacin group the blood flow velocity decreased to 60% of the initial value; the qEEG showed a 0.5 Hz slowing of the alpha peak frequency (P less than 0.01) and a decrease in the power of the alpha band without any change in the delta or theta band. In the hyperventilation group the blood flow velocity decreased to 63% of the initial value and the qEEG showed a marked increase in delta and theta activity (P less than 0.01), but a non-significant change in alpha peak frequency. Indomethacin and hyperventilation caused similar degrees of vasoconstriction; however, the increase in qEEG slow wave activity, which was observed only in the hyperventilation group, is apparently related to metabolic rather than haemodynamic factors.

Adult↗
PubMed1991

Quantitative EEG during progressive hypocarbia and hypoxia. Hyperventilation-induced EEG changes reconsidered.

To investigate the role of cerebral hypoxia as a causative factor in the alteration of the qEEG during hyperventilation, qEEG changes caused by progressive hypocapnia were compared with qEEG changes due to progressive normobaric hypoxia in two parallel groups of 12 and 10 healthy male subjects (age 20-27 years), respectively. In the first group, qEEG records were obtained before and during hyperventilation to pCO2 levels of 4.0, 3.0 and 2.0 kPa. In the second group, the qEEG samples were taken before and during hypoxia with hemoglobin oxygen saturations of 80, 70 and 60%. In both groups, blood flow velocity in the middle cerebral artery was also recorded. Hyperventilation caused an exponential increase in slow activity and a decrease in alpha power. No shift in the alpha mean frequency and alpha peak frequency was observed, except with the pCO2 level of 4.0 kPa, which caused an increase in both variables. Hypoxia with a hemoglobin oxygen saturation of 60% caused a much less pronounced increase in slow activity. No change in total power in the alpha band was found, but both the alpha peak frequency and alpha mean frequency decreased. Lesser degrees of hypoxia caused only minimal EEG changes. Blood flow velocity was decreased by hyperventilation but increased by hypoxia. It is concluded that the EEG changes observed during hyperventilation must mainly or totally be attributed to factors other than cerebral hypoxia.

Adult↗