Electroencephalographic findings in experimentally induced intracranial hypertension.
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Biomedical subjects
Publications and source records attributed to S L Notermans.
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In determining the detectability of brainstem, middle latency and cortical auditory evoked responses in preterm newborns, one has to deal with the ongoing maturation of the auditory system. In the preterm period the detectability of evoked responses is closely related to the appearance of the individual evoked response components. The detectability of the individual evoked response components in preterm infants is important, because low detectability rates make the absence of a particular evoked response component irrelevant with respect to the clinical-neurophysiological correlation. In a longitudinal study we determined the detectability and cumulative detectability, i.e. the presence of individual evoked response components in one or more recordings of evoked response components in 37 low risk preterm infants between 30 and 41 weeks conceptional age (CA). On the basis of their detectability it is concluded that evoked response components, determined between 30 and 34 weeks CA, are generally of limited use for clinical application, except for auditory brainstem response (ABR) components I, IIn, V and Vc and middle latency response (MLR) component Na. Our study made clear that improvement can be achieved by performing more than one examination within a period of approximately 4 weeks between the recording sessions. The cumulative detectability rates after two recordings showed improvement for all components involved in this study. The cumulative detectability rates of ABR components I, II, IIN, III, V, IIc, IIINc, Vc, MLR components Na and P0, and auditory cortical response (ACR) components PbP1 and N2p are sufficient to use as measures in the neurophysiological judgement of functional integrity of the central auditory pathway in preterm infants.
The diagnostic utility of electroneuromyography including F-wave and H-reflex was studied in 68 patients with peripheral polyneuropathy due to nutritional deficiency of thiamine. Out of all the electrophysiologic evaluations assessed, denervation activity in electromyography, prolonged conduction velocity and reduced motor nerve action potentials and prolonged H-reflex latency were the most frequently found abnormal findings, followed by reduced sural nerve action potential and, much less frequently, prolonged F-wave latency. In experimental thiamine-deficiency evoked polyneuropathy in chickens, the prominent abnormal findings were found in the leg muscles such as F-wave pathology and reduction and prolongation of peroneal and sciatic motor nerve action potentials, and also a prolongation of the distal sensory peroneal nerve latency respectively.
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Chickens fed with the same composition of diet as our low income beriberi polyneuropathic patients, developed clinical symptoms of thiamine deficiency in 22.3 +/- 6.3 days. There appeared to be a body store of thiamine which is utilized during a period of deficient intake. Haemoglobin content and serum albumin did not change appreciably during thiamine deficiency. The blood thiamine content was low and the thiamine pyrophosphate (TPP) effect increased to more than 25 percent during the development of the beriberi polyneuropathy, which resumed after one week on thiamine tetrahydrofurfuryl disulfide (TTFD) treatment. However, the clinical features gradually improved after about one month. Neurophysiological findings including somatosensory evoked potentials (SSEPs) and neuromorphological studies of the peroneal and sciatic nerves were compatible with a major degree of axonal degeneration and secondary minimal segmental demyelination. We may conclude that the experimentally induced beriberi polyneuropathy in chickens seems a good model for studying these forms of neuropathy in view of diagnosis and treatment.