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M Emre

Publications and source records attributed to M Emre.

40 records · Page 3Linked to original sources

[Automatic quantification of SEP for continuous patient monitoring].

Parameters presently used to analyse evoked potentials such as amplitude and latency are based on well defined single components, the recognition of which may become arbitrary in severely altered responses. Furthermore, they ignore changes also present in the remainder of an evoked potential wave form. Hence, they are ill suited for monitoring comatose patients or patients during high risk surgery. Alternatively, crosscorrelation analysis may be employed yielding two parameters by comparing the SEP of the patient with a reference response: R, the correlation coefficient, a numerical measure of similarity of the two responses in terms of overall configuration and tau, indicating the time displacement of the main common components of the two signals. A "grand average" evoked potential (SEP) composed of the responses of age and sex matched healthy subjects or in perioperative monitoring the patient's own preoperative response might be used as a reference. By help of continuous averaging of the SEP these two parameters may be determined in real time allowing a more dynamic way of monitoring than by sequential averaging individual responses.

Adult↗

Non-convulsive status epilepticus after abrupt withdrawal of hypnotic-sedative drugs.

Four patients with severe addiction to sedative-hypnotics and with acute withdrawal symptoms of these drugs are described. They developed latent confusional states with characteristic EEG patterns (bilateral slow and sharp waves of high amplitude). Following small doses of benzodiazepines the EEG became normal together with a reduction in the clinical symptoms. It is suggested that the confusional states were of an epileptic nature.

Adult↗

The acute neurotoxicity and effects upon cholinergic axons of intracerebrally injected beta-amyloid in the rat brain.

The acute neurotoxicity and effects upon cholinergic axons of an intracerebrally injected synthetic peptide corresponding to the first 1-40 amino acids of beta-amyloid protein (beta AP1-40) was studied in rats. A synthetic peptide with the reverse sequence (beta AP40-1) or the vehicle alone were injected in the contralateral hemisphere as control. The size of the resulting lesions was quantified in serial sections using an image analyzer. Counts of cholinergic and noradrenergic fibers were also obtained around the lesion area. The results revealed that beta AP1-40 was significantly more toxic than both reverse peptide and the vehicle. The latter two, however, also caused considerable neurotoxicity. beta AP1-40 was toxic to both cholinergic and noradrenergic fibers to the same extent, and this toxicity was limited to the immediate vicinity of the lesion. This study confirms and extends the results of previous studies reporting neurotoxic effects of intracerebrally injected beta-amyloid in the rat. Our results also show that beta AP1-40 itself is not the source of the altered acetylcholinesterase enzyme activity that has been described in the plaques and tangles of Alzheimer's disease.

Acetylcholinesterase↗