Biomedical subjects
Publications and source records attributed to R Besser.
A 20 years old female patient with epileptic seizures (bilateral myoclonus and generalized tonic-clonic seizures (bilateral myoclonus and generalized tonic-clonic seizures) since the age of 13 was treated with valproic acid. Eight hours after 2 of 3 prophylactic antimalarial treatments with mefloquine generalized tonic-clonic seizures occurred. A causal relationship is suggested.
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Two patients with acute severe organophosphate intoxication showed (1) single evoked compound muscle action potentials (CMAP) with repetitive discharges and (2) prominent decremental responses of CMAP with 20 and 50 Hz supramaximal nerve stimulation. Following the intravenous injection of single small doses of pancuronium, marked improvement in these abnormalities occurred and persisted for several hours. We postulate that the physiologic improvement following low-dose pancuronium results from blockade of acetylcholine receptors, especially those located on the terminal axon responsible for antidromic backfiring.
In 19 patients with herpes simplex encephalitis 64 EEG examinations and 36 CT scans have been performed within the first two weeks after onset of clinical symptoms. During the first 10 days periodic discharges were present in 12 patients. At this time CT scan was negative in 5 of them. Five of 7 patients without but only 4 of 12 patients with this EEG pattern survived without clinical abnormalities. Five patients with periodic discharges died during the acute stage of the illness. In patients with poor outcome including major clinical deficit or death periodic discharges were present during successive investigations until day 14. In the group of patients with good clinical improvement these EEG changes were only detected in a single recording until day 7. Periodic discharges have to be considered as an indicator of a poor prognosis whenever they are present for a longer period.
Blood organophosphate (OP) levels, serum butyrylcholinesterase (BChE) activity and electrophysiological neuromuscular transmission following repetitive nerve stimulation at 10 Hz and 50 Hz were studied serially in five patients with severe acute organophosphate intoxication following suicide attempts. Eight to 45 hours after oral ingestion, blood OP levels were elevated, BChE activity was markedly reduced, while repetitive nerve stimulation studies showed no or only mild abnormalities. The latter attained the maximal abnormality 32-69 h after ingestion, when BChE was inactivated further but elevated OP levels had fallen. Recovery from these abnormalities at 10 Hz nerve stimulation occurred within 100-237 h after the intoxication and it was still incomplete at 50 Hz stimulation 48-80 h later. BChE activity varied within a wide range and showed even normal values at both times. Neuromuscular transmission studies proved to be the most useful indicator for determining the severity and time course of organophosphate intoxication.
Acute organophosphate intoxication resulting from suicide attempts in 14 patients produced a series of electrophysiologic abnormalities that correlated with the clinical course. Spontaneous repetitive firing of single evoked compound muscle action potentials (CMAP) was the earliest and most sensitive indicator of the acetylcholinesterase inhibition. A decrement of evoked CMAP following repetitive nerve stimulation was the most severe abnormality. At the height of the intoxication no CMAP was evoked after the first few stimuli. The decrement-increment phenomenon occurred only at milder stages of intoxication and its features are characteristic of acetylcholinesterase inhibition. These electrophysiologic features proved to be the most useful for determining initial severity and clinical course of the acute organophosphate intoxication and differentiated this syndrome from those of myasthenia gravis, Eaton-Lambert syndrome, and botulism.
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Repetitive stimulation of the median nerve elicited a so far unknown course of the muscle action potentials in four patients with organophosphate intoxications. The amplitude of the initial muscle action potential decreased with the second stimulus and gradually increased to normal values by subsequent stimuli. With the second stimulus a loss of the repetitive muscle action potentials occurred. The Decrement-increment phenomenon was seen in early and/or late stages of severe intoxications when fasciculations were prominent. We suppose that the repetitive muscle action potential following the first stimulus results from backfiring. The second orthodromic nerve action potential collides with this antidromic activity leading to a partial extinction. Loss of backfiring with the second stimulus abolishes the phenomenon of collision and enables a recovery of the muscle action potential amplitudes.
The current treatment of spontaneous intracerebral hematomas is reviewed, and the results in the literature as well as our own experience on the subject are discussed. It is evident that modern diagnostic methods and follow-up observation periods have led to a sharp decline in the need for operative treatment. The diverse forms of clinical treatment and the remaining indications for neurosurgical intervention are presented.
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A 72-year-old man had developed amiodarone neuropathy. He was found, at biopsy, to have a fascicular neuroma of his right sural nerve, unassociated with his underlying neuropathy, apparently due to blunt trauma, as electroneurographic needling of this nerve could safely be ruled out by the patient and his physicians. Such fascicular neuromas, which may remain without sensory deficits, may develop at an unknown frequency, and may only be uncovered by biopsy--or autopsy--in a coincidental neuropathic process.
SEP were recorded in 14 patients, who fulfilled the clinical and electroencephalographic criteria of brain death. The results are compared with the respective ones in healthy subjects. Beside the absence of cortical N 20 in each brain dead patient, reduction of amplitude or absence of near field negativity (N 13b) from upper neck regardless of the position of the reference electrode represents the predominant result. The near field potential from the lower neck (N 13a) was unaffected. The counterpart in the far field potential recorded from F z was amplitude reduction of P 13. These results suggest that the dissociation of N 13a and N 13b can confirm the diagnosis of brain death. Moreover these results support the view of two independent generators of N 13a and N 13b despite their identical amplitude and latency.
Neuromuscular transmission was studied in 11 patients with organophosphate intoxication. The compound muscle action potential (MAP) was recorded from the thumb after single, repetitive (1-50 Hz) and paired stimulation. All patients showed a prolonged MAP. The duration increased with the severity of intoxication. The number of peaks varied only slightly. In all cases repetitive stimulation reduced the later components of the MAP. There was no correlation with tetanic fade of the initial negative component. One patient had a pronounced tetanic fade but a slight reduction of repetitive components. In view of experimental studies a combined pre- and postsynaptic effect seems to be responsible.
Early somatosensory evoked potentials to median nerve stimulation were recorded in 6 normal adults from the scalp and the neck. Simultaneous derivations consisted of a recording with a cephalic reference, recordings of both electrodes with a noncephalic reference and an arithmetically subtraction of these potentials. The electrodes were placed over the scalp (P4'), the lower and the upper neck and the reference electrodes over the midfrontal region (Fz), both ears (M1/2) and the contralateral hand. P15/P16 in the P4'-Fz derivation had no identity to the far field potentials (FFP) P13/P14 recorded from the scalp with hand reference. FFP P9 and P11 from the ear lobes was abolished in the P4'-M1/2 derivation and the residual positive waves corresponded to P13 and P14. None of the electrodes picked up a wave equivalent to P15 regardless of the reference electrode. In the neck (CV 7) - scalp derivation NSEP9, 13 and 14 corresponded to the FFP P9, 13 and 14. NSEP11 differed in latency from P11 and N11. There was no latency shift from the lower (CV 7) to the upper (CV 2) neck. NSEP9 and 11 was enhanced in amplitude from CV 7, which resulted from different polarities (N11/P11) over CV 7 and CV 2. These results indicate the necessarity of potential analysis with respect to the activity of the recording electrodes.
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