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Biomedical subjects

R Besser

Publications and source records attributed to R Besser.

At least 37 records · Page 2Linked to original sources
PubMed1989

End-plate dysfunction in acute 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.

Adult↗
PubMed1989

[The decrement-increment phenomenon in disorders of neuromuscular transmission by inhibition of acetylcholinesterase].

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.

Cholinesterase Inhibitors↗
PubMed1989

[Treatment of spontaneous intracerebral hemorrhage--operative or conservative?].

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.

Cerebral Hemorrhage↗
PubMed1988

Traumatic fascicular neuroma.

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.

Aged↗
PubMed1988

Somatosensory evoked potentials aiding the diagnosis of brain death.

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.

Brain Death↗
PubMed1988

[The repetitive muscular action potential in neuromuscular transmission disorders due to acetylcholinesterase inhibition].

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.

Action Potentials↗
PubMed1988

[The effect of a reference electrode on the configuration of somatosensory evoked potentials].

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.

Adult↗
PubMed1987

[Brain death].

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Brain Death↗
PubMed1987

Combined therapy with acyclovir and adenosine arabinoside in herpes simplex encephalitis.

We report a case of herpes simplex encephalitis (HSE) with initial coma and severe left-sided hemiparesis in which combined treatment with adenine arabinoside and acyclovir was followed by complete recovery. This favorable result is discussed in view of the literature of HSE treatment including experimental studies on antiviral activity of both drugs. Combined treatment may be useful in severe cases of HSE.

Acyclovir↗
PubMed1987

Acute trimethyltin limbic-cerebellar syndrome.

An acute limbic-cerebellar syndrome was seen in six industrial workers who inhaled trimethyltin (TMT). Clinical features included hearing loss, disorientation, confabulation, amnesia, aggressiveness, hyperphagia, disturbed sexual behavior, complex partial and tonic-clonic seizures, nystagmus, ataxia, and mild sensory neuropathy. Severity paralleled maximal urinary organotin levels. One patient died and two remained seriously disabled.

Acute Disease↗
PubMed1984

Methyltin intoxication in six men; toxicologic and clinical aspects.

Neurologic and psychiatric symptoms such as headache, tinnitus, defective hearing, changing desorientation and aggressiveness are initial symptoms of methyltin chloride intoxication. Some patients also developed epileptic equivalents, such as dreamy attacks and central ventilation transaminases. Laboratory findings included low levels of serum potassium, leucocytosis and elevated transaminases. The excretion rate of tin in the urine correlated with the severity of the intoxication. There was no measurable effect of plasma separation or d-penicillamine therapy on tin excretion in the urine or on the clinical picture. The long-term prognosis of severely intoxicated persons is poor. Neurohistopathologic findings confirm the animal studies by Brown et al and the severe damage and cell necrosis in the hippocampus area. To prevent such events workers need to be warned of the risk and dangers of working with organo-metallic compounds. The effectiveness of protective clothes and gas masks should be checked. In exposed workers regular testing is advised of tin concentrations in the urine.

Accidents, Occupational↗