Roland Besser

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.

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.

Inactivation of end-plate acetylcholinesterase during the course of organophosphate intoxications

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.

Pancuronium improves the neuromuscular transmission defect of human organophosphate intoxication

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 1ocate.d on the terminal axon responsible for antidromic backfiring.

Brain-stem localization and function

General Considerations.- Rules for Correlating Posterior Circulation Brain and Vascular Lesions.- Contribution of Magnetic Resonance Imaging to the Diagnosis of Brain-Stem and Cerebellar Infarcts.- Multifocal Ischemic Brain-Stem Lesions.- Craniocaudal Disintegration of Neurophysiological Findings in Progressive Coma.- Bilateral Thalamic Infarction: A Contribution to Coma Analysis.- Cerebellar System, Vestibular Function, FAEP.- Topical Signs of Cerebellar Disease.- Is Saccadic Lateropulsion in Wallenbergs Syndrome Caused by a Cerebellar or a Brain-Stem Lesion?.- Paroxysmal Ataxia and Dysarthria with a Single Lesion in the Cerebellar Peduncle.- Preliminary Classification of Vestibular Brain-Stem Disorders.- Electronystagmography: The Answers One Might Get.- Vertigo, Masseter Paresis or Masseter Reflex Abnormality, and Impaired Caloric Response.- Oculomotor Function.- Oculomotor Syndromes in Rostral Brain-Stem Lesions.- The Internuclear Ophthalmoplegias.- Isolated Internuclear Ophthalmoplegia Following Head Injury: Magnetic Resonance Imaging and Neurophysiologic Findings.- Nuclear and Fascicular Oculomotor Nerve Lesions in Brain-Stem Infarcts: A Clinicomorphological Study.- A Case Report Illustrating the Brain-Stem Anatomy of Horizontal Eye Movements.- The Oculo-auricular Phenomenon in Brain-Stem Disease.- Sensory Functions and Trigeminal Reflexes.- Correlation of Somatosensory Evoked Potentials and Somatosensory Findings in Patients with Brain-Stem Lesions.- Functional Anatomy of the Spinal Trigeminal Nucleus.- Somatosensory Evoked Potentials After Trigeminal Stimulation in the Diagnosis of Brain-Stem Lesions.- Diagnostic Value of Trigeminal SEP and the Jaw-Opening Reflex in Brain-Stem Lesions.- The Masseter Reflex in the Topodiagnosis of Brain-Stem Lesions.- The Masseter Inhibitory Reflex in Pontine Lesions.- Diagnostic Localizing Value of the Electrically Elicited Blink Reflex.- Facial Nerve Function and Taste.- Magnetically Evoked Corticofacial Potentials of Orbicularis Oculi Muscle Conditioned by the Electrical Blink Reflex.- Facial Mykokymia in Brain-Stem Disorders.- Persistent Tonic Facial Contraction: A Local Brain-Stem Sign.- One-and-a-half Syndrome and Facial Palsy of Peripheral Type: A Rare Brain-Stem Syndrome.- The Stapedial Reflex in Pontine Lesions.- Taste Disturbance Associated with Paramedian Posterior Thalamo-Subthalamic Artery Syndrome.

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.

Backfiring of the isolated rat phrenic nerve does not collide with impulse propagation following repetitive nerve stimulation at 1–50 Hz

Acetylcholinesterase inhibition with neostigmine in the isolated rat phrenic nerve-hemidiaphragm preparation induced axonal backfiring and repetitive compound muscle action potentials following single nerve stimulation. The duration of backfiring and the repetitive compound muscle action potentials did not exceed 55 ms. With repetitive nerve stimulation at frequencies ranging from 1 to 50 Hz, backfiring was present only with the first stimulus and the amplitude of the second compound muscle action potential was maximally reduced, while the subsequent responses recovered gradually. However, the amplitudes of the concommitant antidromic nerve action potentials remained unchanged during the entire train of stimulation. Lack of nerve action potential amplitude changes and the short duration of backfiring of the first nerve action potential exclude a collision phenomenon of backfiring with the nerve action potential induced by the second stimulus. Moreover, the duration of the repetitive compound muscle action potentials did not exceed the duration of backfiring. Therefore, the prolongation of the muscle membrane refractory period by reexcitation following backfiring cannot explain the decrement of the second compound muscle action potential.

No evidence for efficacy of intrathecal verapamil in the treatment of tonic-clonic status epilepticus

In two patients with refractory generalized tonic-clonic status epilepticus, 15 mg of the calcium antagonist verapamil was given by suboccipital intrathecal administration. During a 2–6-h observation period, seizure frequency did not decrease. However, in one patient, verapamil induced severe hypotension. Subsequent thiopental anesthesia suppressed convulsions immediately. Our results indicate that, in contradistinction to animal studies with different administration techniques, intrathecal administration of verapamil does not produce any anticonvulsant effect in humans.

Polyneuropathy following parathion poisoning.

MeanserumK(mmol/1) 1.9 3-2 40 35-50 Sensory action potential amplitude (, V)t/peak latency (ms) Right median F2-wrist 20/4 0 20/3 4 20/2 8 > 8 Right ulnar F5-wrist 12/3-8 9/2 9 12/1 9 > 7 Right sural 8/5-6 18/3-6 13/3-7 > 5 Compound muscle action potential distallproximal stimulation (mV) Right median (SE APB) 1-5/0-6 4-0/3 8 NT > 3-5 Right ulnar (SE ADM) 0 7/0 6 5 0/4 6 4-5/3-8 > 5 Right lateral popliteal 1-2/1-2 0-8/0-8 1-0/0-9 > 2 (SE EDB) F wave latency (ms) Right median (wrist) 35 32 NT < 31 Right ulnar (wrist) 44 30 29 < 32 Motor conduction velocity (mls) Right median (forearm) 46 49 NT > 48 Right ulnar (forearm) 42 58 55 > 50 Right lat. popliteal 38 43 47 > 39 Distal motor latency (ms) Median 5-8 3-9 NT < 4-8 Ulnar 3.5 3-2 2-4 < 3-5 Lateral popliteal 5.0 6-0 4-1 < 6-5

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.