Electrophysiologic investigation of thallium poisoning

Electrophysiologic findings in thallium intoxication are usually untimely, limited in extent, and often uninformative. This report documents serial conduction and electromyographic findings in a case of thallium poisoning, beginning 10 days after symptom onset and ending 24 months later. Initially, the plantar nerves in the foot demonstrated profound axonal loss while the sural and peroneal nerves were essentially normal. The latter two nerves subsequently underwent axonal loss. Two years were required for the sural and peroneal nerves to display recovery. At 24 months, the plantar nerves continue to remain absent. A primarily distal axonopathy, significantly worse in the lower than upper extremities and requiring more than 2 years for recovery, now documents what was previously speculated: the electrophysiologic course of thallium intoxication. Additionally, this case emphasizes the need to examine the plantar nerves of the foot to avoid missing distal axonopathies during the early course of the disease process. The clinical course and pathophysiology of thallium poisoning are also reviewed.     

Neurofibrillary changes after acute experimental lead poisoning.

Following acute tetraethyllead intoxication in rabbits classic neurofibrillary tangles develop. As studied by electron microscopy, such tangles develop in hydropic degenerating neurons and consist primarily of bundles of 200 A diameter smooth tubules of enormous length. In two of 16 animals a few twisted tubules (periodicity of 800 A) also could be found. The significance of these lead-induced twisted tubules, so characteristic of Alzheimer's pre-senile dementia in man, is discussed.     

Burton's line in lead poisoning

Lead poisoning in both its acute and chronic forms has been recognised since the second century BCE. Lead colic, anaemia, renal tubulopathies and motor neuropathies are well recognised. This paper sketches the early history and remembers the important contribution of Henry Burton, who described the gums to be bordered by a narrow leaden-blue line, about the one-twentieth part of an inch in width, whilst the substance of the gum apparently retained its ordinary colour and condition. The sign though inconstant, is still a valuable clinical clue.     

Experimental chronic lead poisoning.

In the peripheral nerve, the distal part of the nerve fibers was remarkably damaged--periaxial segmental demyelination--while the proximal part of nerve fibers was only slightly affected. In the CNS, perivascular edema of the small blood vessels and capillaries was observed in the cerebral cortex and cerebellar cortex. All endothelial cells of these blood vessels showed a high electron density with many pinocytotic vesicles and ribosomes. Following these changes, the nerve fibers adjacent to the edema were destroyed. The above-mentioned findings seem to indicate that lead induces a toxic effect on the blood vessel and produces perivascular edema in the CNS of adult animals. This may induce brain dysfunction.     

Pathogenetic considerations of pica in lead poisoning

An important factor associated with lead poisoning in children is the habit of eating non-food substances, a condition termed pica. In search for underlying mechanisms involved in the pathogenesis of pica, this investigation presents evidence in support of the hypothesis that in many families failure of normal mother-child interaction, paternal deprivation, culturally dependent maternal oral interests and significant stress factors in the home where abundant lead-containing material is available are etiologically related to the development of pica in lead poisoning. Other factors, which have been thought to be associated with pica, are nutritional deficiencies and maladaptive behavior patterns. A multifocal treatment approach is considered to be most effective.     

Familial lead poisoning from contaminated wine

Three members of a family were found be suffering from lead poisoning of nonindustrial origin, the causative agent being the home-produced wine left to ferment in a glazed earthenware vat. The clinical and neurophysiological features are discussed in the light of similar cases in the literature. Correct diagnosis and early treatment of nonindustrial lead polyneuropathy are often extremely difficult because of the elusive nature of the exposure.

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Sommario Tre componenti di una famiglia hanno sofferto di una intossicazione da piombo di origine industriale da vino prodotto in casa e lasciato fermentare in recipienti di terracotta smaltata. Le caratteristiche cliniche ed elettrofisiologiche dei casi vengono descritti in rapporto con casi analoghi citati dalla letteratura. La diagnosi corretta e il precoce trattamento di queste polineuropatie da piombo non industriale risultano spesso difficili per la natura occasionale dell' azione tossica.

     

Autonomic dysfunction due to lead poisoning

We present a case history of a 24 years old male who developed autonomic dysfunction, intestinal pseudo-obstruction and anemia due to lead poisoning. Concomitant recording of blood levels of lead and autonomic function showed a gradual decline in blood lead level (98.8 microg/dL at week 0, 56 microg/dL at week 6, and 40 microg/dL at week 52) and gradual improvement in autonomic functions. Decrease in blood lead levels with DMSA (Meso-2, 3-dimercaptosuccinic acid) therapy showed improvement in autonomic functions. At week 0, the patient had severe loss of autonomic tone and autonomic reactivity which improved at week 6. At the 52nd week, most of the autonomic parameters had normalized except for the persistence of mild loss of parasympathetic reactivity.     

Electrophysiologic study of Fisher syndrome

Electrophysiologic studies were performed on a 6-year-old girl with Fisher syndrome. We recorded several evoked potentials in this patient: visual evoked potentials, auditory brainstem responses, auditory evoked potentials, short-latency somatosensory evoked potentials, blink reflex elicited by photic stimuli (photo-evoked eyelid microvibration), blink reflex elicited by auditory stimuli (auditory evoked eyelid microvibration), and motor nerve conduction velocity. In our study, photo-evoked eyelid microvibration response was not obtainable; laterality was indicated in visual evoked potential and electroencephalographic studies, and the remaining evoked potentials demonstrated normal responses. The results obtained from the brainstem reflex (photo-evoked eyelid microvibration) suggest that the pathologic focus of Fisher syndrome is located in the midbrain, particularly in the pretectum. It is expected that the combined use of these electrophysiologic techniques may facilitate differentiation between Fisher and Guillain-Barré syndromes.     

Tomaculous neuropathy. Electrophysiologic study

In two cases with recurrent palsies, the results of electrophysiological studies led to nerve biopsy showing typical tomacula. The first case was an inherited neuropathy with liability to pressure palsies. The second case was an apparently sporadic painless recurrent brachial neuropathy. Electrophysiological alterations were diffuse and sensory fibres of the median nerve between index and wrist were the most involved. Conduction blocks were observed without palsy in narrow anatomical passageways where nerve compressions are frequent (ulnar nerve at the elbow, peroneal nerve at the fibula). A compression by a neighbouring anatomical structure could make the prognosis worse and justify nerve decompression. The nerves with slowest conduction have the most important risk of palsy and the patients should be given advice to avoid their compression.     

纳洛酮治疗抗精神病药中毒疗效观察

目的:观察纳洛酮对急性抗精神病药中毒的疗效. 方法:回顾性比较分析85例急性抗精神病药中毒者的临床资料.纳洛酮组加用纳洛酮治疗,常规组以常规治疗. 结果:纳洛酮组有效率明显高于常规组(P<0.01),病死率明显低于常规组(P<0.01),催醒时间明显短于常规组(P<0.01). 结论:纳洛酮治疗急性抗精神病药中毒疗效可靠,不良反应不明显,催醒作用明显,能有效提高急性抗精神病药中毒患者抢救成功率.     

Electrophysiologic study in benign human botulism type B

Conventional electromyography (EMG) and single fiber EMG (SFEMG) were performed in a 64-year-old diabetic woman with mild type B botulism. The main clinical signs were autonomic dysfunction and cranial nerves paresis. Conventional EMG was normal, except for small changes that were consistent with mild mixed peripheral neuropathy in the lower limbs and were related to diabetes. Repetitive stimulation and results of single stimulus before and after full effort were normal. SFEMG showed increased jitter and impulse blocking in clinically normal muscles. The jitter was frequency dependent and improved at a higher innervation rate. Impulse blocking in potentials with only slightly increased jitter was found. The follow-up showed improvement of the jitter in agreement with clinical recovery. Jitter abnormalities were recorded after 16 weeks, when clinical signs of botulism had been reversed to normal. Motor unit fiber density increased progressively, and on examination at 8 weeks, some potentials showed very high jitter values. Both findings might suggest new endplate formation, perhaps due to ultraterminal sprouting development.     

Peripheral polyneuropathy after acute methanol poisoning: Six-year prospective cohort study

BackgroundMethanol is a widely used industrial short-chain aliphatic alcohol with known neurotoxic properties. Mass poisoning outbreaks due to the consumption of methanol-adulterated alcoholic drinks present a challenge to healthcare providers due to the high mortality and serious central nervous system (CNS) damage in survivors. However, the impact of methanol exposure on the peripheral nervous system is unknown.ObjectivesTo investigate the role of acute methanol exposure in the development of peripheral polyneuropathy (PNP) during the years following discharge from the hospital.MethodsA total of 55 patients with confirmed methanol poisoning (mean age of 47.9 ± 3.6 years; 9 females) were examined 4 times within a 6-year prospective longitudinal cohort study. The program included neurological and electromyographic examinations, visual evoked potentials, ocular examinations with retinal nerve fibre layer thickness measurements, brain magnetic resonance imaging, and a series of biochemical and toxicological tests.ResultsPNP was observed in 20/55 (36 %) patients, which, in most of the cases, was mild axonal sensorimotor neuropathy. In 8/55 (15 %) patients, worsening of electromyographic findings was registered during the follow-up period, including 5 cases with newly diagnosed PNP and 3 cases of PNP progression. In one subject, complete reversal of PNP was registered after cessation of alcohol intake. The patients with PNP were significantly older (57.3 ± 5.3 versus 42.5 ± 3.9 years; p < 0.001), with higher blood glucose (5.93 ± 0.97 versus 4.81 ± 0.32 mmol/L; p = 0.035) and lower vitamin B₁ (45.5 ± 7.4 versus 57.5 ± 5.2 ug/L; p = 0.015) concentrations. The number of chronic alcohol abusers was significantly higher in the PNP group (17/20 versus 20/35; p = 0.034). No associations between PNP prevalence/ dynamics and acute parameters of poisoning severity, arterial blood pH (7.26 ± 0.07 with PNP versus 7.18 ± 0.09 without PNP; p = 0.150), or serum methanol (1320.0 ± 700.0 with PNP versus 1430.0 ± 510.0 mg/L without PNP; p = 0.813) and ethanol (460.0 ± 560.0 with PNP versus 340.0 ± 230.0 mg/L without PNP; p = 0.675) concentrations at admission were found. No difference in the number of patients with visual (9/20 with PNP versus 12/35 patients without PNP; p = 0.431) and CNS sequelae (9/20 with PNP versus 15/35 patients without PNP; p = 0.877) of poisoning was present.DiscussionDespite the relatively high number of PNP cases, no association was found between the severity of acute methanol poisoning and the prevalence of PNP and its dynamics during six years of observation. We did not find an association between methanol-induced visual/ brain damage and the prevalence of PNP in survivors of poisoning. A high prevalence of PNP and its progression might be attributed to other causes, mainly a history of chronic alcohol abuse and insufficiently treated diabetes mellitus. Our results highlight the importance of complete cessation of alcohol consumption and better control of glycaemia in diabetic patients in the prevention and treatment of peripheral PNP.