Clinical Neuroscience

[Thallium poisoning induced polyneuropathy - clinical and electrophysiological data]


DECEMBER 20, 2003

Clinical Neuroscience - 2003;56(11-12)

[Introduction - The aim of the study was the electrophysiological investigation of thallium induced polyneuropathy. Beyond the rarity of the illness, the motivation of this work was the possibility of following up the pattern of neuronal damage. Thallium is one of the most toxic heavy metal and its wide use increases the chance of chronic or accidental acute poisoning. The entero-hepatic circulation makes the accumulation of this toxic agent in tissues possible, mostly in neurons, in the epithelial cells of the digestive tract, in the germinative cells of the skin and testicles. In addition to alopecia and digestive complaints, the clinical picture of thallium poisoning is dominated by neurological signs. Severe axonal polyneuropathy develops in almost all cases, with further damage to the retina and impairment of cognitive functions being not unusual. The diagnosis is confirmed by finding high levels of thallium in body fluids, especially in saliva and urine. Case report - Electrophysiological examination of our accidentally poisoned patient revealed severe, sensory-motor, predominant motor axonal polyneuropathy and pointed out some aspects of the pattern of neurotoxic process: the initially distal lesion, the dying-back course and the capacity for regeneration. Conclusion - Because thallium has the same molecular targets as potassium ion thus impairing the energetical supply of the nerve cell, the most effective treatment is carefully loading with potassium. If recognized and treated early, thallium poisoning has a favourable prognosis.]



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Clinical Neuroscience

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Clinical Neuroscience



[Introduction - While it is several decades ago that electrophysiological studies in the early stages after an ischaemic stroke revealed spontaneous activity in the affected muscles, today few data are available on the peripheral changes in later stages after a cerebrovascular event. The aim of this study was to detect electrophysiological signs that could indicate changes at the motor unit level occurring within a longer post-stroke period. Patients and methods - Forty-four patients who had developed hemiparesis after an ischaemic stroke in the area of the middle cerebral artery were involved in the study. Motor and sensory nerve conduction studies and electromyography were carried out on each side on six nerves and in five muscles respectively. Values between the affected and unaffected side were compared by statistical methods. Results - In patients with hemiparesis present for less then nine months, low M wave amplitudes, fibrillation potentials and an increased number of complex motor unit potentials were found on the affected side; in patients with symptoms present for more then nine months the mean duration and size index of the motor unit potentials in the paretic abductor digiti minimi muscle were increased. These data suggest a process of neurogenic type. The signs of distal axonal damage observed in the early period after stroke have been replaced later by chronic neurogenic changes. These changes could be the consequence of spinal motor neuron damage and axonal transport disturbance due to the loss of supraspinal trophic inputs. Conclusion - The correlation between the extent of electrophysiological changes and of the central motor deficit of the patient indicates the importance of delaying this process by appropriate rehabilitation procedures.]