Severe Generalized Polyneuropathy in Lithium Intoxication

Chang, Yang-Chyuan; Yip, Ping-Keung; Chiu, Yi‐Da; Lin, Hao-Yang

doi:10.1159/000116226

Cited by 10 publications

(4 citation statements)

References 9 publications

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“…1 Features of lithium toxicity characteristically include drowsiness, slurred speech, psychomotor slowing, polyneuropathy, and impaired memory and, in severe cases, seizures, coma and death. [2][3][4] Other recognized effects include atrioventricular delay, arrhythmia, and acute renal failure. [5][6][7] Clinical manifestations of lithium toxicity effects may lag behind changes in serum lithium concentrations, due at least in part to delayed distribution into tissues.…”

Section: Introductionmentioning

confidence: 99%

Pattern of lithium exposure predicts poisoning severity: evaluation of referrals to a regional poisons unit

Waring

Laing

Good

et al. 2007

QJM

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Section: Introductionmentioning

confidence: 99%

Pattern of lithium exposure predicts poisoning severity: evaluation of referrals to a regional poisons unit

Waring

Laing

Good

et al. 2007

QJM

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“…in der Zeit des symptomatischen pHPT höher als in den 4 Jahren zuvor, was auf die polyuriebedingte Dehydratation und die dadurch erniedrigte Lithiumclearance zurückzuführen ist (75). Neben der Dehydratation als Risiko für eine Intoxikation sind als zusätzliche Risikofaktoren fLir neurotoxische Lithiumeffekte weibliches Geschlecht, eine neuroleptische Begleitmedikation (13,38) und eine im Einzelfall besondere Empfindlichkeithier die chronische Neuropathie der Beinnerven aufgrund des Kaudasyndromes -zu berücksichtigen (18,38). Die distale Betonung der Paraparese in der zweiten Hälfte des Krankheitsverlaufes, verbunden mit den elektrodiagnostischen Befunden, lassen an das Lithium als einen weiteren metabolischen Faktor rur die Entstehung dieser Paraparese denken.…”

Section: U Leutgebunclassified

“…et aL(18) berichten über einen Fall mit deutlicher Minderung der Reizantwortamplituden in der Neurographie motorischer und sensibler Nerven nach einer Lithiumintoxikation. Die Nervenleitgeschwindigkeiten waren bei ihrer Patientin ebenso wie bei den Intoxikationsfällen von Newman und Saunders(62) und Uchigata et al(87) nur gering erniedrigt bzw.…”

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“…Parallel zu den EMG-Veränderungen beobachteten Brust et al(13) nicht nur hochgradige Paresen, sondern auch einen Verlust der Tiefensensibilität in den Füßen. Auffällig war in den Fällen von Chang et al(18) und Brust et al (13) eine Progredienz der klinischen und elektrodiagnostischen Zeichen der peripheren Neuropathie nach dem Absetzen des Lithiums. Brust et al (13) diskutieren in diesem Zusammenhang eine Fortdauer höherer Lithiumkonzentrationen im Nervengewebe bei bereits wieder normalisiertem Serumspiegel.…”

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Lithium und seine Wirkungen auf das Endokrinium, den Knochen und den peripheren Nerv - eine aktuelle Übersicht

Leutgeb¹

1995

Fortschr Neurol Psychiatr

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Controlled studies in 1990-1992 with Danish, Sardinian, and Hongkong-Chinese patients consistently revealed a prevalence of goiter of about 50% in lithium treated patients. This is far beyond the frequency generally assumed for Germany, the whole country still known to be an endemic goiter area. Hypothyroidism as a side effect of lithium occurs in a clearly different group of patients and is much less frequent, the overall incidence being not substantially different from the incidence in the general population. But the risk of becoming hypothyroid as well as hyperparathyroid during lithium prophylaxis is markedly higher in women over 45 years of age, who in the general population are also prone to both endocrine dysfunctions. Lithium is considered to have a provoking role. Lithium is known to be accumulated in the bone and an impact on bone metabolism was shown in animal studies. The data reviewed prohibit the use of lithium during lactation and enforce strict indication in children. In adults the effect of lithium on bone should be considered only in osteomalacia and severe osteoporosis. This review is illustrated by the case of a 60-year-old woman, who after 4 years of successful treatment with lithiumcarbonate because of schizoaffective psychosis, developed a syndrome of hypercalcemia. Exstirpation of a parathyroid adenoma rendered her normocalcemic. Moreover, a pre-existing diffuse goiter had grown to a large nodular goiter within the course of her 5-year treatment. As she finally became paraparetic, she was admitted to our rehabilitation center for the diseases of the spinal cord. Her paraparesis may have been caused not only by the lithium-induced primary HPT, but in part by lithium itself. There are a few reports on lithium causing peripheral neuropathy at toxic levels. A transient deterioration of a pre-existing neuropathy, as in our case study, may have happened at lithium serum levels not far beyond the upper limit of 0.8 mmol/l.

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Polyneuropathy in lithium intoxication

Vanhooren

Dehaene²,

Zandycke³

et al. 1990

Muscle and Nerve

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Two patients developed acute sensorimotor polyneuropathy after intoxication with lithium carbonate. Nerve conduction studies, electromyography, and sural nerve biopsy proved it to be an axonal neuropathy. Recovery of muscle strength, reflexes, and sensory function started weeks after discontinuation of lithium therapy. One patient fully recovered within a year. In the literature we found nine other cases of lithium polyneuropathy.

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Severe Generalized Polyneuropathy in Lithium Intoxication

Cited by 10 publications

References 9 publications

Pattern of lithium exposure predicts poisoning severity: evaluation of referrals to a regional poisons unit

Pattern of lithium exposure predicts poisoning severity: evaluation of referrals to a regional poisons unit

Lithium und seine Wirkungen auf das Endokrinium, den Knochen und den peripheren Nerv - eine aktuelle Übersicht

Polyneuropathy in lithium intoxication

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