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Acute Vocal Fold Palsy After Acute Disulfiram Intoxication
Abstract
Acute peripheral neuropathy caused by a disulfiram overdose is very rare and there is no report of it leading to vocal fold palsy. A 49-year-old woman was transferred to our department because of quadriparesis, lancinating pain, sensory loss, and paresthesia of the distal limbs. One month previously, she had taken a single high dose of disulfiram (130 tablets of ALCOHOL STOP TAB, Shin-Poong Pharm. Co., Ansan, Korea) in a suicide attempt. She was not an alcoholic. For the first few days after ingestion, she was in a confused state and had mild to moderate ataxia and giddiness. She noticed hoarseness and distally accentuated motor and sensory dysfunction after she had recovered from this state. A nerve conduction study was consistent with severe sensorimotor axonal polyneuropathy. Laryngeal electromyography (thyroarytenoid muscle) showed ample denervation potentials. Laryngoscopy revealed asymmetric vocal fold movements during phonation. Her vocal change and weakness began to improve spontaneously about 3 weeks after transfer. This was a case of acute palsy of the recurrent laryngeal nerve and superimposed severe acute sensorimotor axonal polyneuropathy caused by high-dose disulfiram intoxication.
... Unilateral pallidal lesion was found on MRI scan in a 38-year-old man, whose disulfiram intoxication resulted in cortical decerebration (de Mari et al., 1993). Acute vocal cord palsy (Bae, 2009) and reversible posterior encephalopathy (Coppens et al., 2011) have also been described following disulfiram intoxication. ...
Catatonic syndromes could accompany a variety of psychiatric and medical conditions. The most common conditions underlying catatonia are affective disorders followed by schizophrenia, but several medical conditions including intoxications affecting the central nervous system can also present with catatonic signs and symptoms. Therapeutic doses of disulfiram could induce catatonia with or without accompanying psychosis or mood disorder. A case of disulfiram intoxication manifesting with catatonia is reported here together with a brief overview of the literature. A patient was admitted to the toxicology ward after a suicide attempt with approximately 20 g of disulfiram. On transfer to the psychiatric ward, she was sitting still, in a semi-stuporous state and displayed motiveless resistance to instructions or attempts to move (active negativism). She was unresponsive to most of the questions (mutism), occasionally verbigerated 1-2 words and stared for more than 20 seconds between shifting attention. After developing a comatosus state her treatment continued at the toxicology ward, where a contrast-enhanced computer tomography scan revealed bilateral emollition of 1.5 cm diameter in both nucleus lentiformis at the level of the third ventricle. Following treatment her condition improved and she benefited of rehabilitation facility and a second psychiatric treatment. She was discharged free of neurological and psychiatric symptoms. In conclusion, we underscore the importance of accurate diagnosis of the underlying psychiatric or medical condition when encountering a fast emerging catatonic syndrome and focus first on treating the causative condition while simultaneously attempting symptomatic treatment of catatonia.
Objectives: Disulfiram (DSF) treatment remains a viable option as a treatment for alcohol dependence. There have been concerns about its safety, which are often used as a reason for withdrawing the treatment or as an argument against starting it. How safe is the current prescription of DSF? This paper aims to provide an update of DSF’s safety-related research. Method: A systematic review of the recent literature was drawn from a comprehensive MEDLINE (2000 to 2012) search. Case reports and clinical trials using DSF for the treatment of alcohol and/or cocaine use and/or dependence were reviewed. Result: Within the specified period, there have been 30 case reports and 8 clinical trials regarding DSF’s side effects. One was a longer trial of DSF spanning >50 weeks. The case reports were related to neurological, hepatic, cardiac, dermatological, psychiatric adverse events, neuroimaging findings, and drug-drug interaction. Because of exclusion criteria, adverse events in DSF randomized double-blind clinical trials seem to be less serious and less frequent than adverse events reported postmarketing. Conclusions: With the safety recommendations in place, we consider the administration of DSF to be safe practice and within an acceptable risk profile.
This chapter discusses the adverse effects of miscellaneous drugs, materials, medical devices, and techniques. It has been suggested that there are individual differences in subjective responses to alcohol, and an exaggerated cardiac response to alcohol has been suggested to be a marker of increased sensitivity to its stimulant properties. Cerebellar degeneration has been attributed to alcoholism. The range of adverse reactions to bisphosphonates has been reviewed, with particular emphasis on the association between long-term treatment and osteonecrosis of the jaw, a potentially serious adverse effect that occurs mostly in patients with multiple myeloma or breast cancer. Cyanoacrylates are used in the manufacture of polymers and adhesives. They have long been thought to be linked to malignancies. Visual field defects have been reported after macular hole surgery with indocyanine green-assisted internal limiting membrane peeling in a retrospective review of 140 eyes, in 96 of which indocyanine green 0.25% was used. There were nasal visual field defects in 11 eyes, temporal visual field defects in 7 and concentric visual field defects in 1. In the group in whom indocyanine green is used, the visual field defects were far higher in the left eye than in the right. The authors speculated that the postoperative nasal visual field defects were caused by enhanced toxicity of indocyanine green, resulting from exposure to illumination. It is reported raised serum phosphorus and calcium are associated with arterial calcification and mortality in dialysis patients. Unlike calcium-based binders, sevelamer attenuates arterial calcification, but it is not known whether it affects mortality or morbidity.
There have been several reports of disulfiram intoxication, but little evidence of neurologic conditions resulting from disulfiram-induced brain damage combined with Wernicke encephalopathy-associated lesions. We report a rare patient with both Wernicke encephalopathy and disulfiram intoxication. This 50-year-old woman, who was taking disulfiram for chronic alcohol abuse, presented with an acute confusional state, dysarthria, nystagmus, supranuclear ophthalmoplegia, and paraparesis. Biochemical serum and cerebrospinal fluid analyses were normal. An electromyogram detected a motor polyneuropathy. Cognitive assessment revealed severe impairment of memory, attention, and logical and executive abilities. Magnetic resonance imaging with gadolinium enhancement showed brain lesions consistent with Wernicke encephalopathy, but also symmetric hyperintensities on T2-weighted images in the globus pallidus. Stopping the disulfiram and treating with hydration, high-dose thiamine supplements, and benzodiazepines significantly improved the patient's consciousness and oculomotor function. A magnetic resonance imaging scan after 1 month of treatment showed complete disappearance of the brain lesions and the hyperintensities in the globus pallidus. After a further month of intensive neurorehabilitation, the patient was able to interact with the medical staff, and her neuropsychological tests showed only mild memory impairment. Patients with alcoholism who present at emergency departments are at high risk for misdiagnosis, especially because there is no specific routine laboratory test for detecting asymptomatic disulfiram intoxication. Although uncommon, the combination of Wernicke encephalopathy and disulfiram intoxication should be suspected in patients with alcoholism. The disorder can be detected through a careful history and prompt clinical evaluation, together with characteristic magnetic resonance imaging findings.
Disulfiram is used in the treatment of chronic alcoholism, because of the unpleasant symptoms produced after ethanol intake. Although it is well tolerated in most patients, one in 15,000 patients will develop peripheral neuropathy every year, which is frequently misdiagnosed as alcoholic neuropathy.
We report clinical, laboratory, electrophysiological and histopathological features in a 19-year-old patient who developed an acute distal sensorymotor neuropathy during the treatment of alcoholism. At the end of 4-month treatment with disulfiram 250 mg/day, the patient complained of weakness in distal segments of the lower limbs associated with burning dysesthesias, numbness and pain in the soles of the feet and the legs below the knees; reduction in foot strength, the absence of ankle jerk tendon reflexes, and tactile stocking pin-pick and vibratory sensory impairment in the lower limbs below the knee. Recovery was successful after treatment cessation.
The significance of toxic neuropathy is shown by the fact that the recognition of clinical picture, identifying etiological factors and its elimination may prevent the evolution of polyneuropathy. This allows for more effective treatment of these neuropathies as apposite to idiopathic ones which can be treated only symptomatically. Our case report indicates the possibilities during a period with no serious damage to the axons manifested.
Early assessment of severity and continuous monitoring of patients are the key factors for adequate treatment of acute pancreatitis (AP). The aim of this study was to determine the value of procalcitonin (PCT) and Bedside Index for Severity in Acute Pancreatitis (BISAP) scoring system as prognostic markers in early stages of AP with comparison to other established indicators such as C-reactive protein (CRP) and Acute Physiology and Chronic Health Evaluation (APACHE) II score.
This prospective study included 51 patients (29 with severe AP). In the first 24 h of admission in all patients the APACHE II score and BISAP score, CRP and PCT serum concentrations were determined. The values of PCT serum concentrations and BISAP score were compared with values of CRP serum concentrations and APACHE II score, in relation to the severity and outcome of the disease.
Values of PCT, CRP, BISAP score and APACHE II score, measured at 24 h of admission, were significantly elevated in patients with severe form of the disease. In predicting severity of AP at 24 h of admission, sensitivity and specificity of the BISAP score were 74% and 59%, respectively, APACHE II score 89% and 69%, respectively, CRP 75% and 86%, respectively, and PCT 86% and 63%, respectively. It was found that PCT is highly significant predictor of the disease outcome (p < 0,001).
In early assessment of AP severity, PCT has better predictive value than CRP, and similar to the APACHE II score. APACHE II score is a stronger predictor of the disease severity than BISAP score. PCT is a good predictor of AP outcome.
Zinc intoxication has been reported in cases of dietary supplementation, therapeutic overdose, coin ingestion and chronic use of denture cream. Zinc in excess upregulates copper-binding metallothionein in the gut mucosa, leading to increased elimination of copper and negative copper balance. Copper deficiency may also occur in the absence of zinc intoxication, during long-lasting parenteral nutrition and in malabsorption. It is characterised by haematological abnormalities, including sideroblastic anaemia, neutropenia and myelodysplastic syndrome, possibly related to a decreased activity of reductase enzymes of the mitochondria. Neurological manifestations of copper deficiency typically involve a myelopathy resembling subacute combined degeneration, yet optic and peripheral neuropathies, lower motoneuron degeneration, myopathy and central nervous system demyelination have also been reported.1–5 No case of renal manifestation has been published yet. Because of its core feature of chronic copper overload, Wilson disease (WD) may be considered a low risk for such complications to occur. We report here an original case of copper deficiency in WD related to chronic therapeutic overdose of zinc.
In 1992, a 25-year-old patient was diagnosed as having WD. He had mild cognitive deficit, resting tremor, dystonia, dysarthria, gait impairment and liver cirrhosis. Penicillamine therapy was discontinued after 6 months due to further neurological deterioration. Zinc sulfate in monotherapy was introduced …
Disulfiram is a deterrent agent, prescribed to motivated patients, with their informed consent for the relapse prevention of alcohol dependence (AD).1 Supervised disulfiram treatment has proven efficacy for AD.1 There are reports of unregistered medical practitioners in India prescribing disulfiram surreptitiously.2
Neurotoxic side effects of disulfiram may be abrupt, in the form of fatigue, amnesia, confusion and behavioural changes; subacute in the form of ataxia, stupor, psychosis, seizure and encephalopathy; and chronic in the form of optic neuritis, ptosis and peripheral neuropathy.3 Previous reports of neurological sequelae with disulfiram have highlighted that a high dose of disulfiram, either supervised3 or as a single high-dose suicidal attempt,4 lead to these complications.
We report a case of subacute onset of neurological sequelae with therapeutic doses of disulfiram administered surreptitiously, without medical consultation and recovery within 6 weeks of stopping disulfiram.
A 32-year-old male, with family history of AD in one first-degree relative, personal history of nicotine dependence for 7 years and AD for 9 years presented with complaints of pain in both legs for 10 days, hoarseness of voice and drooping of both eyelids for 8 days.
On repeated enquiry, the patient's wife admitted to …
Disulfiram is a dithiocarbamate drug used for alcohol aversion therapy that produces a distal sensorimotor peripheral neuropathy in certain individuals. Because carbon disulfide, a disulfiram metabolite, produces a peripheral neuropathy clinically similar to disulfiram, it has been postulated that disulfiram neuropathy results from CS2 release in vivo. The current study evaluated the morphological changes produced by disulfiram and the contribution of CS2-mediated protein cross-linking to disulfiram-induced neuropathy. Male Sprague-Dawley rats were administered 1% w/w disulfiram in their feed for 2, 4, 5, or 7 wk, and erythrocyte spectrin, hemoglobin, and neurofilament preparations were isolated and the extent of cross-linking assessed by SDS-PAGE, RP-HPLC, and Western blotting, respectively. Spinal cord and peripheral nerve sections were obtained from separate treated animals and assessed by light and electron microscopy. Significant protein cross-linking was only detected in neurofilament preparations obtained after 7 wk of exposure. Morphological changes were observed after 4 wk exposure and consisted of vacuoles within the Schwann cell cytoplasm and segmental demyelination. No neurofilamentous axonal swellings were detected and no significant changes were observed in the CNS. Because disulfiram neuropathy lacks both the morphological changes and intermolecular cross-linking characteristic of CS2, we conclude that disulfiram neuropathy is not mediated by the axonal toxicant CS2; instead, disulfiram appears to be a primary Schwann cell toxicant. Recognition of a diethylcarbamoyl adduct on globin and axonal proteins presents a novel putative neurotoxic mechanism for disulfiram.
In four patients, sensorimotor polyneuropathy developed during treatment with disulfiram. Each patient began to improve with the cessation of treatment. Clinical, electrophysiologic, and pathologic observations point to a potentially reversible and probably dose-related axonal polyneuropathy.
In four patients, sensorimotor polyneuropathy developed during treatment with disulfiram. Each patient began to improve with the cessation of treatment. Clinical, electrophysiologic, and pathologic observations point to a potentially reversible and probably dose-related axonal polyneuropathy.
Organophosphorous poisoning causing isolated laryngeal paralysis has only been rarely reported before. We describe a case of difficult extubation in a patient with organophosphorous poisoning, the cause of which was found to be bilateral vocal fold palsy. This is a type of intermediate paralysis that recovers with time. Such a condition should be thought of as a cause of dyspnoea or difficult extubation in patients with organophosphorous poisoning.
A 35-year-old man developed a distal sensorimotor polyneuropathy after taking disulfiram, 500 mg daily for five months. His symptoms improved after the drug therapy was discontinued. Clinical, electrophysiological, and pathological observations during the acute stage and during recovery suggest that disulfiram produces a distal axonopathy.
Purpose:
For 40 years, disulfiram has been the alcohol-aversive drug used most frequently by American physicians in the treatment of alcohol dependency disorders. We reviewed the clinical literature regarding the risks, benefits, indications, and efficacy of this controversial drug and summarized current knowledge of this therapy.
Conclusions:
Disulfiram will produce an aversive reaction with ethanol, usually at a dose between 250 mg/day and 500 mg/day, although some patients may not have an aversive reaction at this level. Cardiac, hepatic, and neurologic toxicity can also occur within this dosage range. If disulfiram is to be used, the patient must clearly understand the risks of drinking while taking the drug, and the physician and patient must agree about the need for continued clinical supervision and monitoring for efficacy and side effects. The physician must also recognize that disulfiram is only an adjunctive therapy and that continued support, supervision, and other therapeutic measures are required. Disulfiram is probably effective in reducing the frequency of alcohol consumption in the compliant patient over the short term (e.g., 6 months). Certain subgroups of patients, such as those who are older, those who are more socially stable, and those who are well-motivated, may experience a beneficial effect for longer periods. The drug may be most effective in reducing short-term alcohol consumption when the compliance of the patient is supervised, although consideration of this kind of therapy includes the practical problems of supervising the patient and concerns that the supervising person may be placed in a difficult position. Prescription of disulfiram without accompanying education, counseling, and concomitant alcoholism therapy is not beneficial. Disulfiram has no proven effect on the long-term outcome of alcoholism.
A case of sensorimotor polyneuropathy during disulfiram administration is described. This complication partially resolved after the medication was stopped. Pathological observations revealed axonal changes and neurofilament accumulation was found in a few myelinated and unmyelinated axons.
Disulfiram is used to treat alcoholism and is known to cause peripheral neuropathy: few reports of biopsied human nerves have revealed axonal degeneration and loss of myelinated fibers. We studied a 22-year-old woman with severe sensorimotor neuropathy following treatment with disulfiram for 6 months. Histologic studies of the sural nerve revealed a neurofilamentous axonopathy with rare enlarged axons distended by neurofilaments. Disulfiram is converted enzymatically to carbon disulfide, which causes neurofilamentous distal axonopathy in animals. Similar changes in human nerve after disulfiram administration suggest that carbon disulfide is the toxic agent.
Bilateral vocal cord paralysis is uncommon. Most cases occur secondary to trauma, malignancy, surgery, or intubation. Also, it was reported as a side effect of Vinca alkaloids.
We report a patient with small cell lung cancer who developed bilateral vocal cord paralysis and needed to be intubated after treatment with cisplatin and etoposide. All workups excluded metastases as a cause of bilateral vocal cord paralysis. The patient required tracheostomy; she did not receive any further chemotherapy. After 11 weeks, vocal cord paralysis disappeared, tracheostomy was reversed, and the patient remained symptom free; however, 6 months later, the patient developed brain and liver metastases and died from her disease with no evidence of vocal cord paralysis.
We report a case of reversible bilateral vocal cord paralysis that we believe to be secondary to cisplatin toxicity, which is an undescribed complication of this drug.
Cisplatin can induce reversible bilateral vocal cord paralysis. The concurrent use of cisplatin and etoposide might have contributed to this complication in our patient.
We report the development of stridor and dysphagia in a 5-month-old-infant with acute lymphoblastic leukaemia after the administration of four weekly doses of vincristine during induction therapy. Because direct laryngoscopy revealed bilateral vocal cord paralysis, the patient underwent elective intubation. Extubation was performed 7 days later, after direct laryngoscopy confirmed recovery of vocal cord mobility. Vincristine-induced bilateral recurrent laryngeal nerve paralysis is a rare but potentially life-threatening complication. Therefore, it should be suspected when stridor is present, and clinicians should consider visualization of the airway to establish the cause of upper airway compromise in infants receiving vincristine.
A case of embolic cerebral infarction following disulfiram poisoning.
- Lim S.H.
- Kim H.J.
- Shin H.R.
- Kim C.S.
- Lee J.
- Hah J.S.
- Kim S.J.
Lim SH, Kim HJ, Shin HR, Kim CS, Lee J, Hah JS, Kim SJ. A case of em-bolic cerebral infarction following disulfiram poisoning. J Korean Neurol Assoc. 2001;19:294-297.
A case of embolic cerebral infarction following disulfiram poisoning
- Lim
Cisplatin induced reversible bilateral vocal cord paralysis: an undescribed complication of cisplatin
- Taha