Severe dependency on zolpidem in a patient with multiple sclerosis suffering from paraspasticity

Damm, Julia; Eser, Daniela; Rupprecht, Rainer

doi:10.3109/15622970903369973

Cited by 5 publications

(4 citation statements)

References 16 publications

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“…3,4 To the best of our knowledge, 61 cases of zolpidem misuse have been reported in the literature so far. [5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20][21][22] In most of the these cases, a history of alcohol or drug abuse was already present. Studies in healthy volunteers with no history of drug abuse suggest that zolpidem has only a modest abuse potential.…”

Section: Introductionmentioning

confidence: 99%

Severe Chronic Abuse of Zolpidem in Refractory Insomnia

Chiaro¹,

Castelnovo²,

Bianco³

et al. 2018

Journal of Clinical Sleep Medicine

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Zolpidem is an imidazopyridine nonbenzodiazepine hypnotic drug with a high affinity to the α1 subunit of the gamma amino butyric acid A receptor It is the first pharmacological option in the short-term management of sleep-onset insomnia. Initially considered a safer drug compared to benzodiazepines because of lower liability for abuse and dependence, recently, an increasing body of reports has questioned zolpidem's proneness to misuse. In this report, we describe a case of serious zolpidem abuse requiring pharmacological washout during hospitalization because of previous withdrawal seizures in a patient with chronic sleep-onset and maintenance insomnia.

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Section: Introductionmentioning

confidence: 99%

Severe Chronic Abuse of Zolpidem in Refractory Insomnia

Chiaro¹,

Castelnovo²,

Bianco³

et al. 2018

Journal of Clinical Sleep Medicine

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“…The hypothesis is further emphasized by previous studies that have proved the muscle relaxant action of zolpidem at high doses. It is well-recognized that zolpidem does not have any muscle relaxant activity at therapeutic dose, but high dose zolpidem has been shown to improve the symptoms of spasticity and this effect is attributed to its action on Gabaa receptor with α2-receptor and α3-receptor subunits [9]. Causality assessment of the adverse drug reaction was done to assess the causal relationship of zolpidem with the hyponatremia event using the structured "Probablity scale" system proposed by World Health Organization Collaborating Centre for International Drug Monitoring, the Uppsala Monitoring Centre (WHO-UMC) [10].…”

Section: Discussionmentioning

confidence: 99%

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confidence: 99%

Zolpidem Induced Hyponatremia: a Case Report

Priya

2014

JCDR

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CASE REPORTa 62-year-old male patient, doctor by profession, was admitted with gradual onset of drowsiness, nausea and vomiting of short duration. He was a known case of hypertension, diabetes mellitus and intervertebral disc prolapse of L3 -L4, L4-L5 joints for which midline decompression and laminectomy was done three years back. Despite the surgery, he continued to have low back ache and was later diagnosed with failed back syndrome for which he is on regular orthopaedic follow up.The patient also had a long history of insomnia for which he was receiving benzodiazepine alprazolam at bedtime for more than 10 y. He was initially taking nightly dose of 0.25 mg which he had gradually increased to 0.5 mg and then to 1 mg. He claims to have started taking the drug for sleeping difficulty but later continued it mainly due to pain related insomnia. about three years back, the patient had changed his medication to non-benzodiazepine hypnotic, zolpidem. He had started off with a dose of 5 mg, after which, he had progressively increased the dose to 10 mg and continued it for a period of upto four months before the date of admission for his present complaints. In the last 4 months, he had taken a high dose of 20 mg bed time daily. He was also receiving the combination of gliclazide 40 mg with metformin 250 mg twice daily, metoprolol 25 mg and the fixed drug combination of aspirin 75 mg and atorvastatin 10 mg once daily for the past five years.at admission, clinically the patient was found to be drowsy, arousable and moving all four limbs. He was euvolemic. His blood pressure was 120/80 mmHg. Complete blood counts showed leucocytosis, with a normal urine routine on investigation. biochemically, he had severe hyponatremia, low serum osmolarity, elevated urine spot sodium with normal urine osmolarity [Table/ Fig-1]. Renal, liver and thyroid function tests were normal. Serum cortisol was elevated [Table/ Fig-1] and lipid profile was within normal limits. Random and fasting blood glucose levels were normal. Serum calcium and lactate levels were also normal. blood and urine culture were sterile and ultrasound of the abdomen done showed fatty liver with cholelithiasis and grade I prostatomegaly.He was treated with fluid restriction, 3% saline infusion and vasopressin receptor antagonist, tolvaptan 15 mg once daily for a period of about 10 d for adequate correction of serum sodium in addition to withdrawal of the offending drug. Serial investigations done on the ensuing days showed normalization of sodium levels [ ABSTRACTZolpidem is a non-benzodiazepine hypnotic that acts by binding to (Gabaa) receptor. This is a case report of a patient with chronic insomnia for which he had initially been receiving benzodiazepine hypnotic alprazolam and for the past three years, he had switched himself to non-benzodiazepine hypnotic, zolpidem and had progressively increased the dose to 20 mg. The patient presented with history of drowsiness, nausea and vomiting of short duration. Investigations revealed that the patient had hyponatremia. Dec...

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“…Additionally, intravenous use of zopiclone has been described 22. A recent case report described a patient with multiple sclerosis and paraspasticity taken 700–800 mg zolpidem per day because of perceived myorelaxation 23. These observations strongly suggest that zolpidem at higher doses leads to the same risks and benefits as benzodiazepines.…”

Section: Discussionmentioning

confidence: 99%