Abstract
The discovery that clonazepam prescribed for the treatment of migraines caused obstructive sleep apnea led to a rapid taper of clonazepam and substitution of lorazepam. Lack of accurate knowledge about the different pharmacokinetics and actions of different benzodiazepines at GABA-A receptors and the risks associated with rapid benzodiazepine withdrawal resulted in the development of the benzodiazepine protracted withdrawal syndrome. Moderately severe disability continued after 2 years. Insufficient knowledge about benzodiazepines and their withdrawal is a serious problem as doctors across the world are under extreme pressure to stop prescribing them but do not have an understanding of the potential perils involved. The pathophysiology of protracted withdrawal syndrome remains poorly understood and there is no recognised treatment. Information about appropriate management of withdrawal and the protracted withdrawal syndrome are available on Professor Ashton’s website at www.benzo.org.uk.
Highlights
CASE REPORTA 59-year-old female married with two children was seen by her neurologist for the treatment of migraines and referred for a sleep study
The discovery that clonazepam prescribed for the treatment of migraines caused obstructive sleep apnea led to a rapid taper of clonazepam and substitution of lorazepam
The patient was referred to a pain specialist who used acupuncture to treat the migraines and converted the clonazepam to lorazepam over a period of 17 days
Summary
A 59-year-old female married with two children was seen by her neurologist for the treatment of migraines and referred for a sleep study. The patient was referred to a pain specialist who used acupuncture to treat the migraines and converted the clonazepam to lorazepam over a period of 17 days. A very rapid conversion and an inadequate substitution were made and the patient developed multiple physical symptoms It took more than four months before an addiction specialist instituted appropriate treatment with a low dose of diazepam and recognised the symptoms were due to the benzodiazepine protracted withdrawal syndrome. With an increase in diazepam to 2.5 mg mane and 5 mg nocte, palpitations reduced but xerostomia, severe orthostasis and tachycardia persisted. When these symptoms did not resolve over several months it was felt the patient had developed sensitivity to diazepam. Difficulty with digestion, abdominal pain, palpitations and orthostasis persisted
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