Chronischer Baclofenmissbrauch und Entzugsdelirium (Australian and New Zealand Journal of Psychiatry, 2011)

Chronic baclofen abuse and withdrawal delirium (Australian and New Zealand Journal of Psychiatry, 2011)
Autoren: Julian J. Nasti & Vlasios Brakoulias
(pp, 12.06.2016)

Diese Veröffentlichung wird auch in einem Kommentar in der Rubrik „Schwerpunkte“ erwähnt, dessen Lektüre im Kontext empfehlenswert ist.

Korrespondenz im englischen Original

Baclofen is a GABA-B agonist used for muscle spasticity in disorders such as multiple sclerosis. It has growing applications in the treatment of alcohol dependence [1] and its role in the treatment in other addiction disorders has recently been explored [2,3]. Because of its structural similarity to GABA, baclofen also has GABA-A effects [4] such as sedation and anxiolysis. These GABA-A effects presumably underpin baclofen’s abuse potential: both baclofen overdose with selfinjurious intent [5] and baclofen overdose in a recreational setting have been described [6]. Baclofen withdrawal delirium has been described in other case reports [7]. Often these patients are on intrathecal baclofen pumps for management of severe muscle spasticity or using oral baclofen for the same indication. To our knowledge there have been no reports of withdrawal delirium in a patient chronically abusing baclofen.

We report the case of a 61-year-old lady who presented with agitation. Her past psychiatric history included alcohol dependence precipitated by her marriage breakdown and several episodes of depression. She also had a history of abusing methylphenidate, dexamphetamine and opiate analgesic agents. On initial assessment a provisional diagnosis of mania was made and olanzapine 2.5 mg bis die (bd) and clonazepam 0.5 mg ter die sumendus (tds) were prescribed. Although initially orientated, by day 3 of her admission she remained agitated and was noted to be disorientated with a Mini Mental State Examination score of 25/30. After obtaining further collateral history, we confi rmed that the patient had been acquiring baclofen from a number of general practitioners for a factitious diagnosis of multiple sclerosis. The patient had been taking at least 75 mg of baclofen each day for at least six months and it was likely that the dose had escalated in the week prior to presentation.

The patient apparently felt that baclofen made her ‘ think more clearly ’ . The patient continued to deteriorate and began misidentifying staff members as relatives and
picking things from the air. CT scanning, chest X-ray, blood and urinalysis did not identify any abnormalities. Baclofen 10 mg tds was initiated under the assumption
that the delirium had been precipitated by baclofen withdrawal. Her regular olanzapine dose was increased to 10 mg bd, and PRN clonazepam and diazepam was
continued. The patient further deteriorated following the reintroduction of baclofen, and required seclusion to manage her degree of psychomotor agitation. She was assessed as having cogwheel rigidity of her upper limbs. The baclofen dose was increased to 25 mg tds six days after her admission and all other regular medication was ceased. A temporary improvement in the degree of agitation and perceptual disturbance was observed following the increase in the dose of baclofen, but there was some recurrence of her agitation the following day. Eight days after admission, her degree of agitation and hallucinosis finally abated, and by the ninth day, she was fully oriented to time and place and showed no evidence of delirium. The patient ’ s onset of delirium on day 4 is consistent with published reports of withdrawal from oral baclofen regimes [7]. In the largest case series of baclofen withdrawal, psychiatric symptoms included auditory hallucinations (30.4%), visual hallucinations (56.5%) confusion (47.8%), agitation (56.5%), disorientation (17.4%), and insomnia (17.4%) [7].

All of these symptoms were prominent in our patient. Seizures can also occur. It is noteworthy that our patient did not improve despite signifi cant doses of regular and
PRN benzodiazepines. Theoretically, an improvement would be expected given the near-perfect cross-tolerance between benzodiazepines and baclofen [8]. GABA-B agonists inhibit dopamine release which is known to subserve the rewarding aspects of intoxication [9]. In this patient, who had a history of polysubstance abuse, it is possible that baclofen played a role in preventing relapse to dependence on alcohol and other substances. We believe that our patient ’ s delirium was precipitated by withdrawal from baclofen, and is the first reported case of baclofen withdrawal delirium in the setting of chronic baclofen abuse.

Link zum Abstract

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