CONICET | Buscador de Institutos y Recursos Humanos

Objective: We report the case of a 64-year old woman who developed full-blownparkinsonism after PGB administration.Background: Pregabalin (PGB) is a GABA-analog which binds to the 2- subunit types1 and 2 of the L-type voltage-dependent Ca-channel, inhibiting release ofneurotransmitters such as glutamate, noradrenaline, acetylcholine and Substance P. Itis useful for the treatment of neuropathy pain and some forms of seizures.Methods: A female patient suffering from long-term diabetes treated with daily insulininjections since the age of 40, developed diabetic sensory-motor polyneuropathy andbegan treatment with Gabapentin 300 mg plus amytriptyline 25 mg in 1996 withacceptable pain control and without developing other neurological symptoms. In 2006,she consulted elsewhere and PGB 150 mg was added to her usual medication.Results: Three months later she presented with monotone voice and slurred speech,slight but definitely abnormal loss of facial expression, chin tremor and moderatesymmetric postural-holding and action tremor. Mild to moderate symmetric upper andlower limb rigidity, and mild symmetric slowing and reduction in finger-tapping andhand movement amplitude were also noticed. Gait was normal but slow, with evidentslow and reduced arm swing. Unified Parkinson's disease Rating Scale (UPDRS) motorscore was 27 / 108 points. Clear link to PGB introduction as well as symmetric limbinvolvement and degree of affectation after two months of use, made us suspectdrug-induced parkinsonism and PGB was withdrawn. Six months later the patient hadalmost completely recovered with a UPDRS motor score of 4/108, and three monthsafter that, UPDRS motor score was 0.Conclusions: Though some cases of tremor were reported in clinical trials on PGB, toour knowledge this is the first report of full-blown parkinsonism associated with PGBuse. Vigilance of PGB-treated patients is recommended.

enviar mensaje