Pregabalin Withdrawal Research Articles

Pregabalin withdrawal

Pregabalin withdrawal

Pregabalin withdrawal

Pregabalin withdrawal

Pregabalin withdrawal in patients without psychiatric disorders taking a regular dose of pregabalin: A case series and literature review

Pregabalin is a drug that can cause psychiatric symptoms via pregabalin withdrawal. Prior reports on pregabalin withdrawal have mainly focused on cases with pregabalin dependence or abuse, and little attention has been paid to patients who are prescribed regular doses of pregabalin. Herein, we report three cases of pregabalin withdrawal in patients without psychiatric disorders, taking regular doses of pregabalin, who developed psychiatric symptoms such as insomnia and anxiety after abrupt discontinuation of pregabalin. In addition, we conducted a systematic review of six case reports (previous studies) of pregabalin withdrawal under regular doses of pregabalin. Among the six cases, three patients had no comorbid mental or substance use disorders, the dose of pregabalin ranged from 150 to 600 mg/d, and the duration of pregabalin use ranged from a few weeks to many years. Of these six cases of pregabalin withdrawal, five had psychopathological symptoms, three had vegetative symptoms, and three had neurologic and physical complications. We concluded that since pregabalin withdrawal can occur even with regular doses and short‐term use, clinicians must carefully reduce pregabalin doses when reducing or discontinuing treatment, paying close attention to withdrawal symptoms. Our case series sheds light on the scant evidence from previous research on physical dependence in patients who are taking regular doses of pregabalin. Furthermore, our cases were also valuable in demonstrating that pregabalin withdrawal can occur even after a relatively short period of 2 months.

Pregabalin withdrawal

Pregabalin withdrawal

RETRACTED: Neurotoxic effects of pregabalin dependence on the brain frontal cortex in adult male albino rats

Pregabalin (PGB) is an analog of the inhibitory neurotransmitter gamma-aminobutyric acid. The currently available evidence favors the misuse and abuse potential of PGB. However, its neurotoxicity remains unclear. Therefore, this study assessed the toxic effects of chronic pregabalin dependence as well as withdrawal on the cortical neurons of the frontal lobe. This study included eighty adult male albino rats which were divided into three groups. Group I (Control) included 40 rats and was further subdivided into two equal subgroups (IA and IB) as negative and positive controls. Group II (PGB-dependent) included 20 rats which received PGB starting with the therapeutic dose (300 mg/day), then the doses were gradually increased until they reached the dependent dose (3400 mg/day) by the end of the first month. Further, the dependent dose was given daily for another 2 months. Group III (PGB withdrawal) included 20 rats which received PGB as described in group II. After that, administration of PGB was stopped and the rats were kept for another one month. By the end of the experiment, all animals were sacrificed by cervical decapitation. The specimens were taken from the frontal cortex for histologic and immunohistochemical staining as well as morphometric analysis. Sections of the frontal cortex of group II showed changes in the form of disturbed architectural pattern of cortical layers, apoptotic cells, weak immunoexpression of Bcl-2 and VEGF as well as moderate-strong immunoexpression of iNOS and nestin. These expressions were significantly different from the control groups, but they were non-significant in comparison with group III. These findings indicate that chronic PGB dependence induces neurotoxic effects mainly in the form of neuronal apoptosis, gliosis, and oxidative stress injury of the frontal cortex. The PGB- induced neurotoxic effects persisted after withdrawal. The influence of these neurotoxic effects and their relevance to the cognitive or neurologic disorders in PGB-dependent individuals warrants further research. Furthermore, it is recommended to quantify the behavioral changes related to PGB dependence as well as withdrawal in future studies.

Case Report: the Comorbidity of Pregabalin-Use Disorder and Post-Traumatic Stress Disorder: Clinical and Pharmacological Issues

Owing to its anxiolytic effects, pregabalin is used to treat many distressing symptoms, with various clinical observations supporting its potential benefits in cases of post-traumatic stress disorder (PTSD). However, a decade-long concern has been raised regarding the risk of patient misuse. A 27-year-old immigrant male self-treated with massive doses of pregabalin for at least 6 yr to alleviate his re-experiencing of the past war events he faced in his native country. PTSD and pregabalin-use disorder were diagnosed upon his arrival at our addiction care center. A controlled pregabalin withdrawal failed because the patient switched from this drug to alcohol and methadone available on the street. We therefore organized a hospitalization to provide a controlled methadone delivery and to begin pregabalin withdrawal, enabling thereafter the management of his care to focus on his PTSD. This case report invites clinicians to be cautious in prescribing pregabalin to patients suffering from PTSD, especially to at-risk populations such as migrants. Pregabalin has a positive effect on acute post-traumatic anxiety, but no long-term beneficial impact. As suggested by preclinical studies, pre-existing PTSD could potentiate the development of a pregabalin substance-use disorder.

Pregabalin-associated movement disorders: A literature review.

Central nervous system adverse effects are commonly reported with pregabalin (PGB). On the other hand, movement disorders (MDs) associated with this drug were rarely described. However, their occurrence could significantly affect the quality of life of PGB users. This literature review aims to evaluate the clinical epidemiological profile, pathological mechanisms, and management of PGB-associated MDs. Relevant reports in six databases were identified and assessed by two reviewers without language restriction. A total of 46 reports containing 305 cases from 17 countries were assessed. The MDs encountered were as follows: 184 individuals with ataxia, 61 with tremors, 39 with myoclonus, 8 with parkinsonism, 1 with restless legs syndrome, 1 with dystonia, 1 with dyskinesia, and 1 with akathisia. The mean age was 62 years (range: 23–94). The male sex was slightly predominant with 54.34%. The mean PGB dose when the MD occurred was 238 mg, and neuropathic pain was the most common indication of PGB. The time from PGB start to MD was < 1 month at 75%. The time from PGB withdrawal to recovery was < 1 week at 77%. All the individuals where the follow-up was reported had a full recovery. The most common management was PGB withdrawal. In the literature, the majority of the cases did not report information about timeline events, neurological examination details, or electrodiagnostic studies. The best management for all MDs is probably PGB withdrawal. If the patient is on dialysis program, perhaps an increased number of sessions will decrease recovery time. Furthermore, the addition of a benzodiazepine could accelerate recovery.

Pregabalin withdrawal

Pregabalin withdrawal

First-episode psychosis induced by pregabalin withdrawal: a case report

ABSTRACTPregabalin is a novel isomer of gamma-aminobutyric acid that functions as a major inhibitory neurotransmitter in the brain. It is used daily in medical practice for treating neuropathic pai...

Pregabalin withdrawal

Pregabalin withdrawal

Seizure induced by sudden cessation of pregabalin in a patient with chronic kidney disease

A middle-aged woman with diabetic nephropathy on pregabalin for neuropathic pain presented with a diarrhoeal illness. She was found to have acute on chronic renal impairment with an estimated glomerular...

Manifestations of Pregabalin Withdrawal

Pregabalin is an analog to isobutyl γ-aminobutyric acid (GABA), and is commonly utilized as an anticonvulsant and medication for neuropathic pain. Pregabalin withdrawal has not been well documented, but is commonly described as a constellation of symptoms including anxiety, tachycardia, diaphoresis, nausea, and aggression. We report a case of pregabalin withdrawal with a primary presentation of akathisia, which has yet to be described in current literature.

Acute pregabalin withdrawal: a case report and review of the literature

Objective: Pregabalin is a commonly prescribed GABA analog most commonly used for the treatment of neuralgia. Recently, case reports on pregabalin have been published describing episodes that may be associated with withdrawal-like symptoms after extended or aggressive therapy. This report describes a case in which long term exposure of high dose pregabalin may have resulted in acute withdrawal, and outlines the subsequent medical management of these symptoms. Case Summary: A 61-year-old male presenting with severe agitation presumed to be withdrawal from long term and high dose exposure to pregabalin. Medical management included the use of haloperidol, diphenhydramine, lorazepam and the addition of clonidine over the course of several days for the pharmacological management of withdrawal symptoms. Discussion: Although case reports are available to guide clinicians in the recognition of acute pregabalin withdrawal, definitive evidence on how best to treat these patients remains severely limited. With an increase in the prescribing practices of pregabalin, insight into the acute management by fellow clinicians is further needed.

Spasticity increases during pregabalin withdrawal

Primary objective: To determine whether pregabalin produces long-term spasticity reduction in subjects previously identified as responding in short-term trials.Design, subjects and setting: Prospective service evaluation of patients taking pregabalin for spasticity management for at least 1 year through a tertiary referral rehabilitation clinic. A graduated pregabalin withdrawal was undertaken as part of routine clinical management.Method: Twelve of 19 potential subjects agreed to participate. The primary outcome measures were visual analogue pain and spasticity scores at lowest dose of pregabalin compared to baseline and their choice to resume pregabalin therapy.Results: Mean pre-withdrawal pregabalin dosage was 386 mg/day, decreasing to 70 mg/day at mean lowest dosage. Median subjective spasticity scores increased from 4 at baseline to 6 at lowest dose (p < 0.01) without a significant increase in median pain scores. Two patients with epilepsy, whose other anti-convulsants were not altered, had seizures. Following the evaluation, five subjects chose to return to the original dose, five recommenced pregabalin at a lower dose and two subjects no longer required the drug.Conclusion: Pregabalin withdrawal resulted in self-reports of increased spasticity without a concomitant increase in pain, with 91% choosing to continue pregabalin at the conclusion of the evaluation.

Trouble de la marche révélant un syndrome de sécrétion inappropriée d’hormone antidiurétique associé à la prégabaline

Pregabalin, a molecule with similar structure of GABA neurotransmitter, initially developed as an antiepileptic, is now commonly used in the treatment of painful peripheral neuropathies. We report an 82-year-old man who presented with confusion, urinary incontinence and gait instability. He was receiving pregabalin for a left L5 radicular pain. Laboratory tests at admission revealed a profound hyponatremia (117 mmol/L) that was corrected by fluid restriction and pregabalin withdrawal. According to the patient and laboratory outcome, we established the diagnosis of inappropriate antidiuretic hormone secretion due to pregabalin. The test of Naranjo demonstrated a probable imputability of pregabalin.

Reversible Splenial Lesion Syndrome (RESLES): What's in a Name?

The presence of transient lesions involving the splenium of the corpus callosum (SCC) has been described in patients with encephalitis or encephalopathy of varied etiology. We have termed it RESLES (reversible splenial lesion syndrome). To describe 3 additional patients (2 encephalitis, 1 hypoglycemia) and review the literature to define this syndrome, its etiology, presentation, prognosis, and possible pathophysiological mechanisms. Search of the MEDLINE database from 1966 through 2007. English language article titles and abstracts were screened and the appropriate articles reviewed. Additional articles cited by original references were also reviewed. RESLES is caused by antiepileptic drug withdrawal, infection, high-altitude cerebral edema (HACE), or metabolic disorders (hypoglycemia and hypernatremia). Complete resolution after a variable lapse is the rule. Clinical presentation is nonspecific, without evidence of callosal disconnection syndromes. Neuroimaging shows a nonenhancing, round-shaped lesion centered in the SCC that disappears after a variable lapse. Diffusion studies reveal DW hypersignal with low ADC values, suggestive of cytotoxic edema. Only HACE-related cases and 1 patient with pregabalin withdrawal showed high ADC values, consistent with vasogenic edema. RESLES is a distinct clinicoradiological syndrome of varied etiology and benign course except in those patients with an underlying severe disorder.

Adjunctive pregabalin for uncontrolled partial-onset seizures: findings from a prospective audit

Pregabalin (PGB) was licensed in Europe as an add-on antiepileptic drug (AED) for the treatment of partial-onset seizures in 2004. This audit assessed the response to adjunctive PGB in patients with uncontrolled seizures. PGB was titrated in 135 patients [73 men; 62 women, aged 18-76 (median 44 years) until one of the following occurred: ≥ 6 months' seizure freedom, ≥ 50% or < 50% seizure reduction over 6 months; PGB withdrawal because of adverse effects, lack of efficacy or both. Of the 135 patients, 14 (10.4%) became seizure-free for ≥ 6 months (median PGB dose 300 mg/day; range 75-600 mg). A ≥ 50% seizure reduction occurred in 33 (24.4%) patients; 20 (14.8%) had < 50% reduction. PGB was withdrawn in 68 (50.4%) (40 adverse effects, seven lack of efficacy and 21 both). Commonest problems resulting in withdrawal were sedation (n = 18), weight gain (n = 14) and ataxia (n = 9). There was a positive correlation between increasing dose and weight gain (r = 0.42, P = 0.045). Add-on PGB benefited 50% of patients, but only 10% achieved 6 months' seizure freedom. Adverse effects, most commonly sedation, dose-related weight gain and ataxia, led to drug discontinuation by 45%. Prospective audits of novel AEDs are a useful adjunct to randomized, controlled trials in managing epilepsy.

Tremor Associated With Chronic Inflammatory Demyelinating Peripheral Neuropathy

To report a case of a patient with tremor associated with chronic inflammatory demyelinating neuropathy (CIDP) that improved after treatment with pregabalin. A 68-year-old man diagnosed as having CIDP at age 63 years developed postural and kinetic tremor in both hands at age 64 years. Tremor did not improve with propranolol, primidone, phenobarbital, clonazepam, alprazolam, gabapentin, and topiramate, but improved markedly with pregabalin. Tremor worsened after pregabalin withdrawal and improved again after its reintroduction. Pregabalin could be useful in the treatment of postural tremor associated with CIDP resistant to other therapies.

Pregabalin withdrawal

Pregabalin withdrawal