scholarly journals Pregabalin abuse and toxicity and related factors

2021 ◽  
Vol 9 (1) ◽  
pp. 34-42
Author(s):  
Walla Alelwani ◽  
◽  
Abrar Alkhazindar ◽  
Basmah Alqumaysh ◽  
Dina Kutbi ◽  
...  
Keyword(s):  
Neuropathic Pain ◽  
Side Effects ◽  
Liver Enzymes ◽  
Liver Toxicity ◽  
Aminobutyric Acid ◽  
Gamma Aminobutyric Acid ◽  
Structural Analogue ◽  
Related Factors ◽  
Abrupt Discontinuation ◽  
History Of

Pregabalin is one of a group of gabapentinoids approved by the Food and Drug Administration (FDA) in 2004. It is a capsule medication taken by mouth that is used for the treatment of neuropathic pain. It is a structural analogue of the neurotransmitter gamma-aminobutyric acid (GABA), and it appears to have a spectrum of benefits and harms similar to those of other adjuvant analgesics used to treat neuropathic pain. The most common side effects mentioned in peripheral neuropathy studies are dizziness and somnolence. Pregabalin could cause liver toxicity by increasing the levels of liver enzymes. It can potentially cause vasodilatation and fluid retention in the heart and blood vessels. It may also lead to addiction. The use of Pregabalin is common among patients with a history of substance abuse and psychoactive drug dependence, as euphoria is one of its main side effects. However, abrupt discontinuation from using Pregabalin may cause nausea, insomnia, or headache. The present review evaluates the significant impact of Pregabalin toxicity on liver and heart in patients and misusers. Keywords: Pregabalin, liver toxicity, alanine aminotransferase (ALT), aspartate aminotransferase (AST), creatine kinase (CK), heart failure, addiction.

scholarly journals The effect of baclofen on spontaneous and evoked behavioural expression of experimental neuropathic chronic pain

1999 ◽  
Vol 57 (3B) ◽  
pp. 753-760 ◽  
Author(s):  
TEREZINHA DE JESUS T. SANTOS ◽  
CARLOS M. DE CASTRO-COSTA ◽  
SÍLVIO D. A. GIFFONI ◽  
FRANKLIN J. C. SANTOS ◽  
RODRIGO S. N. RAMOS ◽  
...  
Keyword(s):  
Chronic Pain ◽  
Nervous System ◽  
Neuropathic Pain ◽  
Aminobutyric Acid ◽  
Thermal Stimulus ◽  
Dependent Manner ◽  
Gamma Aminobutyric Acid ◽  
Analgesic Effects ◽  
Nociceptive Stimulus ◽  
Dose Dependent

Baclofen (beta-p-chlorophenyl-GABA) has been used in humans to treat spasticity, as well as trigeminal neuralgia. Since GABA (gamma-aminobutyric acid) has been implicated in inhibitory and analgesic effects in the nervous system, it was of interest to study the effect of baclofen in experimental neuropathic pain. With this purpose, experiments were carried out in 17 neuropathic rats with constrictive sciatic injury, as described by Bennet and Xie (1988), taking as pain parameters scratching behaviour and the latency to the thermal nociceptive stimulus. The results showed that baclofen induces, in a dose-dependent manner, significant decrease (p < 0.05) of scratching behaviour and significant increase (p < 0.05) of the latency to the nociceptive thermal stimulus. The absence of antagonism of naloxone suggested a non-participation of an opioid-mediated mechanism in this analgesic effect of baclofen on experimental neuropathic pain.

Catatonia

2020 ◽  
pp. 437-446
Author(s):  
Max Fink
Keyword(s):  
Rating Scale ◽  
Aminobutyric Acid ◽  
Gamma Aminobutyric Acid ◽  
Separate Entity ◽  
Treatment History ◽  
Past Half Century ◽  
Chemically Induced ◽  
Grand Mal ◽  
History Of ◽  
Past Half

For more than a century, catatonia has been considered a marker of the Kraepelin/Bleuler concept of schizophrenia. However, over the past half-century, it has been increasingly recognized as a separate entity, independently diagnosable and treatable. This chapter explores the diagnosis, treatment, and biological underpinnings of catatonia. Initially, it lists certain motor behaviours whose presentation might indicate catatonia, according to the Catatonia Rating Scale (CRS) such as mutism, delirium, and repetitive rhythmic acts. Through the intravenous administration of certain drugs, such as benzodiazepines, barbiturates, or gamma-aminobutyric acid (GABA) agonists, the effect on the patient’s CRS score is used to confirm the diagnosis. The treatment history of catatonia prior to the discovery of the efficacy of benzodiazepines and induced grand mal seizures (electroconvulsive therapy) is broached, such as chemically induced seizures and amobarbital. Finally, its different presentations are discussed, along with its consideration as a biological fear response.

Anaesthesia for the Growing Brain

2019 ◽  
Vol 25 (19) ◽  
pp. 2165-2170 ◽  
Author(s):  
Divya Raviraj ◽  
Thomas Engelhardt ◽  
Tom G. Hansen
Keyword(s):  
Gabaa Receptors ◽  
Animal Studies ◽  
Paediatric Population ◽  
Aminobutyric Acid ◽  
Gamma Aminobutyric Acid ◽  
Term Outcome ◽  
Long Term Outcome ◽  
Anaesthetic Agents ◽  
History Of

Despite the long history of paediatric anaesthesia, there is still much to be discovered regarding how exposure to anaesthesia affects the developing brain. Given that commonly used anaesthetic agents are thought to exert their effect via N-Methyl-D-Aspartate (NMDA) and gamma-aminobutyric acid A (GABAA) receptors, it is biologically plausible that exposure during periods of vulnerable brain development may affect long term outcome. There are numerous animal studies which suggest lasting neurological changes. However, whether this risk also applies to humans is unclear given the varying physiological development of different species and humans. Human studies are emerging and ongoing and their results are producing conflicting data. The purpose of this review is to summarize the currently available evidence and consider how this may be used to minimize harm to the paediatric population undergoing anaesthesia.

Only Early Intervention with Gamma-Aminobutyric Acid Cell Therapy Is Able to Reverse Neuropathic Pain After Partial Nerve Injury

2001 ◽  
Vol 18 (4) ◽  
pp. 471-477 ◽  
Author(s):  
Leigh Ann Stubley ◽  
Miguel A. Martinez ◽  
Shaffiat Karmally ◽  
Tomas Lopez ◽  
Pedro Cejas ◽  
...  
Keyword(s):  
Neuropathic Pain ◽  
Early Intervention ◽  
Cell Therapy ◽  
Nerve Injury ◽  
Aminobutyric Acid ◽  
Gamma Aminobutyric Acid

scholarly journals Evaluation of seizure treatment in anti-LGI1, anti-NMDAR, and anti-GABABR encephalitis

Neurology ◽  
2019 ◽  
Vol 92 (19) ◽  
pp. e2185-e2196 ◽  
Author(s):  
Marienke A.A.M. de Bruijn ◽  
Agnes van Sonderen ◽  
Marleen H. van Coevorden-Hameete ◽  
Anna E.M. Bastiaansen ◽  
Marco W.J. Schreurs ◽  
...  
Keyword(s):  
Side Effects ◽  
Medical Information ◽  
Autoimmune Encephalitis ◽  
Epileptic Seizures ◽  
Aminobutyric Acid ◽  
Seizure Freedom ◽  
Disease Course ◽  
Gamma Aminobutyric Acid ◽  
Psychotic Behavior ◽  
New Onset

ObjectiveThis nationwide cohort study evaluates seizure responses to immunotherapy and antiepileptic drugs (AEDs) in patients with anti-leucine-rich glioma-inactivated 1 (LGI1), anti-NMDA receptor (NMDAR), and anti-gamma-aminobutyric-acid B receptor (GABABR) encephalitis.MethodsAnti-LGI1, anti-NMDAR, and anti-GABABR encephalitis patients with new-onset seizures were included. Medical information about disease course, AEDs and immunotherapies used, effects, and side effects were collected. Outcome measures were (1) seizure freedom while using AEDs or immunotherapy, (2) days to seizure freedom from start of AEDs or immunotherapy, and (3) side effects.ResultsOf 153 patients with autoimmune encephalitis (AIE) (53 LGI1, 75 NMDAR, 25 GABABR), 72% (n = 110) had epileptic seizures, and 89% reached seizure freedom. At least 53% achieved seizure freedom shortly after immunotherapy, and 14% achieved seizure freedom while using only AEDs (p < 0.0001). This effect was similar in all types (p = 0.0001; p = 0.0005; p = 0.013, respectively). Median time to seizure freedom from AEDs start was 59 days (interquartile range [IQR] 27–160), and 28 days from start of immunotherapy (IQR 9–71, p < 0.0001). Side effects were psychotic behavior and suicidal thoughts by the use of levetiracetam, and rash by the use of carbamazepine. Carbamazepine was more effective than levetiracetam in reducing seizures in anti-LGI1 encephalitis (p = 0.031). Only 1 patient, of 86 surviving patients, developed epilepsy after resolved encephalitis.ConclusionEpilepsy after resolved encephalitis was rare in our cohort of patients with AIE treated with immunotherapy. In addition, seizure freedom is achieved faster and more frequently after immunotherapy. Therefore, AEDs should be considered as add-on treatment, and similar to treatment of other encephalitis symptoms, immunotherapy is crucial.

scholarly journals Receptive-field Size of S1 Cortical Neurones is Altered by Methaqualone via a GABA Mechanism

1990 ◽  
Vol 17 (1) ◽  
pp. 30-34 ◽  
Author(s):  
T.P. Hicks ◽  
T. Kaneko ◽  
J.-I. Oka
Keyword(s):  
Receptive Field ◽  
Gaba Receptor ◽  
Clinical Symptoms ◽  
Aminobutyric Acid ◽  
Field Size ◽  
Body Parts ◽  
Gamma Aminobutyric Acid ◽  
Pharmacological Mechanism ◽  
History Of ◽  
Gaba Receptor Complex

ABSTRACT:Methaqualone (Mtq; quaaludes or 'ludes) is a controlled substance, having a molecular structure related to the imidiazobenzodiazepine series of drugs, that has gained some notoriety recently due to its history of widespread abuse on the street. Users report experiencing peripheral paresthesia and transient numbness on body parts receiving dense cutaneous innervation (lips, fingertips, etc.). Since the receptive-field (RF)-sizes of many primary somatosensory (SI) cortical neurones are controlled by local, gamma-aminobutyric acid (GABA)-mediated inhibitory processes, we tested Mtq to see whether its clinical symptoms might have a basis in an action through central GABA-mediated synaptic processes. This report supports this contention and describes a likely pharmacological mechanism involved as one being related to the Ro 15-1788-sensitive benzodiazepine (Bzd) recognition site(s) of the GABA receptor complex.

Drug Repositioning: Antimalarial Activities of GABA Analogs in Mice Infected with Plasmodium berghei

2020 ◽  
Vol 20 (2) ◽  
pp. 110-121
Author(s):  
Akeem A. Ayankunle ◽  
Olayemi K. Wakeel ◽  
Oyetunji T. Kolawole ◽  
Adesola O. Oyekale ◽  
Olusola Ojurongbe ◽  
...  
Keyword(s):  
Thin Films ◽  
Neuropathic Pain ◽  
Plasmodium Berghei ◽  
Post Infection ◽  
Drug Repositioning ◽  
Aminobutyric Acid ◽  
Gamma Aminobutyric Acid ◽  
Treatment Of Epilepsy ◽  
Development Of Resistance ◽  
Almost All

Background: Drug repositioning is becoming popular due to the development of resistance to almost all the recommended antimalarials. Pregabalin and gabapentin are chemical analogs of gamma- aminobutyric acid (GABA) approved for the treatment of epilepsy and neuropathic pain. Objective: This study investigates acute toxicities and antimalarial activities of pregabalin and gabapentin in the murine malarial model. Methods: Acute toxicities were assessed using the method of Lorke, while curative activities were assessed by the administration of serial doses of pregabalin and gabapentin to Plasmodium berghei infected mice. Pregabalin was further investigated for its prophylactic activity, and curative potential when combined with either artesunate or amodiaquine. All drugs were freshly prepared and administered orally. Thin films were collected, stained, and observed under the microscope for the estimation of parasitemia and calculation of percentage chemoinhibition or chemoprevention. In pregabalin –artesunate or -amodiaquine combination aspect of this study, survival day post-infection (SDPI) was recorded, while parasitemia was re-estimated for animals that survived till day 28. Results: The oral LD50 of gabapentin, as well as pregabalin, was >5,000 mg/kg. Gabapentin at 100 and 200 mg/Kg demonstrated 35.64% and -12.78% chemoinhibition, respectively, while pregabalin demonstrated 75.60% and 100.00% chemoinhibition at doses of 12.5 and 25 mg/Kg, respectively. Moreover, pregabalin at individual doses of 25, 50 mg/Kg, and in combination with either artesunate or amodiaquine demonstrated 100.00% chemoinhibition. In its prophylactic study, pregabalin was found to be 100% chemopreventive at individual doses of 12.5 and 25 mg/Kg. Conclusion: Both GABA analogs have antimalarial properties, but pregabalin proved to be more efficacious.

The Role of Ventral Tegmental Area Gamma-Aminobutyric Acid in Chronic Neuropathic Pain after Spinal Cord Injury in Rats

2018 ◽  
Vol 35 (15) ◽  
pp. 1755-1764 ◽  
Author(s):  
Moon Yi Ko ◽  
Eun Young Jang ◽  
June Yeon Lee ◽  
Soo Phil Kim ◽  
Sung Hun Whang ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Neuropathic Pain ◽  
Ventral Tegmental Area ◽  
Aminobutyric Acid ◽  
Gamma Aminobutyric Acid ◽  
Chronic Neuropathic Pain ◽  
Cord Injury ◽  
Ventral Tegmental

The Spinal Antinociceptive Effect of Nocistatin in Neuropathic Rats Is Blocked by D-Serine

2004 ◽  
Vol 101 (3) ◽  
pp. 753-758 ◽  
Author(s):  
Uta Muth-Selbach ◽  
Eva Dybek ◽  
Katrin Kollosche ◽  
Jens-Ulrich Stegmann ◽  
Holger Holthusen ◽  
...  
Keyword(s):  
Neuropathic Pain ◽  
Antinociceptive Effect ◽  
Receptor Activation ◽  
Aminobutyric Acid ◽  
Gamma Aminobutyric Acid ◽  
Antinociceptive Action ◽  
Glycine Release ◽  
Aspartate Receptor ◽  
Nociceptive Responses ◽  
High Doses

Background The neuropeptide nocistatin (NST) has been implicated in the modulation of nociceptive responses in the spinal cord. Depending on the dose, both pronociceptive and antinociceptive effects have repeatedly been reported. The pronociceptive effect is most likely attributable to inhibition of synaptic glycine and gamma-aminobutyric acid release and a subsequent reduction in the activation of inhibitory glycine and gamma-aminobutyric acid receptors, but the mechanisms of its antinociceptive action have hitherto remained elusive. It has recently been demonstrated that synaptically released glycine contributes to N-methyl-D-aspartate receptor activation. The authors therefore investigated whether a reduction in glycine release might also account for the antinociceptive action of NST in neuropathic rats. Methods The authors analyzed the effects of spinally applied NST in the chronic constriction injury model of neuropathic pain. NST was injected intrathecally from nanomolar to picomolar doses and its effects on thermal paw withdrawal latencies were monitored. Furthermore, we tested whether D-serine (100 microg per rat), a full agonist at the glycine binding site of the N-methyl-D-aspartate receptor, would interfere with the effects of NST. Results At high doses (10 nmol/rat), intrathecally injected NST was pronociceptive, whereas lower doses (1 pmol/rat) elicited antinociception. The antinociceptive, but not the pronociceptive, action was occluded by intrathecal pretreatment with D-serine. L-serine, which does not bind to N-methyl-D-aspartate receptors, affected neither the pronociceptive nor the antinociceptive effect. Conclusions These results demonstrate that NST produces a biphasic dose-dependent effect on neuropathic pain. The spinal antinociception by NST is most likely attributable to inhibition of glycine-dependent N-methyl-D-aspartate receptor activation.

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