topiramate and Parkinson-Disease

The duration and, age of dementia have been linked to a higher risk of seizures. The exact mechanism that drives epileptogenesis in impaired mitophagy and autophagy linked dementia (MAD) is fully defined after reviewing the Scopus, Publon, and Pubmed databases. The epileptogenesis in patients with Alzheimer's disease dementia (ADD) and Parkinson's disease dementia (PDD) is due to involvement of amyloid plaques (Aβ), phosphorylated tau (pTau), Parkin, NF-kB and NLRP3 inflammasome. Microglia, the prime protective and inflammatory cells in the brain exert crosstalk between mitophagy and inflammation. Several researchers believed that the inflammatory brain cells microglia could be a therapeutic target for the treatment of a MAD associated epilepsy. There are conventional antiepileptic drugs such as gabapentin, lamotrigine, phenytoin sodium, carbamazepine, oxcarbazepine, felbamate, lamotrigine, valproate sodium, and topiramate are prescribed by a psychiatrist to suppress seizure frequency. Also, the conventional drugs generate serious adverse effects and synergises dementia characteristics. The adverse effect of carbamazepine is neurotoxic and also, damages haemopoietic system and respiratory tract. The phenytoin treatment causes cerebellar defect and anemia. Dementia and epilepsy have a complicated relationship, thus targeting mitophagy for cure of epileptic dementia makes sense. Complementary and alternative medicine (CAM) is one of the rising strategies by many patients of the world, not only to suppress seizure frequency but also to mitigate dementia characteristics of patients. Therefore our present review focus on the interplay between epilepsy and MAD and their treatment with CAM approaches.

Topics: Anticonvulsants; Carbamazepine; Dementia; Epilepsy; Felbamate; Gabapentin; Humans; Inflammasomes; Lamotrigine; Mitophagy; NF-kappa B; NLR Family, Pyrin Domain-Containing 3 Protein; Oxcarbazepine; Parkinson Disease; Phenytoin; Seizures; Topiramate; Triazines; Ubiquitin-Protein Ligases; Valproic Acid

Tremors can be encountered in a variety of disease states but the most common causes are Parkinson disease and essential tremor. This review was undertaken to highlight advances in the field during the last 12 months.. Kinetic tremor may be more prominent in essential tremor than postural tremor. Clinically Parkinson disease and essential tremor may be confused with each other but it may be possible to distinguish between these two nitrites using sophisticated electrophysiology. Monosymptomatic rest tremor has recently been shown to be associated with decreased fluorodopa uptake on the positron emission tomography scan suggesting its relationship to Parkinson disease.. Significant advances have been made in the understanding of the pathophysiology, genetics and therapy of tremor disorders during the last 12 months. This review will consider Parkinson disease, essential tremor and other tremors and highlight advances in the field.

Topics: Acetates; Amines; Anticonvulsants; Antiparkinson Agents; Cyclohexanecarboxylic Acids; Diagnosis, Differential; Electromyography; Essential Tremor; Fructose; Gabapentin; gamma-Aminobutyric Acid; Humans; Levodopa; Motor Cortex; Muscle, Skeletal; Parkinson Disease; Posture; Primidone; Randomized Controlled Trials as Topic; Severity of Illness Index; Somatosensory Cortex; Topiramate; Tremor

Topics: Amantadine; Anticonvulsants; Antiparkinson Agents; Dose-Response Relationship, Drug; Double-Blind Method; Dyskinesia, Drug-Induced; Female; Follow-Up Studies; Humans; Male; Parkinson Disease; Seveso Accidental Release; Topiramate; Treatment Outcome

The antiepileptic drug topiramate reduces levodopa-induced dyskinesia without exacerbating parkinsonism in animal models. We report a randomized, double-blind, placebo-controlled crossover trial in patients with Parkinson's disease and levodopa-induced dyskinesia.. Fifteen patients with Parkinson's disease and stable levodopa-induced dyskinesia were enrolled into the study, of whom 13 were randomized to topiramate or placebo. The study medication was titrated to 100 mg/day over four weeks, and assessments were carried out after a further two weeks. Dyskinesia severity assessed by a blinded rater from video recordings was the primary outcome measure.. Seven patients (mean age 58.9 ± 12.8 years) completed the study. Patients taking topiramate vs. placebo showed a significant increase in dyskinesia severity compared to baseline (Wilcoxon signed rank test, P = 0.043). Five patients withdrew from the study whilst taking topiramate due to adverse effects.. Topiramate tended to worsen dyskinesia in patients with Parkinson's disease, and was poorly tolerated.

Topics: Adult; Aged; Anticonvulsants; Antiparkinson Agents; Cross-Over Studies; Double-Blind Method; Dyskinesia, Drug-Induced; Female; Fructose; Humans; Levodopa; Male; Middle Aged; Parkinson Disease; Topiramate

Clinicians monitor cognitive effects of drugs primarily by asking patients to describe their side effects. We examined the relationship of subjective perception of cognition to mood and objective cognitive performance in healthy volunteers and neurological patients.. Three separate experiments used healthy adults treated with lamotrigine (LTG) and topiramate (TPM), adults with epilepsy on LTG or TPM, and patients with idiopathic Parkinson's disease. Correlations were calculated for change scores on and off drugs in the first two experiments and for the single assessment in Experiment 3.. Across all three experiments, significant correlations were more frequent (chi(2)=259, P < or = 0.000) for mood versus subjective cognitive perception (59%) compared with subjective versus objective cognition (2%) and mood versus objective cognitive performance (2%).. Subjective perception of cognitive effects is related more to mood than objective performance. Clinicians should be aware of this relationship when assessing patients' cognitive complaints.

Topics: Adult; Affect; Anticonvulsants; Cognition; Cross-Over Studies; Depression; Double-Blind Method; Epilepsies, Partial; Female; Fructose; Humans; Lamotrigine; Male; Neuropsychological Tests; Parkinson Disease; Psychomotor Performance; Quality of Life; Self Concept; Topiramate; Triazines

Topics: Anticonvulsants; Antiparkinson Agents; Disruptive, Impulse Control, and Conduct Disorders; Female; Fructose; Humans; Male; Middle Aged; Parkinson Disease; Severity of Illness Index; Topiramate

L-Dopa-induced dyskinesia in patients with Parkinson's disease can be alleviated by amantadine, an antagonist at N-methyl-D-aspartate glutamate receptors. The antiepileptic drug topiramate, which blocks α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors, has also been shown to reduce dyskinesia. The purpose of this study was to examine the behavioral pharmacology of topiramate alone and in combination with amantadine in animal models of PD and L-dopa-induced dyskinesia. The effects of topiramate (5-20 mg/kg) and amantadine (5-20 mg/kg) on abnormal involuntary movements (the rat homologue of dyskinesia) and Rotarod performance were assessed alone and in combination in the 6-hydroxydopamine-lesioned rat following chronic L-dopa treatment. Dyskinesia, parkinsonian disability, and "on-time" were assessed in the MPTP-lesioned nonhuman primate following administration of topiramate (5-20 mg/kg) and amantadine (0.1-1.0 mg/kg) alone and in combination. Topiramate and amantadine dose-dependently reduced dyskinesia in the 6-hydroxydopamine-lesioned rat, whereas topiramate reduced Rotarod performance; there was no effect on parkinsonian disability in the MPTP-lesioned nonhuman primate, in which both drugs reduced dyskinesia. Topiramate and amantadine exhibited differential antidyskinetic effects on dyskinesia elicited by the dopamine D1 receptor agonist SKF 38393 (2 mg/kg). Subthreshold doses of both drugs in combination had a synergistic effect on dyskinesia in the 6-hydroxydopamine-lesioned rat, with no worsening of motor performance; this effect was confirmed in the MPTP-lesioned nonhuman primate, with a selective reduction in "bad on-time." These data confirm the antidyskinetic potential of topiramate and suggest that combination with low-dose amantadine may allow better reduction of dyskinesia with no adverse motor effects.

Topics: Amantadine; Animals; Antiparkinson Agents; Behavior, Animal; Callithrix; Disease Models, Animal; Dopamine Agonists; Drug Synergism; Dyskinesia, Drug-Induced; Fructose; Levodopa; Male; MPTP Poisoning; Neuroprotective Agents; Parkinson Disease; Rats; Rats, Sprague-Dawley; Topiramate

To report the occurrence of adult-onset (de novo) sleepwalking in a series of 6 patients with idiopathic Parkinson disease (PD).. Case series.. Outpatient clinic for movement disorders.. Of 165 consecutive patients with PD seen for 2 years, 6 patients with adult-onset sleepwalking were identified. These patients underwent a systematic clinical assessment of their extrapyramidal and sleep problems, which included standard questionnaires, clinical examination, and estimation of PD severity (motor score of the Unified PD Rating Scale and Hoehn and Yahr stage). Five of 6 patients had a video-polysomnography recording that was scored according to international criteria.. Patients included 3 women and 3 men with a mean (+/-SD) age of 66 +/- 12 years (range, 46-78 years). The mean (+/-SD) Unified PD Rating Scale score was 25 +/- 9 (range, 10-35) and the mean (+/-SD) Hoehn and Yahr stage was 2.5 +/- 1.0 (range, 1.0-4.0). Medications in these patients included levodopa (n = 6), dopamine agonists (n = 4), selective serotonin reuptake inhibitor antidepressants (n = 3), and hypnotics (n = 3). All patients had at least 1 concomitant sleep-wake disorder, including rapid eye movement sleep behavior disorder (n = 4) and insomnia (n = 4). In 2 of 6 patients, the latency between onset of PD and appearance of sleepwalking was more than 4 years.. Neurodegenerative changes associated with PD at the brainstem level can affect the "ascending" control of state transition (leading to dissociated arousals from non-rapid eye movement and/or rapid eye movement sleep) and the "descending" control of locomotion and muscle tone, together giving rise to various sleep-associated behavioral disturbances including sleepwalking, rapid eye movement sleep behavior disorder, and overlap parasomnia.

Topics: Aged; Anticonvulsants; Dreams; Female; Fructose; Humans; Male; Middle Aged; Parkinson Disease; Polysomnography; Sleep Wake Disorders; Somnambulism; Topiramate

Overactive AMPA receptor-mediated transmission may be involved in the pathogenesis of levodopa-induced dyskinesia. The mechanism of action of the anticonvulsant drug topiramate involves attenuation of AMPA receptor-mediated transmission. In this study, the potential antidyskinetic action of topiramate was examined in the MPTP-lesioned marmoset model of Parkinson's disease and levodopa-induced dyskinesia. Topiramate significantly reduced levodopa-induced dyskinesia, without affecting the antiparkinsonian action of levodopa. Topiramate represents an exciting potential novel therapeutic approach to levodopa-induced dyskinesia in patients with Parkinson's disease.

Topics: Animals; Anticonvulsants; Antiparkinson Agents; Callithrix; Disease Models, Animal; Dyskinesia, Drug-Induced; Fructose; Levodopa; MPTP Poisoning; Parkinson Disease; Topiramate