Recovery function of and effects of hyperventilation on somatosensory evoked high-frequency oscillation in Parkinson's disease and myoclonus epilepsy.
Mochizuki Hitoshi,Machii Katsuyuki,Terao Yasuo,Furubayashi Toshiaki,Hanajima Ritsuko,Enomoto Hiroyuki,Uesugi Haruo,Shiio Yasushi,Kamakura Keiko,Kanazawa Ichiro,Ugawa Yoshikazu
Neuroscience research
To evaluate recovery function of and effects of hyperventilation (HV) on high-frequency oscillations (HFOs) of median nerve somatosensory evoked potential (SEP), we recorded SEPs in 8 Parkinson's disease (PD) patients with enlarged HFOs, 4 myoclonus epilepsy (ME) patients and 10 healthy volunteers (N). SEP was recorded from the hand sensory area contralateral to the median nerve stimulated at the wrist. Responses were amplified with filters set at 0.5 and 3000 Hz. HFOs were obtained by digitally filtering raw SEPs from 500 to 1000 Hz. We measured amplitudes of the N20 onset-peak (N20o-p), N20 peak-P25 peak (N20p-P25p), P25 peak-N33 peak (P25p-N33p), the early (1st-2nd) and late (3rd) HFOs. For the recovery function study, paired-pulse stimuli at various interstimulus intervals (20, 50, 100, 150, 200 and 300 ms) were given. To investigate effects of HV, amplitudes of several components of SEPs recorded after HV were compared with those before HV. In PD and ME, the N20o-p recovery curve showed significantly less suppression as compared with those of N. The P25p-N33p recovery curve of ME showed longer suppression than those of N and PD. There were no significant differences in the early or late HFOs recovery curves among three groups. At the dysinhibited state after HV, the late HFO was reduced in association with a significant enlargement of the N20p-P25p amplitude in normal subjects. This suggests that the late HFOs should reflect bursts of inhibitory interneurons. In the ME patients, the early HFOs significantly decreased by HV. The pattern in ME patients may be explained by a kind of compensation for already enhanced SEPs (giant SEP) in the dysinhibited situation. We conclude that (1) Giant HFOs are normally regulated by inhibitory neuronal systems involving in paired stimulation SEP. (2) The late HFOs must reflect bursts of GABAergic inhibitory interneurons.
Subthalamic nucleus neuronal activity in Parkinson's disease and epilepsy subjects.
Montgomery Erwin B
Parkinsonism & related disorders
Activity from 113 subthalamic nucleus (STN) neurons from two epilepsy patients and 103 neurons from 9 Parkinson's disease (PD) patients undergoing DBS surgery showed no significant differences in frequencies (PD, mean 7.5+/-7.0 spikes/s (sps), epilepsy mean 7.8+/-8.5 sps) or in the coefficients of variation of mean discharge frequencies per 1s epochs. A striking relationship between mean discharge frequencies per 1 s epochs and the standard deviations for both groups were consistent with a random Poisson processes. These and similar findings call into question theories that posit increased STN activity is causal to parkinsonism.
10.1016/j.parkreldis.2007.06.014
[Parkinson's disease and epilepsy].
Jiménez-Jiménez F J,Molina-Arjona J A,Roldan-Montaud A,Fernandez-Ballesteros A,Zancada F,Santos J
Revue neurologique
We report the case of a woman suffering from complex partial seizures who developed Parkinson's disease at the age of 58. Parkinsonian symptoms improved transitorily after complex partial seizures. Although this has been reported after generalized seizures, this case is, to our knowledge, the first description of improvement of parkinsonian symptoms following a complex partial seizure.
Parkinson's disease: less epileptic seizures, more status epilepticus.
Feddersen Berend,Rémi Jan,Einhellig Marion,Stoyke Cordula,Krauss Philipp,Noachtar Soheyl
Epilepsy research
We compared the rate of epilepsy and status epilepticus (SE) in patients with and without Parkinson's disease (PD). Out of 1215 patients with idiopathic PD, 31 had epilepsy and 19 of these had at least one episode of SE (61.3%) compared to 298 of 2537 patients (11.7%; p<0.001) with epilepsy and without concomitant PD. This clinical finding supports the hypothesis that the functional impairment of the basal ganglia in PD patients makes SE more likely.
10.1016/j.eplepsyres.2013.11.013
Letter to the Editor: Increasing incidence of Parkinson's disease in patients with epilepsy: A Nationwide Cohort Study.
Journal of the neurological sciences
We have read with a great deal of interest the article by Hwang et al. (1) and appreciate the authors'' commendable efforts. The article was intelligently written and provides a significant insight into the study carried out by the authors. We greatly acknowledge the brief concepts the authors have shared regarding Parkinson's disease and epilepsy, which are without doubt an asset to the field of neurology. The study has laid a good foundation for future related studies. The article mentions epilepsy as an uncommon comorbidity of Parkinson's disease and the transition of a non-epilepsy brain to an epilepsy brain. It is also mentioned that PD is a progressive neurodegenerative disorder of dopaminergic neurons in the substantia nigra, and the incidence of the two diseases. However, as we assess the article in depth, we have found some shortcomings that would have enhanced the sense and purpose of the study.
10.1016/j.jns.2024.123206
Brain vascularization in deep brain stimulation surgeries: epilepsy, Parkinson's disease, and obsessive-compulsive disorder.
Journal of neurosurgical sciences
BACKGROUND:In our experience, we encountered more blood vessels during deep brain stimulation (DBS) surgeries in epilepsy. In this study, we have quantified and compared the cerebral vascularization in epilepsy, Parkinson's disease (PD) and obsessive-compulsive disorder (OCD). METHODS:A retrospective observational study in 15 epilepsy and 15 PD patients was performed. The amount, location, and size of blood vessels within 5 millimeters (mm) of all DBS electrode trajectories (N.=120) for both targets (anterior nucleus of the thalamus: ANT and subthalamic nucleus: STN) in both patient groups were quantified and compared on a Medtronic workstation (Dublin, Ireland). Additionally, blood vessels in the trajectories (N.=120) of another group of 15 PD (STN) and 15 OCD (ventral capsule-ventral striatum [VC-VS]) patients were quantified and compared (trajectories N.=120), also to the first group. Statistical analyses were performed with SPSS version 27.0 (descriptive statistics, independent samples t-tests, Mann Whitney U Test, ANOVA Test and post-hoc Tukey Test). A P value <0.05 was considered statistically significant. RESULTS:Our results showed a significant greater amount of cerebral blood vessels in epilepsy patients (10 SD±4) compared to PD (PD1 6 SD±1 and PD2 5 SD±3) and OCD (5 SD±1) with P<0.0001. Also, all other subanalyses showed more vascularization in the epilepsy group. CONCLUSIONS:Our results show that the brain of epilepsy patients seems to be more vascularized compared to PD and OCD patients. This can make the surgical planning for DBS more challenging, and the use of multiple trajectories limited.
10.23736/S0390-5616.22.05606-5
Increasing incidence of Parkinson's disease in patients with epilepsy: A Nationwide cohort study.
Journal of the neurological sciences
BACKGROUND:Although epilepsy is an uncommon comorbidity of Parkinson's disease (PD), the exact incidence of PD among the patients with epilepsy is not clarified yet. OBJECTIVES:We aimed to estimate the incidence of PD in patients with epilepsy and explore the association between epilepsy and PD. METHODS:Epilepsy patients enrolled in the National Health Insurance Service Health Screening Cohort (NHIS-HealS) (2002-2013) between 2003 and 2007 were set up as the experimental group. The major outcome was the occurrence of PD. Non-epilepsy patients were obtained through Propensity Score Matching of 'greedy nearest neighbor' algorithm in 1:1 ratio. The Cox Proportional Hazards model was used to calculate PD incidence and hazard ratio (HR). RESULTS:A total of 10,510 patients were finally included in the study, which contained 5255 patients in epilepsy and non-epilepsy groups, respectively. During the follow-up period, 85 patients with Parkinson's disease among 5255 patients with epilepsy and 57 patients with Parkinson's disease among 5255 patients without epilepsy occurred. The 10,000 Person-Year (PY), representing the number of PD patients per 10,000 per year, was 21.38 in the epilepsy group and 11.18 in the non-epilepsy group. When all variables were adjusted, it was found that the epilepsy group had a 2.19 times significantly higher risk of developing Parkinson's disease than the control group (The adjusted HR: 2.19 (95% CI, 1.55-3.12)). CONCLUSION:This study indicates an increased risk of PD in patients with epilepsy. However, further research is needed to prove an exact causal relationship between these two brain disorders.
10.1016/j.jns.2024.122891
Common factors among Alzheimer's disease, Parkinson's disease, and epilepsy: possible role of the noradrenergic nervous system.
Szot Patricia
Epilepsia
The neurodegenerative disorders Alzheimer's disease (AD) and Parkinson's disease (PD) share in common the neuropathologic loss of locus coeruleus (LC) noradrenergic neurons. In addition, these two neurodegenerative disorders share two symptoms that define these disorders: cognitive impairment and depression. The hippocampus is a region that is known to play a role in cognition and depression, and the hippocampus receives sole noradrenergic innervation from LC neurons. However, it is unclear how the loss of LC noradrenergic neurons contributes to these common symptoms in these two disorders. Epilepsy is not considered a neurodegenerative disorder, but the hippocampus is severely affected in temporal lobe epilepsy. Of interest, cognitive impairment and depression are also common comorbid disorders in temporal lobe epilepsy. This article describes common symptoms among these three neurologic disorders and a possible role of the noradrenergic nervous system.
10.1111/j.1528-1167.2012.03476.x
Association Between Antiepileptic Drugs and Incident Parkinson Disease.
JAMA neurology
Importance:Recent studies have highlighted an association between epilepsy and Parkinson disease (PD). The role of antiepileptic drugs (AEDs) has not been explored. Objective:To investigate the association between AEDs and incident PD. Design, Setting, and Participants:This nested case-control study started collecting data from the UK Biobank (UKB) in 2006, and data were extracted on June 30, 2021. Individuals with linked primary care prescription data were included. Cases were defined as individuals with a Hospital Episode Statistics (HES)-coded diagnosis of PD. Controls were matched 6:1 for age, sex, race and ethnicity, and socioeconomic status. Prescription records were searched for AEDs prescribed prior to diagnosis of PD. The UKB is a longitudinal cohort study with more than 500 000 participants; 45% of individuals in the UKB have linked primary care prescription data. Participants living in the UK aged between 40 and 69 years were recruited to the UKB between 2006 and 2010. All participants with UKB-linked primary care prescription data (n = 222 106) were eligible for enrollment in the study. Individuals with only a self-reported PD diagnosis or missing data for the matching variables were excluded. In total, 1477 individuals were excluded; 49 were excluded due to having only self-reported PD, and 1428 were excluded due to missing data. Exposures:Exposure to AEDs (carbamazepine, lamotrigine, levetiracetam, and sodium valproate) was defined using routinely collected prescription data derived from primary care. Main Outcomes and Measures:Odds ratios and 95% CIs were calculated using adjusted logistic regression models for individuals prescribed AEDs before the first date of HES-coded diagnosis of PD. Results:In this case-control study, there were 1433 individuals with an HES-coded PD diagnosis (cases) and 8598 controls in the analysis. Of the 1433 individuals, 873 (60.9%) were male, 1397 (97.5%) had their race and ethnicity recorded as White, and their median age was 71 years (IQR, 65-75 years). An association was found between AED prescriptions and incident PD (odds ratio, 1.80; 95% CI, 1.35-2.40). There was a trend for a greater number of prescription issues and multiple AEDs being associated with a greater risk of PD. Conclusions and Relevance:This study, the first to systematically look at PD risk in individuals prescribed the most common AEDs, to our knowledge, found evidence of an association between AEDs and incident PD. With the recent literature demonstrating an association between epilepsy and PD, this study provides further insights.
10.1001/jamaneurol.2022.4699
Therapeutic applicability of cannabidiol and other phytocannabinoids in epilepsy, multiple sclerosis and Parkinson's disease and in comorbidity with psychiatric disorders.
Basic & clinical pharmacology & toxicology
Studies have demonstrated the neuroprotective effect of cannabidiol (CBD) and other Cannabis sativa L. derivatives on diseases of the central nervous system caused by their direct or indirect interaction with endocannabinoid system-related receptors and other molecular targets, such as the 5-HT receptor, which is a potential pharmacological target of CBD. Interestingly, CBD binding with the 5-HT receptor may be suitable for the treatment of epilepsies, parkinsonian syndromes and amyotrophic lateral sclerosis, in which the 5-HT serotonergic receptor plays a key role. The aim of this review was to provide an overview of cannabinoid effects on neurological disorders, such as epilepsy, multiple sclerosis and Parkinson's diseases, and discuss their possible mechanism of action, highlighting interactions with molecular targets and the potential neuroprotective effects of phytocannabinoids. CBD has been shown to have significant therapeutic effects on epilepsy and Parkinson's disease, while nabiximols contribute to a reduction in spasticity and are a frequent option for the treatment of multiple sclerosis. Although there are multiple theories on the therapeutic potential of cannabinoids for neurological disorders, substantially greater progress in the search for strong scientific evidence of their pharmacological effectiveness is needed.
10.1111/bcpt.13997
The Interplay Among Epilepsy, Parkinson's Disease and Inflammation: Revisiting the Link through Ca/cAMP Signalling.
Bergantin Leandro B
Current neurovascular research
BACKGROUND:Robust evidence has described that Parkinson´s disease (PD) is associated with an increased risk for developing epileptic seizures. In fact, an interplay between PD and epilepsy has been of interest for many years. An emerging hypothesis is that inflammation could link both diseases. OBJECTIVE:Bearing in mind the experience of our group in the field of Ca/cAMP signalling pathways, this article discussed, beyond inflammation, the role of these signalling pathways in this link between PD and epilepsy. METHODS:Publications involving Ca/cAMP signalling pathways, PD, and epilepsy (alone or combined) were collected by searching PubMed and EMBASE. RESULTS:The comprehension of the interplay between PD and epilepsy could improve the drug therapy. In addition, a Ca signalling dyshomeostasis due to Coronavirus disease 2019 (COVID-19), an emerging and rapidly evolving situation, has been reported. CONCLUSION:Thus, this article also debated recent findings about therapeutics involving Ca2+ channel blockers for preventing Ca signalling dyshomeostasis due to COVID-19, including the correlation among COVID-19, epilepsy, and PD.
10.2174/1567202618666210603123345