Are patterns of cortical hyperexcitability altered in catamenial epilepsy?

Ann Neurol

Department of Clinical Neurosciences, St Vincent's Hospital, Fitzroy, Australia; Department of Medicine, University of Melbourne, Parkville, Australia; Electrical and Electronic Engineering, University of Melbourne, Parkville, Australia.

Published: November 2013

AI Article Synopsis

  • Researchers used transcranial magnetic stimulation to study how the menstrual cycle affects brain excitability in women, comparing those with catamenial epilepsy to those without.
  • In healthy women, brain excitability was highest during the follicular phase, while women with epilepsy showed increased excitability during the luteal phase.
  • Overall, menstrual cycle-related changes in cortical excitability were consistent regardless of ovulation status in women with epilepsy, suggesting that hormonal effects might be altered by underlying neural changes in epilepsy.

Article Abstract

Objective: We used transcranial magnetic stimulation to determine menstrual cycle-related changes in cortical excitability in women with and without catamenial epilepsy and investigated whether these changes differed between ovulatory and anovulatory cohorts.

Methods: Healthy nonepilepsy women and women with generalized and focal epilepsy were investigated during ovulatory (n=11, 46, and 43, respectively) and anovulatory (n=9, 42, and 41) cycles. Patients were divided based on seizure pattern into catamenial (C1=perimenstrual, C2=periovulatory, C3=luteal seizure exacerbation), noncatamenial, and seizure free. Cortical excitability was assessed using motor threshold (MT) and paired pulse stimulation at short (2-15 milliseconds) and long (100-300 milliseconds) interstimulus intervals twice, at the (1) late follicular and (2) mid luteal phases of the menstrual cycle.

Results: In controls, cortical excitability was greatest in the follicular study, where intracortical facilitation was increased (p<0.05). The opposite was seen in women with epilepsy, where intracortical facilitation was greatest and intracortical inhibition was least in the luteal studies (p<0.05). There were no differences between the ovulatory and anovulatory groups in any of the cohorts. No changes were observed in MT.

Interpretation: Nonhormonal factors are involved in the cyclicity of cortical excitability across the menstrual cycle. Normal menstrual cycle variations in cortical excitability are altered in a similar pattern in ovulatory and anovulatory women with epilepsy regardless of seizure patterns. The underlying neural changes associated with epilepsy may alter responses to sex hormones. This may be an important underlying mechanism for catamenial seizure clustering.

Download full-text PDF

Source
http://dx.doi.org/10.1002/ana.23923DOI Listing

Publication Analysis

Top Keywords

cortical excitability
12
epilepsy investigated
8
patterns cortical
4
cortical hyperexcitability
4
hyperexcitability altered
4
altered catamenial
4
catamenial epilepsy?
4
epilepsy? objective
4
objective transcranial
4
transcranial magnetic
4

Similar Publications

In early-stage Alzheimer's disease (AD) amyloid-β (Aβ) deposition can induce neuronal hyperactivity, thereby potentially triggering activity-dependent neuronal secretion of phosphorylated tau (p-tau), ensuing tau aggregation and spread. Therefore, cortical excitability is a candidate biomarker for early AD detection. Moreover, lowering neuronal excitability could potentially complement strategies to reduce Aβ and tau buildup.

View Article and Find Full Text PDF

Cortical excitability on sleep deprivation measured by transcranial magnetic stimulation: A systematic review and meta-analysis.

Brain Res Bull

January 2025

Sleep Medicine Center, Mental Health Center, West China Hospital, Sichuan University, Chengdu, China. Electronic address:

Sleep deprivation is a common public problem, and researchers speculated its neurophysiological mechanisms related to cortical excitatory and inhibitory activity. Recently, transcranial magnetic stimulation combined with electromyography (TMS-EMG) and electroencephalography (TMS-EEG) have been used to assess cortical excitability in sleep-deprived individuals, but the results were inconsistent. Therefore, we conducted a meta-analysis to summarize relevant TMS-evoked indices of excitability and inhibition for exploring the cortical effects of sleep deprivation.

View Article and Find Full Text PDF

Corticospinal motor neurons (CSMN), located in the motor cortex of the brain, are one of the key components of the motor neuron circuitry. They are in part responsible for the initiation and modulation of voluntary movement, and their degeneration is the hallmark for numerous diseases, such as amyotrophic lateral sclerosis (ALS), hereditary spastic paraplegia, and primary lateral sclerosis. Cortical hyperexcitation followed by in-excitability suggests the early involvement of cortical dysfunction in ALS pathology.

View Article and Find Full Text PDF

Fragile X autosomal homolog 1 (FXR1), a member of the fragile X messenger riboprotein 1 family, has been linked to psychiatric disorders including autism and schizophrenia. Parvalbumin (PV) interneurons play critical roles in cortical processing, and have been implicated in FXR1-linked mental illnesses. Targeted deletion of FXR1 from PV interneurons in mice has been shown to alter cortical excitability and elicit schizophrenia-like behavior.

View Article and Find Full Text PDF

Introduction: Spasticity is a common complication of stroke, which is related to poor motor recovery and limitations in the performance of activities. Both transcranial magnetic stimulation (TMS) and extracorporeal shockwave therapy (ESWT) are effective treatment methods for poststroke spasticity (PSS). However, there is no existing study exploring the safety and effectiveness of TMS combined with ESWT for PSS.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!