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  1. Article ; Online: Commentary on the Paper "Effect of Seizures on the Developing Brain and Cognition".

    Holmes, Gregory L

    Seminars in pediatric neurology

    2023  Volume 47, Page(s) 101080

    Abstract: Effect of seizures on the developing brain and cognition: Gregory L. Holmes Seminars in Pediatric ...

    Abstract Effect of seizures on the developing brain and cognition: Gregory L. Holmes Seminars in Pediatric Neurology Volume 23, Issue 2, May 2016, Pages 120-126 Epilepsy is a complex disorder, which involves much more than seizures, encompassing a range of associated comorbid health conditions that can have significant health and quality-of-life implications. Of these comorbidities, cognitive impairment is one of the most common and distressing aspects of epilepsy. Clinical studies have demonstrated that refractory seizures, resistant to antiepileptic drugs, occurring early in life have significant adverse effects on cognitive function. Much of what has been learned about the neurobiological underpinnings of cognitive impairment following early-life seizures has come from animal models. While early-life seizures in rodents do not result in cell loss, seizures do result in changes in neurogenesis and synaptogenesis and alteration of excitatory/inhibitory balance, network connectivity and temporal coding. These morphological and physiological changes are accompanied by parallel impairment in cognitive skills. This increased understanding of the pathophysiological basis of seizure-induced cognitive deficits should allow investigators to develop novel targets for therapeutic interventions.
    MeSH term(s) Animals ; Child ; Humans ; Brain ; Seizures/drug therapy ; Cognition ; Epilepsy/complications ; Cognition Disorders ; Anticonvulsants/therapeutic use
    Chemical Substances Anticonvulsants
    Language English
    Publishing date 2023-09-10
    Publishing country United States
    Document type Journal Article
    ZDB-ID 1290000-x
    ISSN 1558-0776 ; 1071-9091
    ISSN (online) 1558-0776
    ISSN 1071-9091
    DOI 10.1016/j.spen.2023.101080
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  2. Article ; Online: Brain Connectivity: When too much of a good thing is not so good.

    Holmes, Gregory L

    Clinical neurophysiology : official journal of the International Federation of Clinical Neurophysiology

    2022  Volume 144, Page(s) 117–118

    MeSH term(s) Humans ; Brain ; Head
    Language English
    Publishing date 2022-10-07
    Publishing country Netherlands
    Document type Editorial ; Comment
    ZDB-ID 1463630-x
    ISSN 1872-8952 ; 0921-884X ; 1388-2457
    ISSN (online) 1872-8952
    ISSN 0921-884X ; 1388-2457
    DOI 10.1016/j.clinph.2022.09.016
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  3. Article ; Online: Interictal Spikes as an EEG Biomarker of Cognitive Impairment.

    Holmes, Gregory L

    Journal of clinical neurophysiology : official publication of the American Electroencephalographic Society

    2021  Volume 39, Issue 2, Page(s) 101–112

    Abstract: Summary: Although interictal spikes (IISs) are a well-established EEG biomarker for epilepsy, whether they are also a biomarker of cognitive deficits is unclear. Interictal spikes are dynamic events consisting of a synchronous discharge of neurons ... ...

    Abstract Summary: Although interictal spikes (IISs) are a well-established EEG biomarker for epilepsy, whether they are also a biomarker of cognitive deficits is unclear. Interictal spikes are dynamic events consisting of a synchronous discharge of neurons producing high frequency oscillations and a succession of action potentials which disrupt the ongoing neural activity. There are robust data showing that IISs result in transitory cognitive impairment with the type of deficit specific to the cognitive task and anatomic location of the IIS. Interictal spike, particularly if frequent and widespread, can impair cognitive abilities, through interference with waking learning and memory and memory consolidation during sleep. Interictal spikes seem to be particularly concerning in the developing brain where animal data suggest that IISs can lead to adverse cognitive effects even after the disappearance of the spikes. Whether a similar phenomenon occurs in human beings is unclear. Thus, although IISs are a clear biomarker of transitory cognitive impairment, currently, they lack sensitivity and specificity as a biomarker for enduring cognitive impairment.
    MeSH term(s) Animals ; Biomarkers ; Brain ; Cognitive Dysfunction/diagnosis ; Electroencephalography ; Epilepsy/diagnosis ; Humans
    Chemical Substances Biomarkers
    Language English
    Publishing date 2021-08-06
    Publishing country United States
    Document type Journal Article
    ZDB-ID 605640-4
    ISSN 1537-1603 ; 0736-0258
    ISSN (online) 1537-1603
    ISSN 0736-0258
    DOI 10.1097/WNP.0000000000000728
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  4. Article ; Online: Drug Treatment of Epilepsy Neuropsychiatric Comorbidities in Children.

    Holmes, Gregory L

    Paediatric drugs

    2020  Volume 23, Issue 1, Page(s) 55–73

    Abstract: There is increasing recognition that epilepsy can be associated with a broad spectrum of comorbidities. While epileptic seizures are an essential element of epilepsy in children, there is a spectrum of neurological, mental health and cognitive disorders ... ...

    Abstract There is increasing recognition that epilepsy can be associated with a broad spectrum of comorbidities. While epileptic seizures are an essential element of epilepsy in children, there is a spectrum of neurological, mental health and cognitive disorders that add to the disease burden of childhood epilepsy resulting in a decreased quality of life. The most common comorbid conditions in childhood epilepsy include depression, anxiety, autism spectrum disorders, sleep disorders, attention deficits, cognitive impairment, and migraine. While epilepsy can result in comorbidities, many of the comorbidities of childhood have a bi-directional association, with the comorbid condition increasing risk for epilepsy and epilepsy increasing the risk for the comorbid condition. The bidirectional feature of epilepsy and the comorbidities suggest a common underlying pathological basis for both the seizures and comorbid condition. While recognition of the comorbid conditions of pediatric epilepsies is increasing, there has been a lag in the development of effective therapies partly out of concern that drugs used to treat the comorbid conditions could increase seizure susceptibility. There is now some evidence that most drugs used for comorbid conditions are safe and do not lower seizure threshold. Unfortunately, the evidence showing drugs are effective in treating many of the childhood comorbidities of epilepsy is quite limited. There is a great need for randomized, placebo-controlled drug trials for efficacy and safety in the treatment of comorbidities of childhood epilepsy.
    MeSH term(s) Adolescent ; Anticonvulsants/pharmacology ; Anticonvulsants/therapeutic use ; Child ; Child, Preschool ; Comorbidity ; Epilepsy/complications ; Epilepsy/drug therapy ; Epilepsy/psychology ; Humans ; Mental Disorders/drug therapy ; Mental Disorders/etiology ; Neuropsychiatry/methods ; Quality of Life/psychology ; Seizures/complications ; Seizures/drug therapy ; Seizures/psychology
    Chemical Substances Anticonvulsants
    Language English
    Publishing date 2020-11-24
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 1492748-2
    ISSN 1179-2019 ; 1174-5878
    ISSN (online) 1179-2019
    ISSN 1174-5878
    DOI 10.1007/s40272-020-00428-w
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  5. Article ; Online: Drug Treatment of Progressive Myoclonic Epilepsy.

    Holmes, Gregory L

    Paediatric drugs

    2020  Volume 22, Issue 2, Page(s) 149–164

    Abstract: The progressive myoclonic epilepsies (PMEs) represent a rare but devastating group of syndromes characterized by epileptic myoclonus, typically action-induced seizures, neurological regression, medically refractory epilepsy, and a variety of other signs ... ...

    Abstract The progressive myoclonic epilepsies (PMEs) represent a rare but devastating group of syndromes characterized by epileptic myoclonus, typically action-induced seizures, neurological regression, medically refractory epilepsy, and a variety of other signs and symptoms depending on the specific syndrome. Most of the PMEs begin in children who are developing as expected, with the onset of the disorder heralded by myoclonic and other seizure types. The conditions are considerably heterogenous, but medical intractability to epilepsy, particularly myoclonic seizures, is a core feature. With the increasing use of molecular genetic techniques, mutations and their abnormal protein products are being delineated, providing a basis for disease-based therapy. However, genetic and enzyme replacement or substrate removal are in the nascent stage, and the primary therapy is through antiepileptic drugs. Epilepsy in children with progressive myoclonic seizures is notoriously difficult to treat. The disorder is rare, so few double-blinded, placebo-controlled trials have been conducted in PME, and drugs are chosen based on small open-label trials or extrapolation of data from drug trials of other syndromes with myoclonic seizures. This review discusses the major PME syndromes and their neurogenetic basis, pathophysiological underpinning, electroencephalographic features, and currently available treatments.
    MeSH term(s) Child ; Humans ; Myoclonic Epilepsies, Progressive/drug therapy ; Research Design
    Language English
    Publishing date 2020-01-08
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 1492748-2
    ISSN 1179-2019 ; 1174-5878
    ISSN (online) 1179-2019
    ISSN 1174-5878
    DOI 10.1007/s40272-019-00378-y
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  6. Article ; Online: Do vaccines cause epilepsy? Review of cases in the National Vaccine Injury Compensation Program.

    Scott, Rodney C / Moshé, Solomon L / Holmes, Gregory L

    Epilepsia

    2023  Volume 65, Issue 2, Page(s) 293–321

    Abstract: Objective: The National Childhood Vaccine Injury Act of 1986 created the National Vaccine Injury Compensation Program (VICP), a no-fault alternative to the traditional tort system. Since 1988, the total compensation paid exceeds $5 billion. Although ... ...

    Abstract Objective: The National Childhood Vaccine Injury Act of 1986 created the National Vaccine Injury Compensation Program (VICP), a no-fault alternative to the traditional tort system. Since 1988, the total compensation paid exceeds $5 billion. Although epilepsy is one of the leading reasons for filing a claim, there has been no review of the process and validity of the legal outcomes given current medical information. The objectives were to review the evolution of the VICP program in regard to vaccine-related epilepsy and assess the rationale behind decisions made by the court.
    Methods: Publicly available cases involving epilepsy claims in the VICP were searched through Westlaw and the US Court of Federal Claims websites. All published reports were reviewed for petitioner's theories supporting vaccine-induced epilepsy, respondent's counterarguments, the final decision regarding compensation, and the rationale underlying these decisions. The primary goal was to determine which factors went into decisions regarding whether vaccines caused epilepsy.
    Results: Since the first epilepsy case in 1989, there have been many changes in the program, including the removal of residual seizure disorder as a vaccine-related injury, publication of the Althen prongs, release of the acellular form of pertussis, and recognition that in genetic conditions the underlying genetic abnormality rather than the immunization causes epilepsy. We identified 532 unique cases with epilepsy: 105 with infantile spasms and 427 with epilepsy without infantile spasms. The petitioners' experts often espoused outdated, erroneous causation theories that lacked an acceptable medical or scientific foundation and were frequently criticized by the court.
    Significance: Despite the lack of epidemiological or mechanistic evidence indicating that childhood vaccines covered by the VICP result in or aggravate epilepsy, these cases continue to be adjudicated. After 35 years of intense litigation, it is time to reconsider whether epilepsy should continue to be a compensable vaccine-induced injury.
    MeSH term(s) Humans ; Child ; Spasms, Infantile ; Compensation and Redress ; Vaccines/adverse effects ; Vaccination/adverse effects
    Chemical Substances Vaccines
    Language English
    Publishing date 2023-12-28
    Publishing country United States
    Document type Journal Article
    ZDB-ID 216382-2
    ISSN 1528-1167 ; 0013-9580
    ISSN (online) 1528-1167
    ISSN 0013-9580
    DOI 10.1111/epi.17794
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  7. Article ; Online: Usefulness of the postkainate spontaneous recurrent seizure model for screening for antiseizure and neuroprotective effects.

    Mikati, Mohamad A / Holmes, Gregory L

    Epilepsia

    2021  Volume 62, Issue 5, Page(s) 1289

    MeSH term(s) Humans ; Neuroprotective Agents/therapeutic use ; Seizures/diagnosis ; Seizures/drug therapy ; Status Epilepticus
    Chemical Substances Neuroprotective Agents
    Language English
    Publishing date 2021-03-29
    Publishing country United States
    Document type Letter ; Comment
    ZDB-ID 216382-2
    ISSN 1528-1167 ; 0013-9580
    ISSN (online) 1528-1167
    ISSN 0013-9580
    DOI 10.1111/epi.16885
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  8. Article ; Online: CBD treatment following early life seizures alters orbitofrontal-striatal signaling during adulthood.

    Cashen, Natalie A / Kloc, Michelle L / Pressman, Davi / Liebman, Samuel A / Holmes, Gregory L

    Epilepsy & behavior : E&B

    2024  Volume 152, Page(s) 109638

    Abstract: Obsessive compulsive disorder (OCD) is a comorbid condition of epilepsy and often adds to the burden of epilepsy. Both OCD and epilepsy are disorders of hyperexcitable circuits. Fronto-striatal circuit dysfunction is implicated in OCD. Prior work in our ... ...

    Abstract Obsessive compulsive disorder (OCD) is a comorbid condition of epilepsy and often adds to the burden of epilepsy. Both OCD and epilepsy are disorders of hyperexcitable circuits. Fronto-striatal circuit dysfunction is implicated in OCD. Prior work in our laboratory has shown that in rat pups following a series of flurothyl-induced early life seizures (ELS) exhibit frontal-lobe dysfunction along with alterations in electrographic temporal coordination between the orbitofrontal cortex (OFC) and dorsomedial striatum (DMS), circuits implicated in OCD. Here, we studied the effects of ELS in male and female rat pups on OCD-like behaviors as adults using the marble burying test (MBT). Because cannabidiol (CBD) is an effective antiseizure medication and has shown efficacy in the treatment of individuals with OCD, we also randomized rats to CBD or vehicle treatment following ELS to determine if CBD had any effect on OCD-like behaviors. While the flurothyl model of ELS did not induce OCD-like behaviors, as measured in the MBT, ELS did alter neural signaling in structures implicated in OCD and CBD had sex-dependent effects of temporal coordination in a way which suggests it may have a beneficial effect on epilepsy-related OCD.
    MeSH term(s) Male ; Female ; Animals ; Rats ; Cannabidiol ; Flurothyl ; Magnetic Resonance Imaging ; Epilepsy ; Seizures/chemically induced ; Seizures/drug therapy
    Chemical Substances Cannabidiol (19GBJ60SN5) ; Flurothyl (9Z467FG2YK)
    Language English
    Publishing date 2024-02-06
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2010587-3
    ISSN 1525-5069 ; 1525-5050
    ISSN (online) 1525-5069
    ISSN 1525-5050
    DOI 10.1016/j.yebeh.2024.109638
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  9. Article ; Online: Coexpressed

    Goudsward, Hannah J / Ruiz-Velasco, Victor / Stella, Salvatore L / Willing, Lisa B / Holmes, Gregory M

    Molecular pharmacology

    2024  Volume 105, Issue 3, Page(s) 250–259

    Abstract: Opioid analgesics are frequently associated with gastrointestinal side effects, including constipation, nausea, dysphagia, and reduced gastric motility. Though it has been shown that stimulation of opioid receptors expressed in enteric motor neurons ... ...

    Abstract Opioid analgesics are frequently associated with gastrointestinal side effects, including constipation, nausea, dysphagia, and reduced gastric motility. Though it has been shown that stimulation of opioid receptors expressed in enteric motor neurons contributes to opioid-induced constipation, it remains unclear whether activation of opioid receptors in gastric-projecting nodose ganglia neurons contributes to the reduction in gastric motility and emptying associated with opioid use. In the present study, whole-cell patch-clamp recordings were performed to determine the mechanism underlying opioid receptor-mediated modulation of Ca
    MeSH term(s) Humans ; Receptors, Opioid, kappa ; Analgesics, Opioid/pharmacology ; Receptors, Opioid, mu/physiology ; Constipation ; Neurons, Afferent ; Receptors, Opioid ; Analgesics/pharmacology
    Chemical Substances Receptors, Opioid, kappa ; Analgesics, Opioid ; Receptors, Opioid, mu ; Receptors, Opioid ; Analgesics
    Language English
    Publishing date 2024-02-15
    Publishing country United States
    Document type Journal Article
    ZDB-ID 124034-1
    ISSN 1521-0111 ; 0026-895X
    ISSN (online) 1521-0111
    ISSN 0026-895X
    DOI 10.1124/molpharm.123.000774
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  10. Book ; Online: Handbook of epilepsy

    Browne, Thomas R. / Holmes, Gregory L.

    2008  

    Author's details Thomas R. Browne, Gregory L. Holmes
    Keywords Epilepsy - handbooks
    Language English
    Size 1 Online-Ressource
    Edition 4th ed.
    Publisher Lippincott Williams & Wilkins
    Publishing place Philadelphia
    Document type Book ; Online
    Note Includes bibliographical references and index
    Remark Zugriff für angemeldete ZB MED-Nutzerinnen und -Nutzer
    ISBN 978-0-7817-7397-3 ; 0-7817-7397-0
    Database ZB MED Catalogue: Medicine, Health, Nutrition, Environment, Agriculture

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