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EPILEPSY: PATIENT AND FAMILY GUIDE. Second Edition. 2002. By Orrin Devinsky Published by F.A. Davis Company. 434 pages. C$40.50 approx
<span title="">2002</span>
<i title="Cambridge University Press (CUP)">
<a target="_blank" rel="noopener" href="https://fatcat.wiki/container/bohgdcojtzgkfpsfbcz5zylemy" style="color: black;">Canadian Journal of Neurological Sciences</a>
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However, in his discussion of drugs for epilepsy, Devinsky does present data on both vigabatrin and clobazam, drugs available in Canada, but not the USA. Overall, this is a very good book. ...
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A Guide to Understanding and Living with Epilepsy, 1994. Edited by Orrin Devinsky. Published by F.A. Davis Company. 347 pages. $C21.00
<span title="">1995</span>
<i title="Cambridge University Press (CUP)">
<a target="_blank" rel="noopener" href="https://fatcat.wiki/container/bohgdcojtzgkfpsfbcz5zylemy" style="color: black;">Canadian Journal of Neurological Sciences</a>
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Edited by Orrin Devinsky. Published by F.A. Davis Company. 347 pages. SC21.00. ...
Devinsky has helped us better understand epilepsy in a generally straight forward and easy to understand format. ...
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Commentary: Medical Marijuana Survey & Epilepsy
<span title="2014-11-20">2014</span>
<i title="Wiley">
<a target="_blank" rel="noopener" href="https://fatcat.wiki/container/wno3bzixffai7cgnpowre7zv2a" style="color: black;">Epilepsia</a>
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The excitable cerebral cortex
<span title="">2009</span>
<i title="Elsevier BV">
<a target="_blank" rel="noopener" href="https://fatcat.wiki/container/sprqq3w7qnbabl7xhdmtiibsfq" style="color: black;">Epilepsy & Behavior</a>
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SUDEP: Advances and Challenges
<span title="2020-10-05">2020</span>
<i title="SAGE Publications">
<a target="_blank" rel="noopener" href="https://fatcat.wiki/container/luknhofbpbhu5nzftjpwxx724m" style="color: black;">Epilepsy Currents</a>
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Epilepsy Currents
1-3
ª The Author(s) 2020
By Orrin Devinsky Department of Neurology, NYU Grossman School of Medicine, NY, NY 10021 Sanjay M. ...
Sisodiya Departments of Clinical and Experimental Epilepsy, UCL Queen Square Institute of Neurology, London, WC1N 3BG, United Kingdom ORCID iD Orrin Devinsky https://orcid.org/0000-0003-0044-4632 ...
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Seizure Clusters: Morbidity and Mortality
<span title="2021-02-16">2021</span>
<i title="Frontiers Media SA">
<a target="_blank" rel="noopener" href="https://fatcat.wiki/container/4kchoxo3jrfubkck3y7nfncina" style="color: black;">Frontiers in Neurology</a>
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Seizure clusters, an intermediate between single seizure and status epilepticus, are associated with morbidity, impaired quality of life, and premature mortality. The relationship between seizure clusters and sudden unexplained death in epilepsy (SUDEP) is poorly understood. Here, we define seizure clusters; review comorbid psychiatric disorders and memory deficits associated with seizure clusters; and review cases of witnessed SUDEP for which seizure frequency prior to death is available.
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<a target="_blank" rel="external noopener" href="https://www.ncbi.nlm.nih.gov/pubmed/33664705">pmid:33664705</a>
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... nts with a history of seizure clusters have a 2.5 fold increased risk for SUDEP, and one third of patients with monitored in hospital SUDEP experienced a cluster of generalized tonic clonic seizures prior to death. Understanding the effects of seizure frequency and duration on SUDEP risk could yield new insights in SUDEP pathophysiology and new targets for intervention.
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Postictal Psychosis: Common, Dangerous, and Treatable
<span title="">2008</span>
<i title="American Epilepsy Society">
<a target="_blank" rel="noopener" href="https://fatcat.wiki/container/luknhofbpbhu5nzftjpwxx724m" style="color: black;">Epilepsy Currents</a>
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Postical psychosis often complicates chronic epilepsy, especially in patients with seizure clusters that include tonic-clonic seizures, bilateral cerebral dysfunction (e.g., bilateral epileptiform activity or history of encephalitis), and a family history of psychiatric illness. Psychosis includes delusions, auditory and visual hallucinations, mood changes, and aggressive behavior. It typically emerges after a lucid interval of hours or days after the last seizure. This treatable disorder is associated with serious morbidity and mortality.
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<a target="_blank" rel="external noopener" href="https://www.ncbi.nlm.nih.gov/pubmed/18330462">pmid:18330462</a>
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Spirituality and Religion in Epilepsy
<span title="">2008</span>
<i title="Elsevier BV">
<a target="_blank" rel="noopener" href="https://fatcat.wiki/container/sprqq3w7qnbabl7xhdmtiibsfq" style="color: black;">Epilepsy & Behavior</a>
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Revered in some cultures but persecuted by most others, epilepsy patients have, throughout history, been linked with the divine, demonic, and supernatural. Clinical observations during the past 150 years support an association between religious experiences during (ictal), after (postictal), and in between (interictal) seizures. In addition, epileptic seizures may increase, alter, or decrease religious experience especially in a small group of patients with temporal lobe epilepsy (TLE).
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<a target="_blank" rel="external noopener" href="https://www.ncbi.nlm.nih.gov/pubmed/18171635">pmid:18171635</a>
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... e surveys have revealed that between .4% and 3.1% of partial epilepsy patients had ictal religious experiences; higher frequencies are found in systematic questionnaires versus spontaneous patient reports. Religious premonitory symptoms or auras were reported by 3.9% of epilepsy patients. Among patients with ictal religious experiences, there is a predominance of patients with right TLE. Postictal and interictal religious experiences occur most often in TLE patients with bilateral seizure foci. Postictal religious experiences occurred in 1.3% of all epilepsy patients and 2.2% of TLE patients. Many of the epilepsy-related religious conversion experiences occurred postictally. Interictal religiosity is more controversial with less consensus among studies. Patients with postictal psychosis may also experience interictal hyper-religiosity, supporting a "pathological" increase in interictal religiosity in some patients. Although psychologic and social factors such as stigma may contribute to religious experiences with epilepsy, a neurologic mechanism most likely plays a large role. The limbic system is also often suggested as the critical site of religious experience due to the association with temporal lobe epilepsy and the emotional nature of the experiences. Neocortical areas also may be involved, suggested by the presence of visual and auditory hallucinations, complex ideation during many religious experiences, and the large expanse of temporal neocortex. In contrast to the role of the temporal lobe in evoking religious experiences, alterations in frontal functions may contribute to increased religious interests as a personality trait. The two main forms of religious experience, the ongoing belief pattern and set of convictions (the religion of the everyday man) versus the ecstatic religious experience, may be predominantly localized to the frontal and temporal regions, respectively, of the right hemisphere.
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Psychotropic Effects of Antiepileptic Drugs
<span title="">2005</span>
<i title="American Epilepsy Society">
<a target="_blank" rel="noopener" href="https://fatcat.wiki/container/luknhofbpbhu5nzftjpwxx724m" style="color: black;">Epilepsy Currents</a>
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Antiepileptic drugs are important psychotropic agents that are commonly used to treat psychiatric disorders. The behavioral effects of antiepileptic drugs may differ between epilepsy and psychiatric patient populations. Randomized, double-blind, controlled data on the psychotropic efficacy of antiepileptic drugs are limited mainly to bipolar disorder. Antiepileptic drugs (AEDs) are psychotropic agents; that is, they act on the mind and can positively or negatively influence behavior. This
<span class="external-identifiers">
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... is expected, given their mechanisms of action, which are to alter ion channel and neurotransmitter system functions and, thereby, modulate the electrochemical systems that underlie behavior. Behavioral effects (e.g., cognitive and mood) associated with AEDs are complex and can vary dramatically between patients. It is currently not possible to predict which patient with epilepsy will tolerate an AED and which one will develop adverse, as opposed to positive, psychotropic effects.
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Cannabinoids and Epilepsy
<span title="2015-08-18">2015</span>
<i title="Springer Nature">
<a target="_blank" rel="noopener" href="https://fatcat.wiki/container/kdrrhvfftvgl3gwbfvw6mg7cra" style="color: black;">Neurotherapeutics</a>
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Orrin Devinsky and Ben Whalley have received research support from GW Pharmaceuticals. ...
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NEUROLOGICAL COMPLICATIONS OF PREGNANCY ADVANCES IN NEUROLOGY. VOLUME 64. 1993. Edited by Orrin Devinsky, Edward Feldman. and Brian Hainline. Published by Raven Press. 286 pages. $C117.00
<span title="">1997</span>
<i title="Cambridge University Press (CUP)">
<a target="_blank" rel="noopener" href="https://fatcat.wiki/container/bohgdcojtzgkfpsfbcz5zylemy" style="color: black;">Canadian Journal of Neurological Sciences</a>
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Vagus nerve stimulation for refractory idiopathic generalised epilepsy
<span title="">2004</span>
<i title="Elsevier BV">
<a target="_blank" rel="noopener" href="https://fatcat.wiki/container/goyr52qsqva27j4bm6yddhuhhi" style="color: black;">Seizure</a>
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We reviewed our experience with vagus nerve stimulation (VNS) in 165 patients with medically refractory epilepsy (138 partial epilepsy (PE), 13 symptomatic generalised epilepsy (SGE), 14 idiopathic generalised epilepsy (IGE)). Average duration of VNS therapy was 21.6 months. A 50% or greater reduction in seizure frequency was achieved in 47.1% of the PE group, 46.1% of the SGE group, and 57.1% of the IGE group. A 50% or greater reduction in seizure frequency and reduced antiepileptic drug (AED)
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... regimen were achieved in: PE (9.4%), SGE (7.7%), and IGE (35.7%). These preliminary results suggest that VNS is an effective therapy for some patients with medically refractory IGE.
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Epilepsy Associated with Systemic Autoimmune Disorders
<span title="2013-04-10">2013</span>
<i title="American Epilepsy Society">
<a target="_blank" rel="noopener" href="https://fatcat.wiki/container/luknhofbpbhu5nzftjpwxx724m" style="color: black;">Epilepsy Currents</a>
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Cortical network underlying speech production during delayed auditory feedback
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<span title="2020-11-11">2020</span>
<i title="Cold Spring Harbor Laboratory">
bioRxiv
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Accurate and fluent production of speech strongly depends on hearing oneself which allows for the detection and correction of vocalization errors in real-time. When auditory feedback is disrupted with a time delay (e.g. echo on a conference call), it causes slowed and stutter-like speech in humans. Impaired speech motor control during delayed auditory feedback is implicated in various neurological disorders ranging from stuttering to aphasia, however the underlying neural mechanisms are poorly
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... nderstood. Here, we investigated auditory feedback control in human speech by obtaining electrocorticographic recordings from neurosurgical subjects performing a delayed auditory feedback (DAF) task. We observed a significant increase in neural activity in auditory sites that scaled with the duration of feedback delay and correlated with response suppression during normal speech, providing direct evidence for a shared mechanism between sensitivity to altered feedback and speech-induced auditory suppression in humans. Furthermore, we find that when subjects robustly slowed down their speech rate to compensate for the delay, the dorsal division of the precentral gyrus was preferentially recruited to support articulation during an early time frame. This recruitment was accompanied by response enhancement across a large speech network commencing in temporal cortex and then engaging frontal and parietal sites. Our results highlight the critical components of the human speech network that support auditory feedback control of speech production and the temporal evolution of their recruitment.
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Neuroinflammation and psychiatric illness
<span title="2013-04-01">2013</span>
<i title="Springer Nature">
<a target="_blank" rel="noopener" href="https://fatcat.wiki/container/jwx5lmmb6ngrnd3sff4t4fohxa" style="color: black;">Journal of Neuroinflammation</a>
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Multiple lines of evidence support the pathogenic role of neuroinflammation in psychiatric illness. While systemic autoimmune diseases are well-documented causes of neuropsychiatric disorders, synaptic autoimmune encephalitides with psychotic symptoms often go under-recognized. Parallel to the link between psychiatric symptoms and autoimmunity in autoimmune diseases, neuroimmunological abnormalities occur in classical psychiatric disorders (for example, major depressive, bipolar, schizophrenia,
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... and obsessive-compulsive disorders). Investigations into the pathophysiology of these conditions traditionally stressed dysregulation of the glutamatergic and monoaminergic systems, but the mechanisms causing these neurotransmitter abnormalities remained elusive. We review the link between autoimmunity and neuropsychiatric disorders, and the human and experimental evidence supporting the pathogenic role of neuroinflammation in selected classical psychiatric disorders. Understanding how psychosocial, genetic, immunological and neurotransmitter systems interact can reveal pathogenic clues and help target new preventive and symptomatic therapies.
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