Electrophysiology of Seizure Disorders May Hold Key to the Pathophysiology of Psychiatric Disorders

Michael Raymond Binder

doi:doi:10.11648/j.ajcem.20190705.11

| Peer-Reviewed

Electrophysiology of Seizure Disorders May Hold Key to the Pathophysiology of Psychiatric Disorders

Michael Raymond Binder

Published in American Journal of Clinical and Experimental Medicine (Volume 7, Issue 5)

Received: 20 August 2019 Accepted: 20 September 2019 Published: 30 September 2019

Views: Downloads:

Download PDF

Share This Article

Twitter
Linked In
Facebook

Abstract

Despite the increasing burden of mental illness, social stigma and fears that psychological and emotional problems are a sign of character weakness prevent most sufferers from seeking treatment. These barriers are reinforced by diagnostic ambiguity, frequent drug side effects, variable treatment success, and a lack of clarity about the cause of mental illness. Much more progress has been made with epilepsy, a closely related group of disorders for which the pathophysiology is better understood. Although psychiatric disorders and seizure disorders are known to be distinctly different conditions, they have many shared features including their disruptive effects on mentation, their migratory nature, and their responsiveness to anticonvulsant drugs. In addition, a comparative analysis of the two disorder-types strongly suggests that they have shared mechanisms of symptom production, symptom progression, and symptom prevention. In this side-by-side comparison of the two disorder-types, I will discuss how the electrophysiological patterns that underlie seizure initiation and migration help explain how psychiatric symptoms develop and morph into one another, thus providing important insights into the pathophysiology of mental illness and potentially serving as a guide to the development of more effective treatments.

Published in	American Journal of Clinical and Experimental Medicine (Volume 7, Issue 5)
DOI	10.11648/j.ajcem.20190705.11
Page(s)	103-110
Creative Commons	This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited.
Copyright	Copyright © The Author(s), 2019. Published by Science Publishing Group

Keywords

Neuronal Hyperexcitability, Pathophysiology of Psychiatric Disorders, Bipolar Spectrum, Mood Cycling, Electrophysiology of Seizures, Kindling, Therapeutic Mechanism of ECT

References

[1]	Sabbatini, RME. The history of shock therapy in psychiatry. http://www.cerebromente.org.br/n04/historia/shock_i.htm. (Accessed 8/23/18).
[2]	Lambrecq V, Villég F, Marchal C, et al. (2012) Refractory status epilepticus: electroconvulsive therapy as a possible therapeutic strategy. Seizure. 21 (9): 661-664.
[3]	Kamel H, Cornes SB, Hegde M, Hall SE, and Josephson SA. (2010) Electroconvulsive therapy for refractory status epilepticus: a case series. Neurocritical Care. 12 (2): 204-210.
[4]	Gillig P, Sackellares JC, and Greenberg HS. (1988) Right hemisphere partial complex seizures: mania, hallucinations, and speech disturbances during ictal events. Epilepsia. 29: 26-29.
[5]	Kaplan PW. (2003) Delirium and epilepsy. Dialogues Clin Neurosci. 5 (2): 187-200.
[6]	Beletsky V and Mirsattari SM. (2011) Epilepsy, mental health disorder, or both? Epilepsy Research and Treatment. 2012 (Article ID 163731).
[7]	Matsuura M, Adachi N, Oana Y, et al. (2004) A polydiagnostic and dimensional comparison of epileptic psychoses and schizophrenia spectrum disorders. Schizophrenia Research. 69 (2-3): 189-201.
[8]	Bromfield EB, Cavazos JE, Sirven JI, editors. (2006) In: An introduction to epilepsy. West Hartford (CT): American Epilepsy Society. Chapter 1: Basic mechanisms underlying seizures and epilepsy.
[9]	Xu Y, Jia Y, Ma J, Hayat T, and Alsaedi A. (2018) Collective responses in electrical activities of neurons under field coupling. https://doi.org/10.1038/s41598-018-19858-1.
[10]	van Campen JS, Jansen FE, Pet MA, et al. (2015) Relation between stress-precipitated seizures and the stress response in childhood epilepsy. Brain. 138 (8): 2234-2248.
[11]	Frucht MM, Quigg M, Schwaner C, and Fountain NB. (2000) Distribution of seizure precipitants among epilepsy syndromes. Epilepsia. 41 (12): 1534-1539.
[12]	Ferlisi M and Shorvon S. (2014) Seizure precipitants (triggering factors) in patients with epilepsy. Epilepsy and Behavior. 33: 101-105.
[13]	McKee HR and Privitera MD. (2017) Stress as a seizure precipitant: Identification, associated factors, and treatment options. Seizure. 44: 21-26.
[14]	Lawn N, Lieblich S, Lee J, and Dunne J. (2014) Are seizures in the setting of sleep deprivation provoked? Epilepsy & Behavior. 33: 122-125.
[15]	Coffey CE, Figiel GS, Weiner RD, and Saunders WB. (1990) Caffeine augmentation of ECT. American Journal of Psychiatry. 147 (5): 579-585.
[16]	Winston AP, Hardwick E, and Jaberi N. (2005) Neuropsychiatric effects of caffeine. Advances in Psychiatric Treatment. 11 (6): 432-439.
[17]	Vezzani A. (2005) Inflammation and epilepsy. Epilepsy Curr. 5 (1): 1-6.
[18]	Bowcut JC and Weiser M. (2018) Inflammation and schizophrenia. Psychiatric Annals. 48 (5): 237-243.
[19]	Raison CL and Miller AH. (2015) Anti-Inflammatory agents as antidepressants: truth or dare. Psychiatric Annals. 45 (5): 255-261.
[20]	Maguire J and Salpekar JA. (2013) Stress, seizures, and hypothalamic-pituitary-adrenal axis targets for the treatment of epilepsy. Epilepsy and Behavior. 23 (3): 352-62.
[21]	Flores BH and Gumina HK. (2003) The neuropsychiatric sequelae of steroid treatment. Department of Psychiatry and Behavioral Sciences, Stanford University, Stanford, CA.
[22]	Bough KJ and Rho JM. (2007) Anticonvulsant mechanisms of the Ketogenic Diet. Epilepsia. 48 (1): 43-58.
[23]	Bostock ECS, Kirkby KC, and Taylor BVM. (2017) The current status of the Ketogenic Diet in psychiatry. Front Psychiatry. 8 (43): 1-40.
[24]	Ingram J, Zhang C, Cressman JR, et al. (2014) Oxygen and seizure dynamics: I. experiments. J Neurophysiol. 112 (2): 205–212.
[25]	Hufner K, Brugger H, Kuster E, et al. (2018) Isolated psychosis during exposure to very high and extreme altitude – characterization of a new medical entity. Psychological Medicine. 48 (11): 1872-1879.
[26]	Mazarati A, Shin D, Auvin S, Caplan R, and Sankar R. (2007) Kindling epileptogenesis in immature rats leads to persistent depressive behavior. Epilepsy Behav. 10: 377–383.
[27]	Goddard GV. (1967) Development of epileptic seizures through brain stimulation at low intensity. Nature. 214: 1020-1021.
[28]	Verrotti A, D’Egidio C, Agostinelli S, Verrotti C, and Pavone P. (2012) Diagnosis and management of catamenial seizures: a review. Int J Women’s Health. 2012; (4): 535–541.
[29]	Finocchi C and Ferrari M. (2011) Female reproductive steroids and neuronal excitability. Neurol Science. 32 (Suppl 1): 31-35.
[30]	Luoma JI, Stern CM, and Mermelstein PG. (2012) Progesterone inhibition of neuronal calcium signaling underlies aspects of progesterone-mediated neuroprotection. The Journal of Steroid Biochemistry and Molecular Biology. 131 (1-2): 30–6.
[31]	Stein DG. (2008) Progesterone exerts neuroprotective effects after brain injury. Brain Research Reviews. 57 (2): 386–97.
[32]	Devinsky O, Cilio MR, and Friedman D. (2014) Cannabidiol: Pharmacology and potential therapeutic role in epilepsy and other neuropsychiatric disorders. Epilepsia. 55 (6): 791-802.
[33]	Sankaranarayanan A, Wilding H, Neill E, and Castle D. (2018) A critical systematic review of evidence for cannabinoids in the treatment of schizophrenia. Psychiatric Annals. 48 (5): 214-213.
[34]	Zuardi A, Shirakawa I, Finkelfarb E, and Karniol I. (1982) Action of cannabidiol on the anxiety and other effects produced by delta-9-THC in normal subjects. Psychopharmacology (Berl). 76 (3): 245-250.
[35]	Papanicolaou J, Summers RJ, Vajda FJ, and Louis WJ. (1982) Anticonvulsant effects of clonidine mediated through central alpha2-adrenoceptors. Eur J Pharmacol. 77 (2-3): 163-166.
[36]	Kontaxakis V, Markianos M, Markidis M, and Stefanis C. (1989) Clonidine in the treatment of mixed bipolar disorder. Acta Psychiatrica Scandinavica. 79 (1): 108-110.
[37]	Farook JM, Krazem A, and Barron S. (2008) Acamprosate attenuates the handling induced convulsions during alcohol withdrawal in Swiss Webster mice. Physiol Behav. 95 (1- 2): 267-279.
[38]	Mason BJ and Heyser CJ. (2010) Acamprosate: a prototypic neuromodulator in the treatment of alcohol dependence. CNS Neurol Disord Drug Targets. 9 (1): 23-32.
[39]	Maremmani AGI, Bacciardi S, and Maremmani I. (2014) Six-month outcome in bipolar spectrum alcoholics treated with acamprosate after detoxification: a retrospective study. Int J Environ Res Public Health. 11 (12): 12983-12996.
[40]	Hertzman M, Patt IS, and Spielman LA. (2009) Open-label trial of acamprosate as a treatment for anxiety. Prim Care Companion J Clin Psychiatry. 11 (5): 267.
[41]	Schwartz TL, Siddiqui UA, Raza S, and Costello A. (2010) Acamprosate calcium as augmentation therapy for anxiety disorders. Annals of Pharmacotherapy. 44 (12): 1930-1932.
[42]	Borowicz KK, Sêkowski A, Drelewska E, and Czuczwar SJ. (2004) Riluzole enhances the antiseizure action of conventional antiepileptic drugs against pentetrazole-induced convulsions in mice. Pol J Pharmacol. 56: 187-193.
[43]	Zarate C. (2008) Riluzole in psychiatry: a systematic review of the literature. Expert Opin Drug Metab Toxicol. 4 (9): 1223-1234.
[44]	Deepmala, Slattery J, Kumar N, et al. (2015) Clinical trials of N-acetylcysteine in psychiatry and neurology: A systematic review. Neuroscience and Biobehavioral Reviews. 55: 294- 321.
[45]	Standley CA, Irtenkauf SM, and Cotton DB. (1995) Anticonvulsant effects of magnesium sulfate in hippocampal- kindled rats. Journal of Biomedical Science. 2 (1): 57-62.
[46]	Eby GA and Eby KL. (2006) Rapid recovery from major depression using magnesium treatment. Medical Hypotheses. 67 (2): 362-370.
[47]	El Idrissi A, Messing J, Scalia J, and Trenkner E. (2003) Prevention of epileptic seizures by taurine. Advances in Experimental Medicine and Biology. 526: 515–25.
[48]	Kong WX, Chen SW, Li YL, et al. (2006) Effects of taurine on rat behaviors in three anxiety models. Pharmacol Biochem Behav. 83 (2): 271–276.
[49]	Lundberg L. (2011) A modeling study of effects of polyunsaturated fatty acids on neuronal excitability: implications in epilepsy. Master ́s Thesis in Computer Science at Stockholm University, Sweden.
[50]	Peet M and Stokes C. (2005) Omega-3 fatty acids in the treatment of psychiatric disorders. Drugs. 65 (8): 1051-1059.
[51]	Lian X-Y, Zhang Z, and Stringer JL. (2006) Anticonvulsant and neuroprotective effects of ginsenosides in rats. Epilepsy Res. 70 (2-3): 244-56.
[52]	Stringer JL. (2009) Ginseng and other herbal treatments for epilepsy. Encyclopedia of Basic Epilepsy Research. pp. 1445-1450.
[53]	Khan AW, Khan A, and Ahmed T. (2016) Anticonvulsant, anxiolytic, and sedative activities of Verbena Officinalis. Front Pharmacol. 7: 499.
[54]	Perviz S, Khan H, and Pervaiz A. (2016) Plant alkaloids as an emerging therapeutic alternative for the treatment of depression. Front Pharmacol. 7: 28.
[55]	Zhu HL, Wan JB, Wang YT, et al. (2013) Medicinal compounds with antiepileptic/anticonvulsant activities. Epilepsia. 55 (1): 12463.
[56]	Peng WH, Lo KL, Lee YH, Hung TH, and Lin YC. (2007) Berberine produces antidepressant-like effects in the forced swim test and in the tail suspension test in mice. Life Sciences. 81 (11): 933-938.
[57]	Ben-Menachem E. (2002) Vagus-nerve stimulation for the treatment of epilepsy The Lancet Neurology. 1 (8): 477-482.
[58]	Grimonprez A, Raedt R, Baeken C, Boon P, and Vonck K. (2015) The antidepressant mechanism of action of vagus nerve stimulation: evidence from preclinical studies. Neuroscience and Biobehavioral Reviews. 56: 26–34.
[59]	Laxpati NG, Kasoff WS, and Gross RE. (2014) Deep brain stimulation for the treatment of epilepsy: circuits, targets, and trials. Neurotherapeutics. 11 (3): 508-526.
[60]	Holtzheimer PE and Mayberg HS. (2011) Deep brain stimulation for psychiatric disorders. Annu Rev Neurosci. 34: 289-307.
[61]	Lado FA and Moshé SL. (2008) How do seizures stop? Epilepsia. 49 (10): 1651-54.
[62]	Johnstone T, van Reekum CM, Urry HL, Kalin NH, Davidson, RJ. (2007) Failure to regulate: counterproductive recruitment of top-down prefrontal-subcortical circuitry in major depression. J. Neuroscience. 27 (33): 8877-8884.
[63]	Leuchter AF, Cook IA, Hunter AM, Cai C, Horvath S. Resting-state quantitative electroencephalography reveals increased neurophysiologic connectivity in depression. PLoS One. 2012; 7 (2): 1-13.e32508.
[64]	Strakowski SM, Adler CM, […], Townsend JD, et al. (2012) The functional neuroanatomy of bipolar disorder: a consensus model. Bipolar Disord. 14 (4): 313-25.
[65]	Parmar A and Sarkar S. (2016) Neuroimaging Studies in Obsessive Compulsive Disorder: A Narrative Review. Indian J Psychol Med. 2016 Sep-Oct; 38 (5): 386-394.
[66]	Binder MR. (2019) The multi-circuit neuronal hyperexcitability hypothesis of psychiatric disorders. AJCEM. 7 (1): 12-30.
[67]	Post RM. (2007) Kindling and sensitization as models for affective episode recurrence, cyclicity, and tolerance phenomena. Neuroscience & Biobehavioral Reviews. 31 (6): 858-873.
[68]	Wada JA, Sato M, and Corcoran ME. (1974) Persistent seizure susceptibility and recurrent spontaneous seizures in kindled cats. Epilepsia. 15 (4): 465-478.
[69]	Fuchs E and Flügge G. (2003) Chronic social stress: effects on limbic brain structures. Physiology & Behavior. 79 (3): 417-427.
[70]	Mehler B, Reimer B, Coughlin JF, and Dusek JA. (2009) Impact of Incremental Increases in Cognitive Workload on Physiological Arousal and Performance in Young Adult Drivers. Transportation Research Record: Journal of the Transportation Research Board. (2138): 6-12.
[71]	Hargreave, E. (2006). The Neuroplasticity Phenomenon of Kindling. http://hargreaves.swong.webfactional.com/kindle.htm. (Accessed 5/19/18).
[72]	Vannucchi G, Masi G, Toni C, et al. (2014) Bipolar disorder in adults with Asperger’s syndrome: a systematic review. J Affect Disord. 168: 151-160.
[73]	Courchesne E, Mouton PR, Calhoun ME, et al. (2011) Neuron number and size in prefrontal cortex of children with autism. JAMA. 306 (18): 2001-2010.
[74]	Rane P, Cochran D, Hodge SM, et al (2015) Connectivity in autism: a review of MRI connectivity studies. Harvard Review of Psychiatry. 23 (4): 223-244.
[75]	Smith SJM. (2005) EEG in neurological conditions other than epilepsy: when does it help, what does it add? Neurology, Neurosurgery & Psychiatry.
[76]	Grunze HCR. The effectiveness of anticonvulsants in psychiatric disorders. Dialogues Clin Neurosci. 2008; 10 (1): 77-89.
[77]	Ferreira MAR, O’Donovan MC, [...], and Sklar P. (2008) Collaborative genome-wide association analysis supports a role for ANK3 and CACNA1C in bipolar disorder. Nat Genet. 40 (9): 1056-1058.
[78]	Yuan A, Yi Z, Wang Q, et al. (2012) ANK3 as a risk gene for schizophrenia: new data in Han Chinese and meta analysis. Am J Med Genet B Neuropsychiatr Genet. 159B (8): 997-1005.
[79]	Lopez AY, Wang X, Xu M, et al. (2017) Ankyrin-G isoform imbalance and interneuronopathy link epilepsy and bipolar disorder. Mol Psychiatry. 22 (10): 1464–1472.
[80]	Green EK, Grozeva D, Jones I, et al., Wellcome Trust Case Control Consortium, Holmans PA, Owen MJ, O'Donovan MC, and Craddock N. (2010) The bipolar disorder risk allele at CACNA1C also confers risk of recurrent major depression and of schizophrenia. Mol Psychiatry. 15 (10): 1016-1022.
[81]	Liu Y, Blackwood DH, Caesar S, et al. (2011) Meta-analysis of genome-wide association data of bipolar disorder and major depressive disorder. Mol Psychiatry. 16 (1).
[82]	Iqbal Z, Vandeweyer G, van der Voet M, et al. (2013) Homozygous and heterozygous disruptions of ANK3: at the crossroads of neurodevelopmental and psychiatric disorders. Human Molecular Genetics. 22: 1960-1970.
[83]	Subramanian J, Dye L, and Morozov A. (2013) Rap1 signaling prevents L-type calcium channel-dependent neurotransmitter release. Journal of Neuroscience. 33 (17): 7245.
[84]	Santos M, D'Amico D, Spadoni O, et al. (2013) Hippocampal hyperexcitability underlies enhanced fear memories in TgNTRK3, a panic disorder mouse model. Journal of Neuroscience. 33 (38): 15259-15271.
[85]	Contractor A, Klyachko VA, and Portera-Cailliau C. (2015) Altered neuronal and circuit excitability in fragile X syndrome. Neuron. 87 (4): 699-715.
[86]	O’Brien NL, Way MJ, Kandaswamy R, et al. (2014) The functional GRM3 Kozak sequence variant rs148754219 affects the risk of schizophrenia and alcohol dependence as well as bipolar disorder. Psychiatric Genetics. 24: 277–278.
[87]	Schizophrenia Working Group of the Psychiatric Genomics Consortium: Ripke S, Neale BM, [...], and O’Donovan MC. (2014) Biological insights from 108 schizophrenia-associated genetic loci. Nature. 511 (7510): 421-427.
[88]	Freedman R, Coon H, Myles-Worsley M, et al. (1997) Linkage of a neurophysiological deficit in schizophrenia to a chromosome 15 locus. PNAS. 94 (2): 587–592.
[89]	Pizzarelli R and Cherubini E. (2011) Alterations of GABAergic signaling in autism spectrum disorders. Neural Plast. 1011: 157193.

Cite This Article

Plain Text BibTeX RIS

APA Style

Michael Raymond Binder. (2019). Electrophysiology of Seizure Disorders May Hold Key to the Pathophysiology of Psychiatric Disorders. American Journal of Clinical and Experimental Medicine, 7(5), 103-110. https://doi.org/10.11648/j.ajcem.20190705.11

Copy | Download

ACS Style

Michael Raymond Binder. Electrophysiology of Seizure Disorders May Hold Key to the Pathophysiology of Psychiatric Disorders. Am. J. Clin. Exp. Med. 2019, 7(5), 103-110. doi: 10.11648/j.ajcem.20190705.11

Copy | Download

AMA Style

Michael Raymond Binder. Electrophysiology of Seizure Disorders May Hold Key to the Pathophysiology of Psychiatric Disorders. Am J Clin Exp Med. 2019;7(5):103-110. doi: 10.11648/j.ajcem.20190705.11

Copy | Download

@article{10.11648/j.ajcem.20190705.11,
  author = {Michael Raymond Binder},
  title = {Electrophysiology of Seizure Disorders May Hold Key to the Pathophysiology of Psychiatric Disorders},
  journal = {American Journal of Clinical and Experimental Medicine},
  volume = {7},
  number = {5},
  pages = {103-110},
  doi = {10.11648/j.ajcem.20190705.11},
  url = {https://doi.org/10.11648/j.ajcem.20190705.11},
  eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.ajcem.20190705.11},
  abstract = {Despite the increasing burden of mental illness, social stigma and fears that psychological and emotional problems are a sign of character weakness prevent most sufferers from seeking treatment. These barriers are reinforced by diagnostic ambiguity, frequent drug side effects, variable treatment success, and a lack of clarity about the cause of mental illness. Much more progress has been made with epilepsy, a closely related group of disorders for which the pathophysiology is better understood. Although psychiatric disorders and seizure disorders are known to be distinctly different conditions, they have many shared features including their disruptive effects on mentation, their migratory nature, and their responsiveness to anticonvulsant drugs. In addition, a comparative analysis of the two disorder-types strongly suggests that they have shared mechanisms of symptom production, symptom progression, and symptom prevention. In this side-by-side comparison of the two disorder-types, I will discuss how the electrophysiological patterns that underlie seizure initiation and migration help explain how psychiatric symptoms develop and morph into one another, thus providing important insights into the pathophysiology of mental illness and potentially serving as a guide to the development of more effective treatments.},
 year = {2019}
}

Copy | Download

TY  - JOUR
T1  - Electrophysiology of Seizure Disorders May Hold Key to the Pathophysiology of Psychiatric Disorders
AU  - Michael Raymond Binder
Y1  - 2019/09/30
PY  - 2019
N1  - https://doi.org/10.11648/j.ajcem.20190705.11
DO  - 10.11648/j.ajcem.20190705.11
T2  - American Journal of Clinical and Experimental Medicine
JF  - American Journal of Clinical and Experimental Medicine
JO  - American Journal of Clinical and Experimental Medicine
SP  - 103
EP  - 110
PB  - Science Publishing Group
SN  - 2330-8133
UR  - https://doi.org/10.11648/j.ajcem.20190705.11
AB  - Despite the increasing burden of mental illness, social stigma and fears that psychological and emotional problems are a sign of character weakness prevent most sufferers from seeking treatment. These barriers are reinforced by diagnostic ambiguity, frequent drug side effects, variable treatment success, and a lack of clarity about the cause of mental illness. Much more progress has been made with epilepsy, a closely related group of disorders for which the pathophysiology is better understood. Although psychiatric disorders and seizure disorders are known to be distinctly different conditions, they have many shared features including their disruptive effects on mentation, their migratory nature, and their responsiveness to anticonvulsant drugs. In addition, a comparative analysis of the two disorder-types strongly suggests that they have shared mechanisms of symptom production, symptom progression, and symptom prevention. In this side-by-side comparison of the two disorder-types, I will discuss how the electrophysiological patterns that underlie seizure initiation and migration help explain how psychiatric symptoms develop and morph into one another, thus providing important insights into the pathophysiology of mental illness and potentially serving as a guide to the development of more effective treatments.
VL  - 7
IS  - 5
ER  -

Copy | Download

Author Information

Michael Raymond Binder

Highland Park Hospital, Highland Park, USA

Download PDF

Sections

Plain Text BibTeX RIS

APA Style

Michael Raymond Binder. (2019). Electrophysiology of Seizure Disorders May Hold Key to the Pathophysiology of Psychiatric Disorders. American Journal of Clinical and Experimental Medicine, 7(5), 103-110. https://doi.org/10.11648/j.ajcem.20190705.11

Copy | Download

ACS Style

Michael Raymond Binder. Electrophysiology of Seizure Disorders May Hold Key to the Pathophysiology of Psychiatric Disorders. Am. J. Clin. Exp. Med. 2019, 7(5), 103-110. doi: 10.11648/j.ajcem.20190705.11

Copy | Download

AMA Style

Michael Raymond Binder. Electrophysiology of Seizure Disorders May Hold Key to the Pathophysiology of Psychiatric Disorders. Am J Clin Exp Med. 2019;7(5):103-110. doi: 10.11648/j.ajcem.20190705.11

Copy | Download

@article{10.11648/j.ajcem.20190705.11,
  author = {Michael Raymond Binder},
  title = {Electrophysiology of Seizure Disorders May Hold Key to the Pathophysiology of Psychiatric Disorders},
  journal = {American Journal of Clinical and Experimental Medicine},
  volume = {7},
  number = {5},
  pages = {103-110},
  doi = {10.11648/j.ajcem.20190705.11},
  url = {https://doi.org/10.11648/j.ajcem.20190705.11},
  eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.ajcem.20190705.11},
  abstract = {Despite the increasing burden of mental illness, social stigma and fears that psychological and emotional problems are a sign of character weakness prevent most sufferers from seeking treatment. These barriers are reinforced by diagnostic ambiguity, frequent drug side effects, variable treatment success, and a lack of clarity about the cause of mental illness. Much more progress has been made with epilepsy, a closely related group of disorders for which the pathophysiology is better understood. Although psychiatric disorders and seizure disorders are known to be distinctly different conditions, they have many shared features including their disruptive effects on mentation, their migratory nature, and their responsiveness to anticonvulsant drugs. In addition, a comparative analysis of the two disorder-types strongly suggests that they have shared mechanisms of symptom production, symptom progression, and symptom prevention. In this side-by-side comparison of the two disorder-types, I will discuss how the electrophysiological patterns that underlie seizure initiation and migration help explain how psychiatric symptoms develop and morph into one another, thus providing important insights into the pathophysiology of mental illness and potentially serving as a guide to the development of more effective treatments.},
 year = {2019}
}

Copy | Download

TY  - JOUR
T1  - Electrophysiology of Seizure Disorders May Hold Key to the Pathophysiology of Psychiatric Disorders
AU  - Michael Raymond Binder
Y1  - 2019/09/30
PY  - 2019
N1  - https://doi.org/10.11648/j.ajcem.20190705.11
DO  - 10.11648/j.ajcem.20190705.11
T2  - American Journal of Clinical and Experimental Medicine
JF  - American Journal of Clinical and Experimental Medicine
JO  - American Journal of Clinical and Experimental Medicine
SP  - 103
EP  - 110
PB  - Science Publishing Group
SN  - 2330-8133
UR  - https://doi.org/10.11648/j.ajcem.20190705.11
AB  - Despite the increasing burden of mental illness, social stigma and fears that psychological and emotional problems are a sign of character weakness prevent most sufferers from seeking treatment. These barriers are reinforced by diagnostic ambiguity, frequent drug side effects, variable treatment success, and a lack of clarity about the cause of mental illness. Much more progress has been made with epilepsy, a closely related group of disorders for which the pathophysiology is better understood. Although psychiatric disorders and seizure disorders are known to be distinctly different conditions, they have many shared features including their disruptive effects on mentation, their migratory nature, and their responsiveness to anticonvulsant drugs. In addition, a comparative analysis of the two disorder-types strongly suggests that they have shared mechanisms of symptom production, symptom progression, and symptom prevention. In this side-by-side comparison of the two disorder-types, I will discuss how the electrophysiological patterns that underlie seizure initiation and migration help explain how psychiatric symptoms develop and morph into one another, thus providing important insights into the pathophysiology of mental illness and potentially serving as a guide to the development of more effective treatments.
VL  - 7
IS  - 5
ER  -

Copy | Download