Neuropsychiatric Symptoms of Epilepsy

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260 C.M. Galtrey and H.R. Cock Table 15.1 (continued) Ref. No Country Epilepsy type Setting Method a [ 17 ] 433 UK Mixed Community longitudinal cohort study Self-report postal questionnaires, two time points 5 months apart. Modeling based on results [ 18 ] 2112 USA Refractory Focal, + auras epilepsy clinic 17 % Self-report questionnaire % patients reporting stress as seizure trigger Neither perceived stress nor anxiety independently influence seizure frequency when depression controlled for Abbreviations : UK United Kingdom, USA United States of America, N/A not available, TLE temporal lobe epilepsy, IGE idiopathic generalized epilepsy a Indicates studies where patients were prospectively identified, although the data was then historical/retrospective 67 %
15 Stress and Epilepsy 261 adherence was reported as similar between groups in the Croatian study. That said, larger population-based studies also support an association. A Danish national registry study, examining the influence of losing a child on the subsequent risk of epilepsy in either parent, demonstrated a significant 50 % increased risk overall in bereaved versus non-bereaved parents, particularly in fathers within the first 3 years. This could not be explained by sociodemographic factors, and is truly population based, though the effects of potential lifestyle confounders such as alcohol and substance abuse, and misdiagnoses could not be excluded [ 22 ]. A retrospective analysis of medical information and duty assignments (combat, maintenance, or administrative) from over 300,000 compulsorily drafted Israeli Defense Forces males followed for 30 months gave conflicting results [ 23 ]: The risk of new onset seizures was slightly (RR 1.29, 95 % CI 1.03–1.62), but significantly ( p = 0.03) higher in the “high stress” combat than other units. However, in those with previous or current epilepsy (some of whom if seizure free, and off treatment with normal EEGs were assigned to combat), there was no identifiable effect on risk of recurrence. There are a smaller number of prospective studies though hampered by a lack of clear definitions and standardized assessment tools. Stressful verbal stimuli presented to healthy controls have been shown to produce subtle EEG changes (narrowing of the bandwidth and regional changes in frequency) of sufficient magnitude that a blinded reviewer could correctly identify 92 % of stress stimuli on EEG alone [ 24 ]. Similarly in people with a variety of epilepsies, stressful interviews induced changes (exaggerated spiking, paroxysmal activity, or epileptiform complexes) in the majority [ 25 ] and there are case series of stress inducing audio/video recordings inducing seizures in patients with temporal lobe epilepsy in particular [ 26 ]. There are few larger or longer term truly prospective studies (Table 15.2 ). These broadly support an association, but have struggled to separate the effects of stress per se from confounders such as sleep deprivation, alcohol, and missing medication, or to separate cause from effect. However, as highlighted by one of the most recent prospective studies, the relationship between, and difficulties distinguishing stress from premonitory sensations and mood is particularly challenging to disentangle [ 27 ]. Thus changes in the brain preceding a seizure might increase patient perceptions of stress and anxiety rather than the converse. Nonetheless, overall there is reasonable support from clinical studies that stress might lower seizure thresholds, on which basis we now proceed to look more closely at putative mechanisms. Mechanisms and Consequences of Stress The definition of stress depends on the context. In lay usage, stress is defined in the Oxford English Dictionary as “A state of mental or emotional strain or tension resulting from adverse or very demanding circumstances.” In the historical scientific study of stress, as reviewed by [ 31 ], Claude Bernard (1865) noted that the maintenance of life is critically dependent on keeping our internal milieu constant
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Neuropsychiatric Symptoms of Neurol
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Health care professionals are start
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Editor Marco Mula Atkinson Morley R
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vi Preface symptoms in patients wit
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viii Foreword I who have an interes
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x Foreword II sion, it is hardly su
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Contents 1 Neurobehavioral Comorbid
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Contributors Naoto Adachi , MD Adac
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Contributors xvii Federica Provini
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2 A. Mazarati and clinical trials.
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4 A. Mazarati a b c Fig. 1.1 Morris
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6 A. Mazarati deficits in MWM perfo
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8 A. Mazarati Fig. 1.3 Behavioral p
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10 A. Mazarati It should be noted t
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12 A. Mazarati up, is followed by t
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14 A. Mazarati opposite terminal ch
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16 A. Mazarati serotonin deficiency
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18 A. Mazarati At the same time, wh
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20 A. Mazarati 14. Cavalheiro EA, N
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22 A. Mazarati 57. Vezzani A, Frenc
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24 A. Mazarati 100. Meyza KZ, Defen
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26 A.M. Kanner and R. Ribot Despite
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28 A.M. Kanner and R. Ribot Common
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30 A.M. Kanner and R. Ribot symptom
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32 A.M. Kanner and R. Ribot Impact
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34 A.M. Kanner and R. Ribot anxiety
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36 A.M. Kanner and R. Ribot 2. Depe
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38 A.M. Kanner and R. Ribot 9. Beck
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40 A.M. Kanner and R. Ribot 56. Faz
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Chapter 3 Mania and Elation Marco M
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3 Mania and Elation 45 A manic epis
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3 Mania and Elation 47 some authors
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3 Mania and Elation 49 antimanic ag
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3 Mania and Elation 51 34. Blumer D
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54 C. Brandt Introduction Anxiety d
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56 C. Brandt diagnosis) and referri
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58 C. Brandt history of several psy
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60 C. Brandt to the speculation tha
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62 C. Brandt Case 4.2 This is a rep
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64 C. Brandt tant temporal lobe epi
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66 C. Brandt 53. Swinkels WA, van E
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Chapter 5 Delusions and Hallucinati
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5 Delusions and Hallucinations 71 P
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5 Delusions and Hallucinations 73 a
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5 Delusions and Hallucinations 75 i
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5 Delusions and Hallucinations 77 a
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5 Delusions and Hallucinations 79 T
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5 Delusions and Hallucinations 81 E
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5 Delusions and Hallucinations 83 f
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5 Delusions and Hallucinations 85 W
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5 Delusions and Hallucinations 87 4
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5 Delusions and Hallucinations 89 9
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92 B. Hermann 60 50 40 30 20 10 0 A
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94 B. Hermann Here we observe a uni
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96 B. Hermann other aspects of memo
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Chapter 7 Aggressive Behavior Hesha
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7 Aggressive Behavior 101 A multice
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7 Aggressive Behavior 103 by inter-
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7 Aggressive Behavior 105 amygdala
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7 Aggressive Behavior 107 It has be
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7 Aggressive Behavior 109 spontaneo
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7 Aggressive Behavior 111 [ 91 ] an
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7 Aggressive Behavior 113 26. Kanne
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7 Aggressive Behavior 115 72. Mula
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Chapter 8 Epilepsy and Sleep: Close
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8 Epilepsy and Sleep: Close Connect
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142 M. Schmutz and motor signs they
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144 M. Schmutz mechanism to be foun
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146 M. Schmutz etiological theory h
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148 M. Schmutz Table 9.2 Clinical c
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150 M. Schmutz When asked to give a
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152 M. Schmutz well [ 64 , 65 ]. Co
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154 M. Schmutz Therapy In 1730, the
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156 M. Schmutz As with other conver
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158 M. Schmutz Acknowledgment I am
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160 M. Schmutz 48. Bewley J, Murphy
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Chapter 10 Consciousness Andrea E.
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10 Consciousness 165 Level and Cont
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10 Consciousness 167 of consciousne
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10 Consciousness 169 During absence
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10 Consciousness 171 EEG was unrema
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10 Consciousness 173 These novel in
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10 Consciousness 175 38. Picard F,
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Chapter 11 Emotion Recognition Stef
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11 Emotion Recognition 179 experien
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11 Emotion Recognition 181 have com
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11 Emotion Recognition 183 emotion
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11 Emotion Recognition 185 signalin
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11 Emotion Recognition 187 Effect o
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11 Emotion Recognition 189 77 ]. Th
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11 Emotion Recognition 191 26. Mele
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11 Emotion Recognition 193 67. Davi
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196 A.A. Sardesai and H. Ring help
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198 A.A. Sardesai and H. Ring Why D
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200 A.A. Sardesai and H. Ring and a
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202 A.A. Sardesai and H. Ring retar
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204 A.A. Sardesai and H. Ring Preva
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208 A.A. Sardesai and H. Ring Parti
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17 The Role of Epilepsy Surgery 311
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Chapter 18 The Role of Antiepilepti
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18 The Role of Antiepileptic Drugs
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Chapter 19 The Role of Stimulation
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19 The Role of Stimulation Techniqu
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Neuropsychiatric Symptoms of Epilepsy

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