Neuropsychiatric Symptoms of Epilepsy

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5 Delusions and Hallucinations 77 a Seizure Pre-ictal sensation Lucid interval Post-ictal confusion Post-ictal psychosis b Seizure Seizure Psychotic symptoms Seizure Fig. 5.1 ( a ) A model of post-ictal psychosis. A pre-ictal sensation ( green line ) may occur preceding a seizure. A post-ictal confusion (=delirium, blue line ) may occur just after the seizure. Thereafter, a short-lasting lucid interval ( purple line ) and post-ictal psychotic symptoms ( red line ) may develop. ( b ) A model of psychotic symptoms during a cluster of seizures. When a cluster of seizures occur, it is difficult to clarify whether psychotic symptoms are pre-ictal, ictal, or post-ictal phenomena. Psychotic symptoms ( bold red line ) may not be clearly differentiated from some preictal sensations, ictal symptoms, post-ictal confusions (deliriums), lucid intervals, and previous/ subsequent psychotic symptoms
78 N. Adachi and N. Akanuma to the difficulties in distinguishing the onset of the psychotic symptoms in relation to the seizures, the validity and usefulness of the terms of ictal and post-ictal psychoses may be reduced, and putting both together under “peri-ictal” psychoses may be more appropriate [ 46 ]. Second, it is questionable that all the cases of ictal and post-ictal psychoses occur under “clear” consciousness. Some may emerge during a prolonged period of ictal or post-ictal confusions, making these episodes closer to delirium. Inter-ictal Phenomena Psychoses can occur without a chronological relationship to seizures. This type of psychoses used to be called “epileptic psychosis” and regarded as the most common form of psychosis in epilepsy. From their large case series, Slater and colleagues [ 58 , 74 ] coined this “schizophrenia-like psychosis in epilepsy,” defining a chronic paranoid state that occurred under clear consciousness in people previously having epilepsy. The onset of the psychosis was not necessarily during or immediately following a seizure. This was later classed “inter-ictal psychosis (IIP)” by Toone [ 17 ] in contrast to PIP. Slater’s criterion is concise and practical, and has been used for approximately four decades. Slater and Roth [ 58 ] stated that psychotic symptoms seen in IIP were proper to epilepsy, rather than universal phenomena in psychoses in general. Their concept was based on three findings: (i) no genetic tendency for psychoses was found, (ii) some psychopathological features were unique to epileptic psychosis, and (iii) psychosis always occurred after the development of epilepsy. As a consequence, the idea that psychoses may be a mere comorbidity in people with epilepsy diminished until population-based studies revealed the bidirectional relationship between epilepsy and psychosis in the twenty-first century. British neuropsychiatrists described qualitative differences in psychopathology between “epileptic” psychosis and schizophrenia as “nonepileptic” functional psychosis [ 58 , 75 , 76 ]. They reported that, when compared with those with schizophrenia, patients with IIP tended to show warmer affect and less personality deterioration, and exhibit paranoid delusions with a religious coloring (a relatively common occurrence of mystical delusional experiences) and more visual hallucinations. Subsequent controlled studies with structured evaluation tools [ 77 –82 ] failed to show distinct qualitative difference in psychopathology between IIP and schizophrenia (Table 5.1 ). These studies employed more scientific approaches than traditional descriptive studies, although they still had several limitations, including binary evaluations, small sample cohorts, or insufficiently controlled clinical conditions. Vulnerability factors for IIP have been reported in three categories: (i) epilepsy related, (ii) brain damage related, and (iii) individual related [ 18 , 83 ]. Epilepsyrelated (epileptic) vulnerability factors include age of onset of epilepsy, type and frequency of seizures, lateralization and localization of epileptogenic regions, and use of antiepileptic drugs. Brain damage related (organic) vulnerability factors consist of lateralization and localization of brain lesions and acquired cognitive impair-
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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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Page 112 and 113: Chapter 7 Aggressive Behavior Hesha
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Page 130 and 131: 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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214 D.W. Dunn and W.G. Kronenberger
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236 A. Guekht Introduction Associat
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238 A. Guekht some studies no assoc
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240 A. Guekht et al. reported that
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242 A. Guekht Hyperhomocysteinemia
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244 A. Guekht Some authors offer ne
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246 A. Guekht 11. Helmstaedter C, F
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248 A. Guekht 52. Bernardi S, Scald
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250 A. Guekht 90. Bandopadhyay R, L
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252 A. Guekht 126. Park IS, Yoo SW,
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254 A. Guekht 163. Bakker A, Krauss
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256 C.M. Galtrey and H.R. Cock Intr
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Chapter 16 Epilepsy in Psychiatric
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16 Epilepsy in Psychiatric Disorder
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Chapter 17 The Role of Epilepsy Sur
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17 The Role of Epilepsy Surgery 305
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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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