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ORIGINAL ARTICLE |
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Year : 2015 | Volume
: 4
| Issue : 2 | Page : 99-103 |
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A clinical study of post-ictal psychoses
Suprakash Chaudhury1, S Rohatgi2, PS Murthy3, Subhas Soren4, Ajay Kumar Bakhla5, Chandra Kiran4
1 Department of Psychiatry, Pravara Institute of Medical Sciences, Rural Medical College, Loni, Maharashtra, India 2 Department of Medicine and Neurology, Armed Forces Medical College, Pune, Maharashtra, India 3 Department of Psychiatry, Santhiram Medical College and General Hospital, Nandyal, Andhra Pradesh, India 4 Department of Psychiatry, Ranchi Institute of Neuropsychiatry and Allied Sciences, Ranchi, Jharkhand, India 5 Department of Psychiatry, Rajendra Institute of Medical Sciences, Ranchi, Jharkhand, India
Date of Web Publication | 16-Jun-2015 |
Correspondence Address: Suprakash Chaudhury Department of Psychiatry, Pravara Institute of Medical Sciences (Deemed University), Rural Medical College, Loni - 413 736, Maharashtra India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/2278-0521.157873
Background: Postictal psychosis (PIP) represents 25% of the psychoses seen in epileptic patients. There is a paucity of Indian studies on PIP. Aim: To study the clinical correlates and treatment response of patients with PIP. Materials and Methods: Consecutive patients with PIP, diagnosed according to criteria of Logsdail and Toone (1988), admitted to two tertiary care teaching hospitals were included in the study with their informed consent. After recording detailed history, examination and investigation patients were treated and followed-up. Results: The study included clinical details of 28 patients (24 male and 4 female) with PIP. Psychoses were usually precipitated by a run of seizures. The seizures were partial complex in 15 and generalised tonic clonic in 13 patients. Follow-up details were available in all cases for periods ranging from 3 months to 2 years. The length of psychosis varied from one to 79 days (mean 20.5 days), although ten patients had recovered within 1 week. All patients were confused at onset of psychosis. The episodes were characterised by pleomorphic psychotic phenomena, dominated by marked and varied mood changes and low incidence of schizophreniform phenomenology. Electroencephalogram (EEG) examination of the patients showed abnormalities in 26 patients, while two had normal EEG. Computed Tomography (CT) scan showed abnormality three patients. All patients received antiepileptic drugs. In addition 17 were treated with antipsychotics, two with antipsychotics plus antidepressants, while two received antipsychotics and ECT. Majority of the patients responded well to therapy though psychoses recurred in two. Two patients developed a chronic psychosis after the first post-ictal episode and continued to show residual symptoms for more than 2-3 months. Conclusion: Post-ictal psychoses are short lasting disorders of good prognosis. Keywords: Clinical presentation, epilepsy, post-ictal psychosis
How to cite this article: Chaudhury S, Rohatgi S, Murthy P S, Soren S, Bakhla AK, Kiran C. A clinical study of post-ictal psychoses. Saudi J Health Sci 2015;4:99-103 |
Introduction | |  |
Epilepsy is an unusual disorder that, at times, is associated with a wide range of specific psychiatric symptoms. These psychiatric symptoms occur on the establishment of a temporal-limbic focus of intermittent excessive neuronal excitatory activity that produces increasingly inhibitory responses. [1] Psychiatric disorders are increasingly being recognized as co-existing with epilepsy. [2],[3] A recent Indian study reported that 42.5% of epilepsy patients attending neurology clinic had a psychiatric disorder including organic depressive disorder (16.98%), mild cognitive disorder (11.3 2%), tobacco abuse/dependence (8.49%), dissociative (conversion) disorder (2.83%), emotionally labile (asthenic) disorder (1.88%) and organic delusional (schizophrenia-like) disorder (0.94%). [4] The association between epilepsy and psychosis has generated considerable discussion since the nineteenth century, and these disorders have been broadly described as 'Psychosis of Epilepsy'. [5] Jean Etienne Esquirol in his classical 1838 article has described acute states of excitation related to seizures. Levin described 52 cases of 'epileptic clouded states' following two or more seizures. [6] A cross-sectional population-based study of epilepsy patients in UK observed that psychiatric disorders occurred twice as often in people with epilepsy. [2] Torta and Keller [7] found that the risk of psychosis in populations of patients with epilepsy may be 6-12 times that in the general population, with a prevalence of about 7-8%. On the other hand two Indian studies reported that epilepsy patients had a lower prevalence of psychotic disorders. [7],[8] A recent systematic review and meta-analysis reported that the pooled estimate of prevalence of psychosis in epilepsy was 5.6% (95% CI: 4.8-6.4) with a high level of heterogeneity. The prevalence of interictal psychosis and postictal psychosis (PIP) was 5.2% (95% CI: 3.3-7.2) and 2% (95% CI: 1.2-2.8) respectively. [9] There is a paucity of Indian studies of this condition and basic information (e.g. type of epilepsy, phenomenology, time course and outcome) is lacking. The present study aimed at determining the clinical correlates and phenomenology of PIP.
Materials and methods | |  |
The present study is a hospital-based longitudinal study. The protocol was submitted to and approved by the institutional ethical committee. Written informed consent was obtained from each subject.
Sample
Consecutive patients, between the age of 18-65 years, admitted to Psychiatry wards of two large tertiary care teaching hospitals with the diagnosis of PIP were included in the study as per the inclusion and exclusion criteria. The diagnosis of epilepsy was made as per International League Against Epilepsy classification by the neurophysician/physician. [10] A diagnosis of PIP was accepted if the following four criteria of Logsdail and Toone [6] were fulfilled:
- The episode of confusion or psychosis manifested immediately upon a seizure or emerged within a week of the return of apparently normal mental function
- The psychosis had a minimum length of 24 hours and a maximum length of 3 months
- The mental state was characterized by one of the following.
- Clouding of consciousness, disorientation or delirium
- Delusions, hallucinations, in clear consciousness
- Mixture of (a) and (b).
- There was no evidence of the following extraneous factors that might have contributed to the abnormal mental state.
- Anticonvulsant toxicity-based on physical examination for evidence of cerebellar dysfunction in each case.
- A previous history of interictal psychosis
- EEG evidence of minor status
- Recent history of head injury, or alcohol or drug intoxication.
Patients with mental retardation or other comorbid psychiatric or physical disorders were not included in the study. Patients having longstanding psychosis and subsequently developed seizures were excluded.
Procedure
After obtaining informed consent, patients were assessed using a specially designed proforma for the study to assess socio-demographic data, age at epilepsy onset, details of epilepsy and anti-epileptic medication, presence of seizure clusters preceding PIP; age at onset of PIP, details of onset of PIP, mode of presentation; family history of psychiatric illness; premorbid personality and social situation; physical examination; psychiatric phenomenology; laboratory examination, EEG findings; results of neuroimaging studies; treatment and follow-up.
Results | |  |
0Socio-demographic and clinical characteristics
There were 28 patients with PIP comprising of 24 males and four females. Average age of the subjects was 31.93 (±10.54) years (range 18-65 years). The average age of onset of epilepsy was 15.36 (±8.12) years (range 4-38 years). The age at onset of first episode of PIP ranged from 17 years to 63 years (mean ± SD, 31.57 ± 10.18 years). The interval between the onset of epilepsy and the first episode of PIP varied from 7-44 years (mean ± SD, 16.18 ± 7.78 years). Six patients had one psychotic episode, nine had two episodes, three had three episodes, and ten had multiple episodes of PIP. Family history revealed that one patient had a father who was said to drink alcohol to excess, and another patient had a brother who suffered from seizures. There was no family history of psychosis. All the patients, except six, were married. Fifteen patients were employed, five worked as farm labourers, four were housewives and four were students.
General characteristics of epilepsy
Thirteen (46.4%) of the 28 patients had primary generalized epilepsy causing grand mal seizures, and the remaining 15 (53.6%) had complex partial seizures.
Seizures prior to the onset of psychosis
In 19 (67.9%) of the patients there was a clear history of an increase in seizure frequency prior to the onset of psychosis. In the remaining patients no reliable history could be obtained.
Features of psychosis
All patients were confused at the onset of the psychosis. This confusion persisted throughout the psychosis in eleven. Two patients were catatonic. Two patients had delusions and thought disorder, while seven patients had only delusions. Persecutory delusions were reported in six patients, these were poorly systematised while one had persecutory ideas. Delusions of reference were observed in two patients. One patient each had grandiose and nihilistic delusions. Eight patients had markedly abnormal mood: elevated in five and depressed in three. Four patients reported visual hallucinations; ten had auditory hallucinations and two somatic hallucinations.
Neurological examination
None of the patients had neurological abnormalities on detailed physical examination.
Investigations
EEG examination of the patients showed abnormalities in 26 (92.9%) patients, while two had normal EEG. CT scan abnormalities were detected in three (15%) of 20 patients: 2 (10%) patients had neurocysticercosis while one had mildly dilated ventricles (post-meningitic).
Treatment
All patients received antiepileptic drugs. Twenty four patients were taking a single antiepileptic drug, while four were on multiple antiepileptics. Carbamazepine, sodium valproate and phenytoin were the commonly prescribed antiepileptics. In addition eleven patients were also prescribed benzodiazepines; 18 were treated with antipsychotics, two with antipsychotics and antidepressants while two received antipsychotics and ECT; two patients received albendazole for neurocysticercosis.
Course and outcome
Nineteen patients had a serious behaviour disturbance while inpatients, including two who made suicide attempts and thirteen who were physically aggressive. The length of psychosis varied from one to 79 days (mean 20.5 days), although 13 of the patients had recovered within one week. Follow-up details were available in all of the patients, for a period of 3 months to 2 years. Two patients developed a chronic psychosis after the first post-ictal episode and continued to show residual symptoms for more than two-three months, but all the rest recovered from the psychotic episode. Two patients had relapse of seizures due to irregular medication, and this led to a relapse of the psychosis in both, but three other patients despite having repeated seizures did not suffer relapse of psychoses.
Discussion | |  |
The lack of awareness of psychiatrists about the importance of epilepsy dates back half a century, when epilepsy became considered an exclusive neurologic disorder. [1] Despite their relatively common occurrence, PIP or other brief psychiatric symptoms occurring post-ictally have not been adequately studied. [6] A study of 114 consecutive outpatients with a history of pharmacoresistant partial epilepsy reported postictal psychotic symptoms in 7 and hypomanic symptoms in 22. [11] Another study of 44 patients with refractory temporal lobe epilepsy found eight patients with PIP and seven patients with chronic psychosis. [12] In the study of Roy et al., four patients (33.3%) had PIP and one patient had chronic psychosis. [8] Logsdail and Toone studied 14 patients and concluded that PIP are defined by their temporal relationship to seizures activity. Psychosis usually occurred after an exacerbation in seizure frequency or intensity and appeared after a lucid interval. The episodes were characterizes by pleomorphic psychotic phenomena occurring either in clear or in clouded consciousness and dominated by marked and varied mood changes. Spontaneous resolution was usual, but with tendency to recur. [6] The findings of the present study are broadly in agreement with the above. In the present study amnesia or partial amnesia for the episode was seen in all the patients but was not highlighted in the earlier studies. In the present study all patients had confusion initially while in an earlier study 21.4% did not show confusion though similar diagnostic criteria were used. [6] CT/MRI scan abnormalities were seen in 10.7% patients compared to higher figures of 41.67-83.33% in earlier studies. [6],[7],[8],[13]
A review of patients of PIP reported that the average age at onset was 38.3 ± 9.8 years and 93% occurred in patients older than 18 years of age. [14] This finding is similar to the results of the present study where the earliest age of onset of psychosis was 17 years and the average age of onset of psychosis was 31.57 ± 10.18 years. However, the interval between the onset of epilepsy and the first episode of ranged from 7-44 years (mean ± SD, 16.18 ± 7.78 years), which was somewhat longer in the present series than in previous reports (range 13-15 years). [14] This longer interval in our patients provides additional evidence of the kindling mechanism in the pathogenesis of psychosis in chronic epileptics through long-term epileptic discharges. While the detailed pathophysiology of psychosis in epilepsy is not known, dopaminergic activity and frontal-subcortical circuits (resembling the present model of psychosis) are believed to be involved. Exploring the pathophysiology of PIP may provide a better understanding of the nature of functional psychosis as in schizophrenia. [14],[15]
Apart from the association of PIP with a long history of epilepsy, some studies have reported a higher risk of PIP in men based on the fact that up to 67% of cases occur in men. [16],[17],[18],[19],[20] In our study, 85% of cases were male which is higher than the earlier reports. [6],[16],[17],[18],[19],[20] However, these are findings from unrepresentative samples and for unambiguous determination of the gender effect further investigation with a larger and representative patient sample is needed. In agreement with some previous studies, [16],[17],[18],[19],[20] no patient with PIP in the present study had a family history of psychosis. The finding of increased seizure frequency prior to the onset of PIP observed in 19 (67.9%) of our patients is also in agreement with number of earlier studies. [6],[14],[16],[17],[18],[19],[20]
Previously reported work has observed an association between PIP and generalized epilepsy, though recent studies reported an association with complex partial seizures. [6],[8] Both these observations are in agreement with our findings. It has also been suggested that PIP episodes may remit spontaneously following the occurrence of further seizure activity, and therefore ECT could be beneficial in refractory states. [6] In the present study of the two patients given ECT one showed a good response while the other responded poorly and so the above suggestion was not supported.
There currently is no internationally accepted syndromic classification of psychosis in epilepsy. Recently a tentative classification has been proposed which classifies psychoses in epilepsy into three groups. Type A psychosis consists of ictal psychosis and PIP, and is characterised by a long epilepsy-psychosis interval and high affinity with TLE. Psychotic episodes which began initially with repetitive episodic interictal psychosis and which ultimately became continuous are classified into Type B psychosis. Patients with Type B psychosis share common clinical properties with Type A, in that the condition is characterized by a long epilepsy-psychosis interval and high affinity with TLE. Type A psychosis can progress to Type B in some cases. In contrast, Type C psychosis is characterized by a short epilepsy-psychosis interval, low affinity with TLE and has a strong genetic predisposition. Therefore, in contrast to Type A and Type B psychoses, elimination of epileptic activity may not improve psychosis in this group. [21]
Although some controversy surrounds the link between psychotic illness and epilepsy, the existence of a PIP (related to the occurrence of seixure activity) and an interictal psychosis (schizophrenia-like, paranoid and affective) is now generally accepted. [22] It is important to determine whether intermittent or brief psychoses are related to seizure activity. Some patients experience time-limited psychoses and do not experience the truly interictal psychosis. The more common interictal form is the persistent psychosis called 'schizophrenia-like psychosis of epilepsy'. These patients often lack the 'negative symptoms' seen in schizophrenia. Whether this syndrome is identical to or different from schizophrenia in the traditional psychiatric sense is undetermined. In a comparison of symptoms, Perez and Trimble observed that 50% of patients with epilepsy and psychosis could be diagnosed as having schizophrenia. [22],[23] In contrast to the above, schizophreniform phenomenology was seen in only 2 (7.14%) patient in the present study. However, this finding is in agreement with a recent study [9] in which none of the PIP patients showed schizophreniform phenomenology while all the interictal psychosis patients showed such symptoms. Recent researchers have also reported the enlargement of amygdala and significant reduction in total brain volume in patients with psychosis of epilepsy as compared to normal controls and TLE without psychoses. [24] In the present series no such correlation was found.
The pathophysiology of PIP is not known. Logsdail and Toone hypothesized that PIP results from increased post-synaptic dopamine sensitivity. [6] This hypothesis was tests using single-photon emission CT and the D 2 ligand [ 123 I] iodobenzamide. Results revealed that patients with epilepsy and psychoses had decreased binding to this ligand, suggesting that there was increased release of endogenous dopamine in the psychotic state. [25] Other theories based on neuroscience research to explain psychosis in epilepsy include the following: 1) subictal discharges in temporal lobe; 2) neuronal exhaustion in cortex similar to Todd's paralysis; 3) transient neurotransmitter/modulator dysfunction involving dopamine, GABA, glutamate, acetylcholine, serotonin, adenosine, endogenous opiates, and nitric oxide; and 4) plastic regenerative changes resulting in 'miswiring'. [26] Some recent studies have emphasized the relevance of autoimmunity to the pathogenesis of both epilepsy and psychosis. Antibodies against synaptic autoantigens (such as the N-methyl-d-aspartate receptor or the voltage-gated potassium channel complex) have been reported in approximately 10% of cases of sporadic epilepsy. These same autoantibodies are known to cause encephalopathy syndromes which feature psychiatric symptoms, usually psychosis, as a prominent part of the phenotype in addition to neurological features such as seizures, movement disorders, and autonomic dysfunction. Based on this it has been hypothesized that PIP may be an autoimmune phenomenon mediated by autoantibodies against synaptic antigens. Long or repeated seizures may cause short-lived blood-brain barrier dysfunction during which the brain becomes exposed to pathogenic autoantibodies. In essence, it has been proposed that PIP is a time-limited, seizure-dependent, autoantibody-mediated encephalopathy syndrome. [27]
There is lack of consensus about treatment of PIP. Abnormalities in the ictal phase are treated in the same way as nonpsychiatric epileptic events. Improving seizure control may treat postictal events. It is pertinent to note here that few antiepileptic drugs, such as phenytoin, carbamazepine, ethosuximide, vigabatrin, zonisamide, levetiracetam and topiramate, have been reported to show adverse psychotropic effects. [28],[29],[30],[31] If these observations are confirmed then these antiepileptics must be replaced on the occurrence of psychosis.
Some experts believe that PIP remits spontaneously even without treatment but the use of effective antipsychotics may shorten the duration. [22] In the present study also 35.7% patients recovered with antiepileptic drugs and benzodiazepines only. For psychosis of longer duration or showing schizophreniform features antipsychotic drugs should be instituted. Medications that lower seizure threshold should be avoided. Reports suggest that the antipsychotics chlorpromazine and clozapine and the anti-depressants maprotiline and clomipramine are associated with increased risk and should be avoided. On the other hand fluphenazine, haloperidol, pimozide, perfenazine, trifluoperazine, risperidone, phenelzine, tranylcypromine, fluoxetine, paroxetine, sertraline, venlafaxine and trazodone, are associated with low seizure risk and should be preferred in treatment of PIP. [31],[32],[33]
Around 10% of patients with PIP may became chronically psychotic and there are documented cases of patients who had multiple episodes of PIP before developing interictal psychosis. Based on this it has been suggested that increased awareness and prompt treatment of PIP may inhibit or prevent development of some instances of interictal psychosis. [34] In the present study also two (7.14%) patients developed a chronic psychosis. This finding indicates that the psychiatrist in addition to the neurophysician should follow-up patients with PIP so that patients receive appropriate treatment thereby improving the long term prognosis and quality of life of these patients.
References | |  |
1. | Blumer D, Montouris G, Davies K. The interictal dysphoric disorder: Recognition, pathogenesis, and treatment of the major psychiatric disorder of epilepsy. Epilepsy Behav 2004;5:826-40. |
2. | Gaitatzis A, Carroll K, Majeed A, W Sander J. The epidemiology of the comorbidity of epilepsy in the general population. Epilepsia 2004;45:1613-22. |
3. | Jackson MJ, Turkington D. Depression and anxiety in epilepsy. J Neurol Neurosurg Psychiatry 2005;76:i45-7. |
4. | Cyriac N, Sureshkumar PN, Kunhikoyamu AM, Girija AS. Social factors and psychopathology in epilepsy. Neurol India 2002;50:153-7.  [ PUBMED] |
5. | Toone BK. The psychoses of Epilepsy. J Neurol Neurosurg Psychiatry 2000;69:1-4. |
6. | Logsdail SJ, Toone BK. Post-ictal psychoses: A clinical and phenomenological description. Br J Psychiatry 1988;152:246-52. |
7. | Shome S, Bhatia MS, Jagawat T, Shome S, Jagawat T. Epilepsy: Pattern and psychiatric comorbidity. Ann Natl Acad Med Sci (India) 1996;32:49-58. |
8. | Roy AK, Rajesh SV, Iby N, Jose JM, Sarma GR. A study of epilepsy-related psychosis. Neurol India 2003;51:359-60.  [ PUBMED] |
9. | Clancy MJ, Clarke MC, Connor DJ, Cannon M, Cotter DR. The prevalence of psychosis in epilepsy; a systematic review and meta-analysis. BMC Psychiatry 2014;14:75. Available form: http://www.biomedcentral.com/1471-244X/14/75 [Last accessed on 2015 Apr 22]. |
10. | Proposal for revised classification of epilepsies and epileptic syndromes. Commission of Classification and Terminology of the International League Against Epilepsy. Epilepsia 1989;30:389-99. |
11. | Kanner AM, Soto A, Gross-Kanner H. Prevalence and clinical characteristics of postictal psychiatric symptoms in partial epilepsy. Neurology 2004;62:708-13. |
12. | Umbricht D, Degreef G, Barr WB, Lieberman JA, Pollack S, Schaul N. Postictal and chronic psychosis in patients with temporal lobe epilepsy. Am J Psychiatry 1995;152:224-31. |
13. | Torta R, Keller R. Behavioral, psychotic, and anxiety disorders in epilepsy: Etiology, clinical features, and therapeutic implications. Epilepsia 1999;40:S2-20. |
14. | Szabo CA, Lancman M, Stagno S. Postictal psychosis: A review. Neuropsychiatry Neuropsychol. Behav Neurol 1996;9:258-64. |
15. | Liu HC, Chen CH, Yeh IJ, Sung SM. Characteristics of postictal psychosis in a psychiatric center. Psychiatry Clin Neurosci 2001;55:635-9. |
16. | Kanner AM, Stagno S, Kotagal P, Morris HH. Postictal psychiatric events during prolonged video-electroencephalographic monitoring studies. Arch Neurol 1996;53:258-63. |
17. | So NK, Savard G, Andermann F, Oliver A, Quesney LF. Acute postictal psychosis: A stereo EEG study. Epilepsia 1990;31:188-93. |
18. | Savard G, Andermann F, Oliver A, Remillard GM. Postictal psychosis after partial complex seizure: A multiple case study. Epilepsia 1991;32:225-31. |
19. | Mendez MF, Grau R. The postictal psychosis in epilepsy: Investigation in two patients. Int J Psychiatry Med 1991;21:85-92. |
20. | Lancman ME, Craven WJ, Asconape JJ, Penry JK. Clinical management of recurrent postictal psychosis. J Epilepsy 1994;7:47-51. |
21. | Kanemoto K, Tadokoro Y, Oshima T. Psychotic illness in patients with epilepsy. Ther Adv Neurol Disord 2012;5:321-34. |
22. | Rayport M, Ferguson SM. Psychosis of epilepsy. In: Ettiger AB, Anner AM, editors. Psychiatric issues in Epilepsy. 1 st ed., Philadelphia: Lippincott, William and Wilkins; 2001. p. 73-94. |
23. | Perez MM, Trimble MR. Epileptic psychosis--diagnostic comparison with process schizophrenia. Br J Psychiatry 1980;137:245-9. |
24. | Tebartz Van Elst L, Baeumer D, Lemieux L, Woermann FG, Koepp M, Krishnamoorthy S, et al. Amygdala pathology in psychoses of epilepsy: A magnetic resonance imaging study in patients with temporal lobe epilepsy. Brain 2002;125:140-9. |
25. | Ring HA, Trimble MR, Costa DC, Moriarty J, Verhoeff NP, Ell PJ. Striatal dopamine receptor binding in epileptic psychosis. Biol Psychiatry 1994;35:375-80. |
26. | Sachdev PS. Alternating and postictal psychosis: Review of a unifying hypothesis. Schizophr Bull 2007;33:1029-37. |
27. | Pollak TA, Nicholson TR, Mellers JD, Vincent A, David AS. Epilepsy-related psychosis: A role for autoimmunity? Epilepsy Behav 2014;36:33-8. |
28. | Weber P, Dill P, Datta AN. Vigabatrin-induced forced normalization and psychosis--prolongated termination of behavioral symptoms but persistent antiepileptic effect after withdrawal. Epilepsy Behav 2012;24:138-40. |
29. | Noguchi T, Fukatsu N, Kato H, Oshima T, Kanemoto K. Impact of antiepileptic drugs on genesis of psychosis. Epilepsy Behav 2012;23:462-5. |
30. | Khan A, Faught E, Gilliam F, Kuzniecky R. Acute psychotic symptoms induced by topiramate. Seizure 1999;8:235-7. |
31. | Krauss G, Theodore WH. Treatment strategies in the postictal state. Epilepsy Behav 2010;19:188-90. |
32. | Pisani F, Oteri G, Costa C, Di Raimondo G, Di Perri R. Effects of psychotropic drugs on seizure threshold. Drug Saf 2002;25:91-110. |
33. | Kanner AM, Gidal BE. Pharmacodynamic and pharmacokinetic interactions of psychotropic drugs with antiepileptic drugs. Int Rev Neurobiol 2008;83:397-416. |
34. | Tarulli A, Devinsky O, Alper K. Progression of postictal to interictal psychosis. Epilepsia 2001;42:1468-71. |
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