Curr Psychiatry Rep (2014) 16:509
DOI 10.1007/s11920-014-0509-1
COMPLEX MEDICAL-PSYCHIATRIC ISSUES (MB RIBA, SECTION EDITOR)
Psychosis and Seizure Disorder: Challenges
in Diagnosis and Treatment
Kamalika Roy & Richard Balon & Varma Penumetcha &
B. Harrison Levine
Published online: 20 September 2014
# Springer Science+Business Media New York 2014
Abstract Psychosis temporally related to seizure episodes
has been a recognized entity with much clinical attention,
yet there are less clear guidelines for treatment. Presence of
perceptual disturbances and cognitive impairment symptoms
make the differentiation between primary psychoses and
seizure- related psychoses blurred. Moreover, there are only
a few reported cases describing clinical presentation, diagnos-
tic dilemma and treatment challenges when these two entities
are present at the same time, with overlapping symptomatol-
ogy. We describe such a case where the presence of these two
problems complicated the diagnoses and the patients subse-
quent management required a very intricate collaboration
between psychiatry and neurology. In addition, we review
available published articles including case reports, studies,
This article is part of the Topical Collection on Complex Medical-
Psychiatric Issues
K. Roy (*)
Department of Psychiatry and Behavioral Neurosciences,
Wayne State University,
WSU Tolan Park Medical Building, 3901 Chrysler Service Drive,
Suite 5A, Detroit, MI 48201, USA
e-mail: kroy@med.wayne.edu
R. Balon
Departments of Psychiatry and Behavioral Neurosciences and
Anesthesiology, Wayne State University,
WSU Tolan Park Medical Building, 3901 Chrysler Service Drive,
Suite 3A, Detroit, MI 48201, USA
e-mail: rbalon@wayne.edu
V. Penumetcha
Department of Psychiatry, St. Mary Mercy Hospital,
36475 Five Mile Road, Livonia, MI 48154, USA
e-mail: penumetv@trinity-health.org
B. H. Levine
3570 E. 12th Ave, Denver, CO 80206, USA
e-mail: harrison@hlevinemd.com
and review articles regarding the diagnosis and treatment of
this complicated clinical presentation. Some of the analyses
were reviewed in detail and resulting outcomes are discussed.
Finally, we review the diagnostic and treatment guidelines in
the context of the presenting case.
Keywords Complex partial seizures . Epilepsy . Psychosis .
Schizophrenia . Ictal . Post ictal . Inter-ictal . Antipsychotics .
Atypical . Anticonvulsants . EEG . MRI . Neurotransmitter .
Seizure threshold
Introduction
Within the scope of the current clinical practice of psychiatry,
we often come across cases presenting with complex behav-
ioral and mood symptoms, which cannot be attributed to a
single diagnostic category. Seizure disorders frequently pres-
ent with subtle psychiatric symptoms. It has been reported that
psychoses resembling a primary psychotic disorder such as
schizophrenia occurs 6-12 times more likely in patients with
epilepsy than in the general population [1]. Seizure-related
psychotic symptoms occur typically during the ictal and
interictal time period. The lucid period between seizure activ-
ity and the onset of psychotic symptoms can present indis-
tinctly by altered consciousness and dysregulated behavioral
symptoms. Moreover pre-existing psychiatric diseases can be
co-morbid with seizure disorders. Thus, even for highly ex-
perienced psychiatrists and neurologists, distinguishing be-
tween these two multifactorial diseases with varied clinical
presentations is inherently distorted, especially when consid-
ering the less distinctive clinical diagnostic criteria and vague
temporal association between seizure episodes and psychosis
episodes. To add to the challenge, most of the commonly used
antipsychotics have been demonstrated to lower seizure
threshold. Some of the anticonvulsants also have been shown
509, Page 2 of 7
to worsen psychosis. This chapter presents a discussion of a
complex case and a review of available literature to illustrate
the need for maximizing the integration between psychiatry
and neurology to improve quality of clinical practice.
Case Report
A 56 year old male with a diagnosis of schizophrenia, stable
on a daily dose of 2 mg risperidone for the past 15 years
presented with symptoms of being in a daze". He was found
by family members in a confused state characterized by se-
lective mutism, withdrawn, isolated attitude, and staring va-
cantly with episodic lip smacking. During those episodes he
would not eat or take his medications and would walk around
or sit alone. He visited religious places and spent many hours
alone before someone would walk him home. These episodes
lasted from a few hours to a few days. There was no history of
bowel or bladder incontinence, jerky limb or trunk movement,
tongue biting, or unconsciousness. The patient was admitted
to an inpatient psychiatry unit with a similar clinical presen-
tation four times within a period of six months. During the
previous hospitalizations, his risperidone dose was increased
from 2 mg daily to 2 mg two times a day and the above-
mentioned symptoms were attributed to the worsening of
negative symptoms of schizophrenia. While in the hospital,
he was seen to be staring vacantly, responding minimally only
after repeated verbal commands, with some lip smacking
movements. On a few occasions he complained of a churning
feeling in his upper abdomen. He also reported having feel-
ings of not knowing where he was. He frequently declared
aloud his religious belief without any context and mentioned
the worship place to be his home as it was more familiar to
him than his home. His family members who reported that the
patient often complained of unfamiliarity in his own house
and walked away from home and wandered around verified
this information. He was not seen to be responding to internal
stimuli. Routine labs and EKG were within normal limits.
Risperidone was resumed and the dose was increased to
3 mg twice daily without any change in symptoms. Proton
pump inhibitor (omeprazole) was added for probable gastro-
esophageal reflux disease (GERD). Because of his inexplica-
ble sudden changes in emotions and behavior neurology was
consulted to evaluate for possible organic causes of his symp-
toms. According to the neurology consultation, no evident
symptoms of generalized seizure were clinically established.
Due to repeated episodic behavioral changes without any
observed psychotic symptoms an EEG was recommended that
revealed sharp wave activity over the left temporo-parietal
region at P3-01 electrodes with phase reversal at F7-T3 with
intermittent diffuse slow wave activity throughout the record-
ing. Subsequently, the patient was treated with a combination
of topiramate 100 mg BID and the episodes of being "in daze"
Curr Psychiatry Rep (2014) 16:509
gradually subsided. The dose of risperidone was slowly ta-
pered down to 2 mg daily over two weeks. Patient remained
free of symptoms during outpatient follow up.
The Authors Observation
& In the above case, mood, behavioral and de-realization
symptoms were assumed to be a part of the primary
psychiatric diagnosis of schizophrenia.
& Imprecision of diagnostic criteria for epilepsy related psy-
chosis made it difficult for clinicians to understand the
differentiation and interplay of the two disorders with
clinical presentations overlap.
& Temporal relationship of the onset of mood and behavioral
symptom with seizure episode was ill defined, further
blurring the differentiation between primary psychosis
and psychosis secondary to epilepsy.
Psychosis of Epilepsy
It has been recognized that there is an increased risk of
schizophrenia-like psychosis in epilepsy patients [2]. The
correlation between these two entities has been discussed for
many decades. Some studies [3] reported that prevalence of
schizophrenia in epilepsy patients ranged from 3 to 7 %. In
comparison, prevalence of schizophrenia in the general pop-
ulation is 1 %. However, the lack of well-defined criteria and
the lack of clearly recognized temporal association of psycho-
sis to seizures make it difficult to make a clear distinction
between the two diseases and to determine the exact preva-
lence psychosis of epilepsy.
There are three types of psychosis related to epilepsy: ictal,
post-ictal, and inter-ictal (chronic episodic). The most com-
mon type is the post-ictal one, with a prevalence of 25 to 30 %
of all psychoses in epilepsy [2]. The differences in presenta-
tion are described in Table 1.
Diagnostic Measures
EEG
Epileptogenic activities on scalp EEGs have often been dem-
onstrated in patients with psychoses of epilepsy. Sharp waves,
spikes, and diffuse non-specific slowing have been reported to
be associated with temporal lobe epilepsy (TLE) with psycho-
ses. However appropriate longitudinal and controlled studies
are necessary to establish their significance.
In the mid nineteenth century, Landolt demonstrated an
interesting observation that the EEGs of patients became
more normal when the mood and psychotic symptoms
Curr Psychiatry Rep (2014) 16:509 Page 3 of 7, 509

Table 1 Different types of epilepsy associated psychoses

ICTAL PSYCHOSIS INTER-ICTAL PSYCHOSIS POST-ICTAL PSYCHOSIS

Temporal Occurs during the Psychosis symptoms chronically linger There is variable lucid interval between the last
association seizures episodes between episodes of seizures seizure episode and onset of mental state changes.
with seizures or cluster of seizures This period varies widely (2.5-48 hours, 12-72 hours)
as described by different authors [3, 4]
Duration Transient Chronic schizophrenia like course, There is a period of post- ictal confusion and lethargy for
described in studies [5, 6] hours to days. Subsequently the psychosis symptoms
develop and last for days to weeks or even longer
[711]
Sympto-matology Agitation, Insidious onset of paranoia and perceptual Depressed affect, mania (grandiose delusions, hyper-
hallucinations, disturbances. Higher incidence of religiosity), aggressiveness, irritability. Perceptive
short lasting negative symptoms like isolation, disturbances and other first rank symptoms like
affective blunting, and cognitive thought insertion or command hallucinations are
impairment have been found in temporal rare [4]
lobe epilepsy (31 %) when compared to
normal controls (8 %) [12]. Concrete
thinking, loosening of association,
incoherence and speech abnormalities
like derailment, neologism, poverty
of speech.
Risk factors Generalized tonic No specific type Age over 30 years [4], Localization related epilepsy, for
to look for clonic seizures example, temporal lope epilepsy [3], with secondary
generalization [3], Family history of mood disorder
[8] and psychosis [13], Evident bilateral or
widespread CNS injury, including encephalitis, head
injury [13]. Bilateral EEG change with slowing [8],
borderline intellectual functioning [13]

develop. He coined it as forced normalization or an inverse
relation between appearance of psychotic symptoms and EEG
abnormality. This could be particularly relevant in-patient
with pre-existing psychotic disorder who develops psychosis
of epilepsy, as in the above-discussed case.
Imaging Studies
There have been many non- specific CT and MRI findings in
patients with epilepsy who presented with psychoses.
Logsdail and Toone [7] showed grey matter abnormality on
CT scan in patients with epilepsy related psychoses. In another
study [14], association has been demonstrated between left
sided mesial temporal sclerosis and resistant temporal lobe
epilepsy and post-ictal psychosis. In a retrospective MRI
study [15] total brain volume was significantly less in the
TLE with psychosis group compared to the TLE group and
control group. There was also a significant enlargement of
amygdala on both sides in the TLE with psychosis groups,
when compared to the TLE alone group and healthy controls.
Proposed Mechanism and Underlying Pathology
& The concept of kindling mechanism has been studied in
some animal models [16], where repetitive electrical
discharges have been shown to propagate in specific path-
ways facilitating inter-ictal psychosis.
& Changes in neurotransmitters have been proposed to be a
possible mechanism of action. Especially changes in sen-
sitivity of post-synaptic dopamine receptors (supported by
a SPECT study using [123] iodobenzamide [17]), increase
in turnover of GABA, reduction in aspartate and gluta-
mate [18] have been proposed in the pathogenesis of
psychosis related to seizures.
& Anomaly in axonal sprouting from the dentate granular
cells has been proposed to be responsible for development
of seizures [19]. Increased expression of mRNA for c-fos
and nerve growth factor (NGF) by recurrent seizures has
been shown to be responsible for aberrant regeneration
and mis-wiring of glutaminergic presynaptic mossy fiber,
resulting in psychosis [20].
& Cortical dysgenesis in different forms has been reported to
be present in both the disease entities. Heterotropia of grey
matter and hippocampal neuronal loss and sclerosis in
CA1 area have been shown in 20-50 % patients with
temporal lobe epilepsy [20]. Similarly problems in migra-
tion of primitive neurons in the hippocampus, resulting in
disorganized pyramidal cell layer have been demonstrated
in schizophrenia patients [21].
& Acquired insults through birth trauma, minor anoxia, viral
and other brain infections, and head injury can cause
509, Page 4 of 7
synaptic reorganization in susceptible brain areas, espe-
cially limbic cortex. This, in turn, changes the plasticity of
neurons and causes neurochemical changes in catechol-
amines and glutamate and GABA receptor sensitivity
resulting in seizures. Environmental threats like lack of
sleep, food and stress have been mentioned to be the
precipitating factors for schizophrenia-like-psychosis in
patients with a latent seizure disorder [22]. An attempt to
integrate all these hypotheses is shown in Fig. 1.
Management of Complex Presentation where both Psychosis
and Seizures are Present
Concerns about Antipsychotic Use
Most of the first generation and many of the second-
generation antipsychotics lower the seizure threshold. Cloza-
pine has been shown to be the most likely agent associated
with increased seizure activity. A study using case/non-case
method tried to find out the association between seizures and
antipsychotic drug exposure [23]. It was shown that the
second generation antipsychotic (SGA) group might have a
higher risk of seizure than the first generation antipsychotic
(FGA) group, mostly but not exclusively due to clozapine.
Previous studies have demonstrated a clear dose dependent
relation between clozapine and risk of seizures [24, 25]. Many
of them suggested a clear evidence of dose-related effect on
Fig. 1 Composite model for
pathophysiology of seizure with
psychosis
Curr Psychiatry Rep (2014) 16:509
seizure threshold above a dose range of 500-600 mg daily.
Among other second-generation antipsychotics, risperidone
and quetiapine are shown to have the lowest risk of lowering
the seizure threshold. Among first generation antipsychotics,
chlorpromazine is reported to be most strongly associated with
seizure risk. There has been at least one of chlorpromazine
associated myoclonic status epilepticus at a daily dose of
37.5 mg [26]. At least two cases were reported showing an
association between aripiprazole and seizure induction [27].
A cohort study of 323 hospitalized psychiatric patients
(293 received antipsychotics and 30 did not receive any anti-
psychotics) was performed in McLean Hospital to show ef-
fects of different commonly used antipsychotics on the EEG
[28]. The study found the highest risk of EEG abnormality
with clozapine and olanzapine, moderate risk with risperi-
done, and lowest risk with quetiapine and loxapine (Table 2).
Clinical factors like hypertension and increased age were
significantly associated with EEG abnormalities.
Interestingly, another study of 70 patients with epilepsy and
psychiatric symptoms showed no definite association between
seizure frequency and use of antipsychotic drugs within clin-
ical dose range [29]. Also there has been little evidence on
how the seizure threshold lowering effect correlates with
actual seizure episodes clinically.
So there is a need for a large randomized control study of
different antipsychotic medications, especially atypicals with
a comparison with healthy controls to validate the seizure-
lowering threshold of the commonly used antipsychotics.
Curr Psychiatry Rep (2014) 16:509 Page 5 of 7, 509

Table 2 Cohort study [28] dose and risk of EEG abnormality associated with commonly used antipsychotics. Adapted with permission from Centorrino
F, Price BH et al., EEG Abnormalities during treatment with typical and atypical antipsychotics, Am J Psych, 2002; 159(1):109-115

Antipsychotic Regimen N Dose (mg/kg/day)a EEG Score Risk of EEG Abnormality Risk of Severe EEG
(0=no abnormality, 3=severe abnormality)b (score>0)c Abnormalityd (%)

Mean SD Mean SD % 95 % Cl

Agents (in order of decreasing risk)

Clozapine 17 3.7 2.5 0.94 1.09 47.1 20.6-73.5 5.9
Olanzapine 13 2.8 1.2 0.77 1.09 38.5 7.9-69.1 7.7
Trifluoperazine 11 3.4 1.6 0.64 1.03 36.4 2.5-70.3 9.1
Mesoridazine 3 1.4 0.6 0.33 0.58 33.3 0.0-100.0 0.0
Risperidone 25 4.0 2.0 0.56 0.96 28.0 9.1-46.9 4.0
Fluphenazine 18 8.0 5.2 0.33 0.69 22.2 0.8-43.5 0.0
Thiothixene 9 3.3 1.5 0.56 1.13 22.2 0.0-56.1 11.1
Combination 24 5.9 2.6 0.42 0.88 20.8 3.3-38.4 4.2
Perphenazine 70 3.1 1.7 0.30 0.70 14.3 5.9-22.7 1.4
Chlorpromazine 14 3.0 2.1 0.21 0.58 14.3 0.0-35.3 7.1
Thioridazine 23 2.0 1.3 0.22 0.60 13.0 0.0-27.9 0.0
Haloperidol 55 3.8 3.0 0.13 0.47 7.3 0.2-14.4 0.0
Loxapine 4 3.7 3.4 0.00 0.00 0.0 0.0 0.0
Quetiapine 5 2.4 2.0 0.00 0.00 0.0 0.0 0.0
Pimozide 1 7.5 2.00
Molindone 1 0.8 0.00
Type
Typical 214 3.6 2.9 0.27 0.69 14.5 9.7-19.2 1.9
Atypical 79 4.1 2.3 0.63e 0.99 31.6 f
4.2-42.1 5.1
Potency
High 220 4.0 2.9 0.34 0.79 17.7 12.6-22.7 2.7
Low 73 3.0 2.3 0.42 0.83 23.3 13.4-33.2 2.7
All antipsychotics 293 3.8 2.8 0.36 0.80 19.1 14.6-23.6 2.7
No antipsychotic 30 0.27 0.69 13.3 0.4-26.2 0.0
a
Value in chlorpromazine equivalents; for specific agents, dose data are for subjects given only the indicated antipsychotic
b
For specific drugs given to at least five patients, there was a nonsignificant difference in scores (F=2.19, df=11, 272, p=0.15)
c
Significant difference in risk among specific drugs (2 =34.7, ddf=12, p=0.004)
d
Spike discharges or spike-and-wave activity (score=3)
e
Significantly higher score than that of subjects given typical antipsychotics (2 =10.9, df=1, p<0.001)
f
Significantly higher abnormality risk than that of subjects given typical antipsychotics (2 =11.9, df=1, p<0.001)

Concern about Alternative Psychosis
Following Landolts description of forced normalization in
partial seizures in the mid nineteenth century (see above),
many authors have described less abnormal EEGs obtained
with the emergence of anxiety symptoms and dissociative
states. Almost all anticonvulsants, including valproate have
been anecdotally linked with induced affective and behavioral
changes and relative normalization of EEG when used for
treating seizure disorder. This phenomenon is called alterna-
tive psychosis, a term coined by Tellenbach. Vigabantrin
[30], an irreversible GABA inhibitor and zonisamide [31],
phenytoin and primidone [32], valproate and carbamazepine
[30] have also been shown to carry an increased risk of
psychosis. There is no consensus on treating anticonvulsant
induced psychosis with antipsychotics. A few cases have been
reported where anticonvulsant related psychosis was success-
fully treated with a low dose of risperidone [33].
Treatment Recommendations
Seizure related psychosis in absence of comorbid primary
psychiatric disorder:
& Fifteen percent of patients with chronic inter-ictal psycho-
sis improve without any antipsychotic medication [34].
509, Page 6 of 7
However some studies showed [35] that early intervention
with antipsychotic medications reduced the duration of
inter-ictal psychosis.
& Consent for antipsychotic medication has to be obtained
and its discussion should focus on balancing risks versus
benefits.
& Psychosocial interventions and psycho-education (e.g.,
discussing the association of seizure disorder and psycho-
sis, side effect of medications such as antipsychotics) are
important. Family members should be involved in
psycho-education sessions and invited to ask questions.
& Drug interaction between psychotropic medications and
anticonvulsant agent should be considered, e.g.: carba-
mazepine is known to be an enzyme inducer and can
lower the level of some antipsychotics. When valproate
is used for mood stabilization in a patient who is on
lamotrigine to treat a seizure disorder, the lamotrigine dose
should be reduced by 50 % as valproate induces the UDP
glucuronyl transferase enzyme, which metabolizes
lamotrigine.
& Some authors suggested that risperidone has minimal sei-
zure threshold lowering effect and should be safe to use [36].
& A case of psychotic symptoms associated with the com-
bination of valproate and lamotrigine in a patient with
epilepsy has been reported [37]. This can be attributed to
the synergistic effect of these two medications. So it may
be prudent to avoid using this combination for treatment
of seizures in a patient with comorbid schizophrenia.
& There is minimal data available regarding duration of treat-
ment with antipsychotics. However it is often seen that
chronic inter-ictal psychosis has a prolonged course and thus
continued if not lifelong treatment may be necessary [34].
& Anticonvulsant and antipsychotic regime should be sim-
plified with slow dose titration, close monitoring for any
potential drug interactions and side effects.
Conclusion
Understanding of Current Knowledge in the Perspective
of the Reported case
& In the reported case, diagnostic challenges were barriers to
adequate treatment and symptom management. Co-
existence of two equally heterogeneous and multifactorial
disorders made it an enigma at least initially, resulting in
multiple inpatient psychiatric hospitalizations.
& Lack of clear guidelines about temporal relationship of the
seizure and psychotic symptoms and lack of definitive
diagnostic tools made the diagnoses and treatment more
challenging. The sharp spikes and diffuse slowing on the
Curr Psychiatry Rep (2014) 16:509
EEG could also be attributed to the use of antipsychotics
on which patient was for many years preceding the com-
mencement of his new symptoms.
& A very intricate balance had to be maintained to consider
the seizure lowering effects and psychosis inducing effects
of both the classes of drugs.
& Close collaboration between neurology and psychiatry
with day-to-day symptom monitoring and an integrative
multidisciplinary team approach were proven to be helpful
for optimum patient care.
Future Directions
More evidence-based guidelines for diagnosis of epilepsy
related psychosis should be clearly formulated. Further re-
search is needed to develop diagnostic and predictive tools
for psychosis of epilepsy such as long term EEGs, imaging
methods to study the neural correlates. More sensitive and
specific diagnostic tools need to be explored, as most of the
current tools do not have a great specificity. Similarly, for
treatment, larger randomized controlled and blinded studies
are needed to clearly demonstrate comparative effects of dif-
ferent antipsychotics on seizure threshold and possible occur-
rence of actual seizure episode.
Compliance with Ethics Guidelines
Conflict of Interest Kamalika Roy, Richard Balon, Varma
Penumetcha, and B. Harrison Levine declare that they have no conflict
of interest.
Human and Animal Rights and Informed Consent This article does
not contain any studies with human or animal subjects performed by any
of the authors.
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