The Psychoses of Epilepsy a Neurological Disease

Super Memory Formula

Natural Dementia Treatment Ebook

Get Instant Access

E. S. Krishnamoorthy and R. Seethalakshmi

INTRODUCTION

A close association between psychoses and epilepsy has been known since 1854 confirmed by the fact that the early mental hospitals in Europe had special wards dedicated to epilepsy. The early proponents of psychosis of epilepsy (POE) included Kraepelin (1918) who believed that the "dementia" resulting from epilepsy was different from "dementia praecox" or schizophrenia. This was further affirmed by Vorkastner (1918) and Krapf (1928) who clarified that schizophrenialike symptoms might follow epilepsy and that these need to be differentiated from true schizophrenia. Contrary to this, Glaus (1931) and Gruhle (1963) opined that the schizophrenic symptoms of epilepsy could be true independent schizophrenia. In 1860, with the description of alternating psychosis, this relationship underwent some radical thinking, and sadly petered out until the 1950s when the term schizophrenia-like psychosis of epilepsy (SLPE) was coined by Slater et al. (1963).

Throughout its history, however, POE has been largely considered an epileptic equivalent; both Falret (1854) and Morel (1873) employed terms such as "larval epilepsy", "epileptic mania", and "grands maux intellectuals". This chapter will attempt to justify a neurological diagnosis of the psychoses of epilepsy. This will be argued in two parts — in the first, we will endeavor to establish POE as a distinctive entity different from functional psychoses with schizophrenia as the gold standard. The second part of the discussion will entail neurological explanations of POE.

THE PSYCHOSES OF EPILEPSY

Among the most systematic descriptions of POE is the categorization based on the temporal relationship of the psychosis to the ictus.

Psychiatric Controversies in Epilepsy

Copyright © 2008 by Elsevier Inc. All rights of reproduction in any form reserved.

1. Ictal psychosis: This can be defined as a nonconvulsive status epilepticus with symptoms resembling psychosis; ictal psychosis is associated with concurrent electrographic ictal patterns. The psychosis is usually brief, lasting from hours to days. The manifestation may not always be truly psychotic — consciousness is altered during the episode, insight is usually maintained and delusions and hallucinations are often absent during lucid periods, although there have been several reports of hallucinations (visual and auditory, and somesthetic), paranoia and bizarre psychotic-like catatonic behavior (Kaplan, 2002) during active episodes of ictus.

2. Postictal psychosis (PIP): Postictal psychotic episodes are brief psychotic episodes that occur in close proximity to seizure clusters. PIP can also be associated with a recent exacerbation in seizure frequency that may be related to withdrawal of anticonvulsants. Between the last seizure and the psychosis there is usually a nonpsychotic lucid period, which can range from 12 to 72 h to a week. Similar to ictal psychoses, consciousness may be clouded. Unlike ictal psychosis, however, in PIP true psychotic symptoms are dominant throughout the episode. These are pleomorphic in nature and include persecutory, grandiose, referential, somatic, and religious delusions, catatonic features, and hallucinations. The presentation may additionally be colored with affective symptoms including both manic and depressive symptoms. Schneiderian first rank symptoms that are considered pathognomonic of schizophrenia have also been described rarely. These symptoms usually resolve within a few days.

3. Interictal psychosis.

Chronic (also called SLPE): The principle characteristics of the "schizophrenialike psychoses of epilepsy' were first described as follows (Toone, 1991):

1. Among patients with epilepsy, a schizophrenia-like syndrome occurs more commonly than chance would predict.

2. While the condition shares many of the characteristics of schizophrenia, many experts feel that it is distinguishable from that condition based on certain clinical features: the relative preservation of affect, the relative absence of negative symptoms and cognitive deterioration; the preservation of the personality in between episodes and the near total absence of hebephrenic features.

3. Temporal lobe epilepsy (TLE) is overrepresented.

4. A family history of schizophrenia occurs with no greater frequency than in the general population.

5. The onset of seizures almost invariably precedes the development of psychotic symptoms, usually by an interval of several years.

6. Within the various combinations of epilepsy subtypes and psychosis subtypes, a schizophrenia-like syndrome is usually associated with a dominant temporal lobe focus.

The phenomenon of forced normalization epitomizes the antagonistic relationship between psychosis and seizures. It can be defined as "the phenomenon characterized by the fact that, with the occurrence of psychotic states, the electroencephalogram (EEG) becomes more normal or entirely normal, as compared with previous and subsequent EEG findings." A recent diagnostic guideline suggests behavioral change including psychosis accompanied by over 50% reduction of EEG ictal activity or caregiver report of complete cessation of seizure activity (Krishnamoorthy and Trimble, 1999 ; Krishnamoorthy et al., 2002).

Relationship between schizophrenia (psychosis) and POE

Schizophrenia is considered the archetypal psychotic illness. The other primary psychotic illnesses include brief psychotic disorder, and schizophreniform disorder and schizoaffective disorder which differs from schizophrenia in being predominantly disorders of mood. The question "does POE warrant the distinction of being a separate psychotic entity?" begs answering, given that schizophrenia despite being a discrete nosological entity in psychiatry is acknowledged as having a number of subtypes with widespread phenomenological correlates. To that end, we will examine the epidemiological evidence for an association between epilepsy and psychosis and phenomenological evidence for distinctions between POE and schizophrenia.

Epidemiological issues

Schizophrenia is estimated to have a prevalence of 0.5—1% in the general population; the prevalence of psychotic disorders is likely to be much higher. Epilepsy has a point prevalence of 0.4—1% in the general population, and the lifetime risk of having at least one unprovoked seizure is 5—10%. A number of studies have suggested prevalence rates of schizophrenia within an epileptic population varying between 3% and 7% (Toone, 2000). The overall evidence suggests that schizophrenia-like psychosis is 6—12 times more likely to occur in people with epilepsy than in the general population. Further, when compared with other neurological disorders (e.g., migraine), the prevalence of schizophrenia in people with epilepsy has been found to be nine times higher (Mendez et al., 1993) . A standardized incidence ratio of 1.48 for all epilepsy and 2.35 for psychomotor epilepsy argues strongly for epilepsy as a risk factor for schizophrenia, establishing beyond any reasonable doubt that epilepsy is a risk factor for the development of psychosis.

Schizophrenic-like psychosis of epilepsy (SLPE) is a unique disorder and not an artifact of random association. About 12.5—25% of POE is usually PIP (Adachi et al., 2002); 6.4-10% individuals with epilepsy can develop PIP (Sachdev, 1998). Forced normalization or the alternative psychosis of epilepsy is considerably less frequent with only 3 among 697 individuals demonstrating POE in Schmitz's (1998) study.

Phenomenological variations between POE and schizophrenia

SLPE primarily differs from schizophrenia in the severity of symptoms — quantitatively rather than qualitatively (Toone et al., 1982;Tadokoro et al., 2007). Although SLPE and schizophrenia seem alike in their phenomenology, subtle differences have been identified. SLPE is characterized by an increased frequency of perse-cutory and referential delusions while the incidences of catatonia and negative symptoms have been observed to be higher in schizophrenia. The higher preponderance of affective symptoms and the pleomorphic nature of SLPE also make it different from schizophrenia. In PIP, individuals report grandiose and religious delusions; on the other hand perceptual delusions and second-person hallucinations are less common. Additionally, individuals with SLPE do not demonstrate "affective flattening" and asociality that are common features in schizophrenics; establishment of interpersonal rapport and empathy has been found to be easier as compared to schizophrenics, especially in the earlier stages.

The age at onset in schizophrenia is usually 15—25 years; while in SLPE it has been noted that the psychosis emerges approximately 10—14 years after the onset of the seizure disorder. Individuals with schizophrenia often have greater deterioration in premorbid functioning than individuals with SLPE. These individuals have also been noted to have paranoid or schizoid premorbid personalities. On the contrary, individuals with SLPE have personalities characterized by obstinacy, egocentricity, and aggressiveness. An increased family history of schizophrenia as compared to the general population has not been noted in individuals with SLPE, again distinguishing this from schizophrenia.

The course of psychosis in SLPE is often varied with episodes presenting with different symptoms. Additionally, affected patients have a better prognosis as compared to schizophrenics and usually respond to lower doses of antipsychotic medications. Indeed, in both PIP and SLPE, adjustments in the dosage of the anti-epileptic drug (AED) may help in alleviation of symptoms. This is unlike "schizophrenia" where antipsychotics form the first line of management. Besides, SLPE is characterized by a lesser degree of cognitive impairment in terms of memory and executive function as compared to schizophrenia; some impairment is similar.

Neuropathological findings relating to medial temporal defects in SLPE have been contradictory (Sachdev, 1998) . Neuroimaging data on the other hand have suggested some interesting evidence (van Elst et al., 2002. Rusch et al., 2004) . SLPE has been associated with increased cerebral volume loss and amygdala enlargement as compared to matched patients without psychosis and healthy volunteers. In contrast to patients with schizophrenia, hippocampal volumes are preserved in patients with POE. Cerebral volume loss is more pronounced in patients with SLPE compared with patients with PIP. This finding has been corroborated in histopathological studies that have demonstrated lesser loss of CA1 neurons in the hippocampus in individuals with POE. EEG studies have also demonstrated similar spike discharges in medial temporal and frontal structures in both schizophrenia and SLPE. Both SLPE and schizophrenia have been reported to have higher than normal levels of dopa decarboxylase activity, possibly the result of suppressed tonic release of dopamine in striatum because of low corticostriatal glutamatergic input (Reith et al., 1994) . A recent magnetization transfer study (Flügel et al., 2006) suggested that SLPE is associated with cortical magnetization transfer ratio (MTR) reductions in the left middle and superior temporal gyri. While superior temporal reductions have been reported in schizophrenia, this entity has more widespread abnormalities including involvement of the frontotemporal regions and medial temporal regions (Foong et al., 2001) . These cortical reductions on MTR are indicative of focal disruption of cortical neurons or dendrites suggesting neurodevelopmental defects. It has been suggested that the functional rather than structural abnormality in SLPE may be left-sided temporal.

TABLE 9.1 Schizophrenia and POE: A comparative analysis

Schizophrenia

SLPE

PIP

Etiology

Biological and psychological factors

The epileptic process?

The epileptic process?

Family history of schizophrenia

Present

Absent

Absent

Phenomenology

Age at onset

15—25 years

Related to age at onset of seizure disorder

Related to the age of onset of seizure disorder?

Premorbid/risk factors

Obstetric complications

Left-sided focus, temporal lobe epilepsy, left-handedness, female sex, presence of a gangliogliomas and focal lesions

Similar to SLPE; the predilection for clustering of seizures is a unique risk factor for POE

Premorbid personality

Paranoid or schizoid traits

Obstinacy, aggressive tendencies, egocentricty, religiosity, affective changes, features of the Geschwind syndrome

Pleomorphic paranoid-affective features, explosive behavior (DSH/self mutilation, etc.); bewilderment

Symptoms

Catatonia and negative symptoms including asociality

Persecutory and grandiose delusions

Grandiose and religious delusions

Treatment

Antipsychotic

AED optimization; antipsychotics

Benzodiazepines; AED optimization; short course of antipsychotics if required

Prognosis

Usually chronic deteriorating

Responds well to medication; remains fairly well integrated overall

Usually one-time; may be recurrent in a proportion; well between episodes; occasionally leads to SLPE

IS POE A NEUROLOGICAL DISEASE?

There is clear epidemiological evidence of an increased prevalence of POE in individuals with complex partial seizures (described in the previous section). FlorHenry (1969a, b) suggested a preponderance of schizophrenia-like symptoms in dominant TLE. Epidemiological studies have identified other risk factors including a severe form of epilepsy involving multiple seizure types, a history of status epilepticus, and resistance to drug treatment. POE has also been associated with comparatively more stigmata of neurological damage including "morbid antecedents such as birth trauma and neurological signs" (Flor-Henry, 1969a, b).

Development of POE

It has been postulated that behavioral changes secondary to seizures could be either a positive effect of seizures — the epilepsy activating the areas mediating the development of psychotic symptomatology (e.g. ictal psychosis), or a negative effect — temporary dysfunction leading to inability to perform behaviors or disinhibition of behaviors such as PIP (Sachdev, 1998).

From an etiopathogenic perspective, it has been hypothesized that POE may be the result of:

1. Neurodevelopmental defect leading to cortical dysgenesis that results in both seizures and psychosis. This has been supported by the increased frequency of alien tissue tumors such as gangliogliomas as compared to mesial temporal sclerosis in individuals with POE. Cryptic insults to the vulnerable brain may lead to further synaptic reorganization and possibly psychosis.

2. Diffuse brain damage leading to seizures and psychosis. This theory borrows from neuropathological evidence in schizophrenia suggesting that psychosis is the result of diffuse brain damage rather than a single area.

PIP has been associated with bitemporal foci lending credence to long-term potentiation (LTP) from recurrent limbic kindling leading to the development of secondary epileptogenic foci. Individuals with PIP have also been shown to have an increased incidence of alien tissue such as gangliogliomas; and have been found to lack in Ammon 's Horn sclerosis. As stated above, SLPE has been associated with left-sided temporal deficits by some investigators. These specific regions were first identified by Flor-Henry (1969a, b) and later corroborated by Perez and Trimble (1980); after all, the temporal lobe has far-reaching connecting circuits extending into almost all affected parts of the brain and this could thus explain the presentation of psychosis in individuals with chronic seizure disorder. Yet, the pathogenic role of the left temporal lobe in SLPE is being increasingly questioned by some authors who have suggested involvement of the basal ganglia and periventricular regions moreso than temporal lobe lesions (Sachdev, 1998).

Various mechanisms have been suggested to explain the development of POE at the neurophysiological level.

Limbic kindling

Of the many neurobiological hypotheses that have been put forward in trying to explain the evolution of POE, kindling is perhaps the most controversial, yet fascinating potential explanation (Krishnamoorthy and Trimble, 1999). Kindling is relatively well accepted as an animal model of epilepsy. Kindling is somewhat less well accepted as an animal model of psychoses. The exploration of its relevance to the POE interface is therefore of interest. Kindling defines a mechanism by which repeated (daily) brief, high-frequency trains of electrical pulses to limbic and cortical areas produce a change in response to the stimulus, such that the latter elicits a motor convulsion that outlasts the stimulus train. Thus, when a current of low amplitude but high pulse frequency is applied to the amygdala, a region of great susceptibility, there is a gradual stepwise progression of behavioral and EEG responses that finally culminate in a full motor seizure. Pharmacologic kindling and behavioral sensitization have been used to explain the development of psychosis in animal models (Stevens and Livermore, 1978' Sato et al., 1990). Based on the animal data (extensively reviewed elsewhere), it has been postulated that the end point for pharmacologic kindling may be a particular form of affective expressions or behaviors, unlike electrical kindling that terminates in a motor seizure (Pollock, 1987' Smith and Darlington, 1996).

Role of neurotransmitters

A number of neurotransmitters have been thought to have a role in POE, of which the principal often cited neurotransmitter is dopamine (Trimble, 1991). Dopamine is an inhibitory neurotransmitter that reduces the hyperexcitability associated with seizures and is also psychogenic in nature. Another hypothesis that has gained credence over the years is the Glutamate-GABA hypothesis. When the affective spectrum of psychoses (to which POE have phenomenological affinity) are considered as a whole, GABAergic preponderance (Benes and Berretta, 2001) and glutamatergic deficit (Meldrum, 2000) are hypothesized as being the common denominator. The significance of course is the underlying antagonism between seizures and psychosis that this implies; an epileptogenic state is the classic neurobiological oxymoron - glutamatergic preponderance and GABAergic deficit. Thus, enhanced glutamatergic excitation is a well known epileptogenic mechanism, particularly at the level of the N-methyl-d-aspartate glutamate (NMDA) receptor. In psychoses, on the other hand, an endogenous antagonist at the NMDA receptor, N-acetyl-aspartyl-glutamate, appears to have enhanced activity. This hypothesized dysfunction of glutamatergic transmission also inter-digitates with the traditional dopamine hypothesis of schizophrenia. Presynaptic dopamine receptors on corticostriatal and limbic glutamatergic terminals provide a negative regulation of glutamate release.

Loss of y-aminobutyric acid (GABA) inhibition is another potential epileptogenic factor; AEDs that increase GABA levels are associated with the development of a psychopathologic state in up to 10% of patients including mood changes, agitation, and even psychotic symptoms of a paranoid nature (Trimble, 1998).

Channelopathy

A recent hypothesis (Krishnamoorthy et al.. 2002) that attempts to explain alternative psychosis or forced normalization gains support from evidence of abnormal ion channels in episodic neurological disorders. Ion channels provide the basis for regulation of excitability in the CNS. Mutations in ion channels have been implicated in various epilepsy syndromes including autosomal dominant nocturnal frontal lobe epilepsy (neuronal nicotinic acetylcholine receptor), benign familial neonatal convulsions (potassium channels), generalized epilepsy with febrile seizures plus (sodium channels or the GABA(A) receptor), and episodic ataxia type-1, which is associated with epilepsy in a few patients (another type of potassium channel). There is a viewpoint gaining ground that paroxysmal psychiatric disorders (bipolar disorder for example) are also a product of malfunctioning ion channels (Amann and Grunze, 2005) . Given that ion channels are expressed in the limbic regions of the brain and that AEDs have an influence on both ion channels and behavior, one may speculate on the role that ion channels have in the development of POE, in particular paroxysmal forms such as the forced normalization/alternative psychosis state, where both seizures and psychotic symptoms appear to be affected by common underlying factors. Unfortunately, at this point, these hypotheses remain unproven.

Excitation—inhibition imbalance (Sachdev, 2007)

In a recent paper, Sachdev (2007) puts forward an interesting hypothesis. Epilepsy can be described as a state in which there is an imbalance in neuronal excitation and inhibition. Seizure termination is an active inhibition resulting from fast inhibitory postsynaptic potential (IPSP) through GABAa receptors, a hyperpolar-izing potential through GABAB receptors and after hyperpolarization produced by calcium-activated potassium currents. The hyperpolarizing pumps can produce prolonged inhibition of neuronal activity in an attempt to maintain homeostasis in the brain, leading to the various postictal states. He concludes that both postictal psychosis and alternative psychosis (forced normalization) are states akin to Todd's paresis; states of postictal cortical inactivation with ongoing subcortical or mesial temporal epileptic activity and cortical inhibition referred to as an "inhibitory surround" in response to ongoing seizures.

Other factors that may have a role in the evolution of psychosis are AEDs (Krishnamoorthy and Trimble, 1999), folic acid deficiency (Levi and Waxman, 1975), laterality of lesion (Flor-Henry, 1969a, b) and the presence of alien tissue in the brain (Taylor, 1975) . The predominance of temporal lobe epilepsy occurring with POE also indicates impairment or defect in these or linked structures supported by the evolving literature implicating mesial temporal structures in the development of psychopathology (Krishnamoorthy, 2007).

POE thus can be considered an important neuropsychiatric sequel of a common neurological condition — epilepsy. Although psychodynamic factors such as the presence of a chronic illness and the sudden cessation of seizures may play some role in the development of interictal psychopathology, the majority of the explanations for POE seem to be neurological in nature and related to the ictal process. While our current understanding about the precise nature of these neurobio-logical processes is limited, this should not deter us from exploring them further given the plethora of molecular, cellular and imaging techniques that are now available to us. That the psychosis of epilepsy is a neurological disease is almost a certainty. Whether this will lead to a better understanding of the neurobiology of psychosis overall and of psychopathology in general is the moot point!

Neurology

- Temporal relationship to ictal events

- Increased prevalence in temporal lobe epilepsy

- EEG changes

- Neuropathological evidence

- Imaging evidence of neurological damage

Adachi , N. , Matsuura, M. , Hara, T., Oana, Y. , Okubo, Y. , Kato, M., Onuma, T. (2002). Psychoses and epilepsy: Are interictal and postictal psychoses distinct clinical entities? Epilepsia 43(12), 1574—1582 , Amann, B., Grunze, H. (2005). Neurochemical underpinnings in bipolar disorder and epilepsy, Epilepsia 46, 26-30,

Benes, F. M., Berretta, S. (2001). GABAerg^c interneurons: implications for understanding schizophrenia and bipolar disorder, Neuropsychopharmacology 25(1), 1-27,

CONCLUSION

Psychiatry

- Psychological reaction to chronic stress

Psychiatry

- Psychological reaction to chronic stress

REFERENCES

Falret, J. P. (1854). Memoire sur la folie ciculaire . Bull Acad Med (Paris) 19, 382-400. Flor-Henry. P. (1969a). Psychosis and temporal lobe epilepsy. Epilepsia 10 , 363-365 . Flor-Henry, P. (1969b). Schizophrenic-like reactions and affective psychoses associated with temporal lobe epilepsy: etiological factors . Am J Psychiatry 126 , 3 . Flügel . D. . Cercignani . M.. Symms . M. R. . Koepp. M. J.. Foong. J. (2006). A magnetization transfer imaging study in patients with temporal lobe epilepsy and interictal psychosis . Biol Psychiatry 59(6). 560-567 .

Foong. J.. Symms . M. R. . Barker. G. J.. Maier. M.. Woermann. F. G.. Miller. D. H.. et al. (2001). Neuropathological abnormalities in schizophrenia: evidence from magnetization transfer imaging .

Brain 124. 882-892 .

Glaus .A. (1931). Uber combinationron schizophrenie and epilepsie . Zentralbe Neurol. Psychiatri 135. 450-550.

Gruhle. H. W. (1936). Uber den wahn bei Epilepsie. ZGesampte Neurol Psychiatry 154. 395-399 . Kaplan . P. W. (2002). Behavioral manifestations of nonconvulsive status epilepticus . Epilepsy Behav 3. 122-139.

Kraepelin, B. (1918). Dementia Praecox. (R. M. Barclay, ed.). Edinburgh : Livingstone. Krapf. E. (1928). Epilepsie und schizophrenie . Arch Psychiatr Nervenkr 83. 547-586. Krishnamoorthy, E. S. (2007). A differential role for the hippocampus and amygdala in neuropsychiatry disorders.J Neurol Neurosurg Psychiatry 78(11), 1165-1166. Krishnamoorthy. E. S.. Trimble. M. R. (1999). Forced normalization: clinical and therapeutic relevance .

Epilepsia 40(Suppl 10). S57-sS64 . Krishnamoorthy. E. S.. Trimble. M. R.. Sander. J. W. A. S. . Kanner. A. M. (2002). Forced normalization at the interface between epilepsy and psychiatry. Epilepsy Behav 3. 3-8 . Levi . R. N^Waxman. S. (1975). Schizophrenia, epilepsy, cancer, methionine and folate metabolism:

Pathogenesis of schizophrenia . Lancet 11 . 11-13 . Meldrum . B. S. (2000). Glutamate as a neurotransmitter in the brain: review of physiology and pathology. J Nutr 130, 1007S-s1015S. Mendez. M. F.. Grau . R.. Doss . R. C.. et al. (1993). Schizophrenia in epilepsy: seizure and psychosis variables . Neurology 43. 1073-1077. Morel . B. A. (1873). Discussion sur l'Epilepsie larvee. Ann Med Psychol 9 . 155-163 . (series 5) Perez. M. M.. Trimble. M. R. (1980). Epileptic psychosis - diagnostic comparison with process schizophrenia. Br J Psychiatry 137, 245-249. Pollock, D. C. (1987). Models for understanding the antagonism between seizures and psychosis. Prog

Neuro-Psychopharmacol Biol Psychiatr 11, 483-504. Reith . J. . Benkelfat. C.. Sherwin . A.. Yasuhara. Y.. Kuwabara. H. . Andermann. F.. Bachneff. S.. Cumming. P„ Diksic . M. . Dyve. S. E.. Etienne. P. . Evans .A. C. . Lal . S.. Shevell . M.. Savard. G.. Wong. D. F„ Chouinard . G.. Gjedde. A. (1994). Elevated dopa decarboxylase activity in living brain of patients with psychosis. Proc Natl Acad Sci USA 91, 11651-11654. Rüsch . N.. van Elst. L. T.. Baeumer. D. . Ebert . D. . Trimble. M. R. (2004). Absence of cortical gray matter abnormalities in psychosis of epilepsy: a voxel-based MRI study in patients with temporal lobe epilepsy. J Neuropsychiatry Clin Neurosci 16. 148-155 . Sachdev. P. (1998). Schizophrenia-like psychosis and epilepsy: the status of the association. Am J Psychiatry 155, 325-336.

Sachdev. P. S. (2007). Alternating and postictal psychoses: review and a unifying hypothesis . Schizophr Bull 33(4). 1029-1037.

Sato. M.. Racine. R. J. . Mclntyre. D. C. (1990). Kindling: basic mechanisms and clinical validity.

Electroencephal Clin Neurophysiol 76, 459-472. Schmitz, B. (1998). Forced normalization: history of a concept. In Forced normalization and alternative psychosis of epilepsy (M. R. Trimble. B. Schmitz, eds), pp. 7-24 . Petersfield . Wrightson Biomedical Publishing.

Slater. E. . Beard. A. W.. Glithero. E. (1963). The schizophrenia-like psychoses of epilepsy, i-v. Br J

Psychiatry 109. 95-150.

Smith . P. F. . Darlington. C. L. (1996). The development of psychosis in epilepsy: a re-examination of the kindling hypothesis . Behav Brain Res 75(1-2). 59-66 .

Stevens .J. R. . Livermore. A. (1978). Kindling of the mesolimbic dopamine system: animal model of psychosis . Neurology 28. 36-46.

Tadokoro.Y. . Oshima. T.. Kanemoto. K. (2007). Interictal psychoses in comparison with schizophrenia — a prospective study. Epilepsia 48(12): 2345—2351.

Taylor. D. C. (1975). Factors influencing the occurrence of schizophrenia-like psychosis in patients with temporal lobe epilepsy. Psychol Med 5 . 249—254 .

Toone. B. K. (1991).The psychoses of epilepsy.J Roy Soc Med 84. 457-459 .

Toone. B. K. (2000).The psychoses of epilepsy.J Neurol Neurosurg Psychiatry 69(1). 1-3 .

Toone. B. K. . Garralda . M. E.. Ron . M. A. (1982).The psychoses of epilepsy and the functional psychoses: a clinical and phenomenological comparison . Br J Psychiatry 141. 256-261.

Trimble . M. R. (1991). The Psychoses of Epilepsy . New York: Raven Press .

Trirnble. M. R. (1998). Forced normalization and the role of anticonvulsants . In Forced normalization and alternative psychoses of epilepsy (M. R. Trimble. B. Schmitz, eds), pp. 169-178. Petersfield : Wrightson Biomedical Publishing .

van Elst. L. T.. Baeumer. D.. Lemieux . L. . Woermann . F. G.. Koepp. M.. Krishnamoorthy. S.. Thompson . P. J . . Ebert. D.. Trimble. M. R. (2002). Amygdala pathology in psychosis of epilepsy: a magnetic resonance imaging study in patients with temporal lobe epilepsy.. Brain 125(1). 140-149 .

Vorkastner, W. (1918). Neurologie Psychiatric Psychologie and Ihren Grenzgebieten.

Was this article helpful?

0 0
Bipolar Disorder Uncovered

Bipolar Disorder Uncovered

If you're wanting to learn about bipolar disorder... Then this may be the most important letter you'll ever read! You are about to take an in-depth look at bipolar disorder. It's all you need to know about bipolar disorder to help you or a loved one lead a normal life. It doesn't matter if you or a loved one have been recently diagnosed or been struggling with bipolar disorder for years - This guide will tell you everything you need to know, without spending too much brainpower!

Get My Free Ebook


Responses

  • lea
    Does forced normalization ever resolve?
    3 months ago

Post a comment