Concluding Remarks Plural Epileptic Psychoses Should Be Understood Under Plural Hypotheses

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Does the psychosis of epilepsy differ from a primary psychotic disorder? Historically, several answers have been presented. As we discussed in the preceding sections, variations of the answer in the negative may be summarized as follows: the coexistence of the two conditions in a single individual is only accidental; epilepsy increases the vulnerability to a primary psychotic disorder; and the two conditions develop from a common etiological factor, but independently. Since Slaters report 40 years ago, the first answer seems to be denied by several studies including large scale epidemiological investigations (Jalava and Sillanpaa, 1996; Bredkjaer et al.; 1998; Qin et al.; 2005). When focused on CP, the increased incidence of psychosis among patients with epilepsy has tended to be explained by one of the latter two answers, both of which presuppose an enhanced susceptibility to schizophrenia in patients with epilepsy. As mentioned in the introduction section, the corollary to these is that epileptic psychosis is nothing but a genuine schizophrenia, which at most may become modified by the presence of epilepsy. Simply stated, Slater seemed to prefer the third alternative and advocated the view that damage to the medial temporal structures, irrespective of genetic or exogenous origin (such as epilepsy), is associated with schizophrenia. Mace pointed out that this simple causal link appears to be increasingly untenable in light of subsequent developments in psychiatry and neurology. However, Slaters fundamental idea outlived decades of dispute, and became modified and innovated by Taylors as well as Stevens' more sophisticated versions of the same line of explanation. While Taylor stressed the ontogenetic rather than anatomical impact of a common pathology leading to both epilepsy and psychosis (Taylor, 1971, 1975; , Stevens proposed that the critical factor causing predisposion to schizophrenic psychoses among some individuals with organically induced psychosis (including epilepsy) is the reactive occurrence of abnormal neuronal regeneration, especially when it coincides with a vulnerable period (Stevens, 1989, 1991; . These more sophisticated versions of the common etiology hypothesis offered some prospect of reconciliation between the second and the third line of explanations. It is important to note here that the leading authors who have discussed CP nearly unanimously presumed that CP is an organically induced schizophrenia in essence.

If we conclude that the essence of epilepsy lies in seizure activity, then the question can be paraphrased as follows: Does psychosis occurring in patients with epilepsy have an intrinsic relationship with seizure activity? While answers in the negative predominate when discussing CP, some kind of intrinsic relationship between seizure and psychosis is difficult to deny with regard to transient epileptic psychosis, especially PIP and alternative psychosis. Very recently, Sachdev (2007) provided a unifying hypothesis related to the pathogenesis of alternative and postictal psychoses, and suggested that the brain s inhibitory processes in response to seizures plays a key role in the development of the psychosis underlying the two conditions. Twenty years before Sachdev, this emphasis on the excessive inhibitory process as a cause of psychosis was suggested by Stevens (1986). Wolf (1991) attempted to explain transient epileptic psychosis in a different way, but also as a phenomenon intrinsically related to seizures, and also contended that some epileptic psychoses, especially alternative psychosis, result directly from a deviant seizure that has spread from an original epileptogenic area. Originally, some areas of the reticular activating system were proposed as the destination for this deviant seizure spread. The shifting peak of seizure activity within the limbic circuit depicted in Figure 8.3 may be regarded as a variant of this deviant seizure spread hypothesis. In this case, however, the septal area was considered as the destined area. Finally, Wiesers hypothesis of limbic status epilepticus (Wieser ;t al. ; 1985) should also be categorized as an affirmative answer to the initial question.

In Table 8.9, the major theories for epileptic psychoses and suitable models for respective theories are concisely summarized. To repeat, previous theories can be divided into two groups. In one group (Table 8.9a, b), psychotic episodes occurring concurrently with epilepsy are regarded as essentially nothing but primary psychotic disorders, while in the other (Table 8.9c, d, e), a direct casual relationship between seizure activity and resultant psychosis is presumed. Figure 8.3 is a bird; eye view, in which subcategories of epileptic psychoses are allocated as a function of association with seizures and TLE. A uniting theory covering all the epileptic psychoses does not seem to exist, and lack of awareness of the limited applicability of a single explanation or theory may lead to serious confusion. Answers to the initial question, "Does epileptic psychosis differ from a primary psychotic disorder?", cannot be given wholly, but only separately one by one. As depicted in Figure 8.3, the answers are shaded from the most notable "Yes" of PIP

Close

Association with TLE

Remote

CP without preceding

AIP episodes

AIP with complete remission (including alternative psychosis)

Remote

Relationship with seizure activity

Close

Figure 8.3 Subcategories of epileptic psychosis as a function of their associations with TLE and seizure activity. CP: Chronic psychosis; AIP: Acute interictal pyschosis; PIP: Post-ictal pyschosis; TLE: Temporal lobe epilepsy.

TABLE 8.9 Major hypotheses for epileptic psychoses and corresponding models a. "Psychodynamic hypothesis" as a risk factor in individuals genetically prone to psychosis (Pond, 1962)

b. Localized pathology of strategic position as a common causative factor (Slater, 1963)

c. Deviant seizure spread (Wolf, 1991)

d. Excessive inhibitory surround (Stevens, 1983)

e. Subclinical limbic status epilepticus (Wieser, 1985)

Chronic epileptic psychosis

Acute interictal psychosis (including alternative psychosis)

Postictal psychosis

Chronic epileptic psychosis

Acute interictal psychosis (including alternative psychosis)

Postictal psychosis to the approximate "No" of CP without preceding AIP, based on how close the association with seizures is. Evidently, plural epileptic psychoses should be understood under plural theories. It is possible that complex interrelationships between various sites within the limbic circuit and excessive inhibitory spread will serve as promising key concepts in future studies, at least for transient epileptic psychoses.

It is interesting that as far back as the mid-19th century, Farlet named PIP as a true epileptic psychosis (Farlet, 1860/1861). The true value of that long-forgotten statement is now becoming more apparent.

The first author is indebted to Dr. Naoto Adachi for his valuable advice and Mrs. Lumina Ogawa for her help in the literature searches.

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