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Although the tradition in modern psychiatry is to adhere to the classification systems such as ICD-10 (WHO, 1992) and DSM-IV (APA, 1994), it is well accepted today that psychopathology in disorders such as epilepsy transcends these conventional descriptions and has unique manifestations that are poorly reflected in these established classifications (Krishnamoorthy 2000). Depressive symptoms and disorders in epilepsy are therefore best classified according to their temporal relationship to the ictus.
1) Pre-ictal depression: prodromal depressive moods or irritability can occur hours to days before a seizure, and are often relieved by the convulsion (Lambert and Robertson 1999, Devinsky and Bear 1991). The 19th century psychiatrist Grule (Grule 1930) quotes “physician and attendants do hope for a seizure in these often very difficult patients, which comes like a salvation for everybody: the patient is much more bearable for weeks thereafter”.
In a prospective study examining prodromal mood changes, Blanchett and Frommer (Blanchett and Frommer 1986) found that most patients reported more depression on the days immediately preceding their seizure than on interictal days, along with an improvement of mood after the seizure. The low mood has been hypothesized to be a symptom of subclinical seizure activity or biological processes involved in the initiation of both depression and seizures.
2) Ictal depression: depression can occur as a part of the ictus itself. Ictal depression classically is of sudden onset and occurs out of context, i.e. is not related to environmental stimuli. It can occur in isolation or within seconds to minutes of a CPS and/or secondarily generalized seizure. Ictal depression appears to be more common in patients with TLE (Williams 1956), in whom rates of over 10% (Weil 1959, Devinsky et al. 1991) have been reported. Williams (Williams 1956) described depression as part of an aura in approximately 1% of his series of 2000 patients. The severity of ictal depression can range from mild feelings of sadness to profound helplessness and despair. Suicide has been reported during ictal depressive episodes (Lim et al. 1986, Betts 1993).
3) Postictal depression: although depression lasting hours to days after seizure has been described in some patients, it is rare to find a patient with postictal depression alone (Blumer 1992). Most patients also experience episodes of interictal depression. Postictal depression occurs more commonly after CPSs originating in the right temporal structures, and more prominently with bilateral limbic dysfunction. It has been postulated that postictal depression is a consequence of the inhibitory mechanisms involved in the termination of the seizures.
Depressive disorders which occur peri-ictally are usually short lasting and self-limiting.
4) Interictal dysphoric disorder: more recently, in 1998, (Blumer, 1998) drew attention to a peculiar mood disorder seen in patients with refractory epilepsy, particularly TLE. Interictal dysphoric disorder is characterized by a constellation of eight symptoms and requires the presence of any three.
Depressive mood
Fear
Paroxysmal irritability
Anergia
Anxiety
Euphoric moods
Pain
Insomnia
Interictal dysphoric disorder is typically of short duration and occurs in various permutation and combinations. These symptoms occur at various intervals and tend to last from hours to two or three days. In women, these symptoms become accentuated in the premenstrual period. Blumer stressed that patients with several of the above symptoms maybe at increased risk of sudden, unexpected suicide attempts and also development of interictal psychosis.
Forced normalization
In the 16th century, Cardenus (Whitwell 1936) wrote about a case of melancholia alternating with epilepsy, describing what is possibly the first case of forced normalization associated with epilepsy. The term forced normalization was coined by Heinrich Landolt (Landolt 1953) and defines a phenomenon characterized by the fact that with the occurrence of psychotic states, the EEG becomes normal or more normal compared to previous recordings. Although forced normalization clinically usually manifests as a schizophrenia-like psychosis, prepsychotic dysphoria and depression have also been reported (Wolf 1984). Several studies have also reported a decrease in seizure frequency prior to the onset of depressive illness (Dongier 1959/60, Flor-Henry 1969). A decrease in the seizure frequency and thus forced normalization can be brought about by (Robertson 1998):
* 1) a spontaneous reduction in seizures,
* 2) antiepileptic drugs,
* 3) temporal lobectomy.
The phenomenon of forced normalization forms an interesting interface between neurology and psychiatry, with various theories being suggested to explain the same. While (Wolf et al. (1991) suggested the condition to be a form of active but restricted subcortical seizure activity, various others have postulated that amygdaloid and limbic kindling might play a role in the development of this phenomenon (Krishnamoorthy, 1998). The roles of the glutamate and the GABA receptors in the mechanisms of epilepsy and psychosis also suggest the possibility of the involvement of various neurotransmitters in forced normalization (Krishnamoorthy 1999). One of the most recent hypotheses put forward to explain the same, digresses towards a more physiological view involving dysfunctions of the ion channels, and suggests that the phenomenon of forced normalization could be a unique kind of channelopathy (Krishnamoorthy 2002).
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