A man in his forties had been repeatedly assessed over a period of 15 years at neurological departments and specialised epilepsy hospitals. The conclusion was always psychogenic, non-epileptic seizures (PNES), but there were no proposals for treatment. Prior to the current treatment he had also undergone several psychiatric assessments, which found the seizures to be dissociative and consistent with psychogenic, non-epileptic seizures. Psychotherapeutic and medical approaches had been ineffective.
Alcohol is known to trigger seizures, exacerbate seizure control in epilepsy patients or induce epilepsy. In every third acute admission after an epileptic attack, more alcohol than normal has been consumed prior to the episode (1). Episodes triggered by fever are also common, but more frequent in children. As a rule these do not cause brain damage (2).
Psychogenic, non-epileptic seizures can be defined as an observable, sudden seizure-like change in behaviour or consciousness which resembles an epileptic seizure but is not accompanied by the EEG changes that are characteristic of epileptic seizures or by other evidence of epilepsy or other somatic causes. However, many believe that cases of acute admissions with major, dramatic, GTC-like seizures where psychiatric examination does not reveal a mental disorder could be classified as conversion/dissociation. As a result these seizures are classified as dissociative/psychogenic non-epileptic seizures.
The differential diagnostic procedure for distinguishing between psychogenic, non-epileptic seizures and epilepsy has improved over the past 30 years, particularly since the introduction of video EEG monitoring (3). The occurrence of psychogenic, non-epileptic seizures in the general population is estimated at about 1.5/100 000 (4, 5) and 25 – 30 % of all those referred to epilepsy centres because of treatment resistant epilepsy receive this diagnosis (6, 7). Inadequate diagnosis can prevent appropriate mapping, processing and treatment of the underlying psychosocial causes, resulting in prolongation of the disorder and associated stigma and of the patient’s status as an invalid. In those cases where ineffective anticonvulsant medication is prescribed, stressful side effects may also occur.
According to ICD -10, dissociative convulsions may «mimic epileptic seizures very closely in terms of movements, but tongue-biting, bruising due to falling, and urinary incontinence are rare, and consciousness is maintained or replaced by a state of stupor or trance.» (9).
A number of studies indicate that bipolar disorders are often underdiagnosed in primary care, partly due to an absence of typical manic symptoms (10, 11). Symptoms such as slightly euphoric mood, unusual irritability and decreased need for sleep over a period of at least four days may be enough to cause suspicion of bipolar disorder (10, 11). Lamotrigin is used both as a mood stabiliser for bipolar disorders and as an anticonvulsant for epilepsy. Existing evidence indicates that bipolar disorders and epilepsy may have some biological mechanisms in common (12, 13).
Our patient had repeated neurological assessments over a period of 15 years at both neurological departments and specialist epilepsy centres. The consensual conclusion was psychogenic, non-epileptic seizures, but there were no treatment proposals. Prior to the present assessment and treatment he had also undergone several psychiatric/psychological assessments, which found the seizures to be psychogenic (dissociative) and consistent with psychogenic, non-epileptic seizures. Psychotherapeutic and medicinal approaches had not been effective.
Bodde et al. (14) outline a five-level model of psychological factors that may be involved in psychogenic, non-epileptic seizures (Box 1). This model resembles other models used to explain somatoform disorders. When applied to our patient, he had a) emotional instability, personality-related defensive tendencies and a bipolar disorder b) problems in regulating everyday stress, c) clear triggering factors in the form of overwork, insomnia and noise and d) the «gain» that the seizures had the effect of diverting the emotions and feelings that arose in the situations in which the seizures occurred (amnesia). The patient’s psychosocial history is thus quite consistent with psychogenic, non-epileptic seizures.
Bodde et al’s five-level model of psychological factors that may be involved in psychogenic, non-epileptic seizures (14).
Psychological factors that may cause the condition, such as sexual abuse and personality disorders.
Vulnerability factors, which may cause a predisposition for psychosomatic reactions, such as a tendency to dissociate and a limited ability to regulate stress or resolve conflicts.
Shaping factors, such as close relatives with similar symptoms.
Triggering factors, such as stress and inter-personal conflict.
Prolongation factors, such as gains in the form of attention and care, plus avoidance of coping and situational challenges.
The earlier psychological assessment of our patient was thorough, but did not lead to effective treatment. When the neurological assessment focuses only on excluding epilepsy, psychogenic, non-epileptic seizures becomes an exclusion diagnosis. A positive diagnosis is necessary in order also to acknowledge and treat the underlying mental disorder. It can be particularly challenging when the responsibility for different aspects of a composite problem fall to different disciplines – in this case, neurology and psychiatry.
Psychogenic, non-epileptic seizures are normally regarded as a condition that should be treated in the field of psychiatry (15). However, our example shows that these patients may fall between the two stools of neurology and psychiatry, instead of these specialities cooperating on assessment and treatment.
The neurological assessments also yielded non-specific EEG findings that were not consistent with «pure» psychogenic, non-epileptic seizures. For example: could the first seizures, which were accompanied by fever, have caused brain damage that the EEG did not reveal?
The stress-vulnerability model, in which an x-axis represents a continuous vulnerability or organicity dimension and a y-axis represents a continuous stress dimension, allows all possible combinations of organicity and stress (16). In this case history, it appears that it may have been difficult to discuss the possible implications of several possible pathological EEG findings while maintaining the diagnosis.
However, existing research has shown that psychogenic, non-epileptic seizures by no means exclude the possibility of comorbid epilepsy. Some studies have shown that up to 50 % of patients with the condition also have comorbid epilepsy, or have had it in the past, and that the epileptic component is severely underdiagnosed (17 – 19).
The comparison between psychogenic, non-epileptic seizures and epilepsy is logical in view of the fact that the most evident clinical manifestation is seizures. In an attempt to understand the pathogenesis in a broader biopsychosocial perspective, a broader differential diagnostic approach should be used.
The treatment with lamotrigin was started after a new psychiatric assessment concluded that the patient’s mental problems were consistent with bipolar disorder type II. At that time the patient had been an invalid for several years because of his seizures.
The relationship between epilepsy and bipolar disorders has been the subject of extensive discussions, particularly in neurological publications. Several studies have found that epilepsy and affective disorders have many common pathophysiological features (20 – 24). Extensive comorbidity of affective disorders, particularly depressions (25), bipolarity (26, 27) and epilepsy, the discovery of an increasing number of common pathogenetic features and the benefit derived from anticonvulsants and antidepressants by patients in both diagnostic groups (28) indicate that these two conditions are more closely related than previously believed.
Our case history, with the effectiveness of lamotrigin, may indicate that psychogenic, non-epileptic seizures should be considered in connection with both fundamental organic brain pathology, which cannot always be detected with existing examination methods, and with bipolar disorders. Our definite recommendation is that the diagnosis and treatment of patients with this condition require close cooperation between neurologists and psychiatrists.