Abstract
Keywords
An epileptic seizure is an abnormal paroxysmal discharge of cerebral neurones that leads to an observable alteration in movement or behaviour or a subjective experience. Precipitation of seizures by a stimulus may be accompanied by deliberate self-induction of attacks [1], implying that the seizure can be obtained on demand, and therefore induced at an opportune time. Fenwick afforded a neurophysiological (albeit theoretical) basis for self-induction [2]. Some patients with epilepsy learn that by a willed action (usually manipulation of attention) they can alter neuronal activities in brain areas surrounding the epileptogenic focus, and produce a seizure [2, 3].
While it is relatively rare self-induction may be underestimated in patients with epileptic photosensitivity [4, 5]. Many sufferers are treated with inappropriately high amounts of anticonvulsant medication because of persistence of seizures. If this persistence is on the basis of selfinduced attacks, psychological treatments may be more appropriate. There are many other reasons for persistence of seizures, including high doses of anticonvulsants, which are themselves epileptogenic.
There have been numerous articles on self-induced epileptic seizures focusing on neurological and neurophysiological manifestations but psychiatric aspects have received scant attention. The focus of this review is hence such aspects and emphasis given to methods of selfinduction, functions and meanings of, and motivations for self induction, on the premise that understanding these will enable the clinician to devise interventions.
Prevalence
The first case of self-induced epileptic seizure was reported by Radovici et al. in 1932 [6]. A review in 1962 reported only 51 cases [7] but by the 1980s there were over 120 published case reports [4, 8] and by 1998 approximately 200 cases of self-induced seizures have been reported [9].
The prevalence varies depending on the setting. Self reported complaints, observation of family and friends, the health care provider's suspicions and mental status testing, and the neurophysiologist's monitoring through video/EEG recording are principal routes to detection. Gastaut found one case in every 1000 epilepsy sufferers [7] while Wadlington and Riley found two cases of selfinduced epileptic seizures based on their analysis of 20 000 EEGs [10].
Self-induction has been most widely studied in photosensitive epilepsy, which of itself is rare, occurring in 2–5% of all individuals with epilepsy [11]. Studies employing telemetric monitoring suggest that 25% of susceptible patients self-induce, if not of seizures at least of discharges [4, 5]. Janz reported 21% of patients with juvenile myoclonic epilepsy induced polyspike-wave discharges and absence or jerks by slowly closing their eyes, or staring at a light and waving a hand in front of the eyes to produce flicker [12]. Jeavons and Harding reported five in a series of 460 photosensitive patients and estimated that 3% of all persons with epilepsy are susceptible to visually induced seizures [13], though these are not necessarily self-induced.
Trenite's study yields two sets of data [11]. The first, based on reports of patients and caregivers, revealed that 35 of the 100 photosensitive patients had a history of self-induction. The second was obtained after all 100 patients were monitored by continuous telemetered EEG and closed circuit TV for 2 hours. Thirty-seven patients demonstrated stereotyped slow eye closure movements (which elicit epileptiform activity) either with or without eyelid flutter and, in one patient, with additional waving of the right hand in front of the eyes. Only five of these 37 admitted the practice of self-induction. Out of the 37, 29 also belonged to first group (i.e. were reported to have a history of self-induction). Apart from the obvious discrepancy between sensitivity to lab flicker stimulation and sensitivity to environmental light stimulation, there is the inevitable contamination of people with non-epileptic phenomena. Another limitation is that ‘self-inducers’ in the laboratory setting may be reacting to the particular set of circumstances (photo-stimuli, complicated machinery, close monitoring) and not self-induce in real life. Eye closure could also be a tic or an involuntary movement aggravated by anxiety.
A survey of 76 patients attending the epilepsy clinic at the Maudsley hospital, indicated that between 25 and 33% were able to generate their own seizures at will [3]. These figures need to be treated with caution because results were obtained from a highly specialized clinic. The figure arrived at in a sample of 100 outpatients with difficult-to-treat epilepsy was 2% by self-report [8], whereas Mostofsky and Loyning found that 8% attending a neurology clinic said they could produce a seizure at will [14]. The disparity is due to differences in the populations (the result of referral patterns) and the inevitable contamination of people with non-epileptic phenomena. Also, self-report of ‘sometimes able to induce a seizure’, is not a proven criterion nor clinically problematic.
It would seem that self-precipitation in photic epilepsy occurs in a tiny proportion of all people with epilepsy, as supported by the low prevalence found in the EEG reports cited, and that it is a rare manifestation of a small subgroup of epilepsies. It is difficult to determine from published papers just what level of clinical difficulty self-induction of seizures actually posed to the patients and clinicians.
Methods of self-induction
Many cases, if not most, are children and particularly those with cognitive impairment (see Table 1). A variety of techniques have been reported. The overwhelming majority (96%) of patients reported are photosensitive and use visual stimuli [9, 15]. Self-induced seizures are most commonly caused by waving a hand with open fingers in front of a light source, blinking (usually in sunlight), or staring at a television set. The first descriptions of photosensitive epilepsy date from before the clinical use of EEG and concern patients who induced attacks in themselves by staring at the sun and waving the outspread fingers of one hand in front of the eyes to produce flicker [6]. Some of these subjects are easily identified by a history of staring at bright lights while waving the spread fingers of one hand in front of the 536 SELF-INDUCED EPILEPTIC SEIZURES eyes [7]. The posture assumed by these patients, with the head slightly bent backward when staring at the sun or at a bright light, and the irresistible attraction toward these visual stimuli, is graphically conveyed by the term ‘sunflower syndrome’, suggested by Ames and Saffer for photic self-induced seizures [16, 17].
Seizure characteristics and other clinical features
More recently, it has been realized that many more photosensitive subjects employ a manoeuvre involving extreme upward deviation of the eyes with slow eyelid closure to induce seizures or epileptiform discharges in themselves [18]. The eye movements may themselves be misinterpreted as an ictal phenomenon [19–21]. These tonic eyeball movements are always associated with spike-and-wave activity in young individuals. As they mature, the movements may persist but no longer elicit epileptiform activity [22]. Darby et al. described seven patients who induced paroxysmal EEG discharges by eye closure (see Table 1) [5]. In no instance had self-induction been suspected prior to the EEG investigation, and to identify the syndrome it may be necessary to monitor the EEG and oculogram for 10 minutes or more [5].
Some patients with television epilepsy are compulsively attracted to the screen [7, 23]. Most are children, with a small preponderance of males. Some of these patients admit to using television as a method of selfinduction [24, 25]. Flickering of the television set has its greatest effect when the patient is close to the screen and the image is out of focus. Patients may cause the television picture to go unstable and then stare at the flickering light that it produces [25]. Others insist that the compulsion is distressing to them but irresistible, and it is uncertain whether or not some instances of compulsive attraction to television are to be regarded as selfinducing behaviour or as ictal phenomena. Other visual methods include blinking [6, 7, 18, 26] and looking at objects which presented horizontal or vertical stripes [27–30].
Also described in the literature were children and adolescents who self-induced epileptic seizures by hyperventilation [8, 31] or by an effort of concentration [32]. The variety of forms of self-stimulation also include apnea or Valsalva manoeuvre [33], bilateral compression of the carotid arteries [34], chewing [35], movement [36], foot rubbing [1] and hyperextension of trunk and neck [37]. These patients who used non-visual methods of self-induction were a different group from the photosensitive epilepsy group.
Interestingly, method of induction may change over time, for example, some patients could adopt hand waving as a method of induction and later use eye closure, which is less noticeable and hence more likely to escape observer detection [35]. A combination of methods can also be used, (e.g. initiating a discharge by eye closure and prolonging or enhancing it by hand waving). Choice of induction method may also be subjected to conditioning. Panayiotopoulos reported a patient who will only use pattern, never light, for selfinduced attacks, and thought that this might be related to the apparently earlier incidence in her life of pattern sensitivity, which resulted in conditioning [27].
Seizure characteristics and other clinical features
Self-induced seizures may occur in individuals with primarily generalized epilepsies and those with focal syndromes, the former are the most common variety in which self induction occurs, particularly those with photosensitive seizures. Most patients with spike induction relating to ocular phenomena showed spikes over the occipital regions or diffuse spike and wave activity. Only a few patients who have exhibited induction of spikes by eye movement have spikes over the frontal region [38]. The frequency of these visually induced attacks depends to a certain extent on the available light intensity, and this may account for the observation that they are commoner in Australia than Great Britain [32]. As with other types of photosensitive epilepsy there is a preponderance of females (see Table 1). Patients who are impulsively attracted to the TV set are predominantly male, have normal intelligence, and usually have tonic-clonic seizures [39].
Visual self-inducers are characterized by exceptionally high light sensitivity, frequent seizures and subnormal intelligence [7]. Patients displaying the ‘sunflower syndrome’ (staring at the sun) are often mentally subnormal [7]. The overrepresentation of patients with learning disability (see Table 1) is not surprising since, anecdotally, self-induction of seizures is often also associated with chronically institutionalized patients, and all of the studies were case reports/series with non-random selection of sample. Many of these children do not have many possibilities for self-satisfaction and have limited ability to play with their body [40]. Children with learning disability also may exhibit repetitive behaviours, and the accidental discovery of a seizure-inducing sequence may be more likely [40]. Interestingly, self-induction seems to occur less often among those with severe mental retardation, suggesting that discovery of the seizure-inducing sequence is not purely serendipity. It is also possible that mental retardation makes the patient less amenable to environmental manipulations and consequently, self-induction is more likely to persist, which in turn increases the chance of detection in prevalence studies.
Earlier studies indicate that the majority of selfinducers were of subnormal intelligence but this may not be necessarily true [9]. Self-induction in individuals with learning disability are probably easier to detect, especially when they tend to produce intermittent retinal stimulation by waving the outstretched fingers in front of the eyes. In general, patients with normal intelligence tend to avoid having their self-induction observed [11] and self-induced behaviours are difficult to record by simultaneous video-EEG recording in these patients.
Ames argues that for some, the apparent inducing behaviour such as hand-waving is in fact a part of the ictus and therefore, questions whether these are true selfinducers [19, 20]. There is evidence that the hand movement, in some patients, is part of the ictus rather than the stimulus [19–21, 39]. Several of the patients in the cinefilms of Ames appear to have eyelid myoclonia on coming out into bright sunlight. Wastell et al. also suggest that in people who induce by eye-closure there is in fact an EEG change before eye closure in the form of a direct current (DC) shift [41]. There is hence contradictory evidence as to the degree of wilfulness or selfinduction of some self-induced seizures. In some cases the attraction to the TV set appears to be less an act of will than a capture of will by subclinical seizure activity [42]. It is likely that there are two groups of patients: true self-inducers and another group, where the hand movements and eye closure are parts of ictal activity [8]. When interpreting the EEG findings, it is important to realize that EEG surface recordings are unlikely to tap activity occurring in the deeper structures of the brain. The surface EEG may be normal in partial elementary and partial complex seizures, and myoclonic seizures.
Reasons for self-induction
There has been considerable speculation on the motivation for self-induction, which often remains unclear, even in cases with normal intelligence. Until one has gained the patient's confidence, any discussion of self-induction generally elicits an indignant denial [35]. Reasons elicited and reported for self-induction of seizures so far include:
Compulsion. Many authors consider auto-induction as a compulsive pleasure-seeking behaviour. Some patients seem almost compelled to do it in the way that some children with television epilepsy seem irresistibly drawn towards a TV set [32]. Heliotropism, defined as a compulsive attraction to the sun or to bright lights (a light-seeking behaviour), is one of the most common triggering manoeuvres. Explanations offered are usually vague, ambiguous or even defensive. Some self-inducers say that they do not like it, but they cannot help indulging in this behaviour. Wilful avoidance of stress or escape from unpleasant situations or boredom. It has been suggested that self-induction of seizures might be a biologic protecting mechanism against unpleasant stimuli, a selfpreserving behaviour. This is consistent with Kretschmer's view that hysterical reactions originated in two instinctive patterns of normal behaviour; the violent motor reaction and the sham-death (immobilization) reflex [43]. Both behaviours occur in response to real or supposed threat and represent mechanisms of adaptation and survival. Patients are usually embarrassed to discuss this habit but may admit to a relief of tension when self-inducing. The rate of self-induction usually increases under stress and frequencies of 100 episodes per hour are not unusual [8]. The ‘adaptive’ aspects include relief of tension and fulfilling the need to ‘restore neuronal homeostasis’. Hedonistic motivations. Some patients induced their seizures because of the resulting pleasant experiences [44], which include pleasurable auras (arising from Old's report on self-induction of epilepsy in rats with electrodes in the hypothalamus [45]) and erotic gratification [46]. When animals are taught to do certain acts, for example lever-pressing, to initiate self-stimulation the animals may work tremendously hard to stimulate themselves, and do little else. Some neglect food, water, and natural functions [47]. The patient described by Klass self-induced her pleasant trance-like states, followed by the stereotypical vision of a dancing couple by having records of music and concentrating intensely [48]. Harley et al. described a 16-year-old male, who was looking into bright sunlight while simultaneously masturbating [23]. The existence of a reward centre in the limbic system is well documented [49], and various stimuli to this area are capable of producing repetitive behaviour such as has been observed in animals. Obtaining a sense of control (mastery) over the seizures. Perhaps the most horrifying aspect of epilepsy from the standpoint of the patient is its unpredictability, and for a significant number of people with epilepsy, seizures may occur anywhere, at any time, with little or no warning. Understandably many sufferers take some comfort from the belief that they can identify circumstances which bring on their attacks [35]. Also, following the epileptic seizures there is increased seizure threshold, (i.e. seizure-free postictal periods). Falconer described a medical man who, if interviewing patients, would retire to a closet to induce seizures as he could then rely on a refractory period [50]. Alternatively, self-induction can be viewed as a counterphobic response. Persons with epilepsy commonly fear death and/or brain damage due to their seizures and some would employ counterphobic mechanisms by repeatedly placing themselves in hazardous situations, and denying the possibility of death by pointedly acting as if epilepsy held no risk at all [51]. Attention-seeking. Most reports of self-inducers reveal other behavioural abnormalities leading to social isolation and learning problems. For instance, Harley et al. described their patients as ‘sensitive children who felt different and inadequate as well as unloved in families where there was relatively little warmth’ [23]. In some instances a clear advantage derives from the self-induced seizures, which may be used to manipulate relatives [52]. Others, such as, self-treatment: One freely admitted to inducing tonic-clonic seizures with television as a ‘do it yourself’ convulsive therapy, which relieved the severe bouts of depression from which she suffered (quoted in Binnie, 1993). Striano et al. report an interesting case, who casually discovered the possibility of provoking his seizures by rubbing his left eye, used the triggering manoeuvre to persuade the skeptical physician of the truthfulness of his disturbances [50].
Management
At the outset, two issues need to be highlighted, the relative rarity of the phenomena and controversy as to whether some self-induced behaviour is actually wilful/ illness behaviour [8]. Thus, neurologists and paediatricians would have to be careful making the diagnosis of self-induction and it is not appropriate to hastily refer onto psychiatrists.
Conventional treatment by anticonvulsants has been reported to yield some positive results. Ames and Enderstein reported some success with clonazepam, and opined that either this drug or nitrazepam or sodium valproate is the most likely to succeed [53]. Aso et al. reported a case of a 5-year-old girl who was suspected to self-induce absence by blinking at sunlight. Although her seizures persisted despite treatment with valproate, the selfinduced behaviour became less prominent [30]. In general, it is crucial to distinguish primarily generalized seizures from focal syndromes, the former being specifically sensitive to clonazepam and other benzodiazepines, sodium valproate and lamotrigine.
Overweg and Binnie noted an analogy between selfinduction and electrical self-stimulation of the brain in experimental animals, a phenomenon that can be suppressed by dopamine antagonists [54]. They therefore attempted therapy with chlorpromazine or haloperidol and reported an improvement in six out of seven patients. Trenite et al. also obtained a reduced incidence of self-stimulation in a controlled trial of pimozide [55]. Drugs that suppress self-stimulation in animals may block the pleasurable response without affecting the response to intermittent photic stimulation, and have partially reduced or completely terminated self-induction [35].
A few patients have responded to psychotherapy [56–58]. Forster suggested treatment by avoidance conditioning and proper encouragement of voluntary inhibition of self-provocation [57]. He describes a regime whereby patients with self-induced seizures were administered skin shocks when they began to undertake seizure-provoking behaviours. However, aversive therapies are open to abuse and their employment in the past with vulnerable individuals (e.g. patients with learning disability) pose ethical dilemmas. Cinciripini et al. used both restraint and reward to reduce seizure frequencies significantly in a 7-year-old child with petit mal seizures, both spontaneous and self-precipitated (by putting his hand in front of a light) [58]. Differential reinforcement consisted of praise for using his hands appropriately, or keeping them flat on the table [58]. In many cases it is necessary to help the family rather than the child, and advise them on how the child and his symptoms should be handled [32]. The patient usually resents pharmacological treatment for this phenomenon and can only be motivated to modify his/her behaviour through social pressure by parents or peers [11].
Some self-inducers can be persuaded to wear dark glasses but the child who takes pleasure in inducing the attacks will seldom be persuaded to wear sunglasses [59]. Takahashi et al. describe the characteristics of photogenic self-induced seizures and their treatment by optical filter and blue-tinted contact lenses in a child with severe myoclonic epilepsy in infancy [60]. Monocular occlusion is rarely successful if the patient is mentally retarded or derives satisfaction from the habit. Such measures might also serve to highlight the fact that the person is handicapped and may have adverse effects on his/her self-esteem.
Self-induced epilepsy is notoriously resistant to therapy [7, 9, 53, 61, 62]. This may in part be due to patients’ reluctance to take medication, but even compliant patients appear refractory to antiepileptic drugs. Possible reasons for the refractoriness to treatment are as follows: (i) Many cases were solely treated by neurologists and paediatricians, and received inadequate psychiatric evaluation. Self-induction of seizures is essentially an abnormal illness behaviour, and secondary gains which maintain the behaviour need to be identified and managed. Liaison model would suggest that much of the interventions would need to be carried out by the neurologist (or in collaboration with a psychiatrist), due to the stigma attached to ‘self-induced’ phenomena (abnormal illness behaviour). (ii) Medications tend to dampen photosensitivity or desire for self-stimulation but fail to address other underlying reasons for self-induction, (e.g. avoidance of stress, need to assume the sick role). As pointed out by Lee et al., behaviour modification is more important than drug treatment in many cases [63]. (iii) Evident in some cases was the failure to engage the patient in treatment, which could be because the approach used was too confrontational and resulted in patients’ defaulting treatment and leaving the service. Photosensitive epilepsies, particularly those with eyelid myoclonus are notoriously difficult to treat, not necessarily due to poor compliance or self-induction but simply because medical therapies are at present inadequate for these seizure types.
Discussion
Conceptual issues
The concept of self-induced seizures rests on the premise that the patient is fully aware of the link between the observed behaviour (e.g. hand waving) and the onset of seizures. Some patients suffer from learning disabilities and are not able to explain why they perform the act. Also many did not admit to voluntary selfinduction some even denying the act. It is hence likely that some may have performed the movement on a voluntary basis without realizing that it would culminate in seizures. The sense of voluntary control is subjective and can only be inferred by an outside observer, giving rise to ready diagnostic confusion of factitious disorder with somatoform disorders. The judgement that symptoms are voluntarily produced is based on observations of behaviour suggesting concealment, after excluding all other possible causes of the behaviour. However, it should be noted that this behaviour has a compulsive quality and hence is voluntary in the sense of being deliberate and purposeful, although implying a lack of full control that is an inherent feature of a ‘compulsive’ behaviour. In some cases, it can be considered as tensionreducing, semivoluntary, not performed in response to an obsession.
The clinician needs to ponder over the following issue: what is the effect desired by the patient? Is it the seizure or altered mental states induced by eye closure or hand movements? Some patients, for instance, admit that they make the hand movements voluntarily to elicit a particular sensation [5]. Alpha waves are best seen with eyes closed and under conditions of physical relaxation and relative mental inactivity. Immediately after eye closure, the alpha frequency may be accelerated for a moment (‘squeak effect’) [64]. Extreme upward gaze is known to facilitate the posterior alpha rhythm and lateral eye deviations may have similar effects. It is hereby postulated that enhanced alpha rhythm (as a result of eye closure) could well serve as a common pathway for the elicitation of paroxysmal EEG activity (not desired by the patient) and mediation of relaxation and pleasant mood (effects desired by the patient). For some cases, a more appropriate and accurate description will be ‘flicker-induced seizures’, ‘hyperventilation-induced seizures’ or ‘head movements–induced seizures’ which refocuses on the behaviour rather than the intention or will.
All studies have used non-random samples and consequently, there is often opportunity sampling (see Table 1). The patients were gathered by anecdotal case reports or carefully sifted subgroups (i.e. photosensitive epilepsy and all types of ‘self-triggers’) and the assessors were not blinded. The accuracy of patients self-reports merits further attention. Non-epileptic seizures have to be excluded and validity of observations strengthened by EEG investigation. Diagnosis of seizures depends on judicious consideration of a full medical, neurological and psychiatric history and examination. There should also be appraisal of the seizure history complemented by ancillary investigation of seizure phenomenology.
This literature review might serve to pilot prospective controlled studies of psychiatric aspects of self-induced seizures in more circumscribed populations, using standard diagnostic criteria, standard assessments and employing suitable controls. It is not clear what proportion of patients with treatment refractory epilepsy and nonepileptic seizures have self-induced epileptic seizures. Of interest would be the evaluation of their temperaments/ personality, as Axis II psychopathology may be present given the manipulative nature of the behaviour in a subgroup of patients. Many of the cases described so far relate to children, adolescents and those suffering intellectual disability. More attention needs to be given to developmental or cognitive issues that may strongly influence the behaviour under investigation. It would also be useful to consider the hypothesis that people with cognitive impairments fail to inhibit behaviours liable to trigger seizures, rather than ‘actively’ engaging in them.
There is a paucity of literature on the treatment modalities used and no definite indication that neurology intervention may be truly benefited by psychiatric intervention. Self-induction of epileptic seizures may become entrenched and the model of abnormal illness behaviour is particularly applicable. Abnormal illness behaviour refers to inappropriate or maladaptive modes of perceiving, evaluating, or acting in relation to one's own state of health [65]. For some patients, the sick role becomes attractive when the demands of life are too difficult to cope with, because of limited emotional resources or the clustering of adverse events. This learned behaviour is in part determined by cultural factors and childhood experiences and is reinforced by the perceived advantages of the sick role (e.g. the attention of others) [66]. Secondary gain is usually not deliberate or conscious and is very difficult to determine with confidence.
Treatment
Self-induction appears to be associated with a wide variety of psychiatric syndromes. Though the behaviour is repetitive, purposeful and intentional, it differs from a ‘classical’ compulsion in several ways. First, ‘classical’ compulsions are often performed in response to an obsession (persistent ideas, thoughts, impulses or images that are intrusive and senseless). Obsessional thoughts in self-inducers were reported less frequently than compulsions, either because they were indeed rarer or because of language difficulties or cognitive impairment made them less accessible. Second, as a person attempts to resist a ‘classical’ compulsion, a sense of mounting inner tension arises. None of the cases reported seem to experience this. It could be because the clinician fails to elicit this. Alternatively, these patients did not always recognize the excessiveness or absurdity of their actions or attempt to suppress them and consequently, anxiety was not a feature of the mental state and distress only occurred when the acts of self-induction were observed or detected by others. Only further systematic research can shed light on these areas. Third, self-induction is sometimes experienced as pleasurable or satisfying (positively reinforcing), and sometimes as discomfort-reducing (negatively reinforcing). This is unlike OCD, where the compulsion is typically experienced as discomfortreducing.
Two subgroups of self-inducers may have an ‘Impulse Control Disorder’. The first subgroup concerns individuals who describe self-induction as a tension-reducing behaviour which is not performed in response to an obsession. The second subgroup consists of self-inducers whose primary motive is self-harm, especially in individuals with learning disability. The essential feature of Impulse-Control Disorders is ‘the failure to resist an impulse, drive, or temptation to perform an act (selfinduction of seizures in this case) that is harmful to the person or to others’ [67]. The individual may feel an increasing sense of tension or arousal before committing the act, and following the act he or she may or may not have feelings of regret, self-reproach, or guilt. Of interest will be further exploration of such cases to see if they all experience a mounting tension before each selfinduction episode and if there was indeed a release of tension or gratification after self-induction.
Self-injurious behaviour has a compulsive quality and is often regarded as a stereotypy [68]. The onset of this behaviour may be associated with minor illnesses, but maintenance is most usually attributed to boredom, selfstimulation or to blocking out external stimuli which are disturbing to the person [68]. Repetitive self-mutilation is described under the rubric of Impulse Control Disorder in DSM-IV. This disorder typically starts in adolescence and is associated with severe psychosocial dysfunction. It is hypothesized that poor affect regulation is the underlying psychopathological mechanism of the disorder [69] and there is sometimes gratification of an unconscious need for self-punishment. Biological aetiology in self-mutilation may include sensory deprivation, serotonergic dysfunction and dysregulation of the central opiate system (self-injurious behaviours are thought to cause the release of endorphins in the body, which have an effect similar to opiates). Repetitive selfmutilation per se has been treated with serotonergic agents such as fluoxetine, or clomipramine and narcotic antagonists like naltrexone. There may be a role for serotonergic agents, in view of the ‘compulsive’ element of self-induced epilpetic seizures.
Both factitious disorders and malingering are characterized by intentional symptom production but differ with respect to the reason(s) for symptom production. Factitious disorders are defined by the intentional production of physical or psychological signs or symptoms, including subjective complaints for the unconscious purpose of assuming the sick role. This definition is in contrast to malingering, where there is intentional symptom production or reporting but the conscious goal of such behaviour is external incentives.
Perhaps the most promising avenue to an explanation of self-induction would be through functional analysis to identify possible determinants and/or consequences of the behaviour for the individual. It would also be useful to consider the hypothesis that people with learning disabilities fail to inhibit behaviours liable to trigger seizures, rather than ‘actively’ engaging in them. The arousal mediation hypothesis may be an explanation for a number of poorly understood behavioural patterns, such as stereotyped behaviours, self-injurious behaviours, other challenging behaviours, and potentially selfinduced seizures.
Behavioural modification, which includes behavioural monitoring, competing response training, and positive reinforcement, has also been shown to be effective in decreasing seizure frequency [70]. In patients with learning disabilities, neurobehavioural limits in ability to process information, solve problems, or initiate behaviour may pose additional barriers to compliance. If secondary gain associated with the self-induction (e.g. attention from parents) can be provided through less maladaptive means, attempts should be made to allow the patient to ‘save face’ while giving up the self-induction.
For the young person presenting with self-induction of seizures, the modality that a psychiatrist would need to practice over and above liaison model is a ‘child and family’ approach – addressing developmental tasks, family dynamics and incorporating age appropriate interventions. With the cognitively impaired patients possibly residing within group home or institution, psychological assessment and therapy involving all the carers of the individual patient may be required.