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Serum prolactin
Serum prolactin rises after tonic-clonic epileptic seizures, peaking between 20 and 30 minutes
following the seizure41. The post-ictal prolactin level should be compared with a baseline
measure taken at approximately the same time of day. A prolactin rise is less reliable
following complex partial seizures, may be absent following serial epileptic seizures or in
status epilepticus, and is not seen following simple partial seizures. False positive rises are
now known to occur following syncope42 and, more significantly, DS43 and the test is falling
out of favour. However, a negative finding after an apparent tonic-clonic seizure may still be
very helpful. A recent study has reported higher creatine kinase levels in patients with tonic-
clonic status compared with DS status but again there were false positives and negatives67.

Psychiatric formulation: an aetiological model of DS

By analogy with epileptic seizures, which are a symptom of paroxysmal neurophysiological
abnormality that may have many causes, a useful model of DS would attempt to account for
the mechanisms underlying individual seizures as well as for background predisposing
factors. As yet there is no widely agreed model. However, many putative risk factors for DS
have now been reported and studies seeking to clarify the psychiatric phenomenology and the
neurophysiology of dissociative states are ongoing.

Dissociation
For practical purposes, dissociation may be defined as a psychologically mediated alteration
of awareness and/or control of neurological function. Some have argued for more specific
uses of the term44, but defined in this way dissociation encompasses a spectrum of mental
processes including normal phenomena, such as focused or divided attention (e.g. ‘domestic
deafness’, mental absorption), and pathological states involving perceptual, cognitive and
motor function. The advantage of such a definition is that, by explicitly assuming (and it is
an assumption) that dissociative disorders lie on a continuum with normal experience, it
facilitates an empathic understanding of what might otherwise seem unintelligible, if not
frankly unbelievable, behaviour. This is equally important for professionals, patients and
carers.

The psychophysiological basis for dissociative states is not understood. Many patients with
DS describe becoming gradually cut off or distant from their environment and experience
symptoms of autonomic arousal during their seizures. This suggests that for some patients,
DS may represent a dissociative response to paroxysmal physiological arousal triggered by
intense emotion. Some patients may even be aware of ‘giving in’ to a trance-like state to
escape from distressing emotions80. Most patients, however, deny emotional symptoms in
their attack (DS may be likened to ‘panic attacks without panic’)66, the hypothesis being that
the triggering emotion is concealed by the dissociative state (for Freud this was the primary
gain of hysterical symptoms). However, clinical experience suggests that a proportion of
patients who initially deny triggers for their attacks are eventually able to recognise highly
specific and emotive cues (for example related to traumatic past experiences). Clearly, this
model of dissociative mechanisms gives rise to a number of testable hypotheses which require
further research.

Predisposing, precipitating and maintaining factors
Studies of psychosocial correlates of DS have revealed a number of potential predisposing,
precipitating and maintaining factors which are summarised in Table 3. Adverse or traumatic
experiences, particularly in childhood, are a common underlying theme. Sexual, physical and
emotional abuse are well replicated associations45-47,68 but other traumatic experiences or
situations that foster enduring low self-esteem, for example being bullied at school or
unrecognised learning difficulties, may be over-represented48. The high prevalence of