Elsevier

Epilepsy & Behavior

Volume 5, Issue 4, August 2004, Pages 517-521
Epilepsy & Behavior

Serum prolactin levels for differentiation of nonepileptic versus true seizures: limited utility

https://doi.org/10.1016/j.yebeh.2004.03.004Get rights and content

Abstract

Frequently occurring nonepileptic psychogenic seizures (PNES) are a cause of substantial morbidity. Differentiation of these from true seizures may sometimes be very difficult. Serum prolactin level estimation following the event has been described as a useful test for this purpose. We conducted this study to assess the role of this test in diagnosis of PNES. Serum prolactin was estimated from venous blood samples of 19 patients (13 females, 6 males) with PNES and 17 patients (5 females, 12 males) with true complex partial seizures with or without secondary generalization. The age range was 12–39 years in the PNES group and 9–42 years in the true seizure group. Five patients (all females) in the PNES group (26.3%) had raised prolactin levels, all of them having greater than twice normal levels. In the true seizure group, 10 of 17 (58.8%) patients had raised levels; only 3 (17.6%) of these had greater than twice normal levels. The difference in percentage of patients with abnormal prolactin levels between these groups was not found to be significant. We demonstrate that serum prolactin level estimation is not a useful method for differentiation of psychogenic nonepileptic from true epileptic seizures.

Introduction

Psychogenic nonepileptic seizures (PNES) are a commonly occurring disorder among patients attending general neurology as well as epilepsy clinics. They can be a cause of significant morbidity affecting usually young individuals of both genders (the most productive population of society). Diagnosis of PNES is often a challenge. Between 9 and 50% of patients referred to specialized epilepsy centers have nonepileptic seizures [1], and in many of these patients both true epileptic and nonepileptic seizures coexist. Patients with PNES may have complex clinical semiology, escaping the suspicion of general physicians, pediatricians, and also trained neurologists, who may continue to treat them with antiepileptic drugs, which are without benefit and carry the risk of adverse drug reactions. Delay in diagnosis may result in progression of the underlying psychiatric illness, leading to resistance to therapy. Early suspicion and establishment of PNES are, therefore, essential in combating this common problem. Video-EEG with induction of events is a very useful method for differentiation of these events versus true complex partial seizures (CPS) and other seizure types [2], [3]. The differential diagnosis between PNES and CPS may pose a challenge, especially if there is rhythmic or violent motor activity during the PNES that obscures the EEG. Also, the facility for this electrophysiological test may not be easily available at most centers in most developing countries. A simpler test, which could easily and certainly differentiate PNES from true CPS, is very desirable, especially at small centers. Raised serum prolactin levels have been described following temporal lobe complex partial seizures and found to be a valuable tool in the differentiation of PNES against CPS [4], [5], [6], [7]. Reports on their sensitivity are conflicting. A few reports, most published several years ago, demonstrate conflicting results regarding utility of this tool in differentiating true seizures from PNES [8], [9]. In previous studies evaluating serum prolactin levels in similar patients, PNES have been diagnosed predominantly with clinical history, without confirmation by video-EEG. We conducted this study with the aim of comparing postictal serum prolactin levels in patients with PNES versus those with CPS, both diagnosed by video-EEG.

Section snippets

Material and methods

We recruited patients attending neurology services at the All India Institute of Medical Sciences from January 2002 to January 2003. Patients were recruited into two groups, PNES and CPS.

Results

There were 19 patients (13 females, 6 males) in the age range 12–39 (mean 20.05 ± 9.5) in the NES group and 17 patients (5 females, 12 males), in the age range 9–42 (mean 22.35 ± 7.07) in the CPS group. The mean duration of illness in the NES group was 3.31 ± 3.88 years (range 0.08–14 years); that for the CPS group was 3.78 ± 6.06 years (range 0.33–19 years) (Table 3).

Nine of the nineteen patients in the NES group had minimal motor activity; i.e., during the major part of their events they would lie

Discussion

We observed no significant difference in the serum prolactin levels estimated within 15–20 min of either PNES or CPS despite marked differences in gender distribution. We also found no correlation between elevated serum prolactin and excessive motor activity in either true or psychogenic events.

Serum prolactin level estimation has been considered one of the methods to be used for differentiation of true CPS from PNES. Many studies addressing this issue have concluded that serum prolactin levels

References (13)

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    There were no pronounced changes in PRL after PNES. Seven articles analyzed statistical differences in PRL levels (Shukla et al., 2004; Aydin et al., 2011; Willert et al., 2004; Tharyan et al., 1988; Alving, 1998; Singh and Jana, 1994; Pritchard et al., 1985); six showed that PRL levels were significantly higher in ES patient groups than in patients with PNES (Aydin et al., 2011; Willert et al., 2004; Tharyan et al., 1988; Alving, 1998; Singh and Jana, 1994; Pritchard et al., 1985). In one study, there was no significant difference in PRL levels between ES and PNES groups (Shukla et al., 2004).

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    Serum prolactin levels rise to concentrations greater than 500 IU/mL in more than 90% of patients after GCTS and 60% of patients after CPS, 10–20 minutes after the attack (Trimble, 1986; Mellers, 2005). Positive results are possible in PNES and are commonly found after syncope (Trimble, 1986; Oribe et al., 1996; Alving, 1998; Shukla et al., 2004). Little is known about prolactin levels after other organic imitators of seizures.

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