Serum prolactin during status epilepticus.

Tomson, Torbjörn; Lindbom, Ulla; Nilsson, Bengt; Svanborg, Eva; Andersson, D. E. H.

doi:10.1136/jnnp.52.12.1435

Cited by 32 publications

(11 citation statements)

References 15 publications

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“…A gradual lessening of the expected prolactin rise occurs when serial epileptic seizures occur one after another: exhaustion of the central pituitary prolactin store may be the cause (Berkovic, 1984). One important implication is that the absence of a prolactin rise accompanying pseudostatus epilepticus is invalidated as the absence of such a rise is the rule in true status epilepticus (Tomson et at., 1989).…”

Section: Neurohuldoral Studiesmentioning

confidence: 99%

Convulsive Pseudoseizures: A Review of Current Concepts

Savard

Andermann

1990

Behavioural Neurology

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Convulsive pseudoseizures thought to represent psychiatric disease can usually be detected early if they are considered in the epileptologist's differential diagnosis. No single diagnostic criterion for this behavioural disorder is known to be pathognomonic. Epilepsy and all physiological explanations have to be thoroughly ruled out and positive evidence of relevant psychopathology has to be gathered. The presence of pseudo seizures often heralds severe psychopathology, most frequently major affective disorder and major personality disorder, and occasionally, factitious disorder. Pseudoseizures can coexist with epileptic seizures and are often triggered by anticonvulsant toxicity. Diagnostic problems are more likely to be encountered in patients with frontal or parietal epilepsies, and in patients whose severe psychopathology is refractory to psychiatric intervention.

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Section: Neurohuldoral Studiesmentioning

confidence: 99%

Convulsive Pseudoseizures: A Review of Current Concepts

Savard

Andermann

1990

Behavioural Neurology

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“…Another possibility is that some of the SUDEPs, being unwitnessed, may have had status epilepticus terminally. This is potentially relevant, as serum prolactin fails to be increased at the end of status epilepticus (37,38).…”

Section: Discussionmentioning

confidence: 99%

Prolactin Levels in Sudden Unexpected Death in Epilepsy

Opeskin

Clarke²,

Berkovic

2000

Epilepsia

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- Summary:Purpose: To assess serum prolactin levels in sudden unexpected death in epilepsy (SUDEP) and control groups to test the hypothesis that if seizures occur routinely as a terminal event in SUDEP, then raised prolactin levels may be an indicator of terminal seizure.Methods: Blood was taken for measurement of prolactin levels from subjects with SUDEP and three control groups. The control groups were those with epilepsy dying from causes other than epilepsy (e.g., ischemic heart disease or injuries), physiologically stressed individuals without epilepsy (they were admitted to the hospital after an acute illness and died after several hours to 3 days), and nonepileptic rapid deaths (these people collapsed suddenly and died at the scene). In the SUDEP group, evidence for terminal seizure was considered to be at least one of the following: body found half on, half off the bed, or urinary incontinence at the scene, or bitten lips or tongue at autopsy.The majority of sudden unexpected deaths in epilepsy (SUDEP) are unwitnessed, and in the absence of a better explanation, death is believed to be the result of a seizure. Clinical evidence for terminal seizure is found in up to about a third of cases (1-5), but whether seizures (either witnessed or unwitnessed) always precede SU-DEP is unknown.Serum prolactin has been observed to increase after generalized tonicklonic seizures (6-10) and complex partial seizures (8,ll-16), and the mechanism by which seizures are proposed to cause prolactin elevation involves propagation of the electrical discharge to the hypothalamus, thereby influencing prolactin release (16). Generally serum prolactin does not rise after simple partial or pseudoseizures (8,9,15,17,18 Results: There was evidence for terminal seizure at the scene or at autopsy in four of the 10 SUDEP cases. Serum prolactin levels were not significantly increased in the SUDEP group compared with the controls. None of the SUDEP subjects, including those with clinical evidence of a terminal seizure, had high prolactin levels characteristic of those observed after seizures in living subjects.Conclusions: Prolactin levels are not raised in SUDEP, even if there is evidence of terminal seizure. As prolactin takes 15-20 min to peak after a seizure in life, there may be insufficient time for a prolactin increase to occur in SUDEP. Thus prolactin levels cannot be used to determine if a deceased individual with epilepsy had a seizure or to answer the broad question whether SUDEP is always associated with a terminal seizure. Key Words: Prolactin-Epilepsy-Sudden unexpected death.The purpose of this study was to examine prolactin levels in SUDEP and control groups. If prolactin was consistently increased in SUDEP cases, but not in controls, then we would infer that terminal seizui-es had occurred in the SUDEP group.

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“…An SEinduced increase in the serum level of neuron-specific enolase has been observed in humans and in animal models [22,23]. The level of prolactin in plasma and serum has also been shown to transiently increase after SE in animals and humans [24,25].…”

Section: Potential Biomarkers In Sementioning

confidence: 97%

“…Serum/brain Increased after traumatic injury; predictive value for epileptogenesis to be determined [20] Prolactin CSF, serum Transiently increased in serum of SE animal model in early epileptogenesis; serum levels in SE patients not increased; predictive value for epileptogenesis to be determined [25,26] S100B = S100 calcium binding protein B; NSE = neuron-specific enolase; GFAP = glial fibrillary acidic protein; UCHL1 = ubiquitin carboxyl-terminal hydrolase L1; MBP = myelin basic protein; miR-9 = microRNA-9; SE = status epilepticus…”

Section: Pattern Combinationmentioning

confidence: 99%

Molecular Biomarkers of Epileptogenesis

Pitkänen

Łukasiuk

2011

Biomarkers Med.

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The heterogeneity of epilepsy syndromes and pathologies creates a great challenge for the search for biomarkers. Not surprisingly, identification of a marker that is specific and sensitive for a given epileptogenic pathology remains an unmet need. There have, however, been several studies of major epileptogenic etiologies like traumatic brain injury that aimed to identify molecular markers in blood and cerebrospinal fluid that predict outcome, by using proteomics and metabolomics. Unfortunately, epileptogenesis has not been analyzed as an outcome measure. Another question to be explored is whether a palette of molecular markers is needed, rather than a single molecule, with each marker probing a different component of epileptogenic pathology. Further, perhaps multiple biomarker platforms (e.g., imaging, proteomics, electrophysiology) should be used in combination and/or in a defined temporal sequence.

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Serum prolactin during status epilepticus.

Cited by 32 publications

References 15 publications

Convulsive Pseudoseizures: A Review of Current Concepts

Convulsive Pseudoseizures: A Review of Current Concepts

Prolactin Levels in Sudden Unexpected Death in Epilepsy

Molecular Biomarkers of Epileptogenesis

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