Serum prolactin in epilepsy and hysteria.

Trimble, M R

doi:10.1136/bmj.2.6153.1682

Cited by 234 publications

(95 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The PRL also rose 20 minutes -83 -after complex partial seizures, but not with simple partial attacks, the latter, by definition, having no alterations of consciousness. These results confirm the findings of others (Trimble 1978a;Abbott et al 1980;Collins et al 1982;Hoppener et al 1982), who found PRL elevation 15 to 20 minutes after major generalised tonic-clonic seizures and ECT, but not with hysterical attacks. Hoppener et al (1982) also reported elevated PRL levels in 8CY/o of patients with complex partial seizures.…”

Section: Gamma-aminobutyric Acid (Gaba)supporting

confidence: 82%

Depression in Patients With Epilepsy

Robertson¹

1984

Clinical Neuropharmacology

View full text Add to dashboard Cite

Section: Gamma-aminobutyric Acid (Gaba)supporting

confidence: 82%

Depression in Patients With Epilepsy

Robertson¹

1984

Clinical Neuropharmacology

View full text Add to dashboard Cite

“…Elevated serum PRL among patients with generalized epileptic seizures (ES) helped distinguish epilepsy from PNES. 88 Many studies have since been conducted measuring PRL among patients with PNES, finding that when PRL did not rise postictally, the average sensitivity to PNES was 89% across the studies. 89 Furthermore, studies of PRL in ES versus PNES have since shown that serum levels are elevated on average in 88% of generalized tonic clonic (GTC) epileptic seizures, in 64% of temporal lobe complex partial epileptic seizures (CPSs), and in 12% of simple partial epileptic seizures.…”

Section: Pnesmentioning

confidence: 99%

Functional Neuroanatomy and Neurophysiology of Functional Neurological Disorders (Conversion Disorder)

Voon¹,

Cavanna²,

Coburn³

et al. 2016

JNP

136

View full text Add to dashboard Cite

Much is known regarding the physical characteristics, comorbid symptoms, psychological makeup, and neuropsychological performance of patients with functional neurological disorders (FNDs)/conversion disorders. Gross neurostructural deficits do not account for the patients' deficits or symptoms. This review describes the literature focusing on potential neurobiological (i.e. functional neuroanatomic/neurophysiological) findings among individuals with FND, examining neuroimaging and neurophysiological studies of patients with the various forms of motor and sensory FND. In summary, neural networks and neurophysiologic mechanisms may mediate "functional" symptoms, reflecting neurobiological and intrapsychic processes. J Neuropsychiatry Clin Neurosci 2016; 28:168-190; doi: 10.1176/appi.neuropsych.14090217 Functional neurological disorders (FNDs; or psychogenic neurological symptoms), also known as conversion disorder, are a classic neuropsychiatric disorder, existing in the border between neurology and psychiatry. Unexplained neurological symptoms are common, occurring in up to one-third of patients in neurological outpatient clinics.1 Relative to disorders such as Parkinson's disease, FND is associated with similar levels of disability and physical quality of life with poorer mental health quality of life. 2 The prognosis is poor, with a recent reviewshowing that up to 40% of patients with FND report similar or worse outcomes at 7-year follow-up. 3 Given the frequency, consequences, prognosis, and burden, FND has been called a "crisis for neurology." 4 Despite this, FND is poorly understood. In the last decade, an increasing number of studies have focused on underlying neurobiological mechanisms. FND is defined in DSM-5 as the presence of one or more symptoms of altered voluntary or sensory function, with clinical findings providing evidence of incompatibility between the symptom and recognized neurological or medical conditions.5 The DSM-5 diagnosis differs from that of the DSM-IV diagnosis of conversion disorder by adding the criterion of incorporating physical diagnostic features and by relegating to the accompanying text the criteria requiring (a) an association with psychological stressors and (b) the exclusion of malingering or factitious disorder to make the diagnosis. DSM-5 FND diagnosis criteria now allow for potential greater interrater reliability, making them appropriate for research studies and greater compatibility with specialtyspecific diagnoses including psychogenic movement disorder (PMD) and psychogenic nonepileptic seizures (PNES). 6The putative biopsychosocial mechanisms underlying FND are complex and have been extensively reviewed.7 Our review focuses on the physiological mechanisms that may underlie FND and does not specifically focus on the extensive literature on the antecedents of early childhood experiences and temperament (Figure 1). At the outset, regarding the proposed model, we acknowledge that predisposing factors for functional neurological symptoms are not limited to genetics, te...

show abstract

“…A five to thirty-fold rise of prolactin above baseline levels can be measured approximately 20 minutes after the majority of tonic clonic generalized seizures, after most complex partial seizures but only after some simple partial attacks. Such a rise is never present after convulsive pseudoseizures (Trimble, 1978(Trimble, , 1986. 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).…”

Section: Neurohuldoral Studiesmentioning

confidence: 99%

Convulsive Pseudoseizures: A Review of Current Concepts

Savard

Andermann

1990

Behavioural Neurology

View full text Add to dashboard Cite

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.

show abstract

Serum prolactin in epilepsy and hysteria.

Cited by 234 publications

References 0 publications

Depression in Patients With Epilepsy

Depression in Patients With Epilepsy

Functional Neuroanatomy and Neurophysiology of Functional Neurological Disorders (Conversion Disorder)

Convulsive Pseudoseizures: A Review of Current Concepts

Contact Info

Product

Resources

About