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P-160 - Bipolar Disorder, Migraine and Epilepsy - a Shared Pathogenesis?

Published online by Cambridge University Press:  15 April 2020

J. Holland
Affiliation:
School of Clinical Medicine, University of Cambridge, Cambridge, UK
R. Doughty
Affiliation:
Psychiatry, South Essex Partnership University Foundation NHS Trust, Bedford, UK
M. Agius
Affiliation:
Psychiatry, South Essex Partnership University Foundation NHS Trust, Bedford, UK Psychiatry, University of Cambridge, Cambridge, UK
R. Zaman
Affiliation:
Psychiatry, South Essex Partnership University Foundation NHS Trust, Bedford, UK Psychiatry, University of Cambridge, Cambridge, UK

Abstract

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Introduction

Bipolar, migraine and epilepsy disorders are often co-morbid conditions. This link may help explain their pathogenesis, diagnosis and treatment. The more understood mechanisms by which epilepsy and migraine arise may offer new insight into bipolar disorder neurobiology. Here, we examine the prevalence of these disorders in a UK community mental health team. We then report on a wide-ranging literature review highlighting shared features of the conditions and suggest how they may develop along a similar pathway.

Objectives

  1. Examine co-morbidity prevalence in Bedford East Community Mental Health Team outpatients.

  2. Identify overlapping aspects of neurobiology.

  3. Explain how these may relate to each other.

Aims

  1. Add to existing co-morbidity data.

  2. Offer insight into bipolar neurobiology.

Methods

Manual search of an outpatient database covering January 2010 to February 2011 (n = 615), identifying cases of bipolar disorder, migraine and epilepsy.

Results

Diagnoses Prevalence

Bipolar 19.8%

Migraine 5.4%

Epilepsy 1.1%

Bipolar + epilepsy 0.16%; 0.82% of bipolar patients.

Bipolar + migraine 1.1%; 5.7% of bipolar patients.

Conclusions

Contrasting with previous studies, co-morbidity was much lower - likely to reflect under-reporting of secondary diagnoses. Most literature supports a connection between the disorders. Common features exist regarding disease course, pharmacological treatment, altered cellular and loss of network stability.

We discuss the relationship between genes and environment, and hence impact on Metabolic factors, Ion Channels and neurotropic factors, which affect network changes, Hyper-excitability,Cellular vulnerability and Loss of ‘stabilising’ circuits. We suggest an accumulating pathological change towards disease and we note accompanying Inflammatory/Immune responses.

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Abstract
Copyright
Copyright © European Psychiatric Association 2012
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