Front Lobe Epilepsy & Bipolar Disorder:Can the Onset of a Manic Phase Trigger a Seizure?
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Q:  Front Lobe Epilepsy & Bipolar Disorder : Can the Onset of a Manic Phase Trigger a Seizure?


I am 21 years old and I was diagnosed with bipolar disorder 8 years ago. I also suffer from frontal and temporal lobe epilepsy (Grand Mal) and even with medication am currently having 1-2 seizures every 4-6 months. I know that bipolar has been linked to temporal lobe epilepsy but is there any indication that it may also have something to do with front lobe epilepsy? Is it also possible that the onset of a manic phase could trigger a seizure out of the temporal lobe?  

Dear Amanda -- 
Good questions, which unfortunately go beyond what we know.  You can tell, from the language in the abstract below, how fuzzy the relationship is. However, you might ask your local librarian to dig up this article for you.  The content should be easier to understand than this summary, I hope.  It's very close to the question you asked about a mania-seizure connection, which (as I read the abstract) has some support in the literature.  As for frontal lobe epilepsy and it's relation to bipolar disorder, all I can tell you there is that the connection I usually hear about is temporal lobe, as reflected also in the abstract. 

 
Epilepsia. 2004;45 Suppl 2:5-14. Related Articles, Links

Neurobiology of seizures and behavioral abnormalities.

Post RM.

Biological Psychiatry Branch, National Institute of Mental Health, National Institutes of Health, Department of Health and Human Services, Bethesda, Maryland 20892-1272, USA. Robert.Post@NIH.gov

Seizures are both caused by and induce a complex set of neurobiological alterations and adaptations. The animal model of amygdala kindling provides insight into the spatiotemporal evolution of these changes as a function of seizure development and progression. Intracellular, synaptic, and microstructural changes are revealed as related to both the primary pathophysiology of kindled seizure evolution and compensatory secondary, or endogenous anticonvulsant adaptations. At the level of gene expression, the balance of these pathological and adaptive processes (as augmented by exogenous medications) probably determines whether seizures will be manifest or suppressed and could account for aspects of their intermittency. As anxiety and emotion modulation are subserved by many of the same neuroanatomic substrates involved in the evolution of complex partial seizures, particularly those of the medial temporal lobe, it is readily conceptualized how vulnerability to a range of psychiatric disorders could be related to the primary or secondary neurochemical alterations associated with seizure disorders. The discrete and methodologically controlled elucidation of the cascades and spatiotemporal distributions of neurobiological alterations that accompany seizure evolution in the kindling model may help resolve some of the difficulty and complexity of elucidating these biobehavioral relationships in the clinic.
 

Good luck with your education about this relationship, and your efforts to manage it. 

Dr. Phelps
 

May, 2005

 

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