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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.
-
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 |