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العنوان
Seretonin in Epilepsy\
المؤلف
Ahmed, Engy Sherif Mohamed.
هيئة الاعداد
باحث / Engy Sherif Mohamed Ahmed
مشرف / Magd Fouad Zakaria
مشرف / Ahmed Abd El Monem Gaber
مناقش / Mohamed Amir Tork
تاريخ النشر
2014.
عدد الصفحات
200P. :
اللغة
الإنجليزية
الدرجة
ماجستير
التخصص
الطب النفسي والصحة العقلية
تاريخ الإجازة
1/1/2014
مكان الإجازة
جامعة عين شمس - كلية الطب - المخ والاعصاب والطب النفسى
الفهرس
Only 14 pages are availabe for public view

Abstract

Epilepsy and depression share an unusually high
coincidence suggestive of a common etiology. Disrupted
production of adult-born hippocampal granule cells in both
disorders may contribute to this high coincidence. chronic
stress and depression are associated with decreased granule
cell neurogenesis. Epilepsy is associated with increased
production – but aberrant integration – of new cells early in
the disease and decreased production late in the disease
also. In both cases, this review suggests these changes in
neurogenesis play important roles in their respective
diseases.also they are both result from dysregulation of
hypothalamo pituitary adreno cortical axis and
corticosteroids.
If there is shared underlying pathology that can lead to
both seizures and depression, then it would be expected that
treatments for one condition would improve the symptoms
of the other. This appears to be the case, since some
treatments for depression are effective against seizures, and
some anticonvulsants are effective in management of
mood/affective disorders.
Exposure to older generations of antidepressants
(notably tricyclic antidepressants and bupropion) can
increase seizure frequency. However, a growing body of
evidence suggests that newer (‘second generation’) antidepressants, such as selective serotonin reuptake
inhibitors or serotonin-noradrenaline reuptake inhibitors,
have markedly less effect on excitability and may lead to
improvements in epilepsy severity.
In general, an increase in extracellular 5-HT levels
inhibits many types of seizures and a decrease does the
opposite (Several anti-epileptic drugs including phenytoin,
carbamazepine, valproic acid, lamotrigine and zonisamide
all cause an increase in extracellular 5-HT, and the elevated
5-HT is thought to contribute to their mechanism of action.
Also sudden unexpected death in epilepsy is one of
epileptic comorbidities has a link to serotonergic pathway,
as the frequency of respiratory arrest is markedly reduced
by pretreatment with SSRIs.