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Title of Thesis

Zaheer Hussain Azeemi
Institute/University/Department Details
University of Karachi/ Department of Physiology
Number of Pages
Keywords (Extracted from title, table of contents and abstract of thesis)
menstruation, seizures, epileptic patients, catamenial epileptics, non-catamenial epileptics, semi-catamenial epileptics, catamenial epileptics, non-catamenial epileptics, epilepsy

The present study is an attempt to determine the alterations influencing the premenstrual exacerbation of primary and secondary generalized tonic-clonic seizures documented previously. All possible ways were employed to minimize the generally described inconsistencies. The epileptic patients (n:433), all women were categorized into two main groups: Group-I (with single seizure frequency pattern) and Group-II (with multiple seizure frequency pattern). Each group comprised catamenial epileptics, non-catamenial epileptics and normal controls. Epileptic women with seizures related/unrelated to a menstruation related cycle phase were suggested to be further classified into three sub-types according to seizure severity/dispersion pattern as: Semi-catamenial, catamenial and non-catamenial epileptics. All patient groups showed significant decrease in plasma calcium. It thus seemed a common etiological factor in seizure disorders. Catamenial epileptic groups of estradiol-17B, prolactin, cortisol, sodium, basal body temperature and fall in plasma calcium, all with concomitant significant exacerbation of seizres. Furthermore, plasma progesterone varied significantly only in catamenial epileptic patients with single seizure frequency pattern; whereas plasma LH was found to be altered in only catamenial epileptic patients with multiple seizure frequency pattern. The present study, thus suggests that the etiological role of both the disturbance in water metabolism and endocrine chages co-exists, in presently studied catamenial epileptic women. Hence, this study provides information of possible interactions present between both sets of etiologies involving alteration in neuronal excitability, gonad-brain relationship, pituitary-adrenal system, pituitary-gonad-adrenal system, and collectively as neuro-hypothalamo-hypophyseo-gonado-adrenal system and collectively as neuro-hypothalamo-hypophyseo-gonado-adrenal system. The neural segment of this system comprised also the alterations in electrolytes which in the present study are suggested to be related on one hand to change in neural excitability and behaviour and on other to systemic changes

The alterations noted in this set of observations, thus, may show their significance in view of excitation/inhibition equilibrium caused by the mentioned set of complex interactions among various substances and physiological factors involved in seizure exacerbation in catamenial epileptics. Probably these changes are either secondary to seizure exacerbations, or some of them are altered, in turn changing the concentrations of other constituents and seizure activity and vice versa, the interpretation of which needs comprehensive studies to be conducted with integrative clinic-experimental approach

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1647.06 KB
S. No. Chapter Title of the Chapters Page Size (KB)
1 0 Contents
137.86 KB
2 1 Introduction 1
36.8 KB
3 2 Review Of Literature 5
170.26 KB
  2.1 Epilepsy 5
  2.2 Catamenial Epilepsy 8
4 3 Materials And Methods 26
289.24 KB
  3.1 Subjects 26
  3.2 Manstrual Cycle 28
  3.3 Clinical And Neurological Tests 29
  3.4 Electroencephalography 32
  3.5 Sample Collection 33
  3.6 Biochemical Tests 33
  3.7 Radioimmunoassay Of Hormones 37
  3.8 Method Of Statistical Analysis And Presentation 66
5 4 Results 67
890.93 KB
  4.1 Clinical And Physiological Determinations 72
  4.2 Hormonal And Biochemical Determinations 128
6 5 Discussion 187
256.81 KB
  5.1 Estrogen 187
  5.2 Progesterone 194
  5.3 Cortisol 198
  5.4 Gonadotrophic Hormones ( Fsh/Lh ) 202
  5.5 Prolactin 205
  5.6 Plasma Sodium 206
  5.7 Basal Body Weight 207
  5.8 Plasma Potassium 208
  5.9 Plasma Calcium 209
  5.10 Basal Body Temperature 211
  5.11 Clinical And Physiological Parameters 212
  5.12 Conclusion 214
7 6 References 220
164.84 KB