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The Ex Factor Guide

The Ex Factor by Brad Browning.
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The Ex Factor Guide Summary


4.8 stars out of 56 votes

Contents: 125 Page E-book
Author: Brad Browning

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Astrologysource Summary

Contents: Membership Site
Author: Deborah Fenlon-Browning
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Price: $16.00

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Treatment of aggression in epilepsy

Care should be taken to establish signs of depression or anxiety, since a close link between these psychopathological states and affective aggression in epilepsy has been established. Both should be treated medically and with psychotherapy at the same time (Goldstein, 1997 Lorenzen, 1973). Behavioural therapy in particular in patients with epilepsy and learning disability has been proven to be very effective (Davis, 1984 Holzapfel, 1998 Rapport, 1983). In the medical treatment of depression in patients with epilepsy, SSRIs or other new antidepressants like venlafaxine should be preferred to the old tricyclic antidepressants (TCA) since the latter are more likely to provoke seizures (Blumer, 1997 Lambert, 1999). In fact, an anticonvulsant effect of SSRIs is well documented in animal models of epilepsy (Browning, 1997 Lu, 1998 Pasini, 1996 Wada, 1995) and is also described in humans (Favale, 1995).

Peripheral mechanisms

Clark, K.B., Smith, D.C., Hassert, D.L., Browning, R.A., Naritoku, D.K. and Jensen, R.A. (1998). Posttraining electrical stimulation of vagal afferents with concomitant vagal efferent inactiva-tion enhances memory storage processes in the rat. Neurobiol Learning Memory, 70, 364-73. Clark, K.B., Naritoku, D.K., Smith, D.C., Browning, R.A. and Jensen, R.A. (1999). Enhanced recognition memory following vagus nerve stimulation in human subjects. Nature Neurosci, 2, 94-8. Krahl, S.E., Clark, K.B., Smith, D.C. and Browning, R.A. (1998). Locus coeruleus lesions suppress the seizure attenuating effects of vagus nerve stimulation. Epilepsia, 39, 709-14.

Summary And Conclusions

Brailowsky, S., Silva, B.C., Menini, C., Riche, D., and Naquet, R. 1989. Effects of localized, chronic GABA infusions into different cortical areas of the photosensitive baboon, Papio papio. Electroencephalogr Clin Neurophysiol 72 147-156. Browning, R.A., Wade, D.R., Marcincyzk, M., Long, G.L., and Jobe P.C. 1989. Regional brain abnormalities in norepinephrine uptake and dopmaine beta-hydroxylase activity in the genetically epilepsy-prone rat. J Pharmacol Exp Ther 249 229-235. Browning, R.A., Wang, C., Lanker, M.L., and Jobe, P.C. 1990. Elec-troshock- and pentylenetetrazol-induced seizures in genetically epilepsy-prone rats (GEPRs) differences in threshold and pattern. Epilepsy Res 6 1-11. Browning, R.A., Wang, C., Nelson, D.K., and Jobe, P.C. 1999. Effect of precollicular transection on audiogenic seizures in genetically epilepsy-prone rats. Exp Neurol 155 295-301. Bourn, W.M., and Garrett, R.L. 1983. Increased susceptibility of audiogenic rats to barbital withdrawal convulsions....


The issue of psychotropic drug treatment of depression in epilepsy is interlinked with that of the proconvulsant or anticonvulsant effects of antide-pressants. Tricyclic antidepressants developed a clinical reputation for convulsant liability soon after their introduction into therapeutics (Dailey and Naritoku, 1996). The concept that antidepressant medications are more likely to produce convulsions in patients with epilepsy than in patients without this disorder is intuitively appealing, and is seemingly compatible with the concept that seizure predisposition is fundamental to the definition of epilepsy. However, it is clear that the biology of seizure predisposition is not a single entity moreover, it is not clear whether the risk of seizure expression arises from the seizure liability itself or from a more complex predisposition inherent in the mechanisms of comorbidity between affective disorders and the epilepsies (Jobe and Browning, 2005).

Caas Craas

As the dosage of GABAAR antagonists is increased, clonic seizures appear. In fact, even though the seizures do not meet the criteria outlined in Table 2 for experimental absence seizures, these clonic seizures are used to screen for antiabsence activity of putative anticonvulsant drugs in the PTZ screening model. With a further increase in dosage, tonic seizures emerge. The CD95 for the induction of clonic seizures with PTZ, bicuculline, and picrotoxin in the mGluR4+ + mice is 45, 4.5, and 1.8mg kg, respectively (Snead et al., 2000). The clonic component observed with intermediate doses of PTZ (40-60 mg kg) may be correlated with the work of Browning and Nelson (1986), who showed that clonus restricted to the face and forelimbs depends on seizure discharge emanating from structures within the fore-brain for expression. Facial clonus mirrors the forebrain involvement and is typical of all rat models of generalized absence seizures (Table 3). The tonic seizures manifested in the face of...

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