Anticonvulsant profile of flunarizine

Anticonvulsant profile of flunarizine

441 62 ANTICONVULSANT PROFILE OF FLUNARIZINE Clincke, G., se, Belgium The effect Ashton, of phenobarbital netrarol), Bode1 of CAM, i.e. ...

77KB Sizes 2 Downloads 164 Views

441

62

ANTICONVULSANT PROFILE OF FLUNARIZINE Clincke,

G.,

se,

Belgium

The

effect

Ashton,

of

phenobarbital

netrarol), Bode1

of

CAM,

i.e.

flu oral

also

D..

flunarizine

(flu)

in

and sodium valproate,has electrically-induced

epilepsy it

the

administration

the

anticonvulsant

action

suggested

flu

that

This uas confirwd

could

comparison

antagonizes clonic

seizures

anticonvulsant

compound of

of Neuropharmacalagy,

with

been assessed

seizures).

preferentially

antagonizes

Department

flu

is

blind

profile

the

tonic

evoked potency

well absorbed.

exceeded

be useful

in double

Its

24 h.

cross-over

In

Both the

in the treatment

stimulation) of

similar contrast

the

to to

and

that

that

induced

stimulation

epilepsy

profile using

Bee:

(CARB). a

with

genetic DIPH and

convulsions.

in both after

in

seen

rat

However,

and dogs.

After

systemicdrug injection

DIPH and CAM the

anticonvulsant

of partial

clinical

resembles of

g-2340

(allyglycine,bicuculline,

convulsions

action

component

Pharmaceutics.

(DIPH). carbamazepine

chemically-induced

by amygdala uas

Janssen

diphenylhydantoin

against

amygdal

(electroshock,

(audiogenic

indicanting that the

63

A. -

Nauquier.

duration

and the duration a single

daily

of

the

of action

dose.

trials.

Brain Ischemia and neurotransmitter changes: relevance to migraine pathophysiology and treatment. Bono G., Micieli G., Nappi G. - Headache Centre - University of Pavia - Italy The role of cerebral hypoxia/ischemia in migraine pathophysiology is still unclear. Similarities and differences between TIAs and migraine attacks, in particular those associated with focal neurological disturbances have been discussed and headache of the Ischemic CerebrovascularDisorders (IO) proposed as a model for investigating these problems. A central neurotransmitter derangement in the events triggering/precipitating ischemia is well known; opioid antagonism by naloxone was found able to reverse focal damage in ICVD patients as well as to shorten migraine prodromes; other events (metabolic) possibly involving hypoxia such as spreading depression of cortical activity have also been proposed. Flunarizine effectiveness in migraine has been ascribed to prevention of hypoxic/ischemic phenomena; a critical rCBF reduction, however, was not demonstrated in common migraine. The present study confirms Flunarizine as a wide spectrum therapy for migraine, without discriminatingbetween clinical forms (classic or common) nor between responders and non-responders characteristics.The results are discussed in the light of a possible action of the drug on neurotransmitters involved in pain control systems and adaptive responses to enviromental stimuli.