G.D. Kotzalidis, V. Orlandi, R. Brugnoli, P. Pancheri - Vol.
7, Dicembre 2001, num.4
Testo
Immagini Bibliografia
Summary Riassunto Indice
Suggerimenti per la neurobiologia
del disturbo di panico: il contributo degli studi clinici
Suggestions for the neurobiology of panic
disorder: the contribution of clinical studies
Clinical studies suggest that the circuitry involved in panic disorder employs
a multitude of neurotransmitters, such as neuropeptides (cholecystokinin and
CRF), serotonin, noradrenaline, and aminoacids (GABA, glutamate and/or aspartate).
In particular, the effectiveness of serotonin transporter inhibitors, such as
the SSRIs and clomipramine, compared to the mixed 5-HT/noradrenaline uptake
inhibitor imipramine, and the relative ineffectiveness of 5-HT1A partial agonists,
suggest that transporter inhibition is the most important mechanism involved
(but the details of its action are at present elusive), with 5-HT2A inhibition
coming next. Generalized activation of all bioamines, such as that occurring
with MAO inhibition, appears to both facilitate and hamper clinical effect.
The importance of the noradrenergic system as the crucial system involved, appears
much weakened by the results of clinical trials of noradrenaline transporter
inhibitors, while alpha2 agonists show only a transient effect. The benzodiazepines
appear to be important through GABAA facilitation, although some benzodiazepines
(alprazolam and clonazepam) fair better than other. Mood stabilisers show limited
efficacy, hence restraining the importance of kindling mechanisms. Psychotherapy
(mostly cognitive) usually potentiates the effect of drugs and might act through
the same or complementary mechanisms to set-off hyperactivity within the "fear
circuitry".
