|
|
Notes:
- Given these preclinical
results, it was postulated that pindolol may augment presynaptic serotonergic
functioning in SSRI-treated patients by taking the negative feedback
loop out of play, while not hindering postsynaptic hippocampal responses
that contribute to the antidepressant effect. Artigas, 1995:969 (5)
- Artigas et al
tested this hypothesis in a pilot study that examined the ability of
pindolol to reduce the latency period in patients with depression who
were being treated with the SSRI paroxetine.
- Inclusion criteria
were as follows: occurrence of a major depressive disorder, with a minimum
Hamilton Rating Scale for Depression (HAM-D) score of 20 and absence
of any physical illness or pregnancy.
- Patients were
prescribed paroxetine (20 mg/d) and pindolol (2.5 mg tid); none of these
patients had received prior treatment.
- This graph shows
the change in HAM-D scores before and after treatment with paroxetine
plus pindolol. These five patients experienced rapid improvement.
- Four of the patients
experienced a complete remission in less than 1 week, and one patient
experienced a partial recovery (reduction of HAM-D score from 27 to
13).
- Two other patients
(not shown in graph) did not improve in 2 weeks. Artigas, 1994:249 (4)
- The data indicate
that pindolol induces a dramatic and rapid improvement of the antidepressant
activity of SSRIs.
- The onset
of action was reduced, and a rapid and full antidepressant response
occured in patients who were resistant to treatment with SSRIs.
- Pindolol thus
appears to make the serotonergic neuron respond to the combination of
pindolol with an SSRI in the same manner that it does following long-term
treatment with an SSRI alone. It induces a response in the unresponsive
neurons of a refractory patient that is not achieved with an SSRI alone.
Artigas, 1994:250
- It has also
been suggested that pindolol blockade of b-adrenergic receptors
may also contribute to the augmenting response. Anderson, 1996:
256 (4)
|
