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Treatments for Depression
We shall now consider how the models of depression outlined above, have
attempted to produce effective methods of treatment for depression.
As always these can be split into medical treatments that assume
physical intervention such as drugs are needed to put right altered
brain chemistry and psychological methods that assume talking cures are
required to put right irrational thinking or solve unconscious
conflicts.
As we shall see, depression is unusual in that both medical and
psychological interventions seem to be crucial and work particularly
well in conjunction with oneanother. This is not always the case, for
example, schizophrenia seems better suited to medical approaches and
phobias and anxiety disorders are mostly best resolved using
psychological. Although this is an over-simplification and others would
undoubtedly disagree.
Medical
treatments
Drugs appear to be the treatment of choice. Go to your GP suffering
from depression and by far the most likely treatment will taking two
tablets a day. However, over the past thirty years the drugs have
changed and the choice has increased and improved. We shall look at
three major categories, two of which have a similar mechanism at the
synapse.
1. MAOIs (monoamine
oxidase inhibitors)
Do exactly what they say on the tin… albeit a rather complex tin!
For example: Nardil (phenelzine) and Iproniazid
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Remember our
American cousins refer to adrenaline as epinephrine (hence the
epi-pen) that releases adrenaline.
Therefore
there should be no surprise to find that noradrenaline becomes
norepinephrine.
Note:
adrenaline is Latin for ‘on the kidney.’
Epinephrine is
Greek for ‘on the kidney.’
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Having been released into the synapse, serotonin and noradrenaline are
quickly broken down by the enzyme monoamine oxidase. This will
obviously reduce the amount of these two chemicals available. MAOIs
inhibit (or prevent) the action of monoamine oxidase so results in
higher levels of serotonin and noradrenaline in the synapse.
Evaluation of MAOIs
These are seen as being the least effective of the anti-depressants.
According to Bennett (2006) they have a 50% success rate.
Side effects include increased blood pressure and increased risk of
cerebral haemorrhage, especially if taken with yeast products, bananas
or fish!
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2. Tricyclics
For example:
Dosulepin
(dothiepin),
imipramine
and
amitriptyline
Serotonin and noradrenaline are released into the synapse. On the
pre-synaptic side there are re-uptake sites that reabsorb the chemicals
very quickly. Tricyclics act by blocking these sites (or channels) so
again result in more of the chemical being available in the synapse for
a longer period of time. Tricyclics (0ften referred to as TCA for
tricyclic antidepressant) are so called because of their three carbon
ring structure.
Evaluation of
tricyclics
They are diagnosed for both mild and severe depression and claim to have
a 60-65% success rate.
However, they are probably the most troublesome of all the
antidepressants usually prescribed. Since they work on serotonin and
noradrenaline pathways they have a number of side-effects, particularly
effecting the heart and arteries. Others include:
Dry mouth
Constipation
-bran cereals, prunes,
fruit, and vegetables should be in the diet
Bladder problems
-emptying the bladder
completely may be difficult
Sexual problems
Blurred vision, dizziness and drowsiness.
However, these pale into insignificance compared to their major side
effect. They are potentially lethal in large doses! Not good to be
prescribed to any patient and certainly not to people suffering from
depression, one of whose symptoms may be thoughts of death and suicide.
Newer tricyclics generally have fewer side effects.
General evaluation of
antidepressants
It is worth pointing out that all of these drugs take weeks to work
which suggests their mechanism of action is far more complex than the
above explanations would seem to suggest. In fact we don’t know exactly
how antidepressants bring about the alteration in mood. As mentioned
earlier when looking at the medical model, SSRIs may work by altering
the serotonin system in the brain. Some even believe that the change is
to neural growth in the hippocampus (which would explain the four or
five week delay).
There are concerns that antidepressants are being over-prescribed
(compare to anxiolytics such as valium in the 1970s). In 2004 a survey
of GPs in the UK found that 80% admitted prescribing Prozac or Seroxat
when patients probably just needed someone to talk to!
SSRIs Next page
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