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Saturday, December 25, 2010

My view on atypical depression

Since I am suffering with atypical depression, I just analysed the mechanism of neurotransmission probably responsible for the observed symptoms like hypersomnia, hyperphagia and leaden paralysis.

The serotonergic neurotransmission may be normal in some areas of the brain (may be ascending 5-HT neurotransmission) and low in some parts of the brain (may be descending 5-HT neurotransmission which may be from prefrontal cortex and orbitofrontal cortex).

Noradrenergic neurotransmission may be normal (if the person is not having trait anxiety) or may be excessive (if the person is having trait anxiety).

Dopamine neurotransmission may be significantly impaired (both D1 and D2 type).

I feel it is the serotonin to dopamine ratio which is critical in some areas of the brain which is responsible for the observed symptoms.

High serotonin and low dopamine condition (improper ratio) might be leading to hypersomnia. Actually hypersomnia is not a condition of motivated willingness to remain in sleep. Rather it is a condition of unable to motivate oneself from getting up from the bed. So, I feel it is a condition of high serotonin and low dopamine. Because, when the sleep is not refreshing much, nobody will be willing to remain in bed for long period of time. It is the low dopaminergic neurotransmission which might be accountable for this.

The same high serotonin to low dopamine ratio would also be responsible for the hyperphagia. Because, serotonergic drugs induce carbohydrate cravings. So, increased serotonin levels would be leading to carbohydrate cravings thus leading to more food intake and weight gain.

The same high serotonin to low dopamine level would also be responsible for the fatigue, tiredness and heaviness in the legs. I suspect a low dopaminergic neurotransmission in basal ganglia.

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