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Seasonal affective disorder

What is seasonal affective disorder?

Seasonal affcetive disorder is a psychiatric  (SAD), or the "winter blues", is a psychiatric disorder where individuals display recurrent depressie symptoms typically during the winter period and in some cases, in the summer. SAD occurs in patients suffering from bipolar or major depressive disorder. Approximately 6% of adults suffer from SAD, and the mean age of SAD presentation is 27 years. Such patients recieve considerably more prescriptions and more frequently referred to secondary care. If the condition presents in childhood, the prevalence of it is equal between both genders. During child bearing age, the chances of suffering from it is four times greater in women. THere's a decreased risk of developing as the patient gets older, where the prevalace between gender are equal

 

As seasonal affective disorder is a variant of depression, typical symptoms remain shared. However sufferers also display atypical symptoms as shown below 

 

Joseph Shildkraut's monamine hypothesis has dominated our understanding of the biogenic causes of the     depression since 1965. The monoamine hypothesis proposes that depression is a consequence of a deficit of monoamines (namely serotonin, and noradrenaline), within certain regions of the brain. Below is a diagram illustrating how this deficit of monamines occur. 

 

 

 

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Monoamine hypothesis 

Limitations to the monoamine theory 

Monoamine oxidase inhibitors and TCA's are used to alleviate depressive symptoms,

Criticism: however after treatment is initiated it takes approximately 2-3 weeks of persistent therapy for depressive symptoms to (disappear)

Possible explanation: this could be due to a secondary brain alterration rather than a drug effect 

 

Criticism: Low  levels of NA and 5- HT do NOT induce a depressive state

Possible explanation: the old antihypertensive reserpine did induce a depressive state in some patients 

 

Criticism: The hypothesis does not explain why antidepressanst are effective in other disorders such as social phobia?  

 

Criticism: why are some drugs that enhance the reuptake of 5-HT effective forms of antidepressants? 

 

Criticism: why levels of 5-HT receptors are decreased, and not increased when the patient undergoes long term Electroconvulsive therapy   

 

 

 

 

Serotonergic transmission

1. Vesicles containing serotonin in the presynpatic neurone are transported to and fuses with PRESYNAPTIC MEMBRANE

Serotonin is then released into the SYNAPSE 

2. These vesicles then bind to serotonergic receptors present on the post synaptic neurone, triggering a nervous impulse. 

3. Serotonin levels decrease: 

Any unbound serotonin present in the synapse is either reabsorbed by the presynaptic neurone, or degraded by monoamine oxidase enzymes (noradrenaline is also degraded by these enzymes), thus causing a decrease in serotonin levels in the synapse. 

Serotonin is responsible for the regulation of: 

  • control of appetite 

  • sleep 

  • mood 

  • pain perception 

  • vomiting 

Noradrenaline is responsible for the regulation of: 

  • arousal 

  • mood

  • drive 

Therefore a DECREASE of these monoamines will negatively affect these functions. 

 

How do antidepressants work?

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