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Mental Health

Seasonal affective disorder (SAD)

Recurrent major depressive disorder with a seasonal pattern usually beginning in fall and continuing into winter months.

Introduction

Recurrent major depressive disorder with a seasonal pattern usually beginning in fall and continuing into winter months.


Aetiology

Those most at risk are female, are younger, live far from the equator, and have family histories of depression, bipolar disorder, or SAD.


Pathophysiology

Phase-shift hypothesis:

Posits that there is an optimal relationship in the alignment of the sleep-wake cycle and the endogenous circadian rhythm. During the fall and winter, as day length shortens, the circadian rhythm begins to drift later with respect to clock time and the sleep-wake cycle. This phase delay is hypothesized to bring about mood symptoms

One method to measure this circadian misalignment is known as the phase-angle difference (PAD), and is calculated as the difference in time between the dim light melatonin onset (DLMO, the time of evening rise in melatonin) and mid-sleep

Proposed pathological mechanisms of Seasonal Affective Disorder: (A) The phase-shift hypothesis. Compared to control individuals (red broken line), in SAD patients (blue broken line) the daily circadian rhythm is delayed with respect to clock time, creating a discordance between the circadian rhythm and the clock time/sleep-wake cycle. The discordance, which essentially produces a winter-long jet lag for patients with SAD, is hypothesized to lead to depressive symptoms. (B) The serotonin hypothesis. In control individuals there is greater binding potential at the pre-synaptic serotonin transporter during fall/winter compared to summer months and in SAD patients, there is even greater binding potential during fall/winter compared to healthy individuals. Greater binding potential is schematized in the figure through the use of greater number and/or thicker representations of the transporters. According to the monoamine hypothesis of depression, if greater binding at the transporter results in greater uptake of serotonin into the presynaptic neuron and less available serotonin in the synapse cleft, the outcome could be the appearance of depressive symptoms in affected individuals. | Campbell, P. D., Miller, A. M., & Woesner, M. E. (2017). Bright Light Therapy: Seasonal Affective Disorder and Beyond. The Einstein journal of biology and medicine : EJBM, 32, E13–E25.

Clinical faetures

Diagnostic and Statistical Manual of Mental Disorders (DSM-5) criteria:

Criteria for depression with a seasonal pattern include having depression that begins and ends during a specific season every year (with full remittance during other seasons) for at least 2 years and having more seasons of depression than seasons without depression over a lifetime.

Seasonal pattern disorders occur most frequently in winter although they can also occur in summer.


Diagnosis

Screening instruments:

  • Seasonal Pattern Assessment Questionnaire (SPAQ): Retrospective, self-administered tool that screens for the existence of SAD and S-SAD.

Management

Treatment approaches typically include combinations of antidepressant medication, light therapy, Vitamin D, and counselling.

Bright light therapy (BLT)

First-line treatment of SAD. BLT may function by either correcting the winter circadian rhythm phase delay or by increasing synaptic serotonin, possibly in the serotonin-rich midbrain, a target of retinofugal pathways or indeed, by both mechanisms
Mechanisms of BLT action based on proposed pathophysiology of Seasonal Affective Disorder: (A) BLT corrects the phase delay. Pre- and post-BLT treatment are displayed as blue and purple broken lines respectively. Morning BLT treatment corrects the phase delay by shifting the circadian rhythm earlier (to the left) leading to less discordance between the circadian rhythm and the clock time/sleep-wake cycle. (B) BLT increases available serotonin. BLT treatment during the fall/winter reduces the serotonin transporter binding potential, theoretically leading to less uptake, and a greater amount of available serotonin in the synaptic cleft. | Campbell, P. D., Miller, A. M., & Woesner, M. E. (2017). Bright Light Therapy: Seasonal Affective Disorder and Beyond. The Einstein journal of biology and medicine : EJBM, 32, E13–E25.

Antidepressant therapy:

SAD, like other depressions, is believed to be associated with a dysfunction in brain serotonin activity. Therefore, second generation antidepressants (SGAs) are preferred.
  • Selective Serotonin Reuptake Inhibitors (SSRIs): Fluoxetine (Prozac)

Vitamin D supplementation:

Many people with SAD and S-SAD have insufficient or deficient levels of Vitamin D abd taking 100,000 IU daily may improve their symptoms

Non-pharmacological management:

  • Cognitive Behavioral Therapy (CBT)
  • Transcendental Meditation (TM) and other forms of mindfulness, yoga, walking, and exercise that is personally enjoyable

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