A SAD story:

Seasonal Affective Disorder

Presented by Dr Pavan Kumar Chaired by Dr Aruna

Definition
Seasonal affective disorder (SAD) is a form of recurrent depressive or bipolar disorder. A syndrome in which depression developed during the autumn or winter and remitted in the spring or summer for at least 2 successive years. 2 subtypes: winter SAD and summer SAD, of which the former is far more frequent. Sub-syndromal SAD is a disorder with similar but milder symptoms that do not affect the patients ability to function.

Classification
SAD is listed as a specifier of either bipolar or recurrent major depressive disorder, with a seasonal pattern of major depressive episodes. The essential feature is the onset and remission of Major Depressive Episodes at characteristic times of the year. In most cases, the episodes begin in fall or winter and remit in spring. Less commonly, there may be recurrent summer depression episodes.

ICD 10
ICD-10 gives only provisional diagnostic criteria for SAD on the grounds that its status is uncertain. SAD is recognized as a form of bipolar affective or recurrent depressive disorder, with episodes of varying severity.

ICD 10 DCR
Seasonal affective disorder (Could be applied to Mood [Affective] Disorder, categories F30.-, F31-, F32.- and F33.-) A. Three or more episodes of Affective Disorder occurring with onset within the same 90-day period of the year for 3 or more consecutive years. B. Remissions also occur within a particular 90-day period of the year. C. Seasonal episodes substantially outnumber non-seasonal episodes that may have occurred.

Rosenthal et al.6 proposed operational criteria for the winter disorder: (1) A history of major affective disorder; (2) Development of such depressive episodes in the autumn or winter and remission by the following spring or summer in at least two consecutive years; (3) The absence of any other psychiatric disorder.

Epidemiology

Prevalence
The prevalence of winter-type seasonal pattern appears to vary with latitude, age, and sex. Prevalence increases with higher latitudes. Younger persons at higher risk for winter depressive episodes. Women - 60%--90% of persons with seasonal pattern The specifier applies to seasonal occurrence of full MDD episodes, some research - seasonal pattern may be - recurrent winter depressive episodes that do not meet criteria for a Major Depressive Episode.

 6 major seasonal patterns identified, winter variety (22%) was the MC, followed by the summer variety (10%). A few cases also during autumn (4%) and spring (2%). Community-based surveys on winter SAD prevalence between 1.3% and 3% in Europe, 2% and 3% in Canada, 0.8% and 9.7% in North America and 0% and 0.9% in Asia.

 During his clinical practice in the Punjab, India (2732N), Gupta observed the following 3 patterns of seasonal affective disorders: (1) hypomania or mania during the summer and depression in winter; (2) hypomania or mania in early winter and depression in middle and late winter and (3) severe depression in summer and hypomania or mania in winter.

Neurobiology

Pathogenesis
The decreasing daylight period as winter approaches -trigger a depressive episode, in people predisposed to winter SAD. No causal relation b/w incidence of winter SAD and the shortage of light or cooler temperatures. Although bright-light exposure is used in treatment, the cause of winter SAD may not be lack of light.

 Winter SAD may be triggered by sensitivity to factors that are common to various forms of RDD, which could be seen as a disorder driven by endogenous annual rhythms and characterized, by disturbed synthesis of indoleamines (melatonin and serotonin) during the year.

Light
Light incident on the retina produces a signal that progresses up the retinohypothalamic tract (RHT) to the suprachiasmatic nucleus (SCN) in the hypothalamus, which is believed to be the principal circadian pacemaker in mammals. melatonin theory of pineal function, which holds that the pineal body acts as a neuroendocrine transducer converting a neural input to hormonal output. High levels of melatonin are secreted during the night and low levels are secreted during the day. In addition to entraining melatonin secretion from the pineal gland, light can have an acute suppressive effect on melatonin. In a prolonged situation of insufficient exposure to light, serotonin might be excessively transformed into melatonin

 Studies , show that there is more to SAD than light exposure since symptoms of seasonality or seasonal mood changes, have been identified in populations located fairly close to the equator.

Melatonin
Melatonin - important for the timing of circadian rhythms and the sleep-wake cycle. Winter SAD was at first believed to be related to abnormal melatonin metabolism, but later findings showed that patients with winter SAD do not have abnormal melatonin secretion. contradictory reports on whether depressed patients with winter SAD show abnormal sensitivity to light, as assessed by the light-induced suppression of melatonin secretion at night.

 A few studies also suggest that depressed patients with winter SAD are relatively insensitive to ambient light during the day, shown by abnormal electro-oculographic ratios. Decreased availability of dopamine in the nervous connections of the eye is thought to be the underlying factor.

Serotonin
Placebo-controlled studies of tryptophan depletion support the hypothesis of disturbed serotonergic activity in winter SAD. Rapid lowering of brain serotonin function by depletion of tryptophan from the diet triggers depressive symptoms in patients with winter SAD during the summer, and in recovered patients with recurrent major depression. A good response to bright-light treatment depends on the availability of serotonin and of catecholamines (dopamine and norepinephrine).

Biological clock
A circadian rhythm is an endogenous rhythm that repeats with a period of about 24 h. Patterns of variation include activity, arousal, psychological performance, consumption of food and water, hepatic metabolism, urine volume and pH, blood pressure, heart rate, acid secretion in the gastrointestinal tract and cortisol secretion. The phaseshift hypothesis states that SAD patients have a circadian pacemaker abnormally entrained relative to external cycles and perhaps to other behavioural cycles.

 Circadian cycles seem to be more elastic across days in patients with winter SAD than in healthy people, deviating more from 24 h and peaking at less regular times disturbed biological rhythms are a consequence of inconsistent resetting of the circadian pacemaker and are worsened by shorter periods of daylight, exposure to cold weather, and ageing. secondary to impaired transmission of serotonin or neuropeptide Y along the afferent pathways to the circadian pacemaker These two neurotransmitters are thought to be essential for regulating mood and appetite, respectively.

Sleep
Since mood is influenced by a complex interaction of circadian phase and the duration of wakefulness, even moderate changes in the timing of the sleep-wake cycle may have profound effects on mood. abnormalities in sleep structure (decreased sleep, increased density of rapid eye movement, and impaired sleep efficiency)

Neuroimaging
globally lower cerebral metabolic rate than healthy people, on PET studies. Only depressed patients with winter SAD had asymmetrical (left more than right) metabolic activity of the medial PFC. They also had increased cerebral blood flow after bright-light treatment, whereas healthy controls had decreased blood flow on SPECT. The increase detected in frontal and cingulate cortices and thalamus was associated with a good response to bright-light therapy. Changes in regional cerebral blood flow of left dorsolateral and medial prefrontal cortical areas are also seen on recovery from major depression.

Molecular genetics
PCR experiments showed that short-allele polymorphism for the serotonin transporter was more common in patients with SAD than in healthy people. Moreover, patients with two long alleles were shown retrospectively to have milder symptoms than those with at least one short allele.

Culture
SAD is a complex disorder and culture also contributes to its aetiology. Kleimann and Good emphasise that the effect of culture on mental illness is important to recognise in studies of aetiology, since being sad at times of the year is acceptable to northern Norwegians, the same type of sadness could be considered depression in an American perspective. Actually, what should be taken into account is the degree of impairment of the signs and symptoms in occupational or social functioning.

Clinical Picture

Clinical picture
The onset typically between age 20 & 30 years, but affected people commonly do not seek psychiatric help for some years. Depressive episodes are generally mild to moderate. Clinical features associated with winter SAD are consistent across patients from different industrialized cultures. atypical depressive symptoms (increased duration of sleep, increased appetite, weight gain, and carbohydrate craving) frequently precede impaired functioning. Somatic symptoms are commonly the presenting complaint. On recovery, improvements in cognitive function are often seen (except in visual or spatial memory), which may be linked to altered cognitive sensitivity to light

 Whereas healthy people report sedation after eating carbohydrates, depressed patients with winter SAD are activated and are less sensitive to the sweet taste. Resting metabolic rates may also be increased in depressed patients with winter SAD secondary to changes in appetite and caloric intake.

 Frequent Social withdrawal; decreased activity; sadness; anxiety Fairly frequent Carbohydrate craving; decreased libido; poor quality of sleep; increased sleep; irritability; increased weight; increased appetite Fairly infrequent Suicidal thoughts; decreased sleep; decreased appetite Infrequent Decreased weight

 Patients with summer SAD are more likely to suffer from agitation insomnia, decreased appetite, and weight loss.

Co-morbidity
Generalized anxiety disorder, simple phobias, and social phobias are the most common co-morbid disorders. Common link is likely to be serotonergic dysregulation, evidence is growing that noradrenergic mechanisms also of importance in SAD Avoidant personality disorder is also common. patients with winter SAD and those with bulimia nervosa have similar attitudes towards eating (reflected as distorted perceptions of body size and shape), but opposite ways of eating (low and high scores of restraint eating behaviours, respectively).

Management

Assessment
The Seasonal Pattern Assessment Questionnaire (SPAQ) is perhaps the most widely studied tool. reported to have a high specificity (94%) for SAD but a low sensitivity (41%) The Seasonal Health Questionnaire has been reported to have higher specificity and sensitivity than the SPAQ

Treatment
Light therapies The treatment of SAD is similar to that for other forms of affective disorder, except that bright-light treatment is recommended as the 1st -line option for winter SAD. Since the inhibiting effect of light can only be obtained with fairly high levels, the timing and spectral composition of the light stimulation is of major importance. peak sensitivity of the circadian and neuroendocrine system is in the bluegreen portion of the visible spectrum

 Depends on the total dose of light (duration X illuminance) and time of day for the light treatment of SAD. Exposure to visible light producing at least 2500 lx at eye level in the morning for 24 h or 10,000 lx for 30 min, at a distance of about 1m from the light device to the face.

 The effects of bright-light treatment are thought to be mediated exclusively by the eyes, not the skin, although this assumption has not yet been verified. Side-effects, including eye-strain and headache, are common but are well-tolerated and seldom lead to cessation. Few reports of manic behavior or suicidal tendencies occurring during bright-light treatment

 Atypical depressive symptoms, rather than the overall severity of a depressive episode, best predict a good response. Comorbid anxiety disorders promote, whereas comorbid personality disorders compromise, the benefit from bright-light treatment. A response to daily sessions is generally seen within 12 weeks. The length of time the effect persists after stopping the treatment differs, but symptoms return for most patients. If treatment is effective, continuation throughout winter is recommended for the best response. After the first 12 weeks, remission can be maintained by exposures given five times a week.

 A dawn simulator and light visors have been developed to decrease time spent in light therapy and to allow the patient to maintain activities during the treatment.

Drug therapies
antidepressants are effective in the treatment of winter SAD. the best choice would then be one of the SSRIs or RIMAs Promising results have been seen for sertraline, a selective serotonin-reuptake inhibitor (SSRI). Bright-light treatment can be supplemented with antidepressant drugs. No harmful drug/light interactions have been reported.

Other therapies
psychological therapies for winter SAD. Cognitive-behavioural and interpersonal therapies. Aerobic exercise and sleep deprivation may be effective.

Follow-up
Follow-up of 511 years since the initial diagnosis, < 1/2 (3842%) of patients routinely experience winter SAD, > 1/3rd (3344%) develop a non-seasonal pattern to subsequent episodes. remaining have only mild symptoms (about 6%) or no symptoms at all (1418%). Studies suggest atypical depressive symptoms are the best predictors of season-bound recurrence

Research
First, the aetiology of winter SAD seems to be more complex. Its genetic basis and pathogenesis has to be explored. Second, the ICD-10 diagnostic criteria for SAD need to be validated. Third, the mechanisms and sites of action of bright-light exposure need to be clarified for specific therapies and the optimum strategies for clinical management to be developed.

ConConclusion clusion
Atypical symptoms which include hypersomnia, hyperphagia, carbohydrate cravings and increased weight. The specific aetiology of SAD remains unclear although the neurotransmitter serotonin may play a significant part. Both phototherapy and some SSRIs (sertraline, fluoxetine) produced a good antidepressant effect and were well tolerated, either alone or in combination. Much research is needed for proper understanding of SAD in future.

THANK U