A presentation on Seasonal Affective Disorder and its management and role of circadian rhythm in SAD.

1. Role Of Circadian
Rhythm In Management Of
Dr. Pushpendra Pushkar, JR
Deptt. Of Pharmacology &Therapeutics

3.  Seasonal affective disorder is a major depression
with a seasonal onset.
 It displays recurring seasonal pattern, typically
starting in the late fall and early winter and going
away during the spring and summer.

4.  Seasonal Affective Disorder (SAD) is not considered
as a separate disorder.
 To be diagnosed with SAD, people must meet full
criteria for major depression coinciding with specific
seasons (appearing in the winter or summer months)
for at least 2 years.

5. WINTER
DEPRESSION

6.  It is a dysfunction of circadian rhythms that occurs more
commonly in the fall and winter months and is believed
to be due to decreased exposure to full-spectrum light.

7.  Production of melatonin by the pineal gland is under
the influence of the suprachiasmatic nucleus of the
hypothalamus (SCN) which receives information
from the retina about the daily pattern of light and
darkness.

8.  This lack of sunlight causes a reduction in serotonin
production and an increase in the level of melatonin.
This produces the symptoms associated with SAD.

9. Symptoms of SAD include:
 Hypersomnia
 Having low energy
 Fatigue, particularly difficulty getting up
in the morning, despite a tendency to
lengthen sleep (up to three hours) in the
winter

10.  Overeating
 Weight gain
 Craving for carbohydrates
 Social withdrawal (feel like “hibernating”)

11.  Measurement of symptom severity is accomplished
by:
 SIGH-SAD
(Structured Interview Guide for the Hamilton
Depression Rating Scale, SeasonalAffective
Disorders version).

12. Risk Factors

13. SAD is more frequent in people who live far north or south
of the equator.

14. Younger adults have a
higher risk of SAD than
older adults. SAD has been
reported even in children
and teens
Average age
for people who
suffer from
SAD is
18-30yrs

15.  Family history. People with a family history of other
types of depression are more likely to develop SAD
than people who do not have a family history of
depression.

16. Mechanism
 There may be several biologic mechanisms
underlying SAD,
 circadian phase delay (the phase shift hypothesis) -
the chief cause in the literature.
 Additional contributing mechanisms may include
 retinal sensitivity to light,
 neurotransmitter dysfunction,
 genetic variations affecting circadian rhythms, and
 serotonin levels.

17. The Dim Light Melatonin Onset
 The human body produces its own melatonin
starting two hours before bedtime, provided the
lighting is dim.
 The DLMO can be operationally defined as the
interpolated time when melatonin levels
continuously rise above 10 pg/mL in plasma or 3
pg/mL in saliva.
 Today, DLMO is considered the best test available, a
“gold standard”, for measuring Melatonin levels and
Circadian Rhythm Disorders.

18.  Either plasma or saliva is collected usually every 30
minutes between 6 PM and bedtime.
 This natural action is known as “dim light melatonin
onset” (DLMO) and helps keep the body on a regular
sleep-wake schedule.

20. Phase Shift Hypothesis
 The leading hypothesis for winter depression (seasonal
affective disorder, or SAD) is the phase shift
hypothesis (PSH).
 The phase shift hypothesis (PSH) which states that
most patients with SAD become depressed in the
winter, at least in part because of a phase delay in
circadian rhythms relative to the sleep/wake cycle.

21.  The prototypical phase-delayed SAD patient has a
dim light melatonin onset (DLMO) that is delayed
with respect to mid-sleep (the mid-point between
sleep onset and sleep offset).

22.  According to the PSH, these patients should
preferentially respond to the antidepressant effects
of bright light exposure when it is scheduled in the
morning so as to provide a corrective phase advance
and restore optimum alignment between the
circadian rhythms tightly coupled to the endogenous
circadian pacemaker and those rhythms that are
related to the sleep/wake cycle.

23. Differential Diagnosis
 Major depressive disorder ( non-seasonal pattern),
 Cyclothymic disorder (bipolar disorder characterized
by distinct episodes of hypomanic symptoms and
depressive symptoms),
 Premenstrual dysphoric disorder (PMDD, similar
to premenstrual syndrome (PMS) but is more
serious,
 Chronic fatigue syndrome (occurs more commonly
in women),
 Hypothyroidism, and
 Drug or alcohol abuse.

25.  There are 3 major types of treatment for SAD:
 Psychotherapy (CBT)
 Pharmacotherapy (Antidepressants such as SSRIs)
 Phototherapy / LightTherapy

26. Phototherapy
 Phototherapy has been a mainstay of treatment for
SAD since the 1980s.
 The idea behind phototherapy is to replace the
diminished sunshine of the fall and winter months
using daily exposure to bright, artificial light.

27. Symptoms of SAD may be relieved by sitting in
front of a light box first thing in the
morning, on a daily basis from the early fall
until spring.

28. Treatment guidelines for patients
with SAD
 Schedule indirect eye exposure, immediately upon
awakening, to a light source of greater than 2500 lux
for 2 hrs daily or 10 000 lux for 20 min daily to increase
the photoperiod of the day.
 The response begins 2 to
4 days after beginning
light therapy and is
usually complete within
2 weeks.

29.  If patients do not respond to treatment, they may
need a longer duration of morning light.
 To avoid relapse, light therapy should continue
through the end of the winter season until
spontaneous remission of symptoms in the spring or
summer.
 To avoid relapse in subsequent years, patients may
start light therapy in the early autumn before the
onset of symptoms.

30.  Light therapy is generally well tolerated.
 Adverse effects may include headache, eye strain,
nausea, agitation, and blurred vision, but these are
usually mild and transient

31. THANK YOU TEACHERS!