4 JOURNAL READING

WEDNESDAY,MAY 13 2020

Presenter : dr Amarwati khairina putri

Moderator: dr.Irina k Nasution, M.Ked( Neu) Sp.S
Introduction
Cluster headache (CH) is a primary headache disorder characterized by excruciating,
strictly unilateral headachesthat are accompanied by cranial autonomic Symptoms

Circadian and circannual rhythmicity is also a characteristic of CH

Circadian rhythmicity is considered a key feature of CH, strongly suggesting hypotha-

lamic involvement in the pathophysiology of this disorder

Hypothesized
that circadian rhythmicity might change in association with disease course and reflect
the disease activity of CH

Aimed
investigate the pattern of circadian rhythmicity in relation to disease progression. In
CH patients participating in a prospective, multicenter registry study, the prevalence
and characteristics of circadian rhythmicity were compared between patients with
different numbers of total lifetime bouts.
Methods
Study design

This study is a part of the Korean Cluster

Headache Registry Study (KCHR), which is a
prospective, longitudinal,multicenter, observa-
tional study that enrolled consecutive patients Patient recruitment was started between Sep-
tember 2016 and February 2017 following the
with CH from 15 hospitals (13 university hospi- IRB approval in each hospital.
tals, including eight tertiary and five secondary
referral hospitals, and two general hospitals) in
Korea

The diagnosis of CH was made by KCHR inves-

Patients who visited the participating hospitals
during the study period and were diagnosed
with CH were recruited for the KCHR study
tigators (experienced neurologists with exper-
tise in headache disorders) based on the most
updated criteria from the International Classifi-
cation of Headache Disorders (ICHD) at the
time of enrollment)
Assessment of circadian rhythmicity

circadian rhythmicity of the current bout was determined by investigators by asking patients if
their attacks in the current bout had a trend toward occurring at the same time of day

patients were observed without preventive or transitional treatment for more than 1 week (at
least 2 weeks of observation was recommended if available) and the presence of circadian
rhythmicity and time of CH attacks were ascertained at visit

Patients with 2 lifetime bouts were asked if they experienced any change in the pattern of cir-
cadian rhythmicity during their disease course.

Patients were instructed to choose one of four answers:

a) stationary:No change between bouts;

b) developing: Becomes more prominent as disease progresses;

c) decreasing: Becomes less prominent as dis-
ease progresses d)variable:
Statistical analysis

It was categorized into 10 groups

(deciles) for categorical analysis, raw
numbers were used for continuous
analysis. To analyze the association
between the presence of circadian
Categorical data are presented as rhythmicity and total lifetime bouts
Student’s t-test, Chi-square test, and
numbers (percentages), and continu- created bar graphs of circadian
Fisher’s exact test were used to com-
ous variables are summarized as me- rhythmicity according to deciles of
pare variables between two groups
dian (interquartile range [IQR]). total lifetime bouts compared the
presence of circadian rhythmicity be-
tween the most advanced (10th
decile) versus the other (1st to 9th
decile) groups using theChi-square
test
Results
Time of day for cluster headache attacks
Time of day for cluster headache attacks in relation to the number of
total lifetime bouts

9
Discussion
• ) the prevalence of circadian rhythmicity did not differ
according to the disease progression, although circadian
rhythmicity was less frequently reported in patients with
the longest disease duration;
The main findings • ) in half of all patients with CH, circadian rhythmicity was
not fixed, but varied from bout to bout; and
• ) the pattern of circadian rhythmicity differed according
to the disease Course

• 58–82% of patients with CH (4,16–19). Our

studyshowed a relatively lower prevalence of cir-
cadian rhythmicity,
Previous studies
• because we assessed the circadian rhythmicity
only in the current bout in order to minimize the
possibility of recall bias
We hypothe- Night attacks were CLOCK (Circadian Lo-
sized that circa- predominant early in comotor Output Cy-
dian rhythmicity the disease course and cles Kaput) gene has
may evolve or in the advanced been reported to be
regress as the course of CH. This pat - associated with diur-
disease pro- tern may indicate a nal rhythmicity of CH
gresses. How- possible evolvement The roles of sleep
ever,the overall and regression of di- phase, melatonin, pi-
prevalence of urnal expression of tuitary adenylate cy-
circadian rhyth- CH, the biological im- clase-activating pep-
micity in the in- plication of which has tide (PACAP), and
dex bout re- not yet been deter- orexin have been sug-
mained un- mined. gested as possible
changed regard- mechanisms of circa-
less of disease dian rhythmicity in CH
Progression
 • A strength of the KCHR study is
that the diagnosis and character-
ization of CH were well verified
by experienced neurologists. Pa-

strength tients were longitudinally fol-

lowed up, which enabled use to
ensure the presence of circadian

s of our rhythmicity in patients who were

uncertain about their pattern of
CH attacks

study
 • First, most of the data were obtained from
patients’ recall of the current bout. This
problem is attributed to two issues: The
lack of definition of circadian rhythmicity
in CH and the ethical issue. Currently, cir-
cadian rhythmicity has not been defined
from a consensus, and it is unknown
whether the circadian rhythmicity occurs
exactly on a 24-hour basis.
• Second, our observational study can only

limitations be hypothesis generating, rather than hy-

pothesis testing. The pathophysiological
aspects of our findings should be further
investigated infuture studies.
• Third, we did not collect information re-
garding the association between previous
treatment and changes of circadian
rhythmicity