Letter to the Editor
International Journal of Stroke
2016, Vol. 11(1) NP5–NP6
! 2016 World Stroke Organization
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DOI: 10.1177/1747493015607502
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Post-stroke hypersomnia
Dear editor,
A 50-year-old right-handed male underwent conservative treatment for management of a spontaneous
pontine hemorrhage (PH) in the tegmentum
(Figure 1a). Four weeks after onset, he was transferred
to the rehabilitation department and complained of
severe post-stroke hypersomnia (PSH) since the onset
of PH (he always fell asleep without external stimulation) and the Epworth Sleepiness Scale score was 18
(full score: 24, cut-off for hypersomnia: 10).
Diffusion tensor imaging data were acquired at four
weeks after onset of PH. Two portions of the ascending
reticular activating system (ARAS) were reconstructed:
the dorsal lower ARAS between the pontine reticular
formation (RF) and the thalamic intralaminar nucleus
(ILN), and the ventral lower ARAS between the pontine RF and the hypothalamus. Narrowing of both
dorsal lower ARASs between the pontine RF and the
thalamic ILN was observed and the ventral lower
ARAS between the pontine RF and the hypothalamus
was not reconstructed on both sides.
These findings indicate injury of both the dorsal
ARAS and ventral ARAS on both sides. However,
the ventral lower ARAS appeared to be more severely
injured than the dorsal lower ARAS. It appeared that
PSH of this patient might be attributed to the injury of
the lower ARAS, particularly the injury of both ventral
lower ARASs, because many studies have reported
close association of the hypothalamus with
hypersomnia.1–3
Hypersomnia (excessive daytime sleepiness) is a
common sequela following stroke: one study reported
persistent hypersomnia in 5.6% of stroke patients. PSH
has been reported in stroke patients with lesions in the
thalamus, hypothalamus, or pons, which suggests the
possibility that involvement of the ascending reticular
activating system might be a pathogenetic mechanism
of PSH1,4,5; however, this has not been clearly
demonstrated.
In conclusion, injury of the dorsal and ventral lower
ARAS was demonstrated in a patient with PSH

following PH. We believe that these injuries of the
ARAS might be a pathogenetic mechanism of PSH.
Declaration of conflicting interests
The author(s) declared no potential conflicts of interest with
respect to the research, authorship, and/or publication of this
article.

Funding
The author(s) disclosed receipt of the following financial support for the research, authorship, and/or publication of this
article: This work was supported by the National Research
Foundation (NRF) of Korea Grant funded by the Korean
Government (MSIP) (2015R1A2A2A01004073).

References
1. Tezer FI, Pektezel MY, Gocmen R, et al. Unusual presentation of hypothalamic hamartoma with hypersomnia in
an adult patient. Epileptic Disord 2014; 16: 366–369.
2. Menzler K, Belke M, Unger MM, et al. DTI reveals hypothalamic and brainstem white matter lesions in patients
with idiopathic narcolepsy. Sleep Med 2012; 13: 736–742.
3. Yassin W, Sugihara G, Oishi N, et al. Hypothalamicamygdalar-brainstem volume reduction in a patient with
narcolepsy secondary to diffuse axonal injury. J Clin Sleep
Med 2015; 11: 581–582.
4. Forcadas MI and Zarranz JJ. Hypersomnia after tegmental pontine hematoma. Neurologia 1995; 10: 307–310.
5. Arpa J, Rodriguez-Albarino A, Izal E, et al. Hypersomnia
after tegmental pontine hematoma: case report. Neurologia
1995; 10: 140–144.

Sung Ho Jang
Department of Physical Medicine and Rehabilitation, College of
Medicine, Yeungnam University, Taegu, Republic of Korea
Chul Hoon Chang
Department of Neurosurgery, College of Medicine, Yeungnam
University, Taegu, Republic of Korea
Young Jin Jung
Department of Neurosurgery, College of Medicine, Yeungnam
University, Taegu, Republic of Korea

International Journal of Stroke, 11(1)

NP6
Jeong Pyo Seo
Department of Physical Medicine and Rehabilitation, College of
Medicine, Yeungnam University, Taegu, Republic of Korea

International Journal of Stroke 11(1)
Corresponding author:
Jeong Pyo Seo, Department of Physical Medicine and
Rehabilitation, College of Medicine, Yeungnam University, 317-1,
Daemyungdong, Namku, Taegu 705-717, Republic of Korea.
Email: raphael0905@hanmail.net

Figure 1. (a) Brain CT images at onset show hematoma located in the pontine tegmentum. T2-weighted brain MR images at
four weeks after onset show a leukomalactic lesion located in the pontine tegmentum. (b) Results of diffusion tensor tractography:
narrowing (arrow) of both dorsal lower ascending reticular activating systems (ARAS) between the pontine reticular formation and
the thalamic intralaminar nucleus and non-reconstruction (arrows) of both lower ventral ARASs between the pontine reticular
formation and the hypothalamus compared with those of a normal subject (45-year-old male). RF: reticular formation, ILN:
intralaminar nucleus.

International Journal of Stroke, 11(1)