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Geriatr Gerontol Int 2016; 16: 1085–1088

L E T T E RS T O T H E E D I T O R
CASE REPORT

Acute pontine
mood only

infarction

Dear Editor,
A 65-year-old male patient presented to Chosun University hospital in Gwangju, South Korea, complaining
of sudden mood swings for 4 days. He was bright and
diligent before the visit. He had become suddenly curt,
unfriendly and lethargic, and then 2 days after, had
more progressive mood swings. Four days earlier, his
usual bright and hard-working demeanor had suddenly
been replaced with a curt and unfriendly attitude. He
had a history of hypertension and type II diabetes for 10
years and 4 years, respectively. The patient did not drink
or smoke.

presenting

with

depressive

Brain magnetic resonance imaging, taken 4 days after
symptom onset, showed a small lesion in the right
pontine tegmentum. It showed high signal intensity in
the diffusion weighted image and low signal intensity in
the apparent diffusion coefficient image. These results
suggested an acute cerebral infarction (Fig. 1a,b). High
signal intensities were observed in the right corona
radiate, and no abnormal findings were detected in
other sites, such as the periventricular area, deep white
matter and subcortical gray matter in T2-weighted
images (Fig. 1c). Magnetic resonance angiography
showed occlusion of the right proximal carotid artery
and left proximal middle cerebral artery (Fig. 1d). The

Figure 1 Magnetic resonance imaging
shows (a) diffusion restriction in the right
pons with diffusion weighted image and (b)
apparent diffusion coefficient image. (c)
Fluid-attenuated inversion recovery image
shows hyperintensity on the right corona
radiata and bilateral periventricular white
matter. (d) Magnetic resonance angiography
shows right proximal carotid artery and left
proximal middle cerebral artery occlusion.

© 2016 Japan Geriatrics Society

doi: 10.1111/ggi.12643

| 1085

HG Kang et al.

Korean version of the Geriatric Depression Scale was
carried out to measure the severity of depression on
hospital day 3. He scored 26 points from a total of 30,
and was diagnosed with severe depression. We prescribed 75 mg of clopidogrel and 30 mg of duloxetine,
to no effect. Duloxetine was replaced with 10 mg of
escitalopram, a selective serotonin reuptake inhibitor.
Afterwards, dysphagia improved completely and depression symptoms also gradually improved. Two weeks
later, his conditions did not require specific attention
and he was discharged.
In this case, a patient with a small pontine infarction
experienced depression only, without other neurological symptoms. It has been reported that in the early
stage of post-stroke depression (PSD) with a left anterior lesion, in the majority of cases, depression is
accompanied by other neurological symptoms. There
has been a previous report of a pontine infarction exhibiting emotional incontinence, but there have not been
any reports of a case manifesting depression only.1 The
prevalence of PSD is approximately 30–50%, 3–6
months after a stroke has occurred.2 PSD occurring
within 2 weeks has been associated with the left cerebral
hemisphere, although these associations were not
observed after 2 weeks to 6 months had passed. Paradoxically, after 6 months, PSD were associated with the
right cerebral hemisphere.3 Recently, it was reported
that PSD is not related with stroke size and location.4
Of the many explanations regarding the pathophysiology of depression, the serotonin theory and norepinephrine theory are currently receiving the most
attention. Serotonin controls emotions, and decreased
levels can cause depression, aggression, anxiety and
bulimia. The increased levels of serotonin, otherwise,
can cause mood elevation and have analgesic effects.
Serotonin is secreted from the raphe nucleus located in
the pontine tegmentum. Serotonin neurons originate
from the raphe nucleus, and relay signals to the frontal
lobe and basal ganglia. Lesions in the former pathway
might cause problems in mood control, whereas lesions
in the latter pathway might result in problems with
motor functions, and cause obsessive–compulsive
thoughts and behavior. The pontine lesion of this
patient might have been located just over the pathway
leading to the frontal lobe, with minimal impact on the
other pathway, resulting in mood symptoms with largely
preserved motor functions. Furthermore, norepinephrine signals originate from the locus coeruleus, which is
also located in the pons. As reduced adrenergic levels
can result in lethargic and avolitic attitudes, the lesion
of this patient might have interfered with adrenergic
signaling.
Because of its complex structure, pontine tegmentum
infarctions could cause various neurological symptoms.

1086

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The fifth, sixth, seventh and eighth cranial nuclei are
located nearby and can be damaged, causing various
symptoms. Damage to the fifth cranial nerve can cause
ipsilateral loss of facial pain sense and paralysis of facial
muscles. Damage to the sixth, seventh and eighth
cranial nerves can cause diplopia, ipsilateral facial nerve
palsy, vertigo and disequilibrium, respectively. Medial
lemniscus damage might cause loss of facial touch
and press sense, and medial longitudinal fasciculus
damage could cause diplopia with eyeball movement
disorder. Damage to the trapezoid body and lateral lemniscus might cause auditory dysfunction, and if the
middle cerebellar peduncle is damaged, ataxia might
occur.
In the present case, an infarction occurred in the
central tegmentum of the mid-pons. The medial longitudinal fasciculus passes to the medial side of the tegmentum, and the fifth cranial nerve and middle
cerebellar peduncle pass to the lateral side of the tegmentum. Therefore, related symptoms did not occur in
the present case. The sixth cranial nerve and medial
lemniscus passes through the central tegmentum in the
caudal pons, but in this case the lesion was located in
the mid-pons, and as the medial lemniscus is located on
the dorsal side of the tegmentum, and the sixth nerve
passes at a lower level than the lesion, related neurological symptoms also did not occur. We have experienced and reported that a pontine cerebral infarction
occurred showing mainly symptoms of depression,
without other concomitant neurological symptoms.

Disclosure statement
No potential conflicts of interest were disclosed.
Hyun Goo Kang,1 Jin Sung Cheong2 and Hoyoung An3
Department of Neurology, Chosun University School of Medicine
and Hospital, Gwangju, 2Department of Neurologya, Wonkwang
University School of Medicine and Hospital, Iksan, and
3
Department of Psychiatry, Asan Medical Center, University of
Ulsan College of Medicine, Seoul, South Korea

1

References
1 Zavoreo I, Basic-Kes V, Bosnar-Puretic M, Demarin V.
Post-stroke depression. Acta Clin Croat 2009; 48: 329–333.
2 Im JM. Study on the Effects of a Gestlat Group Therapy
Program on Geriatric Depression. [Master’s Thesis]:
Sungshin Women’s University; 2003.
3 Kang HJ, Kim SW, Kim JM, Shin IS, Yoon JS. Pathogenesis
of post-stroke depression: a bio-psycho-social integrative
model. J Korean Neuropsychiatr Assoc 2011; 50: 347–353.
4 Carson AJ, MacHale S, Allen K et al. Depression after stroke
and lesion location: a systematic review. Lancet 2000; 356:
122–126.

© 2016 Japan Geriatrics Society