ARTICLE IN PRESS

Case Studies

Twenty-Four Syndrome: An Untold Presentation
of Pontine Hemorrhage
Ummer Karadan, DM (Neurology), Ramesh N. Supreeth, MBBS,
Robin George Manappallil, MD, and Chellenton Jayakrishnan, DM (Neurology)

Pontine hemorrhages are relatively uncommon. Various atypical manifestations
of pontine stroke like eight-and-a-half syndrome, fifteen-and-a-half syndrome, and
sixteen syndrome have been described in the past. We came across a case of pontine
bleed that presented with bilateral facial palsy, bilateral horizontal gaze palsy, and
contralateral sensorineural hearing loss accounting to the hitherto not described
“twenty-four syndrome” with Horner’s syndrome and left hemiparesis. Key Words:
Pontine hemorrhage—facial diplegia—bilateral horizontal gaze palsy—contralateral
sensorineural hearing loss.
© 2017 National Stroke Association. Published by Elsevier Inc. All rights reserved.

Introduction
Primary pontine hemorrhages are relatively rare when
compared to supratentorial cerebral hemorrhage. Because
of the close proximity of pons to the cranial nerve nuclei
and vascular anomalies, patients with primary pontine
hemorrhages show various atypical manifestations. Our
patient presented with facial diplegia, bilateral horizontal gaze palsy, and contralateral sensorineural hearing deficit
with Horner’s syndrome and left hemiparesis following
pontine hemorrhage.

Case Report
A 75-year-old lady was brought with history of giddiness and fall, followed by slurred speech. She was
hypertensive for the past 5 years, on amlodipine 5 mg/
day. She was brought to our hospital within 1 hour of
From the Baby Memorial Hospital, Calicut, Kerala 673004, India.
Received October 15, 2017; revision received November 22, 2017;
accepted December 3, 2017.
Address correspondence to Robin George Manappallil, MD, Internal
Medicine, Baby Memorial Hospital, Mini Bypass Road, Calicut, Kerala
673004, India. E-mail: drrobingeorgempl@gmail.com.
1052-3057/$ - see front matter
© 2017 National Stroke Association. Published by Elsevier Inc. All
rights reserved.
https://doi.org/10.1016/j.jstrokecerebrovasdis.2017.12.007

the incident. On the way, she had 2 episodes of
nonprojectile vomiting, with vomitus containing food particles. On presentation, she was conscious and oriented,
with Glasgow Coma Scale of 15/15. Her heart rate was
100/minute and regular, blood pressure was 220/
110 mmHg, respiratory rate 20/minute with saturation
96% in room air. Neurological examination revealed right
eye ptosis, right pupil miosis, bilateral horizontal gaze
palsy with vertical ocular bobbing and bilateral lower motor
neuron facial palsy (right more than left side). Ocular
pursuit and saccades were impaired bilaterally in vertical plane. Horner’s syndrome was present. Oculocephalic
maneuver and calorie test failed to elicit horizontal ocular
movements. Rinne’s test was positive bilaterally with poorer
air and bone conduction on left side. Weber’s test showed
lateralisation of sound to right ear suggesting left sensorineural hearing loss. She had dysphagia but no palatal
palsy or deviation of uvula. Left upper and lower limb
had decreased tone and power (4/5 by manual muscle
test) with brisk deep tendon reflexes, along with loss of
pain, temperature, vibration, and proprioceptive sensations. Left lower limb had extensor plantar reflex. Other
systemic examinations were normal. Her blood investigations showed reactive leukocytosis. Her renal and liver
functions, electrolytes, calcium, thyroid-stimulating hormone
and hemoglobin A1c were normal. Echocardiography
showed concentric left ventricular hypertrophy.

Journal of Stroke and Cerebrovascular Diseases, Vol. ■■, No. ■■ (■■), 2017: pp ■■–■■

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ARTICLE IN PRESS
U. KARADAN ET AL.

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Figure 1. CT brain showing a hyperdense lesion in the pons suggestive
of hemorrhage. Abbreviation: CT, computed tomography.

Computerizedtomography (CT) of brain revealed an acute
pontine bleed predominantly on the right and extending to the left (Fig 1). From the clinical presentation and
imaging findings, a diagnosis of acute pontine hemorrhage with cranial nerve involvement presenting as a
“twenty-four syndrome” along with Horner’s syndrome and left hemiparesis was made. On admission, her
National Institutes of Health Stroke Scale (NIHSS) score
was 18 and modified Rankin Scale (mRS) was 4. She was
managed with antihypertensives, mannitol, and physiotherapy, and was discharged on day 12 of admission with
National Institutes of Health Stroke Scale and modified
Rankin Scale of 12 and 3, respectively.

Discussion
Cerebrovascular diseases are at a rapid increase in developing countries, with more than 2-fold rise in their
incidence between 1970 and 2008. An incidence of 117
per 1 lakh population has been noted in low- and middleincome countries. Intracerebral hemorrhage (ICH) is the
second most common cause of stroke, following ischemia, accounting for about 10%-20% of all stroke cases.1
About 80% of ICH cases are due to hypertensive atherosclerotic cerebrovascular disease and cerebral amyloid
angiopathy.2 The pathophysiology behind nontraumatic
ICH has been attributed to age-related vessel wall degenerative changes, hypertension, and diabetes, resulting
in the formation of Charcot–Bouchard micro aneurysms
and lipohyalinosis of small arterioles.3
Pontine hemorrhage accounts for 5%-9% of ICH cases,
with incidence being highest between 40 and 50 years
of age. These patients present with acute onset coma, con-

stricted pupils, quadriplegia, and early onset respiratory
arrest and sudden death.4
One-and-a-half syndrome is characterized by horizontal gaze palsy (1) with intranuclear ophthalmoplegia (1/
2) due to a lesion of the paramedian pontine reticular
formation and medial longitudinal fasciculus.5 Eight-anda-half syndrome (7 + 1 + 1/2) was noticed when the lesion
also affects the fascicle of ipsilateral facial nerve in the
region of the facial colliculus, producing an ipsilateral lower
motor neuron facial palsy.6 Such a case was reported by
Nandhagopal and Krishnamoorthy.7 Bae and Song reported a case of fifteen-and-a-half syndrome where the
patient had unilateral one-and-a-half syndrome and bilateral lower motor neuron facial palsy (1 + ½ + 7 + 7).8
A sixteen syndrome characterized by bilateral horizontal gaze palsies and facial diplegia (7 + 7 + 1 + 1) was
observed by Connors et al in a case of pontine
hemorrhage.9
In our case, the patient had predominantly right pontine
hemorrhage with extension to the left resulting in facial
diplegia, bilateral horizontal gaze palsy, and contralateral sensorineural hearing deficit, making it to a twentyfour syndrome (7 + 7 + 1 + 1 + 8) along with Horner’s
syndrome and left hemiparesis. The contralateral sensorineural hearing loss was probably due to involvement
of lateral lemniscus after its decussation at the mid pons.
Expansion of the hemorrhage or perilesional edema crossing midline would have caused the lateral lemniscal
involvement. To the best of our knowledge, such a scenario has not been reported yet.

References
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