Bilateral Medial Medullary Infarction: A Rare and Devastating Stroke Subtype

By Weiwei Gao, Lijuan Cai, Renjing Zhu

Affiliations

1. Department of Neurology, Zhongshan Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, China

doi: 10.29271/jcpsp.2025.06.809

Sir,

Medial medullary infarction (MMI) is an uncommon cerebrovascular disorder, accounting for 0.5–1.5% of all types of cerebral infarction.¹ Bilateral MMI (BMMI) is even rarer, comprising only 14% of MMI cases.² The classic clinical presentation of MMI is Dejerine syndrome, which is characterised by a triad of ipsilateral hypoglossal nerve palsy, contralateral hemiplegia, and contralateral hemisensory disturbance. Compared to unilateral lesions, the clinical manifestations of BMMI are more complex and diverse, including the above-mentioned symptoms as well as respiratory failure, altered consciousness, vertigo, dysphagia, and dysarthria.³

On diffusion-weighted imaging (DWI), BMMI presents as high-signal lesions in the bilateral medial medulla extending dorsally along the midline, forming a characteristic "heart-shaped" or "Y-shaped" appearance. Regarding the pathogenesis of BMMI, current research suggests that it may be related to the extension of atherosclerotic plaques or thrombi from the vertebral artery confluence to the basilar artery region, leading to occlusion of the bilateral vertebral artery perforator openings or atherosclerotic occlusion of their proximal segments.⁴ Clinically, the treatment principles for BMMI do not differ from those for conventional ischaemic stroke. For critically ill patients with respiratory dysfunction, close monitoring of vital signs, assessment of respiratory function, and endotracheal intubation or tracheostomy are necessary to ensure airway patency.

A 39-year male woke up on 30 August 2023 with numbness in his left limbs, which he initially ignored. Six hours later, he developed dysarthria and weakness in his left limbs. He had a history of hypertension and diabetes, along with long-term smoking and alcohol consumption. Upon admission, his vital signs were stable. Neurological examination revealed left central facial palsy, left hemiplegia (Medical Research Council [MRC] grade 4/5), and left hemihypoesthaesia. A positive swallowing test indicated dysphagia. The National Institutes of Health Stroke Scale (NIHSS) score was 7, and the modified Rankin Scale (mRS)  score  was  2.

Initial laboratory tests showed marked hyperglycaemia (fasting blood glucose: 11.65 mmol/L; HbA1c: 12.00%) and dyslipidaemia (total cholesterol: 6.40 mmol/L; triglycerides: 2.94 mmol/L; low-density lipoprotein cholesterol: 5.80 mmol/L). Other routine laboratory parameters were within normal limits. The patient was immediately started on dual antiplatelet therapy and high-intensity statin treatment.

Figure 1: Diffusion-weighted imaging and magnetic resonance angiography. (A) Diffusion-weighted imaging revealing a characteristic "Y-shaped" high signal intensity lesion in the bilateral medial medulla, consistent with acute infarction. (B, C) Three-dimensional time-of-flight magnetic resonance angiography demonstrating no significant stenosis or occlusion of the vertebrobasilar arteries.

Within 24 hours of admission, the patient's neurological function rapidly deteriorated. Left hemiplegia worsened (MRC grade 0/5), and right-sided weakness appeared (MRC grade 3/5). Emergency magnetic resonance imaging (MRI) showed a characteristic "half-Y" sign on DWI, indicating high signal intensity in the bilateral medial medulla (Figure 1). Magnetic resonance angiography (MRA) revealed no apparent vascular abnormalities (Figure 1). By day 3, the patient developed altered consciousness with progressive somnolence. Despite aggressive medical management, the patient's condition continued to deteriorate, ultimately leading to respiratory failure and death on hospital  day  10.

In conclusion, BMMI is characterised by an acute onset and rapid progression, with patients often presenting with severe symptoms such as quadriplegia and respiratory failure, resulting in a poor prognosis. Studies have shown that the mortality rate of BMMI is as high as 23.8%, and the disability rate reaches 61.9%.⁵ Furthermore, early imaging examinations in BMMI  may appear normal or only show scattered punctate lesions, leading to misdiagnosis as Guillain-Barre syndrome, brainstem encephalitis, or acute myelitis. Therefore, for patients with suspected cerebrovascular lesions, clinicians should maintain a high index of suspicion, conduct thorough neurological examinations, and promptly perform cranial DWI and cerebrovascular angiography based on the onset characteristics and disease progression. When necessary, dynamic imaging follow-up should be performed to establish an early diagnosis and implement timely  intervention.

COMPETING   INTEREST:
The  authors  declared  no  conflict  of  interest.

AUTHORS’  CONTRIBUTION:
WG: Data curation, investigation, and manuscript writing.
LC, RZ: Conceptualisation, writing, review, and editing.
All authors approved the final version of the manuscript to be published.

REFERENCES

1. Zhou ZH, Wu YF, Wu WF, Liu AQ, Yu QY, Peng ZX, et al. Giant "heart appearance-like sign" on MRI in bilateral ponto-medullary junction infraction: Case report. BMC Neurol 2020; 20(1):107. doi: 10.1186/s12883-020-01683-7.
2. Akimoto T, Ogawa K, Morita A, Suzuki Y, Kamei S. Clinical study of 27 patients with medial medullary infarction. J Stroke Cerebrovasc Dis 2017; 26(10):2223-31. doi: 10. 1016/j.jstrokecerebrovasdis.2017.05.004.
3. Lu JP, Wu Y, Xiao F, Li HY, Tang QQ. Bilateral medial medullary infarction with distal stenosis of hypoplastic vertebral artery. Chin Med J (Engl) 2019; 132(8):998-9. doi: 10.1097/CM9.0000000000000171.
4. Kim JS, Han YS. Medial medullary infarction: Clinical, imaging, and outcome study in 86 consecutive patients. Stroke 2009; 40(10):3221-5. doi: 10.1161/STROKEAHA. 109.559864.
5. Pongmoragot J, Parthasarathy S, Selchen D, Saposnik G. Bilateral medial medullary infarction: A systematic review. J Stroke Cerebrovasc Dis 2013; 22(6):775-80. doi: 10.1016/j. jstrokecerebrovasdis.2012.03.010.