Lateral medullary infarction presenting only with dermatomal sensory disturbance: a case report

ABSTRACT

The triad of Horner’s syndrome, ataxia and sensory disturbances clinically identifies patients with lateral medullary infarct (LMI). However, dermatomal temperature and pain sensory loss have rarely been reported in patients with LMI. We describe the case of a patient with LMI presenting solely with temperature and pain sensory disorder below the C5 sensory level. Magnetic resonance imaging findings demonstrated a small superficial infarction in the right lateral medulla oblongata, indicating that the sensory deficit was caused by a restricted infarction of the lateral spinothalamic tract. We emphasize the importance of adding LMI to a differential diagnosis of acute dermatomal sensory disturbance without other major symptoms of LMI, such as cranial nerve abnormalities, ataxia and Horner’s syndrome.

INTRODUCTION

Lateral medullary infarct (LMI), also known as Wallenberg syndrome or posterior inferior cerebellar artery syndrome, is the most prevalent brainstem infarction in clinical practice [1]. It is caused by the obstruction or dissection of the vertebral or posterior inferior cerebellar artery of the brainstem [2]. LMI characteristically involves the inferior cerebellar peduncle, lateral spinothalamic tract, trigeminal spinal cord nucleus, solitary nucleus, nucleus ambiguous and descending sympathetic tract fibres. Neurological symptoms characteristically include sensory disturbances (89%), dysarthria (75%), vertigo or nausea (73%), Horner’s syndrome (72%), cerebellar ataxia (69%), dysphagia (57%) and hiccups (15%) [3]. As the nuclei and tracts are densely located within the lateral medulla oblongata, sensory disturbances are often accompanied by other neurological symptoms. However, pure sensory deficits caused by LMI are uncommon [4]. Moreover, isolated dermatomal dissociated sensory deficit mimicking spinal cord lesions have rarely been reported. Here, we report the case of a patient with caudal LMI presenting solely with temperature and pain sensory loss distributed along the dermatome.

CASE REPORT

A 58-year-old woman presented with acute loss of temperature and pain sensation in the left side of her body and in the left limbs following cervical pain. She visited our hospital 3 days after symptom onset. Her medical history included asthma, hyperlipidaemia and hypertension. Her daily medications were prednisolone (3 mg), alfacalcidol (0.5 μg), rupatadine fumarate (10 mg) and rosuvastatin calcium (2.5 mg). On physical examination, she was alert, well-oriented and afebrile with a blood pressure of 140/75 mmHg. She had lost temperature and pain sensation below the left C5 sensory level (Fig. 1A), while her sensations of touch, position and vibration were intact. She showed no symptoms of any cranial nerve abnormalities, muscle weakness, abnormal tendon reflexes, ataxia, Horner’s syndrome or facial sensory loss. Her neurological symptoms were checked by two certificated neurologists.

Figure 1.

Schematic presentation of pain and temperature sensation disorder (A). MRI findings obtained 3 days after symptom onset (B–E). Axial (B) and sagittal (C) diffusion-weighted images showing restricted diffusion in the right caudal lateral medulla (arrows). Axial fluid-attenuated inversion recovery image (D) showing high-intensity areas in the right lateral medulla (arrows). Magnetic resonance angiography findings (E) illustrating the enlargement of the right vertebral artery (arrows). Topography of the lateral spinothalamic tract of the caudal level of the medullary oblongata (F). The grey area representing the presumed ischemic lesion in this case. S, sacral; L, lumbar; T, thoracic; C, cervical.

A blood test revealed normal blood profile with normal coagulation and thyroid, kidney and liver functions. Magnetic resonance imaging (MRI) findings revealed high-intensity signals in the right caudal lateral medulla oblongata on diffusion-weighted imaging (Fig. 1B and C), fluid-attenuated inversion recovery (Fig. 1D) and an enlarged right vertical artery (Fig. 1E). The MRI findings of the cervical spinal cord were normal. Consequently, we diagnosed her with LMI, suspecting right vertebral artery dissection as the aetiological cause. Therefore, we initiated clopidogrel administration (75 mg/day). Her sensory responses gradually improved from the left upper extremity on hospitalization day 3. Then, on hospitalization day 8, her sensory responses of the left lower extremity showed improvement. On hospitalization day 10, she was discharged to her home without any symptoms. At her 1-month follow-up examination, her neurological symptoms had improved substantially without stroke recurrence.

DISCUSSION

Sensory disturbance is the most common manifestation of LMI and occurs in 89% of cases [3]. It is well known that the typical features of sensory disturbance are temperature and pain impairment on the ipsilateral face as well as contralateral limbs/body because LMI affects the ascending lateral spinothalamic tract and trigeminal spiral tract. However, the characteristics of sensory disturbance because of LMI may vary according to its size. With the recent advances in MRI, various patterns of sensory dysfunction have been reported in LMI cases [5, 6]. Kim et al. [6] reported the characteristics of sensory disturbance due to LMI in their case series of 50 consecutive patients. Their respective frequencies were as follows: ipsilateral face and contralateral limb/body disturbances (26%); contralateral face, trunk and limb disturbances (25%); limb/body involvement without trigeminal involvement (21%); bilateral trigeminal-contralateral limb/body disturbances (14%) and trigeminal involvement without limb/body involvement (10%).

Sensory disturbances are often accompanied by other neurological symptoms [3, 5] However, temperature and pain sensory loss on the contralateral trunk distributed along the dermatome without ipsilateral facial sensory loss have poorly been reported.

In this case, the MRI findings revealed a small lesion in the right superficial caudal lateral medullary oblongata (Fig. 1B–E). We speculate that the sensory deficit in this case was related to the somatotopic organization of the lateral spinothalamic tract. The lateral spinothalamic tract is an ascending sensory pathway composed of afferent nerve fibres that carry information regarding pain and temperature in the corresponding limb and trunk. In the spinal cord and brainstem, the ascending sensory nerve fibres from the sacral, lumbar, thoracic and cervical components are arranged from the lateral to the medial direction (Fig. 1F) [7]. Based on her physical symptoms and MRI findings, the lateral infarction restricted to the lateral spinothalamic tract resulted in sensory deficits below the C5 sensory level (Fig. 1F).

CONCLUSIONS

Herein, we report a rare case of a small LMI confined to the lateral spinothalamic tract that subsequently developed into isolated dermatomal sensory loss. Clinicians should consider that LMI may vary in size and clinical symptoms; furthermore, the absence of cranial nerve palsy, ataxia or Horner’s syndrome does not rule out LMI.

CONFLICT OF INTEREST STATEMENT

No conflicts of interest.

FUNDING

No sources of funding.

ETHICAL APPROVAL

This case report was conducted in accordance with the principles of the ethics review board at our hospital.

CONSENT

The patient provided her written informed consent for the anonymized and deidentified reporting of her findings, and publishing this manuscript.

GUARANTOR

Yuriko Aratake.