DISCUSSION
LMS represents a rare manifestation of ischemic stroke, often attributed to thrombotic or embolic events originating in the heart or major arteries. Other etiologies include hemorrhage, vertebral artery dissection, cavernous angioma, and malignancies. Vertebral artery dissection and large artery atherosclerosis emerge as prominent risk factors in most cases recorded in LMS stroke registries. Among younger patients, vertebral artery dissection predominates, especially in those with trauma histories, while in adults, atherosclerosis, particularly hypertension, diabetes, and coronary artery disease, stands out as the primary risk factor. (1,5).
Classic lateral medullary syndrome is caused by damage to various structures, including the trigeminal spinal nucleus and tract, spinothalamic tract, descending sympathetic fibers, inferior cerebellar peduncle, vestibular nuclei, and nucleus ambiguus. Variations arise when vulnerable areas are partially preserved due to residual blood supply or when surrounding regions suffer compromised perfusion(6). Patients with infarctions affecting the caudal medulla primarily often exhibit symptoms such as vertigo, nystagmus, and ataxia due to the involvement of the vestibular nuclei and cerebellar pathways. Rostral lesions that affect the nucleus ambiguus, crucial for motor function of the glossopharyngeal and vagus nerves, can manifest as severe dysphagia and hoarseness, sometimes as the only symptoms. The loss of taste may result from damage to the nucleus solitarius. Ipsilateral facial numbness is caused by damage to the trigeminal spinal nucleus and tract. In certain cases, involvement of the caudal pons can lead to ipsilateral facial weakness via the facial nucleus(4,6).
LMS typically involves lesions confined to the lateral medullary area (referred to as pure LMS), but some patients may exhibit additional infarctions in other regions of the brain (known as LMS plus). According to a study conducted in Korea, out of 248 patients with LMS, 161 (64.9%) presented pure LMS, while 87 (35.1%) showed LMS plus. During hospitalization, patients with LMS plus were more likely to require admission to the intensive care unit (ICU) and were at a higher risk of developing pneumonia compared to those with pure LMS. Furthermore, upon discharge, LMS plus patients had a higher modified Rankin Scale (mRS) score, indicating poorer functional outcomes than LMS pure patients. However, no significant differences were observed in the occurrence of stroke, acute coronary syndrome (ACS), frequency of death, or overall functional outcome during follow-up. However, pure patients with LMS reported a higher prevalence of residual neurological symptoms such as dizziness, dysphagia, and sensory disturbances compared to LMS-plus patients(7). Our patient had LMS plus but had a good functional outcome at follow-up.
The vertebral artery originates from the innominate artery on the right side and the subclavian artery on the left side. It is divided into four segments: V1, V2, V3 and V4. The V4 segment ascends to merge with the contralateral vertebral artery, forming the basilar artery. In particular, only the fourth segment produces branches that supply the brainstem and cerebellum. The proximal segment of the posterior inferior cerebellar artery supplies the lateral medulla, while its distal branches nourish the inferior surface of the cerebellum. Obstruction or thrombosis of the V4 segment can lead to ischemia in the lateral medulla. This results in a characteristic array of symptoms known as lateral medullary syndrome, or Wallenberg syndrome, which includes vertigo, ipsilateral facial numbness, contralateral limb numbness, diplopia, hoarseness, dysarthria, dysphagia, and ipsilateral Horner syndrome. In addition, ipsilateral facial weakness of the upper motor nerve may manifest. Most cases arise from ipsilateral vertebral artery occlusion followed by posterior inferior cerebellar artery occlusion(8).
All suspected acute stroke cases require urgent neuroimaging to rule out alternative diagnoses, such as intracerebral hemorrhage or focal compression. Noncontrast CT is commonly used for this purpose and can help identify patients suitable for thrombolysis(9). CT angiography (CTA) should be considered to detect vertebral artery dissection. However, it is crucial to recognize that neither CT nor CTA is highly sensitive for diagnosing acute posterior fossa ischemic stroke; MRI with diffusion-weighted sequences remains the gold standard, boasting a sensitivity of 83% and specificity of 96%(10). However, even magnetic resonance imaging may be unreliable in acute lateral medullary infarction, with sensitivity decreasing to 72% within 48 hours after symptom onset, underlining the importance of clinical judgment in evaluating these patients(11).
As with other strokes of ischemic origin, the treatment of LMS includes thrombolysis if the patient presents within 4.5 years(9). However, our patient presented during the subacute stage, missing the window for thrombolysis. Consequently, secondary prevention measures were promptly initiated to prevent future strokes. Admitted to the neurology department, she received treatment including statins, low molecular weight subcutaneous heparin, and aspirin. In addition, speech and swallow therapy was administered. Interestingly, after a week of hospitalization, her condition showed significant improvement, with dysarthria and dysphagia nearly resolved. Subsequently, she was discharged to undergo physical rehabilitation. At the 3-month outpatient follow-up, her ataxia resolved and she continued with her rehabilitation program.