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.