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1. Lateral medullary syndrome (Wallenberg syndrome )

2. Introduction This syndrome is most often secondary to intracranial vertebral artery or posterior inferior cerebellar artery occlusion Spontaneous dissections of the vertebral arteries are a common cause

3. The characteristic clinical picture results from damage to a wedge-shaped area of the lateral medulla and inferior cerebellum and consists of several signs: Ipsilateral facial hypalgesia and thermoanesthesia (due to trigeminal spinal nucleus and tract involvement). Ipsilateral facial pain is common

4. Contralateral trunk and extremity hypalgesia and thermoanesthesia (due to damage to the spinothalamic tract). Ipsilateral palatal, pharyngeal, and vocal cord paralysis with dysphagia and dysarthria (due to involvement of the nucleus ambiguus ) Ipsilateral Horner syndrome (due to affection of the descending sympathetic fibers ). Ipsilateral hypohidrosis of the body may occur, probably due to interruption of the mostly uncrossed excitatory sweating pathway, which descends from the hypothalamus through the tegmental area of the mesencephalon and pons and, more caudally, through the posterolateral area of the medulla to synapse with the sympathetic sudomotor neurons of the intermediolateral cell column of the spinal cord

5. Vertigo, nausea, and vomiting (due to involvement of the vestibular nuclei) Ipsilateral cerebellar signs and symptoms (due to involvement of the inferior cerebellar peduncle and cerebellum). Occasionally, hiccups ( singultus ) attributed to lesions of the dorsolateral region of the middle medulla [117] and diplopia (perhaps secondary to involvement of the lower pons).

6. Lateral lesions located in the rostral medulla are associated with more severe dysphagia, hoarseness,and the presence of facial paresis. More caudal lesions situated in the lateral surface of the medulla, correlate with more marked vertigo, nystagmus, and gait ataxia. Lesions that extend more ventromedially cause facial sensory changes on the contralateral side of the lesion

7. The motor system (pyramids), tongue movements,and vibration and position sense are typically spared with lateral medullary lesions because the corresponding anatomic structures are located in the medial medulla. The triad of Horner syndrome, ipsilateral ataxia, and contralateral hypalgesia clinically identifies patients with lateral medullary infarction

8. Rare manifestations of the Wallenberg syndrome include : Wild arm ataxia probably related to involvement of the lateral cuneate nucleus Clumsiness of the ipsilateral upper limb resulting from extension of the injury into the subolivary area. Isolated ipsiversive lateropulsion

9. Patients with the lateral medullary syndrome may complain of a sensation of their bodies being pulled to one side and attempt to counteract this lateropulsion of the body by leaning toward the opposite side. Because of gaze-holding impairment, ocular movements may be similarly affected, with a tendency for the eyes to be “pulled” toward the involved medulla ( lateropulsion or ipsipulsion of eye movements) Patients with Wallenberg syndrome may have permanent saccadic dysmetria ( hypermetria to the side of the lesion and hypometria to targets contralateral to the lesion) and a reduced capability to readjust saccadic amplitude

10. Atherosclerotic occlusion or dissection of the intracranial vertebral artery can lead to a total unilateral hemimedullary (Babinski- Nageotte ) syndrome, a combination of the medial and lateral medullary syndromes Characterized by contralateral hemiplegia and sensory loss of the limbs and trunk, ipsilateral hemiataxia , and facial sensory loss, along with dysphagia, dysphonia, and dysarthria.