Rest of the cranial nerve functions were intact. Neurological examination revealed normal higher mental functions, cranial nerve deficit in the form of absent gag reflex on the left side. On examination, patient had stable vitals with a blood pressure of 130/80 mm Hg and pulse rate of 94/min. There was no history of trauma, fever or self-remitting similar episodes in the past. There was no history of smoking or addiction to any other drug or substance. There was no history of nausea, vomiting, seizure, focal weakness, sensory complaints, difficulty in hearing, drooling of saliva, facial deviation, diplopia or dimness of vision. The first case is about a 30-year-old male who admitted with the complaints of sudden onset dizziness, dysphagia both to solids and liquids, dysarthria and swaying to left while walking for past 2 days. However, to our best of knowledge hyperhomocystinemia presenting as Wallenberg has not been described in literature. ,, Hyperhomocysteinemia generally presents as vascular thrombotic events as stroke, coronary artery disease etc. This has led people to search for novel risk factors like hyperhomocysteinemia which has been at times decribed as a modifiable risk factor. But these risk factors are most of the time not found in patients with young stroke. The classical risk factors described for stroke include diabetes, hypertension and cardiac disease. Hyperhomocysteinemia presenting as Wallenberg syndrome: A report of two cases and review of literature. How to cite this URL: Chabbra P, Gupta N, Garg A, Khurana S. How to cite this article: Chabbra P, Gupta N, Garg A, Khurana S. Keywords: Hyperhomocysteinemia, posterior inferior cerebellar artery, Wallenberg syndrome Therefore, we report two cases of Wallenberg syndrome where patients were found to have hyperhomocysteinemia as a risk factor for the prothrombotic state. However, prothrombotic states rarely present as lateral medullary syndrome. The most common etiology of Wallenberg syndrome being atherosclerotic occlusion of the arteries followed by secondary thrombosis. Manifestations depend on the site of lesion. The clinical manifestations include dysphagia, nausea, vomiting, ataxia, Horner's syndrome, ipsilateral loss of pain and temperature over the face and contralateral loss over the trunk and body etc. The clinical manifestations result from impaired functioning of vestibular nuclei, inferior cerebellar peduncle, central tegmental tract, descending sympathetic fibers, nucleus ambiguus, spinothalamic tracts and spinal trigeminal nucleus. It most commonly results from occlusion of the vertebral artery followed by the PICA. Wallenberg syndrome or lateral medullary syndrome occurs due to infarction of the lateral medulla usually supplied by the posterior inferior cerebellar artery (PICA).
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