Trigeminal nerve (V) - Trismus due to masseter and temporalis hyper contraction Vagus nerve (X) - Ipsilateral/ deficit of reflex cough test Glossopharyngeal (IX) - Ipsilateral absent gag reflex and hoarseness Nucleus ambiguus - Ipsilateral dysphagia, dysarthria, and dysphonia ĭescending Sympathetic - Ipsilateral Horner syndrome Vestibular nucleus - Ipsilateral nystagmus, vertigo, nausea, and vomiting Trigeminal nerve (V) - Ipsilateral loss of pain and temperature on the face Spinothalamic tract - Contralateral impairment of pain and temperature in trunk and limbs Vertigo, nausea and vomiting, and symptoms like skew deviation, diplopia, and severe gait ataxia could be due to the pathology of the vestibular nuclei or vestibular–cerebellar connections. This results in the disinhibition of antidiuretic hormone (ADH) secretion by the pituitary gland causing SIADH. The proposed pathophysiology includes the failure of propagation of non-osmotic stimuli from the carotid sinus through vagal nerve due to the nucleus tractus solitarius lesion in the medulla. Reports exist of SIADH in patients with lateral medullary infarction. Hyponatremia after a brain injury occurs due to the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) and cerebral salt wasting syndrome. The neural structures related to hiccups are unknown, but nucleus ambiguus or adjacent areas that are involved in regulating respiration may have involvement in the generation of the hiccup.
Hiccups are also a clinical feature of the lateral medullary syndrome. These include the nucleus ambiguous and nucleus tractus solitarius and the reticular formation. Dysphagia is due to the involvement of swallowing centers in the dorsolateral medulla oblongata. Pathological processes for the development of lateral medullary syndrome include large-vessel infarction (50%), arterial dissection (15%), small vessel infarct (13%), and cardioembolism (5%).ĭysphagia in LMS involves a lack of coordination in pharyngeal and esophageal phases of swallowing.