Practical cases help you to fully understand the lateral medullary syndrome and its case studies.

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When the patient suddenly vertigos and vomits, what kind of disease might it be? How should we distinguish it from other diseases? What about treatment and prognosis? Let's look at a case. "Yi Mai Tong" was edited. Do not reprint without authorization. A 33-year-old man developed severe dizziness, vomiting and imbalance two days ago. He contracted the disease while preparing breakfast in the kitchen. He suddenly felt dizzy, lost his balance, fell down, and sustained no head injuries. Since then, the patient has a constant sense of rotation and cannot sit on his / her feet without support. The patient complained of vomiting several times and was spontaneous. With the head moving freely, the left half of his face remained numb. In addition, there are mild to moderate left occipital headaches and neck pain, with unknown location. Imperceptibly blurry, stiff neck or photophobia, but he was reluctant to open his eyes because he felt dizzy constantly. The patient's medical history and physical examination denied any previous neck movements or any recent strenuous exercise. No epilepsy or weakness in the limbs. No diplopia, blurred vision or temporary blindness, no swallowing difficulties or hoarseness. No head or neck trauma, no hearing loss or tinnitus, and no upper respiratory infections. There have been no previous episodes of similar dizziness or dizziness, and no fever, ear pain, or ear discharge. He was diagnosed with systemic hypertension 5 years ago and did not take antihypertensive medications regularly. At present, no secondary cause of hypertension has been found. His father also had hypertension, but had no family history of neurological disorders. No history of smoking, drinking or using any illegal drugs. After a neurological examination, the patient did not have a stiff neck. Kernig sign is negative. Mild left upper eyelid drooping, but normal range of motion. The left pupil is smaller than the right pupil, the difference is more pronounced in dim light, and it responds to light. He had a spontaneous nystagmus, beating to the right, not changing direction with his gaze. Both the head pulse test and tilt test were negative. Acupuncture tests showed decreased sensation in the left face and right limb. Mild left central facial paralysis. Vomiting reflexes are normal on both sides. The patient was unable to open his eyes due to severe dizziness. Cardiovascular examination showed abnormally elevated blood pressure at 240/120 nanograms. The rest of the tests were normal. Image examination, brain CT is shown below. Figures 1 and 2 discuss that although the patient's CT findings are normal, the patient is suspected of having lateral medullary syndrome based on the patient's symptoms and signs. A magnetic resonance imaging examination of the patient's brain confirmed a dorsal lateral rostral infarction (Figure 3). Figure 3 Lateral medullary syndrome or Wallenberg syndrome is caused by occlusion of the posterior cerebellar artery or vertebral artery. [1, 2] This results in lateral bulbar infarction with or without the cerebellum. disease Signs and symptoms include dizziness, ipsilateral Horner syndrome, ipsilateral and contralateral body pain and loss of temperature sensation, ipsilateral ataxia, hoarseness and difficulty swallowing. Dizziness, nystagmus and vomiting are caused by involvement of the vestibular nucleus or connection with the cerebellum. [4] Ipsilateral Horner syndrome is caused by a sympathetic descending pathway involved in the lateral reticular structure. [5] The loss of ipsilateral sensation is due to the involvement of the trigeminal nerve descending bundle. The loss of contralateral limb sensation is due to the effect of the ascending thalamus sensory bundle. Ipsilateral ataxia is caused by involvement of the cerebellar foot or spinal cerebellar pathway. Difficulty swallowing and hoarseness are suspected of nuclear involvement. In addition to the typical features of lateral bulbar syndrome, the patient in this case had some abnormal features. Feature 1: The patient did not experience hoarseness or difficulty swallowing. The clinical symptoms of lateral medullary syndrome vary depending on the size and extent of the infarction. [2] Patients with medullary caudal infarction usually have little or no swallowing difficulty and hoarseness. [5] This indicates that the caudal nucleus of the medullary bulb is not directly related to visceral efferent fibers. In most cases of dysphagia and hoarseness, the lesions extend to the head and ventral side of the medulla oblongata. Feature 2: The patient developed mild ipsilateral central facial paleness. It is said that when the lesion extends to the lower pons, ipsilateral peripheral facial incontinence is possible, and the intervention of a cortical-ulnar tract anomalous ring is considered a possible mechanism of ipsilateral central facial incontinence. [5,6] Other changes not found in this patient include loss of lateral position The patient developed mild ipsilateral central facial paleness. It is said that when the lesion extends to the lower pons, ipsilateral peripheral facial incontinence is possible, and the intervention of a cortical-ulnar tract anomalous ring is considered a possible mechanism of ipsilateral central facial incontinence. [5,6] Other changes not found in this patient include loss of lateral position The patient developed mild ipsilateral central facial paleness. It is said that when the lesion extends to the lower pons, ipsilateral peripheral facial incontinence is possible, and the intervention of a cortical-ulnar tract anomalous ring is considered a possible mechanism of ipsilateral central facial incontinence. [5,6] Other changes not found in this patient include loss of lateral position

It has been reported that patients with bilateral sensory disorders have large lesions involving the descending and ascending sensory tracts of the trigeminal nerve, while patients with bilateral sensory disorders have lesions involving the sensory tract of the trigeminal nerve ascending. [5] When first evaluating patients with spontaneous vertigo or acute vertigo (ie, acute vestibular syndrome), doctors must consider that lateral bulbar syndrome is one of the few cases, and acute vestibular neuritis and Meniere's disease are also the first. [7] The typical characteristics of lateral medullary syndrome are worth exploring, especially in patients with acute dizziness, where traditional cardiovascular risk factors exist. Acute vestibular neuronitis is also characterized by acute paroxysmal vertigo, impaired balance, and vomiting. However, limb ataxia, loss of sensation, and Horner syndrome are not secondary causes of vertigo, such as vestibular neuritis, and head pulse test results may be positive. Patients with Meniere's disease often have tinnitus, hearing impairment, and dizziness, as well as other typical neurological features, and should be excluded. Aneurysmal subarachnoid hemorrhage caused by rupture of a posterior communicating aneurysm usually results in dilation of the patient's pupil, but dilation is excluded in this case. [8] Except for normal head CT, the patient did not have a stiff neck and photophobia, and the possibility of bleeding from an aneurysm was very small, so it was ruled out. Brain CT is less sensitive to imaging of the posterior cranial fossa. [9] Once clinical evidence of lateral medullary syndrome is suspected, magnetic resonance imaging of the brain is needed to confirm the diagnosis. Although MRI is sensitive to this disease, no changes were observed in early imaging examinations, which can easily be ignored by imaging doctors. [10] Once the images are confirmed, the patient's potential risk factors and pathogenesis must be investigated. Based on clinical experience, vertebral artery rupture is often considered in young patients with lateral spinal cord syndrome. The patient needs magnetic resonance angiography / angiography. Based on the clinical characteristics of age, left occipital pain, and mild neck pain, the patient met known clinical symptoms associated with arterial rupture. This patient underwent CT angiography and found no vertebral artery rupture and aortic atherosclerosis. Echocardiography revealed concentric left ventricular hypertrophy in patients with hypertension. The electrocardiogram showed no arrhythmia. There were no significant differences in fasting blood glucose, blood lipid levels, and glycated hemoglobin levels. The underlying mechanism of stroke is thought to be small blood vessel disease associated with hypertension. Treatment and prognosis of the lateral bulbar syndrome depend on the duration of the symptoms at the time of diagnosis and the mechanism of the stroke. 3-4 after onset. Patients diagnosed within 5 hours can consider thrombolytic therapy for patients without sandwich causes and contraindications. [11] Outside the time frame of thrombolytic therapy, antiplatelet therapy should be provided, while secondary prevention of cardiovascular disease should be carried out by controlling identified risk factors. Strategies to reduce risk should also include anticoagulation therapy for cardiogenic patients. [11] Thrombolytic therapy is safe in patients with a potential cause of intracranial and external vertebral artery rupture, but the risk of intracranial artery rupture is unknown. For vertebral artery rupture, anticoagulation or antiplatelet treatment usually takes 3-6 months; however, in the case of subarachnoid hemorrhage, expansion of symptomatic aneurysms, or failure of drug treatment, it is necessary to use endovascular treatment or arterial repair Form of surgical intervention. The patient was diagnosed late and could not benefit from thrombolysis. The patient's blood pressure is very high, exceeding the average of 140 nanograms. The patient started intravenous rabevolol treatment and switched to oral antihypertensive drugs. During the course of treatment, the sympathetic nerve pathways of the lateral medulla may be affected, and the patient's blood pressure may fluctuate sharply. Later, when blood pressure was controlled and stabilized, it was changed to oral antiplatelet drugs. Most patients with lateral bulbar syndrome have a good prognosis. In previous case reports, most patients had a good prognosis with only a few sequelae after 3-6 months of follow-up. [2,5] Of the 130 patients, only one died during the acute phase. [2] In this case, the patient initially presents with ataxia and must have support to maintain a sitting position. However, about 7 days after the onset of symptoms, the patient returned to an independent sitting position before discharge, still unable to stand independently, and always fell to the left (the same side as the lesion) when standing. Sequelae. [2,5] Of the 130 patients, only one died during the acute phase. [2] In this case, the patient initially presents with ataxia and must have support to maintain a sitting position. However, about 7 days after the onset of symptoms, the patient returned to an independent sitting position before discharge, still unable to stand independently, and always fell to the left (the same side as the lesion) when standing. Sequelae. [2,5] Of the 130 patients, only one died during the acute phase. [2] In this case, the patient initially presents with ataxia and must have support to maintain a sitting position. However, about 7 days after the onset of symptoms, the patient returned to an independent sitting position before discharge, still unable to stand independently, and always fell to the left (the same side as the lesion) when standing.

The following content of the reference: The following is the original index: Olusegun John Ouluwoller February 14, 2020, a 33-year-old man suddenly cannot stand or sit.