What You Should Know About Wallenberg Syndrome - Oren Zarif - Wallenberg Syndrome

Wallenberg syndrome is a constellation of neurological symptoms caused by a posterior vascular accident. While MRI with DWI is the gold standard for diagnosis, a normal MRI may also indicate the presence of the syndrome. Early diagnosis and treatment are essential, as treatment can save lives. Here are a few things you should know about this disorder. Symptoms of this syndrome may vary from person to person, but early detection is crucial. There is no cure for the syndrome, so treatment should be individualized.

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The clinical diagnosis of Wallenberg syndrome is based on the patient's presenting symptoms, history, and radiographic imaging. Damage to the lateral medulla, inferior cerebellar peduncle, trigeminal nerve, and vagus nerve is a primary cause of the neurological deficits associated with the syndrome. Symptoms of this syndrome include gait instability, hoarseness of voice, and dysphagia.

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Treatment depends on the type of stroke and where in the brain stem the infarction occurred. Early treatment and symptom management can help the patient recover. A feeding tube or speech therapy may be required if swallowing is difficult. Medications may be prescribed for the pain, including the anti-epileptic drug gabapentin. The long-term outlook for patients with Wallenberg syndrome is dependent on how much damage has been done to the brain stem and the location of the infarction. Patients may experience significant neurological disabilities for years.

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While the prognosis of patients with this condition is better than those of other acute ischemic stroke, the outcome is not rosy. Symptoms of Wallenberg syndrome can include gait instability, ataxia, hiccups, and a variety of other neurological issues. Early physical therapy and occupational therapy are vital for post-stroke recovery. And early treatment is the key to preventing any permanent disability. If you are suffering from the effects of Wallenberg syndrome, it is essential that you seek medical treatment as soon as possible.

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The symptoms of Wallenberg syndrome include dysphagia, decreased sense of pain, and a smaller pupil. The patient may also experience a lack of sensation in their extremities, including tinnitus. Recovery time will vary from person to person, but in most cases, it lasts between six weeks and six months. However, patients with more serious damage may have permanent disabilities and require lifelong medical care. While this condition is treatable and manageable, it should not be overlooked.

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A post-mortem of the patient in 1894 performed by Wallenberg confirmed the location of the lesion in the posterior inferior cerebellar artery. Although the exact cause of the syndrome is not known, some risk factors have been linked with the condition. For example, pregnancy and puerperium have been linked to vertebral artery dissection. A physician should consider these factors in young patients when evaluating a patient for Wallenberg syndrome.

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Other symptoms of Wallenberg's syndrome include eye deviation and impaired contralateral pursuit. In most patients, these symptoms occur because of otolithic lesions. These lesions affect the vestibular nuclei of the lateral medullary region and cause a vertical divergence of Hertwig-Magendie. This is a characteristic of this disorder and is not uncommon. There is no known cure for this condition, but early diagnosis and treatment are the best ways to minimize its severity.

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Wallenberg studied medicine in Leipzig and Heidelberg under Erb, writing his thesis on poliomyelitis and returning to Danzig as a physician at the city hospital. He was a prominent physician in Danzig until he suffered a skull base fracture in 1891. He believed that his injury had caused his compulsive personality. He refused several positions in Germany and became the chief physician of the city's hospital. He also served as an advisor to the 17th army during the first world war. His work on the nervous system earned him the Erb medal in 1929.

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LMI also causes a unilateral lesion in WS patients. LMI affects the underlying premotor neurons in the nucleus ambiguus, which appear to be responsible for oropharyngeal swallowing. The affected submental muscles are not innervated at the bulbar level, and may be responsible for the development of WS. Interestingly, while both centers of LMI are affected, the remaining premotor neurons are intact, resulting in an unusually functional dysphagia.