Causes and Treatment of Wallenberg Syndrome - Oren Zarif - Wallenberg Syndrome
There are several causes of Wallenberg syndrome. The most common is a dissection or atherosclerotic occlusion of the posterior inferior cerebellar artery, with lesser cases resulting from embolism or dissection. Some people have additional motor weakness or paralysis in addition to wallenberg syndrome. Smoking and hypertension are known risk factors for this disorder, as are minor neck traumas. However, it is unclear which factor is the most important in determining the symptoms.
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Most people with Wallenberg syndrome experience an ischemic stroke of the brain stem. In such cases, the vertebral artery may be occluded or thrombosed, resulting in a stroke. Less common causes include mechanical trauma to the vertebral artery in the neck or aneurysm, and connective tissue disorders such as multiple sclerosis. The most effective way to determine whether you have a stroke or wallenberg syndrome is to have an MRI with DWI. If the signal in the lateral medulla is low, it is likely to be a lateral medulla infarction.
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Treatment for Wallenberg syndrome is similar to that for acute stroke. Rapid evaluation and treatment are essential to improving the patient's prognosis. During the first few days of treatment, blood thinners are given intravenously to prevent clot formation and propagation.
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Medications are also used to control high blood pressure and cholesterol levels. Pain management is crucial, since pain in patients with wallenberg syndrome can be severe and disabling. Antiseizure and analgesic medications are frequently prescribed to alleviate pain.
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The diagnosis of Wallenberg syndrome is based on a combination of symptoms, the patient's history, and radiographic imaging. Damage to the lateral spinothalamic tracts causes pain and temperature sensory deficits in the ipsilateral face. Infarction of the vestibular nuclei also causes vomiting, nystagmus, and ipsilateral ataxia. Further, infarction of the nucleus ambiguous, which regulates the voice, leads to pharyngeal ataxia, laryngeal ataxia, and dysphagia.
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Compared to other acute ischemic strokes, people with Wallenberg syndrome have a more positive outcome after their stroke. However, the most significant sequela of Wallenberg syndrome is gait instability. Early physical and occupational therapy are necessary for recovery. Patients with this syndrome may experience a gait instability. Some patients may also have hiccups and ataxia. There is no cure for the disorder, but early intervention can improve a patient's quality of life.
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Besides the lateral medullary lesions, Wallenberg's syndrome can cause nystagmus. The abnormalities occur when the contralateral eye is elevated, and the ipsilateral eye is tilted or rotated. Other signs of this syndrome include ipsipulsion, contrapulsion, and head tilt. When the upper pole of the iris is damaged, ipsipulsion of saccades occurs.
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Other symptoms associated with Wallenberg syndrome include sensory deficits on the opposite or same side of the infarcted area. Some patients experience drooping eyelids, small pupils, or facial pain. Hearing loss is a symptom of the condition, as are swallowing problems and slurred speech. Patients can return to oral feeding after a few weeks or months. However, some people will experience a permanent disability.
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Researchers have noted a number of similarities between Wallenberg syndrome and CFN inactivation. In the latter case, a patient with Wallenberg syndrome exhibits abnormal Purkinje cell activity, which would result in a powerful inhibition of the cerebellar nuclei. The effects would be similar to those observed with experimental CFN inactivation. This is why researchers are exploring the treatment for the disorder. These findings are a significant step toward better understanding the causes of Wallenberg syndrome.
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Although no cure exists for Wallenberg syndrome, there are treatments available for patients with the disorder. Research on this disorder is conducted at the National Institute of Neurological Disorders and Stroke (NIH).