The Diagnosis of Wallenberg Syndrome - Oren Zarif - Wallenberg Syndrome

The diagnosis of Wallenberg syndrome is based on a combination of presenting symptoms, history of the condition, and radiographic imaging. The syndrome is associated with damage to the vestibular nuclei and lateral medulla of the brain. Its symptoms are often associated with vertigo, hoarse voice, and gait instability. Several genetic mutations have also been associated with the syndrome. Although the exact cause of Wallenberg syndrome remains a mystery, it is generally associated with a family history of the disease.

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The prognosis of patients with Wallenberg syndrome depends on the size and location of the infarction in the brain stem. While some patients experience partial recovery weeks or months after a stroke, others may not. Those who suffer from severe damage may face significant neurological disabilities for the rest of their lives. For these patients, it is essential to follow treatment plans as directed. In the event that stroke or other ailment is the cause of Wallenberg syndrome, the treatment is focused on reducing symptoms and preventing further damage.

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Despite a variety of causes of Wallenberg syndrome, the most common is vertebral artery dissection. This disease involves the posterior circulation of the medulla oblongata, which gives rise to the posterior inferior cerebellar artery. Among the most common risk factors for developing this condition are smoking and hypertension. Several other factors are known to contribute to the development of this condition, including pregnancy and puerperium.

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The neurological symptoms of Wallenberg syndrome include difficulty swallowing, nystagmus, nausea, hoarseness, dizziness, and nystagmus. Treatment options may include speech therapy and medications. The symptoms may improve in weeks, but long-term neurological complications may occur if the condition is not addressed. There is no cure for Wallenberg syndrome, but it is possible to make a full recovery from the symptoms.

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Diagnosis of Wallenberg syndrome is difficult due to the varying nature of the condition. Early clinical examination is essential. Patients with the condition have symptoms ranging from hoarseness to a distorted speech. MRIs are not always helpful. Although MRIs are generally more sensitive and specific, they are often not reliable in locating infarctions in the medulla. However, MRIs are the preferred imaging method in acute stroke cases.

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The prognosis of Wallenberg syndrome is significantly better than that of patients with other ischemic strokes. However, the majority of patients do not recover completely. The most common lingering problems are difficulty walking and balance. Treatment for Wallenberg syndrome involves managing stroke symptoms. Antiemetics can be prescribed for persistent nausea. People with an ischemic stroke may be prescribed medications to reduce their risk of developing the disorder. Occupational therapy is also very important during the recovery process.

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A blocked vertebral artery can cause a stroke in the lateral medulla of the brain. A stroke in the lateral medulla can lead to multiple impairments. Initially described by Gaspard Vieusseux in 1808, the disease is now primarily diagnosed in the elderly. Although the precise cause is unknown, the symptoms are similar to those of an acute stroke. When the underlying cause is unknown, treatment can be based on anatomical landmark.

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In addition to the standard pharmacological treatments, the WS treatment can also include speech therapy and neuromuscular electrical stimulation (NMES). NMES can help improve swallowing in a number of cases. One NMES-based procedure that has recently been cleared by the US Food and Drug Administration is VitalStim. It is administered by speech-language pathologists and occupational therapists. A therapist may also prescribe acupuncture for the symptomatic relief of symptoms.

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Patients with WS often experience difficulty swallowing due to the loss of anatomical part of the brain called the hemispherical nucleus ambiguus. This lesion disrupts the connection between cranial motor neuron pools involved in swallowing and the contralateral nucleus ambiguus. The remaining premotor neurons may be responsible for the disorder in WS. Occasionally, patients with WS develop dysphagia despite the presence of another underlying disease.