An MRI of the Brain Reveals a Diagnosis of Wallenberg Syndrome - Oren Zarif - Wallenberg Syndrome
The patient presented with severe dizziness, left-sided facial burning sensation, intractable hiccups, and decreased left arm and leg strength. In addition, she experienced difficulty sitting up and leaning to the left. An MRI of the brain revealed a lateral hyperintense lesion at the level of the left posterior medulla, the correct location for a diagnosis of wallenberg syndrome. However, the patient was not able to swallow food or liquids due to the pain.
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While a CT may help pinpoint the location of the infarction, MRI is still the preferred imaging method for acute stroke. This imaging test offers better sensitivity and specificity, but it is not reliable in determining the exact location of the infarction in the medulla. The early clinical examination is therefore crucial to the diagnosis of the syndrome. Further, an MRI may show a diagnosis of WS in a patient with other comorbid conditions.
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While a stroke can be a traumatic event, a person suffering from Wallenberg syndrome may recover on their own. However, the severity of the damage caused by the stroke will determine the treatment options available. A patient may experience temporary improvement in their symptoms, while others may develop significant neurological disabilities that require lifelong medical care. The prognosis of the condition depends on the location and size of the damaged brain stem. If the stroke has caused more damage, however, the patient may be left with a permanent disability.
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Although an ischemic stroke is the most common cause of Wallenberg syndrome, the condition can occur in any part of the nervous system. When blood vessels in the brain stem become occluded or blocked, it results in a syndrome called Wallenberg syndrome. Wallenberg syndrome is often caused by damage to the vertebral arteries and posterior inferior cerebellar artery, but other types of arteries can also be responsible for the syndrome.
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The patient with lateral medullary syndrome usually presents with a headache and ataxia, which are symptoms of damage to the cerebellum. Damage to the hypothalamo-spinal fibers may cause ataxia. In addition, patients with isolated nodulus or tonsilar infarction may also experience nystagmus or unidirectional nystagmus. Despite the lack of specific treatment, patients with lateral medullary syndrome may undergo head impulse tests to measure brain function.
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The primary cause of Wallenberg syndrome is a blockage in the posterior circulation of the medulla oblongata. However, less common causes include atherosclerotic occlusion. Moreover, it is important to note that other factors, such as pregnancy and puerperium, can cause vertebral artery dissection and lead to a diagnosis of wallenberg syndrome. Therefore, it is important to seek appropriate treatment for patients with this disease.
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Among the symptoms associated with this condition, the systolic sound of the cerebelli was detected in the grista occipitalis, the angle of the lower jaw, and the temple. Pulsation of the neck vessels was stronger on the right side of the body than the left. A post-mortem examination performed in 1901 by Wallenberg confirmed the location of the infarct in the posterior inferior cerebellar artery.
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Patients with wallenberg syndrome may display symptoms such as walking with a limp, ataxia of the left extremities, and paresthesia of the left soft palate. The left vocal cord may be paralysed and the patients may have a large, enlarged tongue at rest. Furthermore, they may have sensory or sensitivity disturbances of the first and second branches of the left trigeminal nerve. If the symptoms are severe, the patient should seek medical treatment immediately.
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In addition, the patient's ability to swallow food may be impaired. The patient may have delayed swallowing reflex, which is related to the disruption of premotor neurons in the NA. The electrophysiological findings in the NA may help determine the causes of dysphagia. In the meantime, swallowing therapy may be the first line of treatment for the patient with WS. And the patient may benefit from neuromuscular electrical stimulation (NMES) as well as speech therapy.
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Electrophysiological evaluation of swallowing functions has revealed a strong association between WS and stroke. When the disease develops after a stroke, the central pattern generator of deglutition does not function properly, which leads to delayed rostral elevation. Furthermore, the patient with WS may have difficulty controlling bolus. Moreover, swallowing disorder may occur after hemispheric stroke. The extent of the lesion may determine the severity of the dysphagia in WS and its duration.