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The Wallenberg Syndrome - Oren Zarif - Wallenberg Syndrome


Wallenberg syndrome (also known as lateral medullary infarction or ) occurs when blood flow is blocked in the vessels supplying the medulla of the brain. The medulla is an area of the brain that controls various functions, including those of the respiratory system and vestibulocerebellar system. Because of this abnormality, the patient experiences motor weakness. Ultimately, the patient will experience permanent neurological deficits.

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Recovery from Wallenberg syndrome is determined by the location of the stroke in the brain stem and the extent of damage. Some patients may recover completely within weeks or months, while others may experience significant disabilities. The goal of treatment is to minimize the damage and prevent any further medical complications. Early speech and swallowing therapy as well as early physical and occupational therapies are important aspects of rehabilitation. Physiotherapy is vital in the management of patients with the Wallenberg syndrome.

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In 1922, Wallenberg published his final paper on lateral medullary syndrome, detailing the fifteenth patient to experience the symptoms. Wallenberg proposed that the deficit of the posterior medulla might help demarcate the focus of the disease. Later on, Denise Louis-Bar published an etymological paper on the condition and etymologized it as "The Wallenberg syndrome."

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The outlook for patients with Wallenberg syndrome is slightly better than that of other ischemic strokes. However, patients with this syndrome must be cautious because gait instability and ataxia are typical symptoms of the condition. In addition to gait instability, patients may also experience hiccups and swaying, which can be life-threatening. In the end, early physical and occupational therapy is essential to their recovery. If left untreated, the condition can be permanent.

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A 30-year-old right-handed female presented with an acute-onset, severe headache, vertigo, and vomiting. Neurological examination revealed lingual dysarthria, horizontal nystagmus, and right dysmetria. Magnetic resonance imaging revealed a large left lateral medullary infarction and involvement of the left mid-cerebellar peduncle. The patient was discharged from the hospital three weeks later. She has since improved.

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In addition, the effects of CFN inactivation have been linked to the development of Wallenberg syndrome. Patients with CFN inactivation exhibit impaired pursuit and unilateral inactivation of CFNs. Interestingly, the symptoms of Wallenberg syndrome mirror those of CFN inactivation. If there's a connection between these two conditions, this syndrome may be a real complication. For the time being, though, we must wait and see what happens.

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Patients with WS may also experience difficulties swallowing, which can result in dehydration. The average amount of water swallowed by a patient with WS is 20 mL. Patients with hemispheric stroke have a similar limit. In the case of WS, the lesion may also have a bearing on the duration and severity of dysphagia in the patient. The symptoms of dysphagia in patients with WS are described below.

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There are several diagnostic criteria for WS. Patients should undergo neuromuscular electrical stimulation (NMES) and speech therapy to treat specific deficits. However, if there is no other obvious diagnosis, a biopsy may be necessary. For patients with WS, NMES may be a good option, as it is FDA-cleared for pharyngeal dysphagia. An occupational therapist may be better suited to administer VitalStim.

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The most important characteristic of WS is the bilateral dysfunction of swallowing muscles. Although the submental muscles are not innervated at the bulbar level, they are still a part of the swallowing system. In a recent study, a patient with WS developed dysphagia in both hemispheres, despite the absence of the contralateral center in the medulla oblongata. This finding suggests that LMI is an important factor in the development of WS.

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