Wallenberg syndrome, or lateral medullar syndrome, is the clinical presentation of the infarct in the territory of posterior inferior cerebellar artery. Its signs and symptoms include vertigo, nystagmus, diplopia, ipsilateral Horner syndrome, facial ruddiness and dry skin, dysphonia, dysphagia, dysarthria, ipsilateral loss of gag reflex, ipsilateral ataxia, ipsilateral impaired taste, ipsilateral facial pain and paresthesia, decreased ipsilateral blink reflex, contralateral hypoalgesia and thermoanaesthesia in the trunk and limbs; and ipsilateral facial hypoalgesia and thermoanaesthesia. Neuroanatomical knowledge is essential to its comprehension, study and diagnosis, because the classic neurological manifestations are easy to explain and understand if function and localization of affected anatomical structures are known as if the posterior cerebral circulation is.

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Bases neuroanatómicas del síndrome de Wallenberg

/pdf/neuroanatomical-basis-of-wallenberg-syndrome-buz9p5vk.pdf

Neuroanatomical basis of Wallenberg syndrome

Lateral medullary syndrome (LMS), also called Wallenberg syndrome or posterior inferior cerebellar artery syndrome results from a vascular event in the lateral part of the medulla oblongata. It was named after Adolf Wallenberg (1862-1949), who was a renowned Jewish neurologist and neuroanatomist who practiced in Germany. He first reported the case of LMS. The arteries commonly involved in LMS are the posterior inferior cerebellar artery (PICA) or the vertebral artery. Lateral medullary syndrome characteristically has varied neurologic manifestations. The damage is to the inferior cerebellar peduncle and dorsolateral medulla, descending spinal tract, the nucleus of the trigeminal nerve, nuclei, and fibers of the vagus nerves and glossopharyngeal, descending sympathetic tract fibers, spinothalamic tract, and vestibular nuclei.

pdf/lateral-medullary-syndrome-4ihkemngn9.pdf

Lateral Medullary Syndrome

ResumenEl síndrome de Wallenberg es la presentación clínica más frecuente del evento vascular cerebral en la circulación posterior.Su manifestación clínica incluye una gama diversa de signos y síntomas, la mayor parte de los cuales se explican fácilmente por la correlación anatómica con las estructuras afectadas.Su estudio es un reflejo claro de la importancia de la neuroanatomía en la aplicación clínica.Descrito por primera vez en 1895 

Síndrome de Wallenberg: correlación neuroanatómica

A 47-year-old man with Wallenberg syndrome after a stroke in the territory of the left vertebrobasilar artery and posterior inferior cerebellar artery, presented a week later complaining of visual loss in the left eye. Examination showed corneal anaesthesia associated with a neurotrophic corneal epithelial defect. Corneal involvement secondary to trigeminal neuropathy in Wallenberg syndrome is not frequently reported and may lead to epithelial erosion and neurotrophic keratopathy. Clinicians should be aware that visual loss can occur from a neurogenic basis (e.g., Wallenberg syndrome) due to neurotrophic keratopathy. The use of cocaine, a potential cause of neurotrophic keratopathy, should also be suspected in the appropriate clinical scenario.

/pdf/corneal-involvement-in-wallenberg-syndrome-case-report-and-23999s55ji.pdf

Corneal Involvement in Wallenberg Syndrome: Case Report and Literature Review.

We studied three patients who developed left unilateral punctate keratitis after suffering left-sided Wallenberg Syndrome. A complex evolution occurred in two of them. In all cases, neurophysiological studies showed damage in the trigeminal sensory component at the bulbar level. Corneal involvement secondary to Wallenberg syndrome is a rare cause of unilateral superficial punctate keratitis. The loss of corneal sensitivity caused by trigeminal neuropathy leads to epithelial erosions that are frequently unobserved by the patient, resulting in a high risk of corneal-ulcer development with the possibility of superinfection. Neurophysiological studies can help to locate the anatomical level of damage at the ophthalmic branch of the trigeminal nerve, confirming the suspected etiology of stroke, and demonstrating that prior vascular involvement coincides with the location of trigeminal nerve damage. In some of these patients, oculofacial pain is a distinctive feature.

/pdf/unilateral-punctate-keratitis-secondary-to-wallenberg-1ouij040wn.pdf

Unilateral Punctate Keratitis Secondary to Wallenberg Syndrome

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Unilateral Punctate Keratitis Secondary to Wallenberg Syndrome