Babinski-Nageotte Syndrome Research Articles

Author Response: Teaching NeuroImage: Reinhold Hemimedullary Syndrome.

Author Response: Teaching NeuroImage: Reinhold Hemimedullary Syndrome.

Lateral Medullary Syndrome Presenting as Babinski–Nageotte Syndrome with Ipsilateral Upper Motor Neuron Facial Palsy

Babinski–Nageotte syndrome is one of the variants of lateral medullary syndrome (LMS) with contralateral hemiparesis along with classical LMS findings. The simultaneous occurrence of ipsilateral central facial nerve palsy and contralateral hemiparesis is an extremely rare occurrence in LMS. We report the case of a 46-year-old male who presented with complaints of acute onset of vertigo, right-sided (ipsilateral) Horner syndrome, facial sensory loss, upper motor neuron facial nerve palsy, ataxia, and left hemiparesis (contralateral). Magnetic resonance imaging brain suggested acute infarct of the right dorsal medulla and medial aspect of the right cerebellar tonsil with attenuation of the distal segment of the right vertebral artery and right posterior inferior cerebellar artery.

Babinski-Nageotte Syndrome: Case Report of a rare variant of Lateral Medullary Infarction

Babinski-Nageotte Syndrome (BNS) is a rare variant of lateral medullary infarction, and only a few cases have been reported. In this case, a 52-year-old African-American gentleman presented with acute onset weakness on the left side of the body. On examination, there was a palpable right supraclavicular lymph node. Neurological examination showed right-sided gaze-evoked nystagmus and left hemiparesis with grade 3/5 power. Reflexes were normal except for extensor plantar responses on the left. MRI showed a subacute right-sided lateral brainstem infarct just below the pontomedullary junction with minimal progression in a repeat MRI after 24 hours. Workup for supraclavicular adenopathy with CT chest and CT abdomen and pelvis revealed neither neoplastic nor metastatic disease. Biopsy of supraclavicular lymph node was planned as an outpatient but was deferred as it was presumed to be reactive. He was conservatively managed with daily physiotherapy, aspirin, atorvastatin, and optimal blood pressure control. Babinski-Nageotte syndrome includes all symptoms of the Wallenberg syndrome with contralateral hemiparesis due to a spread of the lateral lesion to the pyramidal tract. Atherosclerotic occlusion and lipohyalinosis of the vertebral artery and posterior inferior cerebellar artery have been identified as the most common causes.

Compression of the medulla oblongata by a fusiform vertebral artery aneurysm presenting as Babinski-Nageotte syndrome in a Filipino male: A case report

Babinski-Nageotte Syndrome (BNS) is one of the brainstem syndromes presenting with classic Wallenberg findings with associated contralateral motor deficit. Based on our literature review, only few cases have been reported and none of them was due to aneurysmal compression of the medulla oblongata. This paper aims to present a case of a 42-year old Filipino male, married, construction worker who manifested with sudden onset of severe headache with associated vertiginous dizziness, dysphagia, dysphonia, nausea, vomiting, and right extremity numbness and hemiparesis.

Babinski-Nageotte Syndrome Diagnosed in Postpartum Period.

Babinski-Nageotte Syndrome (BNS) is one of the brainstem syndromes characterized by muscle weakness in the opposite half of the body with classic Wallenberg findings. According to our literature survey, only a few cases have been reported and none of them was in the postpartum period. We report a case of a typical BNS in a postpartum woman with an ischemic lesion in the medulla oblongata shown on magnetic resonance imaging.

Babinski-Nageotte Syndrome Secondary to Hemorrhagic Medullary Cavernoma in a District Hospital: A Variant of Wallernberg Syndrome

Babinski-Nageotte syndrome is a rare clinical entity in a young healthy individual. This syndrome includes a group of neurological symptoms resulting from injury to both medial and lateral medulla of the brain. It is a variant of Wallernberg syndrome. This case report describes a 27 year old healthy Malay gentleman who presented with a three day history of right facial numbness and weakness associated with left sided body hemiparesis and hemiparethesia. He had obvious right hypoglossal nerve palsy. He also complained of vertigo, dysphagia, dysarthria and vomiting. He denied having any hiccups. Physical examination revealed an obvious right Horner’s syndrome with upper motor neuron right facial nerve palsy. There was no facial tenderness. Motor power of the left upper and lower limbs were graded as 2/5. His gag reflex on the right side was absent with abundant oral secretions. Jerky nystagmus of the right eye at all gazes was seen along with diplopia. A plain computed tomography scan of the brain showed a hyperdense lesion suggestive of hemorrhagic medullary cavernoma. He subsequently developed respiratory distress due to pneumonia in which he required mechanical ventilation. However, he succumbed to his illness due to Extended Spectrum Beta Lactamase (ESBL) Klebsiella pneumonia on day 6 of admission. This crossed finding is diagnostic of Babinski-Nageotte syndrome. The unavailability of Magnetic Resonance Imaging/Angiography facility may provide a diagnostic challenge to elucidate the exact etiology for this syndromein a district hospital.

Opalski’s syndrome: A rare variant of lateral medullary syndrome

Opalski’s syndrome: A rare variant of lateral medullary syndrome

Classical crossed brain stem syndromes: myth or reality?

Numerous crossed brain stem syndromes have been described, especially in the nineteenth century. While these syndromes are passed on in neurological textbooks, their relevance in clinical neurology remains to be elucidated. To investigate the prevalence of classical crossed brain stem syndromes in clinical practice, we prospectively recruited 308 consecutive patients with signs and symptoms indicative of acute brain stem infarction. Standardized high-resolution MR imaging and multimodal electrophysiological brain stem testing were applied to localize the site of the acute lesion. We performed a computer-based correlation of clinical signs and symptoms of our patients to those reported in the original historical publications for more than 25 crossed brain stem syndromes. Fourteen cases matched the clinical criteria of Wallenberg's syndrome, two patients had Babinski-Nageotte's syndrome, two had Raymond-Cestan's, one showed Weber's, and one Claude's syndrome. All other tested syndromes were not present in the cohort. More than 20% of patients showed different, so far unnamed crossed symptom combinations. In conclusion, except for Wallenberg's syndrome, classical crossed brain stem syndromes do not seem to play a relevant role in clinical neurology. Other syndromes may serve as theoretical models only that illustrate possible neuroanatomical connections in the human brain stem. This is complicated, however, by considerable topographic and terminological inconsistencies.

Hemimedullary infarct with ipsilateral hemiplegia: A vertebral artery dissection syndrome?

Background Hemimedullary syndrome is very rare and combines the clinical features of lateral and medial medullary infarctions. In patients with hemimedullary syndrome, the presence of ipsilateral, rather than contralateral hemiplegia, is rare. Objective To describe a patient with an infarction in the right hemimedulla with an ipsilateral motor deficit due to dissection of the right vertebral artery (VA) and to assess whether the ipsilateral hemiplegia may be the result of a specific stroke mechanism. Methods We reviewed the reports of hemimedullary syndrome in the literature and compared the characteristics of patients with dissection of the VA with those with VA atherosclerotic disease. Results In our patient, magnetic resonance angiography showed dissection of the right VA to be the cause of the stroke. In a review of the literature (including our case), hemiplegia was ipsilateral to the infarction in four of the five patients with VA dissection, but contralateral in all six patients with atherosclerotic disease of the VA ( p = 0.01). In all five cases of VA dissection, the right hemimedulla was involved, while, in the six cases of atherosclerotic disease, the left side of the medulla oblongata was affected in five instances and the right side in one ( p = 0.01). Conclusion Dissection of the VA may provoke a hemimedullary lesion at a lower level than atherosclerosis, thus affecting medullary-penetrating branches that irrigate the medulla immediately below the pyramidal decussation. Hemimedullary syndrome accompanied by ipsilateral motor deficit should raise suspicion of dissection of the VA.

Between Wallenberg syndrome and hemimedullary lesion

In comparison with the lateral (Wallenberg), medial (Dejerine) and hemimedullary (Reinhold) medulla oblongata syndromes, the Babinski-Nageotte and Cestan-Chenais syndromes are much less familiar cerebrovascular disorders. While the Babinski-Nageotte syndrome is usually confused with the hemimedullary syndrome, reports of the extremely rare Cestan-Chenais syndrome are missing from the modern neurological literature. The pathological and magnetic resonance imaging (MRI) correlations of the Cestan-Chenais syndrome have not been shown so far. We compared clinical and MRI features of two patients exhibiting classical Babinski-Nageotte and Cestan-Chenais syndromes according to their original descriptions with those of three patients with lateral, medial and hemimedullary syndromes. Our study shows that Babinski-Nageotte syndrome includes all symptoms of the Wallenberg syndrome and additionally contralateral hemiparesis due to a spreading of the "Wallenbergian" lateral lesion to the pyramidal tract. The Cestan-Chenais syndrome includes all symptoms of the Babinski-Nageotte syndrome with the exception of the ipsilateral cerebellary hemiataxia because of sparing of the posterior spinocerebellar tract. The Babinski-Nageotte syndrome is neither clinically nor on MRI identical with hemimedullary syndrome. Hypoglossal palsy, an invariable symptom of hemimedullary lesion is not part of the Babinski-Nageotte syndrome. The contralateral hypesthesia is dissociated in the Babinski-Nageotte syndrome. The Babinski-Nageotte and Cestan-Chenais syndromes are intermediolateral medullary syndromes with all (Babinski-Nageotte) or nearly all (Cestan-Chenais) features of the lateral and some features of the medial medulla oblongata syndromes.

Proximal intracranial territory posterior circulation infarcts in the New England Medical Center Posterior Circulation Registry.

We studied 91 patients with proximal intracranial territory posterior circulation ischemia from the New England Medical Center Posterior Circulation Registry to learn their distribution, underlying cardiovascular causes and longterm outcome. All patients had imaging and vascular studies. Six patients had proximal territory TIAs. Among 85 stroke patients, 52% had infarcts limited to the proximal territory, while 48% also had infarcts in other intracranial posterior circulation territories. Eighty-five percent of proximal territory infarcts were posterior inferior cerebellar artery (PICA) territory cerebellar infarcts and 30% were lateral medullary infarcts. One patient had a hemimedullary syndrome. Six patients had PICA territory cerebellar and lateral medullary infarcts. The most common vascular lesion in lateral medullary infarct patients was ipsilateral intracranial vertebral artery (ICVA) disease (38% isolated ICVA disease) and in PICA territory cerebellar infarcts, extracranial vertebral artery (ECVA) disease (29% isolated ECVA disease). Half of all lateral medullary infarcts were due to a hemodynamic mechanism, most often in situ thrombosis of an ICVA occlusive lesion. Half of all PICA territory cerebellar infarcts were due to intra-arterial embolism and one-fifth to cardiac origin embolism. Embolism was a more frequent cause of proximal territory posterior circulation infarcts than intrinsic ICVA disease. The etiological profiles of lateral medullary and PICA cerebellar infarcts were different. Seventeen percent of all patients died during follow-up (41 months) but mortality related to the acute stroke or new strokes was only 6 percent. The outcome was favorable in the surviving patients; 89% had no or only slight disability.

Babinski-Nageotte syndrome on magnetic resonance imaging.

A 70-year-old woman developed left hypoglossal nerve palsy, a right hemiparesis sparing the face, and a typical left Wallenberg's syndrome. These symptoms resulted from a lesion in the left half of the medulla oblongata, suggesting Babinski-Nageotte syndrome, a rare cerebrovascular disease. This is the first case of ischemic infarction in the territory of the left vertebral artery and posterior inferior cerebellar artery demonstrated on magnetic resonance imaging. Severe bilateral lesions of the distal vertebral arteries demonstrated on digital subtraction angiography may have contributed to the development of this syndrome.

The hemimedullary syndrome: case report and review of the literature

Hemi-infarction of the medulla causes the clinical constellation of symptoms and signs of both the lateral and medial medullary syndromes and nearly always results from occlusion of an intracranial vertebral artery. In the case reported here, with a clinical diagnosis of hemimedullary syndrome, the expected infarction was imaged by magnetic resonance. A review of the literature confirms that the hemimedullary syndrome, in which both medial and lateral syndromes occur simultaneously, is extremely rare, since it yielded only two previous cases with adequate anatomical confirmation.

Babinski and the Plantar Reflex

To the Editor: —I wish to call your attention to an error in the editorial, Babinski and the Plantar Reflex ( JAMA 183: 281 [Jan 26] 1963). As written, one is led to believe that the so-called Babinski-Nageotte syndrome has to do with locomotor ataxia. The latter term refers to ataxia dependent upon loss of sense of position and has historically been linked to tabes dorsalis. The so-called Babinski-Nageotte syndrome is based on a paper read at the Societe de Neurologie de Paris, April 17, 1902, and published under the title Hemiasynergie, lateropulsion et myosis bulbaires avec hemianesthesie et hemiplegie croisees ( Rev Neurol [Paris] 10: 358, 1902). Three patients had been seen but only one case was presented in detail. The patient, a 50-yr-old luetic, had headache, vertigo, dysphagia, nasal regurgitation, and a nasal voice. The palatal reflex was abolished. Sensations of touch and temperature were deficient on the right side