UNASSIGNED: Opalski syndrome is a rare variant of Wallenberg syndrome (lateral medullary syndrome) that demonstrates concomitant ipsilateral hemiplegia due to infarctions within the lateral medulla and the cervical spinal cord, which also extend to the post-pyramidal decussation to affect the corticospinal tract.
UNASSIGNED: A 56-year-old man initially presented with a unilateral headache with right cervical pain. Consequently, he developed symptoms that indicate Wallenberg syndrome: vertigo, dysphonia, dysarthria, right limb ataxia with a tendency to fall, and ptosis, in addition to ipsilateral hemiparesis. The diffusion-weighted imaging MRI (DWI MRI) performed initially demonstrated an acute infarct in the dorsolateral medulla. Accordingly, an axial T2-weighted MRI showed a hyperintense focal region in the same area, even as magnetic resonance angiography (MRA) revealed complete stenosis of the corresponding vertebral artery.
UNASSIGNED: Opalski syndrome can result from different etiologies such as vascular occlusion or dissection. Although symptoms may vary, patients commonly present with sudden weakness, vertigo, and gait instability. Diagnosis often relies on MRI or DW-MRI. Treatment is tailored depending on individual factors and may involve medications and monitoring. Complications like respiratory failure can occur but are not directly linked to Opalski syndrome. Proper management includes addressing ischemic risk factors and ensuring appropriate nutrition.
UNASSIGNED: This case highlights the importance of including Opalski syndrome early in the differential diagnosis of patients with clinically suspected ipsilateral lateral medullary infarction and hyperacute ipsilateral hemiparesis.

Lateral Medullary Syndrome (LMS) poses clinical challenges, often resulting from ischemic events in the medulla oblongata. We present a unique case of LMS in a woman in her 60s with a complex medical history. Alongside neurological deficits, she experienced a transient high-grade atrioventricular block (HgAVB), a rare cardiac manifestation linked to LMS. Given the rarity of simultaneous transient HgAVB with acute lateral medullary infarct, only a handful of case reports documenting similar findings are available in the existing literature. More research and case reporting are needed to better our understanding of this area. The patient\'s condition, marked by a sudden onset of severe headache and left-sided weakness, revealed an acute infarct in the medulla territory. Notably, her HgAVB spontaneously resolved after 72 hours. This case emphasises the crucial need for extended cardiac surveillance in LMS patients due to their susceptibility to life-threatening arrhythmias. The intricate interplay between the brainstem and cardiovascular system highlights autonomic dysregulation as a potential mechanism for cardiac abnormalities. The report advocates for a holistic approach to managing LMS cases, stressing interdisciplinary collaboration for timely diagnosis and intervention, ultimately improving patient outcomes and reducing the risk of fatal arrhythmias.

Lateral medullary infarction (LMI), or Wallenberg syndrome, can develop various symptoms, but it is rare that ipsilateral axial lateropulsion (or body lateropulsion, BL) or atonic bladder (AB) are caused by LMI. This report describes a case of LMI with both BL and AB. A 77-year-old man, with a history of hypertension and diabetes, developed acute left BL and anuresis. A neurological exam showed right gaze nystagmus, slight dysarthria and dysphagia, right dysesthesia in the trunk, and ataxia in the left limbs and trunk. Horner\'s syndrome and paralysis were unremarkable. Brain magnetic resonance imaging revealed hyperintensity in the lateral medulla oblongata. Cystometry revealed AB, although the patient had the urge to urinate. Owing to acute therapy, although trunk ataxia was presented for several months, BL and anuresis were recovered on day 15 and day 35, respectively. Here, we describe the potential mechanisms of BL and AB caused by LMI.

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The purpose of this study was to identify course of the corticobulbar tract and factors associated with the occurrence of facial paresis (FP) in lateral medullary infarction (LMI).
Patients diagnosed with LMI who were admitted to tertiary hospital were retrospectively investigated and divided into two groups based on the presence of FP. FP was defined as grade 2 or more by the House-Brackmann scale. Differences between the two groups were analyzed with respect to anatomical location of the lesions, demographic data (age, sex), risk factors (diabetes, hypertension, smoking, prior stroke, atrial fibrillation, and other cardiac risk factors for stroke), large vessel involvement on magnetic resonance angiography, other symptoms and signs (sensory symptoms, gait ataxia, limb ataxia, dizziness, Horner syndrome, hoarseness, dysphagia, dysarthria, nystagmus, nausea/vomiting, headache, neck pain, diplopia, and hiccup).
Among 44 LMI patients, 15 patients (34%) had FP, and all of them had ipsilesional central-type FP. The FP group tended to involve upper (p < 0.0001) and relative ventral (p = 0.019) part of the lateral medulla. Horizontally large lesion was also related to the presence of FP (p = 0.044). Dysphagia (p = 0.001), dysarthria (p = 0.003), and hiccups (p = 0.034) were more likely to be accompanied by FP. Otherwise, there were no significant differences.
The results of present study indicate that the corticobulbar fibers innervating the lower face decussate at the upper level of the medulla and ascend through the dorsolateral medulla, where the concentration of the fibers is densest near the nucleus ambiguus.

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BACKGROUND: A small lateral medullary lesion could produce isolated impairment of temperature sensation without concomitant impaired pain sensation. However, only one such case has ever been reported, and there are no reports on subjective symptoms and detailed somatosensory testing.
METHODS: Herein, we report the case of a 53-year-old female patient presenting with impaired temperature sensation on the left half of her body, from the neck down, following a small infarction of the right midlateral medulla. The chronological changes in the patient\'s introspection regarding impairment of thermoception and the results of detailed somatosensory tests, including thermal sense, are shown in this report.
CONCLUSIONS: Thorough somatosensory tests, personal descriptions of symptoms, and electrophysiological quantification of similar cases are needed to improve our understanding of the neurological separation of the sensations of pain and temperature at the medullary level.

UNASSIGNED: Cases of pain mimicking trigeminal neuralgia (TN) induced by ischemic stroke in the brainstem have been sparsely reported. The study was to determine the characteristics of symptomatic TN in patients with acute ischemic stroke in the medulla oblongata and pons, and to determine the location of the ischemic lesion associated with the pain.
UNASSIGNED: A total of 6/21 (28.5%) patients with medullary ischemic stroke and 3/34 (8.8%) patients with pontine ischemic stroke who experienced pain mimicking TN between 1 week before and 2 weeks after the stroke onset were enrolled in the study. All patients accepted neuroimaging examinations to determine the location of the ischemic lesion and the etiology of ischemic stroke. The characteristics of pain were recorded and analyzed.
UNASSIGNED: Ischemic lesions of patients who experienced pain mimicking TN were located in the lateral medulla oblongata (n=6), nerve root entry zoo (n=2), and areas involved with the spinal trigeminal tract (n=1) in the pons. Half of the instances of pain induced by medullary ischemic stroke occurred prior to the stroke onset. The branch of V1 was exclusively involved in patients with lateral medullary infarction and the branches of V2 and V3 were typically involved in patients with pontine infarction. The pain was relieved spontaneously (n=4, 44.4%) or was controlled with drugs for neuropathic pain treatment (n=5, 55.5%).
UNASSIGNED: Half of the instances of pain induced by medullary ischemic stroke occurred prior to the stroke onset. Pain mimicking TN might be a premonitory symptom of the medullary ischemic stroke. Pain mimicking TN induced by brainstem infarction has a good prognosis.

UNASSIGNED: Hiccups is a known presentation of lateral medullary infarction. However, the region in the medulla associated with this finding is not clearly known. In this study, we aimed to study the neural correlates of hiccups in patients with lateral medullary infarction (LMI).
UNASSIGNED: This retrospective study included all patients who presented with lateral medullary infarction between January 2008 and May 2018. Patients with hiccups following LMI were identified as cases and those with no hiccups but who had LMI were taken as controls. The magnetic resonance imaging of the brain was done viewed and individual lesions were mapped manually to the template brain. Voxel-based lesion-symptom mapping employing nonparametric permutation testing was performed using MRIcron.
UNASSIGNED: There were a total of 31 patients with LMI who presented to the hospital during the study period. There were 11 (35.5%) patients with hiccups. Using the voxel-based lesion-symptom mapping analysis, the dorso-lateral region of the middle medulla showed significant association with hiccups.
UNASSIGNED: In patients with LMI, we postulate that damage to the dorsolateral aspect on the middle medulla could result in hiccups.

暂无摘要。