Usefulness of thermography for differentiating Wallenberg's syndrome from noncentral vertigo in the acute phase.

OBJECTIVES: Wallenberg's syndrome (WS) is caused by a stroke in the lateral medulla and can present with various symptoms. One of the main symptoms is vertigo, which can be misdiagnosed as noncentral vertigo (NCV). Approximately 90% of the patients with acute WS have a lateral difference in body surface temperature (BST) due to autonomic pathway disturbances from infarction. Additionally, thermography can aid in WS diagnosis; however, whether BST differences occur in patients with acute NCV is unclear. METHODS: This study used thermography to measure the BST of patients with NCV and acute WS to determine the effectiveness of BST to differentiate between the conditions. Forty-eight consecutive patients diagnosed with NCV whose BST was measured using thermography during a hospital visit or admission were enrolled. The left and right BST of four sites (face, trunk, and upper and lower limbs) were measured and compared with obtained BST of nine patients with WS. RESULTS: Twenty-two patients had lateral differences in BST ≥ 0.5°C, three with ≥1.5°C, and none with ≥2.5°C. Only one patient with NCV had lateral differences in BST at two or more ipsilateral sites. When WS differentiated from NCV, a left-right difference ≥0.5°C in two or more ipsilateral sites had a sensitivity of 89% and specificity of 98%, and ≥1.0°C had a sensitivity of 78% and specificity of 98%. DISCUSSION: Acute WS can be differentiated from NCV through BST and the number of sites with lateral differences via thermography, even in rooms where conditions are unregulated.

Case report: Lateral medullary syndrome with eight-and-a-half syndromes.

RATIONALE: Lateral medullary syndrome is caused by atherosclerosis or embolism of the vertebral artery and its branches or the posterior inferior cerebellar artery (PICA).The eight-and-a-half syndrome is a rare pontocerebellar nerve-ocular syndrome presenting as a one-and-a-half syndrome plus ipsilateral seventh cerebral nerve palsy. The dorsolateral medullary syndrome combined with the eight-and-a-half syndromes is even rarer, so it is important to recognize the features of the classical brainstem syndrome and the eight-and-a-half syndromes. PATIENT CONCERNS: Most patients with dorsolateral medullary syndrome combined with eight-and-a-half syndromes have a good prognosis, with recovery occurring within a few weeks to a few months, although a few patients may take longer to recover. DIAGNOSIS INTERVENTIONS: In the course of disease development, the patient developed dysarthria, dysphagia, hypothermia, ipsilateral Horner sign and ataxia. Computed tomography was performed which showed cerebral infarction in the left brainstem. Cranial diffusion-weighted imaging + magnetic resonance angiography showed acute infarction in the left cerebellar hemisphere, with a high probability of severe stenosis or occlusion in the intracranial and proximal segments of the basilar arteries. This supports the diagnosis of dorsolateral medullary syndrome. The patient's limited adduction and abduction of the left eye and limited adduction of the right eye, combined with peripheral paralysis of the affected lateral nerve, supported the diagnosis of eight-and-a-half syndromes. The administration of antiplatelet and anti-ester fixation treatment can effectively improve the symptoms and shorten the course of the disease. OUTCOMES: After antiplatelet and anti-ester fixation treatment, the symptoms improved and the patient was discharged. LESSONS: Dorsolateral medullary syndrome combined with eight-and-a-half syndromes is a rare clinical condition, and therefore more attention should be paid to the early diagnosis and treatment of such patients.

Intrinsic stenosing and occlusive pathologies of the vertebral artery: A narrative review.

Intrinsic pathologies of the vertebral arteries, such as atherosclerosis, dissection, fibromuscular dysplasia, radionecrosis and vasculitis, are important causes of vertebrobasilar insufficiency and cerebrovascular events. This review focuses on non-aneurysmal intrinsic stenosing and occlusive pathologies, covering their epidemiology, diagnosis, and treatment options. It also provides a detailed summary of key clinical presentations and syndromes, including an in-depth examination of lateral medullary syndrome, historically known as Wallenberg's syndrome, which is arguably the most emblematic condition resulting from vertebral artery involvement and is depicted in an illustrative cartoon.

Formation of a Large Fusiform Aneurysm near a Medullary Infarction Caused by Dissection of the Posterior Inferior Cerebellar Artery.

Infarction of the posterior inferior cerebellar artery (PICA) can lead to ischemic stroke in the lateral medullary oblongata. PICA dissection can also elicit an ischemic event in this region, but its detection on radiological images is difficult because of the small diameter of the vessel. We report a case of Wallenberg syndrome due to PICA dissection in a 48-year-old man, which was difficult to diagnose on first admission. He reported sudden onset of sensory disturbance on the right side of his face, ataxic gait, and headache. Brain magnetic resonance imaging (MRI) revealed a fresh cerebral infarct in the right lateral medulla oblongata. Magnetic resonance angiography (MRA) performed at the time of his admission showed no cerebral vessel abnormalities. An MRI study 18 months after the event revealed a fusiform aneurysm on the lateral medullary segment of the PICA, which was extremely close to the cerebral infarct. We concluded that the infarct was due to PICA dissection because of the sudden onset of symptoms and because the infarcted territory of the occluded penetrating branch of the dissecting aneurysm was consistent with Wallenberg syndrome. The aneurysm was trapped and an occipital artery-PICA bypass was placed. At the latest follow-up, 1 year after the procedure, he had no neurological symptoms. Imaging findings at the time of his first admission indicated that the PICA was intact. However, 18 months later, MRI revealed enlargement of an aneurysm at the site of the dissection. A cerebral infarct with headache may indicate PICA dissection.

Topographic Consideration on the Occurrence of Ipsilesional Facial Paresis in Lateral Medullary Infarction.

INTRODUCTION: 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). METHODS: 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). RESULTS: 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. CONCLUSION: 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.

Temporal Characteristics of Penetration and Aspiration in Patients with Severe Dysphagia Associated with Lateral Medullary Syndrome.

To assess the severity and timing of penetration and aspiration (PA) of severe dysphagia after lateral medullary syndrome (LMS) and its association with temporal characteristics. We performed videofluoroscopic swallowing studies (VFSS) in 48 patients with LMS and severe dysphagia and 26 sex- and age-matched healthy subjects. The following temporal measures were compared between groups: velopharyngeal closure duration (VCD); hyoid bone movement duration (HMD); laryngeal vestibular closure duration (LCD); upper esophageal sphincter (UES) opening duration (UOD); stage transition duration (STD) and the interval between laryngeal vestibular closure and UES opening (LC-UESop). The association between temporal measures and Penetration-Aspiration Scale (PAS) scores was analyzed. Differences in timing measures were compared between subgroups (safe swallows, and swallows with PA events during and after the swallow). PAS scores ≥ 3 were seen in 48% of swallows (4% occuring before, 35% occurred during and 61% after the swallow) from the LMS patients. Significantly longer STD and LC-UESop were found in the patients compared to the healthy subjects (p < 0.05). Significant negative correlations with PA severity were found for HMD, LCD, and UOD. Short UOD was the strongest predictor with an area under the receiver-operating-characteristic curve of 0.66. UOD was also significantly shorter in cases of PA after the swallow (p < 0.01). Patients with LMS involving severe dysphagia exhibit a high frequency of PA (mostly during and after swallowing). PA events were associated with shorter UOD, HMD, and LCD. Notably, shortened UOD appears to be strongly associated with PA.

Vertebral artery dissection induced lateral medullary syndrome characterized with severe bradycardia: a case report and review of the literature.

BACKGROUND: Lateral medullary syndrome is the most common type of brainstem infarction. Lateral medullary syndrome results in damage to the corresponding cranial nerve nuclei and the nucleus tractus solitarius, with vertigo, ipsilateral ataxia, crossed sensory disturbances, Horner's sign, bulbar palsy, and other underlying symptoms or signs. However, cases with cardiac arrhythmia and other autonomic dysfunctions as the primary manifestations are less common. Clinically, sudden death occasionally occurs in patients with lateral medullary syndrome, which may be associated with severe cardiac arrhythmia. These patients may suffer in life-threatening arrhythmia and even cardiac arrest, and vital signs should be closely monitored to prevent sudden death. In younger patients, vertebral artery dissection is the most common cause. CASE DESCRIPTION: Here, we present a case of lateral medullary syndrome caused by vertebral artery dissection with severe bradycardia. The patient was a 49-year-old man who was admitted with "sudden onset of numbness in the left limbs and right side of the face for 1 hour". Electrocardiogram (ECG) monitoring showed a repeated heart rate decrease to as low as 23 beats/min, followed by a gradual increase in heart rate to 35-55 beats/min after 2-3 seconds. Head magnetic resonance imaging (MRI) examination revealed right dorsolateral cerebral infarction of the medulla oblongata. Digital subtraction angiography (DSA) revealed a right vertebral artery dissecting aneurysm. We performed an emergency placement of a temporary pacemaker, followed by conservative treatment with platelet aggregation inhibitors, vascular softening agents and improved collateral circulation. Elective spring coil embolization of the vertebral artery dissecting aneurysm and stent implantation were performed. At outpatient follow-up, the patient had a good prognosis. CONCLUSIONS: Clinical management of patients with lateral medullary syndrome should be prioritized, with close cardiac monitoring at the early stages of observation and pacemaker placement and tracheal intubation as required to prevent adverse events.

Association of Vertebral Artery Hypoplasia and Vertebrobasilar Cerebrovascular Accident.

Background and Objectives: Vertebral artery hypoplasia (VAH) is a controversial risk factor for cerebral infarction. The aim of this study was to analyze the prevalence of vertebral artery hypoplasia and to evaluate its association with vertebrobasilar cerebrovascular accidents. Materials and Methods: The study was conducted in the Neurology Departments of the Republican Vilnius University Hospital from 2015 to 2020. Data of 742 subjects (133 patients with posterior circulation infarction or vertebral artery syndrome (PCI/VAS), 80 patients with anterior circulation infarction (ACI) and 529 control subjects with no symptoms of cerebrovascular accident) were analyzed. Ultrasound examination of the extracranial internal carotid and vertebral arteries (VA) was performed, risk factors were recorded. Results: The mean age of the subjects was 64.51 ± 13.02 years. In subjects with PCI/VAS the diameter of VA was smaller, and the prevalence of VAH was higher compared to those in subjects with ACI and in the control group. A higher degree of VAH in subjects younger than 65 years of age increased the risk of PCI/VAS. Subjects with non-dominant VA diameter of 2.7-2.9 mm had 2.21 times higher risk of PCI/VAS, subjects with non-dominant VA diameter of 2.5-2.6 mm had 2.36 times higher risk of PCI/VAS, and subjects with non-dominant VA diameter of 2.2-2.4 mm had 4.12 times higher risk of PCI/VAS compared with subjects with non-dominant VA diameter of ≥3 mm. Among patients with PCI/VAS those with VAH had lower rates of ischemic heart disease compared with patients with normal VA diameter. There was no difference in the rates of other risk factors between PCI/VAS patients with and without VAH. Conclusions: Vertebral artery hypoplasia is not a rare finding in individuals without symptoms of cerebrovascular accident, but more frequent in patients with vertebrobasilar cerebral infarction or vertebrobasilar artery syndrome. Vertebral artery hypoplasia can be considered a risk factor for posterior circulation infarction in subjects under 65 years of age.

Sinus arrest following acute lateral medullary infarction.

Lateral medullary syndrome (LMS) is an ischemic stroke of the medulla oblongata that involves the territory of the posterior inferior cerebellar artery. LMS is often missed as the cause of autonomic dysregulation in patients with recent brain stem stroke. Due to the location of the nucleus tractus solitarius (NTS), the dorsal vagal nucleus, and the nucleus ambiguous in the lateral medulla oblongata, patients with LMS occasionally have autonomic dysregulation-associated clinical manifestations. We report a case of LMS-associated autonomic dysregulation. The case presented by recurrent syncope, requiring permanent pacemaker placement. This case shows the importance of recognizing LMS as a potential cause of life-threatening arrhythmias, heart block, and symptomatic bradycardia. Extended cardiac monitoring should be considered for patients with medullary strokes.