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.

Midlateral medullary infarction presenting with isolated thermoanaesthesia: a case report.

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. CASE PRESENTATION: 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.

Neuroanatomical basis of Wallenberg syndrome.

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.

El síndrome de Wallenberg, o síndrome bulbar lateral, es la manifestación clínica del infarto en el territorio de irrigación de la arteria cerebelosa posteroinferior. Su presentación incluye vértigo, nistagmo, diplopía, síndrome de Horner, rubicundez y anhidrosis facial homolateral, disfonía, disfagia, disartria, pérdida homolateral del reflejo nauseoso, ataxia homolateral, disgeusia homolateral, dolor y parestesia faciales homolaterales, pérdida o disminución homolateral del reflejo corneal, hipoalgesia y termoanestesia de tronco y extremidades contralaterales, hipoalgesia y termoanestesia facial homolateral. El conocimiento neuroanatómico es imprescindible para su comprensión, estudio y diagnóstico, ya que sus manifestaciones neurológicas clásicas son fácilmente explicables y entendibles si se conocen la función y la localización de las estructuras anatómicas afectadas, así como la irrigación cerebral posterior.

Fatal Progression of Gorham-Stout Disease with Skull Base Osteomyelitis and Lateral Medullary Syndrome.

Gorham-Stout disease (GSD) is a rare condition in which spontaneous, progressive resorption of bone occurs. There are no previous reports of patients with fatal progression of GSD with skull base osteomyelitis (SBO) and lateral medullary syndrome (LMS). We present the case of a 27-year-old man diagnosed with GSD with involvement of the maxillofacial bones and skull base. The patient developed SBO; LMS resulted from progressive osteolysis, and the patient died of associated brainstem stroke. Careful follow-up with special emphasis on the early detection of intracranial complications is critical in patients presenting with progressive GSD with involvement of the skull base.

[Lateral medullary stroke with extracranial course of the postero- inferior cerebellar artery]. / Accidente cerebrovascular bulbar lateral con trayecto extracraneal de la arteria cerebelosa póstero-inferior.

We present two cases of lateral medullary stroke in subjects with extracranial trajectory of the postero-inferior cerebellar artery. Case 1: a 21-year-old male who presented ataxia and right dysmetria after cervical trauma in a rugby match. Case 2: 56-year-old woman, who started with vertigo and left hemiparesis after intense physical effort. In both cases, the angiographic studies showed an extracranial trajectory of the posterior inferior cerebellar artery. This vessel rarely originates below the foramen magnum, in close relationship with the first three cervical vertebrae and the atlanto-axial joint. At this level, it is exposed to mechanical damage causing dissection, such as direct trauma, abrupt cervical manipulation or prolonged cephalic extension. Therefore, this association should be considered in patients with stroke of the lateral region of the bulb and extracranial trajectory of the posterior-inferior cerebellar artery.

Accidente cerebrovascular bulbar lateral con trayecto extracraneal de la arteria cerebelosa póstero-inferior / Lateral medullary stroke with extracranial course of the postero- inferior cerebellar artery

Presentamos dos casos de accidente cerebrovascular en sujetos con trayecto extracraneal de la arteria cerebeloso póstero-inferior. Caso 1: varón de 21 años, quien presentó ataxia y dismetría derecha luego de un traumatismo cervical en un partido de rugby. Caso 2: mujer de 56 años, quien inició con vértigo y hemiparesia izquierda luego de esfuerzo físico intenso. En ambos casos, los estudios angiográficos mostraron un trayecto extracraneal de la arteria cerebelosa póstero-inferior. Este vaso raramente se origina por debajo del foramen magno, en relación cercana con las primeras tres vértebras cervicales y la articulación atlanto-axial. En este nivel, está expuesta a daño mecánico causante de disección, como por ejemplo trauma directo, manipulación cervical abrupta o extensión cefálica prolongada. Por lo tanto, en pacientes con accidente cerebrovascular de región lateral de bulbo y trayecto extracraneal de la arteria cerebelosa póstero-inferior se debería considerar esta asociación.

We present two cases of lateral medullary stroke in subjects with extracranial trajectory of the postero-inferior cerebellar artery. Case 1: a 21-year-old male who presented ataxia and right dysmetria after cervical trauma in a rugby match. Case 2: 56-year-old woman, who started with vertigo and left hemiparesis after intense physical effort. In both cases, the angiographic studies showed an extracranial trajectory of the posterior inferior cerebellar artery. This vessel rarely originates below the foramen magnum, in close relationship with the first three cervical vertebrae and the atlanto-axial joint. At this level, it is exposed to mechanical damage causing dissection, such as direct trauma, abrupt cervical manipulation or prolonged cephalic extension. Therefore, this association should be considered in patients with stroke of the lateral region of the bulb and extracranial trajectory of the posterior-inferior cerebellar artery.

Posterior Meningeal Artery Origin Patterns among 300 Cases and Their Clinical Importance.

BACKGROUND AND PURPOSE: The posterior meningeal artery (PMA) is known as a dura mater-nourishing vessel. We encountered a patient with Wallenberg syndrome during transarterial embolization of the PMA associated with the dural arteriovenous fistula (DAVF). METHODS: After development of Wallenberg syndrome in the patient, we assessed origins of the PMA patterns in 300 cases and divided them into 3 types. CASE PRESENTATION: A 63-year-old man was incidentally diagnosed as having transverse-sigmoid sinus DAVF with a cortical venous reflux. During the transarterial embolization, the patient complained of vertigo and numbness of the right extremities. Postoperatively, the patient exhibited Wallenberg syndrome. Diffusion-weighted magnetic resonance imaging showed a high-intensity area on the lateral side of the right medulla. CONCLUSIONS: While performing arterial embolization of the PMA that directly originates from the intracranial vertebral artery, the possibility of deficient brainstem nourishment must be considered.

Contraversive ocular tilt reaction after the lateral medullary infarction.

INTRODUCTION: The triad of ocular tilt reaction (OTR) is conjugated ocular torsion, skewed deviation, and head tilt. A lesion involving below the inferior pons develops ipsiversive OTR, whereas a lesion above the inferior pons leads to contraversive OTR. A lateral medullary infarction usually causes ipsiversive OTR. This is the first report of contraversive OTR following the lateral medullary infarction. CASE REPORT: A 58-year-old woman was admitted due to sudden-onset vertigo and gait disturbance. A neurological examination revealed OTR to the left side (left head tilt, leftward ocular torsion, and skew deviation). Lateropulsion to the right and dysmetria on the right arm and leg were present. Diffusion-weighted MRI revealed an acute infarction of the right lateral medulla and the posterolateral pons. The patient slowly improved and can walk without sway after 1 week. Neither head tilt nor ataxia was observed after 3 months. CONCLUSIONS: Lateral medullary lesion typically results in ipsilateral OTR. Contraversive OTR of our patient might be derived from the disruption of the cerebellovestibular inhibitory pathway by the lesion in the juxtarestiform body in the lateral medulla.

[Algorithm for the diagnosis of the vertebral artery compression syndrome based on sensitivity of ultrasound and angiographic methods].

The results of sensitivity analysis and ultrasonic techniques hagiographic 150 patients with vertebral artery syndrome caused by compression extravasal (ECVA) segment V(p), who underwent surgery on clinical. In assessing the sensitivity by a static cross-vertebral artery, vessel diameter, the condition of the lumen--Ultrasonic and hagiographic (SAG and MRA) techniques showed the same high sensitivity in the range 85-89% (P > 0.05), and according to such criteria as the dynamic permeability (89.2% vs. 34.2 and 45.5%), the value of ripple vascular (86.3% vs. 58 and 67%), the state of the perivascular tissue USDG figures were significantly higher than the data angiography (82.2% vs. 0 and 29%) (P < 0.05 for all tests). Comparative analysis of selective angiography, enhanced magnetic resonance angiography and ultrasound proposed method allowed us to determine their sensitivity. Thus, the sensitivity of selective angiography in extravasal vertebral artery compression is 57.1%, magnetic resonance angiography--88% and triplex ultrasound-- 91.3%.

[Central respiratory failure occurred in the subacute phase of unilateral Wallenberg's syndrome: a case report].

A 46-year-old man developed central respiratory failure in the subacute phase of unilateral lateral medullary infarction. He complained of sudden headache and nausea at first. Neurological examination revealed Wallenberg's syndrome. Acute right lateral medullary infarction caused by the dissecting right vertebral artery was identified by magnetic resonance images. He was transferred to our hospital on the 3rd day after the onset. He was alert and conscious on admission, and became restless gradually later. He was intubated for sudden respiratory failure on the 9th day. Blood gas analysis showed hypercapnia and hypoxia. Central respiratory failure was indicated by the fact that various examinations showed no change of his infarction, no subarachnoid hemorrhage, or no worsening of pneumonia. Ventilatory support was required for a month because of repetitive CO2 narcosis. He was weaned from the ventilator on the 39th day. Only a few reports are available on central respiratory failure associated with the subacute phase of unilateral medullary infarction. Delayed central respiratory failure may be lethal. Careful observation is required on the subacute phase of Wallenberg's syndrome.

Three cases of Spontaneous Vertebral Artery Dissection (SVAD), resulting in two cases of Wallenberg syndrome and one case of Foville syndrome in young, healthy men.

First patient, presented with sudden onset of headache, left hypoacusia and right hemiparesis, posteriorly developing gaze-evoked nystagmus and worsening right-sided weakness. Diagnosis of vertebral artery dissection and Foville Syndrome were made through clinical assessment and CT-carotid angiogram-MR angiography. Second patient, presented with four episodes of pain over left side of the nose and left eye pain over 1 month; admitted for acute facial pain without limb weakness. During admission, tingling over V1/V2 facial territory, vertigo, hypotension, uvula deviation and right lower limb numbness. CT-carotid angiogram confirmed vertebral artery with dissection. MRI revealed left lateral medullary infarct. Third patient, presented with sudden onset of left facial numbness and right upper limb weakness; 1 day after, right arm and leg hypoesthesia with hoarseness. MRA revealed dissection of left distal vertebral artery and MRI showed infarction in lower medulla oblongata.

[Sequential MRI imaging of progressive bilateral rostro-caudal medullary infarction]. / Infarctus bulbaire paramédian bilatéral d'évolution progressive: à propos de deux cas documentés en imagerie par résonance magnétique séquentielle.

Bilateral medial medullary infarction is exceptional. Initial symptoms can be misleading, even for a trained neurologist. We report two patients who presented progressive quadriplegia, anarthia and dysphagia. Sequential MRI showed progressive constitution of the characteristic "heart appearance" sign.

Dermatomal sensory manifestations in lateral medullary infarction.

A 61-year-old man who experienced a sudden onset of unstable gait followed by nuchal pain was admitted to our department. The neurologic examination revealed right-sided limb ataxia, right partial ptosis, and decreased sensation to 50% of the normal side to pinprick and temperature stimuli on the left side below the level of the T-6 dermatome. A lateral medullary infarction caused by spontaneous vertebral artery dissection was diagnosed by magnetic resonance imaging and computed tomography angiography. In conclusion, lateral medullary infarction is an important entity to consider in the differential diagnosis of dermatomal sensory manifestations.

Ipsilateral sensorimotor deficits in lateral medullary infarction: a case report.

The patient, a 32-year-old man, presented with sudden onset of occipital headache, vertigo, dysarthria, gait ataxia, right Horner syndrome, numbness of the right hand, and mild right hemiparesis. On magnetic resonance imaging, an acute small infarction was located on the right side of the caudal medulla extending dorsomedially. Magnetic resonance angiography showed severe right vertebral artery stenosis. Lateral medullary infarction associated with ipsilateral sensorimotor deficits in the limb is very rare, and the lesion probably involved the ipsilateral dorsal column or decussating lemniscal fibers and corticospinal fibers caudal to the pyramidal decussation or compression of the decussation.

Prediction of dysphagia severity: an investigation of the dysphagia patterns in patients with lateral medullary infarction.

OBJECTIVE: In order to identify the factors that influence the swallowing function in patients who develop Wallenberg syndrome (WS) following lateral medullary infarction (LMI), we examined various patient characteristics, including the passage pattern abnormality (PPA) of a bolus through the upper esophageal sphincter (UES). METHODS: Fifty-four pure LMI patients with dysphagia participated in this study. PPA, defined as the failure of bolus passage through the UES corresponding to the intact side of the medulla, was identified during videofluorographic swallowing evaluations of each patient. On brain magnetic resonance imaging, the subjects' lesions were classified vertically into three levels and horizontally into seven levels in relation to the involvement of the ambiguous and/or solitary nuclei. Logistic regression analyses were performed for age, sex, PPA and the vertical and horizontal sites of the lesions. RESULTS: In terms of severity, 15 subjects were categorized as having mild dysphagia, 26 subjects were categorized as having moderate dysphagia and 13 were categorized as having severe dysphagia. Subjects with cephalic lesions, greater vertical spread of the lesion and PPA were more likely to have severe dysphagia. PPA and a greater vertical spread of the lesion were related to the severity of the functional outcome (p<0.01). The horizontal extent of the lesion was not strongly related to the prognosis. CONCLUSION: The presence of PPA in LMI patients is suggestive of abnormalities in the swallowing pattern and, in turn, damage to the medullary central pattern generator. The presence of PPA and a greater vertical spread of the lesion can be useful predictors of severe dysphagia.

Cardiovascular autonomic function in lateral medullary infarction.

Even though the medulla contains the baroreceptor regulatory centers, few studies have focused on the autonomic dysfunction of lateral medullary infarction (LMI). Therefore, cardiac parasympathetic and sympathetic functions were compared in LMI patients and age-matched controls. We prospectively recruited 25 LMI patients who had ipsilateral Horner's sign and cardiac autonomic function testing without a history of diabetes, cardiac disease, or previous stroke. Parasympathetic function tests included beat-to-beat heart rate variation during deep breathing, 30:15 heart rate ratio testing while standing, and the valsalva ratio. Sympathetic function tests included blood pressure during active standing and sustained handgrip. The composite autonomic score (CAS) was measured as a total of 10 points; parasympathetic dysfunction was designated as ≥3 points in the parasympathetic subscores and sympathetic dysfunction as ≥2 points in the sympathetic subscores. Multiple regression analysis was performed to predict parasympathetic or sympathetic dysfunction. The mean age and stroke risk factors of the study population were not significantly different between the LMI group (n = 25) and control group (n = 29). However, cardiac autonomic functions were significantly different in the groups: parasympathetic dysfunction (14 vs. 4 patients, p = 0.011) and sympathetic dysfunction (3 vs. 13 patients, p = 0.008). In univariate analysis, male-gender (p = 0.011), right-side involvement (p = 0.035) and ventral involvement (p = 0.007) were significantly associated with parasympathetic dysfunction (CAS subscore ≥3). In multivariable analysis, the ventral involvement remained to be the independent predictor for parasympathetic dysfunction (OR 16.0; 95% CI 2.2-118.3, p = 0.007). This study suggests that LMI patients are susceptible to cardiac parasympathetic dysfunction, especially in the ventral medulla.