Medial Medullary Infarction Research Articles

Truncal Ataxia From Infarction Involving the Inferior Olivary Nucleus

Truncal ataxia in medullary infarction may be caused by involvement of the lateral part of the medulla; however, truncal ataxia in infarction involving the inferior olivary nucleus (ION) has received comparatively little attention. We report a patient with truncal ataxia due to medial medullary infarction located in the ION. A lesion in the ION could produce a contralateral truncal ataxia due to increased inhibitoryinput to the contralesional vestibular nucleus from the contralesional flocculus.

Medial medullary infarction with occlusion of distal vertebral arteryand basilar artery: A case report

症例は64歳の男性で，散歩中，突然の右片麻痺と構音障害を自覚し，当院へ緊急入院となった．頭部CTでは明らかな異常所見を指摘できず，MRI拡散強調画像を行ったところ，延髄左傍正中部に淡い高信号域を認めた．発症6日後に行ったMRI拡散強調画像では，延髄左傍正中部に強い高信号域を認めた．発症7日後の脳血管撮影では，左遠位椎骨動脈と脳底動脈で閉塞を認め，これがMMIの原因と考えられた．発症14日後に行ったbasi-parallel anatomical scanning MR imaging （BPAS-MRI）では，左遠位椎骨動脈に狭小化を認めた．MMIの原因として，遠位椎骨動脈の動脈硬化が重要で，多くはbranch occlusionの様式で梗塞を発症するといわれている．われわれの経験から，MMIの症例においてBPAS-MRIを行うことは，MMIの発症機序の推定に有用であることが示唆された．

A Case of Dysphagia Subsequent to Bilateral Medial Medullary Infarction

A Case of Dysphagia Subsequent to Bilateral Medial Medullary Infarction

Medial Medullary Infarction Identified by Diffusion-Weighted Magnetic Resonance Imaging

Objective: To elucidate the frequency and clinical profiles of patients with medial medullary infarction (MMI) identified by diffusion-weighted MRI (DWI). Methods: We assessed the frequency, radiological findings, etiology and clinical features of MMI detected by DWI from our single-center registry of acute ischemic patients. Results: Thirty patients (1.5% of 2,014 with ischemic stroke) had MMI, including isolated unilateral MMI in 26 patients. Lesions were located by DWI in the rostral medulla of 25 patients (83%). Culprit infarcts that were undetectable by DWI in 6 (38%) of 16 patients who were assessed within 24 h after onset were later confirmed as MMI. The major etiological mechanism was small artery occlusion (SAO; 19 patients) and the median initial National Institutes of Health Stroke Scale score was 4 (interquartile range: 3–4.75). The most frequent symptom was contralateral hemiparesis (27 patients). None of the patients fulfilled the classical Dejerine Triad. Twenty-two patients (73%) had a modified Rankin Scale score of ≤2 at 3 months. A patient developed transient ischemic attack within 3 months; none developed recurrent stroke. Conclusions: Rostral medullary infarction with mild neurological deficits resulting from SAO is relatively frequent. Because emergency DWI within 24 h could not detect MMI in one third of the patients, this type of infarction could be misdiagnosed as capsular/pontine lacunae or other neurological disorders.

Medial vestibulospinal tract lesions impair sacculo-collic reflexes

The medial vestibulospinal tract (VST) is known to mediate the vestibular-evoked myogenic potential (VEMP) in the contracting sternocleidomastoid muscle (SCM). To determine whether disruption of the medial VST in the medulla impairs formation of VEMP, we measured VEMP in 14 patients with medial medullary infarction (MMI). VEMP was induced by a short tone burst and was recorded in contracting SCM while patients turned their heads forcefully to the contralateral side against resistance. Normative data were obtained from 47 healthy volunteers. Seven patients (50%) had abnormal VEMP in the side of the MMI lesion, absent in two, decreased in four, and delayed in two. One patient showed both decreased and delayed response. Of the seven patients with abnormal VEMP, five had the lesions that extended to the dorsal tegmentum while five of the seven patients with normal VEMP showed restricted anteromedial lesions mainly involving the pyramids. Spontaneous nystagmus (4/7, 57%), gaze-evoked nystagmus (6/7, 86%), and ocular tilt reaction/tilt of the subjective visual vertical (4/7, 57%) were frequently observed in the patients with abnormal VEMP. The abnormal VEMP in patients with infarctions involving the medullary tegmentum supports that VEMP is mediated by the medial VST descending within the medial longitudinal fasciculus.

Tetraplegia Following Bilateral Medial Medullary Infarction

Bilateral medial medullary infarction is rare. We report a 54-year-old man who presented with a 3-day history of dysarthria and progressive weakness in all four limbs. He suffered from respiratory failure 10 days later. Brain magnetic resonance imaging showed acute infarction of the bilateral medial medulla, characterized by a typical heart-shaped sign. Intravenous heparin was given for his cerebral infarction; the patient survived but with tetraplegia. Respiratory failure caused by bilateral medial medullary infarction can be fatal. With improvements in diagnostic technology, and the application of appropriate respiratory care, the survival rate of patients with bilateral medial medullary syndrome has increased. Early diagnosis with adequate treatment of respiratory symptoms may improve the clinical outcome.

Medial Medullary Infarction

Clinical-imaging correlation and long-term clinical outcomes remain to be investigated in medial medullary infarction (MMI). We studied clinical, MRI, and angiographic data of 86 consecutive MMI patients. The lesions were correlated with clinical findings, and long-term outcomes, divided into mild and severe (modified Rankin scale >3), were assessed by telephone interview. Central poststroke pain (CPSP) was defined as persistent pain with visual numeric scale > or = 4. The lesions were located mostly in the rostral medulla (rostral 76%, rostral+middle 16%), while ventro-dorsal lesion patterns include ventral (V, 20%), ventral+middle (VM, 33%), and ventral+middle+dorsal (VMD, 41%). Clinical manifestations included motor dysfunction in 78 patients (91%), sensory dysfunction in 59 (73%), and vertigo/dizziness in 51 (59%), each closely related to involvement of ventral, middle, and dorsal portions, respectively (P<0.001, each). Vertebral artery (VA) atherosclerotic disease relevant to the infarction occurred in 53 (62%) patients, mostly producing atheromatous branch occlusion (ABO). Small vessel disease (SVD) occurred in 24 (28%) patients. ABO was more closely related to VMD (versus V+VM) than was SVD (P=0.035). During follow-up (mean 71 months), 11 patients died, and recurrent strokes occurred in 11. Old age (P=0.001) and severe motor dysfunction at admission (P=0.001) were factors predicting poor prognosis. CPSP, occurring in 21 patients, was closely (P=0.013) related to poor clinical outcome. MMI usually presents with a rostral medullary lesion, with a good clinical ventro-dorsal imaging correlation, caused most frequently by ABO followed by SVD. A significant proportion of patients remain dependent or have CPSP.

Abnormal Vestibular Evoked Myogenic Potentials in Medial Medullary Infarction

BackgroundThe medial vestibulospinal tract (MVST), which descends in the medial longitudinal fasciculus (MLF), may mediate the vestibular evoked myogenic potentials (VEMPs) in the contracting sternocleidomastoid muscle. We report herein abnormal VEMPs in a patient with medial medullary infarction (MMI) that appeared to involve the MLF.Case ReportA patient with infarction involving the right medial medulla showed decreased p13-n23 amplitude and increased p13/n23 latencies of the VEMPs on the right side. These abnormal VEMPs recorded in an MMI patient support the theory that VEMPs are mediated by the MVST contained within the MLF.ConclusionsVEMPs may represent a valuable tool for investigating vestibular dysfunction originating from the saccule, even in patients with central vestibulopathies, which is not readily defined by conventional vestibular function tests.

Bilateral Medial Medullary Infarction Demonstrated by Diffusion-Weighted Imaging: Case Report

A 78-year-old woman presented with weakness of the extremities, dysarthria, dizziness, and sensory impairment. Magnetic resonance imaging showed acute bilateral medial medullary infarction. Contrast enhanced magnetic resonance angiography demonstrated stenosis or occlusion of both intracranial vertebral arteries. We present a rare case of bilateral medullary infarction seen on diffusion-weighted imaging.

Dysphagia in a Patient with Bilateral Medial Medullary Infarcts

Bilateral medial medullary infarct is a rare stroke syndrome and only a handful of cases have been described. Dysphagia as a manifestation of medullary infarcts is well recognized but often associated with lateral medullary infarct. Bilateral medial medullary infarcts are commonly associated with severe dysphagia in addition to a number of other signs and symptoms. We describe a patient who had bilateral medial medullary infarct with severe dysphagia in addition to quadriplegia and respiratory difficulty, and analyze infarct topography with respect to dysphagia, risk factors, vascular territories involved, and prognosis in view of previously reported cases.

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.

Unusual triad due to a bilateral medial medullary infarction in a 35-year-old man

Unusual triad due to a bilateral medial medullary infarction in a 35-year-old man

Upbeat Nystagmus: Clinicoanatomical Correlations in 15 Patients

Background and PurposeThe mechanism of upbeat nystagmus is unknown and clinicoanatomical correlative studies in series of patients with upbeat nystagmus are limited.MethodsFifteen patients with upbeat nystagmus received full neuro-ophthalmological evaluation by the senior author. Nystagmus was observed using video Frenzel goggles and recorded with video-oculography. Brain lesions were documented with MRI.ResultsLesions responsible for nystagmus were found throughout the brainstem, mainly in the paramedian area: in the medulla (n=8), pons (n=3), pons and midbrain with or without cerebellar lesions (n=3), and midbrain and thalamus (n=1). Underlying diseases comprised cerebral infarction (n=10), multiple sclerosis (n=2), cerebral hemorrhage (n=1), Wernicke encephalopathy (n=1), and hydrocephalus (n=1). Upbeat nystagmus was mostly transient and showed occasional evolution during the acute phase. In one patient with a bilateral medial medullary infarction, the upbeat nystagmus changed into a hemiseesaw pattern with near complete resolution of the unilateral lesion. Gaze and positional changes usually affected both the intensity and direction of the nystagmus. A patient with a cervicomedullary lesion showed a reversal of upbeat into downbeat nystagmus by straight-head hanging and leftward head turning while in the supine position. Gaze-evoked nystagmus (n=7), ocular tilt reaction (n=7), and internuclear ophthalmoplegia (n=4) were also commonly associated with upbeat nystagmus.ConclusionsIn view of the responsible lesions and associated neuro-ophthalmological findings, upbeat nystagmus may be ascribed to damage to the pathways mediating the upward vestibulo-ocular reflex or the neural integrators involved in vertical gaze holding.

Medial medullary infarction: Abnormal ocular motor findings

In 20 consecutive patients with isolated medial medullary infarction, abnormal ocular motor findings included nystagmus (n = 8), ocular contrapulsion (n = 5), and contralesional ocular tilt reaction (n = 2). The nystagmus was ipsilesional (n = 4), gaze-evoked (n = 5), upbeating (n = 4), and hemiseesaw (n = 1). The ocular motor abnormalities may be explained by involvements of the nucleus prepositus hypoglossi, medial longitudinal fasciculus or efferent fibers from the vestibular nuclei, climbing fibers, and cells of the paramedian tracts.

Dysphagia in unilateral medullary infarction

To study dysphagia in pure, unilateral medullary infarction using video fluoroscopic swallowing (VFS) tests and to compare the results between lateral medullary infarction (LMI) and medial medullary infarction (MMI). We studied 46 patients with medullary infarction (37 LMI, 9 MMI). Based on the MRI findings, each LMI was classified rostrocaudally as either a rostral or caudal lesion, and horizontally as either a superficial (lateral + dorsal) or nonsuperficial lesion. Each MMI was assigned to either a deep (lesion extending to the dorsal surface) or superficial lesion group. VFS examination was conducted and an 8-point scale was used for assessing the severity of dysphagia. Based on these results, dysphagia was classified as: 1) problems on timing of hyolaryngeal excursion (PT), and 2) problems on range of hyolaryngeal excursion (PR). Dysphagia was more frequent (p < 0.05) in MMI patients (78%) than in LMI patients (35%). Among the LMI patients, dysphagia was more frequent (p < 0.01) and severe (p < 0.01) in the rostral than in the caudal group and in the nonsuperficial than in the superficial group. In the MMI group, there was no difference in the frequency of dysphagia between the deep and superficial groups. Regarding the characteristics of dysphagia, seven (54%) of the LMI patients had PR, five (38%) had PT, and one (8%) had both. For the MMI patients, PT was frequent (86%) but PR was present in only one patient (14%). Five MMI patients (71%) showed no responses to penetration or aspiration, and silent dysphagia was observed in only four LMI patients (31%). Dysphagia is as frequent and severe in medial medullary infarction (MMI) as in lateral medullary infarction (LMI) patients. The types and characteristics of dysphagia are different between the LMI and MMI patients, implicating the rationale for a different treatment strategy.

Infarcts presenting with a combination of medial medullary and posterior inferior cerebellar artery syndromes

Cerebellar and medial medullary infarctions are well-known vertebrobasilar stroke syndromes. However, their development in a patient with distal vertebral artery occlusion has not been previously reported. A 49-year-old man with longstanding hypertension suddenly developed vertigo, right-sided Horner syndrome, and left-sided weakness. An MRI of the brain showed acute infarcts in the right inferior cerebellum (posterior inferior cerebellar artery territory) and the right upper medial medulla (direct penetrating branches of vertebral artery). Magnetic resonance angiogram showed occlusion of the distal vertebral artery on the right side. Atherothrombotic occlusion of the distal vertebral artery may cause this unusual combination of vertebrobasilar stroke.

Bilateral medial medullary infarction due to bilateral vertebral artery dissection

We describe a 52-year-old woman who experienced transient motor weakness and numbness of the left extremities and presented 2 days later with severe hemiparesis and sensory impairment of the right extremities and right lingual palsy. Magnetic resonance imaging (MRI) revealed bilateral upper medial medullary infarction, primarily in the left ventral portion. The findings of both three-dimensional (3D) computed tomographic and conventional angiography suggested dissection of both intracranial vertebral arteries (VAs). Medial medullary infarction is generally caused by atherosclerosis within a VA or anterior spinal artery. This is the first report of bilateral medial medullary infarction due to dissection of both intracranial VAs.

Spectrum of medial medullary infarction: clinical and magnetic resonance imaging findings

Among 4200 consecutive patients admitted to three hospitals with acute ischemic stroke, we found only 11 patients in whom magnetic resonance imaging (MRI) had proved that they had medial medullary infarction (MMI). In our centers, patients with MMI were less than 1% of those with vertebrobasilar stroke. The infarcts documented by MRI were unilateral in 10 patients and bilateral in one. On clinico-topographical analysis there were four clinical patterns: (1) Classical Dejerine's syndrome was the most frequent, consisting of contralateral hemiparesis, lemniscal sensory loss and ipsilateral lingual palsy in 7 of the eleven patients. (2) Pure hemiparesis was present in 2 patients; (3) Sensorimotor stroke was present in 1 patient with contralateral hemiparesis, hypesthesia and mild decrease in pain sensation without lingual palsy; (4) Bilateral MMI syndrome in 1 patient, accompanied by tetraparesis, bilateral loss of deep sensation, dysphagia, dysphonia and anarthria. Presumed causes of MMI were intrinsic branch penetrator artery disease with concomitant vertebral artery stenosis in 6 of the 11 patients, vertebral artery occlusion in 2, dolichoectatic vertebrobasilar arteries in 2, a source of cardiac embolism in 1. Prognosis at 3 months was favorable in 8 patients, but the patient with bilateral MMI syndrome had persisting motor deficit causing limitation of daily activities, and 2 died from systemic causes. The classical triad of acute MMI facilitates the diagnosis, although the recognition of this syndrome in patients with incomplete manifestations can be difficult and occurs more frequently than commonly thought. Moreover, vertebral artery atherosclerosis and branch atheromatous disease of the penetrating arteries are the main causes of medullary infarction.

Bilateral medial medullary infarction

We present a case of bilateral medial medullary infarction demonstrated by magnetic resonance imaging (MRI) and review 12 previously reported cases. We classify these 13 cases (including the present case) into two groups according to the extent of the ischemic region: type 1, the ischemic lesion developed from the medullary pyramid to the medial longitudinal fasciculus; type 2, the lesion was confined to the medullary pyramid.A 71 year old man presented with slight disturbance of consciousness, dysarthria, disturbance of leftward gaze, no gag reflex and tetraparesis. He developed nearly complete horizontal ophthalmoplegia. MRI revealed upper medial medullary infarction bilaterally that extended to the pontomedullary junction. We propose that the prognosis of type 2 bilateral medial medullary infarction is better than that of type 1. Furthermore, the prognosis of bilateral medial medullary infarction itself may be better than previously indicated.

Differences in long term sensory sequelae between lateral and medial medullary infarction

Differences in long term sensory sequelae between lateral and medial medullary infarction J.S. Kim, S. Choi-Kwon (Seoul, Korea) Background To compare long term sensory sequelae of the lateral medullary infarction (LMI) and medial medullary infarction (MMI). Methods We studied 55 (41 LMI and 14 MMI) patients who were followed up > 6 months. The nature and intensity of sensory symptoms were assessed by McGill-Melzack pain questionnaire and visual analogue scale, respectively. Results After the mean follow up of 21 months, sensory symptoms were the most important, and the second most important sequelae in LMI patients and MMI patients, respectively. In LMI patients, the symptoms were most often described as cold (38%), numb (29%) and burning (27%) while MMI patients described them as numb (60%), squeezing (30%) and cold (10%). LMI patients significantly more often cited cold environment as an aggravating factor, and more often had a delayed-onset pain than MMI patients. Conclusions: The nature, the mode of onset and aggravating factors of the sensory sequelae are different between LMI and MMI patients, which may be related to selective involvement of the spinothalamic tract by the former and the medial lemniscus by the latter. We suggest that the mechanisms for central post-stroke pain may differ according to the site of damages on the sensory tracts. NXY-059: Neuroprotective Effects in a Rat Focal Stroke