Magnetic resonance imaging of medial medullary infarction

Medial medullary infarction is characterized by ipsilateral hypoglossal nerve palsy, contralateral hemiparesis sparing the face, and contralateral disturbance of deep sensation. Although it is possible to make a clinical diagnosis in typical patients, diagnosis is difficult if hypoglossal nerve palsy is absent. We describe a patient with medial medullary infarction without hypoglossal nerve palsy. The patient suffered from left hemiplegia and homolateral disturbance of deep sensation. Magnetic resonance imaging revealed the site of the lesion to be in the medial portion of the upper medulla oblongata. The result of somatosensory evoked potential testing was compatible with disturbance of the medullary medial lemniscus. In a review of the literature, we examined the relation between clinical features and lesion location in 16 patients with medial medullary infarction and compared these to the present patient. Motor paresis was present in every patient, while disturbance of deep sensation was recorded in nine of 13 patients and hypoglossal nerve palsy in six of 14 patients. In atypical patients with medial medullary infarction (such as the present patient), magnetic resonance imaging is necessary to detect the lesion and to make a clinical diagnosis.     

The medullary vascular syndromes revisited

There are two major vascular syndromes of the medulla oblongata: the medial and the lateral. The medial medullary syndrome is characterized by the triad of ipsilateral hypoglossal nerve palsy with contralateral hemiparesis and loss of deep sensation. Lateral medullary infarction commonly presents with Homer's syndrome, ataxia, alternating thermoanalgesia, nystagmus, vertigo and hoarseness. Combinations of the two major syndromes occur as bilateral medial medullary, hemi-medullary and bilateral lateral medullary syndromes. Each of these syndromes frequently manifests with incomplete or atypical findings depending on the extent of the lesion. Magnetic resonance imaging has been useful in the clinical diagnosis of medullary infarctions. The site of the lesion may help predict the arteries involved.     

31例延髓梗死患者的临床分析

目的:根据头颅MRI对延髓梗死病灶的定位并结合延髓的解剖学特点,探讨延髓梗死临床表现的特征.方法:31例急性延髓梗死患者均行头颅MRI检查,对其病灶位置分布、神经系统症状体征,出院当天改良Rankin量表(mRS)评分等指标进行分析.结果:31例急性延髓梗死病例中:外侧延髓梗死(LMI)16例;内侧延髓梗死(MMI)13例;双侧延髓梗死(BMI)2例.LMI组病灶位于延髓背外侧或外侧;MMI组病灶位于延髓腹内侧,且多位于延髓上段.LMI多表现为不典型或部分性的"Wallenberg综合征",最常见的症状或体征为眩晕,Homer征、构音障碍、吞咽障碍、软腭麻痹,肢体共济失调.MMI多表现为感觉运动性卒中(SMS)或纯运动性卒中(PMS),最常见的症状或体征为对侧肢体偏瘫、构音障碍、中枢性面舌瘫.31例延髓梗死患者中,BMI 2例均为双侧MMI,其中1例出现四肢瘫痪、双侧肢体深浅感觉障碍、核间性眼肌麻痹、构音以及吞咽障碍,另1例表现为左侧肢体偏瘫、构音障碍、强哭、强笑等症状体征.结论:典型的延髓梗死综合征在临床上少见,LMI多表现为不典型,部分性的"Wallenberg综合征".而MMI往往与桥脑、基底节区腔隙性梗死的临床表现相似.双侧MMI导致四肢瘫痪等双侧锥体束受损表现,预后较差.     

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.     

Ocular and head movements in infarctions of the thalamic region

Oculomotor disorders in 22 infarctions in the thalamic region are recorded. Clinical examination and electro-oculography (17 cases) showed that paramedian thalamo-subthalamic lesions were responsible for clear deficits: upgaze paralysis and in some cases downgaze paralysis, partial paresis of the oculomotor nerve, deficits of lateral eye movements, myosis, paralysis of head flexion combined with downgaze paralysis. Postero-median choroid artery infarction was associated with upgaze paresis, slight deficit of lateral eye movements and myosis. Postero-lateral choroid artery infarction resulted in a partial visual field defect and in some cases, a contralateral hypometria; myosis was slight and inconstant. Infarctions of the internal capsule (anterior choroid artery, deep branches of the middle cerebral artery) were associated with a deficit of contralateral saccades. Ocular pursuit, when possible, was often saccadic, whatever the site of the infarction. This prevailed with gaze towards the lesion side.     

Medial medullary syndrome with contralateral face hypalgesia: A report of two cases.

Classically, patients with unilateral medial medullary syndromes show contralateral deep sensory loss, contralateral hemiparesis, and ipsilateral tongue paralysis. We encountered two patients with medial medullary syndromes showing hypalgesia of the contralateral face. Both patients had contralateral deep sensory loss and hemiparesis, but no hypoglossal nerve palsy, so it was difficult to establish a medial medullary syndrome from the clinical neurological signs alone. Magnetic resonance images showed that the infarcted areas were located in the ventromedial area of the upper medulla, probably involving the trigeminothalamic tract in the medial lemniscus. We reviewed the reported cases of medial medullary syndromes and summarized their clinical features as well as the topography concerned with the associated sensory disturbances.     

A case of medial medullary infarction with persistent primitive hypoglossal artery]

A 66-year-old woman was admitted to our hospital because of vomiting, dizziness and vertigo. Neurological examination on admission revealed only upbeat nystagmus without cranial nerve symptoms, paresis, cerebellar signs or sensory disturbances. Magnetic resonance(MR) images demonstrated a new T 2 high intensity and T 1 iso-intensity signal lesion in the right upper medial medulla. This medial medullary infarction caused central vestibular dysfunction. MR angiography and digital subtraction angiography demonstrated a persistent primitive hypoglossal artery (PPHA) originating from the right internal carotid artery to the vertebrobasilar artery associated with the stenosis of the right internal carotid artery at the level of the cervical bifurcation. This is the first report of medullary infarction with persistent carotid-basilar anastomosis. We suspected this medullary infarction was caused by artery to artery embolism in the branch of the right vertebral artery through the PPHA distal originated from the stenosis of the right internal carotid artery.     

A case of bilateral lower pons-medial medullary infarction presenting quadriparesis]

Bilateral medial medullary infarction is rare. Only 18 cases have been reported previously. We experienced a case of the bilateral lower pons-medullary infarction. A 63-year-old woman was admitted to our hospital because of moderate left hemiparesis. Hyperreflexia in left limbs and positive Babinski's reflex in left foot was observed. Sensory disturbance was mild left hemihypesthesia (in light touch, postural sense and vibration) without facial involvement. She also had lateral gaze nystagmus, dysarthria, and bilateral decreased gag reflex. Respiratory failure was not observed. A conservative therapy for cerebral infarction was performed. But the hemiparesis was deteriorated and progressed to complete quadriparesis on the 5th day. The brain MRI (T2-weighted image and FLAIR) demonstrated bilateral lower pons-medial medullary infarction on the 9th day. Cerebral angiography and 3D-CT angiography revealed no stenosis or occlusions in the major cerebral arteries. The anterior spinal artery was not evaluated enough because of the arteriosclerosis. The prognosis of this patient was favorable except for the quadriparesis. The severe quadriparesis has not been improved for about 2 years. The bilateral medial medullary infarction was quite rare in the literature. The prognoses of these cases were unfavorable for the respiratory failure. Our case was not fatal because of no respiratory paralysis.     

Isolated medial medullary infarction due to vertebral artery dissection

Abstract. A 54-year-old man developed left hemiparesis and tactile and deep sensory disturbance following onset of rightside cervical pain. These symptoms resulted from an isolated infarct in the right medial area of the upper medulla oblongata and intracranial vertebral artery (VA) dissection. Atherosclerotic disease of the VA is the most common cause of medial medullary infarction. In past reports of isolated medial medullary infarction, only a few cases involved VA dissection.     

Medial medullary infarction: report of three patients presented with central vestibular dysfunction without limb and lingual weakness]

The purpose of this article is to draw attention to atypical presentation of medial medullary infarction (MMI). With advanced imaging techniques, small infarctions occurring in the medulla are more easily identified. It is difficult, however, to make a clinical diagnosis of MMI if both hypoglossal nerve palsy and limb weakness are absent, because motor weakness is considered a cardinal manifestation of MMI. We describe here three patients who developed central vestibular dysfunction due to MMI without limb and lingual weakness. Case 1: A 44-year-old, diabetic woman developed vomiting and numbness on her left upper limb. Examination revealed unidirectional horizontal and rotatory nystagmus beating toward the right side. There were no Horner syndrome and hypoglossal nerve palsy. Barré arm and leg signs and limb ataxia were absent. Romberg sign was negative. Hypesthesia was present on her left forearm, hand, and fingers. Thumb-localizing test was normal. Cranial MRI demonstrated an infarction in the right paramedian region of the upper medulla. MR angiography demonstrated irregularity of the basilar and the left vertebral arteries. Case 2: A 69-year-old woman suffered from dizziness and nausea. She showed unidirectional, left-beating horizontal nystagmus. There were no Horner syndrome and hypoglossal nerve palsy, Barré arm and leg signs, and limb ataxia. MRI disclosed an infarction in the left upper medial medulla. Case 3: A 47-year-old man developed vertigo when turning over in bed. He showed left-beating nystagmus without latency, when lying down. Horner syndrome and hypoglossal nerve palsy were absent MRI showed bilateral MMI, with the right lesion being larger than the left. MR angiography demonstrated a stenosis in the distal portion of the left internal carotid artery but not in the vertebral and basilar arteries and their branches. This case represents central positional vertigo. Vestibular syndrome seen in cases 1 and 2 was incomplete and incongruent, suggesting dysfunction of the central vestibular system. There have been only nine cases of MMI with horizontal nystagmus in primary position, including unidirectional horizontorotatory nystagmus. In these cases, horizontal nystagmus beats toward the side of the lesion. In sharp contrast, horizontal nystagmus typically beats away from the lesion side in cases of Wallenberg syndrome, suggesting different underlying mechanism. Unidirectional horizontal and rotatory nystagmus is generally associated with peripheral vestibular dysfunction. There has been no reported case of MMI presenting with vestibular dysfunction preserving motor power. Thus, this "benign" form of MMI might have been misdiagnosed as peripheral vestibular dysfunction before the era of MRI.     

Paramedian thalamopeduncular infarction: clinical syndromes and magnetic resonance imaging.

We prospectively examined 11 patients with magnetic resonance imaging-documented infarction in the paramedian thalamopeduncular region, which is supplied by the superior mesencephalic and posterior thalamosubthalamic arteries. Variations in the size and rostral-caudal extent of infarction correlated with the following three clinical patterns: (1) With unilateral paramedian mesencephalic infarction, an ipsilateral third nerve paresis was accompanied by mild contralateral hemiparesis or hemiataxia. Contralateral ptosis and impaired upgaze were observed in two patients; one of them showed additional damage to the posterior commissure. (2) With bilateral infarction in the thalamopeduncular junction, involving the mesencephalic reticular formation, supranuclear vertical gaze defects were accompanied by impaired consciousness or memory, and mild aphasia in some patients. Persistent amnesia was observed only when the dominant anterior nucleus or mamillothalamic tract was damaged. (3) With larger thalamopeduncular infarcts, partial or complete third nerve paresis was combined with supranuclear gaze disturbance and delayed contralateral tremor. An unusual gaze disorder, a variant of the vertical "one-and-a-half syndrome," occurred with a small strategically placed lesion at the thalamopeduncular junction, best explained by selective damage to supranuclear pathways or partial nuclear involvement. The primary cause of these infarctions was embolism to the basilar apex or local atheroma at the origin of the posterior cerebral artery.     

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.     

Intermediate medullary infarction: a case report]

A 68-year-old man presented with right eye pain and vertigo. Thereafter, he gradually leaned rightward, then laid down. He felt nausea and vomited. His right upper eyelid drooped and he felt dysethesia of the right hand. On neurological examination, ptosis of his right eye with slightly miotic right pupil, paresis of the right soft palate and hoarseness were noted. Arm deviation test demonstrated rightward deviation. He presented sensory ataxia of the right upper and lower extremities: finger nose test showed mild dysmetria of the right upper extremity, heel knee test demonstrated dysmetria of right lower extremity and these findings worsened when he closed his eyes. He showed mild bending of his bilateral ring and little fingers when he did rapid alternative movement. He leaned rightward when he sat and closed his eyes. Position sense of his right upper and lower extremities was decreased and sometimes he could not answer correctly when asked on which direction his finger pointed. Pinprick sensation was mildly decreased on the left side not including the face. Touch and vibration sense were normal. SEP findings on upper and lower extremity stimulation were normal. MRI of the brain showed T2 high intensity and partially T1 low intensity lesion at the right medulla (Figure). MR angiography showed no apparent lesion of major arteries such as dissection of the vertebral arteries. He complained and presented with hiccup initially. On MRI, the lesion was thought to involve the spinothalamic tract, medial lemniscus and inferior olivary nucleus. Ambiguus nucleus was in the lesion and solitary nucleus near the lesion. There is no report that seems to describe clinical features of a lesion like that in this case. Intermediate medullary infarction may present dissociated sensory disturbance like Brown-Sequard syndrome and position sensory disturbance without disturbance of vibration sense.     

The medial medullary infarction (Dejerine syndrome) following chiropractic neck manipulation]

A-38-year-old man suddenly developed nausea, vomiting and vertigo during chiropractic neck manipulation. This was followed by right hemiplegia, right deep sensory disturbance and left hypoglossal nerve palsy, consistent with the medial medullary infarction (Dejerine syndrome). The MRI revealed infarction at left medial part of the medulla. The vertebral angiogram and MRA showed marked narrowing of the left vertebral artery. X-rays of the cervical spine showed no spondylosis, dislocation nor osteolysis of the odontoid process. The serological studies, including lupus anticoagulant, protein C, and protein S gave normal results. Although vascular accidents involving the brain stem after chiropractic neck manipulation have been reported since Pratt-Thomas and Berger, previous reports are still rare. In them lateral medullary infarction (Wallenberg syndrome) is probably the most common case. On the other hand, medial medullary syndrome (Dejerine syndrome) is absolutely rare. To our knowledge, the only one report has been made by Watanabe and his colleagues before our present case. The mechanism was suggested that rotation and tilting of the neck stretches and compresses the vertebral artery at the cervical joint causing injury to the vessel, with an intimal tearing, dissection, and pseudoaneurysm formation. Consequently, the present case may be caused by injury to the left vertebral artery with an intimal tearing during neck manipulation sufficient to cause disection and subsequent infarction of the brain stem.     

延髓梗死11例患者MRI与临床特点对照研究

目的 探讨延髓梗死患者MRI病灶部位与临床表现特点的关系.方法 总结11例患者的临床症状和体征,对照MRI结果对梗死病灶进行定位,讨论病灶部位与临床表现的关系.结果 延髓外侧梗死5例,延髓内侧梗死6例(其中双侧梗死2例);延髓外侧梗死常见症状是言语不清、眩晕、饮水呛咳、吞咽困难及面部麻木,延髓内侧梗死常见症状是肢体瘫痪、言语不清;延髓外侧梗死常见体征是构音障碍、感觉障碍、Horner征及面瘫,延髓内侧梗死常见体征是肢体瘫痪、周围性舌瘫.结论 不同病灶部位的延髓梗死患者症状、体征各异,借助MRI可帮助诊断.     

Isolated limb sensory disturbance accompanied with sudden deafness from vertebral artery dissection: a case report

A 52-year-old male presented with right sudden deafness and left isolated limb sensory disturbance following posterior neck pain. An examination revealed a mild degree of right sensory neural hearing loss and decreased pain and thermal sensation in the left side below the L3 level. Brain MRI showed a small lesion in the midlateral portion of the right middle-rostral medulla. The combination of the image findings suggests a right lateral medullary infarction caused by a vertebral artery (VA) dissection. In our case, the fibers carrying the modalities of the lateral spinothalamic tract restricted to below the L3 level, sparing other sensations, suggest a selective involvement. This finding suggests that sensory dermatomal representation in the modality may be preserved at least up to the level of the medulla oblongata. Moreover, in our case, the small emboli originating from the dissected VA possibly caused a small selective cochlear infarction. This type of embolism may give rise to various combinations of symptoms depending on the branches involved. For patients with an acute onset of headache or neck pain who present with isolated limb sensory disturbance accompanied by sudden deafness, even without the classical brainstem signs, a VA dissection and medullary infarction should therefore be considered.     

急性双侧半球支配区脑梗死15例临床分析

目的探讨急性双侧大脑半球梗死的临床特点、预后及发病机制。方法对15例急性双侧半球脑梗死患者的危险因素、临床症状和体征、神经影像所见以及结局进行回顾性分析。结果所有患者均有高血压病、糖尿病、心脏病、脑梗死等2种或2种以上疾病,主要表现为突发意识障碍、眼球运动异常以及四肢瘫痪。头部CT或MRI显示双侧额、顶、颞叶或基底节大片状低密度影或异常信号。9例死于脑疝,1例死于颅外并发症,5例出院时呈去皮质状态。结论本文报道15例急性多发性双侧半球梗死系双侧颈内动脉或大脑中动脉的支配区梗死,心源性或主动脉源性栓塞可能是主要的原因。本病预后极差,死亡或植物生存。     

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.     

Magnetic resonance imaging in ischaemic accidents of the brain stem

Seven cases of ischaemic accident affecting the brain stem are reported. There were two lacunar infarctions and five infarctions due to occlusion of major arteries (two lateral medullary infarctions, one pontine infarction and two thalamo-mesencephalic infarctions). In every case the abnormalities detected at MRI were concordant with the clinical findings. The authors underline the value of MRI in establishing clinico-topographic correlations in vivo and in differentiating lacunar infarctions from infarctions due to stenosis of major arteries in the vertebro-basilar system.     

延髓梗死的临床与神经影像学分析(附73例报告)

目的探讨延髓梗死的临床与神经影像学特点。方法回顾性分析73例延髓梗死患者的临床资料和影像学检查结果。结果本组男性53例,女性20例。首发临床表现复杂多样,其中浅感觉障碍41例,眩晕39例,饮水呛咳36例,恶心呕吐32例,吞咽困难31例,构音障碍29例。梗死病灶位于延髓上段27例,中段29例,下段12例,同时累及上段和中段3例,中段和下段2例。病灶位于背外侧61例,腹内侧10例,背内侧2例。表现为经典的延髓综合征共15例,包括Wallenberg综合征12例,Dejerine综合征1例,Avellis综合征1例,Babinski-Nageotte综合征1例。结论延髓梗死常见临床表现是浅感觉障碍和后循环缺血症状,经典延髓综合征少见;延髓梗死以中上段最常见,主要发生于背外侧;头部MRI对延髓梗死的诊断有极其重要的意义。