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Pure midbrain infarction: clinical, radiologic, and pathophysiologic findings.

OBJECTIVE: To describe the clinical features, MRI findings, and the pathogenesis of the pure midbrain infarction. METHODS: Forty patients with infarcts limited to the midbrain were studied. MRI and angiography (mostly MR angiography) were performed in all patients. RESULTS: Clinical manifestations included gait ataxia in 27 (68%) patients, dysarthria in 22 (55%), limb ataxia in 20 (50%), sensory symptoms in 17 (43%), third nerve palsy in 14 (35%), definitive limb weakness (< or =IV/V) in nine (23%), and internuclear ophthalmoplegia in five (13%). According to MRI findings, the lesions were categorized into four groups. The anteromedial group (n = 18) was characterized by oculomotor disturbances (89%), ataxia (89%, bilateral in 17%), and sensory changes (39%) usually restricted to the perioral and hand areas. Lesions restricted to the subcortical area (n = 10) were usually related to small vessel disease (SVD) (78%), whereas those involving the medial surface (n = 8) were caused by large vessel disease (LVD) (78%). The anterolateral group (n = 11) was characterized by ataxia (70%) and definitive hemiparesis (30%) usually caused by LVD (82%). The combined group (n = 6) had frequent oculomotor disturbances (83%), definitive hemiparesis (67%), and ataxia (50%) and was usually associated with LVD (67%). The lateral group (n = 2) was characterized by prominent sensory symptoms. The prognosis was generally good except for one patient with a bilateral lesion. CONCLUSION: Clinical-radiologic correlation study yields four distinct subgroups: anteromedial, anterolateral, combined, and lateral. Large vessel disease and small vessel disease are usual pathogenic mechanisms, whereas cardiogenic embolism is rare.

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Sensory sequelae of medullary infarction: differences between lateral and medial medullary syndrome.

BACKGROUND AND PURPOSE: A comparison between long-term sensory sequelae of lateral medullary infarction (LMI) and medial medullary infarction (MMI) has never been made. METHODS: We studied 55 patients with medullary infarction (41 with LMI and 14 with MMI) who were followed up for >6 months. We examined and interviewed the patients with the use of a structured format regarding the most important complaints, functional disabilities, and the presence of sensory symptoms. The nature and the intensity of sensory symptoms were assessed with the modified McGill-Melzack Pain Questionnaire and the visual analog scale, respectively. RESULTS: There were 43 men and 12 women, with an average age of 59 years. Mean follow-up period was 21 months. The sensory symptoms were the most important residual sequelae in LMI patients and the second most important in MMI patients. In LMI patients, the severity of residual sensory symptoms was significantly related to the initial severity of objective sensory deficits (P<0.05). Sensory symptoms were most often described by LMI patients as numbness (39%), burning (35%), and cold (22%) in the face, and cold (38%), numbness (29%), and burning (27%) in the body/limbs, whereas they were described as numbness (60%), squeezing (30%) and cold (10%), but never as burning, in their body/limbs by MMI patients. LMI patients significantly (P<0.05) more often cited a cold environment as an aggravating factor for the sensory symptoms than did the MMI patients without spinothalamic sensory impairment. The subjective sensory symptoms were frequently of a delayed onset (up to 6 months) in LMI patients, whereas they usually started immediately after the onset in MMI patients. CONCLUSIONS: Our study shows that sensory symptoms are major sequelae in both LMI and MMI patients. However, the nature, the mode of onset, and aggravating factors are different between the 2 groups, which probably is related to a selective involvement of the spinothalamic tract by the former and the medial lemniscus by the latter. We suggest that the mechanisms for the central poststroke pain or paresthesia may differ according to the site of damages on the sensory tracts (spinothalamic tract versus medial lemniscal tract).

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Brainstem reflex circuits revisited.

Our current understanding of brainstem reflex physiology comes chiefly from the classic anatomical-functional correlation studies that traced the central circuits underlying brainstem reflexes and establishing reflex abnormalities as markers for specific areas of lesion. These studies nevertheless had the disadvantage of deriving from post-mortem findings in only a few patients. We developed a voxel-based model of the human brainstem designed to import and normalize MRIs, select groups of patients with or without a given dysfunction, compare their MRIs statistically, and construct three-plane maps showing the statistical probability of lesion. Using this method, we studied 180 patients with focal brainstem infarction. All subjects underwent a dedicated MRI study of the brainstem and the whole series of brainstem tests currently used in clinical neurophysiology: early (R1) and late (R2) blink reflex, early (SP1) and late (SP2) masseter inhibitory reflex, and the jaw jerk to chin tapping. Significance levels were highest for R1, SP1 and R2 afferent abnormalities. Patients with abnormalities in all three reflexes had lesions involving the primary sensory neurons in the ventral pons, before the afferents directed to the respective reflex circuits diverge. Patients with an isolated abnormality of R1 and SP1 responses had lesions that involved the ipsilateral dorsal pons, near the fourth ventricle floor, and lay close to each other. The area with the highest probabilities of lesion for the R2-afferent abnormality was in the ipsilateral dorsal-lateral medulla at the inferior olive level. SP2 abnormalities reached a low level of significance, in the same region as R2. Only few patients had a crossed-type abnormality of SP1, SP2 or R2; that of SP1 reached significance in the median pontine tegmentum rostral to the main trigeminal nucleus. Although abnormal in 38 patients, the jaw jerk appeared to have no cluster location. Because our voxel-based model quantitatively compares lesions in patients with or without a given reflex abnormality, it minimizes the risk that the significant areas depict vascular territories rather than common spots within the territory housing the reflex circuit. By analysing statistical data for a large cohort of patients, it also identifies the most frequent lesion location for each response. The finding of multireflex abnormalities reflects damage of the primary afferent neurons; hence it provides no evidence of an intra-axial lesion. The jaw jerk, perhaps the brainstem reflex most widely used in clinical neurophysiology, had no apparent topodiagnostic value, probably because it depends strongly on peripheral variables, including dental occlusion.

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Diffusion-weighted magnetic resonance imaging in symptomatic vertebrobasilar atherosclerosis and dissection.

BACKGROUND: Acute multiple brain infarction (AMBI) pattern on diffusion-weighted imaging (DWI) is associated with arterial and cardiac sources of embolism. The DWI characteristics of patients with stroke due to vertebrobasilar arterial dissection and atherosclerotic disease have not been reported in detail. OBJECTIVE: To describe the DWI stroke patterns in patients with posterior circulation occlusive disease to determine mechanisms of ischemia. DESIGN: Retrospective analysis of infarct patterns in patients with symptomatic vertebrobasilar disease. SETTING: Large community-based teaching hospital. PATIENTS: Patients admitted with stroke due to vertebrobasilar disease were identified retrospectively. Patients were included if DWI was obtained within 7 days of symptom onset. MAIN OUTCOME MEASURE: Infarct patterns were analyzed according to established templates of vascular territories. RESULTS: Eleven patients with vertebral dissection and 39 patients with atherothrombosis were identified. An AMBI pattern was present in 8 (72%) of 11 patients with arterial dissections and 25 (64%) of 39 patients with atherosclerotic disease (P = .48). Distal embolism to the terminal branches of the basilar artery occurred with equal frequency in both groups and was found in half of all cases. Isolated thalamic infarction did not occur. Pontine infarction was noted in 2 (18%) of 11 patients with dissections and 18 (46%) of 39 patients with atherosclerosis (P = .09). Cerebellar border zone involvement was found in 14 (36%) of 39 patients with atherosclerosis and 4 (37%) of 11 patients with dissections (P = .6). CONCLUSIONS: Large arterial disease is frequently associated with AMBI in the posterior circulation. The incidence of AMBI was comparable to that reported in the anterior circulation. This DWI study supports the importance of embolism as the main mechanism of infarction in patients with vertebrobasilar occlusive disease. On the basis of our experience, large-vessel vertebrobasilar disease rarely causes isolated small-vessel thalamic infarction.

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Topodiagnostic value of blink reflex R1 changes: a digital postprocessing MRI correlation study.

The aim of the study was to investigate the relation of the blink reflex R1 arc to known anatomical brainstem structures. Acute vascular brainstem lesions as identified by magnetic resonance imaging (MRI) of patients with isolated R1 pathology were superimposed into a stereotactic anatomical atlas using a new method of digital postprocessing. Isolated acute brainstem lesions were documented by diffusion-weighted MRI in 12 of 24 patients with unilateral R1 pathology. The lesions were located in the ipsilateral mid- to lower pons. In three patients only, the lesion had partial contact with the principal sensory nucleus of the trigeminal nerve (PSN) on at least one level. In two patients, the lesion involved the medial longitudinal fasciculus. Most lesions were located medially and ventrally to the PSN on transverse slices. Our results underline the high localizing value of changes in the R1 component of the blink reflex in patients with ipsilateral pontine functional deficits. Although available physiological evidence suggests that the R1 component of the blink reflex traverses an oligosynaptic pathway, this MRI study does not support the view that synaptic transmission in the PSN subserves R1. The reflex arc probably descends more medially and ventrally on its course to the facial nucleus.

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Postoperative coma in a patient with complete basilar syndrome after anterior cervical discectomy.

PURPOSE: Ischemic brainstem stroke resulting from occlusion of the basilar artery during cervical spine surgery in a previously asymptomatic patient is a rare event. We report the development of a large ischemic brainstem stroke, resulting from occlusion of the basilar artery during anterior cervical discectomy, in a patient without previous neurological deficit, or signs of vertebrobasilar insufficiency. CLINICAL FEATURES: A 55-yr-old, diabetic and hypertensive male who developed a cervical spine infection, underwent surgery for anterior discectomy at C5-C6. During the 2.5-hr long procedure the patient was lying supine with his neck hyperextended. Except for a temporary reduction in systolic blood pressure, the intraoperative course was uneventful. At the end of surgery the patient remained unconscious with flaccid paralysis in all extremities, fixed pinpoint pupils, low respiratory rate, and no response to painful stimuli. Naloxone administration did not improve the clinical picture, while brain computed tomography showed a large brainstem and cerebellar stroke, implicating basilar artery occlusion. The patient died five days later from stroke complications. Intraoperative surgical manipulation with a severely inflamed vertebral system, as well as prolonged neck hyperextension occluding the blood flow of vertebrobasilar arteries might have contributed to fatal brainstem stroke in this patient. CONCLUSION: Neck surgery carries a potential risk for posterior circulation stroke, and this report heightens awareness of this rare, but serious complication.

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[Classical brain stem syndrome. Definitions and history].

BACKGROUND: Inaccurate definitions of brain stem syndromes in the literature. METHOD: The original publications of the authors during the last century and the early years of this one were studied in relation to the neuro-ophthalmological diagnosis and neuroanatomy. It is the goal of this medico-historical investigation to compare the knowledge available at this time when the first descriptions were made with the clinical experience and understanding of today. RESULTS: The following classical brain stem syndromes are important for an ophthalmologist: diseases with III-paresis: Weber's syndrome (1863, ipsilateral oculomotor paralysis with alternating hemiplegia), Benedikt's syndrome (1889, oculomotor paralysis and crossed hemiparesis with tremor), Nothnagel Claude's syndrome (III-Paresis with alternating ataxia); diseases with VII-paresis: Millard Gubler's syndrome (1856, nuclear 7th nerve palsy with crossed hemiparesis), Foville's syndrome (1858, conjugate lateral gaze paralysis, ipsilateral nuclear palsy of the 7th nerve, crossed hemiparesis); diseases with VI-paresis: Raymond Cestan's syndrome (1895, abducent nerve paralysis with contralateral hemiparesis). Brain stem lesions are also found in Wallenberg's syndrome (1895, Horner's syndrome, absent corneal reflex, lateropulsion of saccadic eye movements, nystagmus, ataxia, dysphagia, hoarseness, sensory loss over the facial region, contralateral dissociated diminished sensibility (hemiparesis), etc.). The following two syndromes do not belong to the above-mentioned classical examples, because lesions of the long tracts of the brain stem are absent. However, since these two syndromes are accompanied by both ocular and neurological signs which indicate typical lesions of the brain stem, they are also mentioned here: Parinaud's syndrome (1883, paralysis of conjugate vertical gaze and paresis of convergence together with additional neuro-ophthalmological signs) and the Koerber Salus Elschnig's syndrome (1903, 1910, 1913, nystagmus retractorius, vertical gaze palsy, pupillary disturbances, and signs of midbrain disease). CONCLUSIONS: The first descriptions of these syndromes, together with the figures illustrating the neuroanatomical findings in these lesions, are helpful for assessing the clinical picture. Some named syndromes which are used today in clinical diagnosis (e.g. Parinaud's syndrome) do not exactly correspond to the first descriptions in the last century.

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Myasthenia mimicking vertebrobasilar stroke.

The advent of thrombolysis has offered a remarkable opportunity for treatment of acute ischemic stroke. Other therapies involving neuro-protection may be forthcoming. These treatments, however, are not without risk, making accurate diagnosis of stroke all the more important. Several conditions may mimic stroke in the emergency department, with myasthenia being an uncommon stroke mimic. We present two cases of myasthenia presenting as posterior circulation stroke. In one case, the tempo suggested basilar thrombosis. Treatment decisions regarding thrombolysis for stroke must be made rapidly. Stroke mimics continue to present a diagnostic challenge, myasthenia included. Accurate diagnosis is essential to avoid unnecessary hazard, as well as to implement effective treatment for the appropriate diagnosis.

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CT study of closure of the hemipharynx with head rotation in a case of lateral medullary syndrome.

In a patient with unilateral pharyngeal paralysis, rotation of the head to the paralyzed side can effectively close the hemipharynx on that side. However, the exact level or place of closure is unknown. Serial computed tomography of the pharynx in a patient with lateral medullary syndrome showed that hemipharyngeal closing occurred at the level of the hyoid bone, or the hypopharyngeal cavity above the pyriform sinus, and that the entire space of the bilateral pyriform sinuses remained open despite the head rotation.

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Spontaneous relapsing and recurring large multiloculated posterior fossa enteric cyst.

Intracranial enterogenous cyst is an uncommon entity. We report a case of enterogenous cyst of the posterior fossa situated posterolateral to the brain stem and extending into the left CP angle cistern. Patient had spontaneous regression and recurrence of the cyst. Clinical features and radiological findings are described. Near total excision of the cyst was carried out through the retro mastoid route. Patient made a good postoperative recovery.

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