A novel perspective for exploring the relationship between cerebral small vessel disease and deep medullary veins with automatic segmentation.

BACKGROUND: This study aimed to establish an intelligent segmentation algorithm to count the number of deep medullary veins (DMVs) and analyze the relationship between DMVs and imaging markers of cerebral small vessel disease (CSVD). METHODS: DMVs on magnetic resonance imaging (MRI) of patients with CSVD were counted by intelligent segmentation and manual counting. The dice coefficient and intraclass correlation coefficient (ICC) were used to evaluate their consistency and correlation. Structural MR images were used to assess imaging markers and total burden of CSVD. A multivariate linear regression model was used to evaluate the correlation between the number of DMVs counted by intelligent segmentation and imaging markers of CSVD, including white matter hyperintensities of the presumed vascular origin, lacune, perivascular spaces, cerebral microbleeds, and total CSVD burden. RESULTS: A total of 305 patients with CSVD were enrolled. An intelligent segmentation algorithm was established to calculate the number of DMVs, and it was validated and tested. The number of DMVs counted intelligently significantly correlated with the manual counting method (r = 0.761, P< 0.001). The number of smart-counted DMVs negatively correlated with the imaging markers and total burden of CSVD (P< 0.001), and the correlation remained after adjusting for age and hypertension (P< 0.05). CONCLUSIONS: The proposed intelligent segmentation algorithm, which was established to count DMVs, can provide objective and quantitative imaging information for the follow-up of patients with CSVD. DMVs are involved in CSVD pathogenesis and a likely new imaging marker for CSVD.

Anatomic and MRI bases for medullary infarctions with patients' presentation.

OBJECTIVE: There is a low incidence of the medullary infarctions and sparse data about the vascular territories, as well as a correlation among the anatomic, magnetic resonance imaging (MRI) and neurologic signs. MATERIALS AND METHODS: Arteries of the 10 right and left sides of the brain stem were injected with India ink, fixed in formalin and microdissected. The enrolled 34 patients with medullary infarctions underwent a neurologic, MRI and Doppler examination. RESULTS: Four types of the infarctions were distinguished according to the involved vascular territories. The isolated medial medullary infarctions (MMIs) were present in 14.7%. The complete MMIs comprised one bilateral infarction (2.9%), whilst the incomplete and partial MMIs were observed in 5.9% and 8.9%, respectively. The anterolateral infarctions (ALMIs) were very rare (2.9%). The complete and incomplete lateral infarctions (LMIs), noted in 35.3%, comprised 11.8% and 23.6%, respectively, that is, the anterior (5.9%), posterior (8.9%), deep (2.9%), and peripheral (5.9%). Dorsal ischemic lesions (DMIs) occurred in 11.8%, either as a complete (2.9%), or isolated lateral (5.9%) or medial infarctions (2.9%). The remaining ischemic regions belonged to various combined infarctions of the MMI, ALMI, LMI and DMI (35.3%). The infarctions most often affected the upper medulla (47.1%), middle (11.8%), or both (29.5%). Several motor and sensory signs were manifested following infarctions, including vestibular, cerebellar, ocular, sympathetic, respiratory and auditory symptoms. CONCLUSIONS: There was a good correlation among the vascular territories, MRI ischemia features, and neurologic findings regarding the medullary infarctions.

Severe Unilateral Proprioceptive Loss in Medullary- Rostral Spinal Cord Infarction. A Posterior Spinal Artery Syndrome.

We draw attention to a unique presentation, severe unilateral loss of limb proprioception, in patients with medullary and rostral spinal cord infarction. Two patients developed acute severe proprioceptive loss in the limbs ipsilateral to infarcts that involved the caudal medulla and rostral spinal cord. They also had symptoms and signs often found in lateral medullary infarction. The proprioceptive loss is attributable to injury to the gracile and cuneate nuclei and/or their projections to the medial lemniscus. The infarct territory is supplied by the posterior spinal branches of the vertebral artery near its penetration into the posterior fossa. The presence of severe ipsilateral proprioceptive loss in a patient with features of lateral medullary infarction indicates involvement of the rostral spinal cord.

Organ blood flow in response to infusion of arginine vasopressin in premature fetal sheep.

BACKGROUND: Arginine vasopressin (AVP) infusion has been shown to be a useful strategy for the management of systemic perfusion failure in premature infants. Our objective was to determine the characteristics of the blood flow redistribution induced by AVP infusion in premature fetal sheep. METHODS: Nine sheep fetuses at 99 to 113 days of gestation were continuously infused with AVP. Measurement of blood flow to individual fetal organs was performed using a colored microsphere technique, with measurements performed at 30 min before and 90 min after the initiation of AVP infusions. RESULTS: The AVP infusion significantly increased blood flow to the medulla oblongata (P < 0.05), and significantly decreased flow to the adrenal glands (from 492.0 ± 239.6 to 364.9 ± 143.3 mL/min/100 g, P < 0.05) and heart (from 592.6 ± 184.5 to 435.6 ± 137.4 mL/min/100 g, P < 0.05). The infusion significantly increased the vascular resistance in adrenal glands, kidneys, ileum, colon, heart, and cerebellum. In the brain, except for the cerebellum, no significant increase in resistance was identified. CONCLUSIONS: There was no significant response to AVP infusion in cerebral blood flow in mid-gestation fetal sheep. Our observations suggest that, under AVP stimulation, the blood flow to the adrenal glands and myocardium might be decreased due to an increase in vascular resistance.

Predictors of Outcome in Patients with Medullary Hemorrhage.

BACKGROUND: Isolated medullary hemorrhage (MH) is an uncommon presentation of spontaneous intraparenchymal hemorrhage. The relationship between MH and neurological outcome is not well known. This study aims to assess predictive parameters for the outcome of medullary hemorrhage. METHODS: We conducted an extensive search of the literature for cases with spontaneous, isolated MH. The study was conducted according to the statement of Preferred Reporting Items for Systematic Reviews and Meta Analysis (PRISMA). Forty-three cases diagnosed by CT or MRI have been reported in the literature, to which we add three confirmed by MRI. The ventrodorsal size of hemorrhage was taken into account as a parameter of outcome. Early neurologic deterioration (END) was defined as an incremental increase in the National Institutes of Health Stroke Scale score by ≥1 point in motor power, or ≥2 points in the total score within the first week after admission. Modified Rankin Score (mRS) 0-2 was presumed as favorable outcome (FO) and mRS 3-6 score as unfavorable outcome (UO) at discharge and at 3 months after stroke. RESULTS: We enrolled 46 patients, and 17 (37%) patients were diagnosed with END. The cause of medullary hemorrhage was mostly vascular malformations, including cavernous malformation (33%) and arteriovenous malformation (11%). In univariate analyses, neither arteriovenous malformations (OR, 1.04; 95%CI, 0.10-10.53; P = 0.68) nor cavernomas (OR, 1.04; 95%CI, 0.22-4.89; P = 0.62) were associated with UO. Acute respiratory distress syndrome was higher in patients with UO group (44%) compared to those with FO group (16%), but this difference did not reach to a significant level (OR, 4.13; 95%CI, 0.85-20.04; P = 0.09). The diameter of hemorrhage was significantly larger (≥1 cm) in patients with UO compared to those with FO (OR, 16.67; 95%CI, 1.87-148.89; P = 0.003). Three months after stroke, 37 patients (80%) had FO and 9 (19.5%) had UO, and 5 (11%) died. Multiple logistic regression analysis using predetermined variables found to be significant in univariate analyses (END, consciousness disturbance at admission, hemorrhage size, and hypertension) showed that END at stroke onset was significantly associated with UO (OR, 4.97; CI95%, 1.13-21.94; P = 0.03). CONCLUSIONS: These results suggest that the END is a predictor for UO in patients with medullary hemorrhage. The extent of the medullary hemorrhage along the conduction tract may contribute to deterioration.

Asymmetry of medullary veins on multiphase CT-angiography in patients with acute ischemic stroke.

BACKGROUND: It was previously demonstrated that decreased cortical venous drainage is a predictive factor of poor clinical outcome in patients with an acute ischemic stroke. The aim of this investigation is to test the hypothesis that the decline in blood flow in medullary veins (MV) on CT angiogram (CTA) of patients with acute ischemic stroke (AIS) can also be predictive of clinical outcome. METHODS: We retrospectively reviewed a database of patients with AIS who were evaluated by multiphase CTA and enrolled individuals with AIS and evidence of occlusion of the intracranial internal carotid artery, the M1 or M2 segment of the middle cerebral artery, or combination of two occlusions. To characterize asymmetry of MV we used similar principle that was previously established for MV on SWI MR-images; asymmetry was defined was presence of 5 or more contrast opacified MV in one hemisphere as compared to the contralateral side. Clinical outcomes were evaluated by mRS in 90 days. The Fisher Exact test was used to examine the significance of the MV asymmetry. Odds ratio and interrater variability were calculated. RESULTS: 66 patients with AIS were included. The presence of asymmetry in MV was associated with the higher frequency of poor clinical outcomes (84.6% vs 50.9%); the OR was 5.3. Interrater agreement in assessment on MV was moderate in our study (κ=0.55). CONCLUSION: This study shows that (a) medullary veins can be reliably assessed on multiphase CTA, (b) in patients with AIS, asymmetric appearance of MV is associated with poor clinical outcome.

Isolated Infarction of the Medullary Pyramid - A Rare Pure Motor Stroke.

Acute pure motor hemiparesis can occur due to a vascular insult along the cortico spinal pathway. Rarely such a stroke can occur as a result of involvement of the pyramids located on the ventral aspect of the medulla. Neurological localization can be difficult in such strokes and moreover they can also pose imaging challenges since they are missed on the CT scans. So far only 4 such cases have been reported in literature. Here we present two cases of pure motor strokes caused by infarction of the medullary pyramids. We have described the anatomical correlates of the symptoms and signs and also highlight the importance of MRI in picking up these rare strokes.

Medullary Compression Due to Ectatic Vertebral Artery-Case Report and Review of Literature.

Medullary compression syndrome due to anomalous course of blood vessels is a rare disease most commonly seen in the adult population. The offending vessels causing this syndrome are mostly posterior inferior cerebellar artery or the vertebral artery. The symptoms of this syndrome vary from most common hypertension to various other neurologic deficits like hemiplegia, dysesthesia, and dysarthria. Intractable dizziness is a rare symptom of this disease. The definite management plan for this disease is microvascular decompression. We present our case of medullary compression syndrome which manifested as intractable dizziness. We describe our experience in the management of this patient as well as present a review of literature of this rare disease.

Contribution of systemic vascular effects to fMRI activity in white matter.

To investigate a potential contribution of systemic physiology to recently reported BOLD fMRI signals in white matter, we compared photo-plethysmography (PPG) and whole-brain fMRI signals recorded simultaneously during long resting-state scans from an overnight sleep study. We found that intermittent drops in the amplitude of the PPG signal exhibited strong and widespread correlations with the fMRI signal, both in white matter (WM) and in gray matter (GM). The WM signal pattern resembled that seen in previous resting-state fMRI studies and closely tracked the location of medullary veins. Its temporal cross-correlation with the PPG amplitude was bipolar, with an early negative value. In GM, the correlation was consistently positive. Consistent with previous studies comparing physiological signals with fMRI, these findings point to a systemic vascular contribution to WM fMRI signals. The PPG drops are interpreted as systemic vasoconstrictive events, possibly related to intermittent increases in sympathetic tone related to fluctuations in arousal state. The counter-intuitive polarity of the WM signal is explained by long blood transit times in the medullary vasculature of WM, which cause blood oxygenation loss and a substantial timing mismatch between blood volume and blood oxygenation effects. A similar mechanism may explain previous findings of negative WM signals around large draining veins during both task- and resting-state fMRI.

Conjugate Eye Deviation Caused by Upper Medial Medullary Infarction: A Case Report.

Conjugate eye deviation (CED) is defined as a sustained shift in horizontal gaze toward 1 side, together with gaze failure to the other side, caused by lesions in the brainstem, basal ganglia, or cortical frontal eye fields. To date, very few reports have described CED in patients with medullary infarction. A 76-year-old woman presented with sudden onset of vertigo and right hemiparesis, accompanied by CED to the right with gaze palsy to the left. Her brain magnetic resonance imaging showed left upper medial medullary infarction involving the left nucleus prepositus hypoglossi (NPH) and adjacent to the left inferior olivary nucleus (ION). After treatments with 200 mg of aspirin and 60 mg of edaravone daily, symptoms gradually improved. The NPH and ION constitute NPH-ION-floccus-vestibular nucleus loop and contribute to the inhibitory mechanisms for horizontal eye movements. In addition, NPH projects excitatory neurons to the contralateral vestibular nucleus. In our case, disorders of the NPH and ION might have dysregulated inhibitory and excitatory projections, and thereby cause CED to the right with gaze palsy to the left. This represents a rare case showing CED to the contralesional side in upper medial medullary infarction.

Medullary infarction causing coexistent SUNCT and trigeminal neuralgia.

Background Short-lasting unilateral neuralgiform headache attacks with conjunctival injection and tearing (SUNCT) or with autonomic symptoms (SUNA) are grouped together within the trigeminal autonomic cephalalgias (TACs). However, the SUNCT and SUNA phenotype and management overlap with those of trigeminal neuralgia (TN). Additionally, a broad variety of cerebral pathologies are reportedly able to trigger either TN- or SUNCT-like pain, and emerging structural neuroimaging findings suggest the possible role of neurovascular conflict with the trigeminal nerve in SUNCT, further supporting aetiological and pathophysiological overlaps among SUNCT, SUNA and TN. Case report We present the first case of coexisting chronic SUNCT- and TN-like phenotypes caused by haemorrhagic infarct of the dorsolateral medulla. Discussion In light of our case, a perturbation of the dorsolateral medullary circuits may constitute an important pathophysiological component, supporting a unifying nosological hypothesis that considers SUNCT, SUNA and TN clinical variants of the same disorder.

Spontaneous Subclavian Artery Dissection Causing Ischemia of the Medulla Oblongata and Cerebellum.

BACKGROUND: Spontaneous subclavian artery dissection is a rare etiology. Spontaneous artery dissection causing brain ischemia is rare in all ischemic strokes. However, in young to middle-aged patients with brain ischemia, spontaneous carotid or vertebral artery dissection causing ischemic stroke accounts for 10-25%. CASE REPORT: A 58-year-old man with a history of hypertension presented to the Emergency Department with a sudden onset of left-arm paresthesia and numbness followed by symptoms of vertigo and vomiting. A neurological examination showed left-arm paresthesia, horizontal-rotational nystagmus, and left-side dysmetria according to a finger-to-nose test. Contrast-enhanced computed tomography showed left subclavian artery dissection. Diffusion-weighted imaging demonstrated hyperintensity in the left medulla oblongata and inferior part of the cerebellum. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: Spontaneous artery dissection is an important etiology of ischemic stroke among young patients. Cervical magnetic resonance angiography is the gold standard for the diagnosis of arterial dissection. Cervical disc disease is a common etiology in a patient with neck and shoulder pain without cause or neurologic symptoms, when cervical MRI is negative, however, spontaneous subclavian artery dissection should be considered in the differential diagnosis when a patient, especially in a case of younger patient, presents with acute new-onset neck and shoulder pain followed by the onset of neurological symptoms.

[The clinical, radiological and prognostic factor analysis of medullary infarction].

OBJECTIVE: To investigate the clinical and radiological features of medullary infarction (MI), and to compare the clinical characteristics of lateral medullary infarction (LMI) and medial medullary infarction (MMI). METHODS: Patients diagnosed as acute MI who were treated from January 2009 to December 2014 in Department of Neurology, Peking University Third Hospital, were retrospectively enrolled in the study and data were analyzed including risk factors, clinical features, laboratory findings, radiological characteristics, etiology and outcomes. RESULTS: A total of 62 cases of MI were enrolled with 48 cases of LMI and 14 cases of MMI , including 2 cases of bilateral MMI. The mean onset age of LMI and MMI was 60.2±12.3 and 56.9±14.2, respectively. The frequently affected location of LMI was the middle and upper part of medulla [40 cases (83.3%)]. The common symptoms and signs of LMI were dizzy (38 cases , 79.2%), sensory disturbance (33 cases , 68.8%), dysarthria ( 32 cases , 66.7%), dysphagia (30 cases , 62.5%), diminished pharyngeal reflex (30 cases, 62.5%), Horner's sign (29 cases, 60.4%), ataxia (26 cases, 54.2%) and nausea or vomiting (25 cases, 52.1%). The frequently affected location of MMI was the upper part of medulla (13 cases, 92.9%). The common symptoms and signs of MMI were motor dysfunction (12 cases, 85.7%), sensory disturbances (11 cases, 78.6%), dizzy (10 cases, 71.4%) and dysarthria (10 cases, 71.4%). Infarctions caused by atherosclerosis were found in 35 cases of LMI (72.9%) and 12 cases of MMI (85.7%). Five cases (10.4%) of LMI died in hospital, while 1 case (7.1%) of MMI died in hospital. No lesion was found in 16 cases (25.8%) by MRI-DWI within the first 24 hours of onset. CONCLUSIONS: Our study showes that the mean onset age of LMI is older than that of MMI. The lesion of LMI is frequently located in the upper and middle medulla, whereas the lesion of MMI is mostly in the upper medulla. The prognosis of LMI is worse than that of MMI. Atherosclerosis of the vertebral arteries is the predominant vascular pathology in MI.

Perfusion weighted imaging in the assessment of the pathology and outcomes of lateral medullary infarction.

This series case report aimed to elucidate the underlying pathology and outcomes of lateral medullary infarction (LMI) using perfusion weighted imaging (PWI). Four patients were diagnosed with LMI based on high-field diffusion-weighted magnetic resonance imaging (MRI-DWI) and PWI. The national institutes of health stroke scale (NIHSS) scores were recorded on days 1, 7, and 30, and the Barthel index was assessed on days 7 and 30. Three patients exhibited relative regional hypoperfusion of medullary lesion in the perfusion maps. Two cases exhibited ipsilateral hypoperfusion in the inferior cerebellum, whereas one patient exhibited a relatively regional hyperperfusion in the medulla oblongata. The LMI patients with a high NIHSS score and low Barthel index on days 7 and 30 exhibited regional hypoperfusion. This report of 4 LMI cases provides preliminary evidence that regional hypoperfusion may contribute to worse outcomes in LMI.

Surgical approaches to IV ventricle--anatomical study.

PURPOSE: Knowledge of anatomy of the IV ventricle is basic to surgical approach of any kind of lesion in its compartment as well as for those located in its neighborhood. The purpose of this study is to demonstrate the surgical approach options for the IV ventricle, based on the step by step dissection of anatomical specimens. METHODS: Fifty formalin-fixed specimens provided were the material for this study. The dissections were performed in the microsurgical laboratory in Gainesville, Florida, USA. RESULTS: The IV ventricle in a midline sagittal cut shows a tent-shaped cavity with its roofs pointing posteriorly and the floor formed by the pons and the medulla. The superior roof is formed by the superior cerebellar peduncles laterally and the superior medullary velum on the midline. The inferior roof is formed by the tela choroidea, the velum medullary inferior, and the nodule. The floor of the IV ventricle has a rhomboid shape. The rostral two thirds are related to the pons, and the caudal one third is posterior to the medulla. The median sulcus divides the floor in symmetrical halves. The sulcus limitans runs laterally to the median sulcus, and the area between the two sulci is called the median eminence. The median eminence contains rounded prominence related to the cranial nucleus of facial, hypoglossal, and vagal nerves. The lateral recesses are extensions of the IV ventricle that opens into the cerebellopontine cistern. The cerebellomedullary fissure is a space between the cerebellum and the medulla and can be used as a surgical corridor to the IV ventricle. CONCLUSIONS: We obtained in this study a didactic dissection of the different anatomical structures, whose recognition is important for addressing the IV ventricle lesions.

Clinical study of 46 patients with lateral medullary infarction.

BACKGROUND: Lateral medullary infarction (LMI) exhibits a variety of clinical features. Various bulbar symptoms can occur in LMI. METHODS: Neuroradiologic findings of 46 LMI patients were examined. Their infarcts were categorized into the rostral, middle, and caudal groups and were further subdivided into the anteromedial, anterolateral, lateral (L), and posterior regions. RESULTS: The middle medulla was the most common site (27 patients). Most lesions affected the L region alone (25 patients). Dysarthria and facial palsy occurred significantly more frequently in the rostral group than those in the caudal group. Severe truncal ataxia was significantly more common in the caudal group than that in the rostral group. Twenty-five of the 28 patients with severe truncal ataxia displayed vestibular symptoms; otherwise, the other 3 patients showed absence of vestibular symptoms. Soft palate paralysis occurred at a significantly high frequency in the patients with dysphagia and hoarseness compared with the patients without these 2 symptoms. Segmental sensory disturbance occurred in 5 patients, 4 of whom exhibited atypical patterns. CONCLUSIONS: The results of our comparisons between the rostral and caudal groups were consistent with those of previous studies. The presence of severe truncal ataxia without vestibular symptoms in LMI was atypical. An analysis of the bulbar symptoms indicated that the extent to which soft palate paralysis contributed to dysphagia was associated with the severity of ischemia in the nucleus ambiguus. The present study showed variability in clinical features of LMI, which was related to differences in the severity and the extent of ischemia in the lateral medulla.

Cardiac wall motion abnormality after bleeding from vertebral artery aneurysms.

OBJECTIVE: Lesions in the medulla oblongata may be causally associated with cardiac wall motion abnormality (WMA). Although subarachnoid hemorrhage (SAH) patients occasionally develop WMA, the relationship between aneurysmal locations and the frequency of WMA has rarely been investigated. The objective of this study was to evaluate whether the frequency of WMA was higher after the rupture of vertebral artery (VA) aneurysms than that of non-VA aneurysms. METHODS: We performed a retrospective chart analysis of 244 SAH patients who underwent transthoracic echocardiography and plasma catecholamine measurements. The frequencies of WMA and electrocardiographic (ECG) abnormalities were compared among patients classified by the location of aneurysms. Multivariate regression analysis was conducted to identify variables correlated with WMA. Furthermore, the relationship between plasma catecholamine levels and aneurysmal locations was evaluated. RESULTS: The frequency of WMA was significantly higher in patients with VA aneurysms than in those with non-VA aneurysms (45 vs. 22 %, p = 0.01). However, there was no significant difference in the frequency of ECG abnormalities. Multivariate regression analysis showed that VA aneurysms (OR, 3.317; 95 % CI, 1.129-9.745), poor-grade SAH (OR, 2.733; 95 % CI, 1.320-5.658) and concomitant hydrocephalus (OR, 3.658; 95 % CI, 1.690-7.917) correlated with WMA. There were no significant intergroup differences in plasma catecholamine levels. CONCLUSION: VA aneurysms are close to several medullary nuclei that integrate autonomic inputs. A transient deformation and ischemia of the medulla oblongata caused by the mechanical stress related to the rupture of a VA aneurysm and/or a concomitant hydrocephalus may be responsible for the disproportionately high frequency of WMA.

Lateral medullary infarction with ipsilateral hemiparesis, lemniscal sensation loss and hypoglossal nerve palsy.

Here, we present a rare case of a lateral medullary infarction with ipsilateral hemiparesis, lemniscal sensation loss and hypoglossal nerve palsy. In this case, we proved Opalski's hypothesis by diffusion tensor tractography that ipsilateral hemiparesis in a medullary infarction is due to the involvement of the decussated corticospinal tract. We found that the clinical triad of ipsilateral hemiparesis, lemniscal sensation loss and hypoglossal nerve palsy, which had been regarded as a variant of medial medullary syndrome, turned out to be caused by lateral lower medullary infarction. Therefore, this clinical triad does not imply the involvement of the anteromedial part of medulla oblongata, when it is hard to distinguish a massive lateral medullary infarction from a hemimedullary infarction merely from MR images. At last, we suggest that hyperreflexia and Babinski's sign may not be indispensable to the diagnosis of Opalski's syndrome and we propose that "hemimedullary infarction with ipsilateral hemiparesis" is intrinsically a variant of lateral medullary infarction.