ABSTRACT
BACKGROUND AND PURPOSE: Few data are available regarding the influence of the timing of ischemic stroke management, such as daytime and nighttime hours, on the delay of mechanical thrombectomy, the effectiveness of revascularization, and clinical outcomes. We aimed to investigate whether admission during nighttime hours could impact the clinical outcome (mRS at 90 days) of patients with acute ischemic stroke treated by mechanical thrombectomy. MATERIALS AND METHODS: We retrospectively analyzed 169 patients (112 treated during daytime hours and 57 treated during nighttime hours) with acute ischemic stroke in the anterior cerebral circulation. The main outcome was the rate of patients achieving functional independence at 90 days (mRS ≤2), depending on admission time. RESULTS: In patients admitted during nighttime hours, the rate of mRS ≤ 2 at 90 days was significantly higher (51% versus 35%, P = .05) compared with those admitted in daytime hours. Patients in daytime and nighttime hours were comparable regarding admission and treatment characteristics. However, patients in nighttime hours tended to have a higher median NIHSS score at admission (P = .08) and to be younger (P = .08), especially among the mothership group (P = .09). The multivariate logistic regression analysis confirmed that patients in nighttime hours had better functional outcomes at 90 days than those in daytime hours (P = .018; 95% CI, 0.064-0.770; OR = 0.221). CONCLUSIONS: In a highly organized stroke care network, mechanical thrombectomy is quite effective in the nighttime hours among acute ischemic stroke presentations. Unexpectedly, we found that those patients achieved favorable clinical outcomes more frequently than those treated during daytime hours. Larger series are needed to confirm these results.
Subject(s)
Ischemic Stroke/surgery , Thrombectomy/methods , Aged , Aged, 80 and over , Female , Humans , Male , Middle Aged , Retrospective Studies , Time Factors , Treatment OutcomeABSTRACT
BACKGROUND AND PURPOSE: The purpose was to evaluate, in a consecutive series of patients with isolated acute retinal ischaemia, the proportion of patients with acute silent brain infarcts (SBIs) on diffusion-weighted imaging (DWI) and to assess risk of recurrence within 3 months. METHODS: In all, 103 consecutive patients with isolated acute retinal ischaemia (central retinal artery occlusion, branch retinal artery occlusion or transient monocular vision loss) were included between January 2015 and December 2016. They all had cerebral magnetic resonance imaging including DWI as well as a standardized aetiological workup and 3 months of follow-up. The presence of DWI-positive cerebral lesions was recorded. Main clinical and radiological characteristics between DWI-positive and DWI-negative patients were compared. RESULTS: Of the 103 patients (including 42 transient monocular vision loss), 20 (19.5%) had SBIs on DWI, which were ipsilateral to the acute retinal ischaemia in 30% and involved different and/or multiple vascular territories in 70% of cases. Ipsilateral carotid stenosis and occlusion were respectively identified in 17 and eight patients whereas cardioaortic embolism was found in 19 patients. Overall, patients with and without acute SBIs were comparable. The topography of SBIs was related to the aetiology of the acute retinal ischaemia. At 3 months of follow-up, one patient suffered from ischaemic stroke and five had recurrent retinal ischaemia. CONCLUSIONS: Irrespective of the baseline characteristics of the patients, SBIs are present in about 20% of patients with isolated acute retinal ischaemia and may be of interest in the aetiological workup. Overall risk of recurrence is low, favoured by rapid aetiological workup and appropriate treatment.
Subject(s)
Brain Ischemia , Stroke , Brain Infarction , Brain Ischemia/complications , Brain Ischemia/diagnostic imaging , Brain Ischemia/epidemiology , Diffusion Magnetic Resonance Imaging , Humans , Ischemia , Prevalence , Retrospective StudiesABSTRACT
The dynamic connectome perspective states that brain functions arise from the functional integration of distributed and/or partly overlapping networks. Diffuse low-grade gliomas (DLGG) have a slow infiltrating character. Here we addressed whether and how anatomical disconnection following DLGG growth and resection might interfere with functional resting-state connectivity, specifically in relation to picture naming. Thirty-nine native French persons with a left DLGG were included. All underwent awake surgical resection of the tumor using direct brain electrostimulation to preserve critical eloquent regions. The anatomical disconnectivity risk following the DLGG volume and the resection, and the functional connectivity of resting-state fMRI images in relation to picture naming were evaluated prior to and three months after surgery. Resting-state connectivity patterns were compared with nineteen healthy controls. It was demonstrated that picture naming was strongly dependent on the semantic network that emerged from the integration and interaction of regions within multiple resting-state brain networks, in which their specific role could be explained in the light of the broader resting-state network they take part in. It emphasized the importance of a whole brain approach with specific clinical data input, during resting-state analysis in case of lesion. Adaptive plasticity was found in secondary regions, functionally connected to regions close to the tumor and/or cavity, marked by an increased connectivity of the right and left inferior parietal lobule with the left inferior temporal gyrus. In addition, an important role was identified for the superior parietal lobe, connected with the frontal operculum, suggesting functional compensation by means of attentional resources in order to name a picture via recruitment of the frontoparietal attention network.
Subject(s)
Brain Neoplasms , Cerebral Cortex/physiopathology , Connectome , Glioma , Nerve Net/physiopathology , Neuronal Plasticity/physiology , Pattern Recognition, Visual/physiology , Adult , Brain Neoplasms/diagnostic imaging , Brain Neoplasms/pathology , Brain Neoplasms/surgery , Cerebral Cortex/diagnostic imaging , Female , Glioma/diagnostic imaging , Glioma/pathology , Glioma/surgery , Humans , Male , Middle Aged , Nerve Net/diagnostic imaging , Neurosurgical ProceduresABSTRACT
In rhythmical movement performance, our brain has to sustain movement while correcting for biological noise-induced variability. Here, we explored the functional anatomy of brain networks during voluntary rhythmical elbow flexion/extension using kinematic movement regressors in fMRI analysis to verify the interest of method to address motor control in a neurological population. We found the expected systematic activation of the primary sensorimotor network that is suggested to generate the rhythmical movement. By adding the kinematic regressors to the model, we demonstrated the potential involvement of cerebellar-frontal circuits as a function of the irregularity of the variability of the movement and the primary sensory cortex in relation to the trajectory length during task execution. We suggested that different functional brain networks were related to two different aspects of rhythmical performance: rhythmicity and error control. Concerning the latter, the partitioning between more automatic control involving cerebellar-frontal circuits versus less automatic control involving the sensory cortex seemed thereby crucial for optimal performance. Our results highlight the potential of using co-registered fine-grained kinematics and fMRI measures to interpret functional MRI activations and to potentially unmask the organisation of neural correlates during motor control.
Subject(s)
Brain Mapping/methods , Cerebellum/physiology , Executive Function/physiology , Frontal Lobe/physiology , Motor Activity/physiology , Nerve Net/physiology , Somatosensory Cortex/physiology , Upper Extremity/physiology , Adult , Biomechanical Phenomena , Cerebellum/diagnostic imaging , Female , Frontal Lobe/diagnostic imaging , Humans , Magnetic Resonance Imaging , Male , Middle Aged , Nerve Net/diagnostic imaging , Time FactorsABSTRACT
BACKGROUND AND PURPOSE: The differential diagnosis of acute cervical pain includes nonvascular and vascular causes such as carotid dissection, carotid occlusion, or vasculitis. However, some patients present with unclassified vascular and perivascular changes on imaging previously reported as carotidynia. The aim of our study was to improve the description of this as yet unclassified clinico-radiologic entity. MATERIALS AND METHODS: From January 2009 through April 2016, 47 patients from 10 centers presenting with acute neck pain or tenderness and at least 1 cervical image showing unclassified carotid abnormalities were included. We conducted a systematic, retrospective study of their medical charts and diagnostic and follow-up imaging. Two neuroradiologists independently analyzed the blinded image datasets. RESULTS: The median patient age was 48 years. All patients presented with acute neck pain, and 8 presented with transient neurologic symptoms. Imaging showed an eccentric pericarotidian infiltration in all patients. An intimal soft plaque was noted in 16 patients, and a mild luminal narrowing was noted in 16 patients. Interreader reproducibility was excellent. All patients had complete pain resolution within a median of 13 days. At 3-month follow-up, imaging showed complete disappearance of vascular abnormalities in 8 patients, and a marked decrease in all others. CONCLUSIONS: Our study improved the description of an unclassified, clinico-radiologic entity, which could be described by the proposed acronym: TransIent Perivascular Inflammation of the Carotid artery (TIPIC) syndrome.
Subject(s)
Carotid Artery Diseases/diagnostic imaging , Vasculitis, Central Nervous System/diagnostic imaging , Adult , Carotid Artery Diseases/diagnosis , Cerebral Angiography , Diagnosis, Differential , Female , Follow-Up Studies , Humans , Magnetic Resonance Angiography , Male , Middle Aged , Neck Pain/diagnostic imaging , Neck Pain/etiology , Nervous System Diseases/diagnostic imaging , Nervous System Diseases/etiology , Observer Variation , Retrospective Studies , Syndrome , Tomography, X-Ray Computed , Vasculitis, Central Nervous System/diagnosisABSTRACT
BACKGROUND AND PURPOSE: Patients with vascular parkinsonism have higher cognitive decline and more basal ganglia lesions. We aimed to evaluate the relationship of cognitive impairment with functional connectivity between the basal ganglia and cingulate cortex in vascular parkinsonism. MATERIALS AND METHODS: Thirty patients (8 with vascular parkinsonism and 22 with Parkinson disease) and 23 controls were enrolled. The Mattis Dementia Rating Scale and the Stroop Task were used to assess cognitive decline. MR imaging examinations included T1-MPRAGE, FLAIR, and resting-state fMRI sequences. MPRAGE was segmented to obtain basal ganglia and cingulate cortex volumes. FLAIR was segmented to obtain white matter hyperintensity lesion volume. Resting-state fMRI sequences were used to compare basal ganglia functional connectivity with the cingulate cortex between patients and controls. RESULTS: Patients with vascular parkinsonism exhibited impaired attention, resistance to interference, and inhibitory control and an increased number of errors on the Stroop Task. They also had higher caudate nucleus and white matter hyperintensity lesion volumes, which were positively correlated (ρ = 0.75, P < .0001). Caudate nucleus functional connectivity with the perigenual anterior cingulate cortex was increased in patients with vascular parkinsonism compared with controls and patients with Parkinson disease, and it was positively correlated with the caudate nucleus volume (ρ = 0.44, P = .016). Caudate nucleus functional connectivity with the posterior cingulate cortex was decreased in patients with vascular parkinsonism compared with controls and negatively correlated with the number of errors on the Stroop test (ρ = -0.51, P = .0003). CONCLUSIONS: In patients with vascular parkinsonism, cognitive decline could be related to changes of caudate nucleus functional connectivity with the cingulate cortex at resting-state, which may be induced by ischemia-related remodelling.
Subject(s)
Basal Ganglia/physiopathology , Brain/physiopathology , Cognitive Dysfunction/physiopathology , Neural Pathways/physiopathology , Parkinson Disease, Secondary/physiopathology , Basal Ganglia/pathology , Brain/pathology , Cognitive Dysfunction/etiology , Female , Humans , Magnetic Resonance Imaging/methods , Male , Middle Aged , Neural Pathways/pathology , Parkinson Disease, Secondary/complications , Parkinson Disease, Secondary/pathologySubject(s)
Brain Neoplasms/diagnostic imaging , Brain Neoplasms/pathology , Hemangioma, Cavernous, Central Nervous System/diagnostic imaging , Hemangioma, Cavernous, Central Nervous System/pathology , Magnetic Resonance Imaging , Adult , Brain/diagnostic imaging , Brain/pathology , Brain Neoplasms/secondary , Breast Neoplasms/pathology , Diagnosis, Differential , Female , Humans , Middle Aged , Young AdultABSTRACT
BACKGROUND AND PURPOSE: Multiple sclerosis (MS) patients can present with atypical cavitary lesions mimicking vanishing white matter disease (VWMD). Our objective was to identify brain magnetic resonance imaging (MRI) findings that differentiate these two disorders. METHODS: A cross-sectional study was performed including 14 patients with MS with cavitary lesions and 14 patients with VWMD. Two neuroradiologists retrospectively reviewed the MRI including at least T1-, T2- and fluid-attenuated inversion recovery weighted images. RESULTS: The main differences included ovoid lesions perpendicular to the lateral ventricle, punctate isolated juxtacortical lesions (both 100% in MS versus 0% in VWMD) and symmetrical infratentorial hyperintensities (0% in MS versus 50% in VWMD). Other statistically significant differences included midbrain (79% in MS versus 29% in VWMD) and thalamus lesions (71% vs. 7%) as well as extensive external capsule involvement (29% vs. 86%) and extensive corpus callosum lesions (64% vs. 100%). Cavitary lesions usually had periventricular predominance in MS (36% vs. 0%) whereas they were more frequently anterior in VWMD (0% in MS versus 57% in VWMD). CONCLUSION: Despite many similar MRI findings, our results suggest that a careful analysis of the morphology and the location of the lesions is helpful to differentiate these distinct disorders.
Subject(s)
Corpus Callosum/diagnostic imaging , Leukoencephalopathies/diagnostic imaging , Magnetic Resonance Imaging/methods , Multiple Sclerosis/diagnostic imaging , Adult , Corpus Callosum/pathology , Cross-Sectional Studies , Diagnosis, Differential , Female , Humans , Leukoencephalopathies/pathology , Male , Middle Aged , Multiple Sclerosis/pathology , Retrospective Studies , Young AdultABSTRACT
BACKGROUND: Progressive multifocal leukoencephalopathy (PML) is an opportunistic demyelinating encephalopathy related to JC virus. Its characteristics on conventional brain MRI are well known and are important for the diagnosis. OBJECTIVE: To analyze SWI hypointensities recently described in U-fibers and cortex adjacent to the white matter lesions of PML. METHODS: Prospective study including four patients with an history of definite diagnosis of PML. Clinical data were collected retrospectively. Brain MRI exams were done on a 3T magnet, including FLAIR, T2 GRE sequences and SWI. RESULTS: Four males were included (mean age: 47 years, mean PML duration: 24.2 months). Immunosuppression was related to AIDS (n=2), natalizumab for multiple sclerosis (n=1), B-cell lymphoma treated by chemotherapeutic agents and rituximab (n=1). All patients had SWI hypointensities in cortex and/or U-fibers adjacent to the white matter lesions. QSM always suggested a paramagnetic effect. CONCLUSION: SWI and T2 GRE hypointensities in cortex and U-fibers adjacent to the white matter lesions seem highly prevalent in PML, irrespective of the delay between PML onset and the MRI. QSM data suggest a paramagnetic effect.
Subject(s)
Brain/diagnostic imaging , Brain/pathology , Leukoencephalopathy, Progressive Multifocal/diagnostic imaging , Leukoencephalopathy, Progressive Multifocal/pathology , Magnetic Resonance Imaging/methods , Humans , Image Processing, Computer-Assisted , Male , Middle Aged , Prospective Studies , Signal Processing, Computer-AssistedSubject(s)
Headache/diagnostic imaging , Hypoglossal Nerve Diseases/diagnostic imaging , Leiomyosarcoma/diagnostic imaging , Neuralgia/diagnostic imaging , Occipital Bone/diagnostic imaging , Skull Base Neoplasms/diagnostic imaging , Aged , Female , Headache/etiology , Humans , Hypoglossal Nerve Diseases/etiology , Leiomyosarcoma/complications , Leiomyosarcoma/secondary , Neuralgia/etiology , Occipital Bone/pathology , Skull Base Neoplasms/complications , Skull Base Neoplasms/secondary , SyndromeABSTRACT
Complications of subarachnoid hemorrhage are the major life threatening and functional components of the follow up of a ruptured aneurysm. Knowing how to identify these is a key challenge. They vary in type throughout the postoperative follow up period. The aim of this article is firstly to list the main complications of the acute phase (rebleeding, acute hydrocephalus, acute ischemic injury and non-neurological complications), the subacute phase (vasospasm) and the chronic phase of subarachnoid hemorrhages: (chronic hydrocephalus and cognitive disorders) and to describe their major clinical and radiological features. Secondly, we describe the long-term follow up strategy for patients who have suffered a subarachnoid hemorrhage and have been treated endovascularly or by surgery. This follow up involves a combination of clinical consultations, cerebral MRI and at least one review angiogram.
Subject(s)
Subarachnoid Hemorrhage/complications , Aneurysm, Ruptured/complications , Aneurysm, Ruptured/diagnosis , Aneurysm, Ruptured/therapy , Brain Damage, Chronic/diagnosis , Brain Damage, Chronic/etiology , Brain Damage, Chronic/therapy , Brain Ischemia/diagnosis , Brain Ischemia/etiology , Brain Ischemia/therapy , Cerebral Angiography , Cognition Disorders/diagnosis , Cognition Disorders/etiology , Cognition Disorders/therapy , Embolization, Therapeutic , Follow-Up Studies , Humans , Hydrocephalus/diagnosis , Hydrocephalus/etiology , Hydrocephalus/therapy , Image Processing, Computer-Assisted , Magnetic Resonance Imaging , Recurrence , Subarachnoid Hemorrhage/diagnosis , Subarachnoid Hemorrhage/therapy , Surgical Instruments , Tomography, X-Ray Computed , Vasospasm, Intracranial/diagnosis , Vasospasm, Intracranial/etiology , Vasospasm, Intracranial/therapyABSTRACT
Etiologic diagnosis of adulthood leukodystrophy is challenging in neurologic practice. We describe here the clinico-radiological features of a novel autosomal dominant leukodystrophy in a single family. Clinical and MRI features were recorded in a three generation family. Exome sequencing was performed in two affected relatives and one healthy member. Four total relatives (3 women and 1 man, mean age at onset: 45, range 32-59) were followed: 2 for migraine and 2 for cognitive loss. MRI features were homogeneous in the four affected relatives: extensive and symmetrical white matter hyperintensities on T2-weighted images, with a posterior predominance, involvement of the middle cerebellar peduncles, corpus callosum and the posterior limb of the internal capsules. An extensive metabolic screening was negative. In addition, sequencing of pathogenic genes involved in dominant leukodystrophies (NOTCH3, LMNB1, GFAP, CSF1R) was negative. No mutation has been identified yet with exome sequencing. This report is peculiar because of dominant inheritance, adult onset, highly homogeneous white matter hyperintensities on T2-weighted MR images, predominant in the middle cerebellar peduncles and posterior part of internal capsule and absence of mutation of the genes involved in dominant leukodystrophies.
Subject(s)
Brain/pathology , Leukoencephalopathies/diagnosis , Magnetic Resonance Imaging , Adult , Exome , Family Health , Female , Genetic Testing , Glial Fibrillary Acidic Protein/genetics , Humans , Lamin Type B/genetics , Leukoencephalopathies/cerebrospinal fluid , Leukoencephalopathies/genetics , Male , Middle Aged , Mutation , Receptor, Notch3 , Receptors, Notch/geneticsABSTRACT
Any dysfunction in olfaction requires a radiological exploration comprising the nasal cavity, the anterior base of the skull, in particular the frontal and temporal lobes. MRI is the reference examination, due to the frontal plane and the T1, T2 volume maps. In the child, aplasia of the olfactory bulbs falls within a polymalformation (CHARGE) or endocrine (Kallman) context. In the adult, rhino sinus disease and meningiomas are the most common etiologies. Frontal or temporal impairment: tumoral or vascular and neurodegenerative disorders (Parkinson's disease) may accompany a loss of olfaction.
Subject(s)
Cranial Nerve Neoplasms/diagnosis , Image Enhancement/methods , Image Interpretation, Computer-Assisted/methods , Magnetic Resonance Imaging/methods , Olfaction Disorders/diagnosis , Olfactory Nerve Diseases/diagnosis , Olfactory Nerve/pathology , Adult , CHARGE Syndrome/diagnosis , CHARGE Syndrome/pathology , Child , Cranial Nerve Neoplasms/pathology , Diagnosis, Differential , Frontal Lobe/pathology , Humans , Kallmann Syndrome/diagnosis , Kallmann Syndrome/pathology , Olfaction Disorders/pathology , Olfactory Bulb/abnormalities , Olfactory Bulb/pathology , Olfactory Nerve Diseases/pathology , Parkinson Disease/diagnosis , Parkinson Disease/pathology , Temporal Lobe/pathologyABSTRACT
The exploration of the chiasmal and retrochiasmal visual pathways is based on magnetic resonance imaging. A bitemporal hemianopsis suggests a lesion of the optic chiasm while homonymous lateral hemianopsis should lead to a search for a lesion of the retrochiasmal visual pathways. The causes of chiasmal impairment are mainly tumoral. The exploration protocol is based on MRI with T1-weighted sagittal sections, then T2- and T1-weighted coronal sections with and without injection. In case of a retrochiasmal syndrome, the MRI exploration protocol is a function of the type of occurrence of the deficiency and the context.
Subject(s)
Image Enhancement/methods , Image Interpretation, Computer-Assisted/methods , Imaging, Three-Dimensional/methods , Magnetic Resonance Imaging/methods , Optic Chiasm/pathology , Optic Nerve Diseases/diagnosis , Optic Nerve Neoplasms/diagnosis , Visual Pathways/pathology , Diagnosis, Differential , Dominance, Cerebral/physiology , Hemianopsia/diagnosis , Hemianopsia/etiology , Hemianopsia/pathology , Humans , Optic Chiasm/surgery , Optic Nerve Diseases/pathology , Optic Nerve Diseases/surgery , Optic Nerve Neoplasms/pathology , Optic Nerve Neoplasms/surgery , Visual Field Tests , Visual Fields/physiology , Visual Pathways/surgeryABSTRACT
Damage to the optic nerve (ON) is characterised by a reduction in visual acuity. Pre-chiasmatic lesions to the optic nerve may be of traumatic, congenital, tumoral (meningioma, glioma), inflammatory or vascular origins. In all cases, MRI is the choice means of exploration, carried out with axial and coronal sections with a thickness of 2.5-3mm and T1 and T2-weighted spin echo sequences. The coronal sections may be carried out with fat signal saturation for an elective study of the size of the retrobulbar portion of the ON.
Subject(s)
Image Enhancement/methods , Image Interpretation, Computer-Assisted/methods , Magnetic Resonance Imaging/methods , Optic Chiasm/pathology , Optic Nerve Diseases/diagnosis , Optic Nerve Neoplasms/diagnosis , Optic Nerve/pathology , Diagnosis, Differential , Guideline Adherence , Humans , Optic Nerve Diseases/pathology , Optic Nerve Injuries/diagnosis , Optic Nerve Injuries/pathology , Optic Nerve Neoplasms/pathology , Sensitivity and Specificity , Visual Acuity/physiologyABSTRACT
INTRODUCTION: Clinical presentation and etiology of localized nontraumatic convexal subarachnoid hemorrhage (cSAH) have been described in a few patients. They differ from those of aneurysmal subarachnoid bleeding which is diffuse. The purpose of this study was to describe the clinical presentation, the radiologic findings and causes of cSAH. METHODS: We selected patients admitted to the neurology department of CHU of Nîmes or Montpellier, from May 2008 to May 2011, who presented with cSAH, observed in a single cortical sulcus unrelated to trauma and identified on brain MRI T2* weighted images as a hyposignal in one sulcus of the convexity. Data collection was retrospective. RESULTS: Twenty-three patients (14 men and nine women) were included. Mean age was 69.5years (range 29-86). Patients had mostly sensory or sensorimotor deficits which was regressive in less than 30minutes, recurrent, and seldom accompanied by headache. Brain MRI allowed the identification of patients with old brain hematomas (n=2), lobar microbleeds (n=7) and superficial cortical hemosiderosis (n=6). The etiologic diagnosis was determined in 43% (n=10/23): cerebral amyloid angiopathy (n=3), reversible cerebral vasoconstriction syndrome (n=2), primary cerebral angiitis (n=1), posterior reversible encephalopathy syndrome (n=1), cortical vein thrombosis (n=3, two of them associated with dural sinus thrombosis). Cerebral angiography was performed in 11 patients and gave the etiologic diagnosis (angiitis, cortical vein thrombosis) in two. Follow-up was available for 16 patients (mean 12months, range 3months to 5years). Etiology was established during follow-up in two patients, both had cerebral amyloid angiopathy diagnosed after recurrent lobar hematomas. CONCLUSIONS: cSAH has various causes, but clinical presentations appear to be relatively stereotyped with recurrent and brief episodes of sensorimotor deficits. A comprehensive assessment and monitoring would lead to an etiologic diagnosis in some patients.