ABSTRACT
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/pathologyABSTRACT
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 AdultSubject(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
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
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
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.
