It suggests the widespread disruption of white matter integrity and prevalent brain degeneration of frontal lobes according to a depressive symptom in narcolepsy.īrain diffusion tensor imaging frontal lobe hypersomnia mood disorder. This tract-based spatial statistics study demonstrated that drug-naïve patients with narcolepsy had reduced fractional anisotropy of white matter in multiple brain areas and significant relationship between increased mean diffusivity of white matter in frontal/cingulate and depression. Among patients, mean diffusivity values of white matter in the bilateral superior frontal gyri, bilateral fronto-orbital gyri and right superior parietal gyrus were positively correlated with depressive mood. Patients and controls showed no differences in mean diffusivity. Compared with controls, patients showed significant decreases in fractional anisotropy of white matter of the bilateral anterior cingulate, fronto-orbital area, frontal lobe, anterior limb of the internal capsule and corpus callosum, as well as the left anterior and medial thalamus. Fractional anisotropy and mean diffusivity images were obtained from whole-brain diffusion tensor imaging, and tract-based spatial statistics were used to localize white matter abnormalities. To investigate brain white matter alterations in drug-naïve narcolepsy patients with cataplexy and to explore relationships between white matter changes and patient clinical characteristics, drug-naïve narcolepsy patients with cataplexy (n = 22) and healthy age- and gender-matched controls (n = 26) were studied. It also raised the necessity to evaluate white matter changes. Those distinct morphometric changes account for problems in wake-sleep control, attention and memory. Cardiovascular changes can occur in association with narcolepsy/cataplexy and should be considered when dealing with patients presenting with these specific clinical signs.ĬSF (cerebrospinal fluid) MUO (meningoencephalitis of unknown origin) REM (rapid eye movement).Functional imaging studies and voxel-based morphometry analysis of brain magnetic resonance imaging showed abnormalities in the hypothalamus-thalamus-orbitofrontal pathway, demonstrating altered hypocretin pathway in narcolepsy. Functional neuroimaging studies have described changes in brain perfusion or glucose metabolism during resting wakefulness, as well as brain. Diffusion tensor imaging (DTI) can identify the microstructural changes in neurons, as indicated by the values obtained for fractional anisotropy (FA) and apparent diffusion. Anatomical data with magnetic resonance imaging have characterized specific alterations in grey and white matter and their potential implications on disease severity. To the best of our knowledge, brain morphological and microstructural differences have never been studied in patients having narcolepsy with and without cataplexy. Although very rare, symptomatic narcolepsy/cataplexy can occur in dogs and can be secondary to brainstem encephalitis. Various brain imaging techniques have been used to study narcolepsy with cataplexy. Repeated MRI revealed marked reduction in the lesion size cerebrospinal fluid analysis revealed no abnormalities. (1) reported magnetic resonance imaging (MRI) abnormalities in the pontine tegmentum of. No relapse occurred over a 32 mo follow-up period from the diagnosis. The neuropathology of narcolepsy is unknown.
Narcolepsy-cataplexy episodes could initially still be triggered by offering food however, they gradually became shorter and less frequent until they completely subsided along with all other clinical signs after 3 wk. The dog was started on immunosuppressive treatment with prednisolone and cytosine arabinoside, which was subsequently switched to cyclosporine.
MRI of the brain and cerebrospinal fluid analysis were compatible with meningoencephalitis of unknown origin affecting the mesencephalon, pons and rostral medulla oblongata. ObjectiveTo investigate brain changes in both basal and cataplectic conditions in awake patients with narcolepsycataplexy.BackgroundRecent insights in. Hematology, serum biochemistry, and thoracic and abdominal imaging were unremarkable.
There was no evidence of arrhythmia on electrocardiography during the episode. A narcolepsy-cataplexy episode with associated hypertension and bradycardia was triggered during examination. A 4 yr old, intact female cocker spaniel was presented for investigation of acute, progressive lethargy/hypersomnia vestibular signs and cataplexy. The authors found significant hypermetabolism in narcolepsy-cataplexy in fully awake condition in the limbic cortex specifically in the anterior and mid. To our knowledge narcolepsy with cataplexy with such severe symptoms and late age of onset has not been previously reported.
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