Brain and nerve = Shinkei kenkyū no shinpo
-
Neuromyelitis optica (NMO) is an inflammatory disease mainly affecting optic and spinal cords, and was originally described by Devic in 1894. There has been long controversy about whether NMO is a subtype of multiple sclerosis (MS) or a distinct disease. In Japan and other Asian countries, relapsing NMO has been called as optic-spinal form of MS (OSMS), but we reported in 2002 that OSMS was heterogeneous and it comprised both typical NMO and MS with optic spinal presentation. ⋯ Those results suggest that astrocytic damage associated with autoimmunity to AQP4 may be involved in the pathogenesis of NMO, which is distinct from MS, primarily demyelinating disease. After the long history of confusion, NMO became clearly discriminated disease from MS. In this review, we focus on the historical changes of the disease concept and new knowledge gained from the clinical or immunological analyses of NMO.
-
Review Case Reports
[Cognitive impairment in patients with idiopathic normal pressure hydrocephalus].
The major cognitive impairment in patients with idiopathic normal pressure hydrocephalus (iNPH) is frontal lobe symptoms, such as psychomotor slowing and impairment of attention, working memory, verbal fluency and executive function. Compared with Alzheimer's disease (AD), frontal lobe symptoms are disproportionately severe and the impairment of memory and orientation is disproportionately mild in patients with iNPH. Concerning memory impairment, recognition memory is relatively preserved compared with recall in iNPH. ⋯ However, in iNPH patients with impairment of memory and either of visuoconstructive or executive function, improvement of overall cognitive deficits after shunt surgery is less, suggesting that a higher degree of neural impairment may identify less reversible injury or that superimposed AD might limit the potential to show improvement. Neuroanatomical bases of cognitive impairment of iNPH are not well documented. However, damage of periventricular structures, such as corpus callosum, frontal subcortical and cortical areas, thalamus, basal ganglia and hippocampus, could be associated with cognitive impairment of iNPH.
-
The failure of axonal regeneration after central nervous system (CNS) injury is thought to be due in part to the expression of molecules inhibitory for axonal growth and/or the lack of neurotrophic factors. Antibody treatment to neutralize axon growth inhibitory activity, and delivery of neurotrophic factor have been attempted extensively to overcome inhibition and augment regeneration of spinal motor pathways. Local delivery of neurotrophins can counteract pathological events and induce a regenerative response after both acute and chronic spinal cord injury. ⋯ The locomotor function of the FGF-2-treated animals was substantially recovered up to extent where the joint of the hind limb moves 6 weeks after transection, but the recovery was not seen at all on the locomotor activity of the vehicle-treated animals. This regeneration might be facilitated by prominant cell growth of fibroblast-like cells markedly enhanced by FGF-2 around the lesion site, because the cells have properties advantageous for neurite outgrowth. FGF-2-induced cells may become a crucial and promising tool to attain successful axonal regeneration.
-
We reported the case of a 77-year-old female who presented with left hypoglossal paresis and dysarthria due to a small cortical infarction. She was admitted to our hospital because of the sudden onset of dysarthria. A neurological examination revealed deviation of the tongue to the left and paretic dysarthria without motor paralysis in the extremities. ⋯ Furthermore, in this patient, dysarthria in this case was more obvious than that of peripheral hypoglossal palsy. Recent electrophysiological has investigation indicates that the corticolingual tract plays a significant role in the presence of pure dysarthria in the stroke patients. This case indicate that cortical infarction in the primary motor cortex may produce isolated hypoglossal nerve paresis and dysarthria due to disruption of the corticolingual tract.