Ectopic expression of α-synuclein affects the migration of neural stem cells in mouse subventricular zone.

α-Synuclein (α-syn) is a key protein in Parkinson's disease (PD), and its abnormal accumulation is implicated only not in the loss of dopaminergic neurons in the substantia nigra but also in impairment of olfactory bulb (OB) in PD. Olfactory dysfunction could arise from these OB changes as an early symptom in PD. We reported previously the impairment of neuronal stem cell (NSC) proliferation in the subventricular zone, which is upstream of OB in PD models. Reduction of NSC generation could potentially lead to olfactory dysfunction, which is commonly associated with and precedes the motor symptoms by several years in PD. Here, we investigated neurosphere formation in vitro and migration of NSCs in vivo after transduction of α-syn-encoding retroviral vector to characterize the function of α-syn in NSC. Over-expression of α-syn caused less effective formation of neurospheres and induced morphological changes. Fluorescence-activated cell sorting showed diminished NSC cell cycle progression induced by over-expression of α-syn. Intriguingly, suppression of NSC migration along the rostral migratory stream was observed when the α-syn-encoding vector was directly injected into the subventricular zone of mice in vivo. These results indicate that α-syn affects the generation of NSC and suggest that this protein could serve as a tool for the design of potentially useful therapy for PD patients.

Segmental zoster paresis of limbs: report of three cases and review of literature.

OBJECTIVES: Segmental zoster paresis is a relatively rare complication characterized by focal motor weakness, which may occur in limbs affected by herpes zoster. We demonstrate the clinical characteristics of segmental zoster paresis by reviewing the cases of 138 patients, including 3 of our patients. CASE REPORT AND REVIEW SUMMARY: We report 3 patients with zoster paresis of the limbs. Patients 1 and 3 showed motor weakness in the left shoulder and arm after developing a herpetic rash in the left C5-C6 dermatomes. Patient 2 showed weakness in the right thigh and groin after a right L2-L3 herpetic eruption. The electromyograms of all 3 patients showed abnormal spontaneous activity in the affected muscles. Intravenous acyclovir and corticosteroid pulse therapy were added to oral antiviral drugs for patients 1 and 2. All 3 patients recovered favorably. Our review of the literature revealed that antiviral treatment may prevent the occurrence of zoster paresis; however, there is insufficient evidence to show what treatment hastens recovery from zoster paresis. CONCLUSIONS: Segmental zoster paresis is still underrecognized by neurologists. Awareness of this disorder is important because it may eliminate unnecessary invasive investigations and lead to appropriate treatment. Further studies on the treatment are necessary.

Isolated proximal leg paresis due to a small cortical infarction.

We describe two patients with small cortical infarcts, who presented with isolated proximal weakness in one of their legs. These lesions were located in the contralateral precentral gyrus, more medial than the precentral knob, but more lateral than the topmost part of the motor cortex. These clinical findings are consistent with the physiological findings of Penfield and Boldrey, and those of recent activation studies by functional MRI. It is clinically important to pay close attention to the contralateral top of the motor cortex when examining pure motor monoparesis of a proximal part of a lower extremity.

Isolated reversible splenial lesion in adult meningitis: a case report and review of the literature.

We report the rare case of a 38-year-old man who suffered from aseptic meningitis. Brain magnetic resonance imaging showed an ovoid lesion with a high signal intensity on T2- and diffusion-weighted images in the splenium of the corpus callosum that completely disappeared within a week. There were no symptoms or signs associated with the lesion, and the prognosis was good. Although rare in adult patients, awareness of a reversible splenial lesion in meningoencephalitis is important.

Correlation between levels of pigment epithelium-derived factor and vascular endothelial growth factor in the striatum of patients with Parkinson's disease.

Parkinson's disease (PD) is caused by progressive degeneration of nigrostriatal dopaminergic neurons and can potentially be treated by intrastriatal delivery of neurotrophic factors. Pigment epithelium-derived factor (PEDF), which exhibits protective effects on various neuronal populations, is up-/down-regulated in the cerebrospinal fluid in some neurodegenerative conditions. Here we investigated the level of PEDF protein in the striatum and immunoreactivity for PEDF in the substantia nigra (SN) of patients with PD to assess its role in the pathophysiology of PD. We also studied changes in PEDF expression in the striatum of the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of PD. We found a transient and rapid up-regulation of PEDF transcripts and a marked increase in immunoreactivity for PEDF protein in response to MPTP administration in mice. However, there were no significant changes in striatal levels of PEDF and immunoreactivity for PEDF in the SN of PD patients compared with age-matched non-PD patients. Intriguingly, the striatal levels of PEDF and vascular endothelial growth factor (VEGF), which has opposite functions to PEDF in terms of angiogenesis and vascular permeability, correlated positively in PD patients. Our results suggest up-regulation of PEDF in response to acute insult to the dopaminergic pathway, but such response might be disturbed in patients with advanced PD. The correlation between PEDF and VEGF striatal levels in PD patients suggests that concerted neurotrophic functions of these factors or structural changes in blood vessel walls play an important role in the pathophysiology of PD.