Assessing bradykinesia in Parkinson's disease using gyroscope signals.

Parkinson's disease (PD) is a neurodegenerative brain disorder that slowly brings on the dopaminergic neurons death. The depletion of the dopaminergic signal causes the onset of motor symptoms such as tremor, bradykinesia and rigidity. Usually, neurologists regularly monitor motor symptoms and motor fluctuations using the MDS-UPDRS part III clinical scale. Nevertheless, to have a more objective and quantitative evaluation, it is possible to assess the cardinal motor symptoms of PD using wearable sensors and portable robotic devices. Unfortunately while there are several research papers on the use of these devices on PD patients, their use is not so common in clinical practice. In this work we recorded specific MDS-UPDRS motor tasks using magneto-inertial devices, worn by seven PD subjects and seven age-matched controls, in order to deeply analyze the kinematic and dynamic characteristics of goal-directed movements of upper limb, in addition to extract quantitative indices (peak velocity, smoothness, etc) useful for the assessment of motor symptoms. Using only gyroscope signals we looked at those parameters useful to assess bradykinesia. We observed parameters changes from OFF to ON phase congruent with the MDS-UPDRS changes, especially in the frequency domain. Our results suggest the prono-supination task is the more consistent to describe the bradykinesia symptom with the gyroscopes. Probably because of the amplitude of the movement performed. Moreover the peak power looks appropriate for bradykinesia symptom evaluation. We can conclude that, similar to the studies in which tremor symptom is evaluated, it is possible to monitor the bradykinesia using few wearable sensors and few simple parameters.

Cellular origin of fundus autofluorescence in patients and mice with a defective NR2E3 gene.

AIM: To characterise new clinical features in a family with enhanced S-cone syndrome (ESCS) and investigate the pathogenesis of these clinical features in the homozygous Nr2e3(rd7) (rd7) mutant mice. METHODS: Four patients from an affected family were included for genotypic and phenotypic study. Eye tissues from rd7 mice were used to detect a possible relationship between macrophages and autofluorescent material by immunohistochemistry (IHC) staining. RESULTS: Homozygous mutation in R311Q in NR2E3 was detected in this family. Colour photographs revealed that white dots do not correlate to hyperautofluorescent spots seen in autofluorescence imaging of the macula. OCT showed rosette-like lesions similar to those found in rd7 mice histology sections. From IHC analysis, we observed that F4/80 (a pan macrophage marker) and autofluorescence were colocalised to the same cells within the retina rosettes. CONCLUSIONS: The retinal structure of a young ESCS patient with homozygous R311Q mutation in the NR2E3 gene is similar to that seen in the rd7 mice. The macrophages were found to contain autofluorescent materials in the retinal rosettes of rd7 mice. These data are consistent with macrophage infiltration contributing to the hyperautofluorescent spots found in our patients.

Antiglaucomatous drugs effects on optic nerve head flow: design, baseline and preliminary report.

PURPOSE: To determine the effect of the most frequent used antiglaucomatous drugs on the optic nerve head flow. To see the response of the autoregulation system in hypertensive, preperimetric and advanced perimetric glaucomas. MATERIALS: In this preliminary report, optic nerve head parameters and retinal perfusion values were measured in 25 healthy controls as well as in 72 glaucomatous optic nerve heads. The glaucomatous sample was divided into three groups: 24 eyes treated with Betaxolol, 24 with Brinzolamide and 24 treated with Brimonidine (each of these groups was conformed by 8 hypertensive glaucomas, 8 preperimetric glaucomas, and 8 perimetric glaucomas). METHODS: Patients were examined with scanning laser Doppler flowmetry (wave length 638 nm), and flow, volume and velocity indices were assessed in each report. Perfusion maps were analyzed with the new SLDF software, version 3.2 (automatic full field perfusion image analizer). Examinations were also performed with the Heidelberg Retina Tomograph (wave length 638 nm), using the new standard reference plane. Visual fields were performed with the Octopus 123 or 101 perimeters, programs Glx and G2, with 3 phases completed. Diurnal pressure curve with applanation tonometry and gonioscopy (for classification) were also performed. RESULTS: In this preliminary report, it was found that eyes in Hypertensive or preperimetric stages of glaucoma, seem to use their regulation systems in order to preserve their optic nerve head circulation, while advanced perimetric glaucomas seem not be able to preserve their optic nerve head flow. And that antiglaucomatous drugs were not able to increase optic nerve head flow neither. DISCUSSION: Optic nerve head blood supplies is regulated by an autoregulation system. This phenomenon may act in normals, hypertensive and preperimetric glaucomas, but it seems not be able to preserve blood flow in advanced glaucomas. Optic nerve head flow returns to normal values with treatment in glaucoma first stages, while it seems that it could not be restored in advanced glaucomas.