Lack of maintenance of gait pattern as measured by instrumental methods suggests psychogenic gait.

Fluctuation is a common feature of all psychogenic gait disorder (PGD) patterns. Whether this fluctuation involves only the degree of impairment or whether it affects the gait pattern itself remains an interesting question. We hypothesize that, on repeated measurements, both normal and abnormal gait may present quantitative differences while maintaining their basic underlying pattern; conversely, in psychogenic gait, the basic pattern appears not to be preserved. Using an optoelectronic system, data acquired from 19 normal subjects and 66 patients were applied to train a neural network (NN) and subsequently classify gait patterns into four different groups (normal, ataxic, spastic-paraparetic and parkinsonian). Five patients who fulfilled clinical criteria for psychogenic gait and six controls were then prospectively evaluated on two separate occasions, three months apart. Normal controls and ataxic, parkinsonian or spastic patients were correctly identified by the NN, and categorized within the corresponding groups at baseline as well as at a three-month follow-up evaluation. NN analysis showed that after three months, no PGD patient preserved the gait pattern detected at baseline, even though this finding was not clinically apparent. Modification of gait pattern detected by repeated kinematic measurement and NN analysis could suggest the presence of PGD, particularly in difficult-to-diagnose cases.

Kinematic study of whole body center of mass position during gait in Parkinson's disease patients with and without festination.

Gait festination (FE) can cause serious disability in Parkinson's disease (PD) patients. It is argued that the center of pressure position (COP) and body center of mass (COM) are possibly implicated in FE pathogenesis. The relationship between them remains unclear. The goal of this study was to determine spatiotemporal relationships between COM and COP in PD and to explore whether FE arises as a consequence of lack of physiological link between COP and COM during step stride. Twenty patients with idiopathic PD, in OFF state and 17-age-matched control subjects completed a 10-m walking protocol. PD patients were divided in two groups: those with FE and those without (NF). COM position, excursion, and its relationship with COP, as well as other kinematic parameters were analyzed. COM displacement along the horizontal and vertical plane was significantly lower in FE patients as was the maximum position on the movement direction axis compared with controls or NF patients. Significant difference in minimal COM position in FE patients was also observed. The percentage of stride time during which COM was situated ahead of COP along the movement axis in FE patients was significantly greater than for controls or NF patients. This would seem to indicate that FE patients are constantly attempting to align COP to COM, causing FE. The explanation might be that FE arises as a postural strategy to align COP within the area of COM displacement. Findings illustrate a putative role for postural strategies in the treatment of FE.

Use of a stenopeic semiocclusor enhances vep diagnosis.

PURPOSE: We conducted a study to assess the capability of a 2-mm stenopeic semiocclusor in improving the sensitivity of the standard full-field pattern-visual evoked potential technique to disclose abnormalities of the pre-chiasmatic visual pathway. METHODS: Nineteen control subjects and fifty-five patients with a diagnosis of definite or probable Multiple Sclerosis (MS) were evaluated. All subjects were seated in front of a 19" TV monitor depicting a black and white square pattern, standard condition (R). Two trials of 100 stimulus repetitions at 1.8 Hz, recording at Oz- Fz were performed for each eye. After two minutes the procedure was replicated using an stenopeic semiocclusor, central field condition (S). The main parameters quantified were the P100 latency in each eye (a) and P100 inter-ocular difference (b). RESULTS: Under condition R abnormalities were detected in 42 patients for parameter "a", and in 39 patients for parameter "b". If both parameters, a + b, were considered 48 patients (87%) showed abnormalities. Under condition S, abnormalities were detected in 49 patients for parameter "a" and 41 patients for parameter "b". When both parameters, a + b, were considered 53 patients (96%) showed abnormalities. DISCUSSION: The main point of interest of this study is the fact that when a pattern reversal stimulus is restricted to the central area the evoked response shows a P100 peak with prolonged latency in comparison to the full-field stimulus. Additionally, used in combination with the standard full-field technique it improves the abnormality detection rate whilst adding little extra time to the procedure.

Pallidotomy in Parkinson's disease improves single-joint, repetitive, ballistic movements, but fails to modify multijoint, repetitive, gestural movements.

We studied 12 non-demented PD patients in on state before and 3 months after posteroventral pallidotomy (PVP), in order to evaluate the effects of surgery upon an unconstrained, multijoint skilled movement as well as a single joint, repetitive, ballistic movement. A Selspot II System was used for three-dimensional data acquisition, processing and reconstruction of limb trajectories. Specific wrist kinematic features of spatial accuracy (linearity and planarity), temporal attributes (acceleration and velocity), spatiotemporal relationships (velocity-curvature coupling), and joint kinematic variables (relationships between wrist and elbow velocities and relative arm angle amplitudes) for each cycle of movement were graphically and numerically analysed. QMC was applied to single joint, repetitive, ballistic movements. QMC significantly improved after PVP (P < 0.0006). However, wrist as well as joint kinematic variables of the gestural movements failed to change significantly after PVP. The lack of improvement of the kinematic abnormalities of the gestural movement in PD patients would indicate that they are unrelated to the basic motor deficit; most likely they are the result of a disruption of a complex of sensorimotor integration processes due to abnormal parieto-frontal basal ganglia interaction.

Limb-kinetic apraxia in corticobasal degeneration: clinical and kinematic features.

Current concepts regarding the organisation of the motor system indicate the existence of a frontoparietal circuit involved in prehension and manipulation, whose damage may result in a motor behavioural disorder strongly resembling the one originally described as limb-kinetic apraxia. To determine the specific clinical and kinematic features of this distinctive praxic disorder, 5 patients with corticobasal degeneration (apraxic group), 5 with Parkinson's disease (nonapraxic group), and 10 control subjects were studied by a comprehensive apraxic battery, three-dimensional motion analysis of manipulative movements and motor evoked potentials. A mathematical model [quality of movement coefficient (QMC)] was applied to quantify differential kinematic characteristics between elementary motor deficits and the praxic disorder. Transcranial magnetic stimulation was used to evaluate corticomotoneural projections and cortical inhibition. All five patients in the apraxic group exhibited a unilateral praxic deficit characterised by derangement of fractionated and segmental finger movements. QMC was significantly greater in apraxic than in nonapraxic patients (P < 0.02), revealing a chaotic movement with marked interfinger uncoordination. Conventional transcranial magnetic stimulation parameters were within normal limits in both groups of patients; however, the silent period was significantly shorter in the apraxic limb when compared with control subjects (P < 0.001). Limb-kinetic apraxia is a distinctive disorder affecting the performance of finger and hand postures and movements over and above a corticospinal or basal ganglion deficit. Disruption of the frontoparietal circuit devoted to grasping and manipulation, together with defective cortical inhibition, which would also interfere with the selection and control of hand muscle activity, are the most likely underlying physiopathological mechanisms of limb-kinetic apraxia in patients with corticobasal degeneration.