Could Parkinson's disease be diagnosed at an early stage by measuring rest tremor under stressed conditions?
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Biomedical subjects
Publications and source records attributed to Farzad Towhidkhah.
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Science of human identification using physiological characteristics or biometry has been of great concern in security systems. However, robust multimodal identification systems based on audio-visual information has not been thoroughly investigated yet. Therefore, the aim of this work to propose a model-based feature extraction method which employs physiological characteristics of facial muscles producing lip movements. This approach adopts the intrinsic properties of muscles such as viscosity, elasticity, and mass which are extracted from the dynamic lip model. These parameters are exclusively dependent on the neuro-muscular properties of speaker; consequently, imitation of valid speakers could be reduced to a large extent. These parameters are applied to a hidden Markov model (HMM) audio-visual identification system. In this work, a combination of audio and video features has been employed by adopting a multistream pseudo-synchronized HMM training method. Noise robust audio features such as Mel-frequency cepstral coefficients (MFCC), spectral subtraction (SS), and relative spectra perceptual linear prediction (J-RASTA-PLP) have been used to evaluate the performance of the multimodal system once efficient audio feature extraction methods have been utilized. The superior performance of the proposed system is demonstrated on a large multispeaker database of continuously spoken digits, along with a sentence that is phonetically rich. To evaluate the robustness of algorithms, some experiments were performed on genetically identical twins. Furthermore, changes in speaker voice were simulated with drug inhalation tests. In 3 dB signal to noise ratio (SNR), the dynamic muscle model improved the identification rate of the audio-visual system from 91 to 98%. Results on identical twins revealed that there was an apparent improvement on the performance for the dynamic muscle model-based system, in which the identification rate of the audio-visual system was enhanced from 87 to 96%.
Cerebellum has been assumed as an array of adjustable pattern generators (APGs). In recent years, electrophysiological researches have suggested the existence of modular structures in spinal cord called motor primitives. In our proposed model, each "adjustable primitive pattern generator" (APPG) module in the cerebellum is consisted of a large number of parallel APGs, the output of each module being the weighted sum of the outputs of these APGs. Each spinal field is tuned by a coefficient, representing a descending supraspinal command, which is modulated by ith APPG correspondingly. According to this model, motor control can be interpreted in terms of the modification of these coefficients. Vector summation of force fields implies that the complex nonlinearities in neuronal behavior are eliminated, causing our model to be simple and linear. The force field vectors, derived from motor primitives, depend on the state of movement and its derivative and the time that causes different repertoire of movement. This is physiologically plausible. Our model agrees with virtual trajectory hypothesis, stating that dynamics are not computed explicitly in central nervous system, but the desired trajectory, is fed into the spinal cord. We think that the dysmetria and the ataxia seen in some cerebellar diseases may be the result of local disruption of some APPGs. Accordingly, determining the exact location of related motor primitives in human spinal cord and stimulating them by functional neurostimulation may provide a good management for these clinical signs. Surely, experimental researches and clinical trials are needed to validate our hypothesis.
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Wind-up is described traditionally as a frequency dependent increase in the excitability of spinal cord neurons, evoked by electrical stimulation of afferent C-fibers. Different kinds of wind-up have been reported, but wind-up of Abeta fibers in hyperalgesic states has gained little attention. In this paper, we present a cybernetic view on Abeta fiber wind-up and consider the involved molecular mechanisms as feedback and feedforward processes. Furthermore, our previous hypothesis, the sprouting phenomenon, is included in this view. Considering the proposed model, wind-up in hyperalgesic states might leave out in three different ways: (1) blocking the NMDA receptors by increasing extracellular Mg2+, 2) blocking the receptors and channels that contribute to Ca2+ inward current, and 3) blocking the Abeta fibers by local anesthetics. It seems that wind-up may be inhibited more effectively by using these three blocking mechanisms simultaneously, because in this case, the feedback process (main controller), the feedforward process (trigger), and Abeta stimulation (trigger) would be inhibited concurrently. Wind up may aggravate the pain in clinical hyperalgesic situations such as post-surgical states, some neuropathic pains, fibromyalgia syndrome, and post-herpetic neuralgia. Surely, clinical studies are needed to validate the effectiveness of our abovementioned suggestions in relieving such clinical pains.
Two main mechanisms have been suggested for the propagation of action potentials in cardiac muscle cells: (1) the free flow of local circuit current through gap junctions and (2) the effect of electrical field. Different evidences confirm each of two mechanisms. We think that gap junctions are not continuously open in a normal heart cycle; instead, they open and close intermittently. In other words, gap junction has a dynamic behavior in each cardiac cycle, managing different routes of propagation in the diverse moments of normal cycle. Gap junctions could be open in phases 0, 1, 3, 4 and close in phase 2 (plateau) of action potential. Whenever gap junction is open, conduction can be fulfilled rapidly by current flow and whenever it is closed, the electrical field will be the main route of propagation. When the prejunctional cell is in the peak of action potential(AP), gap junction is closed and the postjunctional cell should use the electrical field to be stimulated. Then, when the prejunctional cell comes to the end of AP, the gap junction opens and current will potentiate the rising phase of AP in the postjunctional cell. Moreover, this process causes accumulation of calcium in the postjunctional cell near phase 2. We believe that our hypothesis on the mechanism of cardiac action potential propagation may have exciting advantages. This novel view on gap junction dynamic behavior may be useful for better exploitation of drugs or designing new remedies in arrhythmias. We also hypothesize that in conditions as cardiac failure, in which cardiac contractility is diminished and increasing intracellular calcium concentration is needed, gap junction closing drugs may be effective. It is worth noting that future clinical studies are needed to validate these predictions.
Previous studies have shown that the nervous system can produce anticipatory adjustments that alter the mechanical behavior of the arm in order to resist environmental disturbances. In the present paper, we focus on the ability of subjects to transfer acquired stiffness patterns to other parts of the workspace and on the durability of stiffness adaptations. To explore the transfer of stiffness control, subjects were trained at the left of the workspace to resist the effects of a single-axis disturbance that was applied by a robotic device. Following training, they were tested for transfer at the right. One group of subjects experienced similar torques at the left and right of the workspace, whereas the other group of subjects experienced similar forces at the hand. Following the initial training at the left, the observed orientation of the hand-stiffness ellipse rotated in the direction of the disturbance. In tests at the right, transfer was observed only when the direction of disturbance resulted in torques that were similar to those experienced during training. The results thus suggest that under the conditions of this experiment stiffness control is acquired and transfers in a joint- or muscle-based system of coordinates. A second experiment assessed the durability of an acquired stiffness pattern. Subjects were trained on 2 consecutive days to resist a single-axis disturbance. On a third day, the direction of the disturbance was switched by 90 degrees . Substantial interference with the new adaptation was observed. This suggests that stiffness training results in durable changes to the neural signals that underlie stiffness control.
We used a robotic device to test the idea that impedance control involves a process of learning or adaptation that is acquired over time and permits the voluntary control of the pattern of stiffness at the hand. The tests were conducted in statics. Subjects were trained over the course of 3 successive days to resist the effects of one of three different kinds of mechanical loads: single axis loads acting in the lateral direction, single axis loads acting in the forward/backward direction, and isotropic loads that perturbed the limb in eight directions about a circle. We found that subjects in contact with single axis loads voluntarily modified their hand stiffness orientation such that changes to the direction of maximum stiffness mirrored the direction of applied load. In the case of isotropic loads, a uniform increase in endpoint stiffness was observed. Using a physiologically realistic model of two-joint arm movement, the experimentally determined pattern of impedance change could be replicated by assuming that coactivation of elbow and double joint muscles was independent of coactivation of muscles at the shoulder. Moreover, using this pattern of coactivation control we were able to replicate an asymmetric pattern of rotation of the stiffness ellipse that was observed empirically. These findings are consistent with the idea that arm stiffness is controlled through the use of at least two independent co-contraction commands.