Effects of dance therapy on balance, gait and neuro-psychological performances in patients with Parkinson's disease and postural instability

Postural Instability (PI) is a core feature of Parkinson’s Disease (PD) and a major cause of falls and disabilities. Impairment of executive functions has been called as an aggravating factor on motor performances. Dance therapy has been shown effective for improving gait and has been suggested as an alternative rehabilitative method. To evaluate gait performance, spatial-temporal (S-T) gait parameters and cognitive performances in a cohort of patients with PD and PI modifications in balance after a cycle of dance therapy

A Sound-evoked vestibulomasseteric reflex in healthy humans

Averaged responses to loud clicks were recorded in the unrectified and rectified masseter electromyogram (EMG) of 18 healthy subjects. Unilateral clicks (0.1 ms, 3 Hz, 70–100 dB NHL), delivered during a steady masseter contraction, evoked bilateral responses that appeared to consist of 2 components on the basis of threshold, latency, and their appearance in rectified EMG. The lowest threshold response appeared as a p16 wave (onset 11–13 ms) in the unrectified EMG and corresponded with a 10- to 12-ms period of inhibition in the rectified EMG. Higher-intensity clicks recruited an earlier p11 response in the unrectified EMG (onset 7.0–9.2 ms) that sometimes appeared as an initial increase in the rectified EMG before suppression. The amplitude of the p11 wave scaled with background EMG level and was asymmetrically modulated by 30° tilt of the whole body. The threshold of the early p11/n15 wave in masseter was the same as the threshold for click-induced vestibulocollic reflexes. Single motor unit recordings demonstrated that responses in masseters corresponded to a silent period in unit firing that began earlier and lasted longer at 100 dB than at 80 dB. We propose that loud clicks induce 2 partially overlapping short-latency reflexes in masseter muscle EMG: a p11/n15 response, which we suggest is of vestibular origin, and a p16/n21 response, which we suggest is equivalent to the previously described jaw–acoustic reflex

A Short latency vestibulomasseteric reflex evoked by electrical stimulation over the mastoid in healthy humans

We describe EMG responses recorded in active masseter muscles following unilateral and bilateral electrical vestibular stimulation (EVS, current pulses of 5 mA intensity, 2 ms duration, 3 Hz frequency). Averaged responses in unrectified masseter EMG induced by unilateral EVS were examined in 16 healthy subjects; effects induced by bilateral (transmastoid) stimulation were studied in 10 subjects. Results showed that unilateral as well as bilateral EVS induces bilaterally a clear biphasic response (onset latency ranging from 7.2 to 8.8 ms), that is of equal amplitude and latency contra- and ipsilateral to the stimulation site. In all subjects, unilateral cathodal stimulation induced a positive-negative response termed p11/n15 according to its mean peak latency; the anodal stimulation induced a response of opposite polarity (n11/p15) in 11/16 subjects. Cathodal responses were significantly larger than anodal responses. Bilateral stimulation induced a p11/n15 response significantly larger than that induced by the unilateral cathodal stimulation. Recordings from single motor units showed that responses to cathodal stimulation corresponded to a brief (2-4 ms) silent period in motor unit discharge rate. The magnitude of EVS-induced masseter response was linearly related to current intensity and scaled with the mean level of EMG activity. The size of the p11/n15 response was asymmetrically modulated when subjects were tilted on both sides; in contrast head rotation did not exert any influence. Control experiments excluded a possible role of cutaneous receptors in generating the masseter response. We conclude that transmastoid electrical stimulation evokes vestibulomasseteric reflexes in healthy humans at latencies consistent with a di-trisynaptic pathway

Changes in c-fos expression induced by trigeminal nerve stimulation in the rat brain

Epilepsy in many patients remains poorly controlled despite the introduction of new antiepileptic drugs. Stimulation of the vagus nerve (VNS) has become an effective method for desynchronizing the highly coherent neural activity typically associated with epileptic seizures. This technique has been used in several animal models of seizures as well as in humans suffering from drug-resistant epilepsy (DRE). Stimulation of another cranial nerve, the trigeminal nerve (TNS), can also cause cortical and thalamic desynchronization, resulting in a activity reduction of pharmacologically induced-seizure in awake rats. Moreover, the an antiepileptic action of TNS has been shown in clinical studies, reporting TNS efficacy in patients DRE. These observations suggest that like VNS also TNS has a potential as a therapy for the treatment of DRE. Although it has been suggested an antiepileptic action for TNS, little is known about the brain structures that could mediate this phenomenon. Fos is a nuclear protein that is expressed under conditions of high neuronal activity. We utilized Fos immunoreactivity techniques on Sprague-Dawley rat brains to identify regions that are activated by the left trigeminal nerve stimulation. Anesthetized rats were implanted in the infraorbital branch of the trigeminal nerve (ION) with a bipolar electrode connected to a pulse generator. Three days later, the pulse generator was activated for a 3h treatment using stimulation parameters (30 sec ON, 5 min OFF; continuous cycle; 30 Hz, pulse width of 500 μs, 3.5 mA). A sham control group underwent the same surgery but the electrode was connected to a dummy pulse generator. We found that TNS induced specific increases in nuclear Fos immunolabeling in discrete brain structures, including the amygdale and cortical regions compared to control animals. We found a 4 fold increase in the number of Fos positive cells in the amygdala of TNS rats that resulted statistically significant (P<0.0001) compared to control rats. Moreover, the number of Fos positive cells in the right amigdala was 7 folds grater than the number in the left amygdala (P<0.0001). Likewise , the number of Fos positive cells in the somatosensory area of the frontoparetial cortex was increased of 2.8 folds (P<0.01) and again a difference between left and right was evident, being the number of Fos positive cells 6.6 folds grater (P<0.001) in the right cortex. These brain structures activated by TNS could be important for genesis or regulation of seizures. The activation of these structures may play a pivotal role in the antiepileptic effect of TNS that could be used as an adjuvant to drugs and/or VNS in those patients that are refractory to treatment

Reflex responses of masseter muscles to sound

Acoustic stimuli can evoke reflex EMG responses (acoustic jaw reflex) in the masseter muscle. Although these were previously ascribed to activation of cochlear receptors, high intensity sound can also activate vestibular receptors. Since anatomical and physiological studies, both in animals and humans, have shown that masseter muscles are a target for vestibular inputs we have recently reassessed the vestibular contribution to masseter reflexes. We found that high intensity sound evokes two bilateral and symmetrical short-latency responses in active unrectified masseter EMG of healthy subjects: a high threshold, early p11/n15 wave and a lower threshold, later p16/n21 wave. Both of these reflexes are inhibitory but differ in their threshold, latency and appearance in the rectified EMG average. Experiments in healthy subjects and in patients with selective lesions showed that vestibular receptors were responsible for the p11/n15 wave (vestibulo-masseteric reflex) whereas cochlear receptors were responsible for the p16/n21 wave (acoustic masseteric reflex). The possible functional significance of the double vestibular control over masseter muscles is discussed

Modulation of rat medial vestibular nucleus neurone activity by vasopressin and noradrenaline <i>in vitro</i>

In the present study, we examined the effects of bath application of vasopressin and noradrenaline on the spontaneous tonic discharge of medial vestibular nucleus (MVN) neurones and investigated if there is an interaction between the two drugs in an in vitro slice preparation of the rat brainstem containing the MVN. The results showed that vasopressin did not affect the spontaneous discharge rate of MVN neurones when applied either as a 60 s pulse or when the drug continuously perfused the slice for a period of 10 min. In contrast, noradrenaline affected the spontaneous discharge rate of the majority of cells tested (53/60, 88%). Noradrenaline excited the majority (46/53, 87%) of MVN neurones through both α1 and β noradrenergic receptor-linked mechanisms. The remaining cells (7/53, 13%) were inhibited by noradrenaline through an α2 noradrenergic receptor-linked mechanism. Neither the excitatory nor inhibitory effects of noradrenaline were modified by vasopressin when the two drugs were applied together

Melatonin inhibits rat medial vestibular nucleus neuron activity <i>in vitro</i>

The present study evaluated the effects of melatonin on the discharge rate of tonically active medial vestibular nucleus (MVN) neurons in an in vitro slice preparation of the rat dorsal brainstem. The results demonstrated that, when melatonin was applied to the slice for a period of 7–10 min, a decrease in MVN neuron firing rate was observed in 21/58 (36%) of the cells sampled. The inhibitory effects of melatonin were present in synaptic uncoupling condition and were mimicked by 2-iodomelatonin, a non-selective agonist with high affinity for melatonin membrane receptor subtypes (MT1, MT2, MT3). The MT2 receptor antagonists luzindole and 4-phenyl-2-propionamidotetraline and the MT3 receptor antagonist prazosin did not, however, antagonise the inhibitory effects of melatonin, indicating that melatonin may act on MVN neurons through an MT1 receptor-mediated mechanism

Sensorimotor interaction and motor learning in facial muscles

Background and aim: Integration of sensory information with motor output is thought to be important in motor learning. In limb muscles, this is studied using the short afferent inhibition (SAI) paradigm, to assess sensorimotor interaction, and paired associative stimulation (PAS), to evaluate LTP-like plasticity. As far as we know, SAI and PAS paradigms have never been used in the territory of the cranial nerves. The present study was aimed at testing in normal subjects whether sensorimotor interaction and LTP-like plasticity can be observed in facial muscles as well as in limb muscles. Methods: Motor evoked potentials (MEPs) were evoked in the depressor angulis oris (DAO) muscle of 7 subjects. MEPs were recorded from the contralateral DAO at rest and during 10% maximal voluntary contraction (active condition). SAI was tested in 5 subjects, by pairing electrical stimulation (ES, intensity 3 times the perceptual threshold) of the facial nerve, with magnetic stimulation (TMS, 120% of motor threshold intensity) of the facial motor cortex. Intervals between ES and TMS were 5, 10, 15, 20, 25 and 30 ms. The LTP-like plasticity protocol (200 pairs of ES and TMS, 20 ms ISI, at 0.25 Hz) was tested in X subjects by evoking twenty MEPs in both resting and active conditions, before and at 0, 20 and 30 min after paired stimulation. Results: Facial nerve stimulation in the SAI paradigm had no significant affect on MEP amplitude, either in the active or in the relaxed DAO muscle. By contrast MEP amplitude at rest showed a trend of facilitation (p &lt; 0,072) after the PAS protocol administration. When tested at rest this effect was observed at baseline and after 10 min. On the contrary MEP amplitude recorded during activity was significantly enhanced at 10 (p &lt; 0,026) and 30 (p &lt; 0,014) minutes after PAS. There was a significant difference between the time course in resting and active conditions (p &lt; 0,019). Conclusions: These data show that there is no short latency afferent inhibition in the facial motor cortex, yet despite this, there is evidence for maintained LTP-like plasticity. Further studies are needed to understand how and why PAS works in facial muscles despite the absence of SAI. A larger sample is also required to confirm the PAS effect on resting DAO MEPs. A second point to be clarified is why the PAS time course at rest is different from that operating during active condition.</br

Transcutaneous trigeminal nerve stimulation induces a long-term depression-like plasticity of the human blink reflex.

The beneficial effects of trigeminal nerve stimulation (TNS) on several neurological disorders are increasingly acknowledged. Hypothesized mechanisms include the modulation of excitability in networks involved by the disease, and its main site of action has been recently reported at brain stem level. Aim of this work was to test whether acute TNS modulates brain stem plasticity using the blink reflex (BR) as a model. The BR was recorded from 20 healthy volunteers before and after 20 min of cyclic transcutaneous TNS delivered bilaterally to the infraorbital nerve. Eleven subjects underwent sham-TNS administration and were compared to the real-TNS group. In 12 subjects, effects of unilateral TNS were tested. The areas of the R1 and R2 components of the BR were recorded before and after 0 (T0), 15 (T15), 30 (T30), and 45 (T45) min from TNS. In three subjects, T60 and T90 time points were also evaluated. Ipsi- and contralateral R2 areas were significantly suppressed after bilateral real-TNS at T15 (p = 0.013), T30 (p = 0.002), and T45 (p = 0.001), while R1 response appeared unaffected. The TNS-induced inhibitory effect on R2 responses lasted up to 60 min. Real- and sham-TNS protocols produced significantly different effects (p = 0.005), with sham-TNS being ineffective at any time point tested. Bilateral TNS was more effective (p = 0.009) than unilateral TNS. Acute TNS induced a bilateral long-lasting inhibition of the R2 component of the BR, which resembles a long-term depression-like effect, providing evidence of brain stem plasticity produced by transcutaneous TNS. These findings add new insight into mechanisms of TNS neuromodulation and into physiopathology of those neurological disorders where clinical benefits of TNS are recognized