Evaluating the Differential Electrophysiological Effects of the Focal Vibrator on the Tendon and Muscle Belly in Healthy People

OBJECTIVE: To investigate the electrophysiological effects of focal vibration on the tendon and muscle belly in healthy people. METHODS: The miniaturized focal vibrator consisted of an unbalanced mass rotating offset and wireless controller. The parameters of vibratory stimulation were adjusted on a flat rigid surface as 65 microm at 70 Hz. Two consecutive tests on the different vibration sites were conducted in 10 healthy volunteers (test 1, the Achilles tendon; test 2, the muscle belly on the medial head of the gastrocnemius). The Hoffman (H)-reflex was measured 7 times during each test. The minimal H-reflex latency, maximal amplitude of H-reflex (Hmax), and maximal amplitude of the M-response (Mmax) were acquired. The ratio of Hmax and Mmax (HMR) and the vibratory inhibition index (VII: the ratio of the Hmax after vibration and Hmax before vibration) were calculated. The changes in parameters according to the time and site of stimulation were analyzed using the generalized estimating equation methods. RESULTS: All subjects completed the two tests without serious adverse effects. The minimal H-reflex latency did not show significant changes over time (Wald test: chi2=11.62, p=0.07), and between the two sites (chi2=0.42, p=0.52). The changes in Hmax (chi2=53.74, p<0.01), HMR (chi2=20.49, p<0.01), and VII (chi2=13.16, p=0.02) were significant over time with the adjustment of sites. These parameters were reduced at all time points compared to the baseline, but the decrements reverted instantly after the cessation of stimulation. When adjusted over time, a 1.99-mV decrease in the Hmax (chi2=4.02, p=0.04) and a 9.02% decrease in the VII (chi2=4.54, p=0.03) were observed when the muscle belly was vibrated compared to the tendon. CONCLUSION: The differential electrophysiological effects of focal vibration were verified. The muscle belly may be the more effective site for reducing the H-reflex compared to the tendon. This study provides the neurophysiological basis for a selective and safe rehabilitation program for spasticity management with focal vibration.

Neurophysiological aspects and their relationship to clinical and functional impairment in patients with chronic obstructive pulmonary disease

OBJECTIVE: The purpose was to assess functional (balance L-L and A-P displacement, sit-to-stand test (SST) and Tinetti scale - balance and gait) and neurophysiological aspects (patellar and Achilles reflex and strength) relating these responses to the BODE Index. INTRODUCTION: The neurophysiological alterations found in patients with chronic obstructive pulmonary disease (COPD) are associated with the severity of the disease. There is also involvement of peripheral muscle which, in combination with neurophysiological impairment, may further compromise the functional activity of these patients. METHODS: A cross-sectional study design was used. Twenty-two patients with moderate to very severe COPD (>60 years) and 16 age-matched healthy volunteers served as the control group (CG). The subjects performed spirometry and several measures of static and dynamic balance, monosynaptic reflexes, peripheral muscle strength, SST and the 6-minute walk test. RESULTS: The individuals with COPD had a reduced reflex response, 36.77±3.23 (p<0.05) and 43.54±6.60 (p<0.05), achieved a lower number repetitions on the SST 19.27±3.88 (p<0.05), exhibited lesser peripheral muscle strength on the femoral quadriceps muscle, 24.98±6.88 (p<0.05) and exhibited deficits in functional balance and gait on the Tinetti scale, 26.86±1.69 (p<0.05), compared with the CG. The BODE Index demonstrated correlations with balance assessment (determined by the Tinetti scale), r = 0.59 (p<0.05) and the sit-to-stand test, r = 0.78 (p<0.05). CONCLUSIONS: The individuals with COPD had functional and neurophysiological alterations in comparison with the control group. The BODE Index was correlated with the Tinetti scale and the SST. Both are functional tests, easy to administer, low cost and feasible, especially the SST. These results suggest a worse prognosis; however, more studies are needed to identify the causes of these changes and the repercussions that could result in their activities ...

Long term depression of the recurrent inhibition of monosynaptic spinal reflexes after sciatic nerve crush in adult rats / 生理学报

Sciatic nerve injury is a common disease of peripheral nerve in clinic. After nerve injury, there are many dysfunctions in motoneurons and muscles following regeneration. Previous studies mostly investigated the aspects related to the injured nerve, and the effect on the recurrent inhibition (RI) pathway of spine following regeneration was not fully understood. Following reinnervation after temporary sciatic nerve crush, the functional alteration of RI was studied. In adult rats, RI between lateral gastrocnemius-soleus (LG-S) and medial gastrocnemius (MG) motor pools was assessed by conditioning monosynaptic reflexes (MSRs) elicited from the cut dorsal roots and recorded from either the LG-S or MG nerves by antidromic stimulation of the synergist muscle nerve. The following results were obtained. (1) The RI of MSRs in rats was almost lost (<5 weeks) after sciatic nerve crush. Although the RI partially recovered following reinnervation (6 weeks), it remained permanently depressed (up to 14 weeks). (2) Sciatic nerve crush on one side did not affect the contralateral RI. (3) Sciatic nerve crush did not induce any motoneuron loss revealed by immunohistochemistry. Peripheral nerve temporary disconnection causes long term alterations in RI pathway which make up motoneuron's function enhance for the alteration of muscle power and suggests that peripheral nerve injury induces long term plastic changes in the spinal motoneuron circuitry.

Significance of monosynaptic and polysynaptic reflexes in neonatal rat spinal cord in vitro.

Stimulation of a dorsal root in an isolated spinal cord, elicited a monosynaptic reflex (MSR) in the corresponding ventral root at a latency of 3-5 msec and a dorsal root reflex (DRR) in an adjacent dorsal root 2-3 times the latency of MSR. The magnitude of DRR was 10 times smaller than the MSR. These reflexes could be decreased by the agents which suppress synaptic transmission e.g. either by decreasing the [Ca2+]0 or by increasing [Mg2+]0. In the absence of magnesium ([Mg2+]0) in the perfusing medium, the MSR was 15-20% greater in its magnitude and the segmental polysynaptic reflex (PSR) was distinctly seen at 8-10 msec latency. Segmental PSR disappeared when [Mg2+]0 ions are added to perfusing medium probably indicating the involvement of N-methyl-D-aspartate receptors. Further, in this preparation homosynaptic inhibition and pre- or post-synaptic inhibitions could be elicited. This preparation, thus serves as useful model for the study of central synaptic transmission to study the pharmacological or neurotoxic agents.

Thyrotropin releasing hormone-induced potentiation of spinal monosynaptic reflex in rats in vitro.

Superfusion of thyrotropin-releasing hormone (TRH) in neonatal rat spinal cord in vitro produced dose (0.01-1.00 microM) dependent potentiation of monosynaptic reflex (MSR) which was maximum (44% of control) at 1 microM of TRH. But no ventral root depolarization was observed with TRH (1 microM) although potassium concentration out side ([K+]0) when increased produced a depolarization at the magnitude of 0.2 mV/mM of [K+]0. TRH-induced potentiation of MSR was not altered in spinal cords, obtained from the animals pretreated with 5,7-dihydroxytryptamine or 6-hydroxydopamine. Neither serotonin antagonists (spiperone, ketanserin, cyproheptadine or 3-troponyl-indole-3-carboxylate) nor adrenergic antagonists (phentolamine or haloperidol) could attenuate TRH-induced potentiation. Inhibition of MSR observed in the spinal cord elicited by stimulating the adjacent dorsal root was unaffected by TRH. The results suggest that, TRH potentiates MSR by directly acting on the motoneurons, without involving presynaptic serotonergic or catecholaminergic neuronal systems or the disinhibition of pre- or post-synaptic inhibition in the spinal cord.

Role of H-reflex latency studies in the diagnosis of subclinical diabetic neuropathy.

Motor conduction velocity (MCV) in the median, ulnar and peroneal nerves and H-reflex studies have been conducted in 50 diabetics aged 20-65 years and 25 controls. MCV in the upper limb was below the normal range in 16% of diabetics. 28% diabetics showed abnormal MCV in the peroneal nerve. H-reflex abnormality consisting of either prolonged latency or its complete absence could be observed in 54% of diabetics. The results indicate the greater sensitivity of H-reflex in the detection of sub-clinical diabetic neuropathy. Greater prevalence of neuropathy in the early onset diabetes than in the late onset type is also suggested.

Spinal reflex activity in patients with Duchenne, limb-girdle and myotonic muscular dystrophies

La actividad refleja espinal excitatoria e inhibitoria fue estudiada en pacientes con distrofia muscular del tipo Duchenne, de las cinturas y miotónica. Para ello se emplearon técnicas electrofisiológicas que permitieron conocer el comportamiento de las respuestas H y T y del período silente. A esto se sumó la investigación del coeficiente de excitabilidad de la motoneurona espinal alfa. Tanto en la forma de Duchenne como en la de las cinturas el comportamiento reflejo medular, medido a través de las respuestas H y T, sugirió el compromiso de la neurona motora alpha del asta anterior de médula. En los que padecían la forma miotónica, las mismas respuestas se mostraron igualmente alteradas; sin embargo, en este caso, las peculiaridades del comportamiento observado están, más probablemente, ligadas a la modificación anatómica que exhibe el huso neuromuscular en estos pacientes antes que con una lesión primaria de motoneurona. En los tres grupos el coeficiente de excitabilidad estuvo reducido, fundamentalmente en las formas de Duchenne y miotónica. Este hallazgo señala una cierta participación de la corteza cerebral motora en estas enfermedades. No se encontraron diferencias entre controles y probandos en relación al período silente, hecho que sugiró la indemnidad de los circuitos medulares inhibitorios en estos pacientes

Effects and site of action of a single-breath of 100% CO2 on the monosynaptic reflexes in cats.

A single breath of 100% CO2 produces depression of the monosynaptic reflexes, recorded from L7 or S1 ventral root, after stimulation of the Posterior Biceps and Semitendinosus nerve (PBST) in anaesthetised cats. As the depression could not be attributed to the J-reflex(1), the possible site of action of the CO2 induced depression of monosynaptic reflexes was worked out. PBST nerve threshold did not change after CO2 introduction and the depression persisted in paralysed cats under controlled ventilation, thus eliminating the possibility of movement effect of the spinal cord due to tachypnoea. Spinal cord sections at the level of L1 and C1 abolished the depression, whereas the depression persisted in the decerebrate preparation. Thus it is concluded that a single-breath of 100% CO2 depresses the monosynaptic reflexes at the supraspinal level. Blood gas tensions (PO2 and pCO2) measured before and after CO2 introduction showed a shortlasting increase in pCO2 and not much significant change in pO2 compared to the long lasting depression of monosynaptic reflexes.

Limitations in the use of CO2 as a method for studying the J-reflex.

In order to study the J-reflex, monosynaptic reflexes were recorded from L7 or S1 ventral root after stimulation of the posterior biceps, and semi-tendinosus nerve (PBST) from the lower limb in cats anaesthetized with Pentobarbitone sodium. Intratracheal CO2 (60 ml, 100%) depressed the monosynaptic reflexes, and the depression was comparable to the effects of right atrial phenyl diguanide injection. Bilateral vagotomy did not abolish the response showing that the afferent pathway of this depression does not travel via the vagus nerve. Thus it is concluded that CO2 cannot be used to study the J-reflex.