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    Free and supported stance in Parkinson's disease. The effect of posture and 'postural set' on leg muscle responses to perturbation, and its relation to the severity of the disease

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    Upright stance and its reflex control were studied in parkinsonian patients and in age-matched normal subjects. They stood unperturbed on a force-measuring surface (static conditions), or were displaced by movement of a supporting platform (dynamic conditions). During quiet stance the following variables were analysed, with eyes open or closed: position of the centre of foot pressure (CFP), average sway area, length of sway path, amplitude and distribution of tonic leg muscle EMG activity. Perturbations of stance were induced by toe-up or toe-down rotations, and by backward or forward translations of the platform. Amplitude of short, medium and long-latency EMG responses to displacement were measured in the tibialis anterior (TA) and in the three heads of the triceps surae (TS) muscle. The perturbations were produced during both free and supported stance (holding onto a stable structure), under which condition normal subjects suppress medium and long-latency responses. Under static conditions, the only significant finding in parkinsonians was represented by a shift in the position of the CFP. This was correlated with the severity of the disease (Webster scale), the less affected patients being shifted backwards and the more affected patients forwards, with respect to normals. Under dynamic conditions, the reflex responses to perturbations of free stance were similar in both groups. Only the medium-latency burst of gastrocnemius lateralis and the long-latency burst TA evoked by TS stretch were larger in parkinsonians. The amplitude of these responses, as well as of all the others, was not related to the Webster score. Within the patients' group, a relationship between position of CFP and area of EMG burst was found for both medium and long-latency TA responses evoked by forward translation and toe-up rotation, respectively. Under supported conditions, the capability to suppress all medium and long-latency muscle responses to any perturbation was lost or impaired in the parkinsonians. The degree of impairment was unrelated to the position of the CFP, but was significantly related to the severity of the disease. The suppression to 40% (supported/nonsupported), of TA response to toe-down rotation is proposed as the point of separation between normals and parkinsonians. The forward projection of the CFP, occurring in the severe stages of the disease, and the increase in amplitude of some responses to perturbations of free stance might be a compensatory adaptation to the anomalous upright posture

    Shift of activity from slow to fast muscle during voluntary lengthening contractions of the triceps surae muscles in humans

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    1. Raw or rectified and integrated electromyograms (integrated EMGs) of the leg muscles were recorded during (a) isotonic ramp shortening or lengthening contractions consisting of foot plantar flexions against a constant load, or dorsal flexions accomplished by braking the load and yielding to it, respectively, and (b) isometric increasing or decreasing plantar torques accomplished by graded contractions or relaxations of the triceps muscles. 2. During plantar flexions or increasing torques, the EMG of soleus, gastrocnemius lateralis, medialis, and peroneus increased in parallel. During decreasing torques, motor unit derecruitment took place gradually and simultaneously. The tibialis anterior was silent. During dorsal flexions, one of two characteristic patterns was observed in different subjects: (a) soleus was abruptly derecruited at the beginning of the task, while gastrocnemius lateralis (or medialis) exhibited a large recruitment lasting throughout the lengthening contraction; (b) soleus remained active during the task, showing large motor unit potentials, while the gastrocnemius lateralis recruitment was of a lesser extent than in (a). Peroneus derecruitment was gradual and tibialis anterior activity was absent in both cases. 3. The EMG patterns observed during plantar flexions or in increasing and decreasing torques, and the two patterns observed during shortening or lengthening contractions, were closely reproduced during sinusoidal oscillations of the foot or in isometric contractions and relaxations. 4. When recruitment of the gastrocnemius lateralis was present during dorsal flexion, the slope of its integrated EMG envelope was steeper, the higher the velocity of lengthening contraction. The most rapid and the slowest tasks, however, did not require its activation. Gastrocnemius lateralis integrated EMGs of an amplitude similar to those occurring during lengthening contractions were observed only during ballistic plantar flexions. 5. The two patterns of triceps activation occurring during lengthening contraction could be traced to different mechanical characteristics of the soleus muscles, the gastrocnemius lateralis being activated preferentially in subjects with long soleus half-relaxation times, and the soleus in subjects with short soleus half-relaxation times. 6. The soleus and gastrocnemius lateralis H reflexes were tested during shortening and lengthening contractions

    Medium-latency stretch reflexes of foot and leg muscles analysed by cooling the lower limb in standing humans

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    1. In standing subjects, an ankle-dorsiflexing perturbation of the supporting surface evokes a short-latency response (SLR) and a medium-latency response (MLR) to stretch in both soleus (Sol) and flexor digitorum brevis (FDB) muscles. The SLR is the counterpart of the monosynaptic reflex, whilst the MLR might be either mediated by Ia fibres, the delay being due to a long-loop central circuit, or by fibres of slower conduction velocity. Since small afferents are slowed more than large ones by low temperature, a greater latency increment for the MLR than the SLR induced by cooling of the limb would point to a peripheral origin of the MLR. 2. In nine subjects, one limb was cooled by circulating water in a tube wrapped around it for about 120 min. Perturbations were delivered to the same limb prior to and during cooling, and after rewarming. EMG was recorded by surface electrodes from the Sol and FDB muscles. 3. The mean increase in latency of MLRs was significantly greater than that of SLRs in both muscles. On average, the Sol SLR increased from 42.4 to 47.0 ms and the Sol MLR from 72.0 to 82.3 ms. The FDB SLR increased from 58.1 to 66.5 ms and the FDB MLR from 94.9 to 110.5 ms. The mean difference (MLR minus SLR) increased from 29.6 to 35.2 ms for Sol, and from 36.8 to 43.9 ms for FDB at the end of cooling. After 30 min of rewarming, the responses of both muscles recovered towards control values. 4. The greater latency increment of the MLRs than of the SLRs favours the hypothesis of a slower conduction velocity of the responsible afferent fibres. The most likely candidate fibres are the spindle group II afferents

    Medium-latency response to muscle stretch in human lower limb: estimation of conduction velocity of group II fibres and central delay

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    In standing subjects, ankle dorsiflexion evoked short-latency responses (SLRs) at 41 and 57 ms, on the average, in soleus (Sol) and flexor digitorum brevis (FDB), respectively. Medium-latency responses (MLRs) occurred at 70 and 95 ms. The time between the MLRs was 25 ms and between the SLRs was 16 ms. The difference between these two values represents the extra-time to conduct the FDB volley for MLR from distal to proximal muscle, in excess to that for SLR. The velocity of the afferents mediating the FDB MLR (21.4 m/s on average) was estimated by dividing the distance between the two muscles by the sum of the above extra-time and the conduction time of Ia fibres along the same distance. The central delay of FDB MLR (6.7 ms on average) was obtained by dividing the distance between FDB and spinal cord by the sum of afferent and efferent MLR conduction times. The central delay of FDB SLR (1.4 ms) was analogously obtained. These findings give an estimation of the conduction velocity of the group II afferent fibres in humans and support the hypothesis that the FDB MLR is relayed through a spinal oligosynaptic pathway

    Group II spindle fibres and afferent control of stance. Clues from diabetic neuropathy

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    OBJECTIVE: Since patients with large-fibre neuropathy do not show abnormal body sway during stance, the hypothesis was tested that postural control is not impaired until myelinated fibres of medium size are affected. METHODS: In 22 diabetic neuropathic patients and 13 normals, we recorded: (1) body sway area (SA), (2) stretch responses of soleus (Sol) and flexor digitorum brevis (FDB) to toe-up rotation of a platform, (3) Sol and FDB H reflex and FDB F wave, (4) conduction velocity (CV) of tibial, deep peroneal and sural nerve. In patients, detection thresholds for vibration, cooling (CDT), warming and heat-pain (HPDT) were assessed. RESULTS: Body SA was increased in patients with respect to normals. Toe-up rotation elicited short- (SLR) and medium-latency (MLR) responses in Sol and FDB in all normals. In patients, SLR was absent in FDB and reduced in Sol, and MLR was delayed in both muscles; the FDB H reflex was absent. The CV of tibial nerve group II afferent fibres, as estimated from the afferent time of FDB MLR, was reduced in patients. All sensory detection thresholds were increased. Stepwise multiple regression showed that increased SA was explained by increased latency of MLR, decreased CV of group II fibres and augmented CDT and HPDT. CONCLUSIONS: Unsteadiness in diabetic neuropathy is related to alterations in medium-size myelinated afferent fibres, possibly originating from spindle secondary terminations

    Reflex contribution of spindle group Ia and II afferent input to leg muscle spasticity as revealed by tendon vibration in hemiparesis

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    OBJECTIVE: Foot dorsiflexion evokes a short- (SLR) and a medium-latency EMG response (MLR) in the soleus of standing subjects. SLR is mediated by spindle group Ia, while group II fibres contribute to MLR through an oligosynaptic circuit. We studied the effects of Achilles' tendon vibration on both responses in spastic patients to disclose any abnormal excitability of these pathways. METHODS: SLR and MLR were evoked in 11 hemiparetics and 11 normals. The vibration-induced changes in both responses were correlated to the Ashworth score of the affected leg. RESULTS: There were no differences between normals and patients in the size of control SLR or MLR. Vibration decreased SLR to 70% in normal subjects, but increased it to 110% in patients, in both affected and unaffected leg. Vibration did not affect MLR in normals, but increased it to 165% on the affected and 120% on the unaffected side of patients. Ashworth score was solely correlated with the degree of vibration-induced increase of MLR. CONCLUSIONS: While the lack of inhibitory effect of vibration on SLR confirms a reduced inhibitibility of the monosynaptic reflex, the increased MLR indicates a disinhibition of group II pathway in patients, connected to the loss of descending control on group II interneurones. Spastic hypertonia depends on release of group II rather than group Ia reflex pathways. SIGNIFICANCE: These findings give a neurophysiological support for the pharmacological treatment of spastic hypertonia and suggest a method for the assessment of its effects

    Inhibitory effect of the Jendrassik maneuver on the stretch reflex

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    The Jendrassik maneuver (JM) is a method for enhancing sluggish tendon-tap jerks at medical examination. It is the thesis of this paper that JM effects should not be limited to the monosynaptic reflex pathway but extend to the entire response elicited in the stretched muscle. This consists of a short-latency response (SLR) corresponding to the mono- and oligosynaptic reflex and a medium-latency response (MLR) relayed by group-II spindle afferent fibers and likely made of a segmental burst and a transcortical loop. Soleus (Sol) SLR and MLR were evoked by toe-up and tibialis anterior (TA) MLR by toe-down platform rotation in 15 standing subjects and recorded by surface electromyogram (EMG). For each stimulus type, up to 20 perturbations were elicited during i) quiet stance (Control) and while ii) performing JM, iii) leaning forward (FW), iv) holding onto a stable frame (Holding). For each subject, stimulus type and condition, rectified EMG traces were averaged. Based on the comparison of the population grand averages, selective effects of JM on the responses were identified. Appropriate time windows were set for measuring the area of SLR and of the early and late burst of MLR (MLR1 and MLR2). Significant changes in response size, but not latency, were induced by all conditioning procedures. During toe-up, JM slightly increased Sol SLR; FW increased both Sol background activity and SLR; MLR1 was not affected by JM, but increased by FW; MLR2 was strongly diminished by JM and increased by FW. During toe-down, JM did not affect TA MLR1, but strongly diminished MLR2. Under Holding condition, Sol SLR to toe-up was unaffected, but both MLR1 and MLR2 to toe-up and toe-down were diminished, in both Sol and TA. JM selectively decreases the response component (MLR2) starting about 100 ms from onset of the stretch, in both extensor and flexor muscles. Latency and quality of the JM effect on MLR2 indicate that JM operates by gating a long-loop, possibly transcortical pathway. This new information suggests that lesions of cortical areas or descending pathways can exert enhancing effects on muscle tone by removing an inhibitory action on the late component of the stretch reflex
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