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Impaired modulation of quadriceps tendon jerk reflex during spastic gait: differences between spinal and cerebral lesions.

In healthy subjects, functionally appropriate modulation of short latency leg muscle reflexes occurs during gait. This modulation has been ascribed, in part, to changes in presynaptic inhibition of Ia afferents. The changes in modulation of quadriceps tendon jerk reflexes during gait of healthy subjects were compared with those of hemi- or paraparetic spastic patients. The spasticity was due to unilateral cerebral infarction or traumatic spinal cord injury, respectively. The modulation of the quadriceps femoris tendon jerk reflex at 16 phases of the step cycle was studied. The reflex responses obtained during treadmill walking were compared with control values obtained during gait-mimicking standing postures with corresponding levels of voluntary muscle contraction and knee angles. In healthy subjects the size of the reflexes was profoundly modulated and was generally depressed throughout the step cycle. In patients with spinal lesion the reflex depression during gait was almost removed and was associated with weak or no modulation during the step cycle. In patients with cerebral lesion there was less depression of the reflex size associated with a reduced reflex modulation on the affected side compared with healthy subjects. On the 'unaffected' side of these patients reflex modulation was similar to that of healthy subjects, but the reflex size during gait was not significantly different from standing control values. These observations suggest that the mechanisms responsible for the depression of reflex size and the modulation normally seen during gait in healthy subjects are impaired to different extents in spasticity of spinal or cerebral origin, possibly due to the unilateral preservation of fibre tracts in hemiparesis.

Adolescent↗

Jendrassik maneuver vs controlled contractions conditioning the excitability of soleus monosynaptic reflexes.

To analyze the factors that influence the conditioning of monosynaptic reflexes by the Jendrassik maneuver, the latter was replaced by a rapid, isolated, reproducible contraction of the wrist extensors; this procedure facilitated reflexes as effectively as the classical Jendrassik maneuver. The results were expressed quantitatively in relation to maximal motor response to allow comparisons to be made when different test reflexes were used. Identical selective contractions produced results that were reproducible in the same subject from one experiment to another. The facilitation depends on the time interval between the onset of the signal to contract and elicitation of the reflex. It develops in 3 distinct phases: the 1st, of moderate intensity, begins before electromyographic activity in the conditioning muscle; the 2nd, of much greater intensity, comes after the beginning of electromyographic activity, rapidly attains a maximum and then decreases progressively; the 3rd phase, of medium intensity, is stable until the end of the contraction. Facilitation also depends on the amplitude of the conditioned reflex and is most marked for one-half the maximum amplitude value and maximum tendon reflexes. The H-reflex is facilitated to the same extent as a tendon reflex of the same amplitude, but only during the 2nd phase. During the 3rd phase, facilitation of the H-reflex is no longer significant, but that of the tendon reflex is. Facilitation of alpha motoneurones may be assumed to explain the increases in amplitude during the 2nd phase but this mechanism alone cannot account for all the phenomena observed.

Adolescent↗

Characteristic appearances of the H-reflex and F-wave with increased stimulus intensity in patients with cerebrovascular disease.

We experienced H-reflex may be evoked with supramaximal stimulation in patients with cerebrovascular disease (CVD). In this study, we investigated the relationship between the characteristic appearances of H-reflex and F-wave with increased stimulus intensity and neurological signs. We examined the H-reflex and F-wave of the affected arm with increased stimulus intensity during muscle relaxation in 31 patients (17 males and 14 females) with hemiparesis caused by CVD. Mean patient age was 56.0 (range 30-82) years. 30 healthy subjects, mean age of 56.2 (range 28-80) were investigated using the same method as controlled group. H-reflex and F-wave with increased stimulus intensity after the median nerve stimulation at the wrist were recorded from the opponence pollicis muscle on the affected side in patients with CVD or right arm in the healthy subjects. Appearance patterns of the H-reflex and F-wave with increased stimulus intensity was separated into four types. Type 1: F-wave appeared with increased stimulus intensity, but there was no H-reflex. Type 2: H-reflex and F-wave both appeared with increased stimulus intensity, but the F-wave followed disappearance of the H-reflex with increased stimulus intensity. Type 3: H-reflex and F-wave both appeared with increased stimulus intensity, but the F-wave appeared during the H-reflex with increased stimulus intensity. Type 4: Only the H-reflex appeared with increased stimulus intensity, but there was no F-wave. Neurological findings including muscle tone and tendon reflex were also evaluated. Findings on muscle tone and tendon reflex were classified into increased (markedly, moderately and slightly), normal and decreased. Results were analyzed as follows; 1) The characteristic appearances of H-reflex and F-wave in the healthy subjects and 2) The relationship between characteristic appearances of waves with increased stimulus intensity and neurological signs in patients with CVD. 1) Pattern of the H-reflex and F-wave with increased stimulus intensity in all healthy subjects were type 1. 2) Patterns of the H-reflex and F-wave with increased stimulus intensity in patients with markedly increased muscle tone and tendon reflex were almost always type 4. Those with moderately increased signs in this parameter demonstrated type 2 or 3. Those with slightly increased signs in this parameter demonstrated type 1 or 2. Those with normal or decreased signs were type 1. These findings suggest that the characteristic appearances of the H-reflex and F-wave was influenced by grade of neurological signs.

Adult↗

[A case of hereditary motor and sensory neuropathy with pyramidal tract sign, optic nerve atrophy and mental retardation].

The patient was a 61-year-old man who suffered from gait disturbance since childhood. He also had mental retardation. Gait disturbance was slowly progressive. His mother, sister, brother and son of his sister suffered from gait disturbance. On neurological examination, he showed mental retardation, optic nerve atrophy and neural deafness. He also showed severe muscle atrophy and weakness of bilateral lower limbs associated with pes cavus. Muscle tonus of lower limbs and patellar tendon reflex were increased bilaterally. Achilles tendon reflex was absent. Babinski and Chaddock signs were positive. Superficial and deep sensations were almost normal. There were no cerebellar signs. Blood chemistry was normal. On nerve conduction studies, motor nerve conduction velocity of the upper limbs was normal and that of the posterior tibial nerve was decreased; right 36.0m/sec, left 29.7m/sec. Sensory nerve conduction velocity of the median nerve was slightly decreased; right 36.5m/sec, left 45.2m/sec and sural nerve did not respond to electric stimuli. On sural nerve biopsy, the density of myelinated fibers was severely decreased. Onion bulb formation was not observed. We classified this case as hereditary motor and sensory neuropathy (HMSN) type II based on nerve conduction studies and findings from sural nerve biopsy. HMSN with pyramidal tract sign has been classified as type V and HMSN with optic nerve atrophy as type VI. This case had characteristic symptoms as type V and VI. Histopathological findings of HMSN type V and VI have not been established yet. This case might provide an important clue for classification of HMSN.

Hereditary Sensory and Motor Neuropathy↗

[A patient with HTLV I-associated myelopathy (HAM) complaining of burning pain on the bilateral feet: a case report].

A 67-year-old man complained of a burning pain and weakness of bilateral feet after contusion of the left lumbar region. Skin as well as bone dystrophy and disturbance of bladder function were not seen, but low skin temperature was observed in the left lower leg. Glove anesthesia was seen on bilateral feet. Patellar tendon reflex was accentuated but Achilles tendon reflex was diminished, and bilateral Babinski sign was positive. Compression of the spinal cord or spinal root nerve was not noticed by MRI, myelography and myelo-CT (from cervical to lumbar level). We suspected the complex regional pain syndrome type I, and performed sympathetic blockade, but burning pain was not relieved. We looked for spinal tumor, myelitis, collagen disease, vitamin deficiency and malignancy but could not find out any disorder. However, the patient had neuropathic sign in electromyogram, and high anti-HTLV-I antibody titers in blood serum (8192x) and cerebrospinal fluid (256x). We diagnosed this case as HTLV I-associated myelopathy (HAM). He developed, so called, HTLV I-associated pneumonia at 74 years of age. We suggest that HAM may rarely accompany a burning pain and neuropathy (not myelopathy) as main symptoms. The present case suggests that a patient with HAM may develop HTLV I-associated pneumonia during its process; indicating a new concept of this very rare disease.

Aged↗

[A case of herpes zoster myelitis improved with acyclovir].

A case of herpes zoster myelitis improved with acyclovir was reported. A 71-year-old female showed a rash over the S2-4 dermatomes on the right side. After that, paraplegia and dysuria progressed. Patellar tendon reflex was exaggerated, but Achilles tendon reflex was normal. Babinski and Chaddock sign were bilaterally elicited. Superficial sense was markedly decreased below the Th12 dermatome. Vibration sense was slightly decreased but position sense was normal on the lower extremities. Cerebrospinal fluid analysis revealed pleocytosis, and an elevation of IgG and varicella-zoster virus antibody titer. Acyclovir (250 mg bid/day) was given for ten days. Paraplegia, sensory disturbance and dyschezia improved but dysuria did not. In this case acyclovir administration was started on the 18th day after the onset of myelopathy. Early initiation of acyclovir treatment might lead to recovery of dysuria. As the pathogenic mechanism of herpes zoster myelitis is considered to be direct viral invasion of the spinal cord with subsequent necrosis, early initiation of acyclovir treatment is necessary for the recovery.

Acyclovir↗

Differential effects of low-frequency depression, vibration-induced inhibition, and posttetanic potentiation on H-reflexes and tendon jerks in the human soleus muscle.

A comparison was made between the effects of repetition rate, muscle vibration, and tetanic stimulation of the tibial nerve on H-reflexes and tendon (T) jerks elicited in the relaxed soleus muscle of normal human. H- and T-reflexes with electromyographic (EMG) potentials of equivalent amplitude were elicited alternately in the same leg to ensure identical experimental conditions. H- and T-reflexes of identical EMG amplitude showed isometric twitch tensions of identical amplitude and time course. H- and T-reflexes were elicited at different repetition rates ranging from once every 6 s to 2/s. H-reflexes showed a significantly stronger low-frequency depression than T-reflexes. Inhibition of H- and T-reflexes was induced by 2-min vibration at 100 Hz of ankle extensors, ankle flexors, or knee flexors. Vibration of ankle extensors and flexors induced a stronger inhibition than vibration of knee flexors. In all three conditions, inhibition of H-reflexes was stronger than inhibition of T-reflexes. The difference was relatively greater during vibration of ankle extensors and flexors than during vibration of knee flexors. When tested together, the effects of low-frequency depression and vibration-induced inhibition of H- and T-reflexes were found to be independent if reflex amplitudes were expressed as a percentage of the control reflex amplitude. The cessation of vibration of ankle extensors was followed by a gradual recovery of H-reflexes from inhibition. On the contrary, T-reflexes showed a marked potentiation. Such postvibratory effects were generally not observed following vibration of ankle or knee flexors. When postvibratory effects were tested during low-frequency depression, percent postvibratory depression of H-reflexes and percent postvibratory potentiation of T-reflexes were found to be independent of the degree of low-frequency depression. Tetanic stimulation of the tibial nerve for 20 s at 200 Hz resulted in posttetanic potentiation (PTP) of H- and T-reflexes, the former being stronger than the latter. The extent of the changes in H- and T-reflex EMG amplitudes, due to changes in repetition rate, vibration, or tetanic stimulation, was generally inversely related to the intensity of the electrical or mechanical reflex stimuli. The observed discrepancies between the induced changes in H- and T-reflex amplitudes are interpreted in terms of the differences in afferent inputs between the two reflexes that were suggested by Burke and his colleagues (9-11).(ABSTRACT TRUNCATED AT 400 WORDS)

Adolescent↗

[Tonic pupil and tendon areflexia: the Holmes-Adie's syndrome].

The Holmes-Adie syndrome (HAS) is characterised by initially monolateral, then bilateral enlargement of the pupil with delayed responses to near vision and subsequent redilation, and absent tendon reflexes. The diameter of the affected pupil is oval or irregular, sometimes with spontaneous movements of the pupillary sphincter muscle. Reaction to light may require several minutes' exposure to bright light, as it does redilation after a prolonged stay in a dark room. The reaction to near vision is tonic and delayed, as the subsequent redilation. In 10% of cases there is a permanent failure of the pupil to react either to light or to near vision. Absence of deep tendon reflexes is acquired and permanent, most frequently involving the Achilles' tendon reflex. Loss of different degrees of ciliary and spinal ganglia neurons, without evidence of inflammatory findings, are the neuropathological data accounting for the clinical signs of HAS. Polyneuropathies of different origin can be complicated by a symptomatic form of HAS.

Adie Syndrome↗

Is lower leg proprioception essential for triggering human automatic postural responses?

It is unknown to what extent automatic postural responses are triggered by lower leg proprioception. This issue was addressed by studying postural control in five carefully selected patients with subtle diabetic polyneuropathy (restricted to the lower legs) and 15 healthy subjects. All patients had bilaterally absent Achilles tendon reflexes and weak or absent patella tendon reflexes, but muscle strength was fully preserved. Subjects were tested while standing on a supporting, movable force-plate. The contribution of lower leg proprioception to automatic postural responses was investigated by randomly exposing the subjects to either a 4 degrees 'toe-up' rotational perturbation ('normal ankle input'), a simultaneous 4-cm rearward translation and 4 degrees toe-up rotation ('enhanced ankle input'), or a simultaneous 4-cm rearward translation and 4 degrees 'toe-down' rotation ('nulled ankle input'). We recorded surface EMG (stretch reflexes and balance-correcting responses) from leg and trunk muscles, ankle torque and angular velocities of the upper and lower legs and trunk. We argued that automatic postural responses that have abnormally small amplitudes in patients and are modulated in controls with the velocity of different types of ankle rotations must receive a major input from lower leg proprioception. Conversely, automatic postural responses that are weakly modified in amplitude or onset by different ankle perturbations and are present despite nulled ankle inputs and, finally, are unaffected in patients with distal polyneuropathy must be triggered or modulated by inputs other than from lower leg proprioception. Normal postural synergies and strategies were maintained in patients, although within a given synergy the timing and amplitude of some automatic postural responses were abnormal. A few automatic postural responses appeared to be triggered or modulated by lower leg proprioception. Thus, early stretch reflexes in soleus and medial gastrocnemius were severely diminished in patients, while in controls these stretch reflexes were modulated by different ankle perturbations. Furthermore, balance-correcting responses in tibialis anterior were diminished and delayed in patients, while in controls these balance-correcting responses were modulated by different ankle perturbations. Other automatic postural responses were apparently not triggered or modulated by lower leg proprioception, but likely received a major input from more proximal sensory systems. Thus, in both groups prominent balance-correcting responses were present in several muscles (soleus, gastrocnemius, quadriceps, paraspinals and trapezius) during the 'nulled ankle input' condition, where ankle position was stabilised over the first 250 ms. During the 'enhanced ankle input' condition, where prominent ankle dorsiflexion occurred during the first 200 ms, amplitudes of balance-correcting responses were only marginally weaker in patients than in controls. We analysed body segment displacements to unveil the potential nature of proximal triggers for automatic postural responses. As opposed to the 'inverted pendulum' concept of postural control, early movement occurred in the knees, hips and trunk well before the onset of automatic postural responses. For example, during the 'nulled ankle input' condition, the lower leg moved forward with early knee flexion, followed by knee extension. The trunk extended backwards at 80 ms, which was followed by forward flexion. The absent stretch reflex and weaker balance-correcting responses in patients produced changed trunk velocity profiles (mainly a reduced initial backward motion of the trunk), but lower-body segment movements showed no consistent differences between the two groups. Considering these body segment displacements, any automatic postural response with an onset within the first 200 ms could well be triggered by receptors located at the knee, hip or trunk. (ABSTRACT TRUNCATED)

Achilles Tendon↗

Predominant motor symptoms in a 74-year-old man with a small elongation in the spinocerebellar atrophy type 1 gene.

The patient was a 74-year-old man who developed gait and bulbar disturbances, which progressed for several years. His mother and a sister complained of a similar disturbance. On admission, generalized muscle atrophy and weakness were prominent, especially in the distal portions of the legs, with bulbar involvement. The patellar tendon reflexes were retained and the Achilles tendon reflexes were decreased with a positive right Babinski's sign. The ocular movements were restricted in vertical directions and, to a lesser extent, in horizontal directions. Sensory disturbance, ataxia, and extrapyramidal signs were not apparent on admission. A needle electromyogram demonstrated neurogenic changes. The laboratory examination was normal except for elevated blood glucose (320 mg/dL) and creatine kinase (1760 U/L). His general condition deteriorated so rapidly that intractable respiratory distress due to pneumonia led to a fatal outcome. The clinical diagnosis was motor neuron disease, although a familial background and a disturbance in ocular movements might have suggested other possibilities.

Aged↗

A screening test for thyroid function.

The Achilles tendon reflex half relaxation time measurement (ART) has been used by many physicians both as a diagnostic test and for the assessment of progress in thyroid gland malfunction. Reference is made to some results obtained in Melbourne and in other countries using different methods of measurement of the ART for these purposes. In a series of 2064 patients referred to the Shepherd Foundation Centre, the Achilles tendon reflex half relaxation time was measured by means of the SMI Reflexometer and a comparison was made in each case with a laboratory estimation of the T3 resin uptake and T4 total thyroxine iodine and the Free Thyroxine Index (FTI). Reference is made to a survey conducted among referring doctors where opinions were sought as to the clinical usefulness of different tests including the Achilles tendon reflex time measurement.

Achilles Tendon↗

Biomechanic characteristics of patients with spastic and dystonic hypertonia in cerebral palsy.

OBJECTIVE: To determine what biomechanic characteristics of knee joint motion and walking show potential to quantitatively differentiate spasticity and dystonia in cerebral palsy (CP). DESIGN: Descriptive measurement study. SETTING: University hospital. PARTICIPANTS: Seventeen pediatric and adult patients with CP. INTERVENTIONS: Not applicable. MAIN OUTCOME MEASURES: We measured the resistance of the knee joint at different velocities and positions, maximum muscle activation during external motion, amplitude of knee tendon reflexes, maximum isometric flexion and extension torques, velocity of walking, and knee kinematics during the gait cycle. Patients were classified into 2 groups (dystonia or spasticity) if at least 2 of 3 physicians agreed that a prominent component of dystonia was present. RESULTS: Patients with dystonia had a greater degree of co-contraction and an increased resistance to external motion at slow velocities. The tendon reflexes were almost normal in patients with dystonia, whereas they were increased in patients with spasticity. Muscle strength was more impaired in patients with dystonia, probably as a result of greater muscle co-contraction. They also walked slower, with smaller knee ranges of motion, during the stance phase of walking. CONCLUSIONS: The measurement of resistance and of muscle activation during passive motion and tendon reflexes shows potential to differentiate dystonia from spasticity in CP patients with a mixed form of hypertonia. More studies are needed to confirm these results.

Adult↗

Electromechanical analogs of human reflexes.

The conclusion to be drawn from our modeling is that the combined stretch and tendon reflexes alone can endow artificial muscle with a springlike feel as well as give it a baseline tone. In response to questions that motor physiologists often ask as to what variables the system controls, the answer here is clear: the stretch and tendon reflexes act together to maintain both a tension set-point and a length set-point, but in so doing they also give the system a springlike feel because of the existence of a servo error. The main goal of our studies is to understand the integration of reflexes, and thus far we have only begun to explore the two lowest-level spinal reflexes. We are in the process of expanding this work by developing a much more refined arm explicitly modeled after the human arm. This new arm is to be activated by a minimum of 10 muscles, each of which is reflexively driven, and it will allow us to explore the integration of higher-level reflex action such as automatic inhibition of antagonists and facilitation of synergists.

Humans↗

[Familial early onset cerebellar ataxia with hypoalbuminemia].

We describe two brothers with early onset cerebellar ataxia associated with hypoalbuminemia (EOCAH). Choreo-athetoid movements preceded the cerebellar ataxia, and serum pseudocholinesterase elevation preceded the hypoalbuminemia. The parents are first cousins. Patient 1, the 22-year-old elder brother, developed choreoathetoid movements of the neck and extremities at the age of eighteen months. He later developed slowly progressive cerebellar ataxia with decreased tendon reflexes. The choreoathetoid movements ceased at about 16 years of age. A recent examination revealed cerebellar ataxia, action myoclonus of the neck and upper limbs, diminished tendon reflexes, mild sensory disturbance in the lower extremities, and very slight amyotrophy of the feet. Patient 2, the 18-year-old younger brother, developed choreo-athetoid movements at the age of 6 years, followed by slowly progressive cerebellar ataxia with disminished tendon reflexes. No scoliosis, ECG abnormalities, or edema was detected. Serum biochemistry studies revealed elevated pseudocholinesterase (6,226 to 2,390 IU) in the patient's early teens. Serum albumin levels tended to be low (3.7 to 4.1 g/dl). Serum triglyceride and beta-lipoprotein levels were elevated in the patients' late teens. Genetic studies showed slight linkage of D9S15. The maximum lod score was 0.289 (recombination fraction rate was 0.14).

Adolescent↗

Attenuated dynamic responses of primary endings of muscle spindles: a basis for depressed tendon responses in acrylamide neuropathy.

Depressed or lost tendon reflexes commonly observed in patients with peripheral neuropathies may result partly from attenuation of the dynamic discharge from the primary endings of muscle spindles. This possibility was investigated in cats with an experimental neuropathy induced with acrylamide (30 mg/kg/day intramuscularly). Achilles tendon reflexes and the dynamic discharge from primary muscle spindles were evaluated after five or ten injections of acrylamide. After five injections the animals were moderately impaired neurologically, the Achilles tendon reflex was difficult to elicit in 2 of 5 animals, and the dynamic responses of primary endings of soleus muscle spindles to stretch were depressed. Following ten injections of acrylamide the cats were severely impaired neurologically; tendon responses were either absent or difficult to elicit, and the dynamic responses of their muscle spindles to stretch were reduced by 50% (p less than 0.01). Additionally, the spindels responded to stretch with only 20 to 30% the normal number of afferent impulses. These data suggest that lost tendon responses in acrylamide neuropathy result in part from inadequate activation of motoneurons by spindle afferent discharge.

Acrylamides↗

[The Miller-Fisher syndrome (clinical report)].

The authors present a case report of two female patients, aged 16 and 33. Both patients had the same sudden onset of illness, with diplopia and nystagmus and very severe ataxia. The younger patient had absent tendon reflex, while the older one had the tendon reflex preserved. The younger patient had the triparesis present, both patients had no sphincter disorders. They did not have sensibility disturbances, except that the younger patient had hypesthesia of the soft palate (the motor function was preserved). The first patient was somnolent at the beginning. The clinical course being favourable, the younger patient recovered faster than the older one. Electoencephalogram was normal in both patients. CT of the brain was changed at one moment, locking like inflammatory changes. CSF of the younger patient, done twice, was normal. Serologic findings on viruses were normal. Electromyography in both patients showed, beside good motor velocity, the marked sensory velocity which recovered at the control check-ups. The authors present these two cases and they consider the differential-diagnostic difficulties of Fisher's syndrome compared to "brain stem encephalitis".

Adolescent↗

Continuous wavelet transform in the evaluation of stretch reflex responses from surface EMG.

OBJECTIVE: This is the first reported use of the continuous wavelet transform (CWT) of the surface EMG (sEMG) to extract the reflex response to muscle stretch. We used a modulus-based method to estimate instantaneous amplitude-envelopes from ridges of the CWT (referred in this work as sEMG intensity) to extract the dynamic reflex response from sEMG. We tested the method on tendon reflexes where excellent temporal resolution is required to identify the different latency components, and on the tonic stretch reflex (tonic SR) response to an ongoing perturbation that characteristically has a low signal to noise ratio. METHODS: Eight subjects without neurological impairment were subjected to a series of archilles tendon taps and a 2 min continuous perturbation of the ankle using a pseudo-sinusoidal stretch profile containing frequencies from 0.1 to 8.0 Hz. The tendon reflexes were assessed in the soleus muscle at 10% of MVC and the tonic SR in tibialis anterior while the muscle was relaxed, at 5 and 10% of maximal voluntary contraction. Root mean square (RMS) and wavelet ridge extraction was applied to the sEMG signal to extract sEMG amplitudes (RMS) and intensities for all reflexes. To obtain the tonic SR, these estimates and those from the sEMG-RMS were subsequently cross-correlated with the perturbation record to yield 2 sets of estimates of reflex gain and coherence for comparison. RESULTS: The sEMG intensities were highly correlated with the torques resulting from a ramped voluntary contraction. Following tendon taps, the method resolved the M1, M2, M3 response components at accurate latencies and with more complete reconstruction of the components than RMS-derived estimates. The wavelet ridge estimates extracted the tonic SR from resting and contracting muscles with significantly higher coherence than RMS estimates. Reflex gain, when estimated from sEMG intensity or sEMG-RMS, demonstrated similar relationships to the perturbation frequency and background contraction level. When the sEMG intensity reflex gain estimates from different subjects were pooled, they showed significantly lower variance about the mean than gain estimates derived from the rectified sEMG. CONCLUSIONS: Wavelet-ridge extraction provides a valid approach to reflex evaluation from sEMG that does not depend on the absolute amplitude of the potentials measured at the EMG electrodes. This may have substantial advantages in more directly comparing responses between subjects on an absolute frequency scale without the need for normalisation against maximal contraction levels.

Electromyography↗

Modulation of the biceps femoris tendon jerk reflex during human locomotion.

During gait it is generally accepted that there is a reduction in amplitude of H-reflexes as compared to standing. For short-latency stretch reflexes, however, it is less clear whether a similar reduction in reflex gain is present during locomotion. Stretches of constant amplitude are hard to produce under these circumstances and for this reason some previous studies on the biceps femoris (BF) have used "reduced gait" in which the stimulated leg is stepping on the spot while the contralateral leg is walking on a treadmill. With this method it was possible to show that BF tendon jerk reflexes are larger at end swing and therefore are likely to contribute to the EMG burst normally occurring in that part of the step cycle when the BF is rapidly stretched. In the present study two questions were addressed: first, whether the reflex is different in size during gait compared to standing and, second, whether it is modulated in size during the gait cycle not only during reduced but also during normal gait. It was found that during both types of gait there was a general reflex depression with regard to the respective control values obtained during standing at similar EMG activity levels. In previous studies on soleus and quadriceps, discrepancies between EMG activity and reflex amplitude have been ascribed to changes in presynaptic inhibition of Ia terminals mediating the afferent volley of the reflex. Based on the data presented, this may also be true for the BF. In both normal and reduced gait the reflex was similarly modulated in size, showing a maximum at the end of swing. This similarity implies that reduced gait may be useful as an acceptable alternative for normal gait in studies on phase-dependent reflex modulation during locomotion.

Adult↗