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Spinal Cord and Reflexes
Published in Nassir H. Sabah, Neuromuscular Fundamentals, 2020
The H-reflex, or Hoffmann reflex, is elicited by electrical stimulation of a muscle nerve, as illustrated in Figure 11.12. As the stimulus strength is increased from a low level, the largest Ia sensory fibers are stimulated first. This is because the largest fibers have the smallest internal resistance; so, for a given voltage stimulus applied externally to the mixed nerve, the voltage across the axonal membrane of the largest-diameter fibers will reach threshold first (Section 4.3.1). Two APs will be generated in the vicinity of the cathode-stimulating electrode and will travel in opposite directions (Figure 11.12a, top of diagram). The AP that reaches the sensory endings of the primary afferents will simply depolarize these endings temporarily and is extinguished (left-pointing dashed arrow). The AP that travels along an Ia fiber to the spinal cord reaches the synapse of this fiber on an α-motoneuron of the homonymous muscle. The APs generated in the α-motoneurons by the excited Ia fibers will travel along the axons of the α-motoneurons to the muscle, causing it to contract. The EMG recorded is the H-response, illustrated in the top trace of Figure 11.12b. The response shown has a latency of about 20 ms. Of this, about 0.5 ms is the delay at the synapse between the Ia fibers and the α-motoneurons, the rest being propagation time of the APs along the Ia fibers and the axons of the α-motoneurons. When the stimulus strength is large enough to excite all the Ia fibers in the nerve, the H-response reaches its maximum.
Clinical Management of Spasticity and Contractures in Stroke
Published in Anand D. Pandyan, Hermie J. Hermens, Bernard A. Conway, Neurological Rehabilitation, 2018
Judith F. M. Fleuren, Jaap H. Buurke, Alexander C. H. Geurts
With neurophysiological measurement methods, electrical activity of involved muscles is measured. The use of the Hoffmann reflex, the electrical equivalent of the mechanical tendon reflex, has been studied extensively (Voerman et al., 2005). The same accounts for some other electrically elicited reflexes. However, their clinical relevance is limited. The use of surface electromyography (sEMG) for the recording of (reflex) muscle activity during functional tasks or during passive movement can be a valuable addition, when applied in a standardised way. The construct validity is potentially good, as it comes close to the definition of spasticity. However, due to large inter- and intra-subject variability, parameters related to intensity of muscle activity cannot be used reliably. Interpretation of data is mainly dependent on timing parameters, which can be compared to available datasets of healthy subjects during a standardised task, such as walking. Timing errors represent any inappropriate phasing of muscle activity. The activity of any muscle may be prolonged or shortened, continuous or absent. Its onset and cessation may be premature or delayed. Each of these phasing errors may alter the pattern of sequential movements during gait (Perry and Burnsfield, 2010). In the case of “overactivity,” the inappropriate timing may be related to altered reflex threshold values, but it can also be related to abnormal efferent drive (De Niet et al., 2011).
The neck
Published in Ashley W. Blom, David Warwick, Michael R. Whitehouse, Apley and Solomon’s System of Orthopaedics and Trauma, 2017
The Hoffmann sign (elicited by flicking the terminal phalanx of the middle or ring finger to elicit the finger flexor response) and the Trömner sign (flexion of the thumb and index finger in response to tapping the volar surface of the distal phalanx of the middle finger held partially flexed between the examiner’s finger and thumb) are established neurological signs for pyramidal response in the upper extremity and are commonly used as clinical neurological examinations for upper motor neuron lesions above the fifth or sixth cervical segments of the spinal cord. Hyperreflexia and the Hoffmann reflex have the highest sensitivity in patients with cervical myelopathy. These pathognomonic pyramidal signs may be absent in approximately one-fifth of myelopathic patients, but their prevalence is correlated with the severity of myelopathy.
Relationship between soleus H-reflex asymmetry and postural control in multiple sclerosis
Published in Disability and Rehabilitation, 2022
Gregory S. Cantrell, David J. Lantis, Michael G. Bemben, Chris D. Black, Daniel J. Larson, Gabriel Pardo, Cecilie Fjeldstad-Pardo, Rebecca D. Larson
The Hoffmann reflex (H-reflex) is an electrical stimulation-induced analogue of the monosynaptic reflex elicited by activation of group Ia sensory fibers [12]. Maximal H-reflex amplitude (Hmax) compared with maximal motor response (Mmax) resulting from direct activation of alpha-motor neurons has been previously used to assess spinal excitability of motor neurons. Moreover, the soleus H-reflex is one of the more commonly studied reflexes in spinal excitability investigations, due to the convenient accessibility of the tibial nerve [12,13], and was of interest in the present study due to its role in posture. While the soleus H-reflex has been assessed in people with MS [5,14], it has not yet been compared between legs, nor has a potential link between soleus H-reflex asymmetry and postural stability in people with MS been evaluated. Therefore, supported by previous research demonstrating bilateral asymmetries in people with MS, the purpose of this study was to test the hypotheses that the soleus H-reflex differs between legs in people with MS, and soleus H-reflex asymmetry is associated with postural control.
Limb Segment Load Inhibits the Recovery of Soleus H-Reflex After Segmental Vibration in Humans
Published in Journal of Motor Behavior, 2018
Shih-Chiao Tseng, Richard K. Shields
A major focus of translational regenerative research is to advance the understanding of tissue response to environmental mechanical stimuli. Mechanical oscillation (i.e., vibration) has been used to study neural and musculoskeletal adaptations in a range of people; from athletes to individuals with CNS damage from spinal cord injury (SCI) (Gilsanz et al., 2006; Iwamoto, Takeda, Sato, & Uzawa, 2005; Torvinen et al., 2003; Verschueren et al., 2004; Ward et al., 2004). Early studies have shown that vibrating directly over a muscle tendon will produce inhibitory effects on the Hoffmann reflex (H-reflex) (De Gail, Lance, & Neilson, 1966; Fromm & Noth, 1976; Hultborn, Meunier, Pierrot-Deseilligny, & Shindo, 1987; Lance, 1966; Lance, Degail, & Neilson, 1966; Rymer & Hasan, 1981). The inhibitory effect induced by direct tendon vibration is attributed to presynaptic inhibition, the refractory state of Ia afferent fibers, neuronal transmitter depletion at Ia terminals, postsynaptic reciprocal and nonreciprocal Ia inhibition, and effects from cutaneous and other afferent receptors (Stein, 1995).
Identification of an A4V SOD1 mutation in a Chinese patient with amyotrophic lateral sclerosis without the A4V founder effect common in North America
Published in Amyotrophic Lateral Sclerosis and Frontotemporal Degeneration, 2018
Lu Tang, Yan Ma, Xiaolu Liu, Lu Chen, Dongsheng Fan
In this study, we present the first report of a non-Caucasian ALS patient carrying the missense mutation A4V in SOD1 gene. The patient manifested with a typical SOD1-A4V phenotype, which includes aggressive disease progression and predominant involvement of the lower motor neurons. Patients carrying A4V mutations usually have an average survival of 1.4 years, shorter than the 3–5 years in other dominant SOD1 mutations. Of note, when deep tendon reflexes in upper limbs were normal but the same myotomes were wasted, it could be possible that it was apparently “normal” but indicative of upper motor neurons lesion. However, with the negative Hoffmann’s reflex and normal muscle tone in upper limbs, we would prefer to regard it as normal without involvement of upper motor neurons. It is highly likely that this short survival duration is responsible for the fact that despite its severe effect on lower motor neurons, little or no upper motor neuron sign is observed in patients with A4V (10) and A4T (8) mutations.