Let's change deep tendon reflex to muscle stretch reflex

2015 ◽  
Vol 52 (6) ◽  
pp. 1140-1140 ◽  
Author(s):  
Randall L. Braddom
2008 ◽  
Vol 08 (01) ◽  
pp. 75-85 ◽  
Author(s):  
ROBERT LEMOYNE ◽  
FOAD DABIRI ◽  
ROOZBEH JAFARI

The deep tendon reflex is a fundamental aspect of neurological examinations. The severity of and degree of recovery from a traumatic brain injury can be assessed by the myotatic stretch reflex. A hyperactive reflex response is correlated with spasticity, which can also be correlated with the degree of damage to the supraspinal input, in essence assessing the severity of traumatic brain injury. The myotatic stretch reflex is clinically evaluated by the National Institute of Neurological Disorders and Stroke (NINDS) reflex scale (0–4); however, this scale lacks temporal data and may also vary in interpretation. The solution is a fully quantified evaluation system of the myotatic stretch reflex, whereby a patellar hammer's force input is based on original potential energy and a microelectromechanical system (MEMS) accelerometer quantifies the output. The MEMS accelerometer is attached to a set anchor point near the ankle. The reflex amplitude is based on the maximum acceleration of the reflex response. The quantified data collected from MEMS accelerometers are transmitted by a portable computer (i.e. a Pocket PC). This paper describes a device that quantitatively evaluates the reflex response using accelerometers and that demonstrates precision for reproducibility.


2011 ◽  
Vol 11 (03) ◽  
pp. 471-513 ◽  
Author(s):  
ROBERT LEMOYNE ◽  
TIMOTHY MASTROIANNI ◽  
CRISTIAN COROIAN ◽  
WARREN GRUNDFEST

The deep tendon reflex is a fundamental aspect of a neurological examination. The two major parameters of the tendon reflex are response and latency, which are presently evaluated qualitatively during a neurological examination. The reflex loop is capable of providing insight into the status and therapy response of both upper and lower motor neuron syndromes. Attempts have been made to ascertain reflex response and latency; however, these systems are relatively complex, resource intensive, with issues of consistent and reliable accuracy. The solution presented is a wireless quantified reflex device using tandem three-dimensional (3D) wireless accelerometers to obtain response based on acceleration waveform amplitude and latency derived from temporal acceleration waveform disparity. Three specific aims have been established for the proposed wireless quantified reflex device: (1) Demonstrate the wireless quantified reflex device is reliably capable of ascertaining quantified reflex response and latency using a quantified input. (2) Evaluate the precision of the device using an artificial reflex system. (3) Conduct a longitudinal study respective of subjects with healthy patellar tendon reflexes, using the wireless quantified reflex evaluation device to obtain quantified reflex response and latency. Aim 1 has led to a steady evolution of the wireless quantified reflex device from a singular 2D wireless accelerometer capable of measuring reflex response to a tandem 3D wireless accelerometer capable of reliably measuring reflex response and latency. The hypothesis for aim 1 is that a reflex quantification device can be established for reliably measuring reflex response and latency for the patellar tendon reflex, comprised of an integrated system of wireless 3D MEMS accelerometers. Aim 2 further emphasized the reliability of the wireless quantified reflex device by evaluating an artificial reflex system. The hypothesis for aim 2 is that the wireless quantified reflex device can obtain reliable reflex parameters (response and latency) from an artificial reflex device. Aim 3 synthesizes the findings relevant to aim 1 and 2, while applying the wireless accelerometer reflex quantification device to a longitudinal study of healthy patellar tendon reflexes. The hypothesis for aim 3 is that during a longitudinal evaluation of the deep tendon reflex the parameters for reflex response and latency can be measured with a considerable degree of accuracy, reliability, and reproducibility. Enclosed is a detailed description of a wireless quantified reflex device with research findings and potential utility of the system, inclusive of a comprehensive description of tendon reflexes, prior reflex quantification systems, and correlated applications.


2014 ◽  
Vol 46 (3) ◽  
pp. 600-609 ◽  
Author(s):  
ELLEN CASEY ◽  
FARAH HAMEED ◽  
YASIN Y. DHAHER

1978 ◽  
Vol 32 (1) ◽  
pp. 109-113
Author(s):  
Hitoka Doi ◽  
Yoshiyuki Murai ◽  
Yoshigoro Kuroiwa

1980 ◽  
Vol 38 (1) ◽  
pp. 51-61 ◽  
Author(s):  
W. Koehler ◽  
U. Windhorst

2021 ◽  
Vol 15 ◽  
Author(s):  
Rui Wu ◽  
He Lv ◽  
Hui Wang ◽  
Zhaoxia Wang ◽  
Yun Yuan

ObjectivesMitofusin 2 and ganglioside-induced differentiation-associated protein 1 are two main mitochondrial dynamics-related proteins. Dysfunction of these two proteins leads to different subtypes of Charcot–Marie–Tooth disease type 2A (CMT2A) and CMT2K. This study aims to report the pathological difference between CMT2A and CMT2K in a large cohort.MethodsThirty patients with molecularly confirmed CMT2A and nine with CMT2K were identified by next-generation sequencing. Sural nerve biopsies were performed in 29 patients.ResultsThe patients with both diseases showed length-dependent neuropathy with distal weakness, sensory loss, and no deep tendon reflex. Optic neuropathy appeared in 3/30 (10%) patients with CMT2A. Tendon contracture appeared in 4/9 (50.0%) patients with CMT2K. Sural biopsy revealed the loss of both myelinated and unmyelinated nerve fibers. Closely packed, irregularly oriented neurofilaments were observed in axons of unmyelinated nerve fibers in both diseases. Another important finding was the ubiquitous presence of smaller, rounded, and fragmented mitochondria in CMT2A and elongated mitochondria in CMT2K in the myelinated and unmyelinated axons.ConclusionThis study confirmed large diversity in phenotypes between CMT2A and CMT2K. Mitochondrial dynamics-related variations can induce different mitochondrial morphological changes and neurofilament accumulation in axons.


Author(s):  
Uma Datta Gupta ◽  
Tutul Chowdhury

Friedrich's ataxia is a progressive neurodegenerative disease that affects the posterior cord of the spinal tract. We present a case of an 83-year-old male with resting tremor and rigidity that had gradually worsened over the past few years. The patient has been diagnosed with Friedrich's ataxia. Unlike typical Friedrich ataxia, this patient does not have a shortened life expectancy. There is a small percentage of atypical patients demonstrate late-onset of disease, isolated spastic paraparesis without ataxia, and retained or exacerbated deep tendon reflex. Although there is no association between Parkinson's disease and Friedrich's ataxia; in our case, treatment of tremor and rigidity improves the patient's quality of life. 


Author(s):  
Adam Fisch

Chapter 8 discusses the nerve physiology of the spinal canal and muscle, including the muscle stretch reflex, advanced muscle-nerve physiology, and nerve roots and rami.


Sign in / Sign up

Export Citation Format

Share Document