About: Hoffmann's reflex is a research topic. Over the lifetime, 9 publications have been published within this topic receiving 83 citations. The topic is also known as: Hoffmann's reflex & finger flexor reflex.
TL;DR: The presence of a positive Hoffmann’s reflex in asymptomatic patients strongly suggests underlying cervical pathology, but it does not warrant further evaluation with either cervical radiographs or magnetic resonance imaging since the management and clinical course are not affected by positive studies.
Abstract: Study Design. Asymptomatic patients with a positive Hoffmann’s reflex were prospectively studied with cervical radiographs and magnetic resonance imaging. Objectives. To determine a relationship between a positive Hoffmann’s reflex and cervical pathology in asymptomatic patients and to evaluate if further work-up was necessary in this patient population. Summary of Background Data. A positive Hoffmann’s reflex usually implies an upper motor neuron lesion from spinal cord compression. Although this reflex is commonly tested, the significance of this reflex in asymptomatic patients is not known. Methods. Sixteen patients without cervical pain or radiculopathy and a positive Hoffmann’s reflex were prospectively studied with cervical radiographs and magnetic resonance imaging. Positive findings were correlated with a detailed neurologic examination. Results. All 16 patients were asymptomatic. Fourteen patients (87.5%) demonstrated spondylosis on cervical radiographs. The magnetic resonance imaging studies showed pathologic findings in all 16 patients. Fifteen patients (94%) had cervical involvement with cord compression from a herniated nucleus pulposus. The remaining patient had a T5–T6 thoracic disc with resultant compression. No treatment was instituted, and the clinical course of each patient was not affected. Conclusions. Although the presence of cervical cord impingement is extremely high in these patients, no treatment was rendered specifically to address the cervical pathology. Therefore, the presence of a positive Hoffmann’s reflex in asymptomatic patients strongly suggests underlying cervical pathology, but it does not warrant further evaluation with either cervical radiographs or magnetic resonance imaging since the management and clinical course are not affected by positive studies.
TL;DR: The present study induced photothrombotic injury in the rostral and caudal forelimb motor areas of mice and used the rate-dependent depression of Hoffmann’s reflex (H-reflex) as an indicator of spastic symptoms, suggesting that this is a viable animal model of post-stroke spasticity.
Abstract: Abnormal reflexes associated with spasticity are considered a major determinant of motor impairments occurring after stroke; however, the mechanisms underlying post-stroke spasticity remain unclear. This may be because of the lack of suitable rodent models for studying spasticity after cortical injuries. Thus, the purpose of the present study was to establish an appropriate post-stroke spasticity mouse model. We induced photothrombotic injury in the rostral and caudal forelimb motor areas of mice and used the rate-dependent depression (RDD) of Hoffmann's reflex (H-reflex) as an indicator of spastic symptoms. To detect motoneuron excitability, we examined c-fos mRNA levels and c-Fos immunoreactivity in affected motoneurons using quantitative real-time reverse transcription PCR and immunohistochemical analysis, respectively. To confirm the validity of our model, we confirmed the effect of the anti-spasticity drug baclofen on H-reflex RDDs 1 week post stroke. We found that 3 days after stroke, the RDD was significantly weakened in the affected muscles of stroke mice compared with sham-operated mice, and this was observed for 8 weeks. The c-fos mRNA levels in affected motoneurons were significantly increased in stroke mice compared with sham-operated mice. Immunohistochemical analysis revealed a significant increase in the number of c-Fos-positive motoneurons in stroke mice compared with sham-operated mice at 1, 2, 4, and 8 weeks after stroke; however, the number of c-Fos-positive motoneurons on both sides of the brain gradually decreased over time. Baclofen treatment resulted in recovery of the weakened RDD at 1 week post stroke. Our findings suggest that this is a viable animal model of post-stroke spasticity.
TL;DR: Results suggest that high‐fat feeding increases H‐reflex excitability, and further studies are needed to determine whether these changes alter muscle stretch reflex strength and/or balance.
Abstract: Obesity is associated with balance and motor control deficits. We have recently shown that Group Ia muscle spindle afferents, the sensory arm of the muscle stretch reflex, are less responsive in mice fed a high-fat diet. Here we test the hypothesis that reflex excitability to sensory information from Group Ia muscle spindle afferents is altered in a mouse model of diet-induced obesity. We measured the anesthetized Hoffmann's or H-reflex, the electrical analog of the muscle stretch reflex. Adult mice of both sexes were fed a control diet (CD; 10% kcal from fat) or a high-fat diet (HFD; 60% kcal from fat) for 5, 10, or 15 weeks. We used three quantitative measures of H-reflex excitability: (1) H-reflex latency; (2) the percentage of motor neurons recruited from electrical stimulation of Group Ia muscle spindle afferents (Hmax /Mmax ); and (3) rate-dependent depression (RDD), the decrease in H-reflex amplitude to high frequency stimulation (20 stimuli at 5 Hz). A HFD did not significantly alter H latency (P = 0.16) or Hmax /Mmax ratios (P = 0.06), but RDD was significantly lower in HFD compared to CD groups (P < 0.001). Interestingly, HFD males exhibited decreased RDD compared to controls only after 5 and 10 weeks of feeding, but females showed progressive decreases in RDD that were only significant at 10 and 15 weeks on the HFD. These results suggest that high-fat feeding increases H-reflex excitability. Future studies are needed to determine whether these changes alter muscle stretch reflex strength and/or balance and to determine the underlying mechanism(s).
TL;DR: A case of an asthmatic patient who presented with pulseless electrical activity (PEA) and remained in a comatose state following management and showed diffuse cerebral edema secondary to anoxic brain injury on computed tomography scan.
Abstract: Several guidelines and definitions for brain death have been proposed. The Uniform Determination of Death Act (UDDA) in 1980, the American Academy of Neurology (AAN) guidelines in 1995 and the later update in 2010 have all described standards for diagnosing brain death. As brain death testing became more commonly performed, several abnormal reflexive movements were recognized and led to ambiguities that falsely suggested retained brain function. Movements in the upper extremities have been under-recognized. We report a brain-dead patient with finger flexion in the upper extremities with noxious stimulation and suspect a pathogenesis similar to that of Hoffman's reflex sign. We present a case of an asthmatic patient who presented with pulseless electrical activity (PEA). The patient was managed emergently and subsequently deteriorated to a comatose state. She remained in a comatose state following management and showed diffuse cerebral edema secondary to anoxic brain injury on computed tomography (CT) scan. Subsequent apnea testing, transcranial Doppler studies (TCD) and detailed neurological examinations were performed. She was eventually declared brain dead. On nailbed pressure to her fourth finger, she had flexion of her third finger, similar to the finding of a Hoffman's sign in an upper motor neuron injury. We have described this case in detail and reviewed the literature on abnormal movements in brain-dead patients.