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Annals of Physical and Rehabilitation... Jan 2021Functional electrical stimulation (FES) applied to the paretic peroneal nerve has positive clinical effects on foot drop secondary to stroke. (Meta-Analysis)
Meta-Analysis Review
BACKGROUND
Functional electrical stimulation (FES) applied to the paretic peroneal nerve has positive clinical effects on foot drop secondary to stroke.
OBJECTIVE
To evaluate the effectiveness of FES applied to the paretic peroneal nerve on gait speed, active ankle dorsiflexion mobility, balance, and functional mobility.
METHODS
Electronic databases were searched for articles published from inception to January 2020. We included randomized controlled trials or crossover trials focused on determining the effects of FES combined or not with other therapies in individuals with foot drop after stroke. Characteristics of studies, participants, comparison groups, interventions, and outcomes were extracted. Statistical heterogeneity was assessed with the I statistic.
RESULTS
We included 14 studies providing data for 1115 participants. FES did not enhance gait speed as compared with conventional treatments (i.e., supervised/unsupervised exercises and regular activities at home). FES combined with supervised exercises (i.e., physiotherapy) was better than supervised exercises alone for improving gait speed. We found no effect of FES combined with unsupervised exercises and inconclusive effects when FES was combined with regular activities at home. When FES was compared with conventional treatments, it improved ankle dorsiflexion, balance and functional mobility, albeit with high heterogeneity for these last 2 outcomes.
CONCLUSIONS
This meta-analysis revealed low quality of evidence for positive effects of FES on gait speed when combined with physiotherapy. FES can improve ankle dorsiflexion, balance, and functional mobility. However, considering the low quality of evidence and the high heterogeneity, these results must be interpreted carefully.
Topics: Electric Stimulation Therapy; Gait Disorders, Neurologic; Humans; Peroneal Nerve; Physical Therapy Modalities; Stroke; Stroke Rehabilitation; Walking Speed
PubMed: 32376404
DOI: 10.1016/j.rehab.2020.03.012 -
Orthopedic Reviews 2021Peroneal neuropathy is the most common compressive neuropathy of the lower extremity. It should be included in the differential diagnosis for patients presenting with... (Review)
Review
Peroneal neuropathy is the most common compressive neuropathy of the lower extremity. It should be included in the differential diagnosis for patients presenting with foot drop, the pain of the lower extremity, or numbness of the lower extremity. Symptoms of peroneal neuropathy may occur due to compression of the common peroneal nerve (CPN), superficial peroneal nerve (SPN), or deep peroneal nerve (DPN), each with different clinical presentations. The CPN is most commonly compressed by the bony prominence of the fibula, the SPN most commonly entrapped as it exits the lateral compartment of the leg, and the DPN as it crosses underneath the extensor retinaculum. Accurate and timely diagnosis of any peroneal neuropathy is important to avoid progression of nerve injury and permanent nerve damage. The diagnosis is often made with physical exam findings of decreased strength, altered sensation, and gait abnormalities. Motor nerve conduction studies, electromyography studies, and diagnostic nerve blocks can also assist in diagnosis and prognosis. First-line treatments include removing anything that may be causing external compression, providing stability to unstable joints, and reducing inflammation. Although many peroneal nerve entrapments will resolve with observation and activity modification, surgical treatment is often required when entrapment is refractory to these conservative management strategies. Recently, additional options including microsurgical decompression and percutaneous peripheral nerve stimulation have been reported; however, large studies reporting outcomes are lacking.
PubMed: 34745471
DOI: 10.52965/001c.24937 -
Deutsches Arzteblatt International May 2019Foot drop can be caused by a variety of diseases and injuries. Although it is a common condition, its overall incidence has not been reported to date. Foot drop markedly... (Review)
Review
BACKGROUND
Foot drop can be caused by a variety of diseases and injuries. Although it is a common condition, its overall incidence has not been reported to date. Foot drop markedly restricts the everyday activities of persons suffering from it. There is, therefore, a need for an optimized strategy for its diagnosis and treatment that would be standardized across the medical specialties encountering patients with this problem.
METHODS
This article consists of a review on the basis of pertinent publications re- trieved by a search in the Pubmed/MEDLINE and Cochrane databases, as well as a description of the authors' proposed strategy for the diagnosis and treatment of foot drop.
RESULTS
Foot drop can be due to a disturbance at any central or peripheral location along the motor neural pathway that terminates in the dorsiflexor muscles of the foot, or at multiple locations in series. Optimal localization of the lesion(s) is a pre- requisite for appropriate treatment and a successful outcome. The most common causes are L5 radiculopathy and peroneal nerve injury. An operation by a neuro- surgeon or spinal surgeon is a reasonable option whenever there is a realistic chance that the nerve will recover. In our opinion, any patient with a subjectively disturbing foot drop and a clinically suspected compressive neuropathy of the peroneal nerve should be informed about the option of surgical decompression of the nerve at the fibular head, which can be performed with little risk. In case of a permanent foot drop, some patients can benefit from muscle-transfer surgery. For spastic foot drop, the option of botulinum toxin injections should be evaluated.
CONCLUSION
The care of patients with foot drop could be optimized by interdisciplin- ary foot-drop clinics involving all of the relevant specialists. The goals of treatment should always be improved mobility in everyday life and the prevention of falls, pain, and abnormal postures.
Topics: Foot; Gait Disorders, Neurologic; Humans; Peripheral Nerve Injuries; Peroneal Nerve; Peroneal Neuropathies
PubMed: 31288916
DOI: 10.3238/arztebl.2019.0347 -
Nature Communications Nov 2020The lateral parabrachial nucleus (LPBN) is known to relay noxious information to the amygdala for processing affective responses. However, it is unclear whether the LPBN...
The lateral parabrachial nucleus (LPBN) is known to relay noxious information to the amygdala for processing affective responses. However, it is unclear whether the LPBN actively processes neuropathic pain characterized by persistent hyperalgesia with aversive emotional responses. Here we report that neuropathic pain-like hypersensitivity induced by common peroneal nerve (CPN) ligation increases nociceptive stimulation-induced responses in glutamatergic LPBN neurons. Optogenetic activation of GABAergic LPBN neurons does not affect basal nociception, but alleviates neuropathic pain-like behavior. Optogenetic activation of glutamatergic or inhibition of GABAergic LPBN neurons induces neuropathic pain-like behavior in naïve mice. Inhibition of glutamatergic LPBN neurons alleviates both basal nociception and neuropathic pain-like hypersensitivity. Repetitive pharmacogenetic activation of glutamatergic or GABAergic LPBN neurons respectively mimics or prevents the development of CPN ligation-induced neuropathic pain-like hypersensitivity. These findings indicate that a delicate balance between excitatory and inhibitory LPBN neuronal activity governs the development and maintenance of neuropathic pain.
Topics: Animals; Disease Models, Animal; Excitatory Amino Acid Agonists; Excitatory Postsynaptic Potentials; GABA Agonists; Glutamic Acid; Humans; Hyperalgesia; Inhibitory Postsynaptic Potentials; Male; Mice; Mice, Transgenic; Neural Pathways; Neuralgia; Neurons; Nociception; Optogenetics; Parabrachial Nucleus; Peroneal Nerve; Stereotaxic Techniques; gamma-Aminobutyric Acid
PubMed: 33239627
DOI: 10.1038/s41467-020-19767-w