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Journal of Neurology Oct 2021Ataxia is a frequent symptom in neurological cases with many causes. Sensory ataxia (due to involvement of the proprioceptive pathways) is observed in conditions... (Review)
Review
Ataxia is a frequent symptom in neurological cases with many causes. Sensory ataxia (due to involvement of the proprioceptive pathways) is observed in conditions affecting the central nervous system (spinal cord disorder) and the peripheral nervous system (peripheral neuropathy). The latter correspond to what we refer to as 'ataxic neuropathies'. Ataxic neuropathies represent a wide and heterogeneous spectrum of disorders that may affect dorsal root nerves, dorsal root ganglia, nerve trunks, distal nerve endings or all of them together. The identification of a predominant sensory ataxia in a case of peripheral neuropathy should raise the possibility of some specific etiologies. We propose here to present the main causes of ataxic neuropathies, which are identified with diagnostic workflows that are dictated by the topography of the likely sites of lesions in the proprioceptive pathway together with the timing of their occurrence (acute, subacute, or chronic).
Topics: Ataxia; Ganglia, Spinal; Humans; Peripheral Nervous System Diseases; Spinal Nerve Roots
PubMed: 32556571
DOI: 10.1007/s00415-020-09994-y -
CNS Neuroscience & Therapeutics Sep 2019Previous studies have demonstrated that the CXCL12/CXCR4 signaling axis is involved in the regulation of neuropathic pain (NP). Here, we performed experiments to test...
BACKGROUND
Previous studies have demonstrated that the CXCL12/CXCR4 signaling axis is involved in the regulation of neuropathic pain (NP). Here, we performed experiments to test whether the CXCL12/CXCR4 signaling pathway contributes to the pathogenesis of neuropathic pain after spinal nerve ligation (SNL) via central sensitization mechanisms.
METHODS
Neuropathic pain was induced and assessed in a SNL rat model. The expression and distribution of CXCL12 or CXCR4 were examined by immunofluorescence staining and western blot. The effects of CXCL12 rat peptide, CXCL12 neutralizing antibody, CXCR4 antagonist, and astrocyte metabolic inhibitor on pain hypersensitivity were explored by behavioral tests in naive or SNL rats. We measured the expression level of c-Fos and CGRP to evaluate the sensitization of neurons by RT-PCR. The activation of astrocyte and microglia was analyzed by measuring the level of GFAP and iba-1. The mRNA levels of the pro-inflammatory cytokines such as TNF-α, IL-1β, and IL-6 and Connexin 30, Connexin 43, EAAT 1, EAAT 2 were also detected by RT-PCR.
RESULTS
First, we found that the expression of CXCL12 and CXCR4 was upregulated after SNL. CXCL12 was mainly expressed in the neurons while CXCR4 was expressed both in astrocytes and neurons in the spinal dorsal horn after SNL. Moreover, intrathecal administration of rat peptide, CXCL12, induced hypersensitivity in naive rats, which was partly reversed by fluorocitrate. In addition, the CXCL12 rat peptide increased mRNA levels of c-Fos, GFAP, and iba-1. A single intrathecal injection of CXCL12 neutralizing antibody transiently reversed neuropathic pain in the SNL rat model. Consecutive use of CXCL12 neutralizing antibody led to significant delay in the induction of neuropathic pain, and reduced the expression of GFAP and iba-1 in the spinal dorsal horn. Finally, repeated intrathecal administration of the CXCR4 antagonist, AMD3100, significantly suppressed the initiation and duration of neuropathic pain. The mRNA levels of c-Fos, CGRP, GFAP, iba-1, and pro-inflammatory cytokines, also including Connexin 30 and Connexin 43 were decreased after injection of AMD3100, while EAAT 1 and EAAT 2 mRNAs were increased.
CONCLUSION
We demonstrate that the CXCL12/CXCR4 signaling pathway contributes to the development and maintenance of neuropathic pain via central sensitization mechanisms. Importantly, intervening with CXCL12/CXCR4 presents an effective therapeutic approach to treat the neuropathic pain.
Topics: Animals; Benzylamines; Central Nervous System Sensitization; Chemokine CXCL12; Cyclams; Heterocyclic Compounds; Ligation; Male; Neuralgia; Rats; Rats, Sprague-Dawley; Receptors, CXCR4; Signal Transduction; Spinal Cord; Spinal Nerves
PubMed: 30955244
DOI: 10.1111/cns.13128 -
Journal of Neurology Oct 2021The aim of this review was to analyse the pathophysiology of axonal degeneration in Guillain-Barré syndrome (GBS) with emphasis on early stages (≤ 10 days after... (Review)
Review
The aim of this review was to analyse the pathophysiology of axonal degeneration in Guillain-Barré syndrome (GBS) with emphasis on early stages (≤ 10 days after onset). An overview of experimental autoimmune neuritis (EAN) models is provided. Originally GBS and acute inflammatory demyelinating polyneuropathy were equated, presence of axonal degeneration being attributed to a "bystander" effect. Afterwards, primary axonal GBS forms were reported, designated as acute motor axonal neuropathy/acute motor-sensory axonal neuropathy. Revision of the first pathological description of axonal GBS indicates the coexistence of active axonal degeneration and demyelination in spinal roots, and pure Wallerian-like degeneration in peripheral nerve trunks. Nerve conduction studies are essential for syndrome subtyping, though their sensitivity is scanty in early GBS. Serum markers of axonal degeneration include increased levels of neurofilament light chain and presence of anti-ganglioside reactivity. According to nerve ultrasonographic features and autopsy studies, ventral rami of spinal nerves are a hotspot in early GBS. In P-induced EAN models, the initial pathogenic change is inflammatory oedema of spinal roots and sciatic nerve, which is followed by demyelination, and Wallerian-like degeneration in nerve trunks possessing epi-perineurium; a critical elevation of endoneurial fluid pressure is a pre-requisite for inducing ischemic axonal degeneration. Similar lesion topography may occur in GBS. The repairing role of adaxonal Schwann cytoplasm in axonal degeneration is analysed. A novel pathophysiological mechanism for nerve trunk pain in GBS, including pure motor forms, is provided. The potential therapeutic role of intravenous boluses of methylprednisolone for early severe GBS and intractable pain is argued.
Topics: Axons; Guillain-Barre Syndrome; Humans; Neuralgia; Sciatic Nerve; Spinal Nerves
PubMed: 32607643
DOI: 10.1007/s00415-020-10034-y -
Current Opinion in Urology Jul 2020To provide an overview of available electrical stimulation devices in neurogenic patients with lower urinary tract disease. (Review)
Review
PURPOSE OF REVIEW
To provide an overview of available electrical stimulation devices in neurogenic patients with lower urinary tract disease.
RECENT FINDINGS
It is advocated to do more studies in neurogenic patients as results seem promising and useful but most studies did not include neurogenic patients or neurogenic patients were not analyzed or reported separately. Most studies included a small heterogenous neurogenic group with multiple pathophysiologic origin focusing on effect of a treatment instead of results of a treatment in a specific neurogenic group. Neuromodulation or stimulation has the advantage that it acts on different organs, like bladder and bowel, so can treat neurogenic patients, who mostly suffer from multiple organ failure.
SUMMARY
Brindley procedure, sacral neuromodulation (SNM) and posterior tibial nerve stimulation (PTNS) are available for a while already. The Brindley procedure (including sacral anterior root stimulation in combination with a rhizotomy of posterior sacral roots) is developed for selected spinal cord injury patient with a complete spinal injury, and has shown results for many years in neurogenic patients. An alternative to the rhizotomy is not established yet. SNM and PTNS are other modalities that are used in nonneurogenic patients, but are not yet indicated and much studied in neurogenic patients.
Topics: Denervation; Electric Stimulation; Electric Stimulation Therapy; Humans; Implantable Neurostimulators; Lower Urinary Tract Symptoms; Rhizotomy; Sacrococcygeal Region; Spinal Nerve Roots; Tibial Nerve; Urinary Bladder; Urinary Bladder, Neurogenic
PubMed: 32427629
DOI: 10.1097/MOU.0000000000000773 -
Handbook of Clinical Neurology 2024The femoral and obturator nerves both arise from the L2, L3, and L4 spinal nerve roots and descend into the pelvis before emerging in the lower limbs. The femoral... (Review)
Review
The femoral and obturator nerves both arise from the L2, L3, and L4 spinal nerve roots and descend into the pelvis before emerging in the lower limbs. The femoral nerve's primary function is knee extension and hip flexion, along with some sensory innervation to the leg. The obturator nerve's primary function is thigh adduction and sensory innervation to a small area of the medial thigh. Each may be injured by a variety of potential causes, many of them iatrogenic. Here, we review the anatomy of the femoral and obturator nerves and the clinical features and potential etiologies of femoral and obturator neuropathies. Their necessary investigations, including electrodiagnostic studies and imaging, their prognosis, and potential treatments, are discussed in this chapter.
Topics: Humans; Obturator Nerve; Peripheral Nervous System Diseases; Femoral Nerve; Femoral Neuropathy
PubMed: 38697739
DOI: 10.1016/B978-0-323-90108-6.00007-7 -
Neuromodulation : Journal of the... Feb 2024Functional gastrointestinal disorders (FGIDs) are common, and they severely impair an individual's quality of life. The mechanism of pathogenesis and the effective... (Review)
Review
INTRODUCTION
Functional gastrointestinal disorders (FGIDs) are common, and they severely impair an individual's quality of life. The mechanism of pathogenesis and the effective treatments for FGIDs remain elusive. Neuromodulation-a relatively new treatment-has exhibited a good therapeutic effect on FGIDs, although there are different methods for different symptoms of FGIDs.
MATERIALS AND METHODS
We used PubMed to review the history of neuromodulation for the treatment of FGIDs and to review several recently proposed neuromodulation approaches with improved effects on FGIDs.
CONCLUSION
Electroacupuncture, transcutaneous electroacupuncture, transcutaneous auricular vagal nerve stimulation, sacral nerve stimulation (SNS) (which relies on vagal nerve stimulation), and gastric electrical stimulation (which works through the modulation of slow waves generated by the interstitial cells of Cajal), in addition to the noninvasive neurostimulation alternative approach method of SNS-tibial nerve stimulation and transcutaneous electrical stimulation (which is still in its infancy), are some of the proposed neuromodulation approaches with improved effects on FGIDs. This review has discussed some critical issues related to the selection of stimulation parameters and the underlying mechanism and attempts to outline future research directions backed by the existing literature.
Topics: Humans; Quality of Life; Transcutaneous Electric Nerve Stimulation; Gastrointestinal Diseases; Vagus Nerve Stimulation; Spinal Nerves
PubMed: 37690016
DOI: 10.1016/j.neurom.2023.08.001 -
Cells Jul 2021Complete spinal cord injury (SCI) leads to permanent motor, sensitive and sensory deficits. In humans, there is currently no therapy to promote recovery and the only... (Review)
Review
Complete spinal cord injury (SCI) leads to permanent motor, sensitive and sensory deficits. In humans, there is currently no therapy to promote recovery and the only available treatments include surgical intervention to prevent further damage and symptomatic relief of pain and infections in the acute and chronic phases, respectively. Basically, the spinal cord is classically viewed as a nonregenerative tissue with limited plasticity. Thereby the establishment of the "glial" scar which appears within the SCI is mainly described as a hermetic barrier for axon regeneration. However, recent discoveries have shed new light on the intrinsic functional plasticity and endogenous recovery potential of the spinal cord. In this review, we will address the different aspects that the spinal cord plasticity can take on. Indeed, different experimental paradigms have demonstrated that axonal regrowth can occur even after complete SCI. Moreover, recent articles have demonstrated too that the "glial" scar is in fact composed of several cellular populations and that each of them exerts specific roles after SCI. These recent discoveries underline the underestimation of the plasticity of the spinal cord at cellular and molecular levels. Finally, we will address the modulation of this endogenous spinal cord plasticity and the perspectives of future therapeutic opportunities which can be offered by modulating the injured spinal cord microenvironment.
Topics: Animals; Humans; Nerve Regeneration; Neural Stem Cells; Neuroglia; Neuronal Plasticity; Phenotype; Recovery of Function; Spinal Cord; Spinal Cord Injuries; Spinal Nerves
PubMed: 34440655
DOI: 10.3390/cells10081886 -
Physiological Reports Feb 2021This article aims to review studies that have investigated the role of neurons that use the transmitter acetylcholine (ACh) in controlling the operation of locomotor... (Review)
Review
This article aims to review studies that have investigated the role of neurons that use the transmitter acetylcholine (ACh) in controlling the operation of locomotor neural networks within the spinal cord. This cholinergic system has the particularity of being completely intraspinal. We describe the different effects exerted by spinal cholinergic neurons on locomotor circuitry by the pharmacological activation or blockade of this propriospinal system, as well as describing its different cellular and subcellular targets. Through the activation of one ionotropic receptor, the nicotinic receptor, and five metabotropic receptors, the M1 to M5 muscarinic receptors, the cholinergic system exerts a powerful control both on synaptic transmission and locomotor network neuron excitability. Although tremendous advances have been made in our understanding of the spinal cholinergic system's involvement in the physiology and pathophysiology of locomotor networks, gaps still remain, including the precise role of the different subtypes of cholinergic neurons as well as their pre- and postsynaptic partners. Improving our knowledge of the propriospinal cholinergic system is of major relevance to finding new cellular targets and therapeutics in countering the debilitating effects of neurodegenerative diseases and restoring motor functions after spinal cord injury.
Topics: Acetylcholine; Animals; Cholinergic Fibers; Humans; Locomotion; Receptors, Muscarinic; Receptors, Nicotinic; Spinal Cord; Spinal Cord Injuries; Spinal Nerves; Synaptic Transmission
PubMed: 33527727
DOI: 10.14814/phy2.14736 -
Neurology India 2021Occipital neuralgia (ON) is a primary headache disorder characterized by sharp, shooting, or electric shock-like pain in the distribution of the greater, lesser, or... (Review)
Review
BACKGROUND
Occipital neuralgia (ON) is a primary headache disorder characterized by sharp, shooting, or electric shock-like pain in the distribution of the greater, lesser, or third occipital nerves.
AIM
To review the existing literature on the management of ON and to describe our technique of an endoscopic-assisted approach to decompress the GON proximally in areas of fibrous and muscular compression, as well as distally by thorough decompression of the occipital artery from the nerve.
METHODS
Relevant literature on the medical and surgical management of ON was reviewed. Literature on the anatomical relationships of occipital nerves and their clinical relevance were also reviewed.
RESULTS
While initial treatment of ON is conservative, peripheral nerve blocks and many surgical management approaches are available for patients with pain refractory to the medical treatment. These include greater occipital nerve blocks, occipital nerve stimulation, Botulinum toxin injections locally, pulsed radiofrequency ablation, cryoneuroablation, C-2 ganglionectomy, and endoscopic-assisted ON decompression.
CONCLUSION
Patients of ON refractory to medical management can be benefitted by surgical approaches and occipital nerve blocks. Endoscopic-assisted ON decompression provides one such approach for the patients with vascular, fibrous or muscular compressions of occipital nerves resulting in intractable ON.
Topics: Headache; Humans; Nerve Block; Neuralgia; Spinal Nerves; Treatment Outcome
PubMed: 34003169
DOI: 10.4103/0028-3886.315980 -
Joint Bone Spine Mar 2022Compression of roots/nerves can disrupt some of their functions, but does not necessarily cause pain. This is illustrated by the frequency of nearly asymptomatic spinal... (Review)
Review
Compression of roots/nerves can disrupt some of their functions, but does not necessarily cause pain. This is illustrated by the frequency of nearly asymptomatic spinal stenosis or disc herniations. In fact, pain of radiculopathies (and nerve entrapments) may mostly be the consequence of intraneural oedema induced by microscopical venous stasis around roots/spinal ganglia (or nerves) not or poorly shown by imaging. This narrative review first lists arguments for a role of congestion of vasa-nervorum in the pathophysiology of radiculopathies, including those induced by disc herniation and spinal stenosis, but also other sources of overpressures in spinal venous plexuses (pregnancy, vena cava atresia and thrombosis, portal hypertension, epidural varices, arterio-venous fistula, vertebral hemangioma or hemangioblastoma). It also details sources of venous congestion around nerves outside the spine, from pelvis (May-Thurner syndrome, Nut-cracker syndrome) to buttocks (superior and inferior gluteal veins), and even thighs and legs. A better recognition of a preeminent role of venous congestion in radiculopathies, plexopathies, and nerve entrapments, should have major consequences: (i) discard the dogma that compression is mandatory to induce root/nerve suffering, since root/nerve adherences in two locations can impair blood flow in vasa-nervorum through root/nerve stretching; (ii) implementation of sensitive techniques to visualise impingement of blood flow around or within roots and nerves; (iii) better prevention of roots/nerves adherence, or arachnoiditis induced by extravascular fibrin deposition secondary to venous stasis.; (iv) optimizing treatments dampening clot formation and/or extravascular fibrin leakage in the intradural/peridural spaces, or around roots/nerves, like guided injection of tissue plasminogen activator.
Topics: Female; Humans; Hyperemia; Intervertebral Disc Displacement; Pregnancy; Radiculopathy; Spinal Nerve Roots; Tissue Plasminogen Activator
PubMed: 34653602
DOI: 10.1016/j.jbspin.2021.105291