scholarly journals Dorsal Column Stimulation Treats Pain from Chemotherapy-induced, Small Fiber Neuropathy

2017 ◽  
pp. 57-61
Author(s):  
David Dickerson
Keyword(s):  
Spinal Cord ◽  
Dorsal Column ◽  
Nerve Fibers ◽  
Small Fiber Neuropathy ◽  
Autonomic Nerve ◽  
Vitamin Deficiencies ◽  
Small Fiber ◽  
Analgesic Regimen ◽  
Number Of Patients ◽  
Dorsal Column Stimulation

Small fiber neuropathy (SFN) is a disorder of small afferent nerve fibers that can result in debilitating pain and functional limitations. There are many etiologies including, but not limited to, diabetes, vitamin deficiencies, infections, and exposure to neurotoxic drugs such as chemotherapeutics. The constellation of signs and symptoms overlap with other disease states leading to potential misdiagnosis. New tests including histologic studies of skin biopsies and autonomic nerve tests have emerged in the last 20 years improving differentiation between these disease processes and SFN. Multiple chemotherapeutic medications have been implicated in causing SFN, including vincristine which was the causative agent in this case report. The exact incidence of chemotherapy-induced peripheral neurotoxicity (CIPN) is currently unknown, but according to some publications it has been reported to be as high as 40% in patients that have been treated with chemotherapy. As the number of cancer survivors continues to grow, the number of patients with painful SFN will potentially increase. Devising an effective analgesic regimen for patients with painful SFN can be difficult, and often requires the pain physician to employ multiple pharmacologic and non-pharmacologic therapies. Treatments include analgesics from several drug classes: antidepressants, opioids, and anticonvulsants. Often times however, more advanced interventional techniques must be employed as effective pain control may be limited by medication side effects or inadequate return of function. While dorsal column stimulation was approved for a limited number of applications, a number of new applications are reported in the literature. In this paper, we present a case of vincristineinduced SFN successfully treated with neuromodulation via spinal cord stimulator. Key words: Vincristine, vinblastine, chemotherapy- induced neuropathy, chronic pain, spinal cord stimulation, dorsal column stimulation, neuromodulation, small fiber neuropathy, neuropathic pain

scholarly journals Diagnosing small fiber neuropathy in clinical practice: a deep phenotyping study

2021 ◽  
Vol 14 ◽  
pp. 175628642110043
Author(s):  
Nadine Egenolf ◽  
Caren Meyer zu Altenschildesche ◽  
Luisa Kreß ◽  
Katja Eggermann ◽  
Barbara Namer ◽  
...  
Keyword(s):  
Neurological Examination ◽  
Punch Biopsy ◽  
Small Fiber Neuropathy ◽  
Fiber Density ◽  
Axon Reflex ◽  
Small Fiber ◽  
Corneal Confocal Microscopy ◽  
Intraepidermal Nerve Fiber Density ◽  
Number Of Patients ◽  
Skin Punch Biopsy

Background and aims: Small fiber neuropathy (SFN) is increasingly suspected in patients with pain of uncertain origin, and making the diagnosis remains a challenge lacking a diagnostic gold standard. Methods: In this case–control study, we prospectively recruited 86 patients with a medical history and clinical phenotype suggestive of SFN. Patients underwent neurological examination, quantitative sensory testing (QST), and distal and proximal skin punch biopsy, and were tested for pain-associated gene loci. Fifty-five of these patients additionally underwent pain-related evoked potentials (PREP), corneal confocal microscopy (CCM), and a quantitative sudomotor axon reflex test (QSART). Results: Abnormal distal intraepidermal nerve fiber density (IENFD) (60/86, 70%) and neurological examination (53/86, 62%) most frequently reflected small fiber disease. Adding CCM and/or PREP further increased the number of patients with small fiber impairment to 47/55 (85%). Genetic testing revealed potentially pathogenic gene variants in 14/86 (16%) index patients. QST, QSART, and proximal IENFD were of lower impact. Conclusion: We propose to diagnose SFN primarily based on the results of neurological examination and distal IENFD, with more detailed phenotyping in specialized centers.

scholarly journals Intraepidermal Nerve Fibers Are Indicators of Small-Fiber Neuropathy in Both Diabetic and Nondiabetic Patients

Diabetes Care ◽  
2004 ◽  
Vol 27 (8) ◽  
pp. 1974-1979 ◽  
Author(s):  
G. L. Pittenger ◽  
M. Ray ◽  
N. I. Burcus ◽  
P. McNulty ◽  
B. Basta ◽  
...  
Keyword(s):  
Nerve Fibers ◽  
Small Fiber Neuropathy ◽  
Small Fiber

scholarly journals Ca2+ toxicity due to reverse Na+/Ca2+ exchange contributes to degeneration of neurites of DRG neurons induced by a neuropathy-associated Nav1.7 mutation

2015 ◽  
Vol 114 (3) ◽  
pp. 1554-1564 ◽  
Author(s):  
M. Estacion ◽  
B. P. S Vohra ◽  
S. Liu ◽  
J. Hoeijmakers ◽  
C. G. Faber ◽  
...  
Keyword(s):  
Nerve Fibers ◽  
Small Fiber Neuropathy ◽  
Missense Mutations ◽  
Sodium Calcium Exchanger ◽  
Drg Neurons ◽  
Persistent Currents ◽  
Burning Pain ◽  
Reverse Mode ◽  
Small Fiber ◽  
High K

Gain-of-function missense mutations in voltage-gated sodium channel Nav1.7 have been linked to small-fiber neuropathy, which is characterized by burning pain, dysautonomia and a loss of intraepidermal nerve fibers. However, the mechanistic cascades linking Nav1.7 mutations to axonal degeneration are incompletely understood. The G856D mutation in Nav1.7 produces robust changes in channel biophysical properties, including hyperpolarized activation, depolarized inactivation, and enhanced ramp and persistent currents, which contribute to the hyperexcitability exhibited by neurons containing Nav1.8. We report here that cell bodies and neurites of dorsal root ganglion (DRG) neurons transfected with G856D display increased levels of intracellular Na+ concentration ([Na+]) and intracellular [Ca2+] following stimulation with high [K+] compared with wild-type (WT) Nav1.7-expressing neurons. Blockade of reverse mode of the sodium/calcium exchanger (NCX) or of sodium channels attenuates [Ca2+] transients evoked by high [K+] in G856D-expressing DRG cell bodies and neurites. We also show that treatment of WT or G856D-expressing neurites with high [K+] or 2-deoxyglucose (2-DG) does not elicit degeneration of these neurites, but that high [K+] and 2-DG in combination evokes degeneration of G856D neurites but not WT neurites. Our results also demonstrate that 0 Ca2+ or blockade of reverse mode of NCX protects G856D-expressing neurites from degeneration when exposed to high [K+] and 2-DG. These results point to [Na+] overload in DRG neurons expressing mutant G856D Nav1.7, which triggers reverse mode of NCX and contributes to Ca2+ toxicity, and suggest subtype-specific blockade of Nav1.7 or inhibition of reverse NCX as strategies that might slow or prevent axon degeneration in small-fiber neuropathy.

scholarly journals Should Skin Biopsies Be Performed in Patients Suspected of Having Parkinson’s Disease?

2017 ◽  
Vol 2017 ◽  
pp. 1-6 ◽  
Author(s):  
Timo Siepmann ◽  
Ana Isabel Penzlin ◽  
Ben Min-Woo Illigens ◽  
Heinz Reichmann
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Structural Damage ◽  
Later Life ◽  
Nerve Fibers ◽  
Autonomic Nerve ◽  
Diagnostic Tools ◽  
Small Fiber ◽  
Superficial Skin ◽  
Skin Biopsies

In patients with Parkinson’s disease (PD), the molecularly misfolded form of α-synuclein was recently identified in cutaneous autonomic nerve fibers which displayed increased accumulation even in early disease stages. However, the underlying mechanisms of synucleinopathic nerve damage and its implication for brain pathology in later life remain to be elucidated. To date, specific diagnostic tools to evaluate small fiber pathology and to discriminate neurodegenerative proteinopathies are rare. Recently, research has indicated that deposition of α-synuclein in cutaneous nerve fibers quantified via immunohistochemistry in superficial skin biopsies might be a valid marker of PD which could facilitate early diagnosis and monitoring of disease progression. However, lack of standardization of techniques to quantify neural α-synuclein deposition limits their utility in clinical practice. Additional challenges include the identification of potential distinct morphological patterns of intraneural α-synuclein deposition among synucleinopathies to facilitate diagnostic discrimination and determining the degree to which structural damage relates to dysfunction of nerve fibers targeted by α-synuclein. Answering these questions might improve our understanding of the pathophysiological role of small fiber neuropathy in Parkinson’s disease, help identify new treatment targets, and facilitate assessment of response to neuroprotective treatment.

Effects of Induced Hypothermia on Subcortical Evoked Potentials in the Cat

1958 ◽  
Vol 194 (2) ◽  
pp. 423-426 ◽  
Author(s):  
George C. Stevenson ◽  
William F. Collins ◽  
Clark T. Randt ◽  
Thomas D. Saurwein
Keyword(s):  
Spinal Cord ◽  
Evoked Potentials ◽  
Reticular Formation ◽  
Dorsal Column ◽  
Nerve Fibers ◽  
Induced Hypothermia ◽  
Conduction Time ◽  
Midbrain Reticular Formation ◽  
Spinal Cord Dorsal ◽  
Relay Nucleus

The effects of induced hypothermia in the unanesthetized immobilized cat on somatic afferent evoked potentials from the posteroventral lateral nucleus of the thalamus, periaqueductal midbrain reticular formation and dorsal column of the spinal cord were studied in 28 cats. At a rectal temperature of 23°C, marked depression of the responses recorded from all loci was demonstrable. The afferent midbrain reticular formation was demonstrated to be more sensitive to hypothermia than the thalamic relay nucleus. Augmentation of the spinal cord dorsal column evoked potentials was noted between 33°C and 25°C. Conduction time measurements indicated that between 37°C and 27°C the velocity of transmission along the nerve fibers is more affected than transmission across a synapse.

A quantitative method for the assessment of intraepidermal nerve fibers in small–fiber neuropathy

2005 ◽  
Vol 252 (7) ◽  
pp. 789-794 ◽  
Author(s):  
M. Koskinen ◽  
A. Hietaharju ◽  
M. Kyläniemi ◽  
J. Peltola ◽  
I. Rantala ◽  
...  
Keyword(s):  
Quantitative Method ◽  
Nerve Fibers ◽  
Small Fiber Neuropathy ◽  
Small Fiber

scholarly journals Conventional and Kilohertz-frequency Spinal Cord Stimulation Produces Intensity- and Frequency-dependent Inhibition of Mechanical Hypersensitivity in a Rat Model of Neuropathic Pain

2013 ◽  
Vol 119 (2) ◽  
pp. 422-432 ◽  
Author(s):  
Ronen Shechter ◽  
Fei Yang ◽  
Qian Xu ◽  
Yong-Kwan Cheong ◽  
Shao-Qiu He ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Neuropathic Pain ◽  
Spinal Cord Stimulation ◽  
Dynamic Range ◽  
Dorsal Column ◽  
Dependent Manner ◽  
Motor Threshold ◽  
Wide Dynamic Range ◽  
Mechanical Hypersensitivity ◽  
Dorsal Column Stimulation

Abstract Background: Spinal cord stimulation (SCS) is a useful neuromodulatory technique for treatment of certain neuropathic pain conditions. However, the optimal stimulation parameters remain unclear. Methods: In rats after L5 spinal nerve ligation, the authors compared the inhibitory effects on mechanical hypersensitivity from bipolar SCS of different intensities (20, 40, and 80% motor threshold) and frequencies (50, 1 kHz, and 10 kHz). The authors then compared the effects of 1 and 50 Hz dorsal column stimulation at high- and low-stimulus intensities on conduction properties of afferent Aα/β-fibers and spinal wide-dynamic–range neuronal excitability. Results: Three consecutive daily SCS at different frequencies progressively inhibited mechanical hypersensitivity in an intensity-dependent manner. At 80% motor threshold, the ipsilateral paw withdrawal threshold (% preinjury) increased significantly from pre-SCS measures, beginning with the first day of SCS at the frequencies of 1 kHz (50.2 ± 5.7% from 23.9 ± 2.6%, n = 19, mean ± SEM) and 10 kHz (50.8 ± 4.4% from 27.9 ± 2.3%, n = 17), whereas it was significantly increased beginning on the second day in the 50 Hz group (38.9 ± 4.6% from 23.8 ± 2.1%, n = 17). At high intensity, both 1 and 50 Hz dorsal column stimulation reduced Aα/β-compound action potential size recorded at the sciatic nerve, but only 1 kHz stimulation was partially effective at the lower intensity. The number of actions potentials in C-fiber component of wide-dynamic–range neuronal response to windup-inducing stimulation was significantly decreased after 50 Hz (147.4 ± 23.6 from 228.1 ± 39.0, n = 13), but not 1 kHz (n = 15), dorsal column stimulation. Conclusions: Kilohertz SCS attenuated mechanical hypersensitivity in a time course and amplitude that differed from conventional 50 Hz SCS, and may involve different peripheral and spinal segmental mechanisms.

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