Local Anesthetics
Sahab Uddin, Rashid Mamunur in Advances in Neuropharmacology, 2020
From the structural point of view, this amino amide type local anesthetic differs from those of its category in that it has a thiophene group instead of a benzene ring, which gives it greater lipid solubility and potency. Moreover, articaine has an ester group which gives it a lower plasma half-life (20 min) since this compound is rapidly hydrolyzed by the action of nonspecific plasma esterases to its inactive metabolite articainic acid. This rapid metabolism is associated with a reduced risk of systemic toxicity and overdose compared with other amino amide local anesthetics (Yapp et al., 2011). However, several epidemiological studies suggest that articaine has a higher occurrence of causing paresthesia. Paresthesia is an abnormal sensation, usually pricking, tickling, numbness, burning or itching which occurs in hands, feet, toes, fingers, or another part of the body. Comparing articaine 4% and lidocaine 2% associated both local anesthetic drugs with epinephrine 1:100,000, the ratio of suffering from paresthesias after their administration of in a dental procedure is 1/49 for articaine and 1/63 for lidocaine and the duration of paresthesia varies from a few hours to around 20 days (Haas, 2006; Hopman et al., 2017; Malamed et al., 2001).
Peripheral Nerve Microcirculation
John H. Barker, Gary L. Anderson, Michael D. Menger in Clinically Applied Microcirculation Research, 2019
A number of pathologic conditions in the nerve are considered to have a microcirculation component. One of the most common disease entities is nerve compression syndrome. A localized compression of the nerve causes a disruption of blood flow producing at first paresthesias but also numbness, and pain if prolonged. If the compression occurs over extensive periods, the axons become permanently damaged, disrupting transport of materials across the site. Eventually, demyelination and cell death occur distal to the compression site. This disruption may affect proximal sites. Microcirculation changes include increased vascular permeability that may precede changes in flow.19 Higher endoneurial pressure led to lower flow conditions. Much of the evidence for these findings is circumstantial and has not been proved in the clinical situation.
Mitochondrial Dysfunction Affecting the Peripheral Nervous System in Diabetic Neuropathy and Avenues for Therapy
Shamim I. Ahmad in Handbook of Mitochondrial Dysfunction, 2019
DPN has been defined as a “length-dependent, symmetrical sensorimotor polyneuropathy that is attributable to metabolic and micro-vessel alterations, resulting from chronic hyperglycemia exposure (diabetes) and cardiovascular risk covariates” (6). The sensory symptoms spread in a ‘stocking-glove’ distribution, starting in the toes and moving over time to reach the knees, and then moving to the upper limbs. A variety of symptoms may be present that includes prickling and tingling sensations (paresthesias), electric shocks, burning feeling, or pain insensitivity. Hyperalgesia, an increased sensitivity to pain, or allodynia, a painful response to otherwise painless stimuli, are other notable DPN symptoms that are mediated through neuropathy of the small fibers. Of individuals with DPN, 20–30% will suffer from neuropathic pain (5,6,19,24), and this is typically observed to be worse at night. Notably however, the stronger painful symptoms do not appear to directly correlate with severity of damage to axons (4).
Guillain-Barré syndrome after bortezomib therapy in a child with relapsed acute lymphoblastic leukemia
Published in Pediatric Hematology and Oncology, 2022
Valeria Ceolin, Rosita Cenna, Francesca Resente, Manuela Spadea, Franca Fagioli, Nicoletta Bertorello
Peripheral neuropathy (PN) has been described in patients receiving bortezomib, which is predominantly sensory. Symptoms include paresthesia, numbness in distal areas, particularly the lower limbs, burning sensations, dysesthesias, sensory loss, reduced proprioception, vibratory sensation, reduction of deep tendon reflexes and autonomic skin innervation. Neuropathic pain has also been described and happens more frequently than with other neurotoxic drugs.14 PN usually appears after a number of cycles of treatment and is associated with dose accumulation, but symptoms may also appear after the first few doses; recent studies28 did not find a clear linear correlation between the cumulative dose or dose intensity and the severity of polyneuropathy, indicating that certain patients developed a severe polyneuropathy following a relatively low dose of BZM. The pathophysiology of bortezomib induced neuropathy is not completely clear yet. Experimental studies suggest that aggresome formation, endoplasmic reticulum stress, myotoxicity, microtubule stabilization, inflammatory response, and DNA damage could contribute to this neurotoxicity.29
Differential diagnosis of knee pain following a surgically induced lumbosacral plexus stretch injury. A case report
Published in Physiotherapy Theory and Practice, 2019
William R. VanWye, Harvey W. Wallmann, Elizabeth S. Norris, Karen E. Furgal
Neurological findings included an absent left Achilles deep tendon reflex (DTR) (S1-S2) and diminished sensation to light touch on the lateral leg (L5) and foot (S1), plantar surface (S1) and heel (S2) of the foot, and digits I-V (L5-S1) (Figure 1). Neurodynamic testing was assessed via the straight leg raise (SLR) and the seated slump test (Butler, 2000). Both tests produced transient left LE paresthesia (i.e. pins and needles) in a pattern consistent with Figure 1. The SLR test was performed with the patient in supine, spine in neutral. The PT performed passive unilateral hip flexion with the knee extended while holding the ankle in end-range dorsiflexion. The aforementioned symptoms were produced at 60 degrees of hip flexion on the left. The PT repeated this on the right and was able to passively move the LE to 90 degrees of hip flexion without symptoms. The slump test was performed in sitting. The patient was asked to place hands behind the low back, slump the thoracic spine, perform full neck flexion followed by full unilateral knee extension. While holding this position, the patient was asked to perform full ankle dorsiflexion, which produced the aforementioned symptoms on the left, but not on the right. Holding this position and releasing neck flexion abolished the left LE symptoms.
Burst and high frequency stimulation: underlying mechanism of action
Published in Expert Review of Medical Devices, 2018
Shaheen Ahmed, Thomas Yearwood, Dirk De Ridder, Sven Vanneste
A rational way to characterize the stimulation paradigm, including the amplitude, charge per pulse, and the current delivered to the spinal cord, was first described in a report comparing burst SCS with conventional stimulation [21]. For burst stimulation, a low amplitude may exert a suppressing effect while increasing the amplitude may actually be detrimental. The burst waveform delivers pulses at an HF and at an amplitude much lower than tonic stimulation. The average amplitude for burst stimulation is 0.6 mA, ranging from 0.05–1.6 mA, which is significantly lower than the average amplitude for tonic stimulation, i.e. 3.1 mA, ranging from 0.5–3.9 mA. In fact, a recent study involving burst and tonic SCS demonstrated that in a large population, very low amplitudes (0.1 mA) are beneficial [50]. However, the amplitude impacts both the number of fibers recruited and the intensity of paresthesia. Thus, it is necessary to optimize the stimulation paradigm so as to achieve pain suppression without inducing paresthesia.
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