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Facial Neuralgia (Atypical)
Published in Charles Theisler, Adjuvant Medical Care, 2023
Facial neuralgia is a severe stabbing, burning, or shocking pain due to an irritated or damaged nerve. Persistent burning or lancinating paroxysmal pain in the facial region typically follows along the anatomical course of a damaged nerve. When patients present with symptoms and no clear etiology, one should consider neuropathic pain such as sphenopalatine or glossopharyngeal neuralgia in the diagnosis.1
Viral Infections
Published in Ayşe Serap Karadağ, Lawrence Charles Parish, Jordan V. Wang, Roxburgh's Common Skin Diseases, 2022
In younger immunocompetent patients, the total duration of the disease is generally 2–3 weeks, while in elderly patients, it can take greater than 6 weeks for lesions to heal. Pain can last after skin lesions resolve and is called postherpetic neuralgia (PHN); the duration and severity of PHN are variable and often age-dependent. Treatments for postherpetic neuralgia are topical therapy (e.g., lidocaine, capsaicin), tricyclic antidepressants, gabapentin and pregabalin, venlafaxine, and oral analgesics, including opiates.
The middle third of the face
Published in Jani van Loghem, Calcium Hydroxylapatite Soft Tissue Fillers, 2020
Shino Bay Aguilera, Luis Soro, Jani van Loghem
The primary concern with filler injection is the occlusion of arteries whether by external compression or injection of product into the vessel (Figure 9.1). This is especially true of products that are more difficult to dissolve such as calcium hydroxylapatite. Fortunately, vascular occlusion is rare and easily avoided when injecting in the periosteal region, as in the HD-Sculpt technique. Major midface arteries to be aware of, however, are the infraorbital artery, the transverse facial artery, and the tortuous facial artery with anastomosing angular artery. Although less common, piercing injuries to nerves should be avoided, and the primary nerve to be mindful of with this technique is the infraorbital nerve. Injury to this nerve can cause intractable neuralgia for an extended period.
An unusual case of lower trunk brachial plexus zoster reactivation
Published in Case Reports in Plastic Surgery and Hand Surgery, 2023
Samantha J. Burch, Elizabeth Shepard, Angelo B. Lipira
Herpes zoster, or shingles, is a common condition caused by reactivation of the varicella-zoster virus (VZV), a double-stranded DNA alphaherpesvirus [1]. Shingles is characterized by a two to three day prodrome of neuropathic pain prior to the eruption of vesicular skin lesions, although cutaneous findings are not required for diagnosis [2]. These skin lesions classically present in a dermatomal pattern, as VZV remains latent in the dorsal root ganglia after primary infection. While VZV primarily affects sensory nerves, motor weakness may be present in 1–5% of patients with herpes zoster [3]. Segmental Zoster Paresis involves motor weakness in the same dermatomal distribution as the vesicular rash, most commonly affecting the face and upper extremity [4]. Motor symptoms in the upper extremities following herpes zoster can also be classified as a mononeuropathy, radiculopathy, or brachial plexopathy, which are confirmed and monitored by electrophysiologic testing or MRI [3]. In most cases, neuropathic pain and motor symptoms resolve with time, however a subset of patients can experience postherpetic neuralgia (PHN) or persistent motor deficits, for reasons that remain poorly understood [5].
Preparation of uniform-sized GeXIVA[1,2]-loaded PLGA microspheres as long-effective release system with high encapsulation efficiency
Published in Drug Delivery, 2022
Lu Li, Zhiguo Li, Yongxin Guo, Kai Zhang, Weidong Mi, Jing Liu
Currently, the drug of choice for the clinical treatment of chronic neuralgia is opioids. However, opioids are accompanied by a series of adverse reactions such as tolerance and addiction, and they are frequently administered, resulting in poor patient compliance, and there are certain limitations in clinical treatment (Angst & Clark, 2006; Chou et al., 2015; Devereaux et al., 2018). Conotoxin αO-GeXIVA, a 28-amino acid polypeptide found in the marine animal conus in the South country Sea, can achieve an analgesic effect by specifically blocking the α9α10 nAChR receptor, which has attracted widespread attention (Yu et al., 2018; Xu et al., 2020; Wang et al., 2019). Its isomer GeXIVA[1,2] is by far the most active conotoxin (Yousuf et al., 2022), showing excellent analgesic effects in many disease models (Vincler & Mcintosh, 2007; Alsharari et al., 2020; Khan et al., 2002). Notably, no addictive or motor side effects were observed during the treatment period. Therefore, GeXIVA[1,2], as a novel polypeptide compound with unique pharmacological and analgesic effects, is expected to be used in the clinic to improve the therapeutic effect of chronic neuropathic pain.
Investigating the possible pain attenuating mechanisms of pregabalin in chronic constriction injury-induced neuropathic pain in rats
Published in International Journal of Neuroscience, 2019
Renuka Verma, Jasmine Sharma, Nirmal Singh, Amteshwar Singh Jaggi
Neuropathic pain is chronic pain in which a patient experiences severe pain those results from the dysfunction of the somatosensory nervous system [1, 2]. Neuropathic pain can be classified as central neuropathic pain or peripheral neuropathic pain, depending upon the site of injury [3, 4]. Peripheral neuropathic pain is triggered after damage to the peripheral nerves (sensory, motor and autonomic) and it is generally encountered in the patients who have cancer, AIDS, herpes disease, persistent diabetes, lumbar disc syndrome, thoracotomy, mastectomy and sternotomy [5]. Central neuropathic pain is caused due to the dysfunctioning of the central nervous system (the brain and the spinal cord) that may result from the injury of the spinal cord, multiple sclerosis and stroke [6]. The characteristic symptoms of neuropathic pain include hyperalgesia (increased sensitivity to pain stimulus), allodynia (decreased threshold, i.e. increased pain response to stimuli which generally do not provoke pain), dysesthesia (burning pain sensation) and neuralgia (shooting or stabbing pain; electric shock-like pain) [7, 8]. Regardless of the significant prevalence of neuropathic pain, there is still a lack of suitable pharmacological treatment for neuropathic pain. A few therapies available for the treatment of neuropathic pain include anti-epileptic agents including lamotrigine, calcium channel α2-δ ligands like gabapentin and pregabalin, sodium channel antagonists like carbamazepine and NMDA receptor antagonists, mexiletine and topical 5% lidocaine [3].