Academic literature on the topic 'Nerve Compression Syndromes - therapy'

Compressive neuropathies of the forearm are common and involve structures innervated by the median, ulnar, and radial nerves. A thorough patient history, occupational history, and physical examination can aid diagnosis. Electromyography, X-ray, and Magnetic Resonance Imaging may prove useful in select syndromes. Generally, first line therapy of all compressive neuropathies consists of activity modification, rest, splinting, and non-steroidal anti-inflammatory drugs. Many patients experience improvement with conservative measures. For those lacking adequate response, steroid injections may improve symptoms. Surgical release is the last line therapy and has varied outcomes depending on the compression. Carpal Tunnel syndrome (CTS) is the most common, followed by ulnar tunnel syndrome. Open and endoscopic CTS release appear to have similar outcomes. Endoscopic release appears to incur decreased cost baring a low rate of complications, although this is debated in the literature. Additional syndromes of median nerve compression include pronator syndrome (PS), anterior interosseous syndrome, and ligament of Struthers syndrome. Ulnar nerve compressive neuropathies include cubital tunnel syndrome and Guyon’s canal. Radial nerve compressive neuropathies include radial tunnel syndrome and Wartenberg’s syndrome. The goal of this review is to provide all clinicians with guidance on diagnosis and treatment of commonly encountered compressive neuropathies of the forearm.

Since Dandy first reported vascular compression of the trigeminal nerve, the concept of neurovascular compression syndrome for trigeminal neuralgia and hemifacial spasm (HFS) has been accepted, and neurovascular decompression has been performed for this condition. The further investigations indicated that some other clinical syndromes such as glossopharyngeal neuralgia, disabling positional vertigo, tinnitus, geniculate neuarlgia, spasmodic torticolis, essential hypertension, cyclic oculomotor spasm with paresis and superior oblique myokymia also may be initiated by vascular compression of the glosopharyngeal, cochleovestibular, intermediate, accessory, oculomotor and trochlear nerves or the ventrolateral medulla oblongata. In this study several hypotheses regarding the development of cranial nerves vascular compression syndromes are presented. It is also emphasized the value of high-resolution magnetic resonance tomographic angiography for visualization of vascular compression. The most frequent clinical syndromes caused by vascular compression of the cranial nerves are discussed regarding the pathogenesis, symptoms and therapy. We present our series of 124 patients with preoperative evidently positive finding of vascular compression to the trigeminal nerve (MRI). Microvascular decompression (MVD)was performed in all of them. Initial postoperative result was excellent in 110/124 (89%) patients, while in 11/124 (9%) patients the pain relief was satisfactory. In the remaining three patients MVD failed. Recurrence of pain after two years reached 19 %. Complications were related to diplopia associated with transient fourth nerve dysfunction in 5 (4%) patients, facial motor dysfunction in 4 (3%) patients, transient facial hypesthesia in 27 (22%) patients and partially hearing loss in 4 (3%) patients. Cerebellar hemorrhagic infarction occurred in 1 ( 0,8 %) patient and cerebrospinal fluid leaks appeared in two (1,6%) cases. There was no lethal outcome.

The issue of compression ischemic syndromes, in particular, carpal tunnel syndrome, is currently extremely relevant. Prolonged compression of the nerve leads to irreversible consequences and degeneration of its fibers, followed by neurogenic muscle atrophy and permanent loss of function. Standard medical and physical therapy methods of treatment do not always achieve a positive effect. The paper considers the results of the use of phonophoresis of hydrocortisone and fermenkol in 35 patients with carpal tunnel syndrome. Positive dynamics was noted in both groups, which increases the possibility of treatment tactics selection for patients of this profile.

Introduction Neuropathic pain in cancer patients requires a focused clinical evaluation based on knowledge of common neuropathic pain syndromes. Definition Neuropathic pain is a non-nociceptive pain or "differentiation" pain, which suggests abnormal production of impulses by neural tissue that is separated from afferent input. Impulses arise from the peripheral nervous system or central nervous system. Causes of neuropathic pain due to malignancy Neuropathic pain is caused directly by cancer-related pathology (compression/infiltration of nerve tissue, combination of compression/infiltration) or by diagnostic and therapeutic procedures (surgical procedures, chemotherapy, radiotherapy). Mechanisms Pathophysiological mechanisms are very complex and still not clear enough. Neuropathic pain is generated by electrical hyperactivity of neurons along the pain pathways. Peripheral mechanisms (primary sensitization of nerve endings, ectopically generated action potentials within damaged nerves, abnormal electrogenesis within sensory ganglia) and central mechanisms (loss of input from peripheral nociceptors into dorsal horn, aberrant sprouting within dorsal horn, central sensitization, loss of inhibitory interneurons, mechanisms at higher centers) are involved. Diagnosis The quality of pain presents as spontaneous pain (continuous and paroxysmal), abnormal pain (allodynia, hyperalgesia, hyperpathia), paroxysmal pain. Clinical manifestations Clinically, neuropathic pain is described as the pain in the peripheral nerve (cranial nerves, other mononeuropathies, radiculopathy, plexopathy, paraneoplastic peripheral neuropathy) and relatively infrequent, central pain syndrome. Therapy Treatment of neuropathic pain remains a challenge for clinicians, because there is no accepted algorithm for analgesic treatment of neuropathic pain. Pharmacotherapy is considered to be the first line therapy. Opioids combined with non-steroidal antiinflammatory drugs are warrented. If patient is relatively unresponsive to an opioid, a trial with adjuvant analgesics might be considered. Tricyclic antidepressants might be selected for patients with continuous dysesthesia, and anticonvulsants might be used if the pain is predominanty lancinating or paroxysmal. The complexity of neuropathic syndromes and underlying etiologic mechanisms warrant clinical trials to determine appropriate treatment.

Abstract OBJECTIVE: Lesions of the peripheral nervous system result in the loss of sensory and motor function and may in addition be accompanied by severe neuropathic syndromes originating from aberrant axonal regrowth. The transplantation of autologous nerve grafts represents the current “gold standard” during reconstructive surgery, despite obvious side effects. Depending on the demands of the lesion site, various donor nerves may be used for grafting (e.g., the sural, saphenous), sacrificing native functions in their target areas. Recently, several synthetic nerve guide implants have been introduced and approved for clinical use to replace autologous transplants. This alternative therapy is based on pioneering studies with experimental nerve guides. METHODS: We present a comprehensive review of all published human studies involving synthetic nerve guides. RESULTS: Data from some 300 patients suggest that for short nerve defects of a few centimeters, resorbable implants provide promising results, whereas a number of late compression syndromes have been documented for nonresorbable implants. CONCLUSIONS: To treat longer defects, further implant development is needed, a goal that could be achieved, for example, by more closely imitating the intact nerve architecture and regulatory cell-cell interactions.

Aim. Explore different treatment approaches for degenerative-dystrophic damage of the spine and formulate the most effective treatment methods, their stage from accounting pathogenetic basis of pain syndromes.
 Research methods – bibliosemantic, comparative, systemic.
 Results. Diverse treatments for degenerative-dystrophic damage of the spine does not facilitate but even complicates general practitioner’s work due to the fact that information on clinical benefits of various drugs and techniques as well as various types of surgery is too contradictory; there is no single method of consistent, combination therapy for vertebrogenic pain. There is no universal therapy or surgery that would provide sustainable relief of symptoms of nonspecific back pain and/or radicular syndrome. The pathogenesis of development of specific clinical manifestations of the disease and the ratio of clinical manifestations and pathomorphological changes are crucial in choosing the treatment. The general principles of treatment are unchanged: rest, analgesics and movement should be combined in appropriate sanogenic proportions in each case. Reduction of oedema and swelling of the intervertebral disc and the spinal nerve root, nerve endings are crucial in regression of pain syndrome. There is no doubt that nonsteroidal anti-inflammatory drugs (NSAIDs) are the most effective in relieving lumbar and radicular pain at the beginning of treatment. In the absence of significant improvement after the use of NSAIDs and the necessary sanogenic motor loads, a more dynamic treatment should be used. First of all, different methods of local administration of pharmacological drugs: starting with the banal subcutaneous injection of painful areas and finishing with ultrasound and MRI-controlled injections directly into the area around the damaged nerve root, the epidural space, or the facet joint. In most cases, epidural injections can reach areas of disc-radicular conflict – after the drug is injected into the epidural space, favourable conditions are created for diffusion of glucocorticoids (or other pharmacological agents) into surrounding tissues, as well as the nerve root, regardless of its compression or irritation.
 Conclusions. And only after the ineffectiveness of NSAIDs and puncture treatments, as well as epidural injection and in the case of persistent mechanical compression of nerve roots in comparison with clinical manifestations, appropriate surgical treatments, both minimally invasive and open, are necessary.

ABSTRACT Objective: To analyse the anatomical variations of the median nerve motor branches in the elbow region. Methods: Twenty upper limbs of 10 adult male cadavers were prepared by intra-arterial injection of a solution of 10% glycerol and formaldehyde. All cadavers belonged to the institution anatomy laboratory. Results: We found a great variability within the distribution of median nerve branches leading to forearm muscles. Only three limbs (14%) presented the normal standard of innervation described in anatomy treatises. The pronator teres muscle (PTM), flexor carpi radialis (FCR), palmaris longus (PL), and the flexor digitorum superficialis (FDS) received exclusive innervation from the median nerve in all forearms. The anterior interosseous nerve (AIN) also originated from the median nerve in all dissected limbs. Conclusion: A thorough understanding of the anatomy of the median nerve branches is important for performing surgeries such as: approach to the proximal third of the forearm, alleviation of pronator teres and anterior interosseous nerve compression syndromes, and distal nerve transfers. It also enables a better understanding the recovery of muscle function after a nerve injury. Level of Evidence IV, Case series.

The term canalicular neuropathy is applied to nerve lesions arising on nerve segments passing through the osteofibrous canals or other narrow orifices and resulting in nerve compression and entrapment. We studied 31 patients referred to us for non-traumatic canalicular syndromes in the upper limbs. After clinical, electrophysiological and morphological analysis of each case, we emphasize the role of MR imaging in establishing prognosis and selecting treatment. Anatomosurgical specimens correlated well with MR features, whereas there was little correlation between electrophysiological severity and anatomical changes. In summary, canalicular neuropathy is a clinical syndrome. The aim of MR investigation is to document the morphological changes which will serve to institute appropriate treatment. When patients have clinical and electrophysiological evidence of neuropathy without MR demonstration of the nerve lesion, therapy will be conservative, thus saving the cost and risk of surgery. On the other hand, when clinical and electrophysiological findings are flanked by MR demonstration of the neuropathy, the disease is known to be advanced and surgery will be indicated to prevent neurotmesis.