Radicular Neuropathy Research Articles

Historical Course of Neuropsychiatric Effects of Lemon Balm (Melissa Officinalis L.) as a Medicinal Herb

Abstract Affective disorders have become prevalent and costly worldwide chronic conditions. Lemon Balm (Melissa Officinalis L.) is a medicinal plant with beneficial effects on neuropsychiatric disorders. Its potential to specifically treat conditions such as depression and anxiety has been investigated for over 20 centuries. Given the lack of a historical overview of lemon balm in mood disorders, the present review aimed to introduce the historical course of the neuro-psychiatric applications of lemon balm across the centuries. We investigated several viable medieval Arabic sources up to the 15th century, to distinguish the neuropsychiatric applications, especially anxiolytic and anti-depressive effects of lemon balm. In the early centuries, lemon balm was mainly prescribed to treat gastrointestinal disorders. Over time, physicians identified the efficient use of lemon balm in sadness, sleep disorders, anxiety, depression, epilepsy, ischemic stroke, amnesia, sciatalgia, and radicular neuropathy. Importantly, it was established that the therapeutic effects of lemon balm in the field of neuro-psychiatric diseases were emphasized by physicians during the Middle Ages. These findings have since been validated in human clinical trials. Lemon balm has also demonstrated the ability to be utilized in epilepsy, amnesia and ischemic stroke. Based on the extensive history of lemon balm in neuropsychiatry, future investigations could use this knowledge to extensively investigate the potential of lemon balm in neuropsychiatric disorders such as depression and anxiety, and possibly develop an efficient neuropsychiatric remedy.

Clinical Diagnosis and Treatment Recommendations for Adverse Reaction in the Nervous System Related to Immunocheckpoint Inhibitor

免疫检查点抑制剂（immune checkpoint inhibitors, ICIs）可引起神经系统的不良反应，发生率在0.1%-12%，80%发生在应用前4个月内。可以引起神经系统各部位的病变，包括无菌性脑膜炎，脑膜脑炎，坏死性脑炎，脑干脑炎，横贯性脊髓炎等中枢神经系统病变，也可引起颅神经周围神经病、多灶性神经根神经病、格林巴利综合征、脊神经根神经病、重症肌无力、肌病等周围神经病变。对于神经系统的这些并发症，均需要症状体征，并结合影像学、脑脊液细胞学、脑电图或肌电图等检查，除外感染或恶性肿瘤后获得诊断。治疗中，在严重病例需停用ICIs，并用大剂量糖皮质激素或丙种球蛋白治疗和对症支持治疗。在出现神经系统不良反应后，严重病例预后较差。

Unilateral lytic changes over the weight-bearing joint causing severe destruction of ankle joint (atypical Charcot joint) in a girl with congenital insensitivity to pain without anhidrosis (hereditary sensory and autonomic neuropathy type V): Case report and literature review

Background. The presence of Charcot arthropathies, joint dislocations, infections and fractures in a child without evidence of neurological abnormality should give rise to a suspicion of congenital insensitivity to pain (hereditary sensory and autonomic neuropathy). Hereditary sensory and autonomic neuropathy (HSAN) is a rare syndrome characterized by congenital insensitivity to pain, temperature changes and by autonomic nerve formation disorders. HSAN is classified into five types: sensory radicular neuropathy (HSAN I), congenital sensory neuropathy (HSAN II), familial dysautonomia or Riley Day Syndrome (HSAN III), congenital insensitivity to pain with anhidrosis (HSAN IV) and congenital indifference to pain (HSAN V).
 Case presentation. A 13-year old girl first product of a non-consanguineous marriage, presented with malunion of successive fractures or Charcots ankle joint destruction on top of significant lytic changes/osteonecrosis. The patient had sustained many painless injuries resulting in fractures with subsequent disfiguremnt of her ankle joint. Arthropathy of the knees, ankles, tarsal bones and feet without pain associated with obvious changes in the shape of the ankle joint were present. Despite a normal sense of touch in our patient the indifference to pain made her extremely susceptible to breakdown of the skin over the ankle osseous prominences.
 Conclusion. Generally speaking, the orthopaedic management of such patients is extremely difficult since these patients do not restrict the movements of the involved extremity as they lack the inhibitory pain reflex. Interestingly, our attempts for surgical stabilisation of the ankle joints were succsessfull and eventually the girl became able to walk. It is important to anticipate patient and parent education in joint protection and surveillance for injury as the most important component of the treatment plan for these children. We might postulate that the degree of osteolysis of the ankle joint in our present child might be a form of secondary osteolysis.

The Use and Alpha-Lipoic Acid (ALA), Gamma Linolenic Acid (GLA) and Rehabilitation in the Treatment of Back Pain: Effect on Health-Related Quality of Life

The aim of this trial was to evaluate the effects of alpha-lipoic acid (ALA) and gamma-linolenic acid (GLA) and the beneficial effect of physical exercise on positive sensory symptoms and neuropathic pain in patients with compressive radiculopathy syndrome from disc-nerve root conflict. Often these painful syndromes after the acute event, tend to recurr becoming subacute or chronic syndromes that become for the period of interest disabiling is an event very important in these cases proper prevention, based on a maintenance drug therapy and the strengthening exercises of paravertebral muscles, flexibility exercises on the spine and when needed on the reduction of body weight. In this Observational Cohort, two-arm trial, 203 patients were enrolled and divided into two groups, the first, ALA and GLA group, (n = 101) received oral dose of 600 mg of alpha-lipoic acid (ALA) and 360 mg of gamma-linolenic acid (GLA) and a rehabilitation program for six weeks, the second (n = 102) treated with only rehabilitation program. Patients were recruited at the centre of Physical Medicine and Rehabilitation, they underwent a physiatric examination at the primary outcome (t0) and secondary outcomes were recorded at monitoring visits scheduled at two weeks = t1, four weeks = t2, six weeks = t3, and at the same has been administered the following scale: VAS scale, SF-36, Oswestry Low Back Pain Disability Questionnaire, Aberdeen Back Pain Scale (ABPS), Revised Leeds Disability Questionnaire (LDQ), Roland and Morris Disability Questionnaire. Significant improvements was noted in the ALA and GLA group for paresthesia, stabbing and burning pain, as showed by VAS (Visual Analogue Scale), Oswestry Low Back Pain Disability Questionnaire, Aberdeen Low Back Pain Scale; also, improvements of quality of life has been noted, in the same group, as showed by SF-36, LDQ (Revised Leeds Disability Questionnaire), Roland and Morris disability questionnaire. All these outcome measure showed statistically significant decreases. Oral treatment with alpha-lipoic acid (ALA) and gamma-linolenic acid (GLA) for six weeks in synergy with rehabilitation therapy improved neuropathic symptoms and deficits in patients with radicular neuropathy.

Proposal for a standardized protocol for the systematic orofacial examination of patients with Hereditary Sensory Radicular Neuropathy

To apply a standardized protocol for the orofacial evaluation of two adult siblings (one male and one female) with Hereditary Sensory Radicular Neuropathy (HSRN) that presented with dental problems. The systematic evaluation consisted of (a) clinical questionnaire; (b) radiographs [orthopantomography and computarized tomography (CT)]; (c) orofacial psychophysical tests (pain, thermal, mechanical and electrical sensation); and (d) histology of gingiva and pulp (optical and transmission electronic microscopy). The female patient had complete insensitivity to orofacial pain and partial facial heat sensitivity, and received dental treatment without anaesthesia or pain. She had a severe and painless jaw infection due to pulp necrosis in tooth 37. The male patient had partial insensitivity to orofacial pain and required anaesthesia for dental treatment. Histological examination of gingivae and pulpal tissue revealed an altered proportion of unmyelinated and myelinated sensory nerve fibres. * Patients with HSRN may present with significant, silent dental disease. * A standard protocol is helpful when evaluating such patients. * If the opportunity arises, evaluation of pulp tissue may reveal an altered proportion of myelinated and unmyelinated nerve fibres. This may avoid the more estabilished sural nerve biopsy.

Topical high molecular weight hyaluronan reduces radicular pain post laminectomy in a rat model

Topical high molecular weight hyaluronan reduces radicular pain post laminectomy in a rat model

NEUROPATHY AND S.L.E. (REVIEW OF THE LITERATURE AND PERSONAL RESULTS)

In 1950, for the first time, some authors described neuropathy in patients affected by SLE. This manifestation rarely was described like a beginning symptom, its incidence increased during the last ten years (from 1% to 10%).Pathogenesis is usually linked up to the evidence of vasculitic lesions due to the presence of self‐antibodies which precipitation produce vasa nervorum occlusion or promote relasing of inflammatory factors.Neuropathy has until now four well‐known main manifestations:–Sensory‐Motory Polineuropathy: the most frequent assonal, symmetric, distal, and subacute neuropathy.–Radicular Neuropathy: with acute beginning, axonal and demielinating damage with a pathogenesis linked up to the presence of Antifosfolipidi antibodies.–Mononeuropathy Multiplex: it can be a SLE beginning symptom, assonal, also with the involvement of cranial nerves.–Autonomic Neuropathy: it can be isolated or it can be only one manifestation of a wide nervous system involvement.Between Sept. 1998 and Dec. 1999, we studied 30 patients affected by SLE; 5 patients presented a polineuropathy prevalently sensitive, assonal, distal, involving frequently inferior limbs, which represents 16.6% of the population.Even if we think necessary an enlargment of the casistic, we consider appropriate to point to the increase of neuropathy incidence in SLE patients, probably due to a neurological approach. Immunological study of these patients usually doesn't allow a correct evaluation of the peripheral nervous system involvment.Therefore, peripheric and central nervous system complications of SLE must be considered important for the course of the systemic disease and for therapeutic choice.

The gene for hereditary sensory neuropathy type I (HSN–I) maps to chromosome 9q22.1–q22.3

Hereditary sensory neuropathy type I (HSN-I, also known as hereditary sensory and autonomic neuropathy type I (HSAN-I), or hereditary sensory radicular neuropathy) is an autosomal dominant disorder that is the most common of a group of degenerative disorders of sensory neurons. HSN-I was initially recognized as a disease that produced mutilating ulceration leading to amputation of digits (Fig. 1). It was given names such as familial ulcers with mutilating lesions of the extremities and perforating ulcers with osseous atrophy. The disease involves a progressive degeneration of dorsal root ganglion and motor neurons, leading to distal sensory loss and later distal muscle wasting and weakness and variable neural deafness. Sensory deficits include loss of all modalities, particularly loss of sensation to pain and temperature. Skin injuries may lead to chronic skin ulcers, osteomyelitis, and extrusion of bone fragments, especially the metatarsals. Onset of symptoms is in the second or later decades. We undertook a genome screen using linkage analysis in four Australian HSN-I kindreds. We now show that the HSN1 gene maps to an 8-centiMorgan (cM) region flanked by D9S318 and D9S176 on chromosome 9q22.1-q22.3. Multipoint linkage analysis suggests a most likely location at D9S287, within a 4.9-cM confidence interval.

Is there involvement of the central nervous system in hereditary sensory radicular neuropathy?

There is pathological evidence that hereditary sensory radicular neuropathy (HSN type I) is a disorder related to multi-system atrophy with marked cell loss in the cerebral cortex, thalamus, brain stem and cerebellum. We report here a clinical study of a case of HSN-I including audiometric testing, autonomic functions, electromyography, transcranial magnetic stimulation and magnetic resonance imaging of the brain. There were no signs of central nervous system involvement. It is stated that HSN-I remains a disorder of dorsal root ganglia and sensory nerves, leading to painless perforating ulceration and mutilation, within the course of the disease peripheral motor nerve involvement, but without involvement of central motor pathways.

Osteoarthropathy in hereditary sensory radicular neuropathy

A young man had hereditary sensory radicular neuropathy with relapsing ulcer of the foot and, in addition to previously known clinical features, osteoarthropathy with hallux valgus, metatarsus primus varus, exostosis, and pes planus.

Orthopedic Aspects of Congenital Insensitivity to Pain

In an 11-year-old girl with congenital insensitivity to pain, diagnosis depended on three diagnostic features: pain sensation absent from birth; entire body affected; all other sensory modalities and deep tendon reflexes present. The cause of this disease is unknown. Other diseases to be considered when insensitivity to pain is present are diabetes, lues, and syringomyelia. Less common neurologic diseases are congenital sensory neuropathy with or without anhidrosis, familial dysautonomia (Riley-Day syndrome), and sensory radicular neuropathy. The three orthopedic manifestations of congenital insensitivity to pain are recurrent fractures, neuropathic (Charcot's) joints, and osteomyelitis. Management is based on proper appreciation of the disease. Prevention of complications is important. Treatment of fractures and osteomyelitis is straightforward. However, the treatment of neuropathic joints demands caution and is done best nonsurgically.

Hereditary sensory radicular neuropathy. A case report

Hereditary sensory radicular neuropathy. A case report

Hereditary Perforating Ulcers of the Foot

In 4 cases of hereditary sensory radicular neuropathy the loss of pain and thermal sensibility resulting in perforating ulcers starts distally in lower extremities and progresses proximally. It has a sporadic and familial form as well as the hereditary type. In siblings inheritance appeared to be autosomal dominant. By early recognition of the disease and removing pressure from the involved areas, or spreading pressure equally over the foot with proper footwear ulcers are preventable.

HEREDITARY SENSORY NEUROPATHY WITH SPASTIC PARAPLEGIA

Five cases of spastic paraplegia with a progressive symmetrical sensory neuropathy producing ulceration and osteomyelitis of the hands and feet are reported. The pathology in one patient, who died of secondary amyloidosis, was similar to that found by Denny-Brown in hereditary sensory radicular neuropathy with severe loss of posterior root ganglion cells and loss of myelinated fibres in both peripheral nerves and posterior columns of the spinal cord. A sural nerve biopsy in another case showed a striking loss of both myelinated and unmyelinated fibres, with some evidence of degeneration and regeneration. The inheritance is probably by an autosomal recessive gene. The prognosis in the more severe form of the disorder is poor.

Analysis of serum immunoglobulins in hereditary sensory radicular neuropathy

Serum and salivary immunoglobulins were studied in 11 members of a family including 3 patients with hereditary sensory radicular neuropathy (HSRN) in 1 of whom serum immunoglobulins were measured over a period of about 6 years. It was confirmed that serum IgA and IgG levels rose as the disease progressed. Although our results do not agree, in part, with the findings of Whitaker et al. (1974) who reported an increase in IgA alone, the present study suggested that such dysimmunoglobulinaemia deserves further study. Whether dysimmunoglobulinaemia is a primary phenomenon related to the development of HSRN or simply a secondary change remains to be further explored.

Hereditary Deafness and Sensory Radicular Neuropathy

We report a case of radicular sensory neuropathy and deafness. The patients appears to be one of a family in whom several members were similarly afflicted. Thus, this case fits the pattern of hereditary deafness and sensory radicular neuropathy, originally described by Hicks in 1922.

NOTICES OF RECENT PUBLICATIONS

Journal Article NOTICES OF RECENT PUBLICATIONS Get access Hereditary Sensory Radicular Neuropathy. By DAVID C. WALLACE. 1970. Pp. 114. Sydney: Australasian Medical Publishing Co. Ltd. No price stated. R. T. C. PRATT R. T. C. PRATT Search for other works by this author on: Oxford Academic PubMed Google Scholar Brain, Volume 97, Issue 1, 1974, Page 812, https://doi.org/10.1093/brain/97.1.812 Published: 01 January 1974

Hereditary sensory radicular neuropathy. A case report.

Hereditary sensory radicular neuropathy. A case report.

Hereditary sensory radicular neuropathy: an electrophoretic and immunoelectrophoretic study of the blood serum

The protein metabolism in four cases of hereditary sensory radicular neuropathy was studied through the electrophoresis and immunoelectrophoresis of the blood serum. A slight increase of the gammaglobulin content was found in all cases. The immunoelectrophoresis showed an absense of IgA in a case, a slight increase of IgG in all cases, and an absence of IgM in two cases and a marked decrease of this macroglobulin in two cases of the disease and in their healthy parents. Only two patients showed an increase of beta1 lipoprotein.

Congenital Sensory Neuropathy

Congenital sensory neuropathy is a term which is useful to denote a small group of patients in whom pain, temperature, and touch sensibility is absent or diminished on the extremities and varying portions of the trunk. Deep tendon reflexes are absent or hypoactive, and skin or sensory nerve biopsy or both usually reveal some abnormality of neural structures.1,2The condition is sporadic and nonprogressive, unlike hereditary sensory radicular neuropathy, syringomyelia, and the acquired sensory neuropathies. Normal autonomic function distinguishes it from the dysautonomias and an interesting group of recently reported cases of analgesia and hypohidrosis.3,4The presence of the histologic abnormalities mentioned above and involvement of sensory modalities other than pain should adequately separate the condition from congenital indifference to pain, though the information in some case reports is not sufficient to permit this distinction to be made clearly. We report here what we believe to be the