[Clinical effect of acupuncture combined with medication on diabetic peripheral neuropathy and its influence on serum lipid metabolism].

OBJECTIVE: To observe the clinical effect on diabetic peripheral neuropathy (DPN) treated with acupuncture combined with medication and explore its effect mechanism. METHODS: Sixty-two patients of DPN were randomly divided into a combined therapy group (31 cases) and a medication group (31 cases, 2 cases dropped out); besides, 20 healthy subjects were recruited as a normal group. On the base of routine intervention, in the medication group, thioctic acid capsules were administrated orally, 0.2 g each time, 3 times a day. In the combined therapy group, besides the medication as the medication group, acupuncture was performed on bilateral Quchi (LI 11), Waiguan (TE 5), Hegu (LI 4), Tianshu (ST 25), Zusanli (ST 36), Sanyinjiao (SP 6) and Taichong (LR 3) and the needles were retained for 30 min, acupuncture was delivered once daily, 6 times a week. The duration of treatment was 4 weeks in the two groups. The score of Toronto clinical scoring system (TCSS), the nerve conduction velocity of median nerve (MN) and common peroneal nerve (CPN) were observed before and after treatment in the two intervention groups; and the serum lipid metabolism was detected before and after treatment in the two intervention groups and the normal group. RESULTS: Compared with that before treatment, the scores of TCSS were reduced in the combined therapy group and the medication group (P<0.05) after treatment, and the score decrease in the combined therapy group was larger than that of the medication group (P<0.001). The motor nerve conduction velocity and the sensory nerve conductive velocity of MN and CPN after treatment all increased in the combined therapy group and the medication group compared with those before treatment (P<0.05), and the improvements in the combined therapy group were larger than those of the medication group (P<0.001). Before treatment DPN patients had 365 differential lipid metabolites, including sphingosine (SPH, d18:0), involved in the inositol phosphate metabolism, compared with the subjects of the normal group. There were 103 differential lipid metabolites in the medication group before and after treatment, including lysophosphatidyl ethanolamine (LPE, 18:1/0:0), participated in glycerophospholipid metabolism. In the combined therapy group, before and after treatment, there were 99 differential lipid metabolites, including lysophosphatidylcholine (LPC, 18:0/0:0), participated in the neuroactive ligand-receptor interaction. Acupuncture greatly affected 50 lipid metabolites such as lysophosphatidic acid (LPA, 0:0/22:6), LPA(0:0/18:2) and LPC(O-18:0), which was mainly involved in glycerophospholipid metabolism. CONCLUSION: Acupuncture combined with medication ameliorates the symptoms and the nerve conduction velocity in DPN patients, which may be related to the regulation of serum lipid metabolism.

Nerve cross-sectional area in advanced uremic neuropathy: A nerve ultrasound pilot study.

BACKGROUND AND PURPOSE: Uremic neuropathy (UN) is a disabling neuropathy in end-stage kidney disease (ESKD) affecting the majority of patients receiving long-term hemodialysis (HD). One previous nerve ultrasound study reported an increased cross-sectional area (CSA) of the median nerve in moderate UN, while another study found enlarged sural nerves in small-fiber polyneuropathy associated with ESKD. The present cohort study aims to analyze bilateral CSA of multiple nerves in UN. METHODS: Ten nondiabetic ESKD patients with UN on HD for at least 2 years and 10 healthy age-matched controls underwent bilateral ultrasound examinations with CSA measurements in 13 arm and leg nerve sites. Nerve conduction studies (NCS) and the total neuropathy score (TNS) were recorded. Pearson's coefficient and the Mann-Whitney U-test were used to analyze correlations and compare groups. RESULTS: ESKD patients presented advanced neuropathic symptoms (mean TNS 15.9). NCS showed significantly reduced motor and sensory amplitudes in the UN group compared to the control group, and a slightly reduced nerve CSA was observed in 5 of 13 nerve sites (p < .05); the other nerve sites were not enlarged. Sural nerve CSA (p < .05) and sensory amplitude (p < .01) were negatively correlated with the TNS. CONCLUSIONS: Nerve enlargement was not observed in the present study in advanced UN. A reduced nerve CSA observed in the sural nerve suggests an axonal loss associated with long-term HD in ESKD. During clinical workup of an acute disease of the peripheral nervous system in ESKD patients, nerve enlargement might be attributable to other causes than chronic UN.

Pharmacogenomic predictor of long-term residual chemotherapy-induced peripheral neuropathy in ovarian cancer survivors: A substudy of the GINECO Vivrovaire study.

BACKGROUND: Chemotherapy (CT) remains a backbone treatment of epithelial ovarian cancer (EOC) inducing persistent peripheral neuropathy (CIPN). Using a dedicated patient-reported outcome tool, this study investigated persistent CIPN and its pharmacogenetic predictors in a cohort of long-term EOC survivors. METHODS: Vivrovaire was a French multicenter cohort of patients with EOC free of disease 3 years after CT completion. Persistent CIPN was assessed using the FACT/GOG-Ntx4 self-questionnaire. The association of homozygous (hom) or heterozygous (het) single nucleotide polymorphisms (SNPs) in selected genes was evaluated. RESULTS: 130 patients were included with a median time from CT completion of 63 [35-180] months. The median CIPN score was 37 [18-44], with 35 (26.9%) patients reporting severe CIPN (<33). SNPs were identified as follows: CYP2C8 [hom, n = 32 (24.6%)/het, n = 99, (76.2%)]; CYP3A4 [hom, n = 0 (0%)/het, n = 8 (6.2%)], ERCC1 [hom, n = 21 (16.2%)/het, n = 57 (43.8%)], and XPC [hom, n = 45 (34.6%)/het, n = 66 (50.8%)]. In univariate analysis, the identification of ≥1 hom SNP was associated with a lower CIPN score (continuous variable; p = 0.045). Patients harboring hom or het CYP2C8_rs1934951 SNP reported more likely severe CIPN (threshold <33) score (OR 2.482; 95% CI [1.126-5.47], p = 0.024). In the multivariate analyses, age, interval from CT completion, type and number of CT courses were not significantly associated with CIPN score (OR 5.165, 95% CI [0.478-55.83], p = 0.176). CONCLUSIONS: Persistent CIPN is common among ovarian cancer long-term survivors. CYP2C8_rs1934951 SNP may be associated with severe residual CIPN in EOC survivors. More studies are warranted to identify predictive factors of CIPN.

Cardiac autonomic neuropathy in Graves' disease: smoking and age as predictive factors.

BACKGROUND: Hypermetabolic state in Graves' disease (GD) has a great impact on heart homeostasis, acting directly on the heart muscle and modulating the autonomic nervous system. AIMS: To characterize Cardiac Autonomic Neuropathy (CAN) as a possible complication in patients with GD. METHODS: We evaluated euthyroid GD patients and a control group of healthy euthyroid people. CAN was assessed using autonomic tests of cardiovascular reflex and heart rate variability: respiratory, Valsalva, orthostatic and orthostatic hypotension tests, high frequency, low frequency, and very low-frequency bands. Transthoracic echocardiography was performed in GD patients. RESULTS: 60 GD patients and 50 people in control group were assessed. CAN was diagnosed in 20% of GD and 14% in the control group. Among GD, 13.3% presented incipient, and 6.7%, established CAN, while in the control group, it was verified incipient in 8% and established in 6% (p=0.7479). All GD patients with CAN presented an alteration in the deep breathing test. Age and smoking were evidenced as factors associated with the presence of CAN, while higher TRAb values at diagnosis decreased the chance of NAC. CONCLUSIONS: The prevalence of CAN in euthyroid GD patients was 20%. Changes in the cardiac autonomic nervous system were identified, pointing to the importance of evaluating this complication in these patients. Smoking was a predictive factor for CAN, increasing its relationship with conditions that aggravate GD.

The ethanol extract of cocoa pod husk minimizes hyperalgesia and blood glucose levels in diabetic neuropathy model through transient receptor protein vanilloid (TRPV)-1.

Oxidative stress accumulation becomes a pathophysiological factor in diabetic neuropathy (DN), activating TRPV-1. Resveratrol in cocoa pod husk exhibits antioxidant activity that could be beneficial in DN. This study examined how the ethanol extract of cocoa pod husk (EECPH) affects DN in mice by targeting TRPV-1. Cocoa pod husk was extracted using 96 % ethanol with remaceration. The antioxidant activity was measured using DPPH. Mice were induced using alloxan 210 mg/kg BW i.p. At day 14, mice were randomized into seven groups: normal, diabetic, gabapentin 100 mg/kg BW, metformin 250 mg/kg BW, and EECPH (doses 250, 500, and 750 mg/kg BW). Treatments were administered orally, once daily for 14 days. The latency time and blood glucose levels were measured on days 7, 14, 21, and 28. On day 29, mice were sacrificed, and the blood, pancreas, and spinal cord were removed. Malondialdehyde, cholesterol, and serum glutamic oxaloacetic/pyruvic transaminase (SGOT/PT) were examined. Morphology of the spinal cord and pancreas was determined using hematoxylin and eosin staining. The expression of TRPV-1 was assessed using immunohistochemistry. The EECPH dose of 750 mg/kg BW showed the greatest effect in lowering hyperalgesia and blood glucose as well as cholesterol and SGOT/PT in mice. That dose also improved the histology of the pancreas and spinal cord by altering the expression of TRPV-1. It can be concluded that EECPH may lower the expression of TRPV-1 in the pancreas and spinal cord of mice. This activity was responsible of reducing hyperalgesia in DN mice.

The underlying causes, treatment options of gut microbiota and food habits in type 2 diabetes mellitus: a narrative review.

Type 2 diabetes mellitus is a long-lasting endocrine disorder characterized by persistent hyperglycaemia, which is often triggered by an entire or relative inadequacy of insulin production or insulin resistance. As a result of resistance to insulin (IR) and an overall lack of insulin in the body, type 2 diabetes mellitus (T2DM) is a metabolic illness that is characterized by hyperglycaemia. Notably, the occurrence of vascular complications of diabetes and the advancement of IR in T2DM are accompanied by dysbiosis of the gut microbiota. Due to the difficulties in managing the disease and the dangers of multiple accompanying complications, diabetes is a chronic, progressive immune-mediated condition that plays a significant clinical and health burden on patients. The frequency and incidence of diabetes among young people have been rising worldwide. The relationship between the gut microbiota composition and the physio-pathological characteristics of T2DM proposes a novel way to monitor the condition and enhance the effectiveness of therapies. Our knowledge of the microbiota of the gut and how it affects health and illness has changed over the last 20 years. Species of the genus Eubacterium, which make up a significant portion of the core animal gut microbiome, are some of the recently discovered 'generation' of possibly helpful bacteria. In this article, we have focused on pathogenesis and therapeutic approaches towards T2DM, with a special reference to gut bacteria from ancient times to the present day.

Polyneuropathy as an initial manifestation of Hereditary Transtyretin Amyloidosis (ATTRV) in a young patient: Case report of a diagnostic challenge.

We report the case of a 27-year-old man with transthyretin amyloidosis secondary to the p.Val142Ile mutation with an atypical clinical presentation of predominantly lower limb polyneuropathy without cardiac involvement. p.Val142Ile is mainly associated with cardiopathy, whereas the neuropathic phenotype is mainly associated with p.Val50Met. Our patient belongs to a non-endemic region and due to his lack of support network a possible familial component is unknown. His case represents a diagnostic challenge given the wide heterogeneity of clinical manifestations associated with the disease, with other possible diagnoses of polyneuropathy being reasonably excluded according to prevalence and frequency. The particularly unusual genotype-phenotype association distinguishes this case from the classic description of transthyretin amyloidosis secondary to p.Val142Ile.

Leber's hereditary optic neuropathy like disease in MT-ATP6 variant m.8969G>A.

Purpose: To describe a case with Leber's hereditary optic neuropathy (LHON) like optic atrophy in the presence of MT-ATP6 gene variant m.8969G > A. Observations: A 20-year-old patient with a history of mild developmental delay, mild cognitive impairment, and positional tremor presented with subacute painless visual loss over a few weeks. Mitochondrial genome sequencing revealed a variant in MT-ATP6, m.8969G > A (p.Ser148Asn). This variant was previously reported in association with mitochondrial myopathy, lactic acidosis, and sideroblastic anemia (MLASA) and with nephropathy, followed by brain atrophy, muscle weakness and arrhythmias, but not with optic atrophy. Conclusions and importance: Rare variants in MT-ATP6 can also cause LHON like optic atrophy. It is important to perform further genetic analysis of mitochondrial DNA in genetically unsolved cases suspected of Leber's hereditary optic neuropathy to confirm the clinical diagnosis.

Long-term clinical observation of patients with heterozygous KIF1A variants.

KIF1A-related disorders (KRDs) encompass recessive and dominant variants with wide clinical variability. Recent genetic investigations have expanded the clinical phenotypes of heterozygous KIF1A variants. However, there have been a few long-term observational studies of patients with heterozygous KIF1A variants. A retrospective chart review of consecutive patients diagnosed with spastic paraplegia at Miyagi Children's Hospital from 2016 to 2020 identified six patients with heterozygous KIF1A variants. To understand the long-term changes in clinical symptoms, we examined these patients in terms of their characteristics, clinical symptoms, results of electrophysiological and neuroimaging studies, and genetic testing. The median follow-up period was 30 years (4-44 years). This long-term observational study showed that early developmental delay and equinus gait, or unsteady gait, are the first signs of disease onset, appearing with the commencement of independent walking. In addition, later age-related progression was observed in spastic paraplegia, and the appearance of axonal neuropathy and reduced visual acuity were characteristic features of the late disease phenotype. Brain imaging showed age-related progression of cerebellar atrophy and the appearance of hyperintensity of optic radiation on T2WI and FLAIR imaging. Long-term follow-up revealed a pattern of steady progression and a variety of clinical symptoms, including spastic paraplegia, peripheral neuropathy, reduced visual acuity, and some degree of cerebellar ataxia. Clinical variability between patients was observed to some extent, and therefore, further studies are required to determine the phenotype-genotype correlation.

Co-occurrence of glial fibrillary acidic protein astrocytopathy in a patient with Leber's hereditary optic neuropathy due to DNAJC30 mutations.

Leber's hereditary optic neuropathy (LHON) is a mitochondrial disease characterized by visual loss, and rarely associated with extraocular manifestations including multiple sclerosis-like lesions. The association of LHON and neuromyelitis optica spectrum disorders has rarely been reported. Here is reported a case of glial fibrillary acidic protein astrocytopathy presenting with area postrema syndrome in a patient with previously diagnosed recessive LHON due to mutations in the nuclear gene DNAJC30. This case emphasizes the necessity of extensive investigations for other treatable conditions in patients with LHON and otherwise unexplained extraocular involvement and the possibility that also visual symptoms can respond to immune therapy.

Peripheral Neuropathy.

Peripheral neuropathy is a commonly encountered diagnosis in both neurology and primary care office settings. It is important for primary care providers to identify, characterize, and diagnose patients with neuropathy. This study aims to describe the clinical presentation, diagnostic work up, and treatment options for this entity, as well as the identification of atypical features that should prompt specialized laboratory testing, electrodiagnostic testing, and neurologic consultation.

Visual dysfunction and neurodegeneration caused by severe inflammatory optic neuropathy after coil embolization of a paraclinoid aneurysm: illustrative case.

BACKGROUND: Visual impairment due to delayed optic neuropathy is a rare complication of the endovascular treatment of paraclinoid aneurysms. An inflammatory response induced in the treated aneurysm wall is a known mechanism underlying this pathophysiology. The authors describe a case with severe and progressive optic neuropathy leading to neuronal degeneration and severe visual dysfunction. OBSERVATIONS: A 42-year-old female with a history of surgical clipping for a paraclinoid aneurysm presented with a recurrence. Although the patient was unaware of any visual dysfunction, a preoperative ophthalmological examination revealed mild inferior quadrantanopia in the left eye. The coil embolization procedure was uneventful; however, the following day, the patient experienced progressive visual impairment, which worsened despite the initiation of steroid therapy. Ophthalmological examination revealed a severe decrease in visual acuity and further deterioration of the visual field. Magnetic resonance imaging showed remarkable swelling and edema of the left optic nerve adjacent to the treated aneurysm. Despite continued steroid therapy, the patient's visual function did not recover well due to subsequent optic nerve degeneration. LESSONS: Optic neuropathy after endovascular procedures can lead to severe visual dysfunction. Careful management is essential, particularly when treating a symptomatic paraclinoid aneurysm, even if symptoms are only apparent on detailed examination.

Dorsal root ganglion magnetic resonance imaging biomarker correlations with pain in Fabry disease.

Fabry disease is a rare monogenetic, X-linked lysosomal storage disorder with neuropathic pain as one characteristic symptom. Impairment of the enzyme alpha-galactosidase A leads to an accumulation of globotriaosylceramide in the dorsal root ganglia. Here, we investigate novel dorsal root ganglia MR imaging biomarkers and their association with Fabry genotype and pain phenotype. In this prospective study, 89 Fabry patients were examined using a standardized 3 T MRI protocol of the dorsal root ganglia. Fabry pain was assessed through a validated Fabry pain questionnaire. The genotype was determined by diagnostic sequencing of the alpha-galactosidase A gene. MR imaging end-points were dorsal root ganglia volume by voxel-wise morphometric analysis and dorsal root ganglia T2 signal. Reference groups included 55 healthy subjects and Fabry patients of different genotype categories without Fabry pain. In patients with Fabry pain, T2 signal of the dorsal root ganglia was increased by +39.2% compared to healthy controls (P = 0.001) and by +29.4% compared to painless Fabry disease (P = 0.017). This effect was pronounced in hemizygous males (+40.7% compared to healthy; P = 0.008 and +29.1% compared to painless; P = 0.032) and was consistently observed across the genotype spectrum of nonsense (+38.1% compared to healthy, P < 0.001) and missense mutations (+39.2% compared to healthy; P = 0.009). T2 signal of dorsal root ganglia and globotriaosylsphingosine levels were the only independent predictors of Fabry pain (P = 0.047; P = 0.002). Volume of dorsal root ganglia was enlarged by +46.0% in Fabry males in the nonsense compared to missense genotype category (P = 0.005) and by +34.5% compared to healthy controls (P = 0.034). In painful Fabry disease, MRI T2 signal of dorsal root ganglia is increased across different genotypes. Dorsal root ganglion MRI T2 signal as a novel in vivo imaging biomarker may help to better understand whether Fabry pain is modulated or even caused by dorsal root ganglion pathology.

Peripheral Neuropathy Associated with Higher Mortality in Population with Chronic Kidney Disease: National Health and Nutrition Examination Surveys.

Introduction: Peripheral neuropathy (PN), one of the commonest neurological complications of chronic kidney disease (CKD), was associated with physical limitation. Studies showed that a decrease in physical capability in patients with CKD is related with an increased risk of mortality. The objective of our research was to directly explore the relationship between PN and risk of mortality in patients with CKD. Method: 1,836 participants with CKD and 6,036 participants without CKD, which were classified by PN based on monofilament examination in National Health and Nutrition Examination Survey (NHANES), were collected from the 1999 to 2004 National Health and Nutrition Examination Surveys. Multivariable Cox proportional hazard models were conducted to assess the relationships of PN and deaths in patients with CKD and non-CKD. Results: During 14 years of a median follow-up from 1999 to 2015 and 2004 to 2015, 1,072 (58.4%) and 1,389 (23.0%) deaths were recorded in participants with CKD and without CKD, respectively. PN was related with increased all-cause mortality even after adjusting possible confounding factors in population with CKD (hazard ratio [HR] 1.34, 95% confidence interval [CI] 1.17-1.53) and without CKD (HR 1.27, 95% CI 1.12-1.43). And the adjusted HRs (95% CI) for cardiovascular mortality of the people with CKD and without CKD who suffered from PN were 1.42 (1.07, 1.90) and 1.23 (0.91, 1.67), respectively, versus those without PN. Conclusion: PN was related with a higher risk of all-cause and cardiovascular death in people with CKD, which clinically suggests that the adverse prognostic impact of PN in the CKD population deserves attention and is an important target for intervention.

Cross-Sectional Study of the Relationship Between Medial Plantar Nerve Conduction Studies and Severity of Diabetic Neuropathy.

Objective: Diabetic peripheral neuropathy (DPN), a complication of diabetes, is detected only in later stages. Medial plantar nerve (MPL) can identify earlier stages of neuropathy. We evaluated the correlation of MPL sensory nerve action potentials (SNAPs) and severity of DPN measured using the Toronto Clinical Neuropathy Score (TCNS). Methods: In this hospital-based, cross-sectional study, we recruited diabetic subjects referred for suspected DPN. Neuropathy was graded with TCNS. Sural nerve conduction studies were performed using standard techniques. MPL studies were conducted using the modified Ponsford technique. All evaluations were performed on Nihon Kohden (model MEB 9200K). Averaged MPL SNAP was correlated with TCNS using Pearson's correlation coefficient. To estimate a correlation of 0.4 with 80% power (P = 0.05), we needed 46 subjects. Linear regression was conducted to adjust for age, duration, and diabetic control. Receiver operating characteristic (ROC) curve analysis was performed to obtain the cutoff for MPL SNAP values using the Youden index. Results: Fifty-one subjects with a mean age of 53.5 years (8.7) and mean duration of diabetes of 10.2 years (7.2) were included. MPL SNAPs were recordable in 12 patients, and the mean amplitude was 5.15 (2.9) µV. There was correlation between MPL SNAP and TCNS (r = -0.43, P = 0.02). No confounding was seen. Use of MPL SNAP resulted in diagnosis of DPN in an additional six (11.8%) patients. The ROC curve suggested that MPL SNAP cutoff of 1.05 µV had an accuracy of 67% in identifying neuropathy as defined by TCNS. Conclusions: MPL SNAP has a moderate correlation with clinical score and identifies more diabetic neuropathy than sural nerve.

Assessing Nerve Conduction Velocity as a Diagnostic and Prognostic Indicator in Leprosy Patients: A Cross-Sectional Study.

Introduction Hansen's disease is a condition in which patients develop peripheral neuropathy. In 1873, G. H. A. Hansen discovered Mycobacterium leprae, the causative agent of leprosy, a chronic infectious disease. These bacteria influence the peripheral nerves, which is likely to cause neuropathy. Sensory nerve conduction studies were performed in leprosy patients on the upper limb nerves of 30 patients in the rural area of the Wardha district in the Indian population. Methods In this study, we recruited 30 leprosy patients from the Department of Dermatology and A.V.B.R. Hospital, Sawangi Wardha. The patient's nerve conduction velocity (NCV) tests were carried out in the Department of Physiology at J. N. Medical College, Wardha. NCVs were obtained during these three years, beginning in 2009, while performing sensory nerve conduction velocity (SNCV) and motor nerve conduction velocity (MNCV). The latency, amplitude, and NCV parameters were recorded, and the data collection period ended in 2011. In this study, we measured both MNCV and SNCV. Results In our study, impairment of conductional velocity was observed. In leprosy patients, the MNCV values of latency, amplitude, and conductional velocity were 6.61, 3.89, and 46.92 m/s, respectively, whereas the SNCV values were 3.005, 25.17, and 38 m/s, respectively. Based on the results, it appears that the maximal sensory nerve involvement was recorded at 38 m/s conductional velocity. In NCVs, increased latency and decreased conductional velocity were found across the study. Conclusion It was concluded that nerve conduction studies are one of the non-invasive techniques for early diagnosis and management of leprosy. This study should be repeated with a larger sample size and should be multicentric.

Neuropathy in a Patient With Congenital Absence of the Inferior Vena Cava.

Neuropathic pain is a frequent complaint in the neurology clinic. We present a case of a 31-year-old male with congenital absence of the inferior vena cava (AIVC) resulting in venous hypertension who complained of lower extremity pain interfering with his daily activities. His AIVC was thought to be incidental rather than causative of his pain complaints. His examination was consistent with peripheral neuropathy. Simple lifestyle adaptations, such as restriction of physical activity and leg elevation, were sufficient to relieve his symptoms. Recognition of the role of AIVC may have prevented additional invasive procedures in our patient.

Optic Neuritis in Resolving Phase of COVID-19 Infection and Its Management: A Case Report.

Optic neuritis is assumed to be immune-mediated, although the specific antigens that cause demyelination are uncertain. Systemic T-cell activation is detected at the onset of symptoms, which occurs before alterations in cerebrospinal fluid (CSF). The optic nerve disease is a rare disease and can occur in one or both eyes, especially in those with no established inflammatory or autoimmune illnesses. Adult ophthalmic neuritis is usually unilateral and is frequently associated with multiple sclerosis (MS). Generally, it starts as a rapid loss of vision and pain in eye movement. It progresses and achieves the maximal deficiency over a week. The objectives of this paper were to determine the association between coronavirus disease 2019 (COVID-19) and optic neuritis and to study the management of optic neuritis in the resolving phase of COVID-19. A case study was done on a 38-year-old female complaining of sudden diminution of vision in her right eye for one week. She tested positive on the reverse transcriptase-polymerase chain reaction (RT-PCR) test for COVID-19 for which she was managed symptomatically and was started on antiretrovirals. This case report is based on an infrequent COVID-19 complication. It has been proposed that this virus has the probability of manifesting various neurological complications. In our case, optic neuritis occurs mainly three weeks after COVID-19 infection. Our patient was managed by intravenous methylprednisolone injection followed by oral prednisone for 14 days. So, further case studies will be required to support the above treatment plan for optic neuritis caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Unilateral or bilateral optic neuritis can occur as a neurological complication in the resolving stage of COVID-19 infection. Early detection and treatment with steroids can result in the best visual outcome.

Retention of Improved Plantar Sensation in Patients with Type II Diabetes Mellitus and Sensory Peripheral Neuropathy after One Month of Vibrating Insole Therapy: A Pilot Study.

Sensory peripheral neuropathy is a common complication of diabetes mellitus and the biggest risk factor for diabetic foot ulcers. There is currently no available treatment that can reverse sensory loss in the diabetic population. The application of mechanical noise has been shown to improve vibration perception threshold or plantar sensation (through stochastic resonance) in the short term, but the therapeutic use, and longer-term effects have not been explored. In this study, vibrating insoles were therapeutically used by 22 participants, for 30 min per day, on a daily basis, for a month by persons with diabetic sensory peripheral neuropathy. The therapeutic application of vibrating insoles in this cohort significantly improved VPT by an average of 8.5 V (p = 0.001) post-intervention and 8.2 V (p < 0.001) post-washout. This statistically and clinically relevant improvement can play a role in protection against diabetic foot ulcers and the delay of subsequent lower-extremity amputation.

Evaluation of the Effect of Loratadine versus Diosmin/Hesperidin Combination on Vinca Alkaloids-Induced Neuropathy: A Randomized Controlled Clinical Trial.

Neurological injury is a crucial problem that interferes with the therapeutic use of vinca alkaloids as well as the quality of patient life. This study was conducted to assess the impact of using loratadine or diosmin/hesperidin on neuropathy induced by vinca alkaloids. Patients were randomized into one of three groups as follows: group 1 was the control group, group 2 received 450 mg diosmin and 50 mg hesperidin combination orally twice daily, and group 3 received loratadine 10 mg orally once daily. Subjective scores (numeric pain rating scale, douleur neuropathique 4, and functional assessment of cancer therapy/gynecologic oncology group-neurotoxicity (FACT/GOG-Ntx) scores), neuroinflammation biomarkers, adverse drug effects, quality of life, and response to chemotherapy were compared among the three groups. Both diosmin/hesperidin and loratadine improved the results of the neurotoxicity subscale in the FACT/GOG-Ntx score (p < 0.001, p < 0.01 respectively) and ameliorated the upsurge in neuroinflammation serum biomarkers. They also reduced the incidence and timing of paresthesia (p = 0.001 and p < 0.001, respectively) and dysuria occurrence (p = 0.042). Both loratadine and diosmin/hesperidin attenuated the intensity of acute neuropathy triggered by vinca alkaloids. Furthermore, they did not increase the frequency of adverse effects or interfere with the treatment response.