Uncommon cause of trigeminal neuritis and central nervous system involvement by herpes labialis: a case report.

BACKGROUND: Trigeminal neuropathy is characterized by numbness in the region innervated by the trigeminal nerves, with or without neuropathic weakness in the muscles of mastication. Trigeminal neuritis is a form of trigeminal neuropathy in which the lesion is caused by an inflammation. Herein, we report a patient with trigeminal neuritis due to central nervous system (CNS) involvement of herpes labialis (HL) infection, which was successfully treated with anti-viral and anti-inflammatory agents. CASE PRESENTATION: A young healthy female presented with numbness in the left hemiface for two weeks. She had a preceding typical HL infection on left facial lip one week before the sensory symptom onset. Brain magnetic resonance imaging revealed high signal intensities and asymmetrical thickening with enhancement along the cisternal segment of the left trigeminal nerve. Additionally, brain MR angiography showed multifocal stenoses in the M1 segment of the middle cerebral artery and the cavernous portion of the internal carotid artery. Cerebrospinal fluid (CSF) examination showed mild pleocytosis with normal protein level, glucose ratio, but CSF polymerase chain reaction assay for specific anti-viral antibodies including herpes simplex virus was negative, and CSF culture also did not identify a specific pathogen. The results of serologic testing including tumor markers and autoimmune markers were all unremarkable. A tentative diagnosis of trigeminal neuritis as a complication of HL involving the CNS was made considering the clinical, neuroradiological, and laboratory findings of the patient. Therefore, the patient was treated with intravenous methylprednisolone and acyclovir for 10 days. After the treatments, her sensory disturbance was markedly improved. Brain MRI at the 3-month follow-up also demonstrated improvement of previously identified high signal intensity lesions and multifocal intracerebral artery stenoses. CONCLUSION: HL is usually a self-limiting, benign disease without complications, but rarely presents as trigeminal neuritis due to CNS involvement. Therefore, meticulous evaluation may be necessary if trigeminal neuritis or CNS involving symptoms occur after HL.

Donor site morbidity of calcaneal, distal tibial, and proximal tibial cancellous bone autografts in foot and ankle surgery. A systematic review and meta-analysis of 2296 bone grafts.

PURPOSE: This study aims to report on the safety and donor site morbidity of the distal lower extremity (calcaneal, proximal, and distal tibial) cancellous bone autografts. We summarized the findings in a comprehensive infographic illustration. We are unaware of any similar meta-analyses to date. METHODS: Following the PRISMA guidelines, two independent investigators searched MEDLINE (PubMed), EMBASE, SCOPUS, Google Scholar, and Cochrane databases in December 2020 using the following keywords and their synonyms: ("bone graft", "donor site morbidity", "calcaneal graft", "proximal tibia graft", and "distal tibia graft"). Besides, the reference lists from previous review articles were searched manually for eligible studies. The primary outcomes of interest were (1) chronic pain, (2) fracture, and (3) infection, whereas the secondary outcomes were (1) neurological complications, (2) sensory disturbance and hypertrophic scars, (3) other complications such as shoe-wear difficulties and gait disturbance. Inclusion criteria were: studies on complications and adverse events of lower extremity bone autografts (calcaneal, proximal tibial, and distal tibial bone autografts) reporting at least one of the desired outcomes. Studies not reporting any of the outcomes of interest or if the full text is not available in English were excluded. Studies reporting on bone marrow aspirate or autografts for non-orthopedic indications were also excluded. RESULTS: After the removal of duplicates, a total of 5981 studies were identified. After screening those records, 85 studies remained for full-text assessment. Out of those, 15 studies qualified for the meta-analysis with a total of 2296 bone grafts. Out of those grafts, 1557(67.8%) were calcaneal grafts, 625 (27.2%) were proximal tibial grafts, and 114 (5%) were distal tibial grafts. In calcaneal bone grafts, there were 28 cases of chronic pain [1.97%, CI:1.10-2.50%, I2 = 66%], 5 fractures [0.32%, CI: 0.10-0.60%,I2 = 0%], 20 sural neuritis [1.28%, CI:0.70-1.80%, I2 = 0%), and no wound infections. In proximal tibial grafts there were 13 cases of chronic pain [2.08%, CI: 1.01-3.2%, I2 = 34.5%], 1 fracture [0.16%, CI:0.10-0.50%, I2 = 0%], and 3 superficial wound infections [0.48%, CI: 0.10-1.01, I2 = 0%]. In the distal tibial grafts there were no cases of chronic pain or wound infections, 1 fracture [0.90%, CI: 0.80-2.6%, I2 = 0%], and 5 saphenous neuritis [4.5%, CI: 0.70-8.40%, I2 = 65%]. CONCLUSION: Calcaneal, distal tibial, and proximal tibial bone autografts are safe with a low rate of overall and major complications. We report an overall complication rate of 6.8%, which is less than half of that previously reported for iliac crest grafts. The authors recommend using distal lower extremity grafts for foot and ankle primary surgeries instead of iliac crest grafts when indicated. Clinical trials with a large sample size are required.

Oxytocin reverses ethanol consumption and neuroinflammation induced by social defeat in male mice.

Oxytocin (OXT) modulates social interactions, attenuates stressful responses and can decrease drug-seeking and taking behaviors. In previous studies, we observed that social defeat (SD) induced a long-lasting increase in ethanol intake and neuroinflammation in male mice. We also know that OXT blocks the increase in cocaine reward induced by SD. Therefore, in the present study we aimed to evaluate the effect of 1 mg/kg of OXT administered 30 min before each episode of SD on ethanol consumption and the neuroinflammatory response in adult male mice. Three weeks after the last SD, mice underwent oral ethanol self-administration (SA) procedure, and striatal levels of the two chemokines CX3CL1 and CXCL12 were measured after the last SD and at the end of the ethanol SA. OXT administration blocked the increase in voluntary ethanol consumption observed in defeated mice, although it did not affect motivation for ethanol. An increase in the striatal levels of CX3CL1 and CXCL12 was observed in defeated animals immediately after the last defeat and after the ethanol SA. However, defeated mice treated with OXT did not show this increase in the neuroinflammatory response. In conclusion, OXT treatment can be a powerful therapeutic target to reduce the negative effects of social stress on ethanol consumption and the neuroinflammatory process.

Isolated Oculomotor Neuritis After Dengue Fever.

ABSTRACT: We report a rare case of isolated partial left III cranial nerve palsy due to inflammatory oculomotor neuritis after dengue fever with unique neuro-imaging findings of enhancement seen along the entire course of the oculomotor nerve.

Clinical spectrum and prognosis of neurological complications of reactivated varicella-zoster infection: the role of immunosuppression.

Immunosuppressed patients are at higher risk for developing herpes zoster (HZ), and neurological complications are frequent in them. However, the influence of immunosuppression (IS) on the severity and prognosis of neurological complications of varicella-zoster virus (VZV) reactivation is unknown. We studied retrospectively patients with neurological complications due to VZV reactivation who attended our hospital between 2004 and 2019. We aimed to assess the clinical spectrum, potential prognostic factors, and the influence of the immune status on the severity of neurological symptoms. A total of 98 patients were included (40% had IS). Fifty-five patients (56%) had cranial neuropathies which included Ramsay-Hunt syndrome (36 patients) and cranial multineuritis (23 patients). Twenty-one patients developed encephalitis (21%). Other diagnosis included radiculopathies, meningitis, vasculitis, or myelitis (15, 10, 6, and 4 patients, respectively). Mortality was low (3%). At follow-up, 24% of patients had persistent symptoms although these were usually mild. IS was associated with severity (defined as a modified Rankin scale greater than 2) (odds ratio, 4.23; 95% confidence interval, 1.74-10.27), but not with prognosis. Shorter latency between HZ and neurologic symptoms was the only factor associated with an unfavorable course (death or sequelae) (odds ratio, 0.82; 95% confidence interval, 0.71-0.95). In conclusion, the clinical spectrum of neurological complications in VZV reactivation is wide. Mortality was low and sequelae were mild. The presence of IS may play a role on the severity of neurological symptoms, and a shorter time between HZ and the onset of neurological symptoms appears to be a negative prognostic factor.

Intravenous Vitamin C as Ancillary Treatment for Cranial Polyneuritis and Meningitis due to Varicella Zoster Virus Reactivation.

A 65-year-old Japanese woman developed vesicular eruptions on her right ear due to varicella zoster virus (VZV) reactivation, followed by cranial polyneuritis and meningitis affecting her right cranial nerves V, VII, VIII, IX, and X. After acyclovir administration, her facial paralysis worsened. Intravenous methylprednisolone and vitamin C were administered on Day 4 post-admission. Her symptoms steadily improved, and by Day 45 she had fully recovered. Cranial polyneuritis is a rare complication of VZV reactivation, and there is no established method of treatment. This is the first report of full recovery from cranial polyneuritis using intravenous vitamin C as ancillary treatment.

Neuropathic Pain and Itch Mechanisms Underlying Allergic Conjunctivitis.

OBJECTIVE: Among the constellation of symptoms that characterizes allergic conjunctivitis, many (eg, burning and stinging) can be attributed to chronic neuropathic pain. Cumulative data support that these hallmark symptoms might be linked to the effects of allergen-induced neuromodulation. This review investigates the key characteristics of neuropathic itch and pain in allergic conjunctivitis and their underlying pathogenic mechanisms. METHODS: A literature review was conducted using a PubMed search focusing on allergic conjunctivitis, neurogenic inflammation, neuropathic itch, and neuropathic pain. Articles were reviewed, and those discussing clinical course, pathophysiology, and neuronal regulation of chronic neuropathic symptoms as related to allergic disease were summarized. RESULTS: Recent evidence suggests that some symptoms of allergic conjunctivitis may be better represented as a chronic neuropathic disorder. We found that neurogenic mechanisms may have a significant role in chronic ocular surface inflammation from allergic inflammation. Manifestations may be associated with repeated ocular sensory nerve injury leading to an acute-to-chronic transition, which is in turn associated with neuropathologic changes (peripheral and central sensitization), neuronal dysfunction, and spontaneous ocular pain. CONCLUSION: Current goals in the management of allergic conjunctivitis aim to minimize the inflammatory cascade associated with the allergic response in the initial stages of the pathogenic mechanism. Based on the mechanistic data reviewed herein, the recognition that neuronal inflammation explains many of the symptoms in allergic conjunctivitis opens new frontiers for drug discovery.

Use of a modified Outerbridge-Kashiwagi procedure for the treatment of posttraumatic elbow sequelae.

BACKGROUND: To review our 10-year experience treating posttraumatic sequelae of the elbow using a modified Outerbridge-Kashiwagi (O-K) procedure. METHODS: Twenty-one patients with posttraumatic sequelae of the elbow treated using the technique were evaluated clinically using the Mayo Elbow Performance Score, range of motion testing, and pain level. We noted the presence of preoperative and postoperative ulnar nerve symptoms, complications, and reoperations. Open contracture release was selected to address either removal of hardware or ulnar nerve pathology. RESULTS: At a mean of 39 months (range, 12-116 months), the Mayo Elbow Performance Score improved from 52 to 84 (P < .0001) and the mean arc of motion improved from 44° to 98° (P < .0001). At the final follow-up, 90% of patients reported no pain or mild pain, and 81% of patients had a satisfactory objective result. In 15 of 21 cases (71%), it was necessary to mobilize the ulnar nerve. After contracture release, 1 patient developed new onset ulnar nerve symptoms. Three patients underwent reoperation: 2 for recalcitrant contracture and 1 for new onset ulnar nerve symptoms. CONCLUSIONS: The mini-open O-K procedure is safe and effective in restoring function in patients with retained hardware and posttraumatic contracture. Posttraumatic arthritic patients often require both removal of hardware and neurolysis of the ulnar nerve. The mini-open O-K procedure allows complete access to the elbow joint, which facilitates release for both intrinsic and extrinsic contracture.

Major complications after distal biceps tendon repairs: retrospective cohort analysis of 970 cases.

BACKGROUND: The major complication and reoperation rates after distal biceps repair are poorly defined. The purpose of this large retrospective cohort study of distal biceps repairs performed by multiple surgeons within a large orthopedic group was to more clearly define the rates and risk factors of clinically impactful major complications and reoperations. METHODS: All distal biceps tendon repairs performed from January 2005 through April 2017 with a minimum 2-month follow-up were identified using Current Procedural Terminology code 24342. We included 970 patients. The primary outcome measure was the total major complication rate. Reoperations, minor complications, and risk factors were also tracked. RESULTS: Repairs were performed via a single anterior incision in 652 cases and a 2-incision exposure in 318 cases. A 7.5% major complication rate and 4.5% reoperation rate were observed overall. Major complications occurred at the following rates: proximal radioulnar synostosis, 1.0%; heterotopic ossification or loss of range of motion with reoperation, 0.9%; tendon rerupture, 1.6%; deep infection, 0.5%; posterior interosseous nerve palsy, 1.9%; and complex regional pain syndrome, 0.6%. The 2-incision exposure was identified as a significant risk factor for the development of proximal radioulnar synostosis when compared with single-incision repair techniques (P = .0003; odds ratio, 19), occurring in 2.8% of 2-incision exposure cases. Lateral antebrachial cutaneous nerve neuritis or numbness and radial sensory nerve neuritis or numbness were documented more frequently in the postoperative period among patients treated with a single-incision exposure (P < .0001 and P = .034, respectively). CONCLUSIONS: Distal biceps repair is associated with a 7.5% major complication rate and 4.5% reoperation rate. The use of a 2-incision technique for repair increases the risk of radioulnar synostosis.

Group IV nociceptors develop axonal chemical sensitivity during neuritis and following treatment of the sciatic nerve with vinblastine.

We have previously shown that nerve inflammation (neuritis) and transient vinblastine application lead to axonal mechanical sensitivity in nociceptors innervating deep structures. We also have shown that these treatments reduce axonal transport and have proposed that this leads to functional accumulation of mechanically sensitive channels in the affected part of the axons. Though informing the etiology of mechanically induced pain, axonal mechanical sensitivity does not address the common report of ongoing radiating pain during neuritis, which could be secondary to the provocation of axonal chemical sensitivity. We proposed that neuritis and vinblastine application would induce sensitivities to noxious chemicals and that the number of chemo-sensitive channels would be increased at the affected site. In adult female rats, nerves were either untreated or treated with complete Freund's adjuvant (to induce neuritis) or vinblastine. After 3-7 days, dorsal root teased fiber recordings were taken from group IV neurons with axons within the sciatic nerve. Sciatic nerves were injected intraneurally with a combination of noxious inflammatory chemicals. Whereas no normal sciatic axons responded to this stimulus, 80% and 38% of axons responded in the neuritis and vinblastine groups, respectively. In separate experiments, sciatic nerves were partially ligated and treated with complete Freund's adjuvant or vinblastine (with controls), and after 3-5 days were immunolabeled for the histamine H3 receptor. The results support that both neuritis and vinblastine treatment reduce transport of the histamine H3 receptor. The finding that nociceptor axons can develop ectopic chemical sensitivity is consistent with ongoing radiating pain due to nerve inflammation.NEW & NOTEWORTHY Many patients suffer ongoing pain with no local pathology or apparent nerve injury. We show that nerve inflammation and transient application of vinblastine induce sensitivity of group IV nociceptor axons to a mixture of endogenous inflammatory chemicals. We also show that the same conditions reduce the axonal transport of the histamine H3 receptor. The results provide a mechanism for ongoing nociception from focal nerve inflammation or pressure without overt nerve damage.

The Effect of Intra-articular Cocktail Versus Femoral Nerve Block for Patients Undergoing Hip Arthroscopy.

PURPOSE: To compare clinical efficacy and complication rate as measured by postoperative falls and development of peripheral neuritis between intra-articular blockade and femoral nerve block in patients undergoing arthroscopic hip surgery. METHODS: An institutional review board approved retrospective review was conducted on a consecutive series of patients who underwent elective arthroscopic hip surgery by a single surgeon, between November 2013 and April 2015. Subjects were stratified into 2 groups: patients who received a preoperative femoral nerve block for perioperative pain control, and patients who received an intra-articular "cocktail" injection postoperatively. Demographic data, perioperative pain scores, narcotic consumption, incidence of falls, and iatrogenic peripheral neuritis were collected for analysis. Postoperative data were then collected at routine clinical visits. RESULTS: A total of 193 patients were included in this study (65 males, 125 females). Of them, 105 patients received preoperative femoral nerve blocks and 88 patients received an intraoperative intra-articular "cocktail." There were no significant differences in patient demographics, history of chronic pain (P = .35), worker's compensation (P = .24), preoperative pain scores (P = .69), or intraoperative doses of narcotics (P = .40). Patients who received preoperative femoral nerve blocks reported decreased pain during their time in PACU (P = .0001) and on hospital discharge (P = .28); however, there were no statistically significant differences in patient-reported pain scores at postoperative weeks 1 (P = .34), 3 (P = .64), and 6 (P = .70). Administration of an intra-articular block was associated with a significant reduction in the rate of postoperative falls (P = .009) and iatrogenic peripheral neuritis (P = .0001). CONCLUSIONS: Preoperative femoral nerve blocks are associated with decreased immediate postoperative pain, whereas intraoperative intra-articular anesthetic injections provide effective postoperative pain control in patients undergoing arthroscopic hip surgery and result in a significant reduction in the rate of postoperative falls and iatrogenic peripheral neuritis. LEVEL OF EVIDENCE: Level III, retrospective comparative study.

Ocular inflammation induces trigeminal pain, peripheral and central neuroinflammatory mechanisms.

Ocular surface diseases are among the most frequent ocular pathologies, with prevalence ranging from 20% of the general population. In addition, ocular pain following corneal injury is frequently observed in clinic. The aim of the study was to characterize the peripheral and central neuroinflammatory process in the trigeminal pathways in response to cornea alteration induced by chronic topical instillations of 0.2% benzalkonium chloride (BAC) in male C57BL/6J mice. In vitro BAC induced neurotoxicity and increases neuronal (FOS, ATF3) and pro-inflammatory (IL-6) markers in primary mouse trigeminal ganglion culture. BAC-treated mice exhibited 7days after the treatment reduced aqueous tear production and increased inflammatory cell infiltration in the cornea. Hypertonic saline-evoked eye wipe behavior was enhanced in BAC-treated animals that exhibited increased FOS, ATF3 and Iba1 immunoreactivity in the trigeminal ganglion. Ocular inflammation is associated with a significant increase in IL-6 and TNF-α mRNA expression in the trigeminal ganglion. We reported a strong increase in FOS and Iba1 positive cells in particular in the sensory trigeminal complex at the ipsilateral interpolaris/caudalis (Vi/Vc) transition and Vc/upper cervical cord (Vc/C1) regions. In addition, activated microglial cells were tightly wrapped around activated FOS neurons in both regions and phosphorylated p38 mitogen-activated protein kinase was markedly enhanced specifically in microglial cells during ocular inflammation. Similar data were obtained in the facial motor nucleus. These neuroanatomical data correlated with the increase in mRNA expression of pro-inflammatory (TNF-α, IL-6, CCL2) and neuronal (FOS and ATF3) markers. Interestingly, the suppression of corneal inflammation 10days following the end of BAC treatment resulted in a marked attenuation of peripheral and central changes observed in pathological conditions. This study provides the first demonstration that corneal inflammation induces activation of neurons and microglial p38 MAPK pathway within sensory trigeminal complex. These results suggest that this altered activity in intracellular signaling caused by ocular inflammation might play a priming role in the central sensitization of ocular related brainstem circuits, which represents a significant factor in ocular pain development.

Transplantation of cerebellar neural stem cells improves motor coordination and neuropathology in Machado-Joseph disease mice.

Machado-Joseph disease is a neurodegenerative disease without effective treatment. Patients with Machado-Joseph disease exhibit significant motor impairments such as gait ataxia, associated with multiple neuropathological changes including mutant ATXN3 inclusions, marked neuronal loss and atrophy of the cerebellum. Thus, an effective treatment of symptomatic patients with Machado-Joseph disease may require cell replacement, which we investigated in this study. For this purpose, we injected cerebellar neural stem cells into the cerebellum of adult Machado-Joseph disease transgenic mice and assessed the effect on the neuropathology, neuroinflammation mediators and neurotrophic factor levels and motor coordination. We found that upon transplantation into the cerebellum of adult Machado-Joseph disease mice, cerebellar neural stem cells differentiate into neurons, astrocytes and oligodendrocytes. Importantly, cerebellar neural stem cell transplantation mediated a significant and robust alleviation of the motor behaviour impairments, which correlated with preservation from Machado-Joseph disease-associated neuropathology, namely reduction of Purkinje cell loss, reduction of cellular layer shrinkage and mutant ATXN3 aggregates. Additionally, a significant reduction of neuroinflammation and an increase of neurotrophic factors levels was observed, indicating that transplantation of cerebellar neural stem cells also triggers important neuroprotective effects. Thus, cerebellar neural stem cells have the potential to be used as a cell replacement and neuroprotective approach for Machado-Joseph disease therapy.

Neuroinflammation, mitochondrial defects and neurodegeneration in mucopolysaccharidosis III type C mouse model.

Severe progressive neurological paediatric disease mucopolysaccharidosis III type C is caused by mutations in the HGSNAT gene leading to deficiency of acetyl-CoA: α-glucosaminide N-acetyltransferase involved in the lysosomal catabolism of heparan sulphate. To understand the pathophysiology of the disease we generated a mouse model of mucopolysaccharidosis III type C by germline inactivation of the Hgsnat gene. At 6-8 months mice showed hyperactivity, and reduced anxiety. Cognitive memory decline was detected at 10 months and at 12-13 months mice showed signs of unbalanced hesitant walk and urinary retention. Lysosomal accumulation of heparan sulphate was observed in hepatocytes, splenic sinus endothelium, cerebral microglia, liver Kupffer cells, fibroblasts and pericytes. Starting from 5 months, brain neurons showed enlarged, structurally abnormal mitochondria, impaired mitochondrial energy metabolism, and storage of densely packed autofluorescent material, gangliosides, lysozyme, phosphorylated tau, and amyloid-ß. Taken together, our data demonstrate for the first time that deficiency of acetyl-CoA: α-glucosaminide N-acetyltransferase causes lysosomal accumulation of heparan sulphate in microglial cells followed by their activation and cytokine release. They also show mitochondrial dysfunction in the neurons and neuronal loss explaining why mucopolysaccharidosis III type C manifests primarily as a neurodegenerative disease.

Anxiolytic effects of sesamin in mice with chronic inflammatory pain.

OBJECTIVE: Sesamin is known for its role in antioxidant, antiproliferative, antihypertensive, and neuroprotective activities. However, little is known about the role of sesamin in the development of emotional disorders. Here we investigated persistent inflammatory pain hypersensitivity and anxiety-like behaviors in the mouse suffering chronic pain. METHODS: Chronic inflammatory pain was induced by hind paw injection of complete Freund's adjuvant (CFA). Levels of protein were detected by Western blot. RESULTS: Administration of sesamin could induce anxiolytic activities but had no effect on analgesia. In the basolateral amygdala, a structure involving the anxiety development, sesamin attenuated the up-regulation of NR2B-containing N-methyl-d-aspartate receptors, GluR1 subunit of the alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor as well as phosphorylation of GluR1 at Ser831 (p-GluR1-Ser831), and Ca(2+)/calmodulin-dependent protein kinase II (CaMKII-alpha) in the hind paw CFA-injected mice. In the same model, we found that the sesamin blocked the down-regulation of gamma-aminobutyric acid A (GABAA-alpha-2) receptors. CONCLUSION: Our findings show that sesamin reduces anxiety-like behaviors induced by chronic pain at least partially through regulating the GABAergic and glutamatergic transmission in the amygdala of mice.

Management of chronic neuritis with a combination regimen of lower doses prednisolone and methotrexate: a brief report.

INTRODUCTION: Recommended fixed duration prednisolone regimen was not found effective in the treatment of chronic neuritis. Alternate effective treatment was being sought to reduce the deformity in the field of leprosy. OBJECTIVE: We wished to see whether a prolonged course of prednisolone and methotrexate could be of any help for them. METHODOLOGY: In 2012-2014, an open pilot clinical study was undertaken where three chronic neuritic patients were treated with lower doses prednisolone and methotrexate for 12 months and a follow up period was delivered for 12 months. The study was undertaken in one of the outdoor clinics of the university. RESULTS: Complete and permanent remission of neuritis was achieved with appreciable functional recovery. Few mild self-limiting side-effects from prednisolone were observed and there was no side-effects from methotrexate. CONCLUSION: Prolonged course of prednisolone and methotrexate was found safe and effective in treating chronic neuritis.

Air pollution, a rising environmental risk factor for cognition, neuroinflammation and neurodegeneration: The clinical impact on children and beyond.

Air pollution (indoors and outdoors) is a major issue in public health as epidemiological studies have highlighted its numerous detrimental health consequences (notably, respiratory and cardiovascular pathological conditions). Over the past 15 years, air pollution has also been considered a potent environmental risk factor for neurological diseases and neuropathology. This review examines the impact of air pollution on children's brain development and the clinical, cognitive, brain structural and metabolic consequences. Long-term potential consequences for adults' brains and the effects on multiple sclerosis (MS) are also discussed. One challenge is to assess the effects of lifetime exposures to outdoor and indoor environmental pollutants, including occupational exposures: how much, for how long and what type. Diffuse neuroinflammation, damage to the neurovascular unit, and the production of autoantibodies to neural and tight-junction proteins are worrisome findings in children chronically exposed to concentrations above the current standards for ozone and fine particulate matter (PM2.5), and may constitute significant risk factors for the development of Alzheimer's disease later in life. Finally, data supporting the role of air pollution as a risk factor for MS are reviewed, focusing on the effects of PM10 and nitrogen oxides.

Surgical Outcomes for Resection of the Dorsal Exostosis of the Metatarsocuneiform Joints.

A retrospective case series testing the efficacy of surgical resection of the dorsal exostosis deformity of the metatarsocuneiform joints was performed. Surgery was performed in 26 consecutive patients (28 feet), in whom previous conservative therapy had failed. All 26 patients had bursitis at the level of the dorsal exostosis deformity. The patients were separated into 2 groups: group 1, those with bursitis and neuritis before surgery (n = 13; 46.4%), and group 2, those with bursitis without neuritis (n = 15; 53.5%). Both groups were evaluated using an 11-point visual analog scale administered preoperatively and ≤1 year postoperatively. The mean pain rating in the patients with neuritis and bursitis before surgery (7.31 ± 2.8) and in those with bursitis without neuritis (6.67 ± 3.4) had both decreased to 0 at 6 months and 1 year after surgery. After surgery, 7 patients (25.2%) experienced neuritis. Of these 7 patients, 4 (57.1%) had continuation of neuritis that was present before surgery and 3 (42.9%) had an onset of neuropraxia that was secondary to the surgery itself. This might have resulted from retraction of the nerves during spur removal. Eventually, all the cases of neuritis resolved. One patient (3.6%) experienced regrowth of their dorsal exostosis deformity, 1 (3.6%) developed an abscess at the surgical site, and 1 (3.6%) developed pain elsewhere at the Lisfranc joint. All patients were subsequently treated at our institution and were pain free and had returned to full activity within 1 year. These results suggest that resection of the dorsal exostosis deformity of the metatarsocuneiform joints is an effective surgical procedure for patients with this deformity.

[Panuveitis with oral and genital ulcer misdiagnosed as Behcet's disease: two cases report and literature review].

Here we reported two patients who presented with panuveitis and were transferred from ophthalmologists to rheumatologists, for both the patients had oral and genital ulcers. They were misdiagnosed with Behcet's disease at first glance. Two young males presented with acute uveitis with history of recurrent oral and genital ulcers. They initially presented with symptoms and signs resembling Behcet's disease and were treated with systemic steroids with suboptimal responses. Routine laboratory test revealed syphilis and human immunodeficiency virus (HIV) infection. After treatment of penicillin and anti HIV virus therapy, the panuveitis was relived. The other patient was lost in the follow up. Recently epidemiological data indicate that syphilis and HIV infection increase, which can mimic the manifestation of Behcet's disease. Diagnosis of sexual transmitted diseases, such as HIV or syphilis needs to be ruled out in all cases that mimic the clinical feature of Behcet's disease, especially for those who had a history of high risk behaviors. Every patient should have history analysis in detail. Screening of sexual transmitted diseases, such as HIV or syphilis is important especially in those rapid progressive panuveitis. Also, other virus infections, such as cytomegalovirus, epstein-barr virus or Herpes simplex virus can cause mucosa ulcers and uveitis. CD4 T cell count is a very important marker to indicate that the patient has immunodeficiency. Erythema nodosa and pseudofolliculitis are the third common clinical manifestation in Chinese Behcet's disease patients. Rheumatologist should watch out for patients without skin involvement when making the diagnosis of Behcet's disease. Syphilis-associated uveitis usually has a good prognosis. Treatment of antibiotics can get good response, 92% uveitis can be relieved, with 67% improved vision. Acute syphilitic posterior placoid chorioretinitis (ASPPC) is a clinically and angiographically distinct manifestation of ocular syphilis. Systemic glucocorticoid can be used in syphilis induced posterior uveitis, sleritis and optic neuritis, and it can also prevent the Hector's reaction. However, for patients diagnosed with both HIV and syphilis, regular antibiotic can not prevent relapse. So doctors need to follow up them regularly. Patients who present with uveitis, oral and genital ulcers can be easily diagnosed with Behcet's disease. Rheumatologists need to be aware of the reemergence of sexual transmitted disease. High degree of clinical suspicion can allow ophthalmologists and rheumatologists to diagnose and treat the disease early. Correct diagnoses timely can get the good treatment response, and rescue the vision. Treatment with regular antivirus and Penicillin can receive the good response, and moreover glucocorticoid can relieve the inflammation.