Tibial Cortex Transverse Distraction Followed by Open Correction with Internal Fixation for Management of Foot and Ankle Deformity with Ulcers.

OBJECTIVE: To assess the feasibility and results of tibial cortex transverse distraction (TCTD) followed by open correction with internal fixation (OCIF) for foot and ankle deformity with concurrent ulcers. METHODS: A retrospective analysis was conducted. Between 2010 and 2019, a two-stage management of TCTD followed by OCIF was performed in 13 patients (13 feet). There were five males and eight females with a mean age of 33.8 ± 14.6 years. Ten patients had a right-side lesion, and three patients had a left-side lesion. The etiology of deformity included seven cases of congenital neurological disease, one case of Charcot-Marie-Tooth disease, one case of trauma sequelae, and three cases of myelomeningocele. Duration of disease, size of ulcers, surgical procedures, healing time, external fixation time, and complications of these patients were recorded. The Texas wound classification and National Pressure Ulcer Advisory Panel (NPUAP) classification were used for assessing the ulcers. The modified Dimeglio score of deformity and American Orthopeadic Foot and Ankle Society (AOFAS) ankle-hindfoot score were applied to evaluate the status before treatment and the results at final follow-up. RESULTS: The TCTD and wound debridement were performed in all patients, and an additional Ilizarov correction technique was added in two patients. All ulcers were healed in 3 months after first-stage treatment. The median patient self-report time of ulcer healing was 2.0 weeks (IQR, 1.8-3.3). The median external fixation time was 138.0 days (IQR, 134.5-141.5) days. After second-stage operative correction, the patients were followed-up for an average of 28.0 ± 2.9 months. At the final follow-up, the modified Dimeglio score of deformity was decreased from 6.7 ± 2.1 to 1 (IQR, 0.0-1.0), and the mean AOFAS score was improved from 42.9 ± 19.1 to 82.6 ± 7.7. Before the treatment, there were eight patients with severe deformity, four patients with moderate deformity, and one patient with mild deformity. Postoperatively, seven patients were classified as mild deformity and six patients had a postural foot. The results of AOFAS ankle-hindfoot score were defined as excellent in three patients, as good in five, and as fair in five. Complications include one case of mild displacement of the osteotomized cortex and one case of pin-tract infection. No delayed union, nonunion, relapse of ulcers, or deformity were observed. CONCLUSIONS: The two-stage management of TCTD followed by OCIF could be considered as an alternative treatment for foot and ankle deformities combined with chronic ulcers.

Fatigue in patients with hereditary neuropathy with liability to pressure palsies.

OBJECTIVE: Hereditary Neuropathy with Liability to Pressure Palsies (HNPP) is caused by a heterozygous deletion of peripheral myelin protein-22 (PMP22) gene resulting in focal sensorimotor deficits. Our lab has identified a disruption of myelin junctions in excessively permeable myelin that impairs action potential propagation. This mechanism is expected to cause fatigue in patients with HNPP. Therefore, the objective was to characterize fatigue in patients with HNPP and determine the relationship of fatigue to nerve pathology, disability, and quality of life. METHODS: Nine females with HNPP participated in a single visit that included genotyping, nerve conduction studies, neurological exam, quantitative magnetic resonance imaging, and a physical therapy exam incorporating upper and lower extremity function and survey measures of fatigue. This visit was followed by 2 weeks of ecological momentary assessment (wrist-worn device) that captured fatigue ratings five times per day. RESULTS: Participants demonstrated mild neurological impairment (CMTNS: 5.7 ± 2.8), yet reported high fatigue levels (average fatigue intensity over 2 weeks: 5.9 out of 10). Higher fatigue levels were associated with poorer quality of life and more pain. Higher fatigue was associated with significantly greater distal nerve proton density changes on peripheral nerve MRI, which is in line with hyper-permeable myelin in HNPP. INTERPRETATION: Fatigue is common and severe among patients with HNPP whose disabilities are minimal by conventional outcome measures. Therapeutic interventions targeting fatigue have the potential to improve quality of life and may serve as a robust outcome measure to show longitudinal changes for patients with HNPP.

Motor impairment in a rare form of spastic paraplegia (Spoan syndrome): a 10-year follow-up.

BACKGROUND: Spastic paraplegia, optic atrophy and neuropathy (Spoan syndrome) is an autosomal recessive disease with approximately 70 cases recorded in Brazil and Egypt. METHODS: This is a prospective longitudinal study performed with 47 patients affected with Spoan syndrome of seven communities of Rio Grande do Norte (Brazil) to investigate changes in motor function based on comparative data obtained from a 10-year follow-up. RESULTS: The mean age of the participants was 47.21 ± 12.42 years old, and the mean age at loss of ambulation and hand function were 10.78 ± 5.55 and 33.58 ± 17.47 years old, respectively. Spearman's correlation analysis between the score on the Modified Barthel Index and the investigated variables evidenced statistical significance for age (p < 0.001) and right- and left-hand grip strength (p = 0.042 and p = 0.021, respectively). Statistical significance was not evidenced for the remainder of the variables, including age at onset of symptoms (p = 0.634), age at loss of ambulation (p = 0.664) and age at loss of hand function (p = 0.118). CONCLUSIONS: Our analysis allows asserting that the participants exhibited slight dependence until age 35. The greatest losses occurred from ages 35 to 41, and starting at 50, practically all patients become completely dependent. These findings are relevant for determining the prognosis as well as suitable treatment, rehabilitation and assistive technology for these individuals.

Clinical spectrum of AIFM1-associated disease in an Irish family, from mild neuropathy to severe cerebellar ataxia with colour blindness.

Mutations in apoptosis-inducing factor mitochondrion-associated-1 (AIFM1) cause X-linked peripheral neuropathy (Cowchock syndrome, CMT4X); however, more recently a cerebellar presentation has been described. We describe a large Irish family with seven affected males. They presented with a variable age of onset, 18 months to 39 years of age. All developed variably present sensorineural deafness, peripheral neuropathy, cerebellar ataxia, and pyramidal involvement. In addition, three had colour vision deficiency. Scale for the assessment and rating of ataxia ranged 2 to 23/40, while Charcot-Marie-Tooth neuropathy score 2 varied between 7 and 13/36. All individuals had normal cognitive assessment. Neurophysiology demonstrated length-dependent large-fibre sensorimotor axonal neuropathy, with particular involvement of superficial radial sensory responses. Brain imaging, performed in four, revealed varying extent of cerebellar atrophy, and white matter changes in one. Optical coherence tomography was abnormal in one, who had unrelated eye pathology. Four obligate female carriers were assessed clinically, two of them neurophysiologically; all were unaffected. Whole genome sequencing demonstrated a previously reported hemizygous AIFM1 mutation. Analysis for mutations in other genes associated with colour deficiency was negative. AIFM1-associated phenotype in this family demonstrated significant variability. To our knowledge, this is the first report of AIFM1-associated colour blindness. Superficial radial nerve was particularly affected neurophysiologically, which could represent a phenotypic marker towards this specific genetic diagnosis.

Sural nerve pathology in TFG-associated motor neuron disease with sensory neuropathy.

The tropomyosin-receptor kinase fused gene (TFG) functions in vesicles formation and egress at the endoplasmic reticulum (ER). A heterozygous missense mutation c.854C > T (p.Pro285Leu) within TFG has been reported as causative for hereditary motor and sensory neuropathy with proximal predominance. Here, we describe two unrelated Chinese pedigrees with 13 affected members harboring the same variant. The clinical, electrophysiological and pathological findings are consistent with motor neuron disease with sensory neuropathy. The main symptoms were painful muscle cramps, slowly progressive proximal predominant weakness, muscle atrophy, fasciculation and distal sensory disturbance. Electromyography revealed widespread denervation and reinnervation. Sural nerve biopsy revealed severe loss of myelinated fibers. Electron microscopy revealed aggregation of ER with enlarged lumen and small vesicles in the remaining myelinated and unmyelinated axons. The mitochondria are smaller in Schwann cells and axons. Some unmyelinated axons showed disappearance of neurofilament and microtubular structures. This is the first report of c.854C > T mutation within TFG in Chinese population. Our findings not only extend the geographical and phenotypic spectrum of TFG-related neurological disorders, but also confirm the abnormalities of ER and mitochondria in sural nerves.

Anesthetic Considerations of Hereditary Neuropathy With Liability to Pressure Palsies in an Obstetric Patient: A Case Report.

Hereditary neuropathy with liability to pressure palsies is an autosomal dominant condition occurring in up to 16 per 100,000 people and predisposes to neural compressive injury. Given the rarity of this condition, no guidelines currently exist for the anesthetic management of hereditary neuropathy with liability to pressure palsies. We describe the management of analgesia during labor in a woman diagnosed with hereditary neuropathy with liability to pressure palsies and a history of nerve palsy after obstetric anesthesia. Our report highlights the necessity of clinician awareness of hereditary neuropathy with liability to pressure palsies and the anesthetic precautions used to successfully avoid neural injury in this case.

Peripheral neuropathy in diabetes: it's not always what it looks like.

BACKGROUND: Hereditary Neuropathy with liability to Pressure Palsies (HNPP) is an autosomal dominant neuropathy, associated with deletion of the Peripheral Myelin Protein-22 (PMP-22) gene, causing recurrent painless palsies with age of onset between 10 and 30 years old. Only a few cases of Type 2 Diabetes and HNPP have been described and the coexistence of HNPP and Type 1 diabetes has never been reported. CASE REPORT: A 54-year old man with a history of Type 1 diabetes, managed with continuous subcutaneous insulin infusion (CSII), presented with deterioration of long-standing motor and sensory symptoms, previously attributed to golfer's elbow, diabetic neuropathy and spinal degenerative disease. He had multilevel severe spine degenerative changes and L4/L5 and L5/S1 root impingements with a L4/L5 discectomy performed when he was 25 years old. On physical examination he had normal power and distal hypoaesthesia of the digits and plantar aspect of the feet. Investigations revealed normal full blood count, liver and renal function, electrolytes, vitamin B12 and serum folate. He suffered from primary hypothyroidism and thyroid function tests indicated adequate levothyroxine replacement. Nerve conduction studies revealed a generalized demyelinating sensorimotor neuropathy, with more severe involvement of nerves over entrapment sites. Further history that his father suffered from episodes of weakness and numbness was elicited. Genetic analysis revealed one copy of the PMP22 gene at 17p11.2 confirming the diagnosis of HNPP. CONCLUSION: In people with diabetes the evaluation of peripheral neuropathy should include a careful history, a comprehensive physical examination, blood tests and in some cases nerve conduction studies and genetic testing.

Mutations in COA7 cause spinocerebellar ataxia with axonal neuropathy.

Several genes related to mitochondrial functions have been identified as causative genes of neuropathy or ataxia. Cytochrome c oxidase assembly factor 7 (COA7) may have a role in assembling mitochondrial respiratory chain complexes that function in oxidative phosphorylation. Here we identified four unrelated patients with recessive mutations in COA7 among a Japanese case series of 1396 patients with Charcot-Marie-Tooth disease (CMT) or other inherited peripheral neuropathies, including complex forms of CMT. We also found that all four patients had characteristic neurological features of peripheral neuropathy and ataxia with cerebellar atrophy, and some patients showed leukoencephalopathy or spinal cord atrophy on MRI scans. Validated mutations were located at highly conserved residues among different species and segregated with the disease in each family. Nerve conduction studies showed axonal sensorimotor neuropathy. Sural nerve biopsies showed chronic axonal degeneration with a marked loss of large and medium myelinated fibres. An immunohistochemical assay with an anti-COA7 antibody in the sural nerve from the control patient showed the positive expression of COA7 in the cytoplasm of Schwann cells. We also observed mildly elevated serum creatine kinase levels in all patients and the presence of a few ragged-red fibres and some cytochrome c oxidase-negative fibres in a muscle biopsy obtained from one patient, which was suggestive of subclinical mitochondrial myopathy. Mitochondrial respiratory chain enzyme assay in skin fibroblasts from the three patients showed a definitive decrease in complex I or complex IV. Immunocytochemical analysis of subcellular localization in HeLa cells indicated that mutant COA7 proteins as well as wild-type COA7 were localized in mitochondria, which suggests that mutant COA7 does not affect the mitochondrial recruitment and may affect the stability or localization of COA7 interaction partners in the mitochondria. In addition, Drosophila COA7 (dCOA7) knockdown models showed rough eye phenotype, reduced lifespan, impaired locomotive ability and shortened synaptic branches of motor neurons. Our results suggest that loss-of-function COA7 mutation is responsible for the phenotype of the presented patients, and this new entity of disease would be referred to as spinocerebellar ataxia with axonal neuropathy type 3.

Multifocal demyelinating motor neuropathy and hamartoma syndrome associated with a de novo PTEN mutation.

OBJECTIVE: To describe a patient with a multifocal demyelinating motor neuropathy with onset in childhood and a mutation in phosphatase and tensin homolog (PTEN), a tumor suppressor gene associated with inherited tumor susceptibility conditions, macrocephaly, autism, ataxia, tremor, and epilepsy. Functional implications of this protein have been investigated in Parkinson and Alzheimer diseases. METHODS: We performed whole-exome sequencing in the patient's genomic DNA validated by Sanger sequencing. Immunoblotting, in vitro enzymatic assay, and label-free shotgun proteomic profiling were performed in the patient's fibroblasts. RESULTS: The predominant clinical presentation of the patient was a childhood onset, asymmetric progressive multifocal motor neuropathy. In addition, he presented with macrocephaly, autism spectrum disorder, and skin hamartomas, considered as clinical criteria for PTEN-related hamartoma tumor syndrome. Extensive tumor screening did not detect any malignancies. We detected a novel de novo heterozygous c.269T>C, p.(Phe90Ser) PTEN variant, which was absent in both parents. The pathogenicity of the variant is supported by altered expression of several PTEN-associated proteins involved in tumorigenesis. Moreover, fibroblasts showed a defect in catalytic activity of PTEN against the secondary substrate, phosphatidylinositol 3,4-trisphosphate. In support of our findings, focal hypermyelination leading to peripheral neuropathy has been reported in PTEN-deficient mice. CONCLUSION: We describe a novel phenotype, PTEN-associated multifocal demyelinating motor neuropathy with a skin hamartoma syndrome. A similar mechanism may potentially underlie other forms of Charcot-Marie-Tooth disease with involvement of the phosphatidylinositol pathway.

Rigid spine syndrome associated with sensory-motor axonal neuropathy resembling Charcot-Marie-Tooth disease is characteristic of Bcl-2-associated athanogene-3 gene mutations even without cardiac involvement.

INTRODUCTION: Bcl-2-associated athanogene-3 (BAG3) mutations have been described in rare cases of rapidly progressive myofibrillar myopathies. Symptoms begin in the first decade with axial involvement and contractures and are associated with cardiac and respiratory impairment in the second decade. Axonal neuropathy has been documented but usually not as a key clinical feature. METHODS: We report a 24-year-old woman with severe rigid spine syndrome and sensory-motor neuropathy resembling Charcot-Marie-Tooth disease (CMT). RESULTS: Muscle MRI showed severe fat infiltration without any specific pattern. Deltoid muscle biopsy showed neurogenic changes and discrete myofibrillar abnormalities. Electrocardiogram and transthoracic echocardiography results were normal. Genetic analysis of a panel of 45 CMT genes showed no mutation. BAG3 gene screening identified the previously reported c.626C>T, pPro209Leu, mutation. DISCUSSION: This case indicates that rigid spine syndrome and sensory-motor axonal neuropathy are key clinical features of BAG3 mutations that should be considered even without cardiac involvement. Muscle Nerve, 57: 330-334, 2018.

Hereditary neuropathy with liability to pressure palsy in patients under 30 years old: Neurophysiological data and proposed electrodiagnostic criteria.

INTRODUCTION: In young patients with mononeuropathy who lack family history and precipitating factors, hereditary neuropathy with liability to pressure palsy (HNPP) may be a possibility. Our objective is to propose neurophysiological criteria for HNPP in patients <30 years of age. METHODS: We conducted a national multicenter retrospective clinical and neurophysiological study in patients under 30 with genetically confirmed HNPP. RESULTS: All of the 51 patients included in the study had at least 1 demyelinating pattern in 2 asymptomatic nerves, and 3 abnormalities were found in almost 90%, including slowed motor nerve conduction velocity across the elbow in at least 1 ulnar nerve (97.5%), increased distal motor latency (DML) in at least 1 fibular nerve (95.8%), and increased DML in both median nerves (89%). Age influenced DML slightly only in the fibular nerve. DISCUSSION: Dissemination of nerve involvement in HNPP incites to perform a complete nerve conduction study. including bilateral ulnar, fibular, and median nerves. Muscle Nerve 57: 217-221, 2018.

Prospective comparison of acute motor axonal neuropathy and acute inflammatory demyelinating polyradiculoneuropathy in 140 children with Guillain-Barré syndrome in India.

INTRODUCTION: There have been few reports on subtypes of Guillain-Barré syndrome (GBS) in children. We compared clinical and laboratory findings of acute inflammatory demyelinating polyradiculoneuropathy (AIDP) and acute motor axonal neuropathy (AMAN). METHODS: One hundred forty children with GBS were included. Based on nerve conduction study (NCS) findings, patients were subclassified as AIDP, AMAN, acute motor sensory axonal neuropathy (AMSAN), and equivocal. RESULTS: Clinically, 72.1% of patients had pure motor, 24.3% motor sensory, and 3.4% Miller Fisher syndrome. Based on NCS, 67.8% of patients had AIDP, 23.6% had AMAN, and 4.3% had AMSAN. By 3 months, 2.1% patients had died, 47.1% had complete recovery, and 24.3% had poor recovery (wheelchair-bound). Children with AMAN had more frequent lower limb weakness (P = 0.02) and a lower probability of complete recovery (P = 0.01) at 3 months than children with AIDP (56% vs. 30%). DISCUSSION: AIDP is the most common GBS subtype in children. It is characterized by better recovery at 3 months when compared with AMAN. Muscle Nerve 57: 761-765, 2018.

Characterisation of pain in people with hereditary neuropathy with liability to pressure palsy.

Hereditary neuropathy with liability to pressure palsy (HNPP) has historically been considered a pain-free condition, though some people with HNPP also complain of pain. This study characterised persistent pain in people with HNPP. Participants provided cross-sectional demographic data, information on the presence of neurological and persistent pain symptoms, and the degree to which these interfered with daily life. The painDETECT and Central Sensitization Inventory questionnaires were used to indicate potential neuropathic, central sensitisation and musculoskeletal (nociceptive) pain mechanisms. Additionally, participants were asked if they thought that pain was related to/part of HNPP. 32/43 (74%) subjects with HNPP had persistent pain and experience this pain in the last week. Of those with pain, 24 (75%) were likely to have neuropathic pain and 27 (84%) were likely to have central sensitisation. All 32 participants felt that their pain could be related to/part of their HNPP. Significant negative impact of the pain was common. Pain characterisation identified neuropathic pain and/or central sensitisation as common, potential underlying processes. Pain may plausibly be directly related to the underlying pathophysiology of HNPP. Further consideration of including pain as a primary symptom of HNPP is warranted.

A case report of hereditary neuropathy with liability to pressure palsies accompanied by type 2 diabetes mellitus and psoriasis.

RATIONALE: Hereditary neuropathy with liability to pressure palsy (HNPP) is an episodic, multifocal neuropathy, with a typical clinical presentation of recurrent transient pressure palsies, which is induced by a PMP22 deletion. Another neuropathy caused by a PMP22 duplication is Charcot-Marie-Tooth disease type 1A (CMT1A). PMP22 is a gene coding a protein called peripheral myelin protein 22 (PMP22), which plays an essential role in the formation and maintenance of compact myelin. Coexistence of type 2 diabetes mellitus (T2DM) and CMT1A has been reported in many work, however HNPP patients with T2DM are rare, and comorbidity of HNPP and psoriasis has not been reported previously. Electrophysiological features of HNPP has been found progressing with aging. Patient concerns: Here we present a 20-year-old man who exhibited lower extremity weakness and foot drop as the initial manifestation. DIAGNOSES: HNPP was diagnosed on the basis of clinical features, positive sural nerve biopsy findings, and genetic testing results. Moreover, physical examination, blood/urine glucose test, and diabetes-related autoantibodies investigations demonstrated that he had psoriasis and T2DM. The electrophysiological manifestations revealed profound demyelinating injuries and axonal injuries in distal peripheral nerves and facial nerves, which were more severe than general HNPP cases. INTERVENTIONS: The young patient was treated with continuous subcutaneous insulin infusion and blood glucose monitoring, and then transferred to oral acarbose therapy. The psoriatic lesions were treated with calcipotriol ointment. OUTCOMES: In the follow-up, the right leg weakness was alleviated, and his gait was improved. LESSONS: The findings indicate that diabetes mellitus may have an impact on the severity of HNPP. Physicians should consider that worsening of symptoms might result from newly diagnosed diabetes mellitus while treating patients with HNPP.

Squatting-induced bilateral peroneal nerve palsy in a sewer pipe worker.

Compression neuropathy of the common peroneal nerve (CPN) at the fibula head is a common condition, but it has not attracted attention in working environments. Here, we report a 38-year-old sewer pipe worker who presented with bilateral CPN palsy following 6h working with a squatting posture in a narrow sewer pipe. During the work, he could not stretch his legs sufficiently because of the confined space. His symptoms deteriorated with repetition of the same work for 1 week. Motor nerve conduction study showed conduction block at the fibula head of bilateral CPNs, compatible with compression neuropathy at this lesion. Three months after cessation of work requiring the causative posture, his symptoms and neurophysiological abnormalities had resolved completely. Almost all seven of his co-workers presented transiently with similar and milder symptoms, although one showed CPN palsy for 6 months. Prolonged squatting posture in a confined space causes acute compression neuropathy at the fibula head in the CPN. More attention should be paid to 'confined space worker's compression neuropathy'.

Prevalence of thoracic spine lesions masquerading as cauda equina syndrome: yield of a novel magnetic resonance imaging protocol.

Our objective was to describe the yield of actionable thoracic spine lesions for a novel magnetic resonance imaging (MRI) protocol including evaluation of the thoracic spine among patients presenting to the Emergency Department (ED) with symptoms consistent with epidural compression syndrome. Our ED and Department of Radiology together designed a novel rapid MRI protocol entailing 3D volumetric T2 weighted sequences through both the thoracic and lumbar spine obtained in the sagittal plane to assess for both lumbar and thoracic spine lesions. We recorded study outcomes for all patients undergoing this protocol or conventional lumbar MRI during May 2014-May 2015 to determine the prevalence of actionable thoracic spine lesions. We defined an actionable thoracic lesion as any pathology requiring treatment (e.g., medication, admission, surgery) not otherwise indicated on the basis of lumbar spine findings. During the study period, 112 of 124 (90.3%) of ED patients undergoing MRI evaluation for epidural compression syndrome underwent the novel protocol. The remaining patients underwent evaluation of the lumbar spine using only a conventional MRI protocol. Of the 112 patients undergoing the novel protocol, 6 (5.4%) patients had thoracic spine lesions indicating therapy not otherwise indicated by lumbar spine findings. The etiologies of these six lesions were: neoplasms (2), de-myelination (2), compression fracture (1), and degeneration due to pernicious anemia (1). Emergency providers should strongly consider the routine use of MRI protocols including thoracic spine evaluation in patients presenting to the ED with symptoms consistent with epidural compression syndrome.

Actualización en infecciones herpéticas congénitas y neonatales: infección por citomegalovirus y herpes simple / Update on congenital and neonatal herpes infections: infection due to cytomegalovirus and herpes simplex

Los neonatos son una población especialmente susceptible a las infecciones víricas que frecuentemente afectan al sistema nervioso central. Las infecciones herpéticas pueden transmitirse al feto y al recién nacido, y ocasionar cuadros clínicos graves con déficits sensoriales y cognitivos a largo plazo. Dos terceras partes de los neonatos con encefalitis por virus herpes simple y la mitad de los niños con infección congénita sintomática por citomegalovirus desarrollan secuelas, lo cual supone un alto coste sociosanitario a largo plazo. Afortunadamente, el mejor conocimiento de estas infecciones en los últimos años y el desarrollo de tratamientos antivirales efectivos han mejorado el pronóstico de los pacientes. El valganciclovir (32 mg/kg/día en dos dosis durante seis meses) previene el desarrollo de hipoacusia y mejora el pronóstico neurológico en la infección congénita sintomática por citomegalovirus. El aciclovir (60 mg/kg/día en tres dosis durante 2-3 semanas) previene el desarrollo de formas graves en la enfermedad herpética cutánea-ocular-oral, y disminuye la mortalidad y las secuelas en la enfermedad diseminada y localizada en el sistema nervioso central (AU)

Newborn infants are a population which is especially susceptible to viral infections that frequently affect the central nervous system. Herpes infections can be transmitted to the foetus and to the newborn infant, and give rise to severe clinical conditions with long-term sensory and cognitive deficits. Two thirds of newborn infants with encephalitis due to herpes simplex virus and half of the children with symptomatic congenital infection by cytomegalovirus develop sequelae, which results in high community health costs in the long term. Fortunately, the better knowledge about these infections gained in recent years together with the development of effective antiviral treatments have improved the patients’ prognosis. Valganciclovir (32 mg/kg/day in two doses for six months) prevents the development of hypoacusis and improves the neurological prognosis in symptomatic congenital infection due to cytomegalovirus. Acyclovir (60 mg/kg/day in three doses for 2-3 weeks) prevents the development of severe forms in skin-eyes-mouth herpes disease, and lowers the rate of mortality and sequelae when the disease has disseminated and is located in the central nervous system (AU)

Nociceptive and Neuronal Evaluation of the Sciatic Nerve of Wistar Rats Subjected to Compression Injury and Treated with Resistive Exercise.

Background. To investigate the climb stairs resistance exercise on nociception and axonal regeneration in the sciatic nerve of rats. Methods. 24 Wistar rats were divided: control group (CG-no injury), exercise group (EG-no injury with physical exercise), lesion group (LG-injury, but without exercise), and treated group (LEG-injury and physical exercise). LG and LEG were subjected to sciatic nerve compression with hemostat. From the 3rd day after injury began treatment with exercise, and after 22 days occurs the removal of a nerve fragment for morphological analysis. Results. Regarding allodynia, CG obtained values less than EG (p = 0.012) and larger than LG and LEG (p < 0.001). Histological results showed that CG and EG had normal appearance, as LG and LEG showed up with large amounts of inflammatory infiltration, degeneration and disruption of nerve fibers, and reduction of the myelin sheath; however LEG presented some regenerated fibers. From the morphometric data there were significant differences, for nerve fiber diameter, comparing CG with LG and LEG and comparing axon diameter and the thickness of the myelin of the CG to others. Conclusion. Climb stairs resistance exercise was not effective to speed up the regenerative process of axons.