Características Clínicas y Terapéuticas de los Pacientes que Ingresan por Trauma Craneoencefálico en el Complejo Hospitalario Dr. Arnulfo Arias Madrid. 2022 - 2023

Introducción: El trauma craneoencefálico (TCE) se define como una patología caracterizada por la alteración cerebral secundaria a una lesión traumática en la región de la cabeza, con la presencia de alteración de la consciencia y/o amnesia debido al trauma, cambios neurológicos, neurofisiológicos, con posibles fracturas de cráneo o lesiones intra craneanas atribuibles al trauma. Metodología: Es un estudio observacional, descriptivo, prospectivo en pacientes que sufrieron TCE internados en el servicio de neurocirugía en el Complejo Hospitalario Dr. Arnulfo Arias Madrid durante el periodo de marzo de 2022 a febrero de 2023. Resultados: Los resultados de este estudio mostraron que predomina el sexo masculino (78%) sobre el femenino (22%) en pacientes con TCE. Las causas de lesión más comunes fueron caídas de sus pies (27%), caídas de altura (25%) y colisión de moto/automóvil (20%). Las presentaciones clínicas más comunes fueron pérdida de consciencia (49%), amnesia/desorientación (19%) y cefalea (10%). Conclusión: El seguimiento promedio de los pacientes con TCE fue de 16 días. El género masculino fue el más frecuente, con mayor proporción en la edad media y adulta mayor. La etiología principalmente fue por caídas, manifestándose comúnmente por perdida del estado de alerta, y teniendo hallazgos múltiples en la tomografía cerebral. La mayoría de los pacientes se les dio manejo conservador. (provisto por Infomedic International)

Introduction: Cranioencephalic trauma (TBI) is defined as a pathology characterized by cerebral alteration secondary to traumatic injury in the head region, with the presence of altered consciousness and/or amnesia due to trauma, neurological, neurophysiological changes, with possible skull fractures or intracranial lesions attributable to trauma. Methodology: This is an observational, descriptive, prospective study in patients who suffered TBI hospitalized in the neurosurgery service at the Complejo Hospitalario Dr. Arnulfo Arias Madrid during the period from March 2022 to February 2023. Results: The results of this study showed a predominance of male (78%) over female (22%) patients with TBI. The most common causes of injury were falls from their feet (27%), falls from height (25%) and motorcycle/automobile collision (20%). The most common clinical presentations were loss of consciousness (49%), amnesia/disorientation (19%) and headache (10%). Conclusion: The average follow-up of patients with TBI was 16 days. The male gender was the most frequent, with a higher proportion in middle age and older adults. The etiology was mainly due to falls, commonly manifested by loss of alertness, and multiple findings in brain tomography. Most patients were managed conservatively. (provided by Infomedic International)

To evaluate peripheral neuropathy of ulnar sensory nerve through nerve conduction studies in Type 2 diabetic patients

Background: Secretory defects or defects in action of insulin precipitate a condition of chronic hyperglycemia known as diabetes mellitus, a metabolic disorder progressive in nature with long asymptomatic stage. Diabetic neuropathy is the most life threatening complication. Aims and Objectives: Early detection of peripheral neuropathy helps to take remedial measures in controlling the progression of the disease. Materials and Methods: Forty clinically detectable peripheral neuropathy Type 2 diabetic patients and 40 age-matched control subjects were selected for the study and nerve conduction test of ulnar sensory nerve was done and distal latency (DL), sensory nerve action potential (SNAP), and sensory nerve conduction velocity (SNCV) were recorded using RMS-EMG-EP-MAK II machine to predict the extent and type of neuropathy in diabetics. Results: Significant difference (P < 0.05) of DL, SNCV, and SNAP of ulnar sensory nerve was found in clinically detectable peripheral neuropathy group as compared to controls. Predominantly, axonal type (loss of amplitude) of neuropathy was present in study group. Conclusion: Electrophysiological variables of ulnar sensory nerve were affected in most of the subjects suggesting axonal loss and demyelinating changes in the nerve.

Giant axonal neuropathy / 中华神经科杂志

Giant axonal neuropathy is a rare neurodegenerative disease in children, which is autosomal recessive inheritance. Giant axonal neuropathy is caused by homozygous or compound heterozygous mutation in the gigaxonin gene on chromosome 16q23.2. Giant axonal neuropathy is a chronic polyneuropathy that affects both the peripheral and central nervous systems. Axonal loss and the presence of giant axonal swellings filled with neurofilaments on nerve biopsy are the pathologic hallmark of this neurodegenerative disorder. The article describes the pathogenesis, clinical manifestation, diagnosis and differential diagnosis of giant axonal neuropathy, to provide reference for clinical diagnosis and treatment of this disease.

Effects of delayed ramelteon treatment on neurological function and tissue repair after cryogenic traumatic brain injury / 中国药理学通报

:Aim To study the effects of continuous dai¬ly administration of ramelteon starting at the subacute period of cryogenic traumatic brain injury (cTBI) on neurological function and brain tissue repair in mice. Methods Thirty male C57BL/6 mice were randomly divided into sham group, vehicle group and ramelteon treatment groups. The right sensory-motor cortex was damaged by pressing a copper probe precooled by liq¬uid nitrogen onto the skull. Ramelteon ( 10 nig 'kg-1 • d"1) was administered by gavage every day starting at different time points after cTBI (1 h, 1 d,3 d) until sacrifice on day 14. Beam walking test and open field test were used to evaluate the motor function. Toluidine blue staining was used to measure the infarct volume. Immunofluorescence was used to detect the expression of GAP-43 and synaptophysin in peri-infarct area. Mi¬croglia activation was detected using Iba-1. The area and thickness of glial scars were analyzed by detecting GFAP positive areas. Results All three treatment ( 1 h - 14 d, 1 - 14 d, and 3 - 14 d) significantly im¬proved cTBI induced motor dysfunction, reduced the infarct volume, elevated the expression of GAP -43 and synaptophysin, and decreased the area and thick¬ness of glial scar and microglia activation. In addition, all ramelteon treatment groups had similar effects on the above indexes. Conclusions Delayed ramelteon treatment can improve neurological dysfunction after cTBI,and the therapeutic time window can be delayed for up to three days after cTBI. Inhibiting glial scar formation and microglia activation, and promoting ax- onal regeneration and synaptogenesis may contribute to the beneficial effects of ramelteon.

The Mechanism of Brain Injury Induced by Rotational Motion / 医用生物力学

Traumatic brain injury ( TBI ) has caused serious economic and social burdens, but due to its heterogeneity, there is no effective treatment. In TBI with different severity, diffuse axonal injury (DAI) incidenceis high. The investigation on DAI will contribute to the diagnosis and treatment of TBI. In this study, the classification of TBI and the research status of DAI were summarized. The method to judge the severity of TBI and DAI, and animal experimental models and related injury criteria and thresholds were reviewed. The result show that DAI is mainly generated by rotational acceleration and it is related to angular acceleration, angular velocity and duration. Several TBI animal models can induce the pathology of DAI, and inertial rotation models which can produce only rotational acceleration have been developed. However, these models are instantaneous rotation models, and the rotation duration is uncontrollable, thus a longer duration is impossible, and DAI severity under long rotational motion cannot be studied. The study proposes that a new rotation animal model which can control rotation duration should be developed. The development of the animal model and investigation on pathomechanism of the model will contribute to the prevention and treatment of DAI.

Proteína precursora del beta-amiloide (ß-App) y daño axonal difuso tras un traumatismo craneoencefálico: un punto de vista forense / Beta-amiloid precursos protein (ß-App) and diffuse axonal damage after head injuries: a forensic point of view

Resumen La proteína precursora del β- Amiloide (β-APP) es una glicoproteína de membrana y un componente habitual de las neuronas. Tiene funciones en el crecimiento y la adhesión celular tras un traumatismo. Es transportada mediante transporte rápido axonal anterógrado y se acumula dentro de las neuronas cuando se daña citoesqueleto. Este proceso es activo, es decir consume energía. El β-APP no es específico de los traumatismos. Se acumula en cualquier circunstancia en la que se dañen los axones, tal como la hipoxia, alteraciones metabólicas, y cualquier otra causa de edema cerebral y aumento de la presión intracraneal que puedan conducir a un daño axonal difuso (DAI) En el presente estudio estudiamos la expresión de esta proteína en casos de traumatismo cráneo-encefálico con diferente evolución cronológica El daño del citoesqueleto producido por la proteólisis, junto con la alteración de las quinasas y las fosfatasas, aumentan la permeabilidad de la membrana, lo que provoca la entrada de calcio en la célula que, a su vez, activa la calmodulina que hace que los neurofilamentos se compacten, los microtúbulos desaparezcan y se rompa la espectrina. Esta disrupción del citoesqueleto tiene como consecuencia que las sustancias que se transportan a su través, se acumulen, sobre todo en las zonas afectadas por el DAI. Al final de todo este proceso, los axones se rompen, lo que se conoce como axotomía secundaria. El estudio de la acumulación del β-APP es útil para valorar la extensión del DAI y para determinar el tiempo de supervivencia tras el traumatismo o cualquier otro daño cerebral.

Abstract β-Amyloid Precursor Protein (β-APP) is a membrane glycoprotein and a common component of neurons. It is involved in adhesion and cell growth processes after traumatic events. It is carried by anterograde fast axonal transport, and it accumulates inside neurons when the cytoskeleton is damaged. This is a vital biochemical process that consumes energy. β-APP is not specific of traumatic events. It accumulates in any case of axonal damage, whatever its cause may be, like hypoxia, metabolic disorders, and any other circumstances that lead to brain swelling and intracranial pressure rising and in consequence to Diffuse Axonal Injury (DAI). In this study we review the expression of this protein in cases of traumatic brain injury with different chronological evolution. The damage of cytoskeleton due to proteolysis in addition to the disturbance of kinases and phosphatases increase the permeability of the membrane. Calcium gets into the cell and activates calmodulin, thus neurofilaments compact, microtubules disappear and spectrin breaks. This disruption of the cytoskeleton has as consequence that the transported substances accumulate in the most affected areas by DAI. At the end of this process axon breaks, which is known as secondary axotomy. The study of the accumulation of β-APP is useful to assess the extent of DAI and to determine the time elapsed after trauma or another insult to CNS.

Pain abdomen and cardiac arrest as peculiar presenting symptoms in AIDP- AMSAN variety

AIDP (Acute Inflammatory Demyelinating Polyneuropathy) is a heterogenous condition encompassing several variants. It is a post infectious neurological disorder with an autoimmune pathogenesis with molecular mimicry mechanism. They present commonly with symmetrical ascending type paralysis and absent or diminished deep tendon reflexes. Cranial nerve palsies may or may not be present. The diagnosis is based on the clinical signs and symptoms, nerve conduction studies and cerebrospinal fluid analysis. We herewith report a rare case of AIDP, where the patient came walking to the emergency room with pain abdomen as the only complaint and had no neurological deficits at the time of presentation, hours later, the patient went into cardiac arrest, the cause of which was later thought to be dysautonomia and respiratory failure. The next day, patient developed motor weakness and multiple cranial nerve palsies which is an overlap of AMSAN and Acute Ophthalmoplegia. It is extremely uncommon to present with pain abdomen and cardiac arrest as presenting features in AIDP, AMSAN (Acute Motor Sensory Axonal Neuropathy) variety.

Leptomeningeal carcinomatosis presenting with acute motor axonal neuropathy

Leptomeningeal carcinomatosis is a rare, devastating, and mostly late-stage complication of various solid tumors and hematologic malignancies. The diagnosis can be challenging especially if malignancy is not in active phase or treatment was discontinued. A literature search revealed various unusual presentations of leptomeningeal carcinomatosis including cauda equina syndrome, radiculopathies, acute inflammatory demyelinating polyradiculoneuropathy, and others. To the best of our knowledge, this is the first case of leptomeningeal carcinomatosis presenting with acute motor axonal neuropathy variant of Guillain-Barré Syndrome and unusual cerebrospinal fluid findings known as Froin’s syndrome.

Neuropatías periféricas, un enfoque multidimensional y práctico de una compleja condición / Peripheral neuropathies, a multidimensional and practical approach to a complex condition

Resumen Introducción: las neuropatías periféricas comprenden una amplia gama de entidades que afectan uno o múltiples nervios periféricos en cualquiera de sus categorías funcionales. Métodos: revisión de la literatura sobre la temática, mediante la búsqueda de artículos en las bases de datos Pubmed y Google Scholar publicadas en los últimos 21 años, sin restricción idiomática, excluyendo estudios descriptivos y reportes de caso. Resultados: las neuropatías periféricas tienen una prevalencia del 2 % al 3 %, pueden ser causadas por etiologías infecciosas, enfermedades inflamatorias, inmunológicas, trastornos neoplásicos, exposición a tóxicos, fármacos y deficiencias nutricionales. El diagnóstico depende del juicio clínico. La aplicación de estudios de laboratorios y electrodiagnóstico pueden clasificar adecuadamente estas entidades. El tratamiento depende de la entidad subyacente y debe incluir un enfoque multimodal. Conclusiones: establecer estrategias de prevención, detección y tratamiento temprano permite una potencial recuperación y disminuye los costos para el sistema de salud.

Abstract Introduction: peripheral neuropathies comprise a wide range of entities affecting one or multiple peripheral nerves in any of their functional categories. Methods: review of the literature on the subject, by searching for articles in Pubmed and Google Scholar databases published in the last 21 years, without language restriction, excluding descriptive studies and case reports. Results: peripheral neuropathies have a prevalence of 2 % to 3 %, and can be caused by infectious etiologies, inflammatory diseases, immunological, neoplastic disorders, exposure to toxins, drugs and nutritional deficiencies. Their diagnosis depends on clinical judgment. The application of laboratory and electrodiagnostic studies can adequately classify these entities. Treatment depends on the underlying entity and should include a multimodal approach. Conclusions: establishing strategies for prevention, early detection and treatment allows for potential recovery and decreases costs for the health system.

A Young Woman with Leukoencephalopathy and Significant Corpus Callosum Atrophy / 罕见病研究

Adult-onset leukoencephalopathy with axonal spheroids and pigmented glia (ALSP) is a rare autosomal-dominant progressive leukodystrophy, caused by mutations of colony stimulating factor-1 receptor (CSF1R) gene. Age of onset is usually between 40 and 50 years old and the clinical presentations include dementia, apraxia, behavioral changes, pyramidal and extrapyramidal signs. Varying clinical manifestations have led to misdiagnoses. Magnetic resonance imaging (MRI) typically reveals white matter changes with T2-Flair/DWI hyperintensity and atrophy especially for thinning of the corpus callosum. Here, we report a young woman experiencing hypomnesia for 2 years with lower extremities weakness and rigidity for 1 month. Considering the evidence of clinical manifestations, imaging and genetic test, this patient was diagnosed with ALSP.

Effect of draxin knockdown on the projection of 23C10-positive neural fibers in the embryonic chick hindbrain / 解剖学报

[Abstract] Objective To investigate the effects of the downregulation of draxin expression on the projection characteristics of 23C10-positive neural fibers in the chick embryonic hindbrain. Methods The vitro incubation of HH stages 21-22 chick embryonic hindbrain biopsy with alkaline phosphatase (ALP) protein was used as control group. The incubation of HH stages 21-22 chick embryonic hindbrain biopsy with draxin-ALP fusion protein was used as experimental group. The number of embryonic hindbrain for each group was 10. To detect whether 23C10-positive neural fibers could directly bind to draxin protein or not;In ovo electroporation using empty vector in the chick embryonic hindbrain was used as control group. In ovo electroporation with small interfering RNA(siRNA) expressing vector for reducing draxin expression in the chick embryonic hindbrain was used as experimental group. The number of embryonic hindbrain for each group was 18. The effect of the down-regulation of draxin expression and the change of projection characteristics of 23C10-positive neural fibers were observed to check whether the down-regulation of draxin expression would affect the distribution of 23C10-positive fibers. Results Most portion of draxin protein could overlap with 23C10-positive neural fibers in HH stages 21-22 chick embryonic hindbrain biopsies; After expression of the siRNA plasmid against draxin by electroporation, the expression level of draxin protein was significantly reduced, and the distribution of 23C10-positive fibers was scattered in the dorsal hindbrain on the electroporated side at HH stages 25-26 of chick embryos (P < 0. 05) . Conclusion Draxin protein may directly bind to 23C10-positive fibers in hindbrain, and it plays an important regulatory role in the fasciculation of 23C10-positive fibers during chick embryonic development.

Acute motor axonal neuropathy following anti-rabies human diploid cell vaccine: A rare case and review

Rationale: Guillain Barre syndrome (GBS) is an acute neurological illness leading to quadriparesis with respiratory involvement. It can be triggered by infections, vaccinations, surgery, trauma, transplantation and drugs. Anti-rabies cell culture vaccines introduced to overcome the high rate of neurological complications associated with tissue based rabies vaccine, can be very rarely associated with GBS. Patient concerns: A 50-year-old female presented with acute severe upper back pain evolving into pure motor quadriparesis following administration of human diploid cell vaccine for rabies. Diagnosis: Acute motor axonal neuropathy variant of GBS following anti-rabies human diploid cell vaccine. Interventions: Intravenous high dose steroids. Outcomes: Patient recovered completely within 1 month. Lessons: Although anti-rabies cell culture vaccines are highly immunogenic and safe, they are rarely associated with GBS. Clinicians should be aware of this link because prompt diagnosis and treatment can result in complete recovery and avoid complications.

Whole-Brain Direct Inputs to and Axonal Projections from Excitatory and Inhibitory Neurons in the Mouse Primary Auditory Area / 神经科学通报·英文版

Neurons in the primary auditory area (AUDp) innervate multiple brain regions with long-range projections while receiving informative inputs for diverse functions. However, the brain-wide connections of these neurons have not been comprehensively investigated. Here, we simultaneously applied virus-based anterograde and retrograde tracing, labeled the connections of excitatory and inhibitory neurons in the mouse AUDp, and acquired whole-brain information using a dual-channel fluorescence micro-optical sectioning tomography system. Quantified results showed that the two types of neurons received inputs with similar patterns but sent heterogeneous projections to downstream regions. In the isocortex, functionally different areas consistently sent feedback-dominated projections to these neurons, with concomitant laterally-dominated projections from the sensory and limbic cortices to inhibitory neurons. In subcortical regions, the dorsal and medial parts of the non-lemniscal auditory thalamus (AT) were reciprocally connected to the AUDp, while the ventral part contained the most fibers of passage from the excitatory neurons and barely sent projections back, indicating the regional heterogeneity of the AUDp-AT circuit. Our results reveal details of the whole-brain network and provide new insights for further physiological and functional studies of the AUDp.

Alteraciones atípicas del líquido cefalorraquídeo en el Síndrome de Guillain-Barré: Reporte de casos / Atypical Alterations of cerebrospinal fluid in Guillain Barré Syndrome: Cases Reports

RESUMEN El síndrome de Guillain-Barré se caracteriza por presentar una disociación albúmino-citológica en la mayoría de pacientes. La presencia de pleocitosis o hipoglucorraquia puede alejar el diagnóstico, por lo que se recomienda descartar, principalmente, causas infecciosas. Se presentan tres casos cuyos estudios de líquido cefalorraquídeo mostraron pleocitosis linfocítica e hiperproteinorraquia persistente y uno de ellos, además, hipoglucorraquia; fue solamente en análisis posteriores que los tres pacientes presentaron la clásica disociación albuminocitológica. El estudio neurofisiológico en todos ellos demostró asimismo un compromiso axonal. Las alteraciones atípicas en el contexto de parálisis flácida aguda justificarían repetir el análisis de líquido cefalorraquídeo y descartar otras etiologías, pero sin posponer en modo alguno el tratamiento.

SUMMARY Guillain-Barré syndrome shows a cyto-albuminologic dissociation in most patients. Pleocytosis or hypoglycorrhachia may defer the diagnosis, a reason for which an infectious etiology must be ruled out. Three cases of Guillain-Barré are described, whose cerebrospinal fluid tests showed limphocytic pleocytosis and persistently elevated protein concentration, while one of the cases also showed hypoglycorrhachia, and the classic cyto-albuminologic dissociation was only demonstrated in subsequent analysis. The neurophysiologic evaluation revealed an axonal disruption in all the patients. The atypical alterations in the context of acute flaccid paralysis warrant a retesting of the cerebrospinal fluid in order to rule out other etiologies, but without postponing the start of treatment.

Características clínicas y respuesta al recambio plasmático terapéutico en los pacientes con síndrome de Guillain Barré / Clinical characteristics and plasma exchange response in Guillain-Barré patients

RESUMEN El objetivo del estudio fue describir las características clínicas, la respuesta al tratamiento y posibles factores asociados de los pacientes con síndrome de Guillain Barré en el Instituto Nacional de Ciencias Neurológicas. Se realizó un estudio descriptivo sobre egresos hospitalarios durante el periodo 2017-2019. La respuesta al tratamiento se evaluó mediante la escala de discapacidad de Hughes. De los 31 pacientes el 61,3% eran varones, y la edad promedio fue de 50 años. Al ingreso, el 87,1% de pacientes se encontraban en el grado 3 o 4 de la escala de Hughes, la mayoría con compromiso axonal, el cual estuvo asociado a discapacidad. Solo 22 pacientes recibieron recambio plasmático; luego de seis meses el 90,9% disminuyó al menos en un grado en la escala de Hughes y el 42,8% quedaron sin discapacidad. En conclusión, se encontró un predominio del sexo masculino y del compromiso axonal, este último asociado a discapacidad.

ABSTRACT The objective of the study was to describe the clinical characteristics, treatment response and possible associated factors of patients with Guillain-Barré syndrome at the National Institute of Neurological Sciences. A descriptive study on hospital discharges was conducted during the period 2017-2019. Treatment response was evaluated based on Hughes' disability scale. From 31 patients 61.3% were males and the mean age was 50 years. At admission, 87.1% of patients were on grade 3 or 4 of Hughes scale, most of them with axonal compromise which was associated to disability. Only 22 patients received plasma exchange; 6 months thereafter, 90.9% of patients decreased by at least one degree in Hughes scale and 42.8% were left without disability. In conclusion, a male and axonal subtype predominance was found, been the latter associated to disability.

Características clínicas y respuesta al recambio plasmático terapéutico en los pacientes con síndrome de Guillain Barré / Clinical characteristics and plasma exchange response in Guillain-Barré patients

RESUMEN El objetivo del estudio fue describir las características clínicas, la respuesta al tratamiento y posibles factores asociados de los pacientes con síndrome de Guillain Barré en el Instituto Nacional de Ciencias Neurológicas. Se realizó un estudio descriptivo sobre egresos hospitalarios durante el periodo 2017-2019. La respuesta al tratamiento se evaluó mediante la escala de discapacidad de Hughes. De los 31 pacientes el 61,3% eran varones, y la edad promedio fue de 50 años. Al ingreso, el 87,1% de pacientes se encontraban en el grado 3 o 4 de la escala de Hughes, la mayoría con compromiso axonal, el cual estuvo asociado a discapacidad. Solo 22 pacientes recibieron recambio plasmático; luego de seis meses el 90,9% disminuyó al menos en un grado en la escala de Hughes y el 42,8% quedaron sin discapacidad. En conclusión, se encontró un predominio del sexo masculino y del compromiso axonal, este último asociado a discapacidad.

ABSTRACT The objective of the study was to describe the clinical characteristics, treatment response and possible associated factors of patients with Guillain-Barré syndrome at the National Institute of Neurological Sciences. A descriptive study on hospital discharges was conducted during the period 2017-2019. Treatment response was evaluated based on Hughes' disability scale. From 31 patients 61.3% were males and the mean age was 50 years. At admission, 87.1% of patients were on grade 3 or 4 of Hughes scale, most of them with axonal compromise which was associated to disability. Only 22 patients received plasma exchange; 6 months thereafter, 90.9% of patients decreased by at least one degree in Hughes scale and 42.8% were left without disability. In conclusion, a male and axonal subtype predominance was found, been the latter associated to disability.

Role of Bcl-2 adenovirus/E1B 19kD interacting protein 3 in oligodendrocyte apoptosis after diffuse axonal injury / 解剖学报

Objective To investigate the role of Bcl-2 adenovirus/E1B 19kD interacting protein 3 (BNIP3) in oligodendrocyte apoptosis after diffuse axonal injury (DAI) in rats. Methods Seventy-seven male adult Sprague-Dawley rats were randomly divided into sham group (n = 11), DAI group (n = 33), and intervention group (n = 33). DAI model was made referring to modified Marmarou method and the rats in intervention group received intracerebroventricular injection of BNIP3 inhibitor, necrostatin-1 (Nec-1, 30 g/L, 2 μl) immediately after injury. Tested the BNIP3 protein expression, oligodendrocyte apoptosis and myelin histopathology before and after the intervention of Nec-1. Results Compared with the sham group, DAI rats upregulated BNIP3 levels and had positive correlation with cell apoptosis in brainstem. Nec-1 significantly inhibited BNIP3 expression, then decreased the number of apoptotic oligodendrocytes, increased the average absorbance of luxol fast blue (LFB) staining and myelin basic protein (M BP) levels, and alleviated the myelin ultrastructure of DAI rats. Conclusion BNIP3 participate in the DAI-induced apoptosis of oligodendrocytes, and inhibition of BNIP3 can protect oligodendrocytes and myelin sheath from DAI injury.

Sarm1-mediated neurodegeneration within the enteric nervous system protects against local inflammation of the colon

Axonal degeneration is one of the key features of neurodegenerative disorders. In the canonical view, axonal degeneration destructs neural connections and promotes detrimental disease defects. Here, we assessed the enteric nervous system (ENS) of the mouse, non-human primate, and human by advanced 3D imaging. We observed the profound neurodegeneration of catecholaminergic axons in human colons with ulcerative colitis, and similarly, in mouse colons during acute dextran sulfate sodium-induced colitis. However, we unexpectedly revealed that blockage of such axonal degeneration by the Sarm1 deletion in mice exacerbated the colitis condition. In contrast, pharmacologic ablation or chemogenetic inhibition of catecholaminergic axons suppressed the colon inflammation. We further showed that the catecholaminergic neurotransmitter norepinephrine exerted a pro-inflammatory function by enhancing the expression of IL-17 cytokines. Together, this study demonstrated that Sarm1-mediated neurodegeneration within the ENS mitigated local inflammation of the colon, uncovering a previously-unrecognized beneficial role of axonal degeneration in this disease context.

Daño axonal difuso en accidentes de tránsito: Reporte de caso y revisión bibliográfica / Diffuse axonal injury in traffic accidents: Case report and literature review

Resumen Los accidentes de tránsito son una de las principales causas de lesiones y muertes en la población general, se ha descrito que aproximadamente el 60% de las muertes por accidentes de tránsito son ocasionadas por el trauma craneoencefálico, siendo que el daño axonal difuso es una causa frecuente de coma y discapacidad grave. Dentro de los hallazgos más importantes en la autopsia médico legal a nivel macróscopico se encuentran las petequias en cuerpo calloso, hemorragias en sustancia blanca, entre otros y a nivel microscópico se observan edema axonal reactivo diseminado. En el presente artículo se comentará un caso de daño axonal difuso secundario a un accidente de tránsito, además se realizará una revisión del tema abarcando los puntos más importantes a tomar en cuenta desde el punto de vista médico legal.

Abstract Traffic accidents are one of the main causes of injuries and deaths in the general population, it has been described that approximately 60% of deaths from traffic accidents are caused by head trauma, diffuse axonal damage is a cause frequent coma and severe disability after head trauma, among the most important findings in the legal medical autopsy at the macroscopic level are the petechiae in the corpus callosum, hemorrhages in white matter, among others and at the microscopic level disseminated reactive axonal swelling. In this article, a case of diffuse axonal damage secondary to a traffic accident will be discussed, and a review of the subject will be carried out covering the most important points to be taken into account from the legal medical point of view.

Análisis de la confección de los certificados de asistencia de primera intención del lesionado. Matanzas 2015 / Analysis of the preparation of the first intention assistance certificates of the injured party. Matanzas 2015

Resumen Dentro de las actuaciones medicolegales de mayor trascendencia en el delito de lesiones se encuentra la asistencia de primera intención del lesionado con la correspondiente certificación médica inicial. La confección en Cuba del certificado de asistencia de primera intención de un lesionado dista mucho de ser la adecuada, comprobado por diversos trabajos de autores nacionales y extranjeros. La presente investigación tiene como objetivo el análisis de la confección de los certificados de este tipo, realizados en el municipio de Matanzas, Cuba, en el año 2015 para lo cual se utilizaron variables como la descripción anatómica de las lesiones y el pronóstico medicolegal. Para el análisis de los resultados se utilizaron métodos estadísticos como valores porcentuales y tablas de frecuencia. Los resultados obtenidos arrojaron como conclusiones que el desconocimiento de la clasificación de las lesiones según el código penal, las dificultades en la descripción anatómica y en el pronóstico médico legal de las lesiones constituyen las principales deficiencias detectadas.

Abstract Among the most important medical legal actions in the crime of injuries is the first intention assistance of the injured party with the corresponding initial medical certification. The preparation in Cuba of the certificate of first intention assistance of an injured person is far from being adequate, proven by various works by national and foreign authors. The objective of this research is to analyze the preparation of certificates of this type, carried out in the municipality of Matanzas, Cuba, in 2015, for which variables such as the anatomical description of the injuries and the medical-legal prognosis were used. . For the analysis of the results, statistical methods such as percentage values and frequency tables were used. The results obtained yielded as conclusions that the ignorance of the classification of injuries according to the penal code, the difficulties in the anatomical description and in the legal medical prognosis of the injuries constitute the main deficiencies detected.