Factores de riesgo asociados a Pérdida de Sensibilidad Protectora en pacientes con Diabetes en la Unidad Multidisciplinaria de Pie Diabético / Risk factors associated with Loss of Protective Sensitivity in Diabetes patients in the Multidisciplinary Unit of Diabetic Foot

Introducción: Identificar factores de riesgo para pérdida de la sensibilidad protectora es fundamental para prevenir el Pie Diabético. Objetivos: Analizar los factores de riesgo asociados a la pérdida de la sensibilidad protectora en pacientes con diabetes mellitus y sus complicaciones. Materiales y métodos: diseño observacional, de casos y controles. Se incluyó pacientes de ambos sexos, con diabetes mellitus; ≥ 18 años, a quienes se realizó el Test de monofilamento en la Unidad Multidisciplinaria Hospital de Clínicas, de enero 2014 a julio 2019. Factores de riesgo considerados: edad, años de diabetes mellitus, Hba1c, HTA, dislipidemia; se tuvo en cuenta las complicaciones: retinopatía, enfermedad arterial periférica = ITB <0,9 derecho e izquierdo, enfermedad renal= ClCr <60 ml/min/m2 (MDRD), amputaciones (mayores y menores). Resultados: De 100 pacientes; 33% con pérdida de la sensibilidad protectora; edad 59±9,7 años; 55% masculino. Factores de riesgo: edad: 57,7±1,0 años sin pérdida de la sensibilidad protectora y 61,2±9 años con pérdida de la sensibilidad protectora, p=0.08; años de diabetes mellitus 9,4±8,4 vs 11,5± 8,7 p=0,20; HbA1C 8,8± 2,7% vs 9,1±2% p=0,50; HTA 63,5% vs 75,6% p=0,20; dislipidemias 75,9% vs 57,69%, p=0,09; complicaciones con pérdida de la sensibilidad protectora: retinopatía 88% vs 57,5% OR=1,67, p=0,02. ClCr 84±40,3 ml/min vs 90,9±30,4, p=0,40. Enfermedad arterial periférica derecha 27,78% vs 11,1% OR=0,1, p=0,10; enfermedad arterial periférica izquierda 20% vs 7 15,5% OR=1 p=0,60; amputación 17,5% vs 7,9% OR=2,01, p=0,06. Conclusión: con pérdida de la sensibilidad protectora: la edad, años de diabetes mellitus fueron mayores. HTA fue más frecuente y Hba1c más elevada; nefropatía, enfermedad arterial periférica y amputación con mayor frecuencia, todas no significativas. La retinopatía fue más frecuente en forma significativa.

Introduction: Identifying risk factors for loss of protective sensitivity is essential to prevent Diabetic Foot. Objectives: To analyze the risk factors associated with the loss of protective sensitivity in patients with diabetes mellitus and its complications. Materials and methods: observational, case-control design. Patients of both sexes were included, with diabetes mellitus; ≥ 18 years, who underwent the Monofilament Test in the Multidisciplinary Unit Hospital de Clínicas, from January 2014 to July 2019. Risk factors considered: age, years of diabetes mellitus, Hba1c, HT, dyslipidemia; Complications were taken into account: retinopathy, peripheral arterial disease = ABI <0.9 right and left, kidney disease = CrCl <60 ml / min / m2 (MDRD), amputations (major and minor). Results: Of 100 patients; 33% with loss of protective sensitivity; age 59 ± 9.7 years; 55% male. Risk factors: age: 57.7 ± 1.0 years without loss of protective sensitivity and 61.2 ± 9 years with loss of protective sensitivity, p = 0.08; years of diabetes mellitus 9.4 ± 8.4 vs 11.5 ± 8.7 p = 0.20; HbA1C 8.8 ± 2.7% vs 9.1 ± 2% p = 0.50; HTN 63.5% vs 75.6% p = 0.20; dyslipidemias 75.9% vs 57.69%, p = 0.09; complications with loss of protective sensitivity: retinopathy 88% vs 57.5% OR = 1.67, p = 0.02. CrCl 84 ± 40.3 ml / min vs 90.9 ± 30.4, p = 0.40. Right peripheral arterial disease 27.78% vs 11.1% OR = 0.1, p = 0.10; left peripheral arterial disease 20% vs 7 15.5% OR = 1 p = 0.60; 17.5% amputation vs 7.9% OR = 2.01, p = 0.06. Conclusion: with loss of protective sensitivity: age, years of diabetes mellitus were older. HBP was more frequent and Hba1c higher; nephropathy, peripheral arterial disease and amputation with greater frequency, all not significant. Retinopathy was significantly more frequent.

Síndrome de Cotard en una paciente con lupus eritematoso sistémico y meningioma petroclival izquierdo / Cotard's syndrome in a female patient with systemic lupus erythematosus and left petroclival meningioma

El síndrome de Cotard es una entidad rara en la cual el paciente manifiesta ideas delirantes acerca de que se encuentra sin vida o que sus órganos internos se encuentran en estado de descomposición, entre otras alteraciones psicopatológicas. Existen diferentes reportes sobre el síndrome en diversas culturas y poblaciones. Usualmente tiene presentaciones neuropsiquiátricas y se lo identifica acompañando entidades neurológicas, metabólicas, infecciosas, entre otras. A través de este reporte de caso, se presenta una paciente con lupus eritematoso sistémico, que desarrolló este tipo de ideas delirantes y durante su hospitalización se detectó un meningioma petroclival izquierdo. Finalmente, se llegó a la conclusión de que no se encontraba en actividad lúpica y que la ubicación del tumor no sería la causante de la alteración conductual. El Síndrome de Cotard es un trastorno neuropsiquiátrico poco común, que debe ser considerado ante la existencia de ideas delirantes de tipo nihilistas

Cotard's syndrome is a rare entity in which the patient manifests delusional ideas about being lifeless or that his/her internal organs are in a state of decomposition, among other psychopathological alterations. There are different reports in different cultures and populations about the syndrome. It usually has neuropsychiatric presentations and is identified by accompanying neurological, metabolic, and infectious entities, among others. In this case report, a female patient with systemic lupus erythematosus is presented, who developed this type of delusions and during her hospitalization a left petroclival meningioma was detected. Finally, it was concluded that she was not in lupus activity and that the location of the tumor was not the cause of the behavioral alteration. Cotard's syndrome is a rare neuropsychiatric disorder, which should be considered when there are nihilistic delusions

Role of Prenatal Ultrasonography and Amniocentesis in the Diagnosis of Congenital Zika Syndrome: A Systematic Review.

OBJECTIVE: To examine the relationship between prenatal diagnostics (ultrasound examination and amniotic fluid Zika virus testing) and postnatal congenital Zika syndrome abnormalities. DATA SOURCES: Systematic searches were performed in 27 databases, including ClinicalTrials.gov, from inception to July 1, 2019, for articles with the keywords "Zika," "prenatal," "ultrasound," and "amniocentesis." METHODS OF STUDY SELECTION: A total of 3,049 unique records were identified. Two reviewers independently assessed titles, abstracts, and full texts for relevance; 84 articles met the inclusion criteria. These articles describe 402 mother-fetus or mother-neonate dyads; 385 were included in the review of prenatal ultrasound examination, and 56 in the review of amniocentesis (39 in both). TABULATION, INTEGRATION, AND RESULTS: Among 195 fetuses with congenital Zika syndrome findings on prenatal ultrasound examination, postnatal congenital Zika syndrome abnormalities were reported for 153 (78%; 95% CI 7-84%). High proportions of microcephaly (76%; 95% CI 69-82%) and brain abnormalities (78%; 95% CI 69-86%) were confirmed postnatally. Among 190 fetuses without congenital Zika syndrome findings on prenatal ultrasound examination, 17% (95% CI 12-24%) had congenital Zika syndrome abnormalities identified postnatally. Structural congenital Zika syndrome abnormalities were identified postnatally in approximately equal proportions among dyads with and without Zika virus RNA detected in an amniotic fluid specimen (68% and 67%; 95% CI 52-82% and 95% CI 38-88%). In six pregnancies, Zika virus RNA was detected in amniotic fluid but not in a subsequent amniocentesis specimen. CONCLUSION: Prenatal ultrasound examination frequently detects structural findings associated with Zika virus infection; however, not all abnormalities are detected, and some may represent transient findings. As with other congenital infections, prenatal detection may vary with timing of infection, timing of ultrasound examination, technical expertise, and severity of abnormalities. The detection of Zika virus RNA in amniotic fluid in the included studies did not predict the risk for congenital Zika syndrome abnormalities in these cases, and clearance of Zika virus RNA from amniotic fluid appears possible after maternal infection. Diagnostic testing for Zika virus infection remains a shared decision between patients and clinicians, and more data are needed to define clinical predictors that will inform these decisions. SYSTEMATIC REVIEW REGISTRATION: PROSPERO, CRD42018080959.

Vital Signs: Zika-Associated Birth Defects and Neurodevelopmental Abnormalities Possibly Associated with Congenital Zika Virus Infection - U.S. Territories and Freely Associated States, 2018.

INTRODUCTION: Zika virus infection during pregnancy causes serious birth defects and might be associated with neurodevelopmental abnormalities in children. Early identification of and intervention for neurodevelopmental problems can improve cognitive, social, and behavioral functioning. METHODS: Pregnancies with laboratory evidence of confirmed or possible Zika virus infection and infants resulting from these pregnancies are included in the U.S. Zika Pregnancy and Infant Registry (USZPIR) and followed through active surveillance methods. This report includes data on children aged ≥1 year born in U.S. territories and freely associated states. Receipt of reported follow-up care was assessed, and data were reviewed to identify Zika-associated birth defects and neurodevelopmental abnormalities possibly associated with congenital Zika virus infection. RESULTS: Among 1,450 children of mothers with laboratory evidence of confirmed or possible Zika virus infection during pregnancy and with reported follow-up care, 76% had developmental screening or evaluation, 60% had postnatal neuroimaging, 48% had automated auditory brainstem response-based hearing screen or evaluation, and 36% had an ophthalmologic evaluation. Among evaluated children, 6% had at least one Zika-associated birth defect identified, 9% had at least one neurodevelopmental abnormality possibly associated with congenital Zika virus infection identified, and 1% had both. CONCLUSION: One in seven evaluated children had a Zika-associated birth defect, a neurodevelopmental abnormality possibly associated with congenital Zika virus infection, or both reported to the USZPIR. Given that most children did not have evidence of all recommended evaluations, additional anomalies might not have been identified. Careful monitoring and evaluation of children born to mothers with evidence of Zika virus infection during pregnancy is essential for ensuring early detection of possible disabilities and early referral to intervention services.

Vital Signs: Update on Zika Virus-Associated Birth Defects and Evaluation of All U.S. Infants with Congenital Zika Virus Exposure - U.S. Zika Pregnancy Registry, 2016.

BACKGROUND: In collaboration with state, tribal, local, and territorial health departments, CDC established the U.S. Zika Pregnancy Registry (USZPR) in early 2016 to monitor pregnant women with laboratory evidence of possible recent Zika virus infection and their infants. METHODS: This report includes an analysis of completed pregnancies (which include live births and pregnancy losses, regardless of gestational age) in the 50 U.S. states and the District of Columbia (DC) with laboratory evidence of possible recent Zika virus infection reported to the USZPR from January 15 to December 27, 2016. Birth defects potentially associated with Zika virus infection during pregnancy include brain abnormalities and/or microcephaly, eye abnormalities, other consequences of central nervous system dysfunction, and neural tube defects and other early brain malformations. RESULTS: During the analysis period, 1,297 pregnant women in 44 states were reported to the USZPR. Zika virus-associated birth defects were reported for 51 (5%) of the 972 fetuses/infants from completed pregnancies with laboratory evidence of possible recent Zika virus infection (95% confidence interval [CI] = 4%-7%); the proportion was higher when restricted to pregnancies with laboratory-confirmed Zika virus infection (24/250 completed pregnancies [10%, 95% CI = 7%-14%]). Birth defects were reported in 15% (95% CI = 8%-26%) of fetuses/infants of completed pregnancies with confirmed Zika virus infection in the first trimester. Among 895 liveborn infants from pregnancies with possible recent Zika virus infection, postnatal neuroimaging was reported for 221 (25%), and Zika virus testing of at least one infant specimen was reported for 585 (65%). CONCLUSIONS AND IMPLICATIONS FOR PUBLIC HEALTH PRACTICE: These findings highlight why pregnant women should avoid Zika virus exposure. Because the full clinical spectrum of congenital Zika virus infection is not yet known, all infants born to women with laboratory evidence of possible recent Zika virus infection during pregnancy should receive postnatal neuroimaging and Zika virus testing in addition to a comprehensive newborn physical exam and hearing screen. Identification and follow-up care of infants born to women with laboratory evidence of possible recent Zika virus infection during pregnancy and infants with possible congenital Zika virus infection can ensure that appropriate clinical services are available.

Dynamic taste responses of parabrachial pontine neurons in awake rats.

The parabrachial nuclei of the pons (PbN) receive almost direct input from taste buds on the tongue and control basic taste-driven behaviors. Thus it is reasonable to hypothesize that PbN neurons might respond to tastes in a manner similar to that of peripheral receptors, i.e., that these responses might be narrow and relatively "dynamics free." On the other hand, the majority of the input to PbN descends from forebrain regions such as gustatory cortex (GC), which processes tastes with "temporal codes" in which firing reflects first the presence, then the identity, and finally the desirability of the stimulus. Therefore a reasonable alternative hypothesis is that PbN responses might be dominated by dynamics similar to those observed in GC. Here we examined simultaneously recorded single-neuron PbN (and GC) responses in awake rats receiving exposure to basic taste stimuli. We found that pontine taste responses were almost entirely confined to canonically identified taste-PbN (t-PbN). Taste-specificity was found, furthermore, to be time varying in a larger percentage of these t-PbN responses than in responses recorded from the tissue around PbN (including non-taste-PbN). Finally, these time-varying properties were a good match for those observed in simultaneously recorded GC neurons-taste-specificity appeared after an initial nonspecific burst of action potentials, and palatability emerged several hundred milliseconds later. These results suggest that the pontine taste relay is closely allied with the dynamic taste processing performed in forebrain.

Inactivation of basolateral amygdala specifically eliminates palatability-related information in cortical sensory responses.

Evidence indirectly implicates the amygdala as the primary processor of emotional information used by cortex to drive appropriate behavioral responses to stimuli. Taste provides an ideal system with which to test this hypothesis directly, as neurons in both basolateral amygdala (BLA) and gustatory cortex (GC)-anatomically interconnected nodes of the gustatory system-code the emotional valence of taste stimuli (i.e., palatability), in firing rate responses that progress similarly through "epochs." The fact that palatability-related firing appears one epoch earlier in BLA than GC is broadly consistent with the hypothesis that such information may propagate from the former to the latter. Here, we provide evidence supporting this hypothesis, assaying taste responses in small GC single-neuron ensembles before, during, and after temporarily inactivating BLA in awake rats. BLA inactivation (BLAx) changed responses in 98% of taste-responsive GC neurons, altering the entirety of every taste response in many neurons. Most changes involved reductions in firing rate, but regardless of the direction of change, the effect of BLAx was epoch-specific: while firing rates were changed, the taste specificity of responses remained stable; information about taste palatability, however, which normally resides in the "Late" epoch, was reduced in magnitude across the entire GC sample and outright eliminated in most neurons. Only in the specific minority of neurons for which BLAx enhanced responses did palatability specificity survive undiminished. Our data therefore provide direct evidence that BLA is a necessary component of GC gustatory processing, and that cortical palatability processing in particular is, in part, a function of BLA activity.