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The autonomic nervous system (ANS) coordinates multiple reflex actions which are essential for life. The tests employed to evaluate the ANS provide valuable information of the functional state of these reflex arcs. The ideal test should be simple to perform, noninvasive, reproducible, sensitive, specific, safe, and appropriate for longitudinal studies. The availability of computer-based techniques has facilitated the electrophysiological assessment of ANS-mediated reflexes. The information provided by autonomic testing must be analyzed in combination with the clinical history and physical examination of the patient, allowing for a hypothesis that can be tested. Properly performed and interpreted, ANS testing can be used to confirm the presence of an ANS disturbance and the involved functional pathways, as well as the extent, intensity, and site of injury. This chapter describes the most important electrophysiological tests used to evaluate the ANS control of cardiovascular reflexes and sweat gland activity.
Subject(s)
Autonomic Nervous System Diseases , Humans , Autonomic Nervous System Diseases/diagnosis , Autonomic Nervous System Diseases/etiology , Autonomic Nervous System/physiology , ReflexABSTRACT
Impaired gas exchange close to labor causes perinatal asphyxia (PA), a neurodevelopmental impairment factor. Palmitoylethanolamide (PEA) proved neuroprotective in experimental brain injury and neurodegeneration models. This study aimed to evaluate PEA effects on the immature-brain, i.e., early neuroprotection by PEA in an experimental PA paradigm. Newborn rats were placed in a 37°C water bath for 19 min to induce PA. PEA 10 mg/kg, s.c., was administered within the first hour of life. Neurobehavioral responses were assessed from postnatal day 1 (P1) to postnatal day 21 (P21), recording the day of appearance of several reflexes and neurological signs. Hippocampal CA1 area ultrastructure was examined using electron microscopy. Microtubule-associated protein 2 (MAP-2), phosphorylated high and medium molecular weight neurofilaments (pNF H/M), and glial fibrillary acidic protein (GFAP) were assessed using immunohistochemistry and Western blot at P21. Over the first 3 weeks of life, PA rats showed late gait, negative geotaxis and eye-opening onset, and delayed appearance of air-righting, auditory startle, sensory eyelid, forelimb placing, and grasp reflexes. On P21, the hippocampal CA1 area showed signs of neuronal degeneration and MAP-2 deficit. PEA treatment reduced PA-induced hippocampal damage and normalized the time of appearance of gait, air-righting, placing, and grasp reflexes. The outcome of this study might prove useful in designing intervention strategies to reduce early neurodevelopmental delay following PA.
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BACKGROUND: Blink and masseter reflexes provide reliable, quantifiable data on the function of the central nervous system: Delayed latencies have been found in patients with neurocognitive disorder (ND) and type 2 diabetes mellitus (T2DM), but this has not been studied in patients with both pathologies. AIM: To investigate if older adults with ND plus T2DM have prolonged latencies of blink and masseter-reflex and if they were associated with disease progression. METHODS: This cross-sectional study included 227 older adults (> 60 years) from Colima, Mexico. Neurocognitive disorder was identified by a neuropsychological battery test, and T2DM identified by medical history, fasting glucose, and glycosylated hemoglobin. Latencies in the early reflex (R1), ipsilateral late (R2), and contralateral late (R2c) components of the blink reflex were analyzed for all subjects, and 183 subjects were analyzed for latency of the masseter reflex. RESULTS: In 20.7% of participants, ND was detected. In 37%, T2DM was detected. Latencies in R1, R2, and R2c were significantly prolonged for groups with ND plus T2DM, ND, and T2DM, compared with the control group (P < 0.0001). The masseter reflex was only prolonged in older adults (regardless of T2DM status) with ND vs controls (P = 0.030). In older adults with ND and without T2DM, the more the cognitive impairment progressed, the more prolonged latencies in R2 and R2c presented (P < 0.01). CONCLUSION: These findings suggest that blink and masseter reflexes could be used to evaluate possible changes in brainstem circuits in older adults with ND and T2DM.
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[This corrects the article DOI: 10.3389/fnbeh.2022.953157.].
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Reflex-ontogeny and intestinal morphometrics were evaluated in Wistar rats whose mothers were fed on a high-fat diet during the perinatal period. Male pups (n=52) formed four experimental groups: NN (pups from mothers with lab chow diet during gestation and lactation); NH (pups from mothers with lab chow diet during pregnancy and high-fat in lactation); HH (pups from mothers with high-fat diet during gestation and lactation); HN (pups from mothers with high-fat diet during pregnancy and lab chow in lactation). The reflex ontogeny, the maturation of physical characteristics and parameters of somatic growth were evaluated during lactation. In addition, the body mass index (BMI), the specific rate of weight gain (SRWG), the Lee index, the weight of the brain and intestinal parameters were analyzed after weaning. High-fat diet during pregnancy (HH and HN groups) delayed the maturation of reflexes and physical characteristics. The high-fat diet affected somatic growth differently, reducing somatic growth parameters in the groups NH and HH and increasing in the HN group. The highest SRWG was found in group HN. SRWG and BMI were reduced in the groups NH and HH. The relative intestinal weight was reduced in the groups NH, HH and HN. The relative length of small intestine was longer in group HN than in group NN. The total height of the mucosa and size of the villous were lower in group HH than in group NN. In conclusion, high-fat diet promoted negative consequences for the development of the nervous and enteric systems of the offspring(AU)
Ontogenia refleja y morfometría intestinal fueron evaluados en crías de ratas Wistar que fueron alimentadas con una dieta alta en grasas durante el período perinatal. Los descendientes machos (n = 52) formaron cuatro grupos experimentales: NN (hijos de madres que utilizaron alimentos de laboratorio durante la gestación y la lactancia); NH (hijos de madres que comieron dieta de laboratorio durante el embarazo y dieta con un alto contenido de grasas en la lactancia); HH (hijos de madres con una dieta alta en grasas durante el embarazo y la lactancia); HN (hijos de madres que comieron una dieta alta en grasas durante el embarazo y comida de laboratorio durante la lactancia). La ontogenia refleja, la maduración de las características físicas y los parámetros de crecimiento somático durante la lactancia fueron evaluados. Además, el índice de masa corporal (IMC), la tasa específica de aumento de peso (SRWG), el índice de Lee, el peso cerebral y los parámetros intestinales fueron analizados después del destete. La dieta alta en grasas durante el embarazo (grupos HH y HN) retrasó la maduración de reflejos y características físicas. La dieta alta en grasas afectó el crecimiento somático de manera diferente, reduciendo los parámetros de crecimiento somático en los grupos NH y HH y aumentando en el grupo HN. El SRWG más grande se encontró en el grupo HN. El SRWG y el IMC se redujeron en los grupos NH y HH. El peso relativo intestinal se redujo en los grupos NH, HH y HN. La longitud relativa del intestino delgado fue mayor en el grupo HN que en el grupo NN. La altura total de la mucosa y el tamaño de las vellosidades fueron menores en el grupo HH que en el grupo NN. En conclusión, la dieta alta en grasas tuvo consecuencias negativas para el desarrollo de los sistemas nervioso y entérico de la prole(AU)
Subject(s)
Rats , Breast Feeding , Dietary Fats , Gene Ontology , Dietary Sugars , Chronic Disease , ObesityABSTRACT
Abstract Introduction Auditory neuropathy spectrum disorder (ANSD) features the presence of otoacoustic emissions, poor speech identification score and absent auditory brainstem response. Objective The present study was designed to evaluate the functioning of all six semicircular canals in individuals with ANSD and to compare it with those of normalhearing individuals. Methods A total of 50 individuals participated in the present study, in which Group I comprised25normal-hearingindividuals, and GroupII comprised25individualswithANSD. All of the participants underwent case history, pure tone audiometry, immittance, otoacoustic emissions, auditory evoked response and video head impulse test (vHIT). Results The independent sample t-test revealed significantly lower vestibulo-ocular reflex gain values in individuals with ANSD. A presence of 100% corrective refixation saccades was observed in the same group. The Pearson correlation test revealed no significant correlation between vestibulo-ocular reflex (VOR) gain with duration of hearing loss and pure tone thresholds for any of the three orthogonal planes. The chisquared test revealed no association between the VOR gain values and the presence or absence of saccades in any of the semicircular canals (p>0.05). Conclusion Huge percentages of individuals with ANSD have been found to have associated vestibular dysfunction as well. Therefore, the vHIT can be used as one of the important tests of the vestibular test battery to evaluate all six semicircular canals in individuals with ANSD.
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Introduction Auditory neuropathy spectrum disorder (ANSD) features the presence of otoacoustic emissions, poor speech identification score and absent auditory brainstem response. Objective The present study was designed to evaluate the functioning of all six semicircular canals in individuals with ANSD and to compare it with those of normal-hearing individuals. Methods A total of 50 individuals participated in the present study, in which Group I comprised 25 normal-hearing individuals, and Group II comprised 25 individuals with ANSD. All of the participants underwent case history, pure tone audiometry, immittance, otoacoustic emissions, auditory evoked response and video head impulse test (vHIT). Results The independent sample t-test revealed significantly lower vestibulo-ocular reflex gain values in individuals with ANSD. A presence of 100% corrective refixation saccades was observed in the same group. The Pearson correlation test revealed no significant correlation between vestibulo-ocular reflex (VOR) gain with duration of hearing loss and pure tone thresholds for any of the three orthogonal planes. The chi-squared test revealed no association between the VOR gain values and the presence or absence of saccades in any of the semicircular canals ( p > 0.05). Conclusion Huge percentages of individuals with ANSD have been found to have associated vestibular dysfunction as well. Therefore, the vHIT can be used as one of the important tests of the vestibular test battery to evaluate all six semicircular canals in individuals with ANSD.
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Preterm birth and hypoxia-ischemia (HI) are major causes of neonatal death and neurological disabilities in newborns. The widely used preclinical HI model combines carotid occlusion with hypoxia exposure; however, the relationship between different hypoxia exposure periods with brain tissue loss, astrocyte reactivity and behavioral impairments following HI is lacking. Present study evaluated HI-induced behavioral and morphological consequences in rats exposed to different periods of hypoxia at postnatal day 3. Wistar rats of both sexes were assigned into four groups: control group, HI-120 min, HI-180 min and HI-210 min. Neurodevelopmental reflexes, exploratory abilities and cognitive function were assessed. At adulthood, tissue damage and reactive astrogliosis were measured. Animals exposed to HI-180 and HI-210 min had delayed neurodevelopmental reflexes compared to control group. Histological assessment showed tissue loss that was restricted to the ipsilateral hemisphere in lower periods of hypoxia exposure (120 and 180 min) but affected both hemispheres when 210 min was used. Reactive astrogliosis was increased only after 210 min of hypoxia. Interestingly, cognitive deficits were induced regardless the duration of hypoxia and there were correlations between behavioral parameters and cortex, hippocampus and corpus callosum volumes. These results show the duration of hypoxia has a close relationship with astrocytic response and tissue damage progression. Furthermore, the long-lasting cognitive memory deficit and its association with brain structures beyond the hippocampus suggests that complex anatomical changes should be involved in functional alterations taking place as hypoxia duration is increased, even when the cognitive impairment limit is achieved.
Subject(s)
Astrocytes/physiology , Hypoxia-Ischemia, Brain/physiopathology , Animals , Animals, Newborn , Brain/pathology , Cognitive Dysfunction/physiopathology , Female , Gliosis/physiopathology , Hypoxia-Ischemia, Brain/pathology , Male , Maze Learning/physiology , Memory Disorders/physiopathology , Rats, Wistar , Regression Analysis , Time FactorsABSTRACT
A low resting heart rate (HR) would be of great benefit in cardiovascular diseases. Ivabradine-a novel selective inhibitor of hyperpolarization-activated cyclic nucleotide gated (HCN) channels- has emerged as a promising HR lowering drug. Its effects on the autonomic HR control are little known. This study assessed the effects of chronic treatment with ivabradine on the modulatory, reflex and tonic cardiovascular autonomic control and on the renal sympathetic nerve activity (RSNA). Male Wistar rats were divided in 2 groups, receiving intraperitoneal injections of vehicle (VEH) or ivabradine (IVA) during 7 or 8 consecutive days. Rats were submitted to vessels cannulation to perform arterial blood pressure (AP) and HR recordings in freely moving rats. Time series of resting pulse interval and systolic AP were used to measure cardiovascular variability parameters. We also assessed the baroreflex, chemoreflex and the Bezold-Jarish reflex sensitivities. To better evaluate the effects of ivabradine on the autonomic control of the heart, we performed sympathetic and vagal autonomic blockade. As expected, ivabradine-treated rats showed a lower resting (VEH: 362 ± 16 bpm vs. IVA: 260 ± 14 bpm, p = 0.0005) and intrinsic HR (VEH: 369 ± 9 bpm vs. IVA: 326 ± 11 bpm, p = 0.0146). However, the chronic treatment with ivabradine did not change normalized HR spectral parameters LF (nu) (VEH: 24.2 ± 4.6 vs. IVA: 29.8 ± 6.4; p > 0.05); HF (nu) (VEH: 75.1 ± 3.7 vs. IVA: 69.2 ± 5.8; p > 0.05), any cardiovascular reflexes, neither the tonic autonomic control of the HR (tonic sympathovagal index; VEH: 0.91± 0.02 vs. IVA: 0.88 ± 0.03, p = 0.3494). We performed the AP, HR and RSNA recordings in urethane-anesthetized rats. The chronic treatment with ivabradine reduced the resting HR (VEH: 364 ± 12 bpm vs. IVA: 207 ± 11 bpm, p < 0.0001), without affecting RSNA (VEH: 117 ± 16 vs. IVA: 120 ± 9 spikes/s, p = 0.9100) and mean arterial pressure (VEH: 70 ± 4 vs. IVA: 77 ± 6 mmHg, p = 0.3293). Our results suggest that, in health rats, the long-term treatment with ivabradine directly reduces the HR without changing the RSNA modulation and the reflex and tonic autonomic control of the heart.
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Our previous results demonstrated improved cognition in adolescent rats housed in environmental enrichment (EE) that underwent neonatal hypoxia-ischemia (HI). The aim of this study was to investigate the effects of early EE on neurobehavioral development and brain damage in rats submitted to neonatal HI. Wistar rats were submitted to the HI procedure on the 7th postnatal day (PND) and housed in an enriched environment (8th-20th PND). The maturation of physical characteristics and the neurological reflexes were evaluated and the volume of striatum, corpus callosum and neocortex was measured. Data analysis demonstrated a clear effect of EE on neurobehavioral development; also, daily performance was improved in enriched rats on righting, negative geotaxis and cliff aversion reflex. HI caused a transient motor deficit on gait latency. Brain atrophy was found in HI animals and this damage was partially prevented by the EE. In conclusion, early EE stimulated neurobehavioral development in neonate rats and also protects the neocortex and the corpus callosum from atrophy following HI. These findings reinforce the potential of EE as a strategy for rehabilitation following neonatal HI and provide scientific support to the use of this therapeutic strategy in the treatment of neonatal brain injuries in humans.
Subject(s)
Brain/growth & development , Environment , Hypoxia-Ischemia, Brain/rehabilitation , Reflex , Animals , Animals, Newborn , Brain/pathology , Corpus Callosum/growth & development , Corpus Callosum/pathology , Corpus Striatum/growth & development , Corpus Striatum/pathology , Female , Hypoxia-Ischemia, Brain/pathology , Hypoxia-Ischemia, Brain/physiopathology , Male , Neocortex/growth & development , Neocortex/pathology , Organ Size , Rats, WistarABSTRACT
This study was designed to verify whether different lactation conditions influenced nervous system development. The authors used motor tasks to verify changes in exploratory activity and muscle strength of weaned rats from different litter sizes and evaluated the applicability of the grid-walking test for assessing motor abnormalities caused by undernutrition. Alterations in litter size during the suckling period perturbed the nutritional status of pups, which exhibited body weight differences between the groups. Large-litter (L) pups showed significant delays in achieving developmental milestones and neurological reflexes compared to the small-litter (S) and medium-litter (M) pups. The S, M, and L group pups exhibited similar exploratory responses and muscle strength. In the grid-walking and foot-fault tests, the L group pups traveled shorter distances and, consequently, had less footsteps. However, the percentages of foot faults in the L group were higher than S and M groups. These results reflect delayed maturation of structures responsible for sensorimotor responses, such as the cerebellum, because much cerebellar maturation takes place postnatally. This is the first study to report that early undernutrition in pups resulted in suboptimal performances on the grid-walking and foot-fault tests and that the former test was sensitive to alterations caused by nutritional deficiency.
Subject(s)
Malnutrition/complications , Motor Skills Disorders/etiology , Animals , Animals, Newborn/physiology , Female , Male , Malnutrition/physiopathology , Motor Skills Disorders/physiopathology , Muscle Strength/physiology , Neurodevelopmental Disorders/etiology , Neurodevelopmental Disorders/physiopathology , Rats , Rats, Wistar/physiology , Reflex/physiology , Reflex, Startle/physiology , Walking/physiologyABSTRACT
The malnutrition in early life is associated with metabolic changes and cardiovascular impairment in adulthood. Deficient protein intake-mediated hypertension has been observed in clinical and experimental studies. In rats, protein malnutrition also increases the blood pressure and enhances heart rate and sympathetic activity. In this review, we discuss the effects of post-weaning protein malnutrition on the resting mean arterial pressure and heart rate and their variabilities, cardiovascular reflexes sensitivity, cardiac autonomic balance, sympathetic and renin-angiotensin activities and neural plasticity during adult life. These insights reveal an interesting prospect on the autonomic modulation underlying the cardiovascular imbalance and provide relevant information on preventing cardiovascular diseases.
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Neonatal veterinarians still observe higher mortality rates among their patients than those observed among humans. Establishment of a neonatal assessment protocol is fundamental to the identification of the medical status of the neonate and the need for medical intervention. The neonatal Apgar score evaluation, which is commonly used in clinical practice, should be complemented by other methods of analysis. This study proposes, in addition to an Apgar score analysis, the evaluation of laboratory parameters and weight. We believe that knowledge of these reference values is essential for diagnosing at-risk neonates and for establishing suitable treatments.
Subject(s)
Animals, Newborn , Veterinary Medicine/methods , Animals , Animals, Newborn/physiology , Body Weight , Dogs , Female , Practice Patterns, Physicians' , Reference ValuesABSTRACT
AIMS: We evaluated the effect of food restriction (FR) on the various reflexes involved in short term cardiovascular regulation; we also evaluated the contribution of the sympathetic nervous systemand of the plasmatic nitric oxide (NO) in the development of the counterregulatory cardiovascular changes triggered by FR. MAIN METHODS: Female rats were subjected to FR for 14 days, and after this period biochemical measurements of biochemical parameters were performed. For physiological tests, animals were anaesthetised, and a catheter was inserted into the femoral artery and vein for the acquisition of blood pressure and heart hate, and drug infusion, respectively.We then tested the BezoldJarisch reflex, the baroreflex and chemoreflex and the effect of the infusion of adrenergic receptor antagonists in control and food restricted animals. KEY FINDINGS: The rats subjected to severe FR presented biochemical changes characteristic of malnutrition with a great catabolic state. FR also led to hypotension and bradycardia besides reducing the plasmatic concentration of NO. Moreover, activation of the BezoldJarisch reflex induced a more pronounced hypotensive response in animals subjected to FR. Intravenous infusion of a α1-adrenoreceptor antagonist induced a greater hypotensive response and a more pronounced tachycardic response in animals under food restriction,while the infusion of ß-adrenoreceptor antagonist induced lower increases in blood pressure in these animals. SIGNIFICANCE: Our results suggest that an increased α1-adrenoreceptor activity in the resistance arteries coupled with a reduction of plasmatic NO contributes in a complementary manner to maintain the blood pressure levels in animals under FR.
Subject(s)
Blood Pressure , Receptors, Adrenergic, alpha-1/physiology , Animals , Anorexia Nervosa/metabolism , Anorexia Nervosa/physiopathology , Baroreflex , Caloric Restriction , Female , Heart Rate , Nitric Oxide/metabolism , Rats , Rats, Inbred F344ABSTRACT
The rat posterodorsal medial amygdala (MePD) links emotionally charged sensory stimuli to social behavior, and is part of the supramedullary control of the cardiovascular system. We studied the effects of microinjections of neuroactive peptides markedly found in the MePD, namely oxytocin (OT, 10 ng and 25 pg; n=6/group), somatostatin (SST, 1 and 0.05 μM; n=8 and 5, respectively), and angiotensin II (Ang II, 50 pmol and 50 fmol; n=7/group), on basal cardiovascular activity and on baroreflex- and chemoreflex-mediated responses in awake adult male rats. Power spectral and symbolic analyses were applied to pulse interval and systolic arterial pressure series to identify centrally mediated sympathetic/parasympathetic components in the heart rate variability (HRV) and arterial pressure variability (APV). No microinjected substance affected basal parameters. On the other hand, compared with the control data (saline, 0.3 µL; n=7), OT (10 ng) decreased mean AP (MAP50) after baroreflex stimulation and increased both the mean AP response after chemoreflex activation and the high-frequency component of the HRV. OT (25 pg) increased overall HRV but did not affect any parameter of the symbolic analysis. SST (1 μM) decreased MAP50, and SST (0.05 μM) enhanced the sympathovagal cardiac index. Both doses of SST increased HRV and its low-frequency component. Ang II (50 pmol) increased HRV and reduced the two unlike variations pattern of the symbolic analysis (P<0.05 in all cases). These results demonstrate neuropeptidergic actions in the MePD for both the increase in the range of the cardiovascular reflex responses and the involvement of the central sympathetic and parasympathetic systems on HRV and APV.
Subject(s)
Animals , Male , Arterial Pressure/drug effects , Baroreflex/drug effects , Corticomedial Nuclear Complex/drug effects , Heart Rate/drug effects , Neuropeptides/pharmacology , Wakefulness , Analysis of Variance , Angiotensin II/administration & dosage , Brain/anatomy & histology , Cardiovascular System/innervation , Corticomedial Nuclear Complex/metabolism , Hemodynamics/drug effects , Microinjections , Neuropeptides/administration & dosage , Oxytocin/administration & dosage , Parasympathetic Nervous System/drug effects , Rats, Wistar , Statistics, Nonparametric , Somatostatin/administration & dosage , Sympathetic Nervous System/drug effects , Vascular Access DevicesABSTRACT
PURPOSE: The vertebrate inner retina has a subset of intrinsically photosensitive retinal ganglion cells (ipRGCs) that express the nonvisual photopigment melanopsin. The intrinsically photosensitive retinal ganglion cells send light information from the environment to the brain to control, among other parameters, the amount of energy entering the eyes through the pupillary light reflex (PLR). A daily variation in the PLR in both mice and humans has recently been shown, indicating circadian control of this response. In a previous work involving the sensitivity spectra for the PLR, we showed that blind chickens (GUCY1*) display the highest sensitivity to light of 480 nm. The aim of the present study was to evaluate the potential circadian control of PLRs in blind birds under scotopic conditions. METHODS: Circadian PLR was performed on GUCY1* chickens with lights of different wavelengths (white or blue light of 475 nm) under scotopic conditions. RESULTS: We found a significant daily variation in the PLRs of chickens exposed to white or blue light of 475 nm, with increased sensitivity at circadian time 6 during the subjective day. CONCLUSIONS: Our observations clearly point to circadian control of PLRs even in blindness, strongly indicating that both the entry of light into the eyes and its quality are differentially regulated during the day in diurnal animals.
Subject(s)
Blindness/physiopathology , Circadian Rhythm , Pupil/physiology , Reflex, Pupillary/physiology , Retinal Ganglion Cells/physiology , Animals , Chickens , Disease Models, Animal , Light Signal Transduction/physiology , Photic StimulationABSTRACT
Resumen Introducción y objetivos: Determinar la presencia de signos de liberación cortical, asociada a daño de sustancia blanca, es un método clínico de fácil realización. El objetivo es deter minar la presencia de signos de liberación cortical en pacientes con enfermedades mentales y enfermedad cerebrovascular y determinar su utilidad clínica, dado que indica daño cortical. Material y métodos: Se realiza búsqueda de signos de liberación cortical en pacientes hospitalizados en clínica psiquiátrica y hospital general con diagnósticos de trastorno afectivo bipolar (40), depresión (37), esquizofrenia (33), enfermedad cardiovascular (33) y demencia (37). Resultados: Los signos de liberación cortical no tienen igual importancia en la determinación de daño cortical; por ejemplo, se encontró reflejo glabelar en todos los grupos; el de paratonía, especialmente en el grupo con esquizofrenia, y más signos, en el grupo de pacientes con demencia. Conclusiones: Se formula que estos signos implican daño de sustancia blanca subcortical; la aparición de estos signos supone la necesidad de seguimiento de pacientes con diagnósticos de trastorno afectivo bipolar, depresión y esquizofrenia.
Abstract Background and objectives: Determining the presence of cortical release signs associated with white matter damage, is a clinically easy method to perform. The objective of this study is to determine the presence of cortical release signs in patients with mental illnesses and cerebrovascular disease, as well as its clinical usefulness, given that it indicates cortical damage. Material and methods: A review was made of cortical release signs in patients hospitalized in clinical psychiatry and general hospitals with bipolar affective disorder (40), depression (37), schizophrenia (33), cardiovascular disease (33) and dementia (37). Results: The signs of cortical release do not have the same importance as cortical damage. For example, the glabellar reflex was found in all the groups, that of paratonia, particularly in the group with schizophrenia, and others signs in the group of patients with dementia. Conclusions: It is suggested that these signs imply subcortical white matter damage. The appearance of these signs shows the need for a follow up of patients diagnosed with bipolar affective disorder, depression and schizophrenia.
Subject(s)
Humans , Male , Female , Middle Aged , Aged , Schizophrenia , Cerebrovascular Disorders , Mental Disorders , Cortical Spreading Depression , Cardiovascular Diseases , Mood Disorders , Dementia , Depression , Depressive DisorderABSTRACT
Objetivos. A pesar de décadas de investigación en el área de la electromiografía, su empleo en odontología es aún controversial, debido a la baja sensibilidad de las variables estudiadas. Se definió y analizó una nueva variable, que es la capacidad del individuo para controlar su trayectoria muscular durante un esfuerzo voluntario estandarizado, con el objetivo de analizar posibles patrones de normalidad.Métodos. Se utilizó retroalimentación visual para controlar el esfuerzo contráctil de los músculos masetero, trapecio y frontal. Se midió, para cada músculo, el tiempo que cada individuo necesitó para controlar la trayectoria de la actividad motora.Resultados. Se demostró que la capacidad de una persona sana para controlar esa trayectoria era diferente para los músculos inervados por distintos pares craneales. Un posible patrón de normalidad fue más evidente en los músculos maseteros.Conclusiones. Se define y analiza, en un trabajo piloto, una nueva variable para el estudio de la función cráneo-mandibular. Se requerirá un futuro estudio, con una muestra ampliada, para confirmar estos resultados preliminares.
Objectives. Despite decades of research in the area of electromyography, its use in dentistry is still controversial because low sensitivity of the proposed variables. We defined and analyzed a new variable, which is the ability of the subject to control the muscle force trajectory, with the aim to find possible normality patterns.Methods. Real-time visual biofeedback was used to control the muscle force trajectory of the masseter, trapezius and frontal muscles. We measured the time that each individual needed to control the trajectory under a standardized set of experimental conditions.Results. We showed that the ability to control the muscle force trajectory can vary for muscles innervated by different cranial nerves. A possible ¨normality¨ pattern was more evident in the masseter muscle.Conclusions. We defined and analyzed, in a pilot research, a new variable for the study of the craniomandibular function. Further research, with an increased sample size, will be needed in order to confirm these preliminary results.
Subject(s)
Electromyography , Masseter Muscle , Masticatory Muscles/physiology , ReflexABSTRACT
The diastolic pulsatile increase in arterial blood pressure is shown to occur earlier in the aorta than in other arteries. It is thus not a reflection of the systolic pressure wave, as has been generally assumed, but an independent pressure wave produced by the sequential contraction of the arterial tree. Conversely, a systolic pulsatile decrease in the rate of blood pressure rise is also produced by an active relaxation of the arterial tree. Simultaneously with the pulsatile changes in arterial blood pressure, there are corresponding changes in arterial blood flow. All these cyclic changes are reflex responses to decreasing diastolic and increasing systolic baroreceptor firing rates, respectively. The two reflexes contribute, together with the known compliance of the large arteries and the great arteriolar blood flow resistance, to the steadiness of capillary blood flow throughout the systolic and the much longer-lasting diastolic phases of the cardiac cycle.
Subject(s)
Arterial Pressure/physiology , Arteries/physiology , Baroreflex/physiology , Models, Cardiovascular , Pulsatile Flow/physiology , Systole/physiology , Animals , Blood Flow Velocity/physiology , Computer Simulation , HumansABSTRACT
Autosomal recessive cerebellar ataxias are a heterogeneous group of neurological disorders. In 1981, a neurological entity comprised by early onset progressive cerebellar ataxia, dysarthria, pyramidal weakness of the limbs and retained or increased upper limb reflexes and knee jerks was described. This disorder is known as early onset cerebellar ataxia with retained tendon reflexes. In this article, we aimed to call attention for the diagnosis of early onset cerebellar ataxia with retained tendon reflexes as the second most common cause of autosomal recessive cerebellar ataxias, after Friedreich ataxia, and also to perform a clinical spectrum study of this syndrome. In this data, 12 patients from different families met all clinical features for early onset cerebellar ataxia with retained tendon reflexes. Dysarthria and cerebellar atrophy were the most common features in our sample. It is uncertain, however, whether early onset cerebellar ataxia with retained tendon reflexes is a homogeneous disease or a group of phenotypically similar syndromes represented by different genetic entities. Further molecular studies are required to provide definitive answers to the questions that remain regarding early onset cerebellar ataxia with retained tendon reflexes.
.As ataxias cerebelares autossômicas recessivas são um grupo heterogêneo de doenças neurológicas. Em 1981, foi descrita uma entidade neurológica incluindo ataxia cerebelar progressiva de início precoce, disartria, liberação piramidal e manutenção ou aumento dos reflexos tendíneos nos membros superiores e inferiores. Essa síndrome é conhecida como ataxia cerebelar de início precoce com reflexos mantidos. Neste artigo, o objetivo foi chamar a atenção para o diagnóstico de ataxia cerebelar de início precoce com reflexos mantidos como a segunda causa mais comum de ataxia cerebelar autossômica recessiva, após a ataxia de Friedreich, e também realizar um estudo do espectro clínico da síndrome. Doze pacientes de diferentes famílias preencheram os critérios clínicos para ataxia cerebelar de início precoce com reflexos mantidos. Disartria e atrofia cerebelar foram as características mais frequentes. No entanto, não há consenso se a ataxia cerebelar de início precoce com reflexos mantidos é uma doença homogênea ou um grupo de síndromes com fenótipos semelhantes representadas por diferentes entidades genéticas. Estudos moleculares futuros são necessários para fornecer respostas definitivas para as questões pendentes em relação à ataxia cerebelar de início precoce com reflexos mantidos.
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