1,721,153 research outputs found
Functional neuroanatomy of the human pre-Bötzinger complex with particular reference to sudden unexplained perinatal and infant death
No full textThe authors are the first to identify in man the pre-Bötzinger complex, a structure of the brainstem critical for respiratory rhythmogenesis, previously investigated only in rats. The evaluation of the neurokinin 1 receptors and somatostatin immunoreactivity in a total of 63 brains from 25 fetuses, nine newborns and 29 infants, allowed to delineate the anatomic structure and the boundaries of this human neural center in a restricted area of the ventrolateral medulla at the obex level, ventral to the semicompact ambiguus nucleus. The neurons of the pre-Bötzinger complex were roundish in fetuses before 30 gestational weeks and lengthened after birth, embedded in a dendritic system belonging to the reticular formation. Besides, structural and/or functional alterations of the pre-Bötzinger complex were present in a high percentage of sudden deaths (47%), prevalent in late fetal deaths. In particular, different developmental defects (hypoplasia with a decreased neuronal number and/or dendritic hypodevelopment of the reticular formation, abnormal neuronal morphology, immunonegativity of neurotransmitters, and agenesis) were found. The authors suggest that the pre-Bötzinger complex contains a variety of neurons not only involved in respiratory rhythm generation, but more extensively, essential to the control of all vital functions. Sudden death and in particular sudden unexpected fetal death could therefore be ascribed to a selective process when developmental alterations of the pre-Bötzinger complex arise
Imàgenes en cardiologìa
No full textSe trata de una arteria coronaria descendente anterior de un lactante de 3 meses, fallecido por síndrome de muerte súbita del lactante (SIDS), expuesto a humo de tabaco y alimentado con leche materna. Nuestra casuistica ha permitido caracterizar lesiones preateroscleróticas en fetos de madres fumadoras y demostrar asimismo la progresión de dichas lesiones a placas “juveniles” en lactantes de padres fumadores.La primera lesión se evidencia en fetos a término después de la semana 35° y consiste en marcadas alteraciones de la media, que comprometen a la túnica intima y se originan probablemente en la difusión de productos tóxicos provenientes del flujo sanguíneo. Las fibras muscolares lisas se fragmentan en segmentos cilíndricos, pierden su polaridad y se dirigen hacia la íntima, infiltrándola. Esta progresión de la lesión con engrosamiento parietal puede hallarse después de pocas semanas de vida y sería causada verosimilmente por el tabaquismo pasivo y por la ingestión de los productos de la nicotina durante la lactancia
Histopathology of the cardiac conduction system in sudden intrauterine unexplained death
No full textBACKGROUND : Sudden intrauterine unexplained death (SIUD) is one of the most heartbreaking tragedies that any parent can experience. It remains poorly understood and incompletely examined both morphologically and functionally. The aim of this work is to examine the likely role of cardiac conduction system in relation to sudden and unexplained fetal death. METHODS: We analyzed and compared the autopsy results in 15 cases of SIUD (6 males and 9 females, ranging in age from 35 to 40 weeks) and 11 cases of intrauterine explained death (IED). A complete autopsy was performed, focusing on the examination of the cardiac conduction system on serial sections. RESULTS: The following findings were observed: resorptive degeneration (33% of SIUD, 36% of IED), dispersion or septation of the atrioventricular (AV) junction (60% of SIUD, 64% of IED), islands of the conduction system in the central fibrous body (80% of SIUD, 73% of IED), Mahaim fibers (20% of SIUD), cartilaginous metahyperplasia (20% of SIUD, 18% of IED), an AV node (AVN) tongue (13% of SIUD), hemorrhage of the cardiac conduction system (7% of SIUD, 9% of IED), left-sided bifurcation (7% of SIUD), an intramural right bundle (7% of SIUD), central fibrous body hypoplasia (7% of SIUD), and thickening of the conduction system arteries (13% of SIUD). CONCLUSIONS: Most of the abnormal cardiac conduction findings were detected only in SIUD and were absent in controls, i.e., Mahaim fibers, AVN tongue, left-sided bifurcation, intramural right bundle, and central fibrous body hypoplasia. We are convinced that these cardiac conduction abnormalities, in association with altered neurovegetative stimuli, could underlie potentially malignant arrhythmias
MORTE FETALE versus SIDS (Legge n.31)-PATOLOGIE (CONGENITE) DEL SISTEMA NEUROVEGETATIVO E DI CONDUZIONE CARDIACO LEGATE ALL’EMBRIOGENESI E ALLO SVILUPPO NELLA MORTE INSPIEGABILE PERINATALE E NELLA SIDS
No full textL’applicazione della Legge 31/2006 “Disciplina del riscontro diagnostico sulle vittime della sindrome della morte improvvisa
del lattante (SIDS) e di morte inaspettata del feto” ha consentito di sviluppare approfondite indagini anatomo-cliniche.
Attraverso lo studio neuropatologico è stata individuata l’eziopatogenesi sia della morte fetale inaspettata e inspiegabile
che della SIDS. Trattasi di anomalie congenite comuni a queste patologie. L’acquisizione dell’origine comune di tali
patologie consente di unificare l’inquadramento nosografico, anche ai fini di valutazioni epidemiologiche. Nel complesso
le anomalie congenite sono più diffuse nelle morti fetali inspiegabili ante-partum. In tale ambito caratteristico è il difetto
di sviluppo del complesso facciale/parafacciale, modulatore delle attività vitali. Nelle morti fetali intra-partum frequente
è il riscontro di ipoplasia/agenesi del complesso parabrachiale/nucleo di Kölliker-Fuse che presiede all’inizio dell’attività
respiratoria. Nelle morti inaspettate neonatali precoci e nella SIDS le anomalie sono più limitate e comprendono l’ipoplasia
del nucleo arcuato e della formazione reticolare respiratoria. Frequente è il riscontro di vie accessorie atrio-ventricolari,
substrato di aritmie anche mortali da rientro; esse sono spesso associate alle anomalie del sistema nervoso autonom
Proposal of the Acronym “SIUDS” for Unexplained Stillbirths, Like “SIDS”
No full textThe authors, propose that also a sudden death during pregnancy that remains unexplained after an in-depth autopsy, should be considered as a syndrome and referred with the acronym “SIUDS”, e.g., “Sudden Intrauterine Unexplained Death Syndrome”, like “SIDS” for “Sudden Infant Death Syndrome”. This suggested definition is based on the presence in these pathologies of common developmental abnormalities of both the autonomic nervous system and the cardiac conduction system, associated to the same preventable risk factors
Pathology of the central autonomic nervous system in stillbirth
No full textThe aim of this study was to identify in stillbirth a possible involvement of morphological and/or physiological alterations of structures of the central autonomic nervous system in the mechanism of death. The study, including the in-depth histological examination of brainstem and cerebellum, was performed on 42 stillbirths, aged from 22 to 40 gestational weeks, 12 of which were explained and 30 were unexplained deaths. In the sudden unexplained stillbirths a variety of morphological and/or biological abnormalities of different structures and nuclei was found, above all the hypoplasia of the parafacial complex, frequently associated with hypoplasia of the arucate and pre-Bötzinger nuclei, and with thyrosine-hydroxilase immunonegativity in the locus coeruleus. A significant correlation was also observed between the neuropathologic findings and mother’s smoking habit
Fetal arterial changes in response to maternal cigarette smoking: revisiting the natural history of the earliest stage of atherosclerosis
No full textThe current knowledge of the development and progression of atherosclerotic lesions is largely owed to exptl. studies carried out in animals fed a high cholesterol diet. Only a few studies have addressed the atherogenic effects of other important exogenous risk factor, namely cigarette smoking. The results of our research into the effects of cigarette smoking on the fetal arterial wall have demonstrated that the first reactive event is a severe alteration of the architecture of the tunica media, forming perpendicularly oriented columns of smooth muscle cells (SMCs), infiltrating the intima. These histopathol. alterations go hand in hand with a marked change in the biol. homeostasis of the SMCs. Our mol. biol. research has shown that the first reaction of these cells to the nicotine is an intense activation of the c-fos proto-oncogene, followed by the transformation of the SMCs to \"myofibroblasts\", characterized by the presence of b-actin and acquisition of both synthetic and ameboid activity. If the harmful effects of passive smoke persist, the myofibroblasts start to proliferate, as demonstrated by positivity of the PCNA, together with the onset of chromosomal alterations. These peculiar changes of the tunica media are the prerequisites for lipid accumulation that thereafter overwhelm the myofibroblast reaction. [on SciFinder (R)
Cardiovascular pathology of Sudden Perinatal Unexpected Death (SPUD) and Sudden Infant Death Syndrome (SIDS)
No full textPathology of the cardiac conduction system can cause arrhythmias underlying SPUD and SIDS. A total of 38 SPUD and 130 SIDS victims were investigated. A complete autopsy was performed in each case, including in particular close examination of the cardiac conduction system, according to our guidelines. Accessory atrio-ventricular pathways, mainly Mahaim fibers, in 30% of cases; dispersion of His Bundle in 25% and cartilaginous meta-hyperplasia of the central fibrous body in 6% of cases were detected. The accessory fibers, in particular conditions and under autonomic neuronal stimulation, may underlie potentially lethal arrhythmias generally junctional reentrant in nature, being actually the most frequent in fetuses and newborns. In a total of 12 cases a fibromuscular hyperplasia of the pulmonary artery was detected. The fibromuscular hyperplasia of the pulmonary artery alone, might or might not have accounted for the sudden deaths, if it had not been for the concomitant presence of mild hypoplasia of the arcuate nucleus in the brainstem which could have had a triggering role in causing the sudden death. Of particular interest are borderline cases, which histological examination showed neoplastic lesions of the conduction system. The SPUD/SIDS «gray zone», or borderline cases, are described as those cases in which it is difficult to establish whether the pathological findings are sufficiently severe to have caused the death. Parental cigarette smoking is the most important risk factor for unexpected perinatal death and SIDS. Of interest were also the observation of early atherosclerotic plaques already detectable in fetuses and involving also of the sino-atrial and atrio-ventricular arteries
Morphometric characteristics of hepatocellular dysplasia
No full textMorphometric study of liver biopsies from six entities (normal tissue, post-hepatitis cirrhosis, post-alcoholic cirrhosis, cancer-related cirrhosis, hepatocellular adenoma and hepatocellular adenocarcinoma) confirmed that this technique can be a valuable adjunct to histopathologic study in the examination of such specimens. As expected, measurements in cirrhotic nodules showed two populations of cells. The so-called 'large dysplastic cells' had nuclear and cellular areas close to those of normal hepatocytes and should thus bu considered to be hyperplastic elements, not precancerous elements. The smaller dysplastic cells had morphometric values close to those of the corresponding hepatocellular carcinomas, indicating that these cells are the truly precancerous ones. Therefore, while the study confirmed that hepatic cirrhosis is a precancerous lesion, it also showed that the term hepatocellular dysplasia must be restricted to the smaller type of cells found in such nodules
Cardiovascular causes of perinatal loss.
No full textHigh risk changes in the cardiac action, mostly manifesting with arrhythmias, may be caused by microscopic malformation of the conduction system. The finding of accessory AV communications, particularly nodo-fasciculoventricular Mahaim bundles are rather frequent in perinatal loss as well as in SIDS, but a clinicopathological assessment of their lethal arrhythmogenic potential is often impossible. These congenital abnormalities, under particular conditions and/or neurovegetative stimuli, are liable to provoke electrical inhomogeneity, instability, and desynchronization with impeding risk of malignant junctional arrhythmias. Mahaim fibers have been detected in 39% of sudden perinatal death and in 23% of SIDS victims. These lesions have been attributed to the variable outcome of a “resorptive degeneration” process that normally “reshapes” the junctional pathways in the early postnatal period. Another approach to the same problem can be made by taking into consideration the persistence of ontogenically specialized ring tissue, astride the AV annuli or, as seen in neonatal death victims, putting together a sort of “arrhythmogenic interface” with the ordinary myocardium, at the top of the ventricular septum. Also, the central cardiac structure supporting the conduction system, could possibly interfere with the causation of impulses, as in the cases of cartilaginous metaplasia of the fibrous body, detected in 6% of SIDS and in 19% of sudden perinatal victims. Regarding the long QT syndrome, as a favoring condition for ventricular tachycardia-fibrillation with a high risk of sudden cardiac death, one can say that this thesis is losing ground; the implications of the neurovegetative reflex mechanisms, does not correspond to any clear-cut pathologic changes. Early atherosclerotic lesions of the cerebral and coronary arteries, involving also the sino-atrial and atrio-ventricular arteries, significantly associated with maternal cigarette smoking, are common in the perinatal period. Lastly, cases of fibromuscolar hyperplasia of the pulmonary artery were detected
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