Síndrome del niño maltratado: aspectos médico-legales / Battered child syndrome: forensic aspects

El maltrato infantil constituye un problema de profundas repercusiones psicológicas, sociales, éticas, jurídicas y médicas. En el presente trabajo se realiza una revisión histórica, conceptual y médica del problema (AU)

Child abuse is a problem with serious psychological, social, ethic, legal and medical repercussions. In this paper an historical, conceptual and medical review of the problem is performed (AU)

Modelo predictivo de la duración de incapacidad temporal por lumbalgia. Factores determinantes / Predictive model of the duration of temporary disability for low back pain. Decisive factors

Conocer la prevalencia de lumbalgia entre los procesos que originan incapacidad temporal (IT), y determinar su duración media. Construir un modelo que ayude a predecir la duración de IT por lumbalgia. Método: Análisis de los registros de procesos de IT desde 1999 hasta 2003 en la provincia de Córdoba. Estimación a través de modelos de regresión considerando como variable dependiente la duración de la IT por lumbalgia. Resultados: La ciática y el dolor de espalda irradiado y no irradiado, constituyen el 11,7% de todos los procesos que originan IT; y suponen el 14,4% del total de días perdidos por IT. Su duración media (59,56 días) es significativamente mayor que el resto de patologías que causan IT: El medio urbano actúa como factor de protección, disminuyendo la duración de la baja. Los varones tienen una probabilidad incrementada (OR de 1, 103) para finalizar su proceso de IT. Por cada año, se prevé una mayor duración de estos procesos

To know the low back pain prevalence hmong the processes that originate temporary disability (TD), andto determine half duration. To build a model that helps to predict the duration of TD for low back pain. Method: Analysis of the registration of processes of TD from 1999 up to 2003 in Córdoba. Estimate through regression models, considering as dependent variable the duration of the TD for low back pain. Results: The sciatica and the back pain, irradiated and not irradiated, they constitute 11,7% of TD processes; and they suppose 14,4% of the total of days lost by TD. Their half duration (59,56 days) it is significantly bigger that the rest of TD causes. The urban means acts as protection factor, dimishing the duration of the drop. The males have an increased probability (OR 1,103) to conclude their process of TD. For every year, to predict a bigger duration of these processes

Glutamatergic and GABAergic agonists increase [Ca2+]i in avian cochlear nucleus neurons.

Neurons of the avian cochlear nucleus, nucleus magnocellularis (NM), are stimulated by glutamate, released from the auditory nerve, and GABA, released from both interneurons surrounding NM and from cells located in the superior olivary nucleus. In this study, the Ca2+ indicator dye Fura-2 was used to measure Ca2+ responses in NM stimulated by glutamate- and GABA-receptor agonists using a chicken brainstem slice preparation. Glutamatergically stimulated Ca2+ responses were evoked by kainic acid (KA), alpha-amino-3-hydroxyl-5-methylisoxazole-4-propionic acid (AMPA), and N-methyl-D-aspartate (NMDA). KA- and AMPA-stimulated changes in [Ca2+]i were also produced in NM neurons stimulated in the presence of nifedipine, an L-type Ca2+ channel blocker, suggesting that KA- and AMPA-stimulated changes in [Ca2+]i were carried by Ca2(+)-permeable receptor channels. Significantly smaller changes in [Ca2+]i were produced by NMDA. When neurons were stimulated in an alkaline (pH 7.8) superfusate, NMDA responses were potentiated. KA- and AMPA-stimulated responses were not affected by pH. Several agents known to stimulate metabotropic receptors in other systems were tested on NM neurons bathed in a Ca2+ free-EGTA--buffered media, including L-cysteine sulfinic acid (L-CSA), trans-azetidine dicarboxylic acid (t-ADA), trans-aminocyclo-pentanedicarboxylic acid (t-ACPD), and homobromoibotenic acid (HBI). The only agent to reliably and dose-dependently increase [Ca2+]i was HBI, an analog of ibotenate. GABA also stimulated increases in [Ca2+]i in NM neurons. GABA-stimulated responses were reduced by agents that block voltage-operated channels and by agents that inhibit Ca2+ release from intracellular stores. Whereas GABA-A receptor agonist produced increases in [Ca2+]i GABA-B and GABA-C receptor agonists had no effect. There appear to be several ways for [Ca2+]i to increase in NM neurons. Presumably, each route represents a means by which Ca2+ can alter cellular processes.

Study of semen stains by scanning electron microscopy. Influence of their ageing.

In order to evaluate the degree of morphological preservation of human spermatozoa in semen stains, an experimental stain on cotton tissue was made and stored at room temperature for 12 months. Small pieces were cut at different times along this period, fixed in saline formaldehyde solution and examined by scanning electron microscopy. Results revealed that the preservation of spermatozoa integrity is high, which represents an important advantage for its use in Court.

Mitochondrial regulation of calcium in the avian cochlear nucleus.

The role of mitochondria and the endoplasmic reticulum in buffering [Ca2+]i in response to imposed calcium loads in neurons of the chick cochlear nucleus, nucleus magnocellularis (NM), was examined. Intracellular calcium concentrations were measured using fluorometric videomicroscopy. After depolarization with 125 mM KCl, NM neurons demonstrate an increase in [Ca2+]i that returns to near-basal levels within 6 min. Addition of the protonophore carbonylcyanide m-chlorophenylhydrazone (CCCP) dissipated the mitochondrial membrane potential, as evidenced by increased fluorescence when cells were loaded with rhodamine-123. Two micromolar CCCP had minimal effect on baseline [Ca2+]i. However, 2 or 10 microM CCCP interfered with the ability of NM cells to buffer [Ca2+]i in response to KCl depolarization without significantly affecting peak [Ca2+]i. Oligomycin also interfered with postdepolarization regulation of [Ca2+]i, but blocked late (7-8 min postdepolarization) increases in [Ca2+]i caused by CCCP. Thapsigargin had no effect on baseline, peak, or postdepolarization [Ca2+]i in NM cells. These results suggest that normal mitochondrial membrane potential and ATP synthesis play an important role in buffering [Ca2+]i in response to imposed calcium loads in NM neurons. Furthermore, the endoplasmic reticulum does not appear to play a significant role in either of these processes. Thus increases in mitochondrial number and function noted in NM cells after deafferentation may represent an adaptive response to an increased cytosolic calcium load.

Lipomatous hypertrophy of the cardiac interatrial septum.

A case of lipomatous hypertrophy of the cardiac interatrial septum is reported in a 91-year-old man who attempted to commit suicide. The lesion was found incidentally at autopsy. Gross examination showed a 3.5-cm mass, yellow and firm. Histologic study showed a proliferation of mature fat cells and slightly hypertrophic cardiac muscle cells.

Glutamate modulates intracellular Ca2+ stores in brain stem auditory neurons.

1. Fura-2 imaging was used to measure the effects of glutamate on caffeine-sensitive Ca2+ stores in neurons of the avian cochlear nucleus, n. magnocellularis (NM). 2. On average, 100-mM caffeine stimulated a 250-nM increase in intracellular calcium ion concentration {[Ca2+]i} in Ca(2+)-free media; 1-mM glutamate significantly attenuated caffeine-stimulated Ca2+ responses. 3. The metabotropic glutamate receptor agonist, ACPD, also inhibited the caffeine-stimulated rise in [Ca2+]i. 4. Glutamate has an important role in regulating Ca2+ stores in NM neurons. Glutamate-deprivation (viz. cochlear removal) results in a rise in [Ca2+]i that may, in part, be the result of release from Ca2+ stores. We hypothesize that Ca(2+)-induced Ca2+ release stores (CICRs) may be involved in deprivation-induced cell death.

Deafferentation increases the intracellular calcium of cochlear nucleus neurons in the embryonic chick.

1. Ratiometric fura-2 imaging was used to measure the intracellular calcium concentration ([Ca2+]i) of neurons in the embryonic avian cochlear nucleus, nucleus magnocellularis (NM), after an in ovo unilateral cochlea removal (deafferentation). 2. The mean [Ca2+]i of NM neurons receiving normal input was 113 nM. 3. Deafferentation increased the mean [Ca2+]i of NM neurons to 247, 311, 339, and 314 nM at 1, 3, 6, and 12 h after cochlear removal, respectively. These values did not differ significantly. 4. The percent frequency distribution of deafferented NM neuron [Ca2+]i shifts away from normative levels toward higher [Ca2+]i at 1 and 3 h after cochlear removal, but shifts back toward normative levels at 6 and 12 h after cochlear removal. 5. This increased [Ca2+]i following cochlear removal temporally coincides with well-characterized changes in NM neurons following activity deprivation. 6. These data suggest that deregulation of [Ca2+]i homeostasis plays a key role in NM neuron degeneration and death following activity deprivation.

Glutamatergic inhibition of voltage-operated calcium channels in the avian cochlear nucleus.

The auditory nerve serves as the only excitatory input to neurons in the avian cochlear nucleus, nucleus magnocellularis (NM). NM neurons in immature animals are dependent upon auditory nerve signals; when deprived of them, many NM neurons die, and the rest atrophy. Auditory nerve terminals release glutamate, which can stimulate second messenger systems by activating a metabotropic glutamate receptor (mGluR). Therefore, it is possible that the effectors of mGluR-stimulated signal transduction systems are needed for NM neuronal survival. This study shows that mGluR activation in NM neurons attenuates voltage-dependent changes in [Ca2+]j. Voltage-dependent Ca2+ influx was also attenuated by increasing cAMP with forskolin, VIP, or 8-bromo-cAMP, indicating that mGluR activation may stimulate adenylate cyclase. The main results may be summarized as follows. NM neurons possess high voltage-activated Ca2+ channels that were modulated by quisqualate, glutamate, and (+/-)trans-ACPD, in that order of potency. Glutamatergic inhibition of Ca2+ influx was not blocked by L-AP3 or L-AP4, which antagonize the actions of mGluRs in other neural systems; it was blocked by serine-O-phosphate. Finally, the attenuation of voltage-dependent Ca2+ influx was duplicated by cAMP accumulators. Since NM neurons have high rates of spontaneous activity and higher rates of driven activity, the expression of this mGluR turns out to be very valuable: without it, [Ca2+]j could reach lethal concentrations. These results provide an important clue as to the identity of an intracellular signal that may play an important role in NM neuronal survival.

Activation of a metabotropic glutamate receptor increases intracellular calcium concentrations in neurons of the avian cochlear nucleus.

Metabotropic glutamate receptors have been shown to stimulate phosphatidylinositol metabolism, and subsequently liberate Ca2+ from intracellular stores, in a variety of tissue and cell types. We previously demonstrated that glutamate could stimulate phosphatidylinositol metabolism, generating inositol-1,4,5-trisphosphate (IP3), in isolated cochlear nucleus tissue from the chick. Using the calcium indicator dye fura-2 and ratiometric fluorescent imaging, this study examined the ability of glutamate and its analogs to liberate Ca2+ from intracellular stores of neurons of the avian cochlear nucleus, and qualitatively characterized the pharmacological profile of such an action. In normal, Ca(2+)-containing medium, glutamate, kainate (KA), alpha-amino-3-hydroxy-5-methyl-isoxazole-4-propionate (AMPA), NMDA, quisqualate (QUIS), and (+/-)-aminocyclopentane-trans-dicarboxylate (ACPD) elicited increases in intracellular calcium concentrations ([Ca2+]i). In the absence of external Ca2+, glutamate, quisqualate, and ACPD evoked increases in [Ca2+]i. In normal medium, the ionotropic glutamate receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) and the NMDA receptor antagonist 2-amino-5-phosphonovalerate (APV) attenuated but did not abolish the glutamate-evoked response and had no effect on the ACPD-evoked response. The putative metabotropic glutamate receptor antagonist 2-amino-3-phosphonopropionate (AP3) was without effect on the glutamate- and ACPD-evoked increases in [Ca2+]i in Ca(2+)-free medium. We conclude that a metabotropic glutamate receptor (mGluR) is present on cochlear nucleus neurons and is able to stimulate the phosphatidylinositol metabolism--Ca2+ signal transduction cascade.

GABAergic terminals in nucleus magnocellularis and laminaris originate from the superior olivary nucleus.

The auditory brainstem nuclei, angularis (NA), magnocellularis (NM), and laminaris (NL) of the chicken, Gallus, contain terminals that stain for antibodies against the inhibitory neurotransmitter, gamma-aminobutyric acid (GABA). Some of these terminals originate from cells surrounding nucleus magnocellularis. Results from this study indicate that the majority of the GABAergic terminals found in NA, NM and NL originate from the superior olivary nucleus (SON). Injections of cholera toxin and horseradish peroxidase show that superior olivary nucleus (SON) neurons, which respond to pure tones, project bilaterally to NA, NM, and NL. NA and NL are reciprocally connected with the SON. More NA cells project to the SON than NL cells. While SON neurons project to NM, NM neurons do not project axons back to the SON. The configuration of SON terminals in NA, NM and NL matches the pattern of GABA-immunoreactive puncta seen in these three nuclei: they surround individual NM cells, congregate in the dendritic neuropil of NL, and blanket the NA. The data indicate that NA, NM and NL may be affected by two different inhibitory cell types: local interneurons and SON neurons. Patterns of connectivity described in this report suggest that the activity of NA cells could influence NM and NL cell physiology. Specifically, increases in NA cell activity could augment the effects of GABAergic SON neurons on NM and NL. Hence, binaural perception in the chicken may be more dependent upon changes in intensity cues than previously believed.

The morphology of collicular and retinal axons ending on small relay (W-like) cells of the primate lateral geniculate nucleus.

The lateral geniculate nucleus (LGN) of every primate examined contains a set of small relay cells in addition to separate sets of magnocellular and parvocellular relay cells. These small cells receive a direct retinal projection, and an indirect retinal projection via the superior colliculus (SC). Receptive-field analyses of the small LGN cells in the bush baby, a lorisiform primate, indicate that this cell class is composed of subclasses, similar in physiology to cat W cells. In an effort to identify some of these subclasses, we have examined the morphological features of retinal and collicular axonal arbors that end on small W-like cells in the LGN of the bush baby, Galago crassicaudatus. Small cells in this species are found in a prominent pair of koniocellular (K) layers as well as the interlaminar zones (ILZs). Retinal arbors were examined by bulk iontophoretic injection of horseradish peroxidase into the optic tract. Collicular arbors were filled via iontophoretic injection of biocytin into the superficial layers of the SC. Forty-eight axon arbors were completely reconstructed and quantitatively evaluated. Our findings show that retinal and collicular axon terminals differ in morphology on the basis of a number of criteria. Our analyses also suggest that retinal axons may have a stronger influence on K cells and collicular axons have a stronger influence of ILZ cells. The ramifications of these findings are provocative since these small LGN cells are known to project directly to the cytochrome-oxidase (CO) blobs within striate cortex. This relationship suggests that CO blob cells receive complex visual input not only from magnocellular and parvocellular LGN cells, but also from small cell pathways that are differentially influenced by retinal and collicular cells.

Intrinsic connections of layer III of striate cortex in squirrel monkey and bush baby: correlations with patterns of cytochrome oxidase.

This study used biocytin and horseradish peroxidase (HRP) to examine the intrinsic connections of the cytochrome oxidase (CO) rich blob and CO poor nonblob zones within layer III of striate cortex in two primate species, nocturnal prosimian bush babies (Galago crassicaudatus) and diurnal simian squirrel monkeys (Saimiri sciureus). Our main objective was to determine whether separate classes of lateral geniculate nucleus (LGN) cells projected to separate superficial layer zones or layers in either species. There were three significant findings. First, we confirm that layer III consists of three sublayers, IIIA, IIIB, and IIIC in both species. Layer IIIA receives input from layers IIIB, IIIC, and V, with little or no input from LGN recipient layers IV and VI. Layer IIIB receives its input from nearly every cortical layer. Layer IIIC, receives input principally from layers IV alpha [which receives its input from magnocellular (M) LGN cells] and from layers V and VI. Taken together with other findings on the extrinsic connections of these layers, our data suggest that IIIA and IIIC provide output to separate hierarchies of visual areas and IIIB acts as a set of interneurons. Second, we find that, as in macaque monkeys, cells in both IV beta and IV alpha of bush babies and squirrel monkeys project to layer IIIB, converging within the blobs. These results suggest that information from all LGN cell classes [parvocellular (P), M, and the Koniocellular (K) or their equivalents] may be integrated within the blobs. Thus, blobs in all of these primates may perform a function that transcends visual niche differences. Third, our data show a species specific difference in the connections of the IIIB nonblobs; nonblobs receive indirect input via IV alpha from the LGN M pathway in bush babies but receive indirect input via IV beta from the LGN parvocellular (P) pathway in squirrel monkeys. These findings indicate that the role of nonblob zones within striate cortex differs from that of blob zones and takes into account visual niche differences.

Direct W-like geniculate projections to the cytochrome oxidase (CO) blobs in primate visual cortex: axon morphology.

The primate lateral geniculate nucleus (LGN) is composed of large, medium, and small cells located, respectively, in magnocellular (M), parvocellular (P), and specialized layers (intercalated and S-layers in simians, koniocellular (K) layers in prosimians). Several studies have examined the physiology and connections of M and P LGN cells and have concluded that they provide separate contributions to visual perception via separate pathways. Less is known about the structure and contributions of the small LGN cells. This study examined the distribution and structure of K LGN cell axons in the cortex of the prosimian, Galago crassicaudatus. Wheat germ agglutinin conjugated to horseradish peroxidase, or Phaseonlus vulgaris leucoaglutinin, was injected into the LGN K layers to demonstrate the overall axon projection pattern and the details of individual axons, respectively. Location of axons within striate cortex was specified relative to boundaries determined by Nissl or cytochrome oxidase (CO) stains on the same or adjacent sections. Our results show that K LGN axons end as single complex arbors within one CO blob zone in layer III; they never terminate in interblob zones. These axons also emit a collateral in layer I that arborizes more broadly and spans both CO blob and interblob zones. These data, together with data on K cell physiology and intralaminar cortical connections, suggest that the LGN small cell pathway could modulate the activity of the other two pathways in striate cortex and contribute directly to visual perception.

Parallel pathways in macaque monkey striate cortex: anatomically defined columns in layer III.

Visual information reaching striate cortex comes from parallel pathways, and the information is organized, or processed, by the layers and columns of striate cortex. To better understand how this is accomplished anatomically, we asked whether parallel pathways originating in the lateral geniculate nucleus (LGN), and terminating separately in layer IV, remain separate in layer III of macaque monkeys. Layer III is of interest since it may play a special role in color and form vision but not in analysis of visual motion. The chief finding was that cells in "blobs" of layer III that stain densely for cytochrome oxidase receive indirect input, via layer IVC, from both LGN magnocellular (M) and parvocellular (P) cells. This is important because the P and M pathways may represent color/form and motion-processing channels, respectively. Interblob cells receive indirect input, via layers IVC and IVA, from the LGN P cells. Also, as suggested by others, our data demonstrate that layer III can be subdivided. The bottom tier, layer IIIB, receives direct projections from all cortical layers. Output from layer IIIB appears to remain intrinsic to striate cortex. In contrast, the top tier, layer IIIA, receives projections from layer IIIB as well as from layers IVA, IVB (blobs only), and V, but it receives no direct projections from LGN recipient layers IVC and VI. Unlike layer IIIB, the output of layer IIIA reaches extrastriate areas. Thus, impulses arriving from parallel LGN pathways may be recombined through serial stages in striate cortex to produce a set of parallel pathways that are qualitatively different from the original LGN set.

Sudden cardiac death: a comparative study of morphological, histochemical and biochemical methods.

The study deals with the comparison of morphological, histochemical and biochemical methods applied to the detection of myocardial infarction in 150 medico-legal autopsies performed at the Institute of Forensic Pathology in Copenhagen. The study also included an NBT (formazan) test of cardiac cross-sections, and light microscopy and fluorescence microscopy of acridine orange-stained specimens from four different sites of the cardiac musculature. Specimens of myocardium from the same four sites and pericardial fluid were analysed biochemically at the Institute of Legal Medicine in Granada. The K+/Na+ ratio was determined in the myocardial tissue and total creatine phosphokinase activity, creatine phosphokinase isoenzymes (MM, MB and BB) and myoglobin were assayed in pericardial fluid. When the results from Copenhagen and Granada were compared, there was absolute concordance in 96 cases, discrepancy in 53 and one case was inconclusive. After studying the circumstances of death, the number of discrepancies were reduced to 20, so that concordance was reached in 86% of all the cases. The results show that the combination of different methods leads to a diagnosis of myocardial infarction in far more cases than with morphological or biochemical methods alone.

Morphological details of primate axons and dendrites revealed by extracellular injection of biocytin: an economic and reliable alternative to PHA-L.

The objective of this study was to determine if biocytin would reliably label details of distant axons and dendrites when injected extracellularly in primates. Biocytin (2.5-5%) was injected iontophoretically or by pressure into several areas of the visual and somatosensory systems of macaque monkeys, squirrel monkeys, tree shrews and galagos. After survival times that ranged from 9 h to 2 weeks, fine details of anterogradely filled axons and/or retrogradely filled dendrites were reliably revealed with an avidin-biotin-HRP complex (ABC solution) that was enhanced with heavy metals. Biocytin labeling was successfully combined with choline acetyltransferase (ChAT) or cytochrome oxidase (CO) histochemistry to reveal double-labeled cells. Our results show that biocytin is a versatile, easy-to-use label that completely fills cell processes both anterogradely and retrogradely in several primate species.

Injury-induced reorganization of somatosensory cortex is accompanied by reductions in GABA staining.

When a portion of primary somatosensory cortex is deprived of its normal inputs by peripheral nerve transection, intact skin surfaces represented in surrounding cortex come to activate the deprived zone within 2 months. We found that this cortical reorganization was accompanied by a marked decrease in the antibody staining of gamma-aminobutyric acid (GABA) within the deprived sector of cortex in monkeys surviving nerve injury for 2-5 months. In contrast, there were no apparent changes in cytochrome oxidase reactivity in the deprived cortex of these same monkeys. Reduced levels of inhibition could allow previously unexpressed connections to become potent. Thus, the regulation of the expression of GABA appears to be one mechanism for maintaining and altering cortical representations.

Poisoning by thallium. A study of five cases.

Thallium poisoning seldom occurs in Spain. This article reports 5 cases of thallium poisoning, of which 4 of the patients belonged to the same family. The cases occurred in or near Granada between 1985 and 1987. The symptoms were initially gastrointestinal (vomiting, abdominal pain, gastrointestinal haemorrhage, etc.) in the case of the family poisoning, and a sensitive-motor polyneuritis in the fifth case. The diagnosis was established by analysis carried out in the authors' laboratory; urinary thallium concentrations were determined by atomic absorption spectrophotometry with graphite furnace and monovalent hollow cathode lamp. Each case was followed up to confirm the efficacy of the treatment; recovery from the poisoning was complete in all cases after 3 to 9 weeks.