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[A case of dissecting aneurysm of the basilar artery presented as superior pons type of Foville's syndrome].

Here we report a 47-year-old man with dissecting aneurysm of the basilar artery who developed Foville's syndrome due to upper pons involvement. At first he had an abrupt onset of dysarthria and weakness in his left upper and lower extremities during his work. Neurological examination on admission revealed mild disturbance of consciousness, absent light reaction on the left side, hypesthesia of the left face, absent gag reflex, dysarthria, and left hemiparesis with ataxia. On the second hospital day he developed paralysis of conjugate eye movement to the right, left central facial palsy, and left hemiplegia, and hyperhidrosis of the left side of the body. He was diagnosed to have superior pons type of Foville's syndrome. Computed tomography showed low density area in the right upper pons, and the basilar artery had marked lateral shift, dilatation, and calcification. Vertebral angiography demonstrated dissecting aneurysm of the basilar artery. Although it is very rare that dissecting aneurysm of the basilar artery causes the brain stem symptoms, its possibility should be considered when computed tomography shows marked lateral shift, dilatation, and/or calcification of the basilar artery.

Aortic Dissection↗

Detecting the polymorphisms of paraoxonase (PON) cluster in Chinese Han population based on a rapid method.

BACKGROUND: An increased risk of coronary heart disease has been shown to be associated with polymorphisms in PON1 gene in different populations. Polymorphisms in PON2 gene have been associated with the level of plasma lipoproteins and glucose and are thought to play a role in atherosclerosis. METHODS: To detect PONs polymorphisms more rapidly and reliably, we modified and improved the method established by Motti et al. We redesigned the primer for amplifying the common polymorphism at position 311 of PON2, which produced more reliable and efficient amplification. RESULTS: A second common polymorphism at codon 148 was also detected by our new method, as were the 2 polymorphisms in the PON1 gene. The new method allowed identification of 4 polymorphisms (PON1-192, PON1-55, PON2-148 and PON2-311) simultaneously. The PONs genotypes of 82 healthy persons were identified by this method. The allelic frequencies were: PON1-192: Q 46.3%, R 53.7%; PON1-55: L 95.1%, M 4.9%; PON2-148: A 85.4%, G 14.6%; PON2-311: S 77.4%, and C 22.6%, respectively. CONCLUSION: This method represents a simple, economical and time-saving technique to simultaneously detect 4 polymorphisms in the PON cluster. It provides a useful application to enable further study of the relationship between PON1 and PON2 and their role in atherosclerosis.

Aged↗

The effect of peroxisome proliferator-activated receptors alpha (PPARalpha) agonist, fenofibrate, on lipid peroxidation, total antioxidant capacity, and plasma paraoxonase 1 (PON 1) activity.

The aim of this study was to investigate the effect of peroxisome proliferator activated receptors alpha agonist, fenofibrate, on the level of oxidative stress, total antioxidant capacity, and plasma paraoxonase 1 (PON 1) activity in the rat. The adult male Wistar rats received fenofibrate for 7 days. The drug was added to food at concentrations 0.005%, 0.05% and 0.5%, which corresponded to doses of 3, 30 and 300 mg/kg/day, respectively. Fenofibrate treatment dose-dependently reduced plasma concentration of malonyldialdehyde and 4-hydroxydialkenals. The level of these lipid peroxidation products in animals treated with 0.005%, 0.05% and 0.5% fenofibrate was lower than in control group by 52.8%, 62.7% and 87.1%, respectively. Lipid hydroperoxides in plasma decreased by 29.7%, 23.4% and 27.5% in these groups, respectively. The drug had no significant effect on total antioxidant capacity measured as ferric reducing ability of plasma (FRAP). Paraoxon-hydrolyzing activity (PON) of plasma paraoxonase was 81.5% lower in animals receiving 0.05% fenofibrate and 69.2% lower in rats treated with 0.5% fenofibrate than in control. Phenyl acetate hydrolyzing activity (arylesterase, AE) was reduced by 15.2%, 49.6% and 55.8% in rats receiving 0.005%, 0.05% and 0.5% fenofibrate, respectively. PON/AE ratio decreased following 0.05% and 0.5% fenofibrate by 64.9% and 30.4%, respectively. The drug had no significant effect on total plasma triglycerides and cholesterol concentrations. The results indicate that fenofibrate treatment favourably modulates oxidant-antioxidant balance and unfavourably affects plasma PON 1 activity in normolipidemic rats. These effects can contribute to the influence of PPARalpha agonists on pathological processes involved in atherogenesis.

Animals↗

[Polymorphisms screening of PON gene cluster].

To identify all putative functional polymorphisms of PON gene cluster in Chinese Han population. Common polymorphisms of PON1, PON2 and PON3 gene were identified by directly sequencing of genomic DNAs derived from 48 randomly selected patients with coronary heart disease. We designed PCR arrays to amplify regions up to about 1kb upstream from transcription-initiation sites, i.e., putative promoter regions, all exons and adjacent non-coding regions. In a total length of 13.9 kb explored, we identified thirty-one SNPs, of which, 17 were first reported. A new coding polymorphism was detected in PON1 gene, which gives rise to amino acid substitutions of arginine (R) for glycine (G) at codon 160, whereas L54M polymorphism, which is common in white population, was not detected in our Han population. Among the five polymorphisms identified in PON3 gene, one in the promoter regions at position -133 (C/A) was located in a potential binding site for transcription factor LF-A1. Allele frequencies of some polymorphisms are significantly different from those reported in Caucasian populations. Complete or nearly complete association between polymorphisms was frequently observed. The identified multiple putative functional polymorphisms in PON gene cluster and their linkage disequilibrium patterns in combination with the population specific frequencies are of values for futher association studies of PON gene cluster with cardiovascular disease.

Aryldialkylphosphatase↗

Selective impairment of smooth-pursuit eye movements due to an ischemic lesion of the basal pons.

Voluntary and reflex-like eye movements were measured in a patient with an ischemic lesion of the right basal pons. Ipsilateral smooth-pursuit eye movements were predominantly impaired and interrupted by saccades. This profound smooth-pursuit deficit contrasted with only minor abnormalities of visually guided saccades and the vestibulo-ocular reflex. A selective disturbance of smooth-pursuit eye movements due to a lesion of the basal pons in this patient concurs with recent work in monkeys suggesting that smooth-pursuit eye movements are mediated by a parietooccipito-ponto-cerebellar pathway.

Brain Ischemia↗

Distribution of catecholaminergic neuronal systems in the canine medulla oblongata and pons.

The distribution of catecholamine-containing neurons, fibers, and varicosities in the brainstem of both adult and juvenile dogs was mapped in detail with glyoxylic acid histofluorescence. Four separate groups of catecholamine-fluorescent neurons were identified within the canine medulla and pons in locations comparable to the A1, A2, A5, and A6 regions reported in other species. However, aspects of the pattern and density of the catecholaminergic neuronal systems appeared to be unique to the dog. The A1 neurons of the caudal ventrolateral medulla were much more scattered than in rats or rabbits, but relatively similar to cats. In the A2 region of the dorsomedial medulla, catecholaminergic cells and fibers were uniquely distributed compared to other species: fluorescent neurons were scattered only within the dorsal motor nucleus of the vagus, and a distinctive pattern of fibers and varicosities outlined the nucleus of the solitary tract and dorsal motor nucleus of the vagus. The A5 neurons of the rostral ventrolateral medulla appeared at the rostral limit of the A1 region. Fluorescent A5 cells were more sparse than in rats or primates, and were patterned similarly to cats and rabbits. The canine A6 region contained the most extensive and dense grouping of catecholamine neurons and was similar in pattern to the rabbits but less extensive than that seen in cats or primates. An ascending catecholaminergic fiber pathway was traced through the central tegmental field of the canine medulla and pons, with features similar to the primate. The present study provides the first description of the catecholaminergic neuronal systems of the canine medulla.

Animals↗

Topography and synaptology of mamillary body projections to the mesencephalon and pons in the rat.

The anterograde and retrograde transport of horseradish peroxidase conjugated to wheat germ agglutinin (WGA-HRP) was used to study the anatomical organization of descending projections from the mamillary body (MB) to the mesencephalon and pons at light and electron microscopic levels. Injections of WGA-HRP into the medial mamillary nucleus resulted in dense anterograde and retrograde labeling in the ventral tegmental nucleus, while injections in the lateral mamillary nucleus resulted in dense anterograde labeling in the dorsal tegmental nucleus pars dorsalis and dense anterograde and retrograde labeling in the pars ventralis of the dorsal tegmental nucleus. Anterogradely labeled fibers in the mamillotegmental tract diverged from the principal mamillary tract in an extensive dorsocaudally oriented swath of axons which extended to the dorsal and ventral tegmental nuclei, and numerous axons turned sharply ventrally and rostrally to terminate topographically in the dorsomedial nucleus reticularis tegmenti pontis and rostromedial pontine nuclei. The anterograde labeling in these two precerebellar relay nuclei was distributed near the midline such that projections from the lateral mamillary nucleus terminated mainly dorsomedial to the terminal fields of projections from the medial mamillary nucleus. In the dorsal and ventral tegmental nuclei, labeled axon terminals contained round synaptic vesicles and formed asymmetric synaptic junctions primarily with small diameter dendrites and to a lesser extent with neuronal somata. A few labeled terminals contained pleomorphic vesicles and formed symmetric synaptic junctions with dendrites and neuronal somata. Labeled axon terminals were also frequently found in synaptic contact with retrogradely labeled dendrites and neuronal somata in the dorsal and ventral tegmental nuclei. These findings indicate that neurons in the dorsal and ventral tegmental nuclei are reciprocally connected with MB projection neurons. In the nucleus reticularis tegmenti pontis and medial pontine nuclei, labeled axon terminals contained round synaptic vesicles and formed asymmetric synaptic junctions primarily with small diameter dendrites. The present study demonstrates that projections from the medial and lateral nuclei of the MB are topographically organized in the mesencephalon and pons. The synaptic morphology of mamillotegmental projections suggests that they may have excitatory influences primarily on the distal dendrites of neurons in these brain regions.

Afferent Pathways↗

Histochemical mapping of acetylcholinesterase and butyrylcholinesterase in the medulla oblongata and pons of squirrel (Funambulus palmarum).

The distribution of acetylcholinesterase (AChE) and butyrylcholinesterase (BChE) has been investigated in a series of sections passing through the medulla oblongata and pons of the squirrel brain. A comparison of the two enzymes has given an interesting picture of their selective localization in the different nuclei. Marked AChE activity has been observed in the cranial nerve nuclei. BChE activity in various nuclei of the medulla oblongata and pons is variable and occurs diffusely between the cells. Possible reasons pertaining to marked variation in AChE and BChE contents of various nuclei and fiber tracts have been discussed.

Acetylcholinesterase↗

Projections of the bed nucleus of the stria terminalis to the mesencephalon, pons, and medulla oblongata in the cat.

Injections of HRP in the nucleus raphe magnus and adjoining medial reticular formation in the cat resulted in many labeled neurons in the lateral part of the bed nucleus of the stria terminalis (BNST) but not in the medial part of this nucleus. HRP injections in the nucleus raphe pallidus and in the C2-segment of the spinal cord did not result in labeled neurons in the BNST. Injections of 3H-leucine in the BNST resulted in many labeled fibers in the brain stem. Labeled fiber bundles descended by way of the medial forebrain bundle and the central tegmental field to the lateral tegmental field of pons and medulla. Dense BNST projections could be observed to the substantia nigra pars compacta, the ventral tegmental area, the nucleus of the posterior commissure, the PAG (except its dorsolateral part), the cuneiform nucleus, the nucleus raphe dorsalis, the locus coeruleus, the nucleus subcoeruleus, the medial and lateral parabrachial nuclei, the lateral tegmental field of caudal pons and medulla and the nucleus raphe magnus and adjoining medial reticular formation. Furthermore many labeled fibers were present in the solitary nucleus, and in especially the peripheral parts of the dorsal vagal nucleus. Finally some fibers could be traced in the marginal layer of the rostral part of the caudal spinal trigeminal nucleus. These projections appear to be virtually identical to the ones derived from the medial part of the central nucleus of the amygdala (Hopkins and Holstege 1978). The possibility that the BNST and the medial and central amygdaloid nuclei must be considered as one anatomical entity is discussed.

Amygdala↗

Effect of corticosterone on noradrenergic nuclei in the pons-medulla and [3H]NA release from terminals in hippocampal slices.

The aim of the present study was to investigate possible membrane and genomic effects of corticosterone on the noradrenergic system of the rat brain. Corticosterone effects were studied in vivo by treating rats s.c. with 10 mg/kg corticosterone for 7 or 14 days. In the first two experiments corticosterone significantly decreased the noradrenaline (NA) and dopamine (DA) levels in the pons-medulla, an area which contains the A1-A7 noradrenergic cell groups, while the NA and DA levels in the dorsal hippocampus remained unchanged. In a third experiment where the locus coeruleus (LC) and the A1 and A2 nuclei (A1,A2) were analysed separately, NA levels were unchanged but total MHPG levels and the total MHPG/NA ratio were decreased in the A1,A2 area. Chronic corticosterone treatment (14 days) did not alter the alpha 2-adrenoceptor-mediated modulation of [3H]NA release from dorsal hippocampal slices. Neither the spontaneous outflow nor the electrically stimulated release of [3H]NA from dorsal hippocampal slices of untreated rats was affected by exposure of the slices to corticosterone (10(-7) M - 10(-4) M) in the superfusion buffer. Thus, chronic corticosterone treatment of rats altered the noradrenergic system of the pons-medulla, but did not change the alpha 2-adrenoceptor-mediated modulation of NA release in the dorsal hippocampus, a major terminal area of the LC neurons. Corticosterone also did not appear to have a direct membrane effect on the NA terminals in the dorsal hippocampus of the rat.

Animals↗

Antidromal and synaptic activation of neurons of the associative parietal cortex of the cat brain elicited by spike activity from the intrinsic nuclei of the pons.

Acute experiments were performed on cats with intracellular recording of efferent and unidentified neurons of the anterior suprasylvian and posterior lateral gyri of the parietal cortex, to study the antidromal and synaptic responses to stimulation of the lateral and medial groups of intrinsic nuclei of the pons. Oligo- and polysynaptic components were detected, along with complex EPSP due to convergence of axons from fast- and slow-conducting neurons. Antidromal and synaptic responses were demonstrated in the same parietal cortex neurons, demonstrating a double connection between the intrinsic nuclei of the pons and the associated parietal cortex. The possible pathways of these connections are discussed, along with their features and importance in the functioning of pontocortical connections.

Action Potentials↗

Inhibition of medullary reticulospinal neurons by excitation of the dorsolateral parts of the pons which block movement and muscle tone in rats.

Analysis of the response of 128 reticulospinal neurons in the magnocellular and ventral reticular nuclei showed that 36.7% of these cells responded with short-latency (2-4 msec) action potentials and increased their tonic activity in response to electrical stimulation of the central parts of the hypothalamus, which evoked increases in hindlimb muscle tone in rats. These cells completely stopped producing action potentials during electrical stimulation and during chemical stimulation of the dorsolateral parts of the pons, which inhibited movement and muscle tone. A total of 23.4% of the cells produced only short-latency (1-4 msec) action potentials in response to stimulation of the inhibitory parts of the pons. A total of 3.9% of reticulospinal neurons increased their activity during stimulation of the hypothalamic zones and pontine areas of the brain. No responses were obtained from 35.9% of neurons. It is suggested that excitation of pontine structures inhibiting movement and muscle tone may prevent conduction in descending activatory systems from the rostral parts of the brain (which increase muscle tone) to the reticulospinal neurons of the medulla oblongata.

Action Potentials↗

Intra-axial endophytic tumors in the pons and/or medulla oblongata. I. Symptoms, neuroradiological findings, and histopathology in 30 children.

Between August 1987 and June 1994 we operated upon 30 consecutive children suffering from endophytic intra-axial tumors located in the pons and/or medulla oblongata. We present the clinical findings, neuroradiological aspects and histopathological results recorded in these cases. Diagnostic tests included clinical examinations, neurophysiological tests and neuroradiological imaging [magnetic resonance tomography (MRT) in all cases, often combined with cranial computer tomography (CCT)]. The diagnosis was confirmed by histopathological examination of the tumor material obtained by open surgical exploration in all cases. We conclude that a short history and more horizontal growth within the pons are more valuable predictors of the histopathology than differentiation between focal or diffuse growth patterns. MRT has little predictive value for histopathological diagnosis in intra-axial brain stem tumors.

Adolescent↗

Magnetic resonance imaging in autism: measurement of the cerebellum, pons, and fourth ventricle.

Magnetic resonance imaging (MRI) research has suggested that autistic individuals have hypoplasia of cerebellar lobules VI and VII, the pons, and enlargement of the fourth ventricle. Using MRI we measured the mid-sagittal area of these structures in 15 high-functioning autistic males; 15 age- and IQ-comparable male volunteers (control group I); and 15 male volunteers comparable to cases on age and parental socioeconomic status (SES) (control group II). Using ratio measures, cerebellar lobules VI-VII were found to be smaller in autistic subjects than controls in group II but not those in group I. No differences were found after multivariate analysis adjusting for mid-sagittal brain area (MSBA), age, and IQ. The size of the pons and fourth ventricle did not differ between cases and controls, although autistic subjects were noted to have a significantly larger MSBA than subjects in either control group.

Adolescent↗

Effects of intraventricular injection of 6-hydroxydopamine in the developing kitten. III. Histochemical fluorescence and radioautographic studies of the noradrenaline hyperinnervation in the pons.

In the present study, using neonatal intraventricular injections of 6-hydroxydopamine (6-OHDA) and the fluorescence histochemical method for monoamines, it is observed that an extensive plexus of noradrenaline (NA) fibres develops in the pontine region of the cat brain subsequently to the neonatal destruction of the ascending NA bundles and of the NA innervation in the cerebral cortex by the neurotoxin. This plexus is only partly conserved 10 months after the 6-OHDA treatment. Generally, only a limited number of NA perikarya degenerate in the region of the locus coeruleus, the others (nucleus subcoeruleus senso lato) exhibiting the same strong fluorescence as the new NA fibres. Using the radioautographic method after intraventricular injections of [3H]NA, our work demonstrates also the transient disappearance (at least one month) of the uptake of [3H]NA in the pons, whose NA cell bodies and nerve terminals are no longer labeled in the same number as in control animals. The possibility of again labeling significantly NA perikarya and numerous nerve terminals occurred between 3 and 5 months of age, probably indicating both a re-establishment of normal uptake properties in the preserved NA perikarya and nerve terminals and some maturation of the uptake mechanisms in the abnormal NA fibres of the pons. This last observation is at variance with data from newborn animals showing that the uptake of NA develops in parallel with the accumulation of endogenous NA in catecholamine nerve terminals. The present results, however, do corroborate and complement previous biochemical data obtained in the cat after neonatal injection of 6-OHDA.

Aging↗

Cholinergic projections from the midbrain and pons to the thalamus in the rat, identified by combined retrograde tracing and choline acetyltransferase immunohistochemistry.

The distribution of cholinergic neurons in the midbrain and pons which project directly to the thalamus was investigated in the rat using a procedure which allows the simultaneous detection of retrogradely transported horseradish peroxidase (HRP) and immunohistochemical demonstration of choline acetyltransferase (ChAT) in the same neurons. HRP injections were placed in the dorsal half of the anterior third of the thalamus on one side which included the anteroventral nucleus as well as portions of the rostral intralaminar and reticular nuclei. These thalamic nuclei showed the highest density of immunohistochemically detectable cholinergic fibers. Neurons containing both HRP and ChAT, which represented cholinergic neurons projecting directly to the thalamus, were found in the midbrain and pons in the lateral tegmental reticular formation, parabrachial region and lateral dorsal tegmental nucleus. Ipsilateral to the injection site over 91% of the HRP labeled neurons in all of these regions were cholinergic, while an average of 60% of the cholinergic neurons had transported HRP. Contralateral to the injection site 5-6% of the cholinergic neurons in these regions were also retrogradely labeled. These findings demonstrate direct cholinergic projections to the thalamus from neurons in several regions in the tegmentum and suggest that tegmental projections to the thalamus are predominantly cholinergic.

Animals↗

Neurons in the area postrema are the only catecholamine-synthesizing cells in the medulla or pons with projections to the rostral ventrolateral medulla (C1-area) in the rabbit.

We have identified, in the rabbit medulla and pons, neurons which project to the C1-region of the rostral ventrolateral medulla. By combining tyrosine hydroxylase immunohistochemistry with retrograde transport of Fluoro-Gold we determined whether any of the retrogradely labelled neurons synthesize catecholamines. The only doubly labelled cells were located in the area postrema. No other group of catecholamine-synthesizing neurons in either the medulla or the pons was found to project to the C1-area of the rostral ventrolateral medulla. Pharmacological agents which lower arterial pressure by stimulating adrenoceptors in the rostral ventrolateral medulla may act on receptors which are not innervated by catecholamine-synthesizing perikarya located outside the C1-region.

Animals↗

Inhibition of spinal nociceptive transmission from the midbrain, pons and medulla in the rat: activation of descending inhibition by morphine, glutamate and electrical stimulation.

It is generally believed that morphine activates a descending system(s) of inhibition, an effect contributing significantly to the analgesia produced. There has arisen, however, considerable controversy on this point. To address whether morphine inhibits spinal nociceptive transmission when given into the brainstem, the effects of focal electrical stimulation and monosodium S-glutamate (Glu) given in the periaqueductal gray (PAG), the locus coeruleus/subcoeruleus (LC/SC) and/or the nucleus raphe magnus (NRM) on spinal unit responses to noxious heating (50 degrees C) of the skin were examined and compared with effects produced by morphine (Mor). Focal electrical stimulation in 46 sites in the midbrain, dorsolateral pons and ventromedial medulla reliably inhibited unit responses to noxious heating of the skin (mean 34% of control). Microinjections of Glu (50 nmol, 0.5 microliter) were made into 17 sites in the midbrain, 10 sites in the LC/SC and 11 sites in the NRM, inhibiting unit responses to a mean 57% at 22 of the 38 sites of microinjection. Mor (10-20 micrograms, 0.5 microliter) was microinjected into 15 sites in the midbrain, 13 sites in the LC/SC and 11 sites in the NRM, inhibiting unit responses to heat to 63% of control at 24 sites of microinjection. The effects of morphine were shown to be receptor specific by antagonism with naloxone administered either intravenously or into the brainstem at the same site of microinjection as morphine. In 31 sites in the midbrain, dorsolateral pons and ventromedial medulla, microinjections of both Mor and Glu into the same sites attenuated unit responses to heating of the skin to a mean 77% and 71% of control, respectively. The results support the hypothesis that Mor acts supraspinally to modulate spinal nociceptive transmission by activating an endogenous descending inhibitory system(s). Focal electrical stimulation, glutamate and morphine modulated spinal nociceptive transmission by activation of descending inhibitory systems whose cell bodies of origin are in the PAG, the LC/SC or the NRM.

Animals↗