MR imaging of the labral-capsular complex: normal variations

Understanding the normal anatomy of the shoulder and its variations is important for the proper interpretation of MR images. This study was performed to describe variations in the normal labral-capsular complex as seen on MR images. MR images of 52 shoulders in 30 asymptomatic volunteers and 27 shoulders of symptomatic patients who had subsequent arthroscopy and/or reconstructive surgery were obtained with 1.5-T MR. The 52 scans of the asymptomatic group were reviewed by three radiologists in conference, and the assessment of labral shapes and capsular insertions was done by consensus. The 27 MR scans of the shoulders in the symptomatic group were reviewed by one radiologist before and after the asymptomatic cases were interpreted. Differences in these two interpretations were shown on receiver-operating-characteristic curves by using the results of subsequent arthroscopy and surgery as the gold standard. The anterior and posterior parts of the labra, respectively, varied in shape but showed several dominant features: triangular (45%, 73%), round (19%, 12%), cleaved (15%, 0%), notched (8%, 0%), flat (7%, 6%), and absent (6%, 8%). Most capsules inserted anteriorly on the labrum (47%) or glenoid rim (49%). All posterior insertions were on the labrum (100%). Intrinsic labral signal was noted on proton density-weighted images, but never on T2-weighted images. Receiver-operating-characteristic curves from interpretations of the symptomatic and clinical cases made before and after evaluation of the asymptomatic shoulders showed the interpretations improved considerably after scans of asymptomatic volunteers were studied. Our study reveals a wide variability in the MR appearance of the labral-capsular complex in asymptomatic shoulders.     

Sphincter injury after anal dilatation demonstrated by anal endosonography.

Anal dilatation is still used in the treatment of anal fissure and haemorrhoids. Using anorectal physiology and anal endosonography we have studied 12 men presenting with faecal incontinence following anal dilatation. Resting anal pressures were low, pudendal nerve latencies were normal; 11 men had a disrupted internal anal sphincter and in ten this was extensively fragmented. Three also had defects of the external anal sphincter. These findings demonstrate for the first time the nature of the structural injury which may be caused by anal dilatation.     

Extracellular characteristics of putative cholinergic neurons in the rat laterodorsal tegmental nucleus

The extracellular electrophysiological properties of neurons in the laterodorsal tegmental nucleus (LDT), a major source of cholinergic afferents to the thalamus, were studied in chloral hydrate-anesthetized rats. A combination of antidromic activation from the thalamus and histological verification of recording sites was used to correlate the identity of extracellular recordings in the rat LDT with cholinergic neurons in that region. All neurons antidromically activated by stimulation of the anteroventral thalamus were histologically verified to be within clusters of cholinergic (NADPH-d-positive) cells in the LDT or in the adjacent nucleus locus coeruleus (LC). The thalamically projecting LDT neurons had a homogeneous neurophysiological profile consisting of long duration action potentials (mean = 2.5 ms), slow conduction velocities (mean = 0.78 m/s), and lengthy chronaxie values (mean = 0.725 ms). The appearance and axonal characteristics of these neurons resembled those of noradrenergic LC neurons, but the two populations exhibited substantially different spontaneous activity patterns and sensory responsiveness. These characteristics may be useful in the preliminary identification of putative cholinergic neurons in vivo, and thereby provide a foundation for exploring the neuropharmacology, afferent modulation, sensory responsiveness and behavioral correlates of the brainstem cholinergic system.     

The precision of positron emission tomography: theory and measurement

The limits of quantitation with positron emission tomography (PET) are examined with respect to the noise propagation resulting from radioactive decay and other sources of random error. Theoretical methods for evaluating the statistical error have been devised but seldom applied to experimental data obtained on human subjects. This paper extends the analysis in several ways: (1) A Monte Carlo method is described for tracking the propagation of statistical error through the analysis of in vivo measurements; (2) Experimental data, obtained in phantoms, validating the Monte Carlo method and other methods are presented; (3) A difference in activation paradigm, performed on regional CBF (rCBF) data from five human subjects, was analyzed on 1.6-cm diameter regions of interest to determine the mean fractional statistical error in PET tissue concentration and in rCBF before and after stereotactic transformation; and (4) A linear statistical model and calculations of the various statistical errors were used to estimate the magnitude of the subject-specific fluctuations under various conditions. In this specific example, the root mean squared (RMS) noise in flow measurements was about three times higher than the RMS noise in the concentration measurements. In addition, the total random error was almost equally partitioned between statistical error and random fluctuations due to all other sources.     

Multiple sclerosis in Galion, Ohio: prevalence and results of a case-control study.

An investigation of the occurrence of multiple sclerosis (MS) was undertaken in the City of Galion, Ohio, USA, because of a report of an increased number of cases. As of June 1, 1987, there were 18 living cases of MS in Galion and Polk Township, for a prevalence rate of 112 cases per 100,000 population. The expected rate is approximately 65-170 cases per 100,000. In a case-control study, residents of Galion or Polk Township who had MS were compared to residents who did not have MS. The controls were matched to the cases on age and sex and had lived in Galion for at least as long as their matched case. The cases and controls did not differ in the distribution of their present or past Galion addresses, occupational histories or workplace exposures. Cases were more likely to have graduated from high school and college than controls. Cases were more likely than controls to report a history of allergies, to recall two or more relatives who had neurologic diseases that began before their first MS symptoms, to report owning a cat that died of unexplained causes and to recall having received oral polio vaccine. Cases and controls had similar levels of antibodies to measles, chickenpox, cytomegalovirus and the human T-cell lymphotrophic virus I.     

Transport of estrogen-induced oxytocin receptors in the ventromedial hypothalamus.

The modulation of oxytocin (OT) receptors (OTRs) by estrogen was investigated in the ventromedial hypothalamus by in vitro receptor autoradiography. Treatment of ovariectomized and adrenalectomized rats with various doses of estradiol benzoate (EB) increased OTR binding not only in the ventromedial nuclei of the hypothalamus (VMN), but also in the area lateral to the nuclei (IVMN). After a single injection of EB, OTRs first were induced within the ventrolateral parts of the VMN, and only hours later they appeared in the IVMN. This is consistent with the interpretation that OTRs are first induced within the estrogen-sensitive neurons of the ventrolateral VMN and then are transported laterally out of the nuclei. Two additional experiments confirmed this interpretation. First, local infusion of a low dose (10 micrograms) of the neuronal transport inhibitor vinblastine blocked the appearance of OTRs in the IVMN but did not prevent the induction of OTRs by EB within the nuclei. Second, a knife cut placed lateral to the VMN prevented the spread of OTRs out of the nuclei. However, even after treatment with a high dose of EB (2 x 10 micrograms), progesterone (P) was required for a maximal extension of the area covered by OTRs. Thus, the OTR is an estrogen-induced neurotransmitter receptor that is transported to its site of action, the lateral ventromedial hypothalamus, where it is modulated by P and where estrogen-induced OT immunoreactivity is found.     

Single odor-sensitive channels in olfactory receptor neurons are also gated by cyclic nucleotides.

Olfactory transduction is thought to occur by processes that are mainly restricted to the specialized cilia emanating from the distal end of the receptor neuron's single dendrite. The involvement of a cAMP-based second messenger system seems likely, and a cyclic nucleotide-sensitive current has been recorded in patches of membrane from the cilia. However, the small diameter of the cilia and the high density of channels within the membrane limit the application of the patch recording technique in the cilia. We have found that the cAMP-sensitive channels also exist at a much lower density within the far more accessible dendritic membrane. Recording from on-cell patches, we have observed single-channel activity in response to extracellularly applied odor substances. The channels have a single-channel conductance of 40 pS and a reversal potential near 0 mV. These same channels are activated by treatments that elevate intracellular cyclic nucleotide concentrations. The results provide a direct demonstration that the cyclic nucleotide-gated channel is the conductance pathway for the odor-elicited current.     

Regulatory properties of brain glutamate decarboxylase (GAD): the apoenzyme of GAD is present principally as the smaller of two molecular forms of GAD in brain

The apoenzyme of glutamate decarboxylase [enzyme without bound cofactor, pyridoxal 5'-phosphate (pyridoxal-P)] serves as a reservoir of inactive glutamate decarboxylase (GAD) that can be activated when additional GABA synthesis is required. We have investigated which of two molecular forms of GAD is present as apoenzyme in synaptosomes and in cortex, caudate nucleus, hippocampus, and cerebellum of rat brain. Endogenous glutamate apodecarboxylase (apoGAD) was labeled by incubating extracts of synaptosomes or punches of each region with 32P-pyridoxal-P, followed by reduction with NaBH4, to link covalently the 32P-pyridoxal-P to GAD. Proteins were separated by SDS-PAGE. Punches from all four brain regions and forebrain synaptosomes contained two forms of GAD with apparent Mrs of 63 and 65 kDa as identified by immunoblotting with four antiGAD sera. Punches and synaptosomes contained a major 32P-pyridoxal-P-labeled band with an apparent Mr of 63 kDa that was stained on immunoblots by the antiGAD serum 1440 and the monoclonal antibody GAD-6, and a minor labeled band at 65 kDa that was stained by the 1440, 6799, and K2 antisera. Synaptosomes contained remarkably few other strongly labeled proteins, but punches contained several other labeled bands. Three additional lines of evidence indicate that the labeled 63-kDa protein is apoGAD: (1) it was purified by immunoaffinity chromatography with the GAD-1 monoclonal antibody; (2) it yielded one major labeled peptide when digested with chymotrypsin, and that peptide appeared identical in peptide-mapping experiments to the labeled active-site peptide isolated from chromatographically prepared rat brain GAD; and (3) its labeling was selectively blocked by 4-deoxypyridoxine 5'-phosphate, a competitive inhibitor of the binding of pyridoxal-P to GAD.(ABSTRACT TRUNCATED AT 250 WORDS)