Ultrasonographic Identification of Fibromuscular Bands Associated with Neurogenic Thoracic Outlet Syndrome: The "Wedge-Sickle" Sign.

Thoracic outlet syndrome (TOS) is a disorder characterized by compression of the lower trunk of the brachial plexus, most often in association with anomalous congenital fibromuscular bands in the scalenic region. Early diagnosis is important, because the neurologic deficit associated with TOS may be irreversible. Using high-resolution ultrasound, we investigated 20 consecutive patients with clinical signs suggestive of TOS (all females, average age: 40.4 +/- 14.9 y) and 25 control patients. In 19 patients, we identified a hyper-echoic fibromuscular structure at the medial edge of the middle scalene muscle, which indented the lower trunk of the brachial plexus ("wedge-sickle sign"). It was associated with the significant enlargement (p < 0.0001) and hypo-echogenicity of the lower trunk. This novel and distinctive ultrasonographic sign allows pre-surgical identification of anomalous fibromuscular bands causing TOS. It is especially useful in patients without neurologic deficit, in whom the diagnosis may not be as straightforward

A dementia neuropathológiája Parkinson-syndromákban = Neuropathology of dementia in Parkinson's syndromes

Vizsgálatainkban Parkinson-syndromákban (multiszisztémás atrophia, Parkinson-kór, progresszív supranuclearis bénulás, vascularis parkinsonismus (Binswanger-betegség) a dementia neuropathológiai hátterét objektív sejtszámlálási módszerekkel vizsgáltuk, az így kapott adatokat összehasonlítva az adott terület neuropathológiai markereivel. A sejtszámlálást optikai disszektor segítségével végeztük, a neuropathológiai eltéréseket immunhisztokémiai módszerekkel határoztuk meg. Multiszisztémás atrophiában a hippocampalis formatio patológiájának különbségét igazoltuk demens és nem demens betegek között. A subcorticalis magvak sejtszámának különbségét nem igazoltuk. Parkinson- kórban és progresszív supranuclearis paresisben a statisztikai feldolgozáshoz szükséges számú minta összegyűjtése még folyamatban van. Vascularis Parkinson- syndromában kimutattuk a subcorticalis fehérállományi és a corticalis NFT patológia kapcsolatát. Úgy találtuk, hogy a territoriális nagyérbetegségben az oligodendroglia károsodása kisebb mértékű, mint kisérbetegségben. | Using objective stereological cell-counting methods, we studied the neuropathological basis of dementia in Parkinsonian syndromes (multiple system atrophy, Parkinson)s disease, progressivw supranuclear palsy and vascular parkinsonism (Binswanger's disease)) and compared the data with the neuropathological markers of the given area. Optical dissector was used for counting the cells while the neuropathological markers were identified by immunohistochemistry. Our results proved that the pathology of the hippocampal formations is different between the demented and non-demented patients with multiple system atrophy. The number of the neurones in the subcortical nuclei was similar. The number of the cases in Parkinson?s disease and in progressive supranuclear palsy is need to be increased The correlation of the cortical neurofibrillary pathology and the subcortical white matter pathology was proved in vascular Parkinsonian- syndrome. We found that the damage (tau pathology) of the oligodendroglial cells is less severe in territorial infarctions than in subcortical small vessel disease

The significance of ultrasonographic carpal tunnel outlet measurements in the diagnosis of carpal tunnel syndrome.

OBJECTIVE: A retrospective study to investigate the utility of ultrasonographic carpal tunnel outlet measurements in the diagnosis of carpal tunnel syndrome (CTS). METHODS: 118 hands of 87 patients with electrophysiologically confirmed CTS and 44 control hands of 23 subjects were assessed. Cross-sectional areas (CSA) of the median nerve were measured at the tunnel inlet, outlet, and forearm. Longitudinal diameters (LAPD) were measured at the inlet, proximal tunnel, distal tunnel, and outlet. RESULTS: CSA at the outlet (median: 18mm2) and its palm-to-forearm-ratio (median: 2.7) were significantly larger than CSA at the inlet (median: 15mm2) and its wrist-to-forearm-ratio (median: 2.2) (p<0.001). 27% of the hands showed enlargement only at the outlet versus 13% only at the inlet. LAPD jump was significantly greater, suggesting relief of higher pressure, at the outlet/distal tunnel versus inlet/proximal tunnel (p<0.001). CONCLUSION: Median nerve enlargement in CTS is greater at the tunnel outlet than at the inlet. We postulate that this is explained by the progressive increase of pressure within the tunnel from proximal to distal. SIGNIFICANCE: The addition of CSA outlet measurements to inlet measurements increased CTS ultrasonographic diagnostic sensitivity and accuracy by 15% and 10%, respectively

Ultrasonographic identification of nerve pathology in neuralgic amyotrophy: Enlargement, constriction, fascicular entwinement and torsion.

Objective: To characterize the ultrasonographic findings on nerves in neuralgic amyotrophy. Methods: Fourteen patients with neuralgic amyotrophy were examined using high resolution ultrasound. Results: Four types of abnormalities were found: 1. Focal or diffuse nerve / fascicle enlargement (57%), 2. incomplete nerve constriction (36%), 3. complete nerve constriction with torsion (50%) (hourglass-like appearance), and 4. fascicular entwinement (28%). Torsions were confirmed intraoperatively and occurred on the radial nerve in 85% of the patients. A significant correlation was found between no spontaneous recovery of nerve function and constriction / torsion / fascicular entwinement (p=0.007). Conclusion: Ultrasonographic nerve pathology in neuralgic amyotrophy varies in order of severity from nerve enlargement to constriction to nerve torsion, with treatment moving from conservative to surgical. We postulate that the constriction caused by inflammation is the precursor of torsion and that the development of nerve torsion is facilitated by rotational movements of limbs. This article is protected by copyright. All rights reserved

Szérumbiomarkerek akut lumbalis-lumbosacralis fájdalomban

Inflammation contributes to the pathogenesis of low back pain and sciatica. Growing evidence suggests that elevated levels of some inflammatory biomarkers are associated with these conditions. Much of the research evaluating the association between pro- and anti-inflammatory cytokines, chemokines, other regulatory molecules, and low back pain and sciatica, focused on patients with chronic low back pain, while fewer studies addressed the issue of detectable biomarkers in the acute phase. Previous studies suggest that pro-inflammatory cytokines such as TNF-alpha, IL-6, and IL-8 and anti-inflammatory IL-4 and IL-10 play an important role in the inflammatory response following intervertebral disc herniation. According to the approach of personalized medicine it is important to identify subsets of patients within the acute patient group regarding etiology, prognosis and treatment. In addition, if we can identify subgroups based on levels of pro-inflammatory biomarkers, where inflammation may be the leading cause of pain, we assume that this subgroup would likely be effectively treated with anti-inflammatory medication. The efficacy of TNF-alpha inhibitors and IL-6 inhibitors in treating low back pain and sciatica has already been tested in clinical trials, but further studies are required. Overall, identification of circulating biomarkers of acute low back pain and sciatica may assist in refining personalized diagnosis and treatment. Further research is needed to evaluate the role of inflammation in acute low back pain and sciatica, to identify what methods are appropriate for evaluation in clinical practice, and whether there are biomarkers of prognostic value in these patients

Expression of kynurenine aminotransferase in the subplate of the rat and its possible role in the regulation of programmed cell death

The neurons of the transient subplate zone, considered important for the prenatal development of the cerebral cortex, were shown here to express kynurenine aminotransferase (KAT)-I from embryonic day (E) 16 until postnatal day (P) 7 in the rat. No other cells of brain tissue exerted KAT-I immunoreactivity during this period. From P3 on, the neurons of the subplate gave rise to KAT-I immunoreactive, varicose axons, which entered the thalamus and terminated around thalamic nerve cells that are devoid of KAT-I immunoreactivity. Other subplate markers displayed a different expression pattern during development. Thus, subplate neurons displayed parvalbumin (PV) immunoreactivity from E16 to P10 and an intense NPY immunoreaction from P7 to P1. They also exhibited nitric oxide synthase immunoreactivity from E16 to P10, whereas on the surface of the subplate neurons, the 0 subunit of the nicotinic acetylcholine receptor (nAChR) was present from P1 to P10. The cells of Cajal-Retzius were nAChR-immunoreactive during this period. Between P1 and P7, the perikarya of subplate neurons also showed an intense immunoreaction with the N-methyl-D-aspartate (NMDA) receptor subtype R2A. After the first postnatal week, many of the KAT-I positive subplate neurons display a gradual decrease of immunoreactivity and undergo programmed cell death. Since KAT-I persists in the subplate through the period E16-P7, we conclude that KAT-I is a useful and reliable subplate marker in the rat. Since it is assumed that migration of nerve cells is regulated by NMDA receptors, and since kynurenic acid - the only naturally occurring NMDA receptor antagonist - is synthesized by KAT, we suggest that a temporary breakdown of the delicate equilibrium between NMDA and KAT might induce abnormal neuronal migration, giving rise to developmental abnormalities