[Abduction/external rotation immobilization after primary traumatic anterior shoulder dislocation: which ortheses are suitable?]. / Abduktions-/Außenrotationsimmobilisation nach primärtraumatischer anteriorer Schulterluxation: Welche Orthesen sind geeignet?

BACKGROUND: Immobilization of the shoulder in 60 ° external rotation and 30 ° abduction after primary anterior shoulder dislocation has been shown to allow anatomical reduction and potential healing of the capsule-labrum complex. The purpose of the present study was to evaluate commercially available shoulder braces concerning functionality and comfort as well as for potential problems. METHODS: In this study ten healthy subjects (6 female, 4 male and average age 23 years) tested four braces: 1. Omo Immobil (Ottobock), 2. Quadrat (DJO Global), 3. MP Airplane Axilla (Horst Rattenhuber GmbH) and 4. ARC XR (Bledsoe Brace Systems) with respect to functionality and comfort. Each subject completed simulated activities of daily living (ADLs) and a the end of each ADL the subject evaluated comfort, difficulty of the activities and potential pain on a points scale. The position or the change of the position were controlled by digital photographs. Additionally it was checked whether the subjects could actively change the position of the brace contrary to the desired position. RESULTS: Braces 3 and 4 were rated significantly more comfortable (p < 0.05). Even the difficulty of the activities was rated lower and in particular putting on and taking off the braces was assessed to be significantly easier in comparison to braces 1 and 2. In addition, differences of potential pain were statistically significant and pain was experienced only with braces 1 and 2. The measuring of the position showed no significant differences (p > 0.05). For braces 1 and 2 the active change of the position by subjects was significantly higher and the arm could be rotated more against the favored position (p < 0.05). Between braces 3 and 4, there were no statistical differences during the whole evaluation. CONCLUSIONS: Ortheses where the main joint is positioned in and not in front of the axilla or which can ensure a jointless stabilization of the shoulder or which allow an improved position by an additional sling on the opposite shoulder, are most qualified for immobilization of the shoulder in an external rotation/abduction position with respect to functionality and comfort.

Potential and current use of N-methyl-D-aspartate (NMDA) receptor antagonists in diseases of aging.

The N-methyl-D-aspartate (NMDA) receptor complex is a subtype of glutamate receptor and its dysfunction is involved in many neurological disorders associated with aging, including chronic pain, depression, stroke and Parkinson's disease. Multiple clinical trials using NMDA receptor antagonists have been aborted mainly due to the severe psychomimetic adverse effects of these drugs that occur before concentrations can reach an adequate level in the brain. In this review, we present the evidence that clinically safer NMDA antagonists such as memantine and nitroglycerin, and the combination drug nitro-memantine, are promising as drugs in treating neurodegenerative diseases.

BID mediates neuronal cell death after oxygen/ glucose deprivation and focal cerebral ischemia.

Mitochondria and cytochrome c release play a role in the death of neurons and glia after cerebral ischemia. In the present study, we investigated whether BID, a proapoptotic promoter of cytochrome c release and caspase 8 substrate, was expressed in brain, activated after an ischemic insult in vivo and in vitro, and contributed to ischemic cell death. We detected BID in the cytosol of mouse brain and primary cultured mouse neurons and demonstrated, by using recombinant caspase 8, that neuronal BID also is a caspase 8 substrate. After 2 h of oxygen/glucose deprivation, BID cleavage was detected in neurons concurrent with caspase 8 activation but before caspase 3 cleavage. Bid(-/-) neurons were resistant to death after oxygen/glucose deprivation, and caspase 3 cleavage was significantly reduced; however, caspase 8 cleavage did not differ from wild type. In vivo, BID was cleaved 4 h after transient middle cerebral artery occlusion. Infarct volumes and cytochrome c release also were less in Bid(-/-) mice (-67% and -41%, respectively) after mild focal ischemia. These findings suggest that BID and the mitochondrial-amplification pathway promoting caspase activation contributes importantly to neuronal cell death after ischemic insult.

Molecular basis of NMDA receptor-coupled ion channel modulation by S-nitrosylation.

Several ion channels are thought to be directly modulated by nitric oxide (NO), but the molecular basis of this regulation is unclear. Here we show that the NMDA receptor (NMDAR)-associated ion channel was modulated not only by exogenous NO but also by endogenous NO. Site-directed mutagenesis identified a critical cysteine residue (Cys 399) on the NR2A subunit whose S-nitrosylation (NO+ transfer) under physiological conditions underlies this modulation. In cell systems expressing NMDARs with mutant NR2A subunits in which this single cysteine was replaced by an alanine, the effect of endogenous NO was lost. Thus endogenous S-nitrosylation can regulate ion channel activity.

Neuroprotection by the NMDA receptor-associated open-channel blocker memantine in a photothrombotic model of cerebral focal ischemia in neonatal rat.

Excessive accumulation of glutamate or other excitatory amino acids and the subsequent overactivity of NMDA receptors is currently thought to lead to neuronal injury in cerebral ischemia. Therefore, antagonists of the NMDA receptor may offer an approach for the treatment of ischemic brain injury. Dizocilpine (MK-801), an NMDA receptor-associated channel blocker, protects neurons in several rodent stroke models. However, this drug has numerous side effects and causes apoptosis of neonatal neurons. Recently, another NMDA receptor-associated channel blocker, memantine, has been shown to ameliorate NMDA-receptor mediated neurotoxicity in neuronal cell cultures and in focal cerebral ischemia models in adult rats without substantial side effects. Memantine has been used clinically in the treatment of Parkinson's disease and spasticity for a number of years. Here we tested the effects of memantine on focal stroke caused by photochemical thrombosis in neonatal rats and demonstrated a neuroprotective effect of memantine in this model. We also found excellent correlation between infarct size determined by magnetic resonance imaging (MRI) and histopathological analysis in the same animals. A single pre-ischemic dose of memantine (20 mg/kg) given 15 min prior to induction of stroke reduced the infarct size by 36.3% when compared to control animals treated with normal saline (P < 0.0001). At this dosage, memantine manifests few, if any, neurobehavioral side effects. Thus memantine appears to be both safe and effective in neonatal as well as adult animal models of stroke.

Increased impulsivity after injected alcohol predicts later alcohol consumption in rats: evidence for "loss-of-control drinking" and marked individual differences.

A delay-of-reward paradigm was used to assess impulsivity in rats. Previous research with this paradigm has found that normally occurring impulsivity scores predict magnitude of voluntary alcohol intake. The authors' primary findings were (a) injected alcohol produced a dose-dependent increase in impulsivity, (b) varying the intervals between alcohol and testing yielded orderly effects, (c) there were extreme individual differences in impulsive reactivity to alcohol, (d) these individual differences did not reflect differences in alcohol pharmacokinetics, (e) subject selection procedures ensured that differences in impulsive reactivity to alcohol were independent of significant variations in baseline impulsivity scores, and (f) individual differences in impulsive reactivity to injected alcohol strongly predicted magnitude of voluntary alcohol intake. The findings are discussed in terms of evidence for a dysfunctional alcohol-induced positive feedback loop ("loss-of-control drinking"), alcohol disinhibition, and the relationship between impulse control and the regulation of alcohol consumption.

Posterior leukoencephalopathy without severe hypertension: utility of diffusion-weighted MRI.

OBJECTIVE: Standard MRI confirms the diagnosis of posterior leukoencephalopathy syndrome (PLES), recently associated with an increasing number of medical conditions. In PLES, T2-weighted MRI demonstrates hyperintensity spreading out from posterior brain regions; the pathophysiology remains mysterious. In the acute setting, diffusion-weighted imaging (DWI), but not standard MR imaging, can distinguish ischemic injury from those conditions known to cause vasogenic brain edema. DWI is potentially valuable in understanding the pathophysiology of PLES and in diagnosing patients who do not have previously known risk factors. METHODS: Serial CT and MRI studies (including DWI, apparent diffusion coefficient [ADC] maps, and, in one instance, perfusion-weighted imaging) were performed in three female patients with a neurologic syndrome consistent with PLES while hospitalized for treatment of other conditions. RESULTS: None of the patients had previously described risk factors for PLES; all had only mild elevations in blood pressure. MRI showed large, abnormal, T2 hyperintense regions in the posterior cerebrum with corresponding hyperintensity on ADC maps-signal characteristics predominantly consistent with vasogenic edema. There were also smaller patchy posterior cortical regions with decreased ADC and bright DWI consistent with infarction in one, and dramatic conversion of a large region to an ischemic pattern in another. CONCLUSIONS: ADC maps and DWI can successfully differentiate PLES from early cerebral ischemia, thus playing a pivotal role in treatment decisions. PLES is associated with a wider variety of conditions than has been previously reported and is not always reversible. Hyperintense DWI signal in patients with the syndrome likely marks a tissue stage of permanent brain injury.

Vasopressin opposes locomotor stimulation by ethanol, cocaine and amphetamine in mice.

The effects of arginine8-vasopressin on the stimulation of locomotor activity induced by ethanol, cocaine and amphetamine were examined in DBA/2N mice. Locomotor activity was measured by photocell beam interruption for a period of 45 min following ethanol, cocaine or amphetamine administration. Pretreatment with vasopressin alone in a dose of 2 (but not 1) microg/mouse s.c. reduced locomotor activity. The low dose of vasopressin did not modify the stimulation of locomotor activity induced by i.p. administration of ethanol in doses of either 1.5 or 2 g/kg. The high dose of vasopressin reduced locomotor activity induced by both doses of ethanol, in an apparently additive manner. Cocaine in doses of 15 and 20 mg/kg strongly stimulated locomotor activity, but this stimulation was completely antagonized by pretreatment with 1 microg of vasopressin. Similarly, the stimulation of locomotor activity induced by amphetamine (5 mg/kg) was also blocked by pretreatment with vasopressin. These findings raise the possibility that the effect of vasopressin varies with the extent and nature of dopaminergic involvement in the drug-induced stimulation of activity. For drugs like cocaine or amphetamine which stimulate locomotor activity primarily through the mesolimbic dopaminergic system, vasopressin can completely antagonize the stimulation. For ethanol, which stimulates locomotor activity through action on a number of other neurotransmitters as well as dopamine, vasopressin treatment only reduces its stimulation of locomotor activity in an additive manner. These results suggest a close interaction between vasopressin and dopamine action.

Sensory alien hand syndrome: case report and review of the literature.

An 81 year old right handed woman developed a left alien hand syndrome characterised by involuntary movements of choking and hitting the face, neck, and shoulder. The patient showed multiple disorders of primary sensation, sensory processing, hemispatial attention, and visual association, as well as a combination of sensory, optic, and cerebellar ataxia (triple ataxia) of the left arm in the absence of motor neglect or hemiparesis. Imaging studies disclosed subacute infarction in the right thalamus, hippocampus, inferior temporal lobes, splenium of corpus callosum, and occipital lobe due to right posterior cerebral artery occlusion. This rare syndrome should be considered as a "sensory" or "posterior" form of the alien hand syndrome, to be distinguished from the "motor" or "anterior" form described more commonly.

Differential response to ethanol, pentobarbital and morphine in mice selectively bred for ethanol sensitivity.

Males of two lines of mice, long sleep (LS) and short sleep (SS), that had been selectively bred for their differential sensitivity to ethanol-induced sleep, were examined for their responses to the hypothermic and analgesic effects of ethanol, pentobarbital and morphine, and to the cataleptic effect of morphine. SS mice were found to be less sensitive than the LS animals to ethanol but not pentobarbital-induced analgesia and hypothermia. The SS animals were also less sensitive to morphine-induced hypothermia, but were, by contrast, more sensitive than their LS counterparts to morphine-induced analgesia, while no line differences existed with respect to catalepsy. The rate of morphine disappearance from the blood was somewhat higher in the LS animals but this difference is probably too small to account for the observed differential responses to morphine.

Alcohol is an effective cue in the conditional control of tolerance to alcohol.

To assess the effectiveness of a pharmacological cue as a conditional stimulus in the Pavlovian model of drug tolerance, two groups of Wistar rats received equal numbers of IP injections of a low and a high dose of alcohol. One group (Paired) received a low dose (0.8 g/kg) of alcohol followed 60 min later by the high dose (2.5 g/kg). Another group (Unpaired) received the low and high doses on an unpaired basis. When tested for tolerance to the hypothermic effect of the high dose of alcohol, only the Paired group showed tolerance, and only if the low dose preceded the high. When a saline injection preceded the high dose injection, the Paired group showed a loss of tolerance. The Paired group also showed a compensatory hyperthermia following the low dose injection. Animals from the Paired group that received repeated administrations of the low dose followed by saline, showed a significant extinction effect as compared with animals that received repeated saline injections only. These findings support the Pavlovian model of conditional tolerance, extending the realm of effective conditional stimuli to include a low dose of a drug.