Endovascular treatment of patients with chronic cerebrospinal venous insufficiency and multiple sclerosis.

Multiple sclerosis (MS) is an inflammatory demyelinating disease of the central nervous system (CNS) by an unknown pathogenesis. MR venography and postmortem studies have demonstrated a topographic correspondence between multiple sclerosis (MS) plaques and the cerebral venous system pathology. In recent observational studies performed on patients from distinctive gene pools, the prevalence of chronic cerebrospinal venous insufficiency (CCSVI) in MS ranged from 56% to 100%. Endovascular treatment (percutaneous transluminal angioplasty (PTA) with or without stenting) of CCSVI was reported to be feasible with a minor complication rate. In 4 patients with different forms of multiple sclerosis venography was performed that revealed stenosis of the proximal region of the jugular vein (right or left). Percutaneous transluminal balloon angioplasty (PTA) was performed in all patients. There were no complications and mean stenosis was reduced after PTA from 59.75% to 36.75%. Follow-up included clinical observations and magnetic resonance imaging (MRI). In all the cases we observed positive remission of the disease, the first ever documented case of MRI index improvement. PTA seems to be an effective treatment for patients with CCVI and multiple sclerosis, However, randomized studies are warranted to establish the efficacy of this new treatment for MS.

Quantitative differences among EMG activities of muscles innervated by subpopulations of hypoglossal and upper spinal motoneurons during non-REM sleep - REM sleep transitions: a window on neural processes in the sleeping brain.

In the rat, a species widely used to study the neural mechanisms of sleep and motor control, lingual electromyographic activity (EMG) is minimal during non-rapid eye movement (non-REM) sleep and then phasic twitches gradually increase after the onset of REM sleep. To better characterize the central neural processes underlying this pattern, we quantified EMG of muscles innervated by distinct subpopulations of hypoglossal motoneurons and nuchal (N) EMG during transitions from non-REM sleep to REM sleep. In 8 chronically instrumented rats, we recorded cortical EEG, EMG at sites near the base of the tongue where genioglossal and intrinsic muscle fibers predominate (GG-I), EMG of the geniohyoid (GH) muscle, and N EMG. Sleep-wake states were identified and EMGs quantified relative to their mean levels in wakefulness in successive 10 s epochs. During non-REM sleep, the average EMG levels differed among the three muscles, with the order being N>GH>GG-I. During REM sleep, due to different magnitudes of phasic twitches, the order was reversed to GG-I>GH>N. GG-I and GH exhibited a gradual increase of twitching that peaked at 70-120 s after the onset of REM sleep and then declined if the REM sleep episode lasted longer. We propose that a common phasic excitatory generator impinges on motoneuron pools that innervate different muscles, but twitching magnitudes are different due to different levels of tonic motoneuronal hyperpolarization. We also propose that REM sleep episodes of average durations are terminated by intense activity of the central generator of phasic events, whereas long REM sleep episodes end as a result of a gradual waning of the tonic disfacilitatory and inhibitory processes.

Inhibition of pontine noradrenergic A7 cells reduces hypoglossal nerve activity in rats.

Noradrenergic (NE) excitatory drive maintains activity of hypoglossal (XII) motoneurons during wakefulness. In predisposed persons, sleep-related decrements of NE cell activity may contribute to hypotonia of upper airway muscles innervated by XII motoneurons. The goal of this study was to determine whether NE neurons of the pontine A7 group, an anatomically identified source of NE projections to the XII nucleus, provide significant, endogenous NE excitatory drive to XII motoneurons. In anesthetized rats, we microinjected clonidine (0.75 mM, 20-40 nl), an alpha(2)-adrenergic receptor agonist that inhibits pontine NE cells, aiming at the A7 region. Nine injections were placed within 0.4 mm from the A7 group identified using tyrosine hydroxylase immunohistochemistry: they reduced XII nerve activity by 31.3+/-2.8% (standard error) and decreased the central respiratory rate by 6%. Another 21 injections, including eight placed near NE cells of the sub-coeruleus region, were made at distances over 0.5 mm from the A7 group and they did not alter either XII nerve activity or respiratory rate. In control experiments, clonidine injections into the A7 group preceded by injections of an alpha(2)-receptor antagonist, RS-79948, did not change XII nerve activity. Four experiments with unilateral clonidine injections into the A7 region and with Fos immunohistochemistry used as a marker of cell activity revealed that the percentage of Fos-positive A7 cells was significantly reduced on the injected side. There was also a significant positive correlation between Fos expression in A7 cells and XII nerve activity. Thus, decrements of NE excitatory drive from the A7 group may significantly reduce XII nerve activity. In obstructive sleep apnea patients, in whom the muscles innervated by XII motoneurons act as upper airway dilators, this may contribute to sleep-related respiratory disorders.

Fos expression in pontomedullary catecholaminergic cells following rapid eye movement sleep-like episodes elicited by pontine carbachol in urethane-anesthetized rats.

Pontine noradrenergic neurons of the locus coeruleus (LC) and sub-coeruleus (SubC) region cease firing during rapid eye movement sleep (REMS). This plays a permissive role in the generation of REMS and may contribute to state-dependent modulation of transmission in the CNS. Whether all pontomedullary catecholaminergic neurons, including those in the A1/C1, A2/C2 and A7 groups, have REMS-related suppression of activity has not been tested. We used Fos protein expression as an indirect marker of the level of neuronal activity and linear regression analysis to determine whether pontomedullary cells identified by tyrosine hydroxylase (TH) immunohistochemistry have reduced Fos expression following REMS-like state induced by pontine microinjections of a cholinergic agonist, carbachol in urethane-anesthetized rats. The percentage of Fos-positive TH cells was negatively correlated with the cumulative duration of REMS-like episodes induced during 140 min prior to brain harvesting in the A7 and rostral A5 groups bilaterally (P < 0.01 for both), and in SubC neurons on the side opposite to carbachol injection (P < 0.05). Dorsal medullary A2/C2 neurons did not exhibit such correlation, but their Fos expression (and that in A7, rostral A5 and SubC neurons) was positively correlated with the duration of the interval between the last REMS-like episode and the time of perfusion (P < 0.05). In contrast, neither of these correlations was significant for A1 /C1 or caudal A5 neurons. These findings suggest that, similar to the prototypic LC neurons, neurons of the A7, rostral A5 and A2/C2 groups have reduced or abolished activity during REMS, whereas A1 /IC1 and caudal A5 neurons do not have this feature. The reduced activity of A2/C2, A5 and A7 neurons during REMS, and the associated decrements in norepinephrine release, may cause state-dependent modulation of.transmission in brain somato- and viscerosensory, somatomotor, and cardiorespiratory pathways.

Compartment syndrome, rhabdomyolysis and risk of acute renal failure as complications of the urological surgery.

Current knowledge related to the risk of CS when operating in these positions (Lloyd Davies and Trendelenburg tilt) is such that it can be deemed negligent to keep patients in this position (with legs higher than the heart) when not absolutely necessary. If it means repositioning and redraping, thus adding a few extra minutes to the episode and costing a small amount in additional drapes, surely this is a small price to pay for excellent perioperative care? If repositioning is impossible to execute, the head-down tilt position should be reversed every two hours, for a short period of time, to allow more natural perfusion of the lower limbs to occur. Raza et al recommend that if the anticipated procedure duration is beyond four hours, the legs should be removed from supports every two hours for a short period to prevent reperfusion injury. The use of Allen stirrups is preferred to calf supports or metal skids. Turnbull and Mills suggest that we should certainly review our use of compression stockings and intermittent compression devices when operating on patients in the Lloyd Davies position. It will be deemed negligent to misdiagnose (ie: mistake for a DVT) or delay treatment (by prolonged re-assessment) of CS postoperatively when patients have been subjected to prolonged surgery in these abnormal positions. Delayed or missed diagnosis may not only be limb-threatening (and cause a very protracted hospital stay)--it can be life-threatening. With today's current knowledge, surgeons undertaking prolonged surgery in abnormal positions must be aware of this, fortunately rare, complication. Practice guidelines within perioperative care should reflect current knowledge and ensure that risk is minimized. Patients who take legal action if they have experienced this condition may be awarded substantial costs against negligence if lack of care can be proven or diagnosis has been delayed.

Creatine kinase mb, cardiac troponin T and cardiac troponin I as the markers of rhabdomyolysis in chronic hemodialysis patients.

We designed this study to compare serum markers of myocardial injury creatine kinase MB (CK-MB), as well, as serum contractile proteins, especially cardiac troponin T (cTnT) and cardiac troponin I (cTnI) in dialysis patients without acute ischemic heart disease. 24 patients on chronic hemodialysis were studied by history and physical examination, electrocardiography, and two-dimensional echocardiography. These patients had no evidence of ischemic heart disease. Biochemical markers were measured in serial predialysis blood samples with specific monoclonal antibody-based immunoassays. For several patients at least one sample measured above the upper reference limit: CK-MB, 7 of 24 (30%); ELISA cTnT, 17 of 24 (71%); Enzymun cTnT, 3 of 18 (17%); and cTnI, 1 of 24 (4%). Chronic dialysis patients without acute ischemic heart disease frequently had increased serum CK-MB and cTnT. Our finding are in agreement with the conclusions that cTnT and CK-MB detected in the serum of patients on chronic hemodialysis originates from the skeletal muscle and not from the heart.

[The role of opioid system in the regulation of the sleep-wakefulness cycle].

In chronic experiments influence of single administration of various doses of morphine (0.5, 2.0 and 3.0 mg/kg) on general behavior, structural organization of the sleep-waking cycle and some EEG and somato-vegetative parameters was studied in the cats. Intraperitoneal administration of morphine elicits numerous autonomic disorders, psychic derangement and complete deterioration of the sleep-waking cycle structure. The result certify that single administration of morphine induces activation of the opiate receptors in various structures of the brain, which entails deviations of behavioral and EEG parameters, activation of the structures responsible for initiation of behavioral waking, suppression of activity in those structure, which control the slow wave sleep triggering mechanisms, deterioration of the sleep quality and significant elevation of emotional tension against the baseline. On the basis of obtained data it is suggested that the opioid system plays an important role in the sleep-waking cycle regulatory mechanisms and other forms of brain integrative activity in general.