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The average age was 56.5. The clinical findings were of ptosis of the eyelids and diplopia. All seven patients were treated with pyridostigmine. In six cases prednisone was also given and in one patient thymectomy was done. There was a satisfactory result in all cases.
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We searched the Cochrane Neuromuscular Disease Group Specialized Register (12 October 2010), the Cochrane Central Register of Controlled Trials (CENTRAL) (12 October 2010, Issue 4 2010 in the Cochrane Library), MEDLINE (January 1966 to September 2010) and EMBASE (January 1980 to September 2010).
The data demonstrate that alterations in neuroendocrine function are associated with deployment to the Gulf War and post-deployment musculoskeletal symptoms, but not PTSD. Additional studies are needed to examine the relationship of enhanced glucocorticoid responsivity to deployment exposures and chronic unexplained medical symptoms in Gulf War veterans.
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One of the six patients with slow transit constipation reported improvement of symptoms and had concurrently weaned anti-psychotic medications. Pyridostigmine was ceased in the remaining five patients due to lack of efficacy and/or side effects. Four patients proceeded to surgery for refractory symptoms. All seven patients with pseudo-obstruction had some improvement of symptoms with few side effects. Of these, two later had surgery for recurrent symptoms.
These results suggest that MuSK-Ab-positive MG patients exhibit unique and hyperactive responses to AChEIs. Furthermore, R-CMAP and DIP development on a standard AChEI dose may be a distinct neurophysiologic feature indicative of MuSK-Ab-positive MG.
Growth hormone (GH) plasma concentrations reflect a balance between stimulation via GH-releasing hormone and inhibition by somatostatin. Cholinergic agonists enhance GH release by inhibiting somatostatin secretion and in health, stimulated GH release undergoes diurnal variation. We investigated the influence of cortisol on pyridostigmine-induced GH responses by testing six patients with DSM-III-R major depression at 09.00 and 14.00 h. There were no differences in GH responses to pyridostigmine between 09.00 and 14.00 h despite a preservation of the circadian variation of cortisol levels. If cortisol plays an important role in regulating cholinergic activity one would expect the diurnal variation of pyridostigmine-induced GH release to be preserved. As it is not, a reasonable assumption to make is that the muscarinic supersensitivity observed in depression may be independent of the prevailing steroid milieu.
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The role of somatostatinergic tone (SST) in growth hormone (GH) neuroregulation in children with chronic renal failure (CRF) and short stature (mean height standard deviation score -3.47) was investigated. Ten children (9 males, 1 female), mean age 13.4 years (range 8-17 years), five with renal transplants (TP) and five on chronic haemodialysis (HD), underwent three separate investigations: (1) measurement of spontaneous GH secretion: (2) measurement of GH after infusion of GH releasing hormone (GHRH); (3) measurement of GH following treatment with pyridostigmine bromide (PD) and subsequent infusion of GHRH. All patients showed normal or exaggerated spontaneous nocturnal GH secretion (mean concentration values ranging between 3.8 and 19.07 ng/ml). In four of ten patients GHRH was not able to cause an increase in GH levels (mean peak GH 7.35 +/- 2.05 ng/ml) while PD pretreatment reinstated the GH response to GHRH (mean peak GH 55.25 +/- 17.23 ng/ml) in these children. In the other patients in whom GHRH-induced GH release was normal or exaggerated (mean peak GH 42.0 +/- 13.8 ng/ml). PD did not potentiate the GH response to GHRH (mean peak GH 54.83 +/- 7.88 ng/ml). These different types of responses were observed both in TP and HD patients. Our data indicate that: (1) PD potentiates the response to GHRH only when GHRH alone is not able to cause GH release, suggesting that SST is already reduced in patients with a normal or exaggerated GH response to GHRH; (2) in CRF patients the SST can be either reduced or increased, at least during the daytime.
One hundred and forty patients who underwent laryngeal microsurgery with the use of rocuronium as a neuromuscular blocking agent, without the use of a neuromuscular monitoring device, were retrospectively investigated. The patients were randomly chosen among all the patients who met the inclusion criteria at a tertiary university hospital between July 2013 and February 2015 and were allocated to group S (sugammadex group) or group P (pyridostigmine group) according to the neuromuscular reversal agent administered. Five patients were excluded from analysis and 135 patients completed the study. Primary outcome was extubation time. Secondary outcomes were anaesthesia time, the correlation between anaesthesia time and extubation time, the total amount of rocuronium, and postoperative adverse events in the post-anaesthesia care unit (PACU).
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Myasthenia gravis is one of the most satisfying neurological disorders to treat. There are few other conditions in which therapeutic intervention can take a patient from being bed-bound and ventilated to normality. Most patients present with less severe symptoms, but even mild extraocular muscle weakness can be profoundly disabling. The standard therapeutic approach is successful for most patients, which can make the non-specialist neurologist somewhat blasé about its management. However, panic can set in when the standard approach fails. Failure is often the result of incorrect diagnosis, or inappropriate use of first-line treatments. This article outlines the main reasons for failure and gives advice on alternative therapeutic strategies.