Sphincter of Oddi dysfunction produces acute pancreatitis in the possum.
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BACKGROUND: Sphincter of Oddi dysfunction has been implicated as a cause of various forms of acute pancreatitis. However, there is no direct evidence to show that sphincter of Oddi dysfunction can cause obstruction of trans-sphincteric flow resulting in acute pancreatitis. AIMS: To determine if induced sphincter of Oddi spasm can produce trans-sphincteric obstruction and, in combination with stimulated pancreatic secretion, induce acute pancreatitis. METHODS: In anaesthetised possums, the pancreatic duct was ligated and pancreatic exocrine secretion stimulated by cholecystokinin octapeptide/secretin to induce acute pancreatitis. In separate animals, carbachol was applied topically to the sphincter of Oddi to cause transient sphincter obstruction. Sphincter of Oddi motility, trans-sphincteric flow, pancreatic duct pressure, pancreatic exocrine secretion, plasma amylase levels, and pancreatic tissue damage (histology score) were studied and compared with variables in ligation models. RESULTS: Acute pancreatitis developed following stimulation of pancreatic exocrine secretion with peptides after pancreatic duct ligation (p<0.05). Neither pancreatic duct ligation nor stimulation of pancreatic exocrine secretion with cholecystokinin octapeptide/secretin alone resulted in acute pancreatitis. Topical carbachol stimulated sphincter of Oddi motility abolished trans-sphincteric flow, and increased pancreatic exocrine secretion (p<0.05) and pancreatic duct pressure to levels comparable with pancreatic duct ligation (p<0.001). Carbachol application (with or without combined peptide stimulation) elevated plasma amylase levels (p<0.01) and produced pancreatic tissue damage (p<0.05). Decompression of pancreatic duct ameliorated these effects (p<0.05). CONCLUSION: Induced sphincter of Oddi dysfunction when coupled with stimulated pancreatic secretion causes acute pancreatitis. This may be an important pathophysiological mechanism causing various forms of acute pancreatitis. (+info)
The anatomy of the metacarpo-phalangeal joints, with observations of the aetiology of ulnar drift.
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One hundred normal fingers were dissected and arthrographs obtained by injection of chromopaque-gelatin mixture, allowing comparison between the radiographic and macroscopic configuration of the synovial capsule. Synovial recesses protruding from each side of every metacarpo-phalangeal joint were found in relation to the collateral ligaments and corresponding exactly with the site of radiological erosions. A group of bursae lying on the superficial aspect of collateral ligaments were also demonstrated. A rudimentary intra-articular meniscus was found. The results of examination of the insertions of the interossei showed differences from traditional descriptions. The cause of rheumatoid deformity was suggested to be the rheumatoid process arising in the lateral recesses and lateral bursae, weakening the collateral ligaments, which give way in the directions of the deforming forces. These are derived from the long flexor tendons, which were shown to exert an ulnar and volar strain on the metacarpo-phalangeal joint of every finger during grip. (+info)
Endocannabinoids control spasticity in a multiple sclerosis model.
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Spasticity is a complicating sign in multiple sclerosis that also develops in a model of chronic relapsing experimental autoimmune encephalomyelitis (CREAE) in mice. In areas associated with nerve damage, increased levels of the endocannabinoids, anandamide (arachidonoylethanolamide, AEA) and 2-arachidonoyl glycerol (2-AG), and of the AEA congener, palmitoylethanolamide (PEA), were detected here, whereas comparable levels of these compounds were found in normal and non-spastic CREAE mice. While exogenously administered endocannabinoids and PEA ameliorate spasticity, selective inhibitors of endocannabinoid re-uptake and hydrolysis-probably through the enhancement of endogenous levels of AEA, and, possibly, 2-arachidonoyl glycerol-significantly ameliorated spasticity to an extent comparable with that observed previously with potent cannabinoid receptor agonists. These studies provide definitive evidence for the tonic control of spasticity by the endocannabinoid system and open new horizons to therapy of multiple sclerosis, and other neuromuscular diseases, based on agents modulating endocannabinoid levels and action, which exhibit little psychotropic activity. (+info)
Division of C8 nerve root for treatment of spastic cerebral palsy in the upper limbs: a preliminary report.
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OBJECTIVE: To investigate the effect of C8 nerve root division on the treatment of spastic cerebral palsy in the upper limbs. METHODS: Two patients were treated with division of the C8 never root. Supraclavicular incision was made to expose the C5-T1 nerve roots. The intraoperative electromyographic recording technique was used to monitor the responses from the flexor digitorum and flexor carpi ulnaris muscle groups simultaneously. The C5-T1 nerve roots were stimulated and the evoked muscle amplitude potentials (EMAP) were recorded from the muscle groups. The EMAP of the muscle groups obtained during electrical stimulation of the C8 nerve root was the largest, which was used as the basis for C8 nerve root division. RESULTS: Division of the C8 nerve root slightly affected the function of the upper limb, and reduced the muscle tone of the flexor wrist and digitorum. CONCLUSION: Division of the C8 nerve root can reduce the muscle tone of the flexor wrist and digitorum in a short time. The long-term effects need to be followed up further. (+info)
Myospasm of internal anal sphincter in children.
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OBJECTIVE: To introduce a common but not well-recognized acute abdominal disease in children. METHODS: Thirty-eight children with spasm of the internal anal sphincter were reviewed. RESULTS: The main symptom was the sudden onset of continuous pain in the lower abdomen with paroxysmal exacerbation. The typical sign was the dilation of the sigmoid colon with tenderness aggravated by pressure. Plain X-ray films showed dilation of the sigmoid colon and rectum. The symptoms could be relieved by digital rectal examination or a glycerin suppository. CONCLUSIONS: It is the temporary achalasia of the internal anal sphincter that causes acute abdominal pain. (+info)
Risk factors for stiffness of the wall of the thoracic aorta in patients with mild atherosis.
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Previous studies have suggested that aging is associated with progressive arterial stiffness and widening of the pulse pressure, and pulse pressure has been found to be a risk factor of cardiovascular diseases. However, the effects of age, blood pressure (including pulse pressure) or atherogenic factors on thoracic aortic wall stiffness in patients with mild atherosis are unclear, so the present study used transesophageal echocardiography to examine 103 consecutive patients with various cardiovascular diseases. The extent of atherosis was evaluated in terms of intima-medial thickness (IMT), and 2 indices of wall stiffness in the aorta were calculated: elastic modulus and stiffness parameter (beta). In subjects with mild atherosis (IMT <1.0mm), age, body mass index, systolic blood pressure, pulse pressure, triglyceride level, and hypertension were factors significantly associated with high wall stiffness, and multiple logistic stepwise analysis revealed that age, pulse pressure, and triglyceride level were particularly significant. (+info)
The use of intravenous nitroglycerin in a case of spasm of the sphincter of Oddi during laparoscopic cholecystectomy.
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Spasm of the sphincter of Oddi still occurs during cholecystectomy. Some reports indicate that the spasm, induced by morphine, can be reversed by injection of naloxone, nalbuphine, and glucagon. Others maintain that nitroglycerin or nifedipine can relax the sphincter of Oddi muscle. We recently encountered spasm of the sphincter of Oddi during a laparoscopic cholecystectomy and treated it successfully with intravenous nitroglycerin. (+info)
Flaccid paraplegia: a feature of spinal cord lesions in Holmes-Adie syndrome and tabes dorsalis.
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In a patient with Holmes-Adie syndrome, and in another with tabes dorsalis, a transverse cord lesion resulted in a severe, but flaccid paraplegia with absent tendon reflexes. Flexor spasms were severe in both patients, but spasticity was absent. The significance of these observations is discussed in relation to the functional and anatomical disorder in these two syndromes. (+info)