Complication caused by use of fibrin glue in vessel transposition for trigeminal neuralgia

A 64-year-old man underwent microvascular decompression of the left superior cerebellar artery (SCA) for left trigeminal neuralgia (TN) using a sling of Teflon tape fixed to the tentorium with fibrin glue. The TN disappeared immediately after surgery, but recurred unusually rapidly at 2 weeks later at the same intensity as before. Second surgery revealed the SCA was suspended from the tentorium, but the trigeminal nerve was stretched and displaced superolaterally because of adhesion to the superior petrosal vein. The adhesion was thought to involve the fibrin glue used during the sling retraction procedure. The nerve was meticulously dissected from the adhesion, and the trigeminal nerve was placed in the correct position. The postoperative course was uneventful, and the TN disappeared completely. We recommend that the smallest amount of the fibrin glue possible be used to avoid adhesion to the surrounding neurovascular elements.     

Neutralization of blood group A-antigen by a novel anti-A antibody: overcoming ABO-incompatible solid-organ transplantation

BACKGROUND: The major barrier to ABO-incompatible solid-organ transplantation is acute humoral rejection. It is known to be triggered by antidonor blood group A/B antibodies, which might bind to A/B-antigen on the endothelium of the graft. Various strategies to reduce antiblood group antibody by overcoming ABO-incompatible transplantation have been tried. However, antigen-suppressing procedures have not been performed. METHODS: We produced a novel anti-A antibody (K7508) by immunizing mice with salivary mucin of a blood group A individual, thereby clarifying that blood group A-antigen is expressed in endothelial cells of the liver. We investigated whether K7508 can mask A-antigen on the cells in vitro. Next, we immunized mice with A-antigen-expressing cells coated with K7508 or its Fab fragment, and measured anti-A antibody production in the mice. RESULTS: Blood group A-antigen-expressing cells, such as blood group A-red blood cells (A-RBCs) and A431 cells, coated with K7508 were not recognized by another anti-A antibody in flow cytometry, indicating that A-antigen was masked by K7508 in vitro. The A-antigen on the paraffin-embedded liver tissue was also masked by K7508. Furthermore, the production of anti-A antibody in mice immunized with A-antigen-expressing cells coated with K7508 or its Fab fragment was significantly suppressed compared to that in mice immunized with non-coated cells alone, indicating that A-antigen was neutralized by K7508 in vivo. CONCLUSIONS: The neutralization of blood group antigen by antiblood group antibody and especially its Fab fragment might represent one strategy to overcome ABO-incompatible organ transplantation.     

Association of cavernous malformation within vestibular schwannoma: immunohistochemical analysis of matrix metalloproteinase-2 and -9

A 65-year-old man presented with a rare case of cavernous malformation with hemorrhage located within vestibular schwannoma. He had suffered hearing impairment for 20 years, and was admitted to our hospital with vertigo and ataxic gait. Neurological examination revealed hearing loss, facial nerve paresis, and left cerebellar ataxia. Magnetic resonance imaging demonstrated a left vestibular schwannoma 35 mm in diameter, as well as a heterogeneous area associated with hypointense rim within the tumor, indicating intratumoral hemorrhage. Subtotal removal of the tumor together with the fibrously encapsulated hematoma was performed through a left retrosigmoid craniotomy. Histological examination of the surgical specimen revealed cavernous malformation within vestibular schwannoma. Immunohistochemistry for matrix metalloproteinase (MMP)-2 and -9, and tissue inhibitors of metalloproteinase-2 showed strong expression in the endothelial cells of the cavernous malformation, but not in the interstitial structures. His symptoms significantly improved after surgery and he underwent gamma-knife therapy for the residual tumor. Cavernous malformations may show dynamic characteristics such as repeated hemorrhage and de novo formation. MMP-2 and -9, which are implicated in angiogenesis and hemorrhage, may be upregulated in such tumors.     

Rapid revascularization after therapeutic parent artery occlusion for a large intracavernous carotid artery aneurysm

A 21-year-old woman presented with an unruptured large intracavernous aneurysm, which was spontaneously revascularized via unusual collateral pathways a short time after extracranial-intracranial bypass and surgical ligation of the proximal internal carotid artery. The patient had been treated for a large basilar trunk aneurysm with intraaneurysmal embolization using Guglielmi detachable coils, and an intracavernous carotid artery aneurysm treated conservatively. Two years later, the patient presented with right abducens nerve palsy, and was referred to our hospital. She had small nevi in the right forehead and eyelid. Cerebral angiography revealed enlargement of the intracavernous aneurysm. Superficial temporal artery-middle cerebral artery bypass followed by surgical carotid artery ligation were performed, and good patency of bypass and disappearance of the aneurysm were confirmed by intraoperative angiography. However, follow-up magnetic resonance angiography and cerebral angiography on the 20th postoperative day revealed revascularization of the internal carotid artery and the intracavernous carotid artery aneurysm via unusual collateral pathways. Subsequently, the recurrent aneurysm and the recanalized internal carotid artery were occluded by endovascular procedures. Histological examination of the nevus showed lack of properly organized vascular structures, and the diagnosis was angiodysplasia. The early development of unusual collateral pathway, and aneurysm formation at a young age might be related to the angiodysplasia. Revascularization is possible within a short time even in cases of intracavernous carotid artery aneurysm successfully treated with surgical ligation of the parent artery.     

Psychogenic urinary dysfunction: a uro-neurological assessment

AIMS: The diagnosis of psychogenic urinary dysfunction (PUD) is one of exclusion, particularly from urologic and neurologic causes, and is usually accompanied by more obvious psychologic/ psychiatric features. We here describe patients with PUD who were diagnosed in our uro- neurological laboratory. MATERIALS AND METHODS: We reviewed the digitized records of 2,300 urodynamic cases treated in the past 6 years to identify patients who fulfilled the diagnostic criteria of PUD. All 2,300 patients had completed a urinary questionnaire and undergone both electromyography (EMG)-cystometry and a detailed neurological examination. In addition, pressure-flow analysis, neurophysiology tests including sphincter EMG analysis, and MRI of the brain and spinal cord were performed as applicable. RESULTS: PUD was seen in 16 cases (0.7%): 6 men, 10 women, mean age 37 years. Lower urinary tract symptoms (LUTS) included overactive bladder (OAB) alone in 5, difficult urination alone in one, and both in 10. LUTS commonly occurred in particular situations, for example, OAB only while riding the train. Some patients showed extremely infrequent toileting. The urodynamic findings were normal except for increased bladder sensation (50%) for OAB and acontractile detrusor (31%) for difficulty. The final diagnosis was conversion reaction in six followed by anxiety in four. CONCLUSIONS: PUD patients experienced the situational occurrence of OAB and/or difficult urination and, in some patients, extremely infrequent toileting. The main urodynamic abnormalities were increased bladder sensation and acontractile detrusor. However, even in cases suggestive of PUD, a non-PUD pathology behind the symptoms should be explored.     

Alpha 1-adrenoceptor agonists protect against stress-induced death of neural progenitor cells

Here, we show that alpha(1)-adrenoceptor agonists suppress stress-induced death of mouse embryonic brain-derived neural progenitor cells (NPCs). NPCs highly expressed both alpha(1A)- and alpha(1B)-adrenoceptor genes, whereas the gene encoding alpha(1D)-adrenoceptor was expressed at low levels. Application of the alpha(1)-adrenoceptor agonists phenylephrine and cirazoline significantly promoted cell survival of embryonic NPCs that had been exposed to stress, as measured by a lactate dehydrogenase release assay, but had no remarkable effect on differentiation of the NPCs. Both phenylephrine and cirazoline protected NPCs from death induced by growth factor deprivation, N2 nutrient deprivation, tunicamycin treatment or staurosporine treatment. Phenylephrine and cirazoline treatments both maximally reduced stress-induced cell death by approximately 60% but did not change the percentage of undifferentiated cells as measured by nestin staining. Moreover, phenylephrine and cirazoline treatments did not affect the cellular activities of caspase-3 and caspase-7 but markedly reduced propidium iodide penetration into the cytoplasm, suggesting that alpha(1)-adrenoceptor agonists inhibit caspase-3/7-independent death of the embryonic NPCs.     

Effects of Exercise Training on Blood Lipids and Lipoproteins in Children and Adolescents

The following review aims to describe what is known about the effects of exercise training in children and adolescents on the following blood lipids and lipoproteins: total cholesterol (TC), high density lipoprotein cholesterol (HDL-C), low density lipoprotein cholesterol (LDL-C), and triglycerides (TG). Only studies that described mode, frequency, duration and intensity of the exercise were included in the review. The results of the studies reviewed were equivocal. Clearly the effects of exercise training on the blood lipid and lipoprotein levels of normolipidemic children and adolescents are equivocal. Of the 14 studies reviewed, six observed a positive alteration in the blood lipid and lipoprotein profile, four of the studies observed no alteration in the blood lipid and lipoprotein profile and one study observed a negative effect on HDL-C but an overall improvement in the lipid and lipoprotein profile due to the decrease in the TC/HDL ratio. It appears that methodological problems present in the majority of the exercise training studies limits the ability to make a conclusive, evidence based statement regarding the effect exercise training has on blood lipid levels in normolipidemic children. Most of the research design flaws can be linked to one or more of the following: small numbers of subjects in each study, low or no representation of girls, inclusion of both boys and girls in the subject pool, inclusion of boys and girls at different maturational stages in the subject pool, exercise training regimes that do not adequately control for exercise intensity, exercise training regimes that do not last longer than 8 weeks and exercise training studies that do not have an adequate exercise volume to elicit a change. Ideally, future research should focus on longitudinal studies which examine the effects of exercise training from the primary school years through adulthood.

Key points

• Exercise training has limited to no effect on blood lipid levels in children and adolescents.
• Few well controlled studies have been done to examine the effect exercise training has on selected cardiovascular risk factors and those studies that have been completed contain methodological flaws which makes interpretation of the results difficult.
• More studies, particularly those of a longitudinal design, are required before a conclusion can be drawn regarding the effects exercise training has on selected cardiovascular risk factors in children and adolescents.

Key words: Cardiovascular risk factors, children, adolescents, aerobic exercise training