Biomedical subjects

C Y Hsu

Publications and source records attributed to C Y Hsu.

At least 127 records · Page 7Linked to original sources

PubMed1997

Regulation of cytokine-induced iNOS expression by a hairpin oligonucleotide in murine cerebral endothelial cells.

Inducible nitric oxide synthase (iNOS) is expressed in response to cytokines by a number of cell types participating in CNS inflammation, including brain cerebral endothelial cells. NF-kappaB, a transcription factor, mediates effector actions of pro-inflammatory cytokines. A combination of tumor necrosis factor alpha (TNF-alpha) and interferon gamma (IFN-gamma) enhanced the expression of iNOS in murine cerebral endothelial cells (MCECs). In an attempt to modulate TNF-alpha+IFN-gamma induced expression of iNOS in MCECs, we designed a double-strand hairpin (hp) oligonucleotide carrying the NF-kappaB motif. This hp oligonucleotide inhibited NF-kappaB binding activity and decreased both iNOS mRNA and protein expression induced by TNF-alpha+IFN-gamma. As a control, a mutant hp oligonucleotide was without effect. The present study confirms the role of transcription factor NF-kappaB in iNOS expression induced by TNF-alpha+IFN-gamma in MCECs. More importantly, it demonstrates that an appropriately designed hp oligonucleotide is an effective tool to modulate iNOS expression and may be of potential pharmacological use.

Animals↗

PubMed1997

Assay of bropirimine in rat plasma by means of robotic solid-phase extraction and high-performance liquid chromatography.

A rapid and simple high-performance liquid chromatography (HPLC) method incorporating automated solid-phase extraction (SPE) is described for the determination of bropirimine, 2-amino-5-bromo-6-phenyl-4(3H)-pyrimidinone, in plasma samples from various species. Using an automated sample processor, plasma samples were loaded onto C18 SPE columns and the drug eluted with ethanol-methylene chloride (10:90, v/v). The extracts were analyzed by reversed-phase HPLC using a C8 column with a mobile phase consisting of acetonitrile-water-trifluoroacetic acid (20:80:0.1, v/v/v). The UV absorbance of the column effluent was monitored at a wavelength of 292 nm. Linear calibration curves were obtained in the range of 0.01 to 22 micrograms/ml. Precision (< or = 4% relative standard deviation) and accuracy (< or = 5% error) were acceptable at the concentrations evaluated. Application of this method to the quantitation of bropirimine in rat plasma for a toxicokinetic/bioavailability study is reported.

Administration, Oral↗

PubMed1997

Loss of expression of the p16 gene is frequent in malignant skin tumors.

Expression of the p16 gene from 30 malignant skin tumors has been surveyed by immunohistochemical assay. Gene point mutations were detected by DNA direct sequencing and the mRNA level of gene expression was measured by RT-PCR. A silent point mutation of the p16 gene was found in only one patient. However, loss of expression of the p16 gene was noticed in 23 of 29 samples (79.3%). Correlation between loss of expression of the p16 gene and metastasis is significant (p = 0.0036). These findings suggest that loss of expression of the p16 gene may play a critical role in tumor progression of malignant skin tumors.

Adenocarcinoma↗

PubMed1997

Quantitative regional brain water measurement with magnetic resonance imaging in a focal ischemia model.

Therapeutic approaches to cerebral edema require an understanding of both the magnitude and location of changes in brain water content. It is desirable to have a sensitive, accurate means of measuring brain water noninvasively so that effective therapies for cerebral edema in stroke, head trauma, and other conditions can be investigated. In this work, a three-dimensional magnetic resonance imaging technique that is able to provide both spin density and T1 simultaneously is described. This method was used to quantitate regional changes in brain water content in a rat model of focal cerebral ischemia. Brain water contents estimated from both relative spin density and relative T1 measurements made in vivo were compared with ex vivo measurements of relative tissue water content based on the wet-dry technique. Correlation coefficients of 0.95 and 0.98 were obtained between the wet-dry measurements and magnetic resonance measurements of T1 and spin density, respectively. Notably, the slope of the relationship between T1 and tissue water content changed dramatically after the injection of a paramagnetic contrast agent while precontrast and postcontrast spin density measurements remained essentially invariant. In addition, a plot of absolute spin density (obtained by normalizing spin density from agar gelatin phantoms of different water contents to the spin density of a sample of 100% water) was linearly related to wet-dry measurements with a slope of 0.99 (R2 = 0.99).

Animals↗

PubMed1997

Quantitative measurements of regional cerebral blood volume using MRI in rats: effects of arterial carbon dioxide tension and mannitol.

A three-dimensional (3D) T1-weighted sequence was used to acquire high spatial resolution whole brain images in rats before and after the injection of an intravascular contrast agent. These T1-weighted images were used to estimate regional cerebral blood volume (rCBV) as a percentage of blood volume in each voxel. Ventilation was manipulated to investigate the effects of altered arterial carbon dioxide tension (PaCO2) on rCBV. In addition, different doses of a hypertonic mannitol solution were used to investigate the sensitivity of the proposed method in a serial monitoring paradigm. An rCBV of 2.40% +/- 0.34% was obtained before any physiological manipulation, in good agreement with literature values using alternative techniques. Using this method, it was found that there exists a linear relationship between PaCO2 and rCBV (R2 = 0.77) and that rCBV increased in a dose and time dependent fashion in mannitol-treated rats. High signal-to-noise was available due to the substantial increase in blood signal from the intravascular contrast agent.

Animals↗

PubMed1997

Endogenous repair after spinal cord contusion injuries in the rat.

Contusion injuries of the rat thoracic spinal cord were made using a standardized device developed for the Multicenter Animal Spinal Cord Injury Study (MASCIS). Lesions of different severity were studied for signs of endogenous repair at times up to 6 weeks following injury. Contusion injuries produced a typical picture of secondary damage resulting in the destruction of the cord center and the chronic sparing of a peripheral rim of fibers which varied in amount depending upon the injury magnitude. It was noted that the cavities often developed a dense cellular matrix that became partially filled with nerve fibers and associated Schwann cells. The amount of fiber and Schwann cell ingrowth was inversely related to the severity of injury and amount of peripheral fiber sparing. The source of the ingrowing fibers was not determined, but many of them clearly originated in the dorsal roots. In addition to signs of regeneration, we noted evidence for the proliferation of cells located in the ependymal zone surrounding the central canal at early times following contusion injuries. These cells may contribute to the development of cellular trabeculae that provide a scaffolding within the lesion cavity that provides the substrates for cellular infiltration and regeneration of axons. Together, these observations suggest that the endogenous reparative response to spinal contusion injury is substantial. Understanding the regulation and restrictions on the repair processes might lead to better ways in which to encourage spontaneous recovery after CNS injury.

Animals↗

PubMed1997

Neuronal apoptosis and necrosis following spinal cord ischemia in the rat.

We examined the characteristics of neuronal death induced by ischemia in the spinal cord. Spinal cord ischemia was induced in Long-Evans rats by occlusion of the descending aorta with a 2F Fogarty catheter for 20 min (model 1) or more limited aortic occlusion (15 min) coupled with blood volume reduction (model 2); rats were sacrificed 6 h-7 days later. The animals developed variable paraparesis in model 1 and reliable paraplegia in model 2. The extent of histopathological spinal cord damage, being maximal in the lumbar cord, correlated well with the severity of paraparesis. Two distinct types of spinal cord neuronal death were observed, consistent with necrosis and apoptosis. Neuronal necrosis was seen in gray matter laminae 3-7, characterized by the rapid (6 h) onset of eosinophilia on hematoxylin/eosin-stained sections, and gradual (1-7 days) development of eosinophilic ghosting. Although TUNEL positivity was present, disintegration of membranes and cytoplasmic organelles was seen under electron microscopy. Neuronal apoptosis was seen after 1-2 days in dorsal horn laminae 1-3, characterized by both TUNEL positivity and electron microscopic appearance of nuclear chromatin aggregation and the formation of apoptotic bodies. DNA extracted from the ischemic lumbar cord showed internucleosomal fragmentation (laddering) on gel electrophoresis. These data suggest that distinct spinal cord neuronal populations may undergo necrosis and apoptosis following transient ischemic insults.

Animals↗

PubMed1997

Neuronal cell death in the ischemic spinal cord: the effect of methylprednisolone.

BACKGROUND: Cell death occurs by either necrosis or apoptosis. The role of apoptosis in the neuronal degeneration after ischemia remains to be defined. We studied (1) the nature of neuronal death and (2) the neuroprotective action of methylprednisolone in a rat model of spinal cord ischemia. METHODS: Spinal cord ischemia was induced in adult Long-Evans rats by occluding the aortic arch for 14 minutes and simultaneously equilibrating the femoral artery pressure to the atmospheric pressure. Twenty rats were subjected to ischemia without treatment and another twenty to ischemia after treatment with methylprednisolone (30 mg/kg, 4 hours before ischemia). The animals were sacrificed and the lumbar spinal cords were examined on postoperative days 1 and 2. RESULTS: On day 1, neurons with morphology indicative of apoptosis were present in the gray matter. Their numbers increased from the ventral to the dorsal location. There were significantly fewer apoptotic neurons in the dorsal horn of the methylprednisolone-treated animals. DNA obtained from the spinal cord of untreated rats on days 1 and 2 showed laddering after electrophoresis, a feature of apoptosis. Pretreatment with methylprednisolone inhibited the development of DNA laddering. Methylprednisolone treatment was not associated with significantly improved neurologic function in the postoperative period. CONCLUSIONS: Apoptotic neuronal death occurs in the rat spinal cord after transient ischemia and is attenuated by pretreatment with methylprednisolone.

Animals↗

PubMed1997

Protection of rat spinal cord from ischemia with dextrorphan and cycloheximide: effects on necrosis and apoptosis.

OBJECTIVE: We examined the characteristics of neuronal cell death after transient spinal cord ischemia in the rat and the effects of an N-methyl-D-aspartate antagonist, dextrorphan, and a protein synthesis inhibitor, cycloheximide. METHODS: Spinal cord ischemia was induced for 15 minutes in Long-Evans rats with use of a 2F Fogarty catheter, which was passed through the left carotid artery and occluded the descending aorta, combined with a blood volume reduction distal to the occlusion. The rats were killed after 1, 2, and 7 days. Other groups of rats were pretreated with dextrorphan (30 mg/kg, intraperitoneally, n = 7), cycloheximide (30 mg, intrathecally, n = 7), or vehicle (saline solution, n = 12) and killed after 2 days. RESULTS: This model reliably produced paraplegia and histopathologically distinct morphologic changes consistent with necrosis or apoptosis by light and electron microscopic criteria in different neuronal populations in the lumbar cord. Scattered necrotic neurons were seen in the intermediate gray matter (laminae 3 to 7) after 1, 2, and 7 days, whereas apoptotic neurons were seen in the dorsal horn laminae 1 to 3 after 1 and 2 days. Deoxyribonucleic acid extracted from lumbar cord showed internucleosomal fragmentation (laddering) on gel electrophoresis indicative of apoptosis. The severity of paraplegia in the rats treated with dextrorphan and cycloheximide was attenuated 1 day and 2 days after ischemia. The numbers of both necrotic and apoptotic neurons were markedly reduced in both dextrorphan- and cycloheximide-treated rats. CONCLUSIONS: The results suggest that both N-methyl-D-aspartate receptor-mediated excitotoxicity and apoptosis contribute to spinal cord neuronal death after ischemia and that pharmacologic treatments directed at blocking both of these processes may have therapeutic utility in reducing spinal cord ischemic injury.

Animals↗

PubMed1997

The clinicopathological characteristics of gonadotroph cell adenoma: a study of 118 cases.

Gonadotroph cell adenoma was the most common pituitary adenoma, constituting 35% of the pituitary adenomas in our series of 339 patients with surgically removed pituitary adenomas from June 1987 to December 1995. The average age of these patients was 53 years, with a male predominance (1.5:1). The most common neurological symptoms were visual symptoms and headache. Amenorrhea and galactorrhea were recorded in 41% and 14%, respectively, of the female patients of reproductive age. Oncocytic change of varying degrees was seen in 69% of the tumors, and the average age of these patients (56 years) was older than those who had no such change (47 years) (P < .005). Five types of gonadotroph cell adenomas were recognized; they were tumors that contained (1) betaFSH, betaLH, and alphaSU, (2) betaFSH and betaLH, (3) betaFSH and alphaSU, (4) betaFSH, and (5) alphaSU. The immunostaining of betaFSH-containing cells was usually diffuse, whereas staining of betaLH- or alphaSU-containing cells was usually focal. Double immunostaining showed the immunoreactive cells containing one or any combination of the gonadotropin subunits. Increases in serum gonadotropin levels were only seen in 35% of the patients with gonadotroph cell adenoma. There was no correlation between serum hormonal levels and immunostaining results. Of the 33 recurrent cases, significant decrease or total absence of immunoreactivity of one or more hormone subunits in subsequent biopsy specimens were seen in three cases.

Adenoma↗

PubMed1997

Identification of a promoter for the latent membrane protein 1 gene of Epstein-Barr virus that is specifically activated in human epithelial cells.

Latent membrane protein 1 (LMP 1) is one of two Epstein-Barr virus (EBV)-encoded proteins that expressed in nasopharyngeal carcinoma (NPC) cells. Previous studies showed that a 3.5-kb transcript of the LMP 1 gene, in addition to the 2.8-kb transcript, was detected in a B95-8-EBV-containing, nude mice-passaged NPC tumor, C15. This indicated that a transcript was initiated from a region 5' to the putative promoter, ED-L1. We have isolated an EBV variant from a NPC tissue, and this virus strain contained a more pathogenic LMP 1 gene. DNA sequence analysis of the 5'-upstream region showed distinct variations as compared to that of B95-8 strain. To test if the LMP 1 gene of the NPC strain also contained an upstream promoter, we generated a series of deletion plasmids encompassing positions -1,030 to +20 of the LMP 1 promoter and tested for their abilities to drive the expression of the reporter gene in human epithelial cell lines, C-33A and NPC-TW076. We found that the region between -643 and -496 contained a promoter activity that was approximately five-fold higher than the putative promoter, ED-L1. This region between -643 and -496 was designated as ED-L1E. C-33A cells containing the genomic clone pT7(E) or the clone that had deleted a 94-bp ED-L1 sequence (delta94) was used to determine the transcription initiation sites by RNase protection assay. Results showed that a transcription initiation site was located at nucleotide 170,099 ("A") of EBV genome. The transcript was expressed in NPC biopsies and in human primary normal epithelial cells transfected with pT7(E) and delta94, respectively, as examined by reverse transcriptase-polymerase chain reaction (RT-PCR) analysis. Furthermore, the ED-L1E was not regulated by the EBV-encoded nuclear antigen 1-mediated transcriptional enhancer family of repeats (FR) in C-33A cells. Our results suggested that the ED-L1E was specifically activated in epithelial cells. The biological significance of the selective usage of the ED-L1E promoter was discussed.

B-Lymphocytes↗

PubMed1997

Pilot study of concurrent chemotherapy and radiotherapy for stage IV nasopharyngeal cancer.

Nasopharyngeal carcinoma (NPC) is a more radio- and chemosensitive tumor than all other head and neck cancers. Between September 1991 and December 1992, a total of 19 patients (13 men and six women; median age, 44 years) with AJCC stage IV NPC were entered into a pilot study of concurrent chemoradiotherapy. Pathology showed either poorly differentiated epidermoid carcinoma or undifferentiated carcinoma. Radiotherapy was delivered using a telecobalt unit and 10-MV x-rays and by conventional fractionation (1.8-2.0 Gy/fraction, 5 fractions/week). The total doses delivered were 70-75 Gy to the primary tumor and neck positive region, and 50-55 Gy to the neck negative area. Chemotherapy with cisplatin (10 mg/m2/day, days 1-5) and 5-fluorouracil (500 mg/m2/day, continuously infused for 5 days) was administered concurrently during weeks 1 and 5 of radiotherapy. The major toxicities were mucositis (42% had grade III and 58% grade II) and leukopenia (nadir white blood cells <3,000/mm3 in eight of 19). Although four patients required a delay in their second cycle of concurrent chemotherapy or had their radiotherapy interrupted for 1 week, all 19 patients completed the planned treatment and achieved a 100% complete response rate. After a median follow-up period of 42 months, one patient suffered from neck recurrence plus distant metastasis, and three patients developed distant metastases alone. The 3-year overall and disease-free survival rates are 89.5% and 83.3%, respectively. Our data indicated that concurrent chemoradiotherapy for advanced NPC is both feasible and effective, with acceptable toxicities. A phase III randomized trial to compare the efficacy of concurrent chemoradiotherapy and radiotherapy alone deserves to be studied further.

Adolescent↗

PubMed1997

Cell death suggestive of apoptosis after spinal cord ischemia in rabbits.

BACKGROUND AND PURPOSE: After spinal cord ischemia, some neurons remain viable after an ischemic insult but may be at risk of dying during reperfusion. We searched for morphological and biochemical features of apoptosis, which is a mechanism of delayed neuronal death, in a rabbit model of spinal cord ischemia. METHODS: The infrarenal aorta of White New Zealand rabbits (n = 24) was occluded for 40 minutes using a loop tourniquet. Rabbits were killed after 12, 24, or 48 hours (n = 8 per group). The loop was placed but never tightened in sham-operated rabbits (n = 6). The lumbar segment of the spinal cord (L5 to L7) was used for morphological studies, including hematoxylin and eosin staining and a modified terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end-labeling (TUNEL) staining method. Electron microscopy was used to examine ultrastructural morphology. In addition, lumbar tissue was used for biochemical investigation of DNA laddering by agarose gel electrophoresis. RESULTS: After ischemia, the affected areas contained neurons with positive TUNEL staining. Positive neurons were located in laminae III to IX, although most were concentrated in the intermediate and ventral areas. Adjacent sections stained with hematoxylin and eosin exhibited ischemic cell changes (red and ghost neurons), while apoptotic bodies were also apparent. In addition, electron microscopy of ischemic tissue samples exhibited ultrastructural characteristics of apoptosis, including nuclear condensation and relatively normal organelle morphology. Finally, isolated DNA revealed a ladder on agarose gel electrophoresis, indicating DNA fragmentation into approximately 180 multiples of base pairs. CONCLUSIONS: Spinal cord ischemia in rabbits induces morphological and biochemical changes suggestive of apoptosis. These data raise the possibility that apoptosis contributes to neuronal cell death after spinal cord ischemia.

Animals↗

PubMed1997

Spinal cord ischemic injury. Development of a new model in the rat.

BACKGROUND AND PURPOSE: Spinal cord ischemic injury (SCII) with resulting paralysis is a major cause of morbidity after operations on the thoracic aorta. Since the vascular supply to the spinal cord is similar in rats and humans, the rat appears important for studies of mechanisms of injury and development of therapeutic strategies to avoid this complication. METHODS: In group A rats, we induced SCII using a previously described method, by occluding the descending thoracic aorta for 15, 20, 24, or 30 minutes with the inflated balloon of a 2F Fogarty catheter inserted through the femoral artery. In group B, the catheter was inserted through the left common carotid artery, and the aorta was occluded just distal to the carotid origin for 20 minutes. In group C, in addition to the procedure described for group B, hypovolemia was induced during a 12-minute period of aortic occlusion by equilibrating the left femoral artery pressure to the atmospheric pressure. The motor function of the hind limbs and the associated spinal cord histopathology were studied. RESULTS: At 96 hours, 9 of 10 rats in group C were paraplegic. This rate was significantly higher than that of group A (1 of 21, P = .00000) or group B (4 of 10, P < .03). In all groups, the histopathological changes became more severe from the rostral to the caudal direction along the spinal cord and from the peripheral to the central location in transverse sections. CONCLUSIONS: The combination of aortic arch occlusion with induced hypovolemia resulted in a reproducible model of SCII in rats.

Animals↗

PubMed1997

Prolongation and enhancement of postischemic c-fos expression after fasting.

BACKGROUND AND PURPOSE: A rapid but transient expression of c-fos after cerebral ischemia has been extensively documented. However, the mechanism of this induction and whether induction of c-fos is neuroprotective or detrimental to the brain after ischemia is presently not clear. Fasting before transient cerebral ischemia has been shown to reduce delayed neuronal necrosis and infarct volume. The purpose of the present study was to examine the effect of preischemic fasting for 24 hours on the expression of c-fos after transient focal cerebral ischemia. METHODS: Focal cerebral ischemia was induced by temporary occlusion of the right middle cerebral artery and both common carotid arteries for 60 minutes. Male Long-Evans rats weighting 250 to 300 g were randomly divided into two groups: fed (control group) and food deprived for 24 hours (fasted group) before ischemic surgery. Infarct volumes were measured on the basis of triphenyltetrazolium chloride-delineated infarct areas, and plasma glucose levels were determined by the glucose oxidase method. Temporal and spatial expression of c-fos was assessed by Northern blot analysis, in situ hybridization, and immunohistochemistry. RESULTS: Fasting for 24 hours before 60 minutes of ischemia resulted in a 26.6% decrease in preischemic plasma glucose levels and a 74.5% reduction in infarct volumes in the fasted group compared with the control group. A rapid but transient induction of c-fos mRNA was observed in the ischemic cortex in control animals after 60 minutes of ischemia. Fasting not only prolonged but also enhanced the intensity of c-fos expression in the ischemic cortex. Regional c-fos expression was also different between these two groups. CONCLUSIONS: The results support the contention that c-fos expression may be compatible with its purported neuroprotective role in selected experimental paradigms. The signaling mechanisms underlying the effect of fasting and subsequent lowering of plasma glucose levels on postischemic c-fos expression remain to be explored.

Animals↗

PubMed1997

Multiple-dose mannitol reduces brain water content in a rat model of cortical infarction.

BACKGROUND AND PURPOSE: Repeated use of mannitol in the setting of ischemic infarction is a controversial and poorly defined therapeutic intervention. The purpose of this study was to examine the effects of repeated mannitol infusions on brain water content and tissue pressure in a well-defined rat model of focal ischemic stroke. METHODS: Mannitol infusions (0.5, 1.5, or 2.5 g/kg) were given by intravenous bolus 4 or 24 hours after 90-minute transient cortical ischemia in the territory of the right middle cerebral artery in rats and every 4 hours thereafter for a total of 24 hours. Fluid replacement was limited to 0.5 mL i.v. isotonic saline administered immediately after each mannitol dose. Control rats received 0.5 mL i.v. saline at the same intervals and were otherwise under ad libitum conditions. Water contents (percent H2O) of whole hemispheres and of cortical biopsies were measured with the wet-dry method, and blood samples were analyzed for plasma osmolality and chemistries. In a subgroup of rats, tissue pressure was also measured within the hemisphere ipsilateral to the infarct. RESULTS: Repeated mannitol infusions resulted in a dose-dependent increase in plasma osmolality and a dose-dependent decrease in the percent H2O of the ischemic middle cerebral artery cortex and ipsilateral hemisphere. In contrast, percent H2O of the contralateral cortex and hemisphere was significantly decreased only in the groups given the highest dose of mannitol (2.5 g/kg). Mannitol infusions at a dose of 1.5 g/kg begun 24 hours after reperfusion were also associated with a significant reduction of tissue pressure. CONCLUSIONS: In a rat model of ischemic cortical infarction, repeated mannitol infusions resulted primarily in a decrease in the percent H2O of the infarct and ipsilateral hemisphere, as well as decreased tissue pressure.

Animals↗

PubMed1997

Prospective comparison of laparoscopic and traditional colposuspensions in the treatment of genuine stress incontinence.

OBJECTIVE: To compare prospectively the results of laparoscopic and traditional colposuspensions in the treatment of genuine stress incontinence and to evaluate the efficacy, technique, and functional and anatomical changes after these two procedures. MATERIALS AND METHODS: Ninety-two patients with urodynamically proven genuine stress incontinence participated in this study, with 46 patients randomly allocated to laparoscopic colposuspension, and the other 46 patients to the traditional procedures. All patients had repeat studies at least 3 months after operation. RESULTS: The bladder neck position was significantly elevated after operation either at rest or during straining in both groups (all p < 0.001), but it was higher in the traditional group than the laparoscopy group during straining (p < 0.05). Comparison of urodynamics before and after operation in both groups showed significantly increased minimal urethral resistance and improved pressure transmission ratios at the proximal urethra (Q2). The blood loss was less in the laparoscopy group. The duration of bladder drainage after laparoscopic colposuspension was shorter, and was not affected by subsequent laparotomy. The operative time was almost the same. The success rate of the laparoscopy group was lower than that of the traditional group (80.4% vs. 95.6%, p = 0.044). The complication rates were 10.8% and 17.4% respectively. CONCLUSION: Laparoscopic colposuspension is an effective method for the treatment of GSI, as documented by anatomical and functional assessments. However, the success rate is still lower than for the traditional procedure.

Adult↗

PubMed1997

Postoperative MRI of anorectal malformation.

Twenty-five patients who had pull-through rectum (PTR) surgery, some of whom suffered from fecal incontinence, soiling or constipation were studied by magnetic resonance imaging (MRI) postoperatively. MRI demonstrated 14 patients with proper placement of the PTR between the puborectal muscle and external sphincter muscle; four patients with improper placement of the PTR outside the puborectal muscle and external sphincter muscle (one with excess perirectal fat); one patient with disruption of the puborectal muscle and external sphincter muscle; three with hypoplasia of the puborectal muscle and external sphincter muscle; three with asymmetric placement of PTR in the levator ani (one with excess perirectal fat). MRI also depicted seven patients with spine anomalies; five with tethered cord; and 10 with genitourinary tract anomalies. The patients with correct location of PTR all had good fecal continence except three patients (two with soiling and one with constipation) who had tethered cord and ganglion cell dysfunction at the PTR. The patients with improper placement of PTR or poorly developed pelvic muscles all had fecal incontinence. Our study emphasizes that MRI can depict the causes of postoperative incontinence, detect anomalies and help to plan further surgery.

Adolescent↗