Biofeedback is the treatment of choice for functional defecation disorders such as idiopathic chronic constipation and neurogenic fecal incontinence. The pre-existing biofeedback systems have many disadvantages. The aims of current project are, first, to develop the biofeedback system into the application software in the Windows environment, and, second, to assess the possibility of clinical usage for patients with functional defecation disorders. The hardware and software of the BASCO (Biofeedback Anal Sphincter Control) system were based on the signal measurement and signal processing of anal sphincter EMG (Electromyography). BASCO system was applied to 5 normal healthy controls and 20 patients with functional defecation disorders. Patients group was categorized as constipation group (N1=15) and incontinence group (N2=5). With use of current system, EMG-based biofeedback therapy was performed, and the outcome was analysed. Anal EMG signal data was processed by the software, and displayed in the monitor of personal computer. The software of EMG-display and database management were adequately operated. In N1 group, a paradoxical elevation or equalized activity of anal EMG pattern was shown in the simulated defecation. In N2 group, low electrical activity was shown. These findings were used for the EMG-based biofeedback therapy as a pilot study. The clinical symptoms were improved in 12 of N1 group and 3 of N2 group in the period of 3.7 (range, 1~12) months follow-up. In Conclusion, newly-developed BASCO system was adequately operated in the volunteer and patients groups. The multi-tasking and multi-processing functions were adequately shown in the real time. Current results could be used for clinical appraisal. Specifically, this system could be used for the practical application of biofeedback therapy in the patients with chronic constipation or fecal incontinence.
Anal Canal* ; Biofeedback, Psychology* ; Constipation ; Defecation* ; Fecal Incontinence ; Follow-Up Studies ; Humans ; Microcomputers ; Pilot Projects ; Volunteers

No abstract available.
Humans ; Survival Rate*

PURPOSE: To realistically map the electric fields of biological tissues using a diffusion tensor magnetic resonance electrical impedance tomography (DT-MREIT) method to estimate tissue response during electrical stimulation. METHODS: Imaging experiments were performed using chunks of bovine muscle. Two silver wire electrodes were positioned inside the muscle tissue for electrical stimulation. Electric pulses were applied with a 100-V amplitude and 100-μs width using a voltage stimulator. During electrical stimulation, we collected DT-MREIT data from a 3T magnetic resonance imaging scanner. We adopted the projected current density method to calculate the electric field. Based on the relation between the water diffusion tensor and the conductivity tensor, we computed the position-dependent scale factor using the measured magnetic flux density data. Then, a final conductivity tensor map was reconstructed using the multiplication of the water diffusion tensor and the scale factor. RESULTS: The current density images from DT-MREIT data represent the internal current flows that exist not only in the electrodes but also in surrounding regions. The reconstructed electric filed map from our anisotropic conductivity tensor with the projected current density shows coverage that is more than 2 times as wide, and higher signals in both the electrodes and surrounding tissues, than the previous isotropic method owing to the consideration of tissue anisotropy. CONCLUSIONS: An electric field map obtained by an anisotropic reconstruction method showed different patterns from the results of the previous isotropic reconstruction method. Since accurate electric field mapping is important to correctly estimate the coverage of the electrical treatment, future studies should include more rigorous validations of the new method through in vivo and in situ experiments.
Anisotropy ; Diffusion Tensor Imaging ; Diffusion* ; Electric Conductivity* ; Electric Impedance ; Electric Stimulation* ; Electrodes ; Magnetic Resonance Imaging ; Methods ; Silver ; Water*

No abstract available.
Biopsy* ; Hematuria*

The electrical conductivity is a passive material property primarily determined by concentrations of charge carriers and their mobility. The macroscopic conductivity of a biological tissue at low frequency may exhibit anisotropy related with its structural directionality. When expressed as a tensor and properly quantified, the conductivity tensor can provide diagnostic information of numerous diseases. Imaging conductivity distributions inside the human body requires probing it by externally injecting conduction currents or inducing eddy currents. At low frequency, the Faraday induction is negligible and it has been necessary in most practical cases to inject currents through surface electrodes. Here we report a novel method to reconstruct conductivity tensor images using an MRI scanner without current injection. This electrodeless method of conductivity tensor imaging (CTI) utilizes B1 mapping to recover a high-frequency isotropic conductivity image which is influenced by contents in both extracellular and intracellular spaces. Multi-b diffusion weighted imaging is then utilized to extract the effects of the extracellular space and incorporate its directional structural property. Implementing the novel CTI method in a clinical MRI scanner, we reconstructed in vivo conductivity tensor images of canine brains. Depending on the details of the implementation, it may produce conductivity contrast images for conductivity weighted imaging (CWI). Clinical applications of CTI and CWI may include imaging of tumor, ischemia, inflammation, cirrhosis, and other diseases. CTI can provide patient-specific models for source imaging, transcranial dc stimulation, deep brain stimulation, and electroporation.
Animal Experimentation* ; Animals* ; Anisotropy ; Brain ; Deep Brain Stimulation ; Diffusion ; Electric Conductivity ; Electrodes ; Electroporation ; Extracellular Space ; Fibrosis ; Human Body ; Inflammation ; Intracellular Space ; Ischemia ; Magnetic Resonance Imaging* ; Methods

OBJECTIVE: The purpose of this study was to titrate the nerve block effect of phenol with different concentrations of phenol solution by electrophysiological and mechanical measurements. METHOD: Right tibial nerves of twenty three adult rabbits were blocked by phenol solution with different concentrations (3%, 5%). Nerve conduction study for compound muscle action potential (CMAP), tension by electrical stimulation, and stiffness (slope) of stretch reflex of the triceps surae were performed after nerve block (4 weeks, 8 weeks, 16 weeks). The ratios of each values of right limb to those of left limb were used to evaluate the nerve block effect. RESULTS: The ratios of CMAP amplitude, tension, and slope of 3% group were 0.36, 0.55, and 0.56 at 4 weeks and those of 5% group were 0.21, 0.25, and 0.58. There were statistically significant differences of the CMAP amplitude and tension ratios, however there was no statistically significant difference of the slope ratio between two groups at 4 weeks. The ratios of CMAP amplitude, tension, and slope of 5% phenol group were increased with time. CONCLUSION: Nerve block effects by 5% phenol solution were greater than 3%. These data suggest that nerve block effect can be titrated with concentration of phenol solution.
Action Potentials ; Adult ; Electric Stimulation ; Extremities ; Humans ; Nerve Block* ; Neural Conduction ; Peripheral Nerves* ; Phenol* ; Rabbits ; Reflex, Stretch ; Tibial Nerve

Four small breed dogs were admitted with seizures. Magnetic resonance imaging (MRI) of the brain revealed dilation of the olfactory bulb cavity as well as enlargement of the lateral ventricles. These findings demonstrate that dilation of the olfactory bulb cavity can occur concurrent with hydrocephalus. This is the first description of the clinical and MRI features of dilation of the olfactory bulb cavity concurrent with hydrocephalus in dogs.
Animals ; Dilatation, Pathologic/veterinary ; Dog Diseases/*pathology ; Dogs ; Female ; Hydrocephalus/complications/pathology/*veterinary ; Magnetic Resonance Imaging/veterinary ; Male ; Olfactory Bulb/*pathology ; Seizures/pathology/veterinary

According to the recently published reports about mitochondrial diseasbl the clinical manifestations are more various than expected. There have been no clinical studies covering whole spectrum of mitochond7iral disease except a few case reports in our country. The authors performed this studies to understand the various clinical and laboratory findings of mitochondrial disease and the usefulness of current tools for the diagnosis of mitochondrial diseases. We reviewed retrospectively the clinical, laboratory and pathologic findings of mitochondrial disease. The diagnosis of mitochondrial disease was based on clinical manifestations, 'ragged-red fiber' in Gomori stainging, and/or abnormal mitochondrial morphologies on electron microscopy. Twenty one patients were diagnosed as mitochondrial disease. Their clinical diagnosis included 7 MELAS (mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes); 3 MERRF (myoclonic epilepsy with ragged red fibers); 2 KSS (Kearns-Sayre syndrome); 7 CPEO (chronic progressive external ophthalmoplegia); and 2 mitochondrial myopathy. The usefulness of electrodiagnostic studies, such as EMG, NCV and FEG, were limited in some patients. The muscle biopsy showed ragged red fibers in 10 of 15 sampled examined. Eleven patients had abnormal serum lactic acid level. The authors found that the mitochondrial disease revealed broad clinical spectrum and clinically available diagnostic tests, such as serum lactate and light microscopic examination showed limited value. Therefore, to evaluate the mitochondrial dysfunction with systemic involvement may be desirable to depend on sensitive and specific methods including succinate dehydrogenase (SDH) staining, electron microscopy and biologic studies of mitochondrial DNA.
Acidosis, Lactic ; Biopsy ; Diagnosis ; Diagnostic Tests, Routine ; DNA, Mitochondrial ; Epilepsy ; Humans ; Lactic Acid ; MELAS Syndrome ; MERRF Syndrome ; Microscopy, Electron ; Mitochondrial Diseases* ; Mitochondrial Myopathies ; Muscular Diseases ; Ophthalmoplegia, Chronic Progressive External ; Retrospective Studies ; Succinate Dehydrogenase

The aim of the present study was to assess the clinical and histopathological findings in a canine model of ischemic stroke. Cerebral ischemic stroke was induced by middle cerebral artery occlusion in four healthy beagle dogs using silicone plugs. They showed neurological signs of forebrain dysfunction such as reduced responsiveness, head turning, circling, postural reaction deficits, perceptual deficits, and hemianopsia. These signs gradually regressed within 4 weeks without therapy. On magnetic resonance imaging, T2 hyperintensity and T1 hypointensity were found in the cerebral cortex and basal ganglia. These lesions were well-defined and sharply demarcated from adjacent brain parenchyma with a homogenous appearance. No abnormalities of the cerebrospinal fluid were observed. At necropsy, atrophic and necrotic lesions were observed in the cerebral cortex. The cerebral cortex, basal ganglia, and thalamus were partially unstained with triphenyl-tetrazolium chloride. Histopathologically, typical features of infarction were identified in cortical and thalamic lesions. This study demonstrates that our canine model resembles the conditions of real stroke patients.
Animals ; Behavior, Animal/physiology ; Brain/metabolism/pathology ; Cerebral Infarction/*etiology/*pathology ; Cerebrospinal Fluid/chemistry/cytology ; Disease Models, Animal ; *Dogs ; Infarction, Middle Cerebral Artery/*complications/*pathology ; Magnetic Resonance Imaging ; Male

BACKGROUND: Current dilemma working with surgically-induced OA (osteoarthritis) model include inconsistent pathological state due to various influence from surrounding tissues. On the contrary, biochemical induction of OA using collagenase II has several advantageous points in a sense that it does not involve surgery to induce model and the extent of induced cartilage degeneration is almost uniform. However, concerns still exists because biochemical OA model induce abrupt destruction of cartilage tissues through enzymatic digestion in a short period of time, and this might accompany systemic inflammatory response, which is rather a trait of RA (rheumatoid arthritis) than being a trait of OA. METHODS: To clear the concern about the systemic inflammatory response that might be caused by abrupt destruction of cartilage tissue, OA was induced to only one leg of an animal and the other leg was examined to confirm the presence of systemic degenerative effect. RESULTS: Although the cartilage tissues were rapidly degenerated during short period of time upon biochemical induction of OA, they did not accompanied with RA-like process based on the histology data showing degeneration of articular cartilage occurred only in the collagenase-injected knee joint. Scoring evaluation data indicated that the cartilage tissues in non-induced joint remained intact. Neutrophil count transiently increase between day 8 and day 16, and there were no significant change in other complete blood count profile showing a characteristics of OA disease. CONCLUSION: These study shows that biochemically induced cartilage degeneration truly represented uniform and reliable OA state.
Animals* ; Blood Cell Count ; Cartilage ; Cartilage, Articular ; Clothing ; Collagenases* ; Digestion ; Inflammation ; Joints ; Knee Joint ; Leg ; Models, Animal* ; Neutrophils ; Osteoarthritis* ; Regeneration