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Objectives: Accurate neurological diagnoses are often difficult to make due to the complexity of the neuroanatomy involved. This study was performed to evaluate the usefulness of a computer system with easily retrievable anatomical information as a support for arriving at more accurate anatomic diagnoses. Patients and methods: Anatomical information from an initial physical examination was programmed into a computer with stored neuroanatomical charts of the brain, spinal cord and peripheral nerves. The information generated a graphic display of possible lesions with suggestions for further examination. These suggestions were then followed and further data entered. This data entry generated a new graphic display with reduced lesion possibilities. Iterations were then followed to narrow the possibilities for diagnosis further, until a final anatomical diagnosis was reached. This method was applied to three hypothetical examples and a number of clinical cases. Here we report three clinical cases in which this method was particularly useful in making a diagnosis. Results: Using computer iterations, the system was able to pinpoint one or more presumptive causative lesions in the CNS or PNS based on known neuronal pathways or nuclei. Conclusion: The results indicate that suitably used, computer memory, by virtue of its large capacity, accuracy and fast recall, can supplement human memory in reaching accurate anatomical diagnoses of neurological lesions.

Terminal Schwann cells (TSCs) that cover motor neuron terminals are known to play important roles in maintaining neuromuscular junctions, as well as in the repair process after nerve injury. However, molecular characteristics of TSCs remain unknown, because of the difficulties in analyzing them due to their paucity. We have established a method of selectively and efficiently collecting TSCs so that cDNA analysis can be done properly. The expression of 1–2% of whole mRNAs was compared between myelinating Schwann cells (MSCs) and TSCs, and it turned out that approximately one-third of the bands could be categorized as cell-type-specific bands. TSCs thus constitute a distinct entity from the viewpoint of gene expression. As one of the cDNA clones belonging to TSC-specific bands was identified homocysteine-responsive ER-resident protein (Herp), and in situ hybridization confirmed that Herp mRNA is expressed in TSCs on motor nerve terminals but not in MSCs, both in developing and adult rats. In conclusion, we have been able to identify Herp as a novel molecular marker for TSCs.

The blood-nerve barrier in peripheral nerves is important for maintaining the environment for axons. Breakdown of the barrier by nerve injury causes various pathologies. We hypothesized that the breakdown and recovery of the blood-nerve barrier after injury are associated with the changes in the expression of intercellular junctional proteins. To test this hypothesis, we induced crush injuries in the rat sciatic nerve by ligation and analyzed spatiotemporal changes of claudin-1, claudin-5, occludin, VE-cadherin, and connexin43 by immunoconfocal microscopy and morphometry and compared them with changes in the permeability of the blood-nerve barrier by intravenous and local administration of Evans blue-albumin (EBA). On day 1 after removal of the ligature EBA leaked into the connective tissue in the endoneurium and then the leakage gradually decreased and disappeared on day 7. On day 1 claudin-1, claudin-5, occludin, VE-cadherin, and connexin43 had totally disappeared from the perineurium and endoneurium. Thereafter, claudin-1, claudin-5, occludin, and VE-cadherin recovered from day 2, whereas connexin43 was redetected on day 5. These results indicate that the breakdown and following recovery of the blood-nerve barrier are closely associated with changes in the expression of claudins, occludin, VE-cadherin, and connexin43 and that the recovery time course is similar but nonidentical.

Synaptosomal-associated protein 25 has been regarded as one of the target-associated soluble N-ethylmaleimide-sensitive fusion attachment protein receptors essential for exocytosis of vesicles in synapses. We have previously reported that cleavage of syntaxin, which is another target-associated soluble N-ethylmaleimide-sensitive fusion attachment protein receptor, with botulinum neurotoxin C1 resulted in inhibition of neurite extension and morphological changes including growth cone collapse and large vacuole formation. As an attempt to explore the mechanism of growth cone extension, we examined the ultrastructural localization of synaptosomal-associated protein 25 in growth cones with or without treatment of botulinum neurotoxin A, which cleaves synaptosomal-associated protein 25. In dorsal root ganglion neurons, light microscopy demonstrated synaptosomal-associated protein 25 immunoreactivity throughout the neurons, including the cell bodies, neurites and growth cones. Using electron microscopy, gold signals immunoreactive for synaptosomal-associated protein 25 were identified diffusely in the cytoplasm of the growth cones. In contrast, in PC-12 cells, a large number of gold signals were localized on the plasma membranes. High levels of signal were also found in the cytoplasm in the central region of the growth cones. We also confirmed that botulinum neurotoxin A treatment reduced neurite extension by about 50%. However, both in dorsal root ganglion neurons and in PC-12 cells we found no differences in the ultrastructure nor in the localization of synaptosomal-associated protein 25 between growth cones with and without toxin treatment. These results indicate that cleavage of synaptosomal-associated protein 25 inhibits growth cone extension in a manner different than that of syntaxin cleavage. The results of this study suggest the possibility that synaptosomal-associated protein 25 is involved in growth cone extension through a process independent of vesicle fusion.

The distribution of protein kinase C (alpha, beta, gamma subtypes) was studied using immunocytochemical techniques in normal nerve fibers and in regenerating sprouts (growth cones) from the nodes of Ranvier following crush injuries to the rat peripheral nervous system. In normal nerves, for each protein kinase C subtype, immunoreactivity was present in both myelinated and unmyelinated axons. In myelinated axons, immunoreactivity for all three subtypes was patchy in the axoplasm and diffuse in the subaxolemmal peripheral zones. No immunoreactivity was found in the microtubule and neurofilament (cytoskeletal) domain. In contrast, in unmyelinated axons, immunoreactivity was distributed diffusely in the axoplasm. Schwann cells of myelinated fibers exhibited protein kinase C immunoreactivity, but those of unmyelinated fibers did not. In regenerating nerves, early sprouts and growth cones extending through the crushed site along Schwann cell basal laminae exhibited intense immunoreactivity for all three subtypes. Immunoreactivity was distributed diffusely throughout the axoplasm of the regenerating sprouts (growth cones), in which microtubules and neurofilaments were very rare. Thus, the subcellular localization of the protein kinase C immunoreactivity in growth cones of early regenerating nerves differed from that of normal parent axons. These findings suggest that protein kinase C (alpha, beta and gamma subtypes), whose subcellular distribution becomes more extensive in regenerating axons, may have important functional roles in axonal sprouting and in the regulation of growth cone activity in the peripheral nervous system.

Many techniques and instrument systems have been developed for performing arthroscopic Bankart repair using a suture anchor. The suture anchor procedure relies on a secure knot, which does not become entangled in the anterior portal. A newly devised anterior portal technique can solve this problem. We have used this technique for arthroscopic Bankart repair using suture anchor. This technique may be useful for any type of suture materials such as SLAP lesion.

Following crush injury of rat sciatic nerve, strong synaptophysin immunoreactivity was demonstrated in the regenerating sprouts that emerged from the proximal nodes of Ranvier and in their growth cones that extended through the space between Schwann cell basal lamina and myelin sheath of the parent axon. These findings suggest that synaptophysin is involved in the growth regulation of regenerating sprouts.