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A 52-year-old man developed sudden occipital headache followed by vomiting and vertigo. On admission, he displayed right Horner syndrome with ipsilateral reduced facial sensation to pain and temperature that crossed in the body, affecting the left limbs. In addition, he had right hemiparesis. Diffusion weighted magnetic resonance images showed a high intensity lesion localized in the lower and right lateral medulla oblongata. Magnetic resonance angiography showed severe luminal stenosis in the right vertebral artery and T2-weighted sampling perfection with application optimized contrasts using different flip angle evolution (SPACE) showed arterial wall expansion. T1-weighted SPACE showed subacute intramural hematoma at that point, suggesting arterial dissection. First described in 1946, Opalski syndrome is considered a variant of Wallenberg syndrome with ipsilateral hemiparesis. This motor impairment is considered as a result of extension of the ischemia from the lateral medulla to the upper cervical cord involving corticospinal fibers caudal to pyramidal decussation. This case adds information regarding the anatomy of the pyramidal decussation.

Hippocampal cholinergic neurostimulating peptide (HCNP), originally purified from the hippocampus of young rats, enhances the cholinergic development of rat medial septal nuclei in vitro. This report concerns the determination of the HCNP content of the cerebrospinal fluid (CSF) of 173 clinically, and of 22 clinico-pathologically defined patients. A radioimmunoassay was used throughout. The HCNP level was relatively uniform among the clinically defined patients; for almost all non-Alzheimer's patients, the level fell within the range delimited by +/- 2 SD of the mean for all patients taken together, and none of them had a level above this range. By contrast, the early-onset Alzheimer's disease patients could be divided on the basis of their HCNP level into two groups, one with high levels (markedly above the mean +/- 2SD range), and the other with levels similar to those of the other patients. The analysis of the CSF samples obtained postmortem revealed that Group I Alzheimer-type dementia (ATD) patients with clinico-pathologically established diagnoses had a strikingly higher level of HCNP than patients with either Group II ATD or cerebral vascular disease. These results suggest that HCNP is involved in certain pathophysiological alterations associated with dementia, and that its determination may be useful in patient evaluation. Copyright 1998 Lippincott Williams & Wilkins

Hippocampal cholinergic neurostimulating peptide (HCNP) is a novel undecapeptide purified from the hippocampus of young rats. The peptide stimulates cholinergic phenotype development in the rat medial septal nucleus in vitro. Here, we have focused on the mechanism of release of the peptide from the hippocampus, by applying tissue culture techniques. Quantitation of HCNP in the culture supernatant after chemical stimulation was carried out by RIA, and by a combination of HPLC and RIA. We found that the N-methyl-D-aspartate (NMDA) receptor specifically mediates release of the deacetylated form of HCNP from the culture. Our results suggest that during the early development of hippocampal neurons, the peptide is released by NMDA receptor activation, and that it may be involved in mediating the effect of activity-dependent cues on developing septal cholinergic neurons.

A rare case of mixed connective tissue disease (MCTD) with acute polyradiculoneuropathy is reported. A 23-year-old woman presented with high body temperature, arthralgia and a headache, and developed gait disturbance two weeks later. She had many clinical features common to patients with MCTD. Her neurological manifestations were diagnosed as acute polyradiculoneuropathy based on the clinical picture, combined with supportive ancillary data, including cerebrospinal fluid (CSF) analysis, electrophysiological evaluation, sural nerve biopsy, peroneus brevis muscle biopsy, and magnetic resonance imaging (MRI). Her neurologic deficits, as well as associated laboratory findings, were improved by corticosteroid therapy.

This report concerns the distribution of the hippocampal cholinergic neurostimulating peptide (HCNP) in tissues and organs of 11-day-old Wistar rats. HCNP, originally isolated and purified from the hippocampus of young rats, is an undecapeptide (acetyl-Ala-Ala-Asp-Ile-Ser-Gln-Trp-Ala-Gly-Pro-Leu). HCNP distribution was investigated by using immunohistochemical techniques, employing an affinity-purified rabbit antibody that specifically recognizes HCNP and its 21-kDa precursor protein. Positively stained cells were detected in a variety of tissues and organs, including salivary gland, small intestine, colon, pancreas, bronchiole, adrenal gland, testis, as well as several others. The nerve fibres around blood vessels of almost all organs expressed HCNP. Our results suggest that HCNP or its precursor, or both, may have a specific function not only in the central nervous system, but also in the peripheral nervous system, and possibly in certain specialized duct and gland cells as well.

This report concerns the demonstration of hippocampal cholinergic neurostimulating peptide (HCNP), its deacetylated analogue (free HCNP) and HCNP precursor protein in rat tissues. To avoid possible enzymatic degradation during sample manipulation, tissue extracts were prepared under acidic conditions using trifluoroacetic acid. The tissue contents of free HCNP and of precursor protein were determined by radioimmuno-assay (RIA) using two antibodies with different specificities, and by a combination of HPLC and RIA. Free HCNP was detected in neuronal and renal tissues, but not in liver. All tissues examined had measurable amounts of HCNP precursor protein. The concentrations of free HCNP and precursor in neuronal tissues were inversely related to the age. These results suggest that the deacetylated analogue of HCNP and its precursor protein may have significant physiological functions, especially in the central nervous system of young animals.

The effect of buprenorphine on the interdigestive myoelectric complex (IMC) was studied by gastrointestinal electromyogram in 3 mature mongrel dogs. The electromyograms were used to study the IMC cycle and total elapsed time (TET). Buprenorphine had very strong hyperkinetic action on the gastrointestinal tract at doses of 1 and 2 micrograms/kg which revealed phasic contraction, but since this action disappeared when atropine was administered. The phasic contraction originated in the upper jejunum just under the ligament of Treitz and then showed a migration pattern of J-->D and J-->I in 11 out of 23 cases (47.8%), D-->J-->I in nine cases (39.1%), J-->D-->J-->I in one case and no response in two cases. TET (min) showed a mean value of 90.3 +/- 11.2 (n = 23), which was not significantly different from the controls (106.1 +/- 14.3) (n = 24), but tended to be longer (0.1 > p > 0.05). After administration of buprenorphine at a dose of 20 micrograms/kg, phasic contraction migrated to ileum, which was disappeared an interval of 6-7 hours until next IMC. At low doses of buprenorphine were administered after a meal, the postprandial pattern was restored and converted to fasted pattern only one IMC cycle. Buprenorphine is partial agonist for the mu receptor. Ahmad et al. (1989) reported that alpha 2 adrenergic receptor and opiate receptors (mainly mu) were presented in submucosal plexus. In concludes that alpha 2 adrenergic activity and other humoral factors seems to take an important role for the initiation of phasic contraction and to control maintenance of IMC cycle.

Segments and Thirty-Vella type loops of the small intestine of dogs were prepared, and the excitation propagation pattern of the interdigestive migrating electric complex (IMEC) was observed by electromyography. The nerve regulatory mechanism in intestinal movement was investigated. The results indicated that first, the frequency of the basic electric rhythm (BER) is controlled so that a downward gradient is formed from the upper to the lower intestine, but this gradient continues to be controlled by a two-dimensional control mechanism involving parietal factors and extrinsic nerves due to transection of the intestines and damage to the extrinsic nerves in the dominant region. However, propagation of the IMEC in the small intestine appeared to be regulated by a combination of the two-dimensional control mechanism involving extrinsic and parietal nerves corresponding to the BER control mechanism. It was clear that the propagation mechanism of IMEC is related to the BER frequency, and propagation of the IMEC is downward in accordance with the frequency gradient of BER.

An immunohistological study using a Leu 7 antibody, which is a marker for human NK and K cells, was carried out in two cases of gastric carcinomas with prominent reactive hyperplasia. The patients were a 72-year-old man and a 55-year-old man who had shown good postoperative courses in spite of the advanced stage of their tumors. There were many scattered Leu 7 positive cells in the lymphoid hyperplasia, predominantly in the germinal centers and the peri-follicles. The number of Leu 7 positive cells were even more pronounced in a patient whose condition was more advanced. These findings suggest that lymphoid hyperplasia, particularly with regard to the NK and K cell response, plays a significant role in the clinical benignity of the tumors.

To study the motility functions after transection and anastomosis of the intestinal tract, the interdigestive action potential was induced experimentally and observed in the small intestines of conscious fasted dogs. When the intestinal tract was transected, the frequency gradient of the basic electric rhythm was disturbed even in cases of subsequent anastomosis. Differences arose in the frequency as upper and lower part of anastomosis, and it did not return to normal. The spike potential which appeared with the building up of the basic electric rhythm was propagated to the distal intestine in a normal course after transection of the intestinal tract according to observations centered on propagation of the IMEC. The propagation velocity of the IMEC gradually drops from the proximal jejunum toward the terminal ileum in the nonmanipulated intestine, while in the intestine undergoing transection and anastomosis, the velocity of propagation was reduced by half in the area of anastomosis, and tended to be even lower in cases of a double section and two anastomoses of the distal intestine. However, the total elapsed time in the small intestine was not extended by much. A new electric complex appeared from the stump of the distal intestine when the intestine was subjected to transection, and a stimulation which is involved in the appearance of the spike potential was formed.

This report deals with a histologic demonstration of a combined tumor of early signet ring cell carcinoma and lymphoma of the stomach in a 52-year-old Japanese man. The Gastric carcinoma was found by a systemic work up for a tonsillar lymphoma. The relationship between the malignant lymphomas of the stomach and of the tonsil is not clear in this case. The carcinoma and lymphoma of the stomach were both small, and the depth of invasion was localized to the mucosa and submucosa, respectively. The lymphoma was observed just beneath the cancer and was a diffuse, large cell type, and of the same histologic typing as the tonsillar lymphoma. Based on the broader size of the carcinoma, it is considered that the carcinoma probably induced the lymphoma in the stomach. This of an early combined tumor of carcinoma and lymphoma of the stomach is, to our knowledge, the first to be reported in the literature.

Two cases of an undifferentiated carcinoma of the stomach have been investigated by conventional histologic, immunohistochemical, and ultrastructural methods. The patients were a 73-year-old man and 65-year-old man. A postoperative histological examination of the resected stomach of each patient disclosed large areas of an undifferentiated carcinoma which were relatively well demarcated from areas of the adenocarcinoma. In the undifferentiated carcinomatous areas, the reticulin fiber stain was epithelial in pattern, and mucin staining proved negative. Similarly both Grimelius and Fontana-Masson staining also negative. In like manner immunostains using cytokeratin , vimentin , IgG, IgA, s-100 protein, and NSE were all negative, and an electron microscopic study showed no neurosecretory granules or mucin secretory granules. Based on these findings, the diagnosis of either a malignant lymphoma or small cell anaplastic carcinoma could be excluded, and thus an undifferentiated carcinoma was the determination.