High Cervical Disc Lesions in Elderly Patients – Presentation and Surgical Approach

Summary  The incidence of high cervical disc lesions is extremely rare, and the mechanism of their development is unclear. We report these three cases, and discuss the possible mechanisms. We also describe surgical strategies for these lesions.  The first and second cases were an 82-year-old male and an 84-year-old male with retro-odontoid disc hernia. The third was an 83-year-old female with a herniated disc at C2/C3. To investigate Aetiological mechanisms of these lesions, we examined the findings on cervical images in extension and flexion, and compared the results in a younger than 80-year-old group and an older than 80-year-old group.  The patients underwent surgery via a posterolateral intradural approach. Wide laminectomy and incision of the dentate ligaments enabled access to the ventral space of the upper cervical spinal canal and sufficient decompression. All patients became ambulatory postoperatively without special fixation of the cervical spine. In the younger group, the level mostly loaded during cervical movement was C5/6, however, the levels in the older group were C2/3 and C3/4.  In elderly patients, less mobilization of the middle and/or lower cervical spine due to spondylotic change causes overloading at higher levels resulting in high cervical disc lesions. Retro-odontoid disc lesions can be caused by a herniated disc at C2/C3, which migrates upward. Regarding surgical strategy, the posterolateral intradural approach is less invasive and more advantageous for these lesions.     

Portal blood flow and liver regeneration in auxiliary partial orthotopic liver transplantation in a canine model

Functional competition has been shown to lead to a detrimental outcome in auxiliary liver transplantation. We evaluated the interaction in auxiliary partial orthotopic liver transplantation between the native liver and the graft in terms of portal flow and regeneration. The need for diversion of the portal flow to the graft was also assessed. Reduced-size liver grafts were transplanted orthotopically after partial hepatectomy in beagles. There were two groups: the preserved group, where portal inflow to the native liver was preserved, and the ligated group, where it was interrupted. Portal flow was measured serially and liver regeneration was evaluated on postoperative day 5. Functional competition was not observed in the preserved group. On the other hand, ligation of the native liver portal vein had no obviously detrimental effects on the remnant native liver. This leads to the conclusion that the portal vein to the native liver can be safely ligated to prevent functional competition.     

Rapid progression of pituitary hyperplasia in humans with primary hypothyroidism: demonstration with MR imaging.

PURPOSE: To use magnetic resonance (MR) imaging to evaluate the morphologic changes of the pituitary gland during the development of hypothyroidism. MATERIALS AND METHODS: Fourteen patients who had undergone thyroidectomy were evaluated before radioactive iodine 131 therapy. In each patient, MR imaging and measurement of serum hormone levels were performed twice: 5 weeks before 131I treatment as the "euthyroid state" with thyroid hormone supplementation and on the day of 131I treatment as the "hypothyroid state" after a 3-week depletion of thyroid hormone supplements. Nine healthy volunteers also underwent MR imaging twice at an interval of 5 weeks. Pituitary volume and the relative signal intensity ratio of the anterior pituitary to the pons were measured. The shape and signal intensity of the pituitary gland were also visually assessed. The paired Student t test was used to evaluate the significance of the data. A P value less than .05 indicated a statistically significant difference. RESULTS: The patients had significantly larger pituitary volume in the hypothyroid state than in the euthyroid state both quantitatively (P < .001) and visually. No significant differences were found in the relative signal intensity ratios of the anterior pituitary to the pons. In healthy volunteers, no significant differences in pituitary volumes or signal intensity were found between the two MR images. CONCLUSION: Rapid progression of hyperplasia of the anterior pituitary may occur with acute development of hypothyroidism.     

Post-traumatic pituitary apoplexy--two case reports

A 60-year-old female and a 66-year-old male presented with post-traumatic pituitary apoplexy associated with clinically asymptomatic pituitary macroadenoma manifesting as severe visual disturbance that had not developed immediately after the head injury. Skull radiography showed a unilateral linear occipital fracture. Magnetic resonance imaging revealed pituitary tumor with dumbbell-shaped suprasellar extension and fresh intratumoral hemorrhage. Transsphenoidal surgery was performed in the first patient, and the visual disturbance subsided. Decompressive craniectomy was performed in the second patient to treat brain contusion and part of the tumor was removed to decompress the optic nerves. The mechanism of post-traumatic pituitary apoplexy may occur as follows. The intrasellar part of the tumor is fixed by the bony structure forming the sella, and the suprasellar part is free to move, so a rotational force acting on the occipital region on one side will create a shearing strain between the intra- and suprasellar part of the tumor, resulting in pituitary apoplexy. Recovery of visual function, no matter how severely impaired, can be expected if an emergency operation is performed to decompress the optic nerves. Transsphenoidal surgery is the most advantageous procedure, as even partial removal of the tumor may be adequate to decompress the optic nerves in the acute stage. Staged transsphenoidal surgery is indicated to achieve total removal later.     

Antiulcer effect of lafutidine on indomethacin-induced gastric antral ulcers in refed rats.

Lafutidine is a new type antiulcer agent with antisecretory and gastroprotective activities. We investigated the effect of lafutidine on indomethacin-induced antral ulcer in refed rats. Subcutaneous indomethacin injection resulted in the formation of gastric antral ulcer. Lafutidine (1-10 mg/kg, p.o.) reduced the area of ulcer in a dose-dependent manner when administered immediately after the indomethacin injection. Capsaicin at 3 mg/kg, p.o. and 16,16-dimethyl prostaglandin E2 at 3 microg/kg, p.o. also reduced the ulcer area. Chemical deafferentation of capsaicin-sensitive neurons or N(G)-nitro-L-arginine treatment aggravated the ulcer formation and abolished the preventive effect of lafutidine and capsaicin. After the induction of gastric ulcer, lafutidine given twice daily for 2.5 days reduced the area of ulcer in a dose-dependent manner with a significant effect at 10 mg/kg, p.o., as compared with that of the control group. In chemically-deafferentated rats, lafutidine did not show any healing effect. Cimetidine (30 mg/kg, p.o.) and famotidine (1 mg/kg, p.o.) had no significant effect on indomethacin-induced antral ulcer. These results may suggest that lafutidine, unlike cimetidine and famotidine, can prevent the indomethacin-induced antral ulcer formation and accelerate the healing of the ulcer in refed rats through mechanisms involving the capsaicin-sensitive afferent neurons and nitric oxide.     

Inhibition by alkylamines of NADPH oxidase through blocking the assembly of enzyme components.

Alkylamines inhibit NADPH oxidase both in intact neutrophils and in a cell-free system. The aim of this study was to examine the mechanism underlying this inhibitory effect. Among alkylamines with different chain lengths, the C12 compound (laurylamine) showed the greatest inhibitory effect on the cell-free NADPH oxidase activity induced by arachidonic acid (AA) in the presence of GTPgammaS. The inhibition was overcome by further addition of AA, and it was observed irrespective of whether laurylamine was added before or after the enzyme activation by AA. When added prior to the enzyme activation, laurylamine blocked translocation to the membrane of all three cytosolic components (p47-phox, p67-phox and rac) in a cell-free translocation assay. When added after the activation, laurylamine released only rac from the membrane. Laurylamine did not inhibit the reduction of cytochrome c by xanthine oxidase, suggesting that it does not have superoxide-scavenging activity. These results indicate that laurylamine inhibits both the activation process of NADPH oxidase and the activated enzyme itself by blocking the assembly of the oxidase components.     

Delayed image of iodine-123 iomazenil as a relative map of benzodiazepine receptor binding: The optimal scan time

Delayed single-photon emission tomograpic (SPET) images after an intravenous bolus injection of iodine-123 iomazenil have been used as a relative map of benzodiazepine receptor binding. We determined the optimal scan time for obtaining such a map and assessed the errors of the map. SPET and blood data from six healthy volunteers and five patients were used. A three-compartment kinetic model was employed in simulation studies and analyses of actual data. The simulation studies suggested that, in the normal brain, the scan time at which a single SPET image best represented the relative receptor binding was 3.0–3.5 h post-injection. This finding was supported by actual data from the volunteers. The simulation studies also suggested that the optimal scan time was not greatly changed by the variability of the input functions, and that the error in the SPET image contrast in the vicinity of the optimal scan time was not increased by changes in the tracer kinetics in the entire brain. The SPET image contrast in the patients at 3.0 h post-injection agreed well with the reference receptor binding estimated by kinetic analysis, with a mean error of 3.6%. These findings support the use of a single SPET image after bolus injection of [¹²³I]iomazenil as a relative map of benzodiazepine receptor binding. For this purpose, a SPET scan time of 3.0-3.5 h post-injection is recommended.     

Phenotypic shift in human differentiated gastric cancers from gastric to intestinal epithelial cell type during disease progression

Background. The phenotypic expression of tumor cells is widely thought to resemble that of the tissue of origin. In the present study, to assess phenotypic changes that occur with disease progression, we investigated human differentiated gastric cancers at different depths of invasion for component cancer cell types. Methods. Using a combined mucin histochemical and immunohistochemical approach, we classified surgical specimens of 301 differentiated gastric cancers into three types: gastric epithelial cell (G) type, intestinal epithelial cell (I) type and mixed gastric and intestinal (GI) type, according to the phenotypic differentiation of the component cancer cells. The relation between the phenotypic type of cancer and their depth of invasion was evaluated. Results. The proportion of G type cancers was 41.4% in early (tumor invasion of mucosa or submucosa) cases, decreasing to 22.2% in advanced (tumor invasion of muscularis propia or deeper) cases, whereas the proportion of I type cancers increased with progressive disease from 23.5% to 31.1% (P < 0.01). Cancers invading the subserosa or deeper included more I type cases and fewer G type than cancers limited to the mucosa (P < 0.01). In most cases of each phenotypic type, intestinal metaplasia was recognized in the surrounding background mucosa, but no clear relation was shown between the phenotype of cancers and the degree of intestinal metaplasia in the background mucosa, suggesting that intestinal metaplasia is not always a preneoplastic lesion. Conclusions. A phenotypic shift from G to I type expression was observed with the progression of human differentiated gastric cancers. Intestinalization may occur independently in cancerous and noncancerous gastric mucosa. Received for publication on May 1, 1998; accepted on Oct. 22, 1998     

Atrophy of the corpus callosum associated with a decrease in cortical benzodiazepine receptor in large cerebral arterial occlusive diseases

OBJECTIVES: It remains controversial whether selective neuronal ischaemic change develops in patients with occlusion of the large cerebral arteries. Previous studies have shown atrophy of the corpus callosum with reduced cortical oxygen metabolism in large cerebral arterial occlusive diseases, which might be indirect evidence of loss of the neurons in cortical layer 3. Recent studies of patients with ischaemic cerebrovascular diseases have demonstrated reduced central benzodiazepine receptor (BZR) binding in the normal appearing cortical areas, which might be more direct evidence of changes of the neurons. Although pathophysiology of the decreased BZR is unclear, a decrease in the cortical BZR binding with neuronal loss would cause atrophy of the corpus callosum. The purpose of this study was to determine whether atrophy of the corpus callosum is associated with a decrease in cortical BZR binding in large cerebral arterial occlusive diseases. METHODS: Seven patients with occlusive diseases of the middle cerebral or internal carotid artery and only minor subcortical infarctions were studied. Single photon emission tomographic images of (123)I labelled iomazenil (IMZ) obtained 180 minutes after injection were analysed for BZR binding. The midsagittal corpus callosum area/skull area ratio (on T1 weighted magnetic resonance images) was compared with the cerebral IMZ uptake/cerebellar IMZ uptake ratio. RESULTS: Compared with 23 age and sex matched control subjects, the patients had significantly decreased callosal area/skull area ratio. The degree of corpus callosum atrophy was significantly and strongly (rho=0.99, p<0.02) correlated with that of the decreases in the mean cerebral cortical IMZ uptake ratio. CONCLUSION: Corpus callosum atrophy may occur in association with a decrease in cortical BZR binding in large cerebral arterial occlusive diseases. Corpus callosum atrophy with decreased cortical BZR binding might reflect cortical neuronal damage in large cerebral arterial occlusive diseases.