Modified cervical laminoforaminotomy based on anatomic landmarks reduces need for bony removal.

We describe a modified keyhole laminoforaminotomy (LF) using anatomic landmarks on the posterior aspect of the cervical vertebral body to decompress the intervertebral foramen with minimal bone removal. Twenty-four procedures were performed at C3-4, C4-5, and C5-6; 12 at C6-7; and 3 at C7-Tl. Facets and laminae structures were identified based on relative surgical perspectives. Bony resection was limited as follows: 1) inferior limit; inferior border of the superior facet; 2) superior limit, superior border of the superior facet; 3) lateral limit, a vertical line linking the junction of the lamina-facet to the lateral end of the superior limit; and 4) lateral aspect of the dural sac. Fluoroscopy was used to confirm that the intervertebral space was reached. The amount of bony removal was quantified for the superior and inferior laminae and facets. The length of the exposed nerve root was measured. The intervertebral foramen was exposed and the intervertebral disc reached in all specimens. Fluoroscopy showed that the center of the exposure remained at the same height with the intervertebral space. The mean length of the nerve root was 4.6 mm; the mean percentage of bony resection was 21.8%, 7.5%, 11.3%, and 11.5% for the superior and inferior laminae and facets, respectively. Opening the intervertebral foramen posteriorly consistently exposed sufficient nerve root length and allowed access to the intervertebral disc. The technique offers the most direct and safest method of decompressing the intervertebral foramen while minimizing bony resection. This simple surgical procedure may help reduce postoperative morbidity.     

Obstructive jaundice--an unusual complication of duodenal tuberculosis: treatment with transhepatic balloon dilatation

This is a report of a patient on treatment for duodenal tuberculosis, who developed obstructive jaundice due to a benign stricture of the terminal common bile duct. This complication of duodenal tuberculosis, to our knowledge, has not been reported before. Percutaneous, transhepatic balloon dilatation of the stricture alleviated the jaundice.     

Dipyridamole alone or combined with low-dose acetylsalicylic acid inhibits platelet aggregation in human whole blood ex vivo.

1. In a randomized, double-blind trial we compared the inhibition of the platelet-vessel wall interactions in whole blood ex vivo. There were four groups of 24 healthy volunteers each of whom were treated orally for 3.5 days with either 200 mg dipyridamole (sustained release preparation), 25 mg acetylsalicylic acid, both drugs combined or placebo twice daily. 2. The mean area of all platelets/aggregates was reduced by 6.2% +/- 4.2% (+/- s.e. mean) by placebo (n = 23), 19.8% +/- 6.7% by dipyridamole (n = 22), 53.7% +/- 4.9% by acetylsalicylic acid (n = 23) and 71.4% +/- 3.7% by the combination of both drugs (n = 24), when compared with total inhibition of aggregation by EGTA. Thus, low-dose acetylsalicylic acid inhibited aggregation (P less than 0.001). 3. Dipyridamole reduced the size of platelet aggregates (P less than 0.01, two-fold analysis of variance). The reduction was correlated with the individual dipyridamole plasma levels (P less than 0.05, analysis of covariance). The subgroup of large and very large thrombi being formed was also reduced by dipyridamole (P less than 0.05). 4. This ex vivo study demonstrates that dipyridamole alone inhibits formation of thrombi on subendothelial matrix and enhances the inhibitory effect of low dose acetylsalicylic acid in this model of thrombosis.     

A human recessive neurosensory nonsyndromic hearing impairment locus is a potential homologue of the murine deafness (dn) locus

A locus for recessive neurosensory nonsyndromic hearing impairmentmaps to chromosome 9q13–q21 in two regionally separateconsanguineous families from India. Each family demonstratesa LOD score greater than 4.5 to this region. D9S15, tightlylinked to the Friedreich's ataxia locus, a region that has beendefined with over 1 Mb of YAC contig information and severalexpressed sequences, is one of the flanking markers. In mice,the deafness (dn) locus maps to mouse chromosome 19 and flankingloci are syntenic to human chromosome 9q11–q21. The dnmouse is a potential model for the hearing impairment foundin both these families.