Balloon Test Occlusion of the Carotid Artery: Internal Validation of Predictive Results.

AIM: To develop a protocol of balloon test occlusion (BTO) to perform single-photon emission computed tomography (SPECT) only in cases that require it by using mean stump pressure (MSTP). MATERIAL AND METHODS: BTO was performed in 52 consecutive patients (derivation group). Using the derivation group data, a protocol was created and applied to 55 consecutive patients (validation group). RESULTS: In the derivation group, all patients with MSTP ≥65 mmHg had an ischemic tolerance, whereas those with MSTP ?45 mmHg were considered ischemic intolerant. Based on these results, we developed a protocol wherein MSTP between 45 mmHg and 65 mmHg was defined as "ischemic borderzone" and SPECT was performed in these cases. Using this protocol, BTO was performed in the validation group and 19 patients were treated with parent artery occlusion with or without bypass. In two cases that did not follow the protocol, the occurrence of hypoperfusion caused cerebral infarction after treatment. However, if this protocol had been followed for all cases, no false-negative cases of BTO would have occurred. CONCLUSION: By measuring MSTP and identifying the approximate ischemic tolerability, the current protocol can identify cases requiring SPECT, which is particularly reliable but complicated. Moreover, this protocol would be especially useful for reducing false-negative cases of BTO.

Usefulness of dual and fully automated measurements of cerebral blood flow during balloon occlusion test of the internal carotid artery.

BACKGROUND: This study was conducted to show the reliability of fully automated quantification of regional cerebral blood flow (rCBF) in balloon occlusion test (BOT) of the internal carotid artery (ICA). We also shows the usefulness of ratio of rCBF during BOT to rCBF at rest (BOT/rest ratio = rCBF during BOT/rCBF at rest) rather than asymmetry index (AI) during BOT (AI = occluded-side rCBF/contralateral rCBF). METHODS: In the last 2 years, we performed the BOT on 10 consecutive patients (4 with intracranial aneurysms and 6 with head and neck tumors). During the BOT, mean stump pressure (MSTP) of the ICA was monitored. We measured cerebral blood flow (CBF) with technetium-99m hexamethylpropylene amine oxime single-photon emission computed tomography at rest and during BOT. rCBF was determined using 3-dimensional stereotaxic region of interest template (3DSRT) which automatically divided CBF into 12 segments. We defined hypoperfusion segment as BOT/rest ratio <0.9 or AI <0.9. RESULTS: When the BOT/rest ratio was used as a hypoperfusion parameter, the number of hypoperfusion segments was significantly greater in patients with an MSTP ≤50 mm Hg than in patients with an MSTP >50 mm Hg. However, only AI during BOT did not reflect MSTP significantly. CONCLUSIONS: The evaluation of CBF changes in BOT using 3DSRT and the BOT/rest ratio were useful because of objective comparison.

Deficiency of the tensin2 gene in the ICGN mouse: an animal model for congenital nephrotic syndrome.

The ICGN mouse is a model for nephrotic syndrome (NS) which presents with proteinuria, hyperlipidemia, and edema. In this study we attempted to identify the gene(s) responsible for NS. By analyzing albuminuria in 160 (ICGN x MSM)F(1) x ICGN backcross progenies, we found that NS in the ICGN mouse is caused by more than one gene. We then performed a quantitative trait locus (QTL) analysis and detected a QTL with a very high LOD score peak in the telomeric region of Chr 15. By analyzing the nucleotide sequence of 22 genes located close to the QTL, we found that the tensin2 gene of the ICGN mouse possessed an 8-nucleotide deletion mutation in exon 18, leading to a frameshift and giving rise to a terminal codon at a premature position. Analyses of in situ hybridization and immunohistochemistry revealed that tensin2 was expressed in podocytes and tubular epithelial cells in normal mice but not in the ICGN mouse. These data raise the possibility that a mutation of the tensin2 gene is responsible for NS of the ICGN mouse and tensin2 is a prerequisite for the normal kidney function.