Paradoxical worsening of spasticity and pain in the lower extremities after increasing the dose of intrathecal baclofen--case report.

OBJECTIVES: Some patients with spasticity and pain in the extremities fail to respond to increases in the dose of intrathecally delivered baclofen. MATERIALS AND METHODS: We report a 78-year-old man with severe spasticity and pain in the lumbar region and both lower extremities because of ossification of the posterior longitudinal ligament, spinal canal stenosis, and cerebral infarction. He was severely disabled and bedridden. Earlier surgical interventions (spinal cord stimulation and deep brain stimulation) had failed. RESULTS: He underwent a screening test for intrathecal baclofen (ITB) therapy. The intrathecal injection of 50 µg baclofen severely aggravated his spasticity and pain and concomitantly elicited myoclonic-like involuntary movements in both lower extremities. Although 25 µg baclofen produced similar results, overt improvements were obtained with 12.5 µg, and he underwent implantation of an ITB pump. His spasticity and pain responded to initial daily doses of 12.5 µg. To obtain further improvements, we gradually increased the daily dose to 40 µg; however, this severely increased his spasticity and pain in both lower extremities and concomitantly elicited myoclonic-like involuntary movements. He is being maintained on a daily dose of 20 µg/day. CONCLUSIONS: We suggest that in patients who experience symptom aggravation at increased ITB doses, potential causative factors and ITB system malfunction should first be ruled out, and consideration should then be given to decreasing the ITB dose.

Low-dose of statin treatment improves cerebrovascular reactivity in patients with ischemic stroke: single photon emission computed tomography analysis.

BACKGROUND: Statins, 3-hydroxy-3-methylglutaryl-coenzymeA reductase inhibitors, have pleiotropic effects that are independent of their cholesterol-lowering activities. For example, they improve vascular endothelial function and exert anti-inflammatory effects. In large clinical trials they reduced the incidence of stroke and myocardial infarction; however, little is currently known regarding the mechanism or mechanisms underlying their clinically confirmed stroke protection. PATIENTS AND METHODS: We assessed 10 patients who had experienced a stroke at least 6 months earlier; they received low-dose (5 mg) simvastatin. Using our triple-injection technetium 99m-ethylcysteinate dimer method, we determined their cerebral blood flow and cerebrovascular reactivity. A second assessment of at-rest cerebral blood flow and cerebrovascular reactivity was performed 4 or more months (mean 6 months) after the start of statin administration. We used acetazolamide (1 g) as the vasodilator. The region of interest was the middle cerebral artery territory on a 3-dimensional stereotaxic region of interest template. RESULTS: Statin administration did not significantly affect the regional cerebral blood flow at rest. Before statin treatment, the patients' vasoreactivity, determined by the triple-injection technetium 99m-ethylcysteinate dimer method, demonstrated delayed, poor, or near-normal response patterns. Statin treatment improved vasoreactivity in all patients. Their mean serum total cholesterol level before statin administration was 200 mg/dL (range 187-256 mg/dL). Statin treatment significantly reduced their mean serum total cholesterol to 180 mg/dL (range 128-220 mg/dL) (P < .01). CONCLUSIONS: The clinically confirmed stroke protection activity exerted by statins may be attributable to improved cerebrovascular reactivity.

Evaluation of delayed appearance of acetazolamide effect in patients with chronic cerebrovascular ischemic disease: feasibility and usefulness of SPECT method using triple injection of ECD.

UNLABELLED: The purpose of this study was to verify the feasibility and usefulness of a new SPECT method, called triple injection of (99m)Tc-ethylcysteinate dimer (TIE), in evaluation of the delayed or poor appearance of acetazolamide (ACZ) effects in patients with chronic cerebral ischemic disease. METHODS: Three equal-volume splits of (99m)Tc-ethylcysteinate dimer were intravenously administered, and 1,000 mg ACZ were used as a vasodilator. A middle cerebral artery territory in the lateral ventricle was used as a region of interest. The data at rest and at 7.5 and 20 min after ACZ challenge (ACZ 7.5 and ACZ 20, respectively) were obtained by dynamic SPECT, and a time response curve to ACZ was obtained through the relative ratio of regional counts to the data at rest, not through regional cerebral blood flow. Nine cases of complete occlusion of the internal carotid artery (IC) and 6 cases of severe IC stenosis were analyzed. RESULTS: In 12 healthy volunteers (24 cerebral hemispheres) using a placebo (negative control), the values at rest and at rest 7.5 and rest 20 (corresponding to ACZ 7.5 and ACZ 20, respectively) were 100%, 100.4% +/- 2.8%, and 99.6% +/- 3.6%, respectively, indicating the accuracy of the TIE method. In a positive control using 24 normal cerebral hemispheres, prompt maximal vasoreactivity at ACZ 7.5 (124.5% +/- 8.0%) was confirmed, as was continuous vasoreactivity until ACZ 20 (130.1% +/- 12.8%). The values between ACZ 7.5 and ACZ 20 were not statistically different. Patients with complete IC occlusion exhibited a poor response at ACZ 7.5 despite a normal response at ACZ 20 (delayed response). Furthermore, in patients with severe IC stenosis, restoration of cerebrovascular reactivity after carotid endarterectomy was confirmed not only at ACZ 20 but also at ACZ 7.5. CONCLUSION: The TIE method using SPECT may be a potentially useful and sensitive strategy in clinical evaluation of the delayed or poor appearance of ACZ effects in patients with chronic cerebrovascular ischemic disease.