Brain SPECT and transcranial doppler ultrasound in vasospasm-induced delayed cerebral ischemia after subarachnoid hemorrhage.

Clinical vasospasm, or delayed ischemia-related neurologic deficits, is the prime determinant of morbidity and mortality after subarachnoid hemorrhage. The diagnosis of clinical vasospasm has been based mainly on clinical observations. Noninvasive techniques for evaluating vasospasm have great promise in supplementing the detailed neurologic examination and assessing the effects of therapy. The clinical utility of single-photon emission computed tomography (SPECT) of regional cerebral blood flow and transcranial Doppler ultrasound (TCD) in the evaluation of cerebral vasospasm after subarachnoid hemorrhage was reviewed in 40 patients. The combination of these noninvasive tests was valuable for the investigation of the dynamic anatomic and functional aspects of vasospasm. TCD proved helpful in monitoring for vascular narrowing by measurements of blood flow velocity. Brain SPECT ascertained the effects of vasospasm on regional cerebral blood flow. In the diagnosis of clinical vasospasm, or delayed ischemic deficits, brain SPECT was more sensitive and specific than TCD. The combination of SPECT and TCD was useful in the assessment of the effect of cerebral angioplasty on hemodynamics and perfusion in the attempt to avert infarction.

Bone matrix and mineral abnormalities in postmenopausal osteoporosis.

Iliac crest biopsies from 56 postmenopausal osteoporotic females with spontaneous compression fractures and decreased total body Ca were compared to similar tissue from 48 normal controls. Biopsies were analyzed for bone density, Na, Ca, Mg, P, Co3, and hydroxyproline (OH-P). From the results OH-P/matrix, % mineral, and the ion content of the mineral were calculated. osteoporotic subjects showed decreased bone density, % mineral in bone, and OH-P in the bone matrix. Within the mineral, CO3 and Ca/P were decreased, while Na and Mg were increased. Statistical analysis showed that matrix OH-P and % mineral varied independently, and therefore the patients were separated into 4 subgroups: Group Ia: decreased matrix OH-P with normal % mineral (n = 9), Group Ib: decreased matrix OH-P with decreased % mineral (n = 5), Group IIa: normal matrix OH-P with normal % mineral (n = 33), Group IIb: normal matrix OH-P with decreased % mineral (n = 9). Decreased % mineral was associated with decreased bone density and an increase in Na and Mg in the mineral, which suggests skeletal Ca deficiency. Decreased matrix OH-P was associated with decreased bone density and, in the low % mineral group, with decreased mineral CO3 and Ca/P, suggesting a mineral of decreased mean crystal size. When both abnormalities coexisted (Group Ib), the greatest reduction in total body Ca was seen. Patients with normal matrix and normal % mineral (Group IIa) still had decreased bone density. The results suggest that in a large, clinically homogeneous population of postmenopausal osteoporotic women, 4 subgroups can be identified by differences in chemical composition of iliac crest biopsies.

Reduction in high density lipoproteins by anabolic steroid (stanozolol) therapy for postmenopausal osteoporosis.

The effects of stanozolol, 17-methyl-2H-5 alpha-androst-2-eno [3,2-c] pyrazol-17 beta-ol, on lipoprotein levels were assessed in a short-term (6 wk) prospective study of 10 normolipidemic, postmenopausal, osteoporotic women. While total cholesterol and triglyceride levels remained constant, equal and offsetting responses were seen in low density lipoprotein (LDL) cholesterol (+30.9 +/- 28.1 mg/dl [mean +/- S.D.], p less than 0.01, a 21% increase) and high density lipoprotein (HDL) cholesterol (-32.5 +/- 11.9 mg/dl [mean +/- S.D.], p less than 0.001, a 53% decline). Hence the LDL/HDL ratio increased dramatically, from 2.5 +/- 0.7 to 6.8 +/- 2.5. Within HDL, stanozolol was associated with a greater decline in HDL2 (from 26.0 +/- 7.4 mg/dl to 3.8 +/- 1.9 mg/dl, p less than 0.001, an 85% decrease) than HDL3 (which diminished from 35.7 +/- 3.2 to 24.1 +/- 5.8 mg/dl. p less than 0.001, a 35% decrease). The major HLD apolipoproteins also declined (A-I by a mean of 41% and A-II by 24%, both p less than 0.001). Postheparin hepatic triglyceride lipase increased (off treatment 74 +/- 42 nmole free fatty acid min-1 mole-1, on treatment 242 +/- 110, n = 6, p = 0.06). All changes were reversed by 5 wk following termination of the drug. These lipoprotein changes suggest caution in the long term prescription of stanozolol, particularly in those without overriding clinical indications for its use.

Evaluation of noninvasive tests of cardiac damage in suspected cardiac contusion.

Nonpenetrating trauma to the chest can result in cardiac damage that may be overlooked because of associated injuries and the lack of obvious thoracic injury. The clinical diagnosis of important cardiac damage in this setting is difficult. We evaluated noninvasive tests for detecting myocardial damage in 100 patients with severe, nonpenetrating chest trauma. The noninvasive tests included serial ECG, serial total CPK and CPK-MB enzymes, continuous Holter monitor recording to detect dysrhythmia, and technetium-99m pyrophosphate scintigraphy. Peak CPK-MB elevations occurred in 72 patients. ECG abnormalities were noted in 70 patients, and 27 patients had Lown grade 3 or greater dysrhythmias. Fifteen patients died and all had autopsies. The noninvasive abnormalities were nonspecific and did not reflect myocardial contusion that led to clinically important cardiac complications.