Imaging of stroke: Part 2, Pathophysiology at the molecular and cellular levels and corresponding imaging changes.

OBJECTIVE: Stroke is the third leading cause of death and the leading cause of severe disability. During the "decade of the brain" in the 1990s, the most promising development was the treatment of acute ischemic stroke. It is thought to result from a cascade of events from energy depletion to cell death. In the initial minutes to hour, clinical deficit does not necessarily reflect irreversible damage. The final outcome and residual deficit will be decided by how fast reperfusion is achieved, which in turn depends on how early the diagnosis is made. This article explains the pathophysiology of stroke at the molecular and cellular levels with corresponding changes on various imaging techniques. CONCLUSION: The pathophysiology of stroke has several complex mechanisms. Understanding these mechanisms is essential to derive neuroprotective agents that limit neuronal damage after ischemia. Imaging and clinical strategies aimed at extending the therapeutic window for reperfusion treatment with mechanical and pharmacologic thrombolysis will add value to existing treatment strategies. Acute ischemic stroke is defined as abrupt neurologic dysfunction due to focal brain ischemia resulting in persistent neurologic deficit accompanied by characteristic abnormalities on brain imaging. Knowledge of the pathophysiologic mechanisms of neuronal injury in stroke is essential to target treatment. Neuroprotective and thrombolytic agents have been shown to improve clinical outcome. Physiologic imaging with diffusion-weighted imaging (DWI) and perfusion CT and MRI provide a pathophysiologic substrate of evolving ischemic stroke.

Associations of birthweight and gestational age with reproductive and metabolic phenotypes in women with polycystic ovarian syndrome and their first-degree relatives.

CONTEXT: Low birthweight has been associated with metabolic and reproductive abnormalities in adults. OBJECTIVE: The aim of the study was to examine the relationship between birthweight and gestational age and its association with reproductive and metabolic phenotypes in women with PCOS and their first-degree relatives. DESIGN AND SETTING: We conducted a family-based study of PCOS at an academic health center. PATIENTS OR OTHER PARTICIPANTS: A total of 1038 individuals (845 females and 193 males) from the cohort and 168 controls participated in the study. MAIN OUTCOME MEASURES: The association between birthweight and familial phenotype was measured. RESULTS: Self-reported and actual birthweight were highly correlated [Spearman correlation coefficient (r) = 0.81; 95% CI, 0.66, 0.89; P = 0.001) and concordant (concordance correlation coefficient = 0.86; 95% lower limit = 0.78). We noted that birthweight for both genders in PCOS families and controls fell within the 10th and 90th percentiles for gestational age based on U.S. population norms. The 50th percentiles for a gestational age of 40 wk were very similar (3409 g in PCOS, 3455 g for controls, and 3495 g for the United States). There were no significant associations between phenotype and birthweight in PCOS probands. Furthermore, there were not any significant relationships between phenotype and birthweight in female or male family members of the PCOS probands. CONCLUSIONS: Birthweight in PCOS families mirrors control and U.S. population data, even corrected for gestational age, and has no substantive association with reproductive and metabolic abnormalities in women with PCOS, their female relatives, or their male relatives.

Postpartum sacral fracture in a 30-year-old female.

Possible causes of sacral and low back pain in the postpartum patient include sacroiliac joint dysfunction, sacroiliitis, lower lumbar diskitis, and irritation of the sciatic nerve. Postpartum stress fracture is a recognized cause of pain that should be considered in the differential diagnosis of the postpartum patient's low back pain. Several case reports of postpartum stress fracture are now in the literature (1, 2, 3, 4, 5, 6, 7, 8). A 30-year-old female presented postpartum with pain in the coccyx region that was most severe nine weeks after the uneventful spontaneous vaginal delivery of her first child. Imaging with computed tomography (CT) obtained 36 days after delivery demonstrated bilateral sclerosis in the lower sacrum. Plain film radiographs may not demonstrate this finding. Both magnetic resonance imaging (MRI) and CT are sensitive for sacral stress fracture.