Rapid MRI of the molecular diffusion of water demonstrated cerebral infarcts in 32 patients. We studied these patients at various times following the onset of ischemic symptoms and found that diffusion-weighted imaging revealed the infarcts sooner than conventional T2-weighted spin-echo imaging did; four hyperacute infarcts were shown only by diffusion-weighted imaging. Acute infarcts had lower apparent diffusion coefficients (ADCs) than noninfarcted regions did. This relative difference in ADC reached a nadir in the first 24 hours and rose progressively thereafter. Chronic infarcts showed a relative increase in diffusion and were readily distinguishable from acute infarcts. The technique takes less than 2 minutes to apply using a standard 1.5-tesla scanner in the clinical setting. Diffusion-weighted imaging has the potential to play a role in improving the early anatomic diagnosis of stroke and therefore in the development and implementation of early stroke interventions.

The authors assessed regional cerebral blood flow dynamics with magnetic resonance (MR) imaging enhanced with gadolinium diethylenetriaminepentaacetic acid (DTPA). After bolus administration of Gd-DTPA, rapid T2*-weighted gradient-echo images were acquired. Image acquisition time ranged from 2 to 3 seconds. The signal intensity (SI) of brain tissue and blood vessels markedly decreased during the first pass of contrast agent through the brain due to the local field inhomogeneity caused by the concentrated paramagnetic contrast agent. The method was used in 18 subjects with no cerebrovascular disease and 32 patients with stroke, vascular stenosis, arteriovenous malformation, and cerebral neoplasm. Comparison with intracranial angiography was performed in three patients and with single-photon emission computed tomography of blood flow in four. The change in T2* relaxation rate was approximately linearly related to the dose of contrast agent. The SI change increased as the echo time was lengthened. Regions in cerebral infarcts, metastases, and arteriovenous malformations showed different enhancement patterns than those of edema around a lesion and of normal brain tissue. Abnormal circulation times in patients with vascular stenoses were demonstrated. The method provides information about cerebral blood flow dynamics not available from conventional MR imaging and MR angiography.

Background: Intracranial arteries in the subarachnoid space may compress the brain parenchyma and cranial nerves. Most arterial compressive lesions have been attributed to dolichoectasia in the vertebral-basilar system, and prior reports have concentrated on the pressure effects of basilar artery ectasia. Much less is known about vertebral artery compression of the medulla. Objective: To describe a series of patients with vertebral arteries compressing the medulla oblongata. Design: Prospective case studies. Setting: Tertiary care center. Patients: Nine symptomatic patients, 4 men and 5 women, between the ages of 32 and 79 years. Main Outcome Measures: Clinical phenomena, radiographic findings, treatment, and outcomes. Results: We found that compression most commonly occurs at the ventrolateral surface. The clinical features can be transient or permanent and are predominantly motor and cerebellar or vestibular, but a poor correlation exists between the clinical findings and the severity or extent of impingement. The vertebral arteries were angulated, tortuous, or dilated but not necessarily dolichoectatic to cause obvious indentation. Seven patients were treated with antiplatelets and anticoagulants or analgesics, whereas 2 underwent microvascular decompression, resulting in temporary or no relief. One surgical patient developed cranial nerve complications. Among the medically treated patients, none had progression of deficits, and those with single episodes had no recurrence of symptoms. Conclusion: This study is the largest collection, to our knowledge, of patients with medullary vascular compression. Further studies are needed to estimate its frequency, natural course, and preferred management.

Dynamic contrast-enhanced T2-weighted magnetic resonance (MR) imaging and MR angiography (MRA) were used to evaluate cerebral blood volume and the intracranial arterial system in 34 patients within 48 hours after the onset of cerebral ischemia. In 24 of the patients, an abnormality identified on T2-weighted images corresponded to the acute clinical deficit. Intracranial MRA demonstrated occlusions or severe stenoses of major vessels supplying the area of infarction in 16 of these patients, and decreased blood volume correlated well with MRA abnormalities. Infarcts less than 2 cm in diameter were not reliably shown with MRA or blood volume studies. Correlation between lesions seen with MRA and decreased blood volume in acute infarcts was good, and both techniques demonstrated lesions early in the clinical course. By providing information about hemodynamics not available with conventional T1- or T2-weighted images, MRA and dynamic MR imaging could prove helpful in describing the pathophysiologic characteristics of stroke and in guiding early therapeutic intervention.

Reproductive and sexual dysfunction in men with epilepsy has been attributed to androgen deficiency. Low serum free testosterone (FT) levels occur in both hypogonadotropic and hypergonadotropic hypogonadism. Antiepileptic drugs (AEDs) have been implicated. Proposed mechanisms include induction of increased sex hormone binding globulin (SHBG) resulting in decreased FT, as well as dysfunction or premature aging of the hypothalamopituitary-gonadal axis. In an investigation comparing serum reproductive steroid levels among 20 men receiving phenytoin (PHT) monotherapy for complex partial seizures, 21 untreated men with complex partial seizures, and 20 age-matched normal controls, total estradiol levels were significantly higher in the PHT group (56.3 +/- 29.4 pg/ml, mean +/- SD) than in the untreated (32.4 +/- 27.4 pg/ml, p less than 0.01) and normal control (34.3 +/- 12.7 pg/ml, p less than 0.05) groups. The physiologically active non-SHBG-bound serum estradiol levels were also significantly higher in the medicated group (45.1 +/- 21.7 pg/ml) than in the untreated (29.9 +/- 17.2 pg/ml, p less than 0.01) and normal control (31.1 +/- 11.4 pg/ml, p = 0.05) groups. These findings suggest that PHT may lower FT by induction of aromatase, enhancing FT conversion to estradiol, as well as SHBG synthetase. Estradiol exerts a potent inhibitory influence on luteinizing hormone secretion and has been suggested to play a major role in negative feedback in men as well as women. Suppression of LH secretion results in hypogonadotropic hypogonadism. Chronically low FT leads to testicular failure and hypergonadotropic hypogonadism. Finally, estradiol has been shown to produce premature aging of the hypothalamic arcuate nucleus, which secretes gonadotropin-releasing hormone.