Subcortical infarctions, transcranial Doppler, and cerebral vasomotor reactivity.
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Biomedical subjects
Publications and source records attributed to D A Dulli.
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Although anterior circulation transient ischemic attacks (TIAs) tend to be more common in patients with extra- cranial carotid arterial disease than in those with intracranial carotid or middle cerebral arterial disease, the authors recently encountered 4 patients with both recurrent, stereotypical TIAs as well as isolated stenosis of their petrous internal carotid artery (ICA). While the gold standard for establishing the diagnosis of intracranial large-artery disease has always been conventional angiography, magnetic resonance angiography changes, confirmed with intra-arterial digital subtraction angiography in 2 of these patients, were quite sufficient to define the occlusive disease in each of the cases. Petrous ICA stenosis is not uncommon, but it has often been overshadowed by the search for extracranial ICA disease that might be amenable to surgical reconstruction.
Although acute stroke is a common presentation to an emergency room, the presentation of a patient with acute ischemic stroke, within a limited time window as an appropriate candidate for cerebral thrombolysis, is not common. In many of these patients, their candidacy can be improved through community education toward emergent transfer to an emergency room if they manifest symptoms of stroke. This would improve the "symptom-to-door" time. Another goal is to improve the recognition and approach of the hospital itself toward improving the "door-to-drug" time in appropriate patients. The obstacle to this second goal does not seem to be a nihilistic or evasive attitude on the basis of this study. Contrary to what was expected, enthusiasm for the use of cerebral thrombolysis was found in emergency physicians of all hospital categories, particularly of small remote hospitals. Instead, educational initiatives should focus on the facilitation of protocols for present and future ischemic stroke therapy, particularly in larger remote facilities that may be more self-dependent in their approach to acute stroke. An equally important focus should be toward more active participation by local neurologists who may be available for acute stroke care. Further, as this study demonstrates a correlation between the involvement of a local neurologist and the use of a stroke protocol, neurologists of non-tertiary facilities should be recruited to participate in these educational initiatives.
OBJECTIVE: To critically evaluate the literature regarding naratriptan's clinical pharmacology, efficacy, safety, and indications. DATA SOURCE: A MEDLINE search was conducted for the period from January 1990 to June 1998. Key words used included naratriptan, triptan, serotonin agonists, migraine, and migraine therapy. In addition, pertinent references cited in articles obtained from MEDLINE and product information for triptans were reviewed. STUDY SELECTION AND DATA EXTRACTION: All original and review articles and abstracts pertaining to naratriptan were reviewed, as were product information extracts. Clinical trials of naratriptan were critically reviewed and compared with pertinent clinical trials of other oral triptans. DATA SYNTHESIS: The treatment of migraine has been dramatically improved with the use of sumatriptan, other triptans, and serotonin-receptor subtype 1B and 1D agonists. Drawbacks to these medications, however, have included poorly tolerated adverse effects and the recurrence of the migraine. Naratriptan has been recently approved for acute oral migraine therapy. In two Phase III trials of naratriptan compared with placebo, relief at four hours was obtained in 60% and 68% of patients using the 2.5-mg dose, with recurrence of headache in 24 hours in 27% and 28% of patients. The data on migraine recurrence were similar to those of other oral triptans; the efficacy of naratriptan at two hours was not specifically analyzed. Adverse effects of naratriptan were similar to placebo, and its tolerability seemed superior compared with studies of other oral triptans. CONCLUSIONS: Naratriptan is a promising new oral therapy for acute migraine; it may successfully treat patients who poorly tolerate other triptan therapies or have longer duration migraine headaches.
Nine patients (group A) were found on magnetic resonance angiography (MRA) to have excessive carotid artery, vertebral artery, and vertebrobasilar junction tortuosity. A control group (group B) were age- and sex-matched to group A patients, were selected randomly from our MRA or stroke data banks, and had not undergone MRA for evaluation of migraine, "carotidynia," or pulsatile tinnitus. Factors more prevalent in group A patients included migraine, chronic daily headache, carotidynia, pulsatile tinnitus, and a positive family history of headache. Factors more prevalent in group B patients included a positive family history of stroke, large-vessel atherosclerosis, and scan evidence of ischemic infarctions; many group B patients had undergone MRA for stroke or transient ischemic attack evaluation. Men were slightly underrepresented at 44%, and were younger than women (34 +/- 6 years vs. 43 +/- 3 years; p = 0.01). Relationships in this preliminary study between arterial tortuosity and migraine seem evident.
This study measured the responses of both extracranial (internal carotid arteries) and intracranial (middle cerebral/angular, basilar arteries) intravascular arterial volume flow rates to acetazolamide using phase-contrast magnetic resonance angiography. Twenty-eight newly studied patients were subdivided into four groups: Group I--Nonocclusive, asymptomatic (n = 7, or 14 carotid and middle cerebral/angular artery sides); Group II--unilateral carotid transient ischemic attacks, nonhemodynamic (embolic), varying stenoses (n = 11); Group III--unilateral carotid transient ischemic attacks, hemodynamic, varying stenoses (n = 5); and Group IV--unilateral carotid occlusion, asymptomatic (n = 5). The data were separated into nonischemic and ischemic sides so as to illustrate group differences based on vasodilatory responses to acetazolamide. For example, the percent change in volume flow rates over baseline values for the ischemic-side middle cerebral arteries of Group III was significantly the lowest of all of the vasodilatory responses (-25 +/- 11% vs 40 +/- 14% for group II ischemic middle cerebral/angular artery sides, p = 0.008). Group III patients also had significantly lower standing blood pressures (p = 0.012), higher number of transient ischemic attacks (p = 0.008), and shorter duration of events (p = 0.013). Determinations of volume flow rate continue to assist in determining the degree of hemodynamic compromise of a particular vascular territory.
BACKGROUND: Activated protein C resistance (APC-R) due to factor V Leiden has recently been established as an important risk factor for cerebral venous thrombosis (CVT). The clinical significance of abnormal or borderline functional APC-R in the absence of factor V Leiden is uncertain. Our observations suggest that APC-R due to mechanisms other than factor V Leiden may also contribute to the development of CVT. CASE DESCRIPTIONS: We describe three women who had superior sagittal and lateral sinus thrombosis while taking oral contraceptives and had a number of additional risk factors for CVT. Each had APC-R for different reasons. CONCLUSIONS: Inherited thrombophilia, including APC-R, should be looked for in all patients with CVT. Functional APC-R is a highly prevalent coagulopathy, but the reasons for this abnormality are diverse; abnormal and borderline functional APC-R results should be supplemented by DNA analysis for the presence of factor V Leiden.
Nineteen patients with strictly unilateral ischemic stroke as determined by clinical examination, computed tomography, magnetic resonance imaging, and standard angiography underwent cerebral blood flow (CBF) analysis using fluorine 18 fluoromethane and positron emission tomography. Mean flow values for averaged hemispheric, infarct, and homologous contralateral regions of interest (ROIs) were determined. All patient CBF values were significantly below comparable CBF ROIs in neurologically normal controls using Wilcoxon's two-sample rank testing. Multiple regression analysis disclosed a significant correlation between contralateral CBF are both localized CBF in the infarct ROI and patient age. Correlations between contralateral CBF and dependency score or severity of neurologic deficit at time of positron emission tomography, expired PCO2, mean arterial blood pressure, serum glucose or hematocrit, risk factor score, and number of days studied after stroke were not statistically significant. Although we did not identify the biologic mechanisms involved, we conclude that CBF reduction contralateral to a strictly unilateral ischemic infarction is due to a combination of aging and transhemispheric diaschisis.
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