Biomedical subjects
Publications and source records attributed to N M Ramadan.
Headache is a common, although under-emphasized, feature of ischemic cerebrovascular disease. In this review, we summarize the literature on the clinical features of headache in ischemic cerebrovascular disease (Part I) and elaborate upon the underlying mechanisms of the head pain (Part II--December issue).
In part I, the prevalence and clinical characteristics of headache in ischemic cerebrovascular disease were reviewed. In this part, we describe the potential mechanisms of head pain and the value of the headache symptom as a predictor of stroke type, location and vascular territory.
The authors investigated early human focal ischemia with phosphorus-31 nuclear magnetic resonance spectroscopy at 1.89 T to characterize the temporal evolution and relationship of brain pH and phosphate energy metabolism. Data from 65 symptomatic patients were prospectively studied; none of the patients had had ischemic stroke in the internal carotid artery territory before. Twenty-eight neurologically normal individuals served as control subjects. Serial ischemic brain pH levels indicated a progression from early acidosis to subacute alkalosis. When acidosis was present there was a significant elevation in the relative signal intensity of inorganic phosphate (Pi) and significant reductions in signal intensities of alpha-adenosine triphosphate (ATP) and gamma-ATP compared with those of control subjects. Ischemic brain pH values directly correlated with the relative signal intensity of phosphocreatine (PCr) and the PCr index and inversely correlated with the signal intensity of Pi. There was a general lack of correlation between either ischemic brain pH or phosphate energy metabolism and the initial clinical stroke severity. The data suggest a link between high-energy phosphate metabolism and brain pH, especially during the period of ischemic brain acidosis, and the authors propose that effective acute stroke therapy should be instituted during this period.
The authors propose that patients who suffer from migraine with aura have a susceptibility to spontaneous neuronal discharges and subsequent spreading depression. This is based upon a state of central neuronal excitability involving the excitatory neurotransmitter glutamate, in combination with supersensitivity of the N-méthyl-D-aspartate (NMDA) receptor. This hypersusceptibility is supported by increased turnover of high-energy phosphates, low intracellular Mg2+ and large amplitude depolarizing waves on magnetoencephalography (MEG).
Patients with carotid artery occlusive disease (CAOD) may be at increased risk of iatrogenic cerebral hypoperfusion. Using the 133xenon-inhalation technique, we evaluated the effects of enalapril on regional cerebral blood flow (CBF) in 14 patients with chronic hypertension, 7 with CAOD and 7 without CAOD (no CAOD). Regional CBF and blood pressure were measured before and 60 minutes after a single dose of enalapril. Changes in mean arterial pressure after enalapril were not significantly different between the two groups: CAOD -4.67 +/- 8.7 mm Hg, no CAOD -6.18 +/- 8.2 mm Hg. Changes in mean CBF after enalapril were also not statistically different: CAOD -1.0 +/- 3.9, no CAOD 1.0 +/- 2.8. In the CAOD group only, however, changes in CBF were significantly related to increasing age (r = -0.9253, p less than 0.01), such that in patients 65 years or older CBF tended to decrease, whereas in younger patients it increased. Elderly patients with CAOD may be at increased risk of iatrogenic cerebral hypoperfusion, and it may be appropriate to evaluate prospectively the effects of antihypertensive medications on CBF.
A 34-year-old woman developed severe and incapacitating positional headaches two weeks following a minor head trauma. Lumbar punctures demonstrated unmeasurable or very low CSF pressures. Gadolinium-enhanced cranial MRI showed diffuse enhancement of thickened meninges, suggesting inflammation. One year later, MRI was normal.
Dynamic cerebral blood flow (CBF) studies using acetazolamide or hypercapnia as a vasodilatory challenge have attempted to evaluate intracranial hemodynamics. We report two patients with asymptomatic internal carotid artery occlusion in whom the vasodilatory stimulus was a single oral dose of antihypertensive medication (prazosin hydrochloride or enalapril maleate). In both patients, changes in regional CBF occurred that were larger than those seen in nine normal controls. One patient experienced an improvement in regional CBF with a reduction in probe pair asymmetry. In the other patient, who had bilateral carotid artery disease, a decrease in regional CBF in all 16 probes (mean decrease 12 percent) and an accentuation of the predose asymmetry were observed. Both patients remained asymptomatic throughout the study. Assessing these effects on cerebral circulation may help identify patients at risk for iatrogenic focal cerebral ischemia and provide information regarding the functional status of the cerebral vasculature.
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We report three cases of cervical internal carotid artery (ICA) dissection, which presented with visual symptoms resembling the migraine aura. When prolonged and especially when associated with other neurologic symptoms, such transient and positive visual phenomena can be manifestations of ICA dissection that mimic migraine.
This article explores the hypothesis that migraine with aura is associated with a state of central neuronal hyperexcitability. The authors propose that this central neuronal hyperexcitability involves overactivity of the excitatory amino acids, glutamate, and possibly aspartate. Stimuli that activate the migraine attack evoke neuronal depolarization, slow depolarization shifts, and spreading suppression of spontaneous neuronal activity possible by glutamate and K+ dependent mechanisms. A low brain Mg2+ and consequent reduced gating of glutamatergic receptors may provide the link between the physiologic threshold for a migraine attack and the mechanisms of the attack itself by promoting glutamate hyperactivity, neuronal hyperexcitability, and susceptibility to glutamate-dependent spreading depression.
Brain magnesium was measured in migraine patients and control subjects using in vivo 31-Phosphorus Nuclear Magnetic Resonance Spectroscopy. pMg and pH were calculated from the chemical shifts between Pi, PCr and ATP signals. Magnesium levels were low during a migraine attack without changes in pH. We hypothesize that low brain magnesium is an important factor in the mechanism of the migraine attack.
Brain magnesium was measured in migraine patients and control subjects using in vivo 31-Phosphorus Nuclear Magnetic Resonance Spectroscopy. pMg and pH were calculated from the chemical shifts between Pi, PCr and ATP signals. Magnesium levels were low during a migraine attack without changes in pH. We hypothesize that low brain magnesium is an important factor in the mechanism of the migraine attack.
MRI is becoming the imaging modality of choice in patients with ischemic cerebrovascular disease although CT is still the test of choice to exclude acute hemorrhagic stroke. We have briefly reviewed characteristic features of ischemic and hemorrhagic cerebrovascular disease as well as vascular anomalies as seen on MRI. In time MRS should provide useful noninvasive metabolic data to complement the anatomical data in patients with cerebrovascular disease.
STUDY OBJECTIVE: To determine the short-term effects of antihypertensive therapy on cerebral blood flow (CBF). DESIGN: Prospective, observational study. SETTING: A university-affiliated teaching hospital. PATIENTS: Twenty-four patients (age range 53-85 yrs) with chronic hypertension, nine of whom had carotid artery occlusive disease (CAOD). INTERVENTIONS: The CBF (xenon-133 inhalation technique) and blood pressure were measured before and at 60 minutes after administration of antihypertensive therapy. MEASUREMENTS AND MAIN RESULTS: Age was inversely related to the change in CBF in patients with CAOD (p < 0.01). In all patients, the change in CBF after taking antihypertensive drugs was significantly inversely associated with baseline CBF (p < 0.01). Changes in regional CBF, measured by asymmetry scores, were significantly greater in patients with CAOD than in those without CAOD (p < 0.05). CONCLUSIONS: Elderly patients with occlusive extracranial cerebrovascular disease are at risk of drug-induced changes in both mean and regional CBF, and may benefit from a CBF assessment before being prescribed antihypertensive therapy.
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