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Biomedical subjects

N M Ramadan

Publications and source records attributed to N M Ramadan.

15 recordsLinked to original sources
PubMed1992

Transcranial Doppler to evaluate the effects of antihypertensive medication on cerebral blood flow velocity.

The effect of oral nifedipine on cerebral blood flow velocity was studied in six elderly hypertensive patients using transcranial Doppler. Serial measurements of blood pressure (BP), middle cerebral artery (MCA) flow velocity and nifedipine serum concentrations were obtained over an 8-hour period. The authors found a significant inverse relationship between MCA velocities and nifedipine concentrations, independent of BP changes. These results are consistent with a direct vasodilatory effect of nifedipine on cerebral vessels and support the use of TCD in pharmacodynamic investigations of the cerebral vasculature.

Aged↗
PubMed1992

TCD and headache.

Explore the source record for details and available documents.

Blood Flow Velocity↗
PubMed1992

Headache in ischemic cerebrovascular disease. Part I: Clinical features.

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).

Brain Ischemia↗
PubMed1992

Human focal cerebral ischemia: evaluation of brain pH and energy metabolism with P-31 NMR spectroscopy.

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.

Acidosis↗
PubMed1992

NMR spectroscopic and magnetoencephalographic studies in migraine with aura: support for the spreading depression hypothesis.

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).

Cortical Spreading Depression↗
PubMed1992

Cerebral blood flow changes with enalapril.

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.

Age Factors↗
PubMed1991

Meningeal enhancement and low CSF pressure headache. An MRI study.

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.

Adult↗
PubMed1991

Assessing the effects of antihypertensive medication on cerebral blood flow: demonstration in internal carotid artery occlusion.

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.

Aged↗
PubMed1990

The concept of migraine as a state of central neuronal hyperexcitability.

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.

Adult↗
PubMed1989

Low brain magnesium in migraine.

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.

Adult↗
PubMed1989

Low brain magnesium in migraine.

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.

Adult↗
PubMed1989

Magnetic resonance and clinical cerebrovascular disease. An update.

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.

Animals↗