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ABSTRACT: Cabergoline is a potent, D2-selective new dopamine agonist with a half-life of 65 hours. We report two cases and review the literature on cabergoline in prolactinomas. Cabergoline appears to be more effective and better tolerated than bromocriptine, compliance may be improved, and costs are comparable. In cases of bromocriptine failure, unusually high starting doses of cabergoline may be necessary. Cabergoline may eventually replace bromocriptine as the drug of choice in prolactinomas.
07/2009; 22(1):37-46.
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ABSTRACT: Leber's Hereditary Optic Neuropathy is a mitochondrial genetic disorder that causes acute to subacute bilateral central loss of vision. It typically presents in young men in their second or third decade of life and onset later in life is rare. We describe a case of a 58-year-old man with late onset of LHON and discuss the importance of suspecting the diagnosis in appropriate cases.
07/2009; 32(1):41-42.
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ABSTRACT: Statins have recently been shown to exert neuronal protection in ischemic stroke. Reactive oxygen species, specifically superoxide formed during the early phase of reperfusion, augment neuronal injury. NADPH oxidase is a key enzyme for superoxide production. The present study tested the hypothesis that atorvastatin protects against cerebral infarction via inhibition of NADPH oxidase-derived superoxide in transient focal ischemia. Transient focal ischemia was created in halothane-anesthetized adult male Sprague-Dawley rats (250-300 g) by middle cerebral artery occlusion (MCAO). Atorvastatin (Lipitor, 10 mg/kg sc) was administered three times before MCAO. Infarct volume was measured by triphenyltetrazolium chloride staining. NADPH oxidase enzymatic activity and superoxide levels were quantified in the ischemic core and penumbral regions by lucigenin (5 microM)-enhanced chemiluminescence. Expression of NADPH oxidase membrane subunit gp91(phox) and membrane-translocated subunit p47(phox) and small GTPase Rac-1 was analyzed by Western blot. NADPH oxidase activity and superoxide levels increased after reperfusion and peaked within 2 h of reperfusion in the penumbra, but not in the ischemic core, in MCAO rats. Atorvastatin pretreatment prevented these increases, blunted expression of membrane subunit gp91(phox), and prevented translocation of cytoplasmic subunit p47(phox) to the membrane in the penumbra 2 h after reperfusion. Consequently, cerebral infarct volume was significantly reduced in atorvastatin-treated compared with nontreated MCAO rats 24 h after reperfusion. These results indicate that atorvastatin protects against cerebral infarction via inhibition of NADPH oxidase-derived superoxide in transient focal ischemia.
AJP Heart and Circulatory Physiology 12/2006; 291(5):H2210-5. · 3.71 Impact Factor
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ABSTRACT: Inducible NO synthase (NOS)-derived peroxynitrite (ONOO-) during ischemia/reperfusion contributes to ischemic brain injury. However, inducible NOS (iNOS) regulation in ischemic stroke remains unknown. Tetrahydrobiopterin (BH4) is an essential cofactor for NOS activity. The present study tested the hypothesis that inhibition of endogenous BH4 rate-limiting enzyme GTP cyclohydrolase I (GTPCH I), and thus BH4 synthesis, reduces cerebral infarction via inhibiting iNOS and ONOO- in transient focal ischemia.
Focal ischemia (2 hours) was created in adult male Sprague-Dawley rats (250 to 300 g) by middle cerebral artery occlusion (MCAO). Rats were treated 12 hours before MCAO with vehicle or diamino-6-hydroxypyrimidine (DAHP; 0.5 g/kg IP), a selective GTPCH I inhibitor. Brains were harvested 24 hours after reperfusion for assays of infarct volume, blood-brain barrier (BBB) permeability, GTPCH I activity, BH4 levels, GTPCH I and NOS mRNA, protein expression, and superoxide anion (O2*-) and ONOO- levels.
Endogenous GTPCH I activity, BH4 levels, iNOS activity, and (O2*- and ONOO- levels were all augmented after ischemia/reperfusion. DAHP treatment significantly reduced GTPCH I activity, resulting in decreased BH4 levels, iNOS activity, and ONOO- levels. Consequently, DAHP treatment significantly reduced the infarct size compared with the nontreated group (22.3+/-5.6 versus 38.3+/-7.4%; n=6; P<0.05). Similarly, BBB permeability was significantly reduced after DAHP pretreatment compared with the control group (4.11+/-0.22 versus 7.78+/-0.44 microg/g tissue; n=5; P<0.05).
These results demonstrate that blockade of endogenous brain BH4 synthesis attenuates cerebral infarction via inhibiting iNOS and ONOO-, which may provide a mechanistic basis of novel therapeutic strategies for ischemic stroke.
Stroke 01/2006; 36(12):2705-11. · 5.73 Impact Factor
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Archives of Ophthalmology 09/2005; 123(8):1155. · 3.71 Impact Factor
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Roy W Beck,
Craig H Smith,
Robin L Gal,
Dongyuan Xing,
M Tariq Bhatti,
Michael C Brodsky,
Edward G Buckley,
Georgia A Chrousos,
James Corbett,
Eric Eggenberger, [......],
John L Keltner,
Mark J Kupersmith,
Neil R Miller,
Pamela S Moke,
Sarkis Nazarian,
Silvia Orengo-Nania,
Peyer J Savino,
William T Shults,
Jonathan D Trobe,
Michael Wall
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ABSTRACT: Participants enrolled in the Optic Neuritis Treatment Trial have been observed for more than a decade to assess the relationship between optic neuritis and the development of clinically definite multiple sclerosis.
To assess neurologic disability 10 to 12 years after an initial episode of optic neuritis.
Longitudinal follow-up of a clinical trial.
Fourteen Optic Neuritis Treatment Trial clinical centers performed standardized neurologic examinations, including an assessment of neurologic disability.
One hundred twenty-seven patients who had developed clinically definite multiple sclerosis.
Functional Systems Scale and Expanded Disability Status Scale.
The disability of most patients was mild, with 65% of patients having an Expanded Disability Status Scale score lower than 3.0. The degree of disability appeared to be unrelated to whether the baseline magnetic resonance imaging scan was lesion-free or showed lesions (P =.51). Among patients with baseline lesions, the degree of disability was unrelated to the number of lesions that were present on the scan (P =.14). Two patients died owing to severe multiple sclerosis, one of whom had no lesions revealed on the baseline scan.
Most patients who develop clinically definite multiple sclerosis following an initial episode of optic neuritis will have a relatively benign course for at least 10 years.
Archives of Neurology 10/2004; 61(9):1386-9. · 7.58 Impact Factor
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Roy W Beck,
Robin L Gal,
M Tariq Bhatti,
Michael C Brodsky,
Edward G Buckley,
Georgia A Chrousos,
James Corbett,
Eric Eggenberger,
James A Goodwin,
Barrett Katz, [......],
Neil R Miller,
Pamela S Moke,
Sarkis Nazarian,
Silvia Orengo-Nania,
Peter J Savino,
William T Shults,
Craig H Smith,
Jonathan D Trobe,
Michael Wall,
Dongyuan Xing
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ABSTRACT: To assess visual function more than 10 years after an episode of optic neuritis in patients enrolled in the Optic Neuritis Treatment Trial.
Longitudinal follow-up of a randomized clinical trial.
Vision testing included measures of visual acuity, contrast sensitivity, and visual field. Quality of life was assessed with the National Eye Institute Visual Function Questionnaire.
Examinations were completed on 319 patients. In most patients, visual function test results in the eyes that experienced optic neuritis at study entry ("affected eyes") were normal or only slightly abnormal after 9.9 to 13.7 years. Visual acuity in the affected eyes was >or=20/20 in 74%, 20/25 to 20/40 in 18%, <20/40 to 20/200 in 5%, and <20/200 in 3%. On average, visual function was worse in patients with multiple sclerosis (MS) than in those without MS. Recurrent optic neuritis in either eye occurred in 35% of patients. Such attacks were more frequent in patients with MS (P <.001). The National Eye Institute Visual Function Questionnaire scores were lower when visual acuity was abnormal and when MS was present.
Most patients retained good to excellent vision more than 10 years after an attack of optic neuritis. Recurrences were more frequent in patients with MS.
American Journal of Ophthalmology 01/2004; 137(1):77-83. · 4.22 Impact Factor
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ABSTRACT: Migraineurs with visual aura are highly susceptible to illusions and visual distortion and are particularly sensitive to a pattern of regularly spaced parallel lines or stripes.
To determine whether the high degree of susceptibility to illusions and visual distortion in migraineurs with aura is associated with hyperneurological activity of the occipital cortex.
In order to investigate any relationships among neuronal activity, spatial frequency of square-wave gratings, and self-described visual distortion, we investigated the neuronal and psychophysical responses to square-wave gratings in migraineurs with visual aura and in nonheadache controls.
Square-wave gratings provoked various types of visual distortion and illusions and induced a hyperneuronal response in the visual cortex of migraineurs with visual aura, a response that strongly depended upon the stimulus spatial frequency.
The hyperneuronal activity of the occipital cortex is consistent with general cortical hyperexcitability in migraine.
Headache The Journal of Head and Face Pain 07/2003; 43(6):664-71. · 2.52 Impact Factor
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Roy W Beck,
Jonathan D Trobe,
Pamela S Moke,
Robin L Gal,
Dongyuan Xing,
M Tariq Bhatti,
Michael C Brodsky,
Edward G Buckley,
Georgia A Chrousos,
James Corbett, [......], David I Kaufman,
John L Keltner,
Mark J Kupersmith,
Neil R Miller,
Sarkis Nazarian,
Silvia Orengo-Nania,
Peter J Savino,
William T Shults,
Craig H Smith,
Michael Wall
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ABSTRACT: To identify factors associated with a high and low risk of developing multiple sclerosis after an initial episode of optic neuritis.
Three hundred eighty-eight patients who experienced acute optic neuritis between July 1, 1988, and June 30, 1991, were followed up prospectively for the development of multiple sclerosis. Consenting patients were reassessed after 10 to 13 years.
The 10-year risk of multiple sclerosis was 38% (95% confidence interval, 33%-43%). Patients (160) who had 1 or more typical lesions on the baseline magnetic resonance imaging (MRI) scan of the brain had a 56% risk; those with no lesions (191) had a 22% risk (P<.001, log rank test). Among the patients who had no lesions on MRI, male gender and optic disc swelling were associated with a lower risk of multiple sclerosis, as was the presence of the following atypical features for optic neuritis: no light perception vision; absence of pain; and ophthalmoscopic findings of severe optic disc edema, peripapillary hemorrhages, or retinal exudates.
The 10-year risk of multiple sclerosis following an initial episode of acute optic neuritis is significantly higher if there is a single brain MRI lesion; higher numbers of lesions do not appreciably increase that risk. However, even when brain lesions are seen on MRI, more than 40% of the patients will not develop clinical multiple sclerosis after 10 years. In the absence of MRI lesions, certain demographic and clinical features seem to predict a very low likelihood of developing multiple sclerosis. This natural history information is a critical input for estimating a patient's 10-year multiple sclerosis risk and for weighing the benefit of initiating prophylactic treatment at the time of optic neuritis or other initial demyelinating events in the central nervous system.
Archives of Ophthalmology 07/2003; 121(7):944-9. · 3.71 Impact Factor
