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Biomedical subjects

M Leopold

Publications and source records attributed to M Leopold.

6 recordsLinked to original sources

The interrelations of migraine, vertigo, and migrainous vertigo.

OBJECTIVE: To assess the prevalence of migrainous vertigo in patients with migraine and in patients with vertigo according to explicit diagnostic criteria that are presented for discussion. METHODS: The authors prospectively evaluated 200 consecutive patients from a dizziness clinic and 200 patients from a migraine clinic for migrainous vertigo based on the following criteria: 1) recurrent vestibular symptoms (rotatory/positional vertigo, other illusory self or object motion, head motion intolerance); 2) migraine according to the criteria of the International Headache Society (IHS); 3) at least one of the following migrainous symptoms during at least two vertiginous attacks: migrainous headache, photophobia, phonophobia, visual or other auras; and 4) other causes ruled out by appropriate investigations. In addition, the authors compared the prevalence of migraine according to the IHS criteria in the dizziness clinic group with a sex- and age-matched control group of 200 orthopedic patients. RESULTS: The prevalence of migraine according to the IHS criteria was higher in the dizziness clinic group (38%) compared with the age- and sex-matched control group (24%, p < 0.01). The prevalence of migrainous vertigo was 7% in the dizziness clinic group, and 9% in the migraine clinic group. In 15 of 33 patients with migrainous vertigo, vertigo was regularly associated with migrainous headache. In 16 patients, vertigo occurred both with and without headache, and in two patients headache and vertigo never occurred together. The duration of attacks varied from minutes to days. CONCLUSION: These results substantiate the epidemiologic association between migraine and vertigo and indicate that migrainous vertigo affects a significant proportion of patients both in dizziness and headache clinics.

Adult↗

Cu(II) potentiation of alzheimer abeta neurotoxicity. Correlation with cell-free hydrogen peroxide production and metal reduction.

Oxidative stress markers as well as high concentrations of copper are found in the vicinity of Abeta amyloid deposits in Alzheimer's disease. The neurotoxicity of Abeta in cell culture has been linked to H(2)O(2) generation by an unknown mechanism. We now report that Cu(II) markedly potentiates the neurotoxicity exhibited by Abeta in cell culture. The potentiation of toxicity is greatest for Abeta1-42 > Abeta1-40 >> mouse/rat Abeta1-40, corresponding to their relative capacities to reduce Cu(II) to Cu(I), form H(2)O(2) in cell-free assays and to exhibit amyloid pathology. The copper complex of Abeta1-42 has a highly positive formal reduction potential ( approximately +500-550 mV versus Ag/AgCl) characteristic of strongly reducing cuproproteins. These findings suggest that certain redox active metal ions may be important in exacerbating and perhaps facilitating Abeta-mediated oxidative damage in Alzheimer's disease.

Amyloid beta-Peptides↗