The objective of this study is to investigate relationship between migraine and cerebral infarction in young people. Patients aging 16-44 years, referred for stroke and age- and gender-matched controls were investigated for migraine following the International Headache Society criteria. Included people were 314 strokes and 314 controls. Each group consisted of 150 men and 164 women. Of the 105 persons with migraine (16.7%), 57 had migraine with aura (9.1%). In women, migraine with aura was related to stroke [35 women among strokes (21.3%) vs. 9 among controls (5.5%), P < 0.0001], whereas migraine without aura was not. After multivariate analysis, migraine with aura remained independently associated with stroke together with hypertension, and the estro-progestinic utilization. In men, migraine was not associated with stroke. In conclusion, migraine with aura appears to be associated with ischemic stroke in young women, independently from other common risk factors.

Recent evidences of a predisposing genetic factor associated with Alzheimer's disease (DAT) suggests that important alterations may be expressed in tissues other than the brain. We present morphological and biochemical studies on muscle obtained from ten patients with Alzheimer's disease and coeval controls. Muscle biopsy examination showed an increased subsarcolemmal mitochondrial oxidative activity in three patients. The biochemical studies showed an increased oxidative enzyme activity only in the DAT group. The CoQ10 level, studied so far in three DAT patients, was greatly reduced (approximately 50%) compared with controls. Possible new peripheral markers in Alzheimer's disease will be discussed.

This chapter investigates adrenal medulla autograft in three parkinsonian patients using two different approaches. For this new neurosurgical approach to Parkinson disease (PD), representing the first attempt to clinical neural grafting, the “open” technique is adopted that appeared to be the most effective and could be considered the standard technique against which the following variations would have to be evaluated. The features of three selected patients are (1) fully informed consent to the procedure with good compliance of patient and family, (2) age lower than 55 years, (3) PD or Parkinsonism rated between stages 3–5 of the modified Hoehn and Yahr scale, (4) good response to L-dopa with severe “on-off’ phenomena or painful dyskinesia and dystonias, and (5) apparent impossibility to withdraw L-dopa without a severe impairment of motor performance. Pre- and post-operative pharmacotherapy has followed the principle of administering the lowest adequate doses (particularly with L-dopa) to obtain the best therapeutic response. Immediately after operation therapy has been administered only as least as required, leaving L-dopa as the drug of last resort. Comparison between optimal treatment regimens before and six months after operation are presented in the chapter.

We tested the efficacy of coenzyme Q10 (ubidecarenone, CoQ10) therapy in patients with Kearns-Sayre syndrome and other mitochondrial myopathies with chronic progressive external ophthalmoplegia (CPEO). We treated seven patients for 1 year with daily oral administration of 120 mg of CoQ10. Throughout the treatment most of our patients showed a progressive reduction of serum lactate and pyruvate levels following standard muscle exercise and generally improved neurologic functions. The ECG and echocardiogram showed no significant changes in our patients. None of our patients showed any improvement in ptosis and CPEO.

In an open‐label study, we substituted conventional levodopa plus benserazide: 100/25 (Madopar) with a controlled‐release form (HBS) in 18 fluctuating parkinsonian patients for 24 months. Significantly positive results were obtained in both peak‐dose and diphasic dyskinesias up to 12 months of treatment; morning akinesias were also improved up to 6 months. A general trend of deterioration, compared to the first 3–6 months of HBS treatment, was observed in “off” fluctuations after 1 year: akinesias due to a delayed response worsened after 1 year of treatment also when compared with the conventional treatment. Positive results were obtained with new HBS on standard Madopar‐related psychiatric disorders.

It is possible to grow functional primary dissociated cultures and explants from stereotactic biopsies of human parkinsonian caudate nuclei. Two major classes of cells were identified on morphological grounds. The culture cells appear to be stimulated by an unidentified soluble factor(s) obtained from human fetal neuronal cells in vitro. Culture of primary neuronal and glial cells from human adult cerebral nuclei seems to be a useful tool for several research purposes and in particular for studying both trophic factor action and target effects on afferent neurons for prospective human brain grafting.

This chapter discusses the grafting potential of human fetal adrenal tissue with the recognition of the high growth potential and functional plasticity of the tissue, when compared to the adult tissue and by the data expressed in the literature that favors the use of young or fetal tissue donors. The in vitro models studied provide a convenient method for expeditiously assessing the potential of human fetal adrenal medullary tissue for grafting in the parkinsonian patients. The results show that human fetal adrenal medullary cells can be isolated and grown in vitro to identify their essential nutritional requirements. Fetal human adrenal medullary cells do not seem to need nerve growth factor (NGF) for process formation and neuronal phenotype expression, while adult human adrenal medullary cells are more resistant to the enzymatic dissociation and require NGF for neurite extension in culture. The viability of cultured human fetal chromaffin cells in media with 10% cerebrospinal fluid (CSF) suggests that placing a graft in the periventricular or intraventricular regions may guarantee the growth and survival of the transplant.

We report biochemical, immunological, and morphological findings in a patient with fatal Kearns‐Sayre syndrome. Histochemical and biochemical findings from muscle biopsy specimens obtained 7 years aprt documented the disease's evolution from a mild mitochondrial disorder affecting a small proportion of muscle fibers to a severe disorder affecting a large proportion of muscle fibers. Cytochrome c oxidase activity in muscle declined profoundly as the disease progressed, although the level of enzyme protein was normal, as shown by immunochemical techniques. Other organs were severely affected by the disease. Examination of postmortem tissue showed spongiosis in the frontal cortex, diffuse loss of Purkinje cells in the cerebellum, liver steatosis, and heart fibrosis with mitochondrial abnormalities. Cytochrome c oxidase activity was only slightly reduced in these organs.

Annals of the New York Academy of SciencesVolume 495, Issue 1 p. 771-773 Human Fetal Adrenal Medulla for Transplantation in Parkinsonian Patients GIANNI PEZZOLI, GIANNI PEZZOLI Institute of Neurology University of Milan Medical School Milan 20122, ItalySearch for more papers by this authorVINCENZO SILANI, VINCENZO SILANI Institute of Neurology University of Milan Medical School Milan 20122, ItalySearch for more papers by this authorENRICO MOTTI, ENRICO MOTTI Institute of Neurosurgery University of Milan Medical School Milan 20122, ItalySearch for more papers by this authorCLAUDIO FERRANTE, CLAUDIO FERRANTE Institute of Neurology University of Milan Medical School Milan 20122, ItalySearch for more papers by this authorANTONIO PIZZUTI, ANTONIO PIZZUTI Institute of Neurology University of Milan Medical School Milan 20122, ItalySearch for more papers by this authorANDREA FALINI, ANDREA FALINI Institute of Neurology University of Milan Medical School Milan 20122, ItalySearch for more papers by this authorANNA ZECCHINELLI, ANNA ZECCHINELLI Institute of Neurology University of Milan Medical School Milan 20122, ItalySearch for more papers by this authorFRANCO MAROSSERO, FRANCO MAROSSERO Institute of Neurosurgery University of Milan Medical School Milan 20122, ItalySearch for more papers by this authorGUGLIELMO SCARLATO, GUGLIELMO SCARLATO Institute of Neurology University of Milan Medical School Milan 20122, ItalySearch for more papers by this author GIANNI PEZZOLI, GIANNI PEZZOLI Institute of Neurology University of Milan Medical School Milan 20122, ItalySearch for more papers by this authorVINCENZO SILANI, VINCENZO SILANI Institute of Neurology University of Milan Medical School Milan 20122, ItalySearch for more papers by this authorENRICO MOTTI, ENRICO MOTTI Institute of Neurosurgery University of Milan Medical School Milan 20122, ItalySearch for more papers by this authorCLAUDIO FERRANTE, CLAUDIO FERRANTE Institute of Neurology University of Milan Medical School Milan 20122, ItalySearch for more papers by this authorANTONIO PIZZUTI, ANTONIO PIZZUTI Institute of Neurology University of Milan Medical School Milan 20122, ItalySearch for more papers by this authorANDREA FALINI, ANDREA FALINI Institute of Neurology University of Milan Medical School Milan 20122, ItalySearch for more papers by this authorANNA ZECCHINELLI, ANNA ZECCHINELLI Institute of Neurology University of Milan Medical School Milan 20122, ItalySearch for more papers by this authorFRANCO MAROSSERO, FRANCO MAROSSERO Institute of Neurosurgery University of Milan Medical School Milan 20122, ItalySearch for more papers by this authorGUGLIELMO SCARLATO, GUGLIELMO SCARLATO Institute of Neurology University of Milan Medical School Milan 20122, ItalySearch for more papers by this author First published: June 1987 https://doi.org/10.1111/j.1749-6632.1987.tb23735.xCitations: 4AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL No abstract is available for this article. References 1 Freed, W. J., J. M. Morihisa, H. E. Spoor, B. J. Hoffer, L. Olson, A. Seiger & R. J. Wyatt 1981. Nature 292: 351– 352. 2 Ungerstedt, U. 1976. Pharmacol. Ther. B 2: 37– 40. 3 Freed, W. J. 1983. Biol. Psychiatry 18: 1205– 1267. 4 Silani, V., G. Pezzoli, A. Falini, E. Motti, A. Pizzuti, C. Ferrante, A. Zecchinelli, F. Marossero & G. Scarlato. J. Neurol 1986. Submitted for publication. Citing Literature Volume495, Issue1Cell and Tissue Transplantation into the Adult BrainJune 1987Pages 771-773 ReferencesRelatedInformation

Cardiac Improvement after Coenzyme Q10 Treatment in Patients with Kearns-Sayre Syndrome: PP286 L. Bet;N. Bresolin;A. Binda;F. Nador;C. Ferrante;G. Comi;G. Scarlato; Neurology