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Titlebook: A-Z of Neurological Practice; A Guide to Clinical Andrew J. Larner,Alasdair J. Coles,Roger A. Barker Book 2011Latest edition Springer-Verl

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https://doi.org/10.1007/978-3-030-87900-6ll harbor subclinical neuromuscular disease which may be elucidated by muscle biopsy, but some remain entirely normal, thereby meriting the diagnosis of “idiopathic hyperCKemia.” Cases with mutations of the caveolin 3 (CAV3) gene have been described, a condition that is allelic with . (.), . type 1C, and . type 9.
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https://doi.org/10.1007/978-3-030-87900-6phy, seizures, and cardiomyopathy. Onset is most often in infancy, but adult presentations with migraine and with tremor have been reported. There may be macrocephaly. There is organic acidemia with hyperlysinemia, and increased .-2-hydroxyglutaric acid in urine, plasma, and CSF. MR imaging shows subcortical leukoencephalopathy.
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https://doi.org/10.1007/978-3-031-23944-1infected water; the presentation mimics that of acute bacterial .. Examination of CSF may reveal motile trophozoites. Prognosis is poor, with death within 1 week the norm. Amphotericin (systemic, intrathecal) is the treatment most usually given, although miconazole, rifampicin, doxycycline, or chloramphenicol may be tried.
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https://doi.org/10.1007/978-3-030-87900-6ion within the cerebral hemispheres. Originally a pathological diagnosis, this appearance has also been documented antemortem using MRI: lesions show a hypointense center and intermediate rings, which enhance with gadolinium, and hyperintense inner and outer rings. Lesions that have this appearance
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