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  • Book
    Pier Paolo Maria Menchetti, editor.
    Contents:
    Anatomy of cervical spine
    Biomechanical evaluation of cervical spine Imaging
    Anesthesiology procedures involved on cervical spine
    Pain management of cervical spine disease
    Percutaneous procedures in cervical disc herniation treatment
    Endoscopy in cervical spine surgery
    Percutaneous posterior facet augmentation in cervical foraminal stenosis
    Anterior cervical decompression and fusion
    Anterior approach and autologous interbody fusion
    Role of cages in anterior cervical surgery
    Cervical prosthetic discs
    Role of materials in cervical spine fusion
    Biomechanical engineering in choice of different stiffness material
    C1-C2 posterior approach
    Screwing of the dens epistropheus
    Transarticular posterior screw fixation
    Posterior open door approach
    Vertebral compression fracture on cervical spine
    Corpectomy in cervical bone metastasis
    Trigeminal neuralgia surgery
    Robotics in cervical spine surgery
    Postoperative physical therapy rehabilitation.
    Digital Access Springer 2016
  • Book
    Herbert C. Brown.
    Print 1980
  • Article
    Seipel JH, Fisher R, Blatchley RJ, Floam J, Bohm M.
    J Clin Pharmacol. 1977 Feb-Mar;17(2-3):140-61.
    The effects of prolonged betahistine administration were studied in institutionalized geriatric patients with particularly severe and long-standing arteriosclerotic dementia. Thirty received betahistine hydrochloride (SERC) or placebo orally in fixed dosage for six months on a double-blind basis and were followed by ward behavioral and psychometric ratings. Six others received active medication and were additionally followed by intracranial rheoencephalography (IREG). Thirty patients successfully completed the two studies. No adverse effects ascribable to the drug were encountered. The results show that betahistine caused definite, strong, and highly significant cerebral and scalp arterial vasodilation and circulatory improvement and that these caused equally definite, strong, and highly significant global improvement in the patients' dementias. Bethahistine, thus, acts in humans as a potent and efficacious cerebral and peripheral microcirculatory and arterial vasodilator which can significantly improve cerebrovascular insufficiency and any associated dementia, no matter how severe either may be and despite the possible presence of large-vessel disease. These improvements sometimes were detected within two weeks or less, developed rapidly to maxima by about 90 days, and were sustained quite well there-after by continued therapy, They may, however, be drug dependent as they regressed in two patients following withdrawal. Various mechanisms whereby a microcirculatory vasodilator can cause arterial vasodilation are considered. The evidence apparently favors that prolonged microcirculatory vasodilatation can cause secondary passive arterial responses. The possibility that the IREG contains external carotid contamination is again examined. Significant discrepancies between the scalp and IREG effects of bethahistine indicate, however, that the response of any such component was negligible within experimental error and that the component, itself, must have comprised but a small percentage of the IREG. Since the circulatory responses detected by the IREG thus arose essentially completely from the effects of betahistine on the cerebral circulation alone, this appears to be the first direct demonstration that cerebral circulatory improvement can cause improvement in mental function in patients with even severe, longstanding, and apparently clinically irreversible arteriosclerotic dementia and that such improvements can be effected pharmacologically.
    Digital Access Access Options