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- BookPier 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. - ArticleSeipel 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.