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Optical coherence tomography (OCT) provides tissue morphology imagery at much higher resolution than other imaging modalities such as MRI or ultrasound, and the machines are comparatively cheaper. It is an easy technique to perform; is non-ionizing, and therefore safe. These benefits are driving a rapid transformation of OCT, from its principal application as a research tool, into an extension of the 'neurological examination' in routine office practice. Originally used in assessing the severity of tissue damage and prognosis of multiple sclerosis and various neuro-ophthalmic conditions, OCT is increasingly used in other neurological disorders such as Parkinson's disease, ALS, and Alzheimer's disease. This book is the first comprehensive review of the use of OCT in neurological diseases. The coverage includes a description of the technique and its utilization in a variety of neurologic conditions. Essential reading for neurologists, neuro-ophthalmologists, and neuroradiologists wanting an introductory account of the clinical applications of OCT.
Cyclophosphamide is employed in autoimmune neuropathies, and vasculidities such as Wegener's granulomatosis and polyarteritis nodosa. Mycophenolate mofetil (Cellcept) is a potent immunosuppressant and has been used increasingly in post-transplant patients because it is considered less toxic than azathioprine and cyclophosphamide. Methotrexate is a general immunosuppressant that acts primarily by inhibition of dihydrofolate reductase. Azathioprine (Imuran) is a purine analog that is metabolized to 6-mercaptopurine and thioinosine acid, which compete with DNA nucleotides, causing immunosuppression. This chapter lists randomized trials of immunosuppressives in multiple sclerosis (MS). In the right patient, cyclophosphamide has been demonstrated effective, while work with methotrexate and mycophenolate mofetil has been less conclusive. Azathioprine also is likely to have a favorable effect on MS, and is relatively safe. Recent novel uses of immunosuppressives in active patients, or new disease populations have broadened the possible uses of these drugs.
There is increasing evidence for the role of activated microglia in the neurotoxic pathways of Alzheimer's disease (AD). Amyloid-β1-42 is a potent activator of microglia (Benveniste et al., 2001), causing them to release pro-inflammatory cytokines including IL-6, IL-1β, TNF-α among others. A peripheral blood marker reflecting CNS inflammatory processes would be useful for treatment development, but the search for such an in vivo marker has been elusive. Peripheral blood and CSF levels of pro-inflammatory cytokines do not consistently differ in AD and controls (reviewed in Rosenberg, 2005). Both microglia and peripheral blood mononuclear cells (PBMCs) release pro-inflammatory cytokines when exposed to immunologic stimuli including lipopolysaccharide (LPS) and phytohemagglutinin (PHA). There are recent data suggesting that PBMCs from AD patients release more cytokines in this paradigm than normal controls (Reale et al., 2004).
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