A New Breakthrough in the Understanding of the Pathobiology of Stroke

The INR has made a stunning discovery: that the neurological status of patients following stroke, even years after the acute event, may rapidly improve following the use of an anti-TNF therapeutic.

Please see:

  1. Selective TNF Inhibition for Chronic Stroke and Traumatic Brain Injury – An Observational Study Involving 629 Consecutive Patients Treated With Perispinal Etanercept. Edward Tobinick MD, Nancy M. Kim, Gary Reyzin, Helen Rodriguez-Romanacce and Venita DePuy. CNS Drugs. 2012 26(12).
  2. Rapid improvement of chronic stroke deficits after perispinal etanercept: three consecutive cases. Edward Tobinick MD. CNS Drugs. 2011 Feb;25(2):145-155.
  3. Deciphering the physiology underlying the rapid clinical effects of perispinal etanercept in Alzheimer’s disease. Edward Tobinick MD. Curr Alzheimer Res. 2012 Jan;9(1):99-109.

These published results, and the subsequent clinical experience of INR physicians, suggest that excess TNF plays an important role in post-stroke chronic disability and establish the promise that the INR’s patented anti-TNF treatment presents for stroke recovery and stroke rehabilitation. Results can vary, and more than one dose may be necessary for optimal benefit, but these results represent a new breakthrough in the understanding of the neurological basis of chronic brain dysfunction following stroke.

For further detailed information, please visit the INR stroke website, or click here.

Consultation for Stroke at the INR

Patients who have experienced stroke often have weakness or decreased sensation in one half of the body, cognitive or speech difficulties, or other neurological problems that can last for years. Consultation with an INR physician following hospital discharge is encouraged, even if the stroke has occurred years before. Please call the INR ((310) 824-6199 (California) or, in Florida (561) 353-9707 for further information.

What is Stroke?
A stroke occurs when the blood supply to part of the brain is suddenly interrupted or when a blood vessel in the brain bursts, spilling blood into the spaces surrounding brain cells. Brain cells die when they no longer receive oxygen and nutrients from the blood or there is sudden bleeding into or around the brain. The symptoms of a stroke include sudden numbness or weakness, especially on one side of the body; sudden confusion or trouble speaking or understanding speech; sudden trouble seeing in one or both eyes; sudden trouble with walking, dizziness, or loss of balance or coordination; or sudden severe headache with no known cause. There are two forms of stroke: ischemic – blockage of a blood vessel supplying the brain, and hemorrhagic – bleeding into or around the brain, including ICH (intra-cerebral hemorrhage and SAH (subarachnoid hemorrhage).

Chronic neurological consequences of stroke

Although stroke is a disease of the brain, it can affect the entire body. A common disability that results from stroke is complete paralysis on one side of the body, called hemiplegia. A related disability that is not as debilitating as paralysis is one-sided weakness or hemiparesis. Stroke may cause problems with thinking, awareness, attention, learning, judgment, and memory. Stroke survivors often have problems understanding or forming speech. A stroke can lead to emotional problems. Stroke patients may have difficulty controlling their emotions or may express inappropriate emotions. Many stroke patients experience depression. Stroke survivors may also have numbness or strange sensations. The pain is often worse in the hands and feet and is made worse by movement and temperature changes, especially cold temperatures.
Recurrent stroke is frequent; about 25 percent of people who recover from their first stroke will have another stroke within 5 years.

We encourage stroke patients to visit the INR following their hospital discharge to consult with an INR physician.

2012 Scientific Citations to INR Publications

The following are selected publications that have cited scientific publications of the INR® in 2012:

1. Belarbi, K., et al., TNF-alpha protein synthesis inhibitor restores neuronal function and reverses cognitive deficits induced by chronic neuroinflammation. J Neuroinflammation, 2012. 9: p. 23.

2. Bomfim, T.R., et al., An anti-diabetes agent protects the mouse brain from defective insulin signaling caused by Alzheimer’s disease- associated Abeta oligomers. J Clin Invest, 2012. 122(4): p. 1339-53.

3. Butchart, J. and C. Holmes, Systemic and central immunity in Alzheimer’s disease: therapeutic implications. CNS Neurosci Ther, 2012. 18(1): p. 64-76.

4. Cereda, C., et al., The Role of TNF-alpha in ALS: New Hypostheses for Future Therapeutic Approaches, in Amyotrophic Lateral Sclerosis, M.H. Maurer, Editor. 2012, InTech. p. 413-436.

5. Clark, I., et al., Tumor necrosis factor-induced cerebral insulin resistance in Alzheimer’s disease links numerous treatment rationales. Pharmacol Rev, 2012. 64(4): p. 1004-26.

6. Dhawan, G. and C.K. Combs, Inhibition of Src kinase activity attenuates amyloid associated microgliosis in a murine model of Alzheimer’s disease. J Neuroinflammation, 2012. 9: p. 117.

7. Drent, M., E.E. Lower, and J. De Vries, Sarcoidosis-associated fatigue. Eur Respir J, 2012. 40(1): p. 255-63.

8. Ferraccioli, G., et al., Rheumatoid Arthritis and Alzheimer Disease: Possible Cellular and Molecular Links. Gerontology and Geriatric, 2012. 1(1).

9. Gabbita, S.P., et al., Early intervention with a small molecule inhibitor for tumor necrosis factor-alpha prevents cognitive deficits in a triple transgenic mouse model of Alzheimer’s disease. J Neuroinflammation, 2012. 9: p. 99.

10. Gruber, H.E., et al., Genome-wide analysis of pain-, nerve- and neurotrophin -related gene expression in the degenerating human annulus. Mol Pain, 2012. 8(1): p. 63.

11. Hojlund, J., et al., Effect of head rotation on cerebral blood velocity in the prone position. Anesthesiol Res Pract, 2012. 2012: p. 647258.

12. Ingles-Esteve, J., et al., Inhibition of specific NF-kappaB activity contributes to the tumor suppressor function of 14-3-3sigma in breast cancer. PLoS One, 2012. 7(5): p. e38347.

13. Jiang, T., J.T. Yu, and L. Tan, Novel disease-modifying therapies for Alzheimer’s disease. J Alzheimers Dis, 2012. 31(3): p. 475-92.

14. Krishnadas, R. and J. Cavanagh, Depression: an inflammatory illness? J Neurol Neurosurg Psychiatry, 2012. 83(5): p. 495-502.

15. Landoni, V.I., et al., Shiga toxin 1 induces on lipopolysaccharide-treated astrocytes the release of tumor necrosis factor-alpha that alter brain-like endothelium integrity. PLoS Pathog, 2012. 8(3): p. e1002632.

16. Lauterbach, E.C., Psychotropic drug effects on gene transcriptomics relevant to Alzheimer disease. Alzheimer Dis Assoc Disord, 2012. 26(1): p. 1-7.

17. Lima, A. and F. Antunes, Intervention of Physical Medicine and Rehabilitation in Failed Back Surgery Syndrome. Journal of Regional Anaesthesia and Pain Management, 2012. 68: p. 29-30.

18. Maccioni, R.B., et al., In Search of Therapeutic Solutions for Alzheimer’s Disease, in When Things Go Wrong–Diseases and Disorders of the Human Brain, T. Mantamadiotis, Editor. 2012, InTech. p. 125-.

19. Matias-Guiu, J.A. and R. Garcia-Ramos, Primary progressive aphasia: from syndrome to disease. Neurologia, 2012.

20. Montgomery, S.L. and W.J. Bowers, Tumor Necrosis Factor-alpha and the Roles it Plays in Homeostatic and Degenerative Processes Within the Central Nervous System. Journal of Neuroimmune Pharmacology, 2012. 7(1): p. 42-59.

21. Ooi, L., et al., New drugs under development for Alzheimer’s disease, in Advances in Alzheimer’s Disease Management, S. Gauthier and P. Rosa-Neto, Editors. 2012. p. 58-67.

22. Ramesh, V., et al., Disrupted sleep without sleep curtailment induces sleepiness and cognitive dysfunction via the tumor necrosis factor-alpha pathway. J Neuroinflammation, 2012. 9.

23. Santello, M. and A. Volterra, TNF-alpha in synaptic function: switching gears. Trends Neurosci, 2012. 35(10): p. 638-47.

24. Singh, P.L., et al., Current therapeutic strategies for inflammation following traumatic spinal cord injury. Neural Regeneration Research, 2012. 7(23): p. 1812-1821.

25. Steele, M.L. and S.R. Robinson, Reactive astrocytes give neurons less support: implications for Alzheimer’s disease. Neurobiol Aging, 2012. 33(2): p. 423 e1-13.

26. Stringer, M.D., et al., The vertebral venous plexuses: the internal veins are muscular and external veins have valves. Clin Anat, 2012. 25(5): p. 609-18.

27. Tweedie, D., et al., Tumor necrosis factor-alpha synthesis inhibitor 3,6′-dithiothalidomide attenuates markers of inflammation, Alzheimer pathology and behavioral deficits in animal models of neuroinflammation and Alzheimer’s disease. J Neuroinflammation, 2012. 9: p. 106.

28. Wilcock, D.M., Neuroinflammation in the aging down syndrome brain; lessons from Alzheimer’s disease. Curr Gerontol Geriatr Res, 2012. 2012: p. 170276.

29. Woodward, M.C., Drug treatments in development for Alzheimer’s disease. Journal of Pharmacy Practice and Research, 2012. 42(1): p. 58-65.

30. Yoshiyama, Y., V.M. Lee, and J.Q. Trojanowski, Therapeutic strategies for tau mediated neurodegeneration. J Neurol Neurosurg Psychiatry, 2012.