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1. Wojner AW. Optimizing ischemic stroke outcomes: an interdisciplinary approach to post-stroke rehabilitation in acute care. Crit Care Nurs Q. 1996; 19: 47 McGuire JR, Harvey RL. The prevention and management of complications after stroke. Phys Med Rehabil Clin North Am. 1999; 10: 857874. Gelber DA, Jozefczyk P. Management of spasticity in multiple sclerosis. Int J MS Care. 1999; 1: 1621. Gelber DA, Jozefczyk PB. Therapeutics in the management of spasticity. Neurorehabil Neural Repair. 1999; 13: 514. Smith C, Birnbaum G, Carter JL, Greenstein J, Lublin FD, the US Tizanidine Study Group. Tizanidine treatment of spasticity caused by multiple sclerosis: results of a double-blind, placebo controlled trial. Neurology. 1994; 44 suppl 9 ; : S34S43. 6. Nance PW, Bugaresti J, Shellenberger K, Sheremata W, Martinez-Arizala A, the North American Tizanidine Study Group. Efficacy and safety of tizanidine in the treatment of spasticity in patients with spinal cord injury. Neurology. 1994; 44 suppl 9 ; : S44S52. 7. The United Kingdom Tizanidine Trial Group. A double-blind, placebo-controlled trial of tizanidine in the treatment of spasticity caused by multiple sclerosis. Neurology. 1994; 44 suppl 9 ; : S70S78. 8. Wallace JD. Summary of combined clinical analysis of controlled clinical trials with tizanidine. Neurology. 1994; 44 suppl 9 ; : S60S69. 9. Bass B, Weinshenker B, Rice GP, Noseworthy JH, Cameron MG, Hader W, Bouchard S, Ebers GC. Tizanidine vs baclofen in the treatment of spasticity in patients with multiple sclerosis. Can J Neurol Sci. 1988; 15: 1519. Bes A, Eyssette M, Pierrot-Deseilligny E, Rohmer F, Warter JM. A multi-centre, double-blind trial of tizanidine, a new antispastic agent, in spasticity associated with hemiplegia. Curr Med Res Opin. 1988; 10: 709718. Ogawa N, Asanuma M, Hirata H, Ota Z, Yamawaki Y, Yamamoto M. Development of a simple spasticity quantification method: effects of tizanidine on spasticity in patients with sequelae of cerebrovascular disease. J Int Med Res. 1992; 20: 7886. Bohannon RW, Smith MB. Inter-rater reliability of a Modified Ashworth Scale of muscle spasticity. Phys Ther. 1987; 67: 206207. Brott T, Adams H, Olinger C. Measurements of acute cerebral infarction: a clinical examination scale. Stroke. 1989; 20: 864870. Medical Research Council. Aids to the Examination of the Peripheral Nervous System. London, UK: Her Majesty's Stationary Office; 1976.

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For Comments or Questions: Call Craig Stern, PharmD. at 888 ; 701-5438, or E-Mail craig ern propharmaconsultants. From neuron-enriched cultures was also assayed in the same way as astrocyte conditioned medium, and no cysteine or glutathione was detected. This shows that neurons cannot themselves provide thiols but instead rely on astrocytes. We analyzed cysteine and related compounds in rat CSF and in plasma of the carotid artery and internal jugular vein. Our results indicate that cystine is transported from blood to the CNS and that the thiol disulfide exchange reaction occurs in the brain in vivo. Cysteine and glutathione are unstable and oxidized to their disulfide forms under aerobic conditions. Therefore, constant release of glutathione by astrocytes is essential to maintain stable levels of thiols in the CNS." 114. Fonnum F, Lock EA. The contributions of excitotoxicity, glutathione depletion and DNA repair in chemically induced injury to neurones: exemplified with toxic effects on cerebellar granule cells. J Neurochem. 2004 Feb; 88 3 ; : 513-31. PMID: 14720201 "Six chemicals, 2-halopropionic acids, thiophene, methylhalides, methylmercury, methylazoxymethanol MAM ; and trichlorfon Fig. 1 ; , that cause selective necrosis to the cerebellum, in particular to cerebellar granule cells, have been reviewed. All six compounds decrease cerebral glutathione GSH ; , due to conjugation with the xenobiotic, thereby reducing cellular antioxidant status and making the cells more vulnerable to reactive oxygen species. 2-Halopropionic acids and methylmercury appear to also act via an excitotoxic mechanism leading to elevated intracellular Ca2 + , increased reactive oxygen species and ultimately impaired mitochondrial function. We propose that a combination of reduced antioxidant status plus excitotoxicity or DNA damage is required to cause cerebellar neuronal cell death with these chemicals. The small size of cerebellar granule cells, the unique subunit composition of their N-methyl-d-aspartate NMDA ; receptors, their low DNA repair ability, low levels of calcium-binding proteins and vulnerability during postnatal brain development and distribution of glutathione and its conjugating and metabolizing enzymes are all important factors in determining the sensitivity of cerebellar granule cells to toxic compounds." 115. Ehrhart J, Zeevalk GD. Cooperative interaction between ascorbate and glutathione during mitochondrial impairment in mesencephalic cultures. J Neurochem 2003 86 6 ; : 1487-97. PMID: 12950457 "These findings indicate that ascorbate contributes to the maintenance of GSSG GSH status during oxidative stress through scavenging of radical species, attenuation of GSH efflux and redistribution of GSSG to the formation of mixed disulfides. It is speculated that these events are linked by glutaredoxin, an enzyme shown to contain both dehydroascorbate reductase as well as glutathione thioltransferase activities." 116. Dringen R, Hirrlinger J. Glutathione pathways in the brain. Biol Chem. 2003 384 4 ; : 505-16. PMID: 12751781 "The antioxidant glutathione GSH ; is essential for the cellular detoxification of reactive oxygen species in brain cells. A compromised GSH system in the brain has been connected with the oxidative stress occuring in neurological diseases. Recent data demonstrate that besides intracellular functions GSH has also important extracellular functions in brain. In this respect astrocytes appear to play a key role in the GSH and ursodiol. 4. Juniper EF, Guyatt GH. Development and testing of a new measure of health status for clinical trials in rhinoconjunctivitis. Clin Exp Allergy 1991; 21: 77-83.

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Tablet friability was closely associated with tablet hardness but showed that there was very low sensitivity to low % solids binder slurry and any percentage of Starch 1500 in the bowl. Only at high % solids and high levels of Starch 1500 in the bowl was there a substantial increase in tablet friability. Again, this is related to the duration of the wet granulation phase and the opportunity for granule growth. High inlet temperatures and the resultant lack of granulation moisture also was shown to affect the friability values.
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