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JOHNSTON MV, SILVERSTEIN FS: Fundamentals of drug therapy in neurology, in Johnston MV, MacDonald RL, Young AB (eds): Principles of Drug Therapy in Neurology Philadelphia, Davis, 1992, pp 1 49 KLAASSEN CD (ed): Casarett and Doull s Toxicology: The Basic Science of Poisons, 6th ed New York, McGraw-Hill, 2001 LEVY BS, WEGMAN DH: Occupational Health: Recognizing and Preventing Work-Related Disease and Injury, 4th ed Philadelphia, Lippincott Williams & Wilkins, 1999 PAYNE R, PASTERNAK GW: Pain, in Johnston MV, MacDonald RL, Young AB (eds): Principles of Drug Therapy in Neurology Philadelphia, Davis, 1992, pp 268 301 PIRODSKY DM, COHN JS: Clinical Primer of Psychopharmacology, 2nd ed New York, McGraw-Hill, 1992 ROM WN (ed): Environmental and Occupational Medicine, 3rd ed Philadelphia, Lippincott-Raven, 1998 ROSENBERG NL: Occupational and Environmental Neurology Boston, Butterworth-Heineman, 1995 SPENCER PS, SCHAUMBURG HH (eds): Experimental and Clinical Neurotoxicology, 2nd ed New York, Oxford, 2000.

Less dif culty attends these diagnoses if paresthesias in the acral extremities, progressive reduction or loss of re exes, and relative symmetry of weakness appear after several days of signs The laboratory tests that af rm the diagnosis of typical GBS give similar but generally milder abnormalities if they are carefully sought in all these variant forms There has been a recent tendency to separate a group of cases with presumed diffuse axonal damage on the basis of an abrupt and explosive onset, severe paralysis, minor sensory features, and the electrophysiologic nding of inexcitability of nerves This axonal type of GBS represents 5 percent (or fewer) of cases but its identi cation has some value in that a poor response to treatment and very protracted recovery are to be expected in most cases This variant is described later.

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OPIATES AND SYNTHETIC ANALGESICS AMERICAN PSYCHIATRIC ASSOCIATION: Practical guidelines for the treatment of substance use disorders Am J Psychiatry 52(suppl):1, 1995 BALL J, ROSS A: The Effectiveness of Methadone Maintenance Treatments New York, Springer Verlag, 1991 BRUST JCM: The nonimpact of opiate research on opiate abuse Neurology 33:1327, 1983 CAM J, FARRE M: Drug addiction N Engl J Med 349:975, 2003 FIELDS HL: Pain New York, McGraw-Hill, 1987 JASINSKI DR, JOHNSON RE, KOCHER TR: Clonidine in morphine withdrawal Arch Gen Psychiatry 42:1063, 1985 MELLO NK, MENDELSON JH: Buprenorphine treatment of cocaine and heroin abuse, in Cowan A, Lewis JW (eds) Buprenorphine: Combatting Drug Abuse with a Unique Opioid Wiley-Liss, 1995, pp 241 287 MONROE JJ, ROSS WF, BERZINS JI: The decline of the addict as psychopath : Implications for community care Int J Addict 6:601, 1971..

To clean manually, use a clean foam-rubber swab or lint-free cloth slightly dampened with distilled water, again following manufacturer s instructions. Most laser cartridges use tape on the cartridge to prevent movement and leakage. Make sure all packing tape is removed from a new print cartridge before installing it. There are several possible causes of blank pages produced by a laser printer. To begin with, check the toner. If the cartridge is empty, replace it. If it is not empty, try replacing the drum. Sometimes drums become unable to hold a charge after time (in some laser printer models, the toner and drum come as an integrated unit). If this does not resolve the problem, use your knowledge of the print process itself. A blank page means a failure of the toner to be attracted to the paper. Perhaps the laser did not discharge areas of the drum. It could also be that the transfer corona wire (or underlying HVPS) did not apply a positive charge to the paper. Unfortunately, these components are difficult to replace, and you could end up sending the printer to a repair shop that specializes in laser printers. Fortunately, almost all laser print problems can be resolved by changing the toner and/or drum.

In a few patients the weakness continues to evolve for 3 to 4 weeks or even longer From this group a chronic form of demyelinative neuropathy (chronic in ammatory demyelinating polyneuropathy, or CIDP) often emerges and an intermediate group that progress for 4 to 8 weeks and then improve can be identi ed (see further on) Acute Axonal Form of Guillain-Barre Syndrome This subject has been alluded to earlier Feasby and colleagues drew attention to an acute are exic polyneuropathy clinically similar to GBS but characterized pathologically by widespread and severe axonal degeneration In their initial report they described ve patients, all with a rapid evolution of polyneuropathy and very slow and poor recovery Unlike the common form of GBS, muscle atrophy in these patients became apparent relatively early in the disease (within weeks) The de ning EMG features were the presence of.

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