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but a fluence of 30 J/cm2 and a 10-mm spot size caused the greatest normalization Histopathologically, while untreated striae appeared thinner but otherwise similar to normal skin, treated striae showed a reduction in the normal papillary patterns of the epidermis Treated striae also showed normal levels of elastin stain in papillary and mid-dermis, revealing thick and thin elastic bers However, untreated striae showed very little uptake of elastin stain, signaling that there were markedly fewer elastin bers present Adverse effects were minimal (transient hypopigmentation, transient hyperpigmentation, mild purpura, mild erythema) but resolved spontaneously Overall, researchers recommended treatment at lowenergy densities and advocated optical pro lometry as a more effective way of assessing improvement67 In 1999, Nouri and colleagues examined the ef cacy of the short-pulsed CO2 laser and the PDL on striae in four patients with skin types IV and VI The CO2 section was treated with the short-pulsed CO2 laser, with a 3-mm spot size at 400 mJ on the rst pass, followed by a second pass at 350 mJ after a saline wash to remove any eschar The second section was a control section The third section was treated with a 585-nm PDL with a 10-mm spot size, and a uence of 3 J/cm2 Results were unfavorable: striae showed no changes or worsened Adverse effects included persistent erythema and hyperpigmentation Because results were so poor, researchers cancelled further trials with additional patients Researchers concluded that for skin types IV to VI, treatment of striae with the short-pulsed CO2 laser or the 585-nm PDL should be avoided or used extremely carefully Researchers advised narrow use of the lasers for striae on skin types I to III71 In 2003, Jimenez and colleagues examined whether the 585-nm PDL would be an effective treatment for striae rubra and alba after two treatments and whether this treatment would affect collagen density Researchers found mixed results At week 12, there was no signi cant difference in decreased area of striae between treated and control groups Less than half of the striae rubra (4/9) and none of the striae alba showed color changes after PDL treatment No signi cant differences were found regarding striae location or age Biopsy samples revealed treated striae had a net increase in collagen content and a net decrease in striae area, while control striae showed a net decrease in collagen content at 12 weeks Adverse effects included hyperpigmentation.

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WHITFIELD CL, CHIEN L, WHITEHEAD JD: Lead encephalopathy in adults Am J Med 52:289, 1972 ARSENIC HEYMAN A, PFEIFFER JB Jr, WILLETT RW, TAYLOR HM: Peripheral neuropathy caused by arsenical intoxication N Engl J Med 254:401, 1956 JENKINS RB: Inorganic arsenic and the nervous system Brain 89:479, 1966 MOYER TP: Testing for arsenic Mayo Clin Proc 68:1210, 1993 MANGANESE

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PEARN J: Neurology of ciguatera J Neurol Neurosurg Psychiatry 70:4, 2001 VENOMS, BITES, AND STINGS CRAWLEY F, SCHON F, BROWN M: Cerebral infarctions: A rare complication of wasp sting J Neurol Neurosurg Psychiatry 66:550, 1999 FELZ MW, SMITH CD, SWIFT TR: A six year old girl with tick paralysis N Engl J Med 342:90, 2000 GARCIA-MONCO JC, BENACH J: Lyme neuroborreliosis Ann Neurol 37: 691, 1995 GOLD BS, DART RC, BARISH RA: Bites of venomous snakes N Engl J Med 347:347, 2002 GRATTAN-SMITH PJ, MORRIS JG, JOHNSTON HM, et al: Clinical and neurophysiological features of tick paralysis Brain 120:1975, 1997 RAHN D, EVANS J (eds): Lyme Disease Philadelphia, American College of Physicians, 1998 METALS AND INDUSTRIAL AGENTS GENERAL DYCK PJ, THOMAS PK, GRIFFIN JW, et al (eds): Neuropathy associated with industrial agents, metals, and drugs, in Peripheral Neuropathy, 3rd ed vol 2 Philadelphia, Saunders, 1993, pp 1533 1581 LEAD AGENCY FOR TOXIC SUBSTANCES AND DISEASE REGISTRY: The Nature and Extent of Lead Poisoning in Children in the United States: A Report to Congress Atlanta: Department of Health and Human Services, 1988 BAGHURST PA, MCMICHAEL AJ, WIGG NR, et al: Environmental exposure to lead and children s intelligence at the age of seven years The Port Pirie Cohort Study N Engl J Med 327:1279, 1992 CANFIELD RL, HENDERSON CR, CERY-SLECHATA DA, et al: Intellectual impairment in children with blood lead concentrations below 10 g per deciliter N Engl J Med 348:1517, 2003 GOLDMAN RH, BAKER EL, HANNAN M, KAMEROW DB: Lead poisoning in automobile radiator mechanics N Engl J Med 317:214, 1987 JORGENSEN FM: Succimer: The rst approved oral lead chelator Am Fam Physician 48:1496, 1993 MAHAFFEY KR: Exposure to lead in childhood N Engl J Med 327:1308, 1992 MAHAFFEY KR, ANNEST JL, ROBERTS J, MURPHY RS: National estimates of blood lead levels: United States, 1976 1980 N Engl J Med 307:573, 1982 MORTENSEN ME, WALSON PD: Chelation therapy for childhood lead poisoning The changing scene in the 1990s Clin Pediatr 32:284, 1993 NEEDLEMAN HL: Childhood lead poisoning Curr Opin Neurol 7:187, 1994 NEEDLEMAN HL, SCHELL A, BELLINGER D, et al: The long-term effects of exposure to low doses of lead in childhood: An 11-year follow-up report N Engl J Med 322:83, 1990 ROGAN WJ, DIERICH KN, WARE JH, et al: The effect of chelation therapy with succimer on neuropsychological development in children exposed to lead N Engl J Med 344:1721, 2001 RUTTER M: Raised lead levels and impaired cognitive/behavioural functioning: A review of the evidence Dev Med Child Neurol 22(suppl 42): 1, 1980.

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