Leiden V Factor and Spastic Cerebral Palsy in Mexican Children Marı ´a de la Luz Arenas-Sordo, 1 Ce ´ sar Zavala-Herna ´ ndez, 2 Ce ´ sar Casiano-Rosas, 3 Elba Reyes-Maldonado, 3 Camilo Rı ´os, 4 Edgar Herna ´ ndez-Zamora, 1 Martha G. Del Valle-Cabrera, 5 and Jesu ´ s K. Yamamoto-Furusho 6 Aim: Cerebral palsy (CP) is a persistent motor disorder that appears before the patient is 3 years old due to a nonprogressive interference in the brain’s development which takes place before the central nervous system growth is complete. Causes of this have been studied, and one that has been proposed for spastic hemiparesis CP is the Leiden mutation of V factor coagulation. We want to know whether this mutation can cause CP in our population. Materials and Methods: We carried out a study of cases and controls with 94 patients with spastic hemiparesis CP and 120 controls as well as their mothers with their controls. Results: None of the patients, their mothers, or controls had the Leiden mutation; however, other risk factors were significant: hypoxia odds ratio (OR) 7.189 (2.546, 20.302) p = 0.0001, smoking OR 16.621 (2.945, 93.818) p = 0.001, maternal infections (urinary or vaginal) OR 7.040 (2.952, 16.789) p = 0.0001, weeks of gestation OR 0.866 (0.7750, 0.999) p = 0.048, and maternal age OR 1.114 (1.031, 1.204) p = 0.006. Conclusion: Leiden mutation of factor V is not an important factor for our Mexican mestizo population; however, there are other important perinatal risk factors. Introduction T he concept of cerebral palsy (CP) has been created to include different neurological sequels that affect our motor sphere. In 1958, the first accepted definition was pub- lished by Mac-Keith and Polani: ‘‘CP is a persistent motor disorder appearing before the age of 3 due to a nonprogres- sive interference in the development of the brain taking place before the growth of the central nervous system is complete’’ (Bax et al., 2005; Morris, 2007). Since then, several definitions have been proposed that blend the original, and diverse classifications pay attention to etiological criteria, functional or clinical-topographic, ac- cording to the predominant motor alteration and its distri- bution (O’Shea et al., 1998; Alberman and Mutch, 2007; Mantovani, 2007; Morris, 2007). In 2004, the meeting that defined and classified CP, which took place in Bethesda, defined it as ‘‘A group of movement development and posture disorders limiting activity due to nonprogressive alterations occurring in the developing brain of the fetus or the small child. The motor disorder is frequently accompanied by alterations in sensitivity, cognition, com- munication, perception, behavior and/or epileptic crises’’ (Bax et al., 2005). Factor V Leiden mutation, named after the Dutch city in which it was first described, is characterized by a mutation, the substitution of adenine for guanine in the 1691 (G1691A) nucleotide of chromosome 1, which synthesizes an abnormal protein, arginine replaced by glutamic acid in the 506 position (Arg506Glu), conditioning resistance to the anticlotting action of activated C protein (APCR). Mutated factor V becomes resistant to the Activated C protein and consequently pro- duces more thrombin and a state of hyper clotting first de- scribed by Dahlba ¨ck et al. (Dahlba ¨ck et al., 1993; Svensson and Dahlba ¨ ck, 1994). Heterozygosis for Leiden Factor V increases vein thrombosis risk by 7 times and 80 times if it is due to a homozygotic state for this factor (Pe ´rez Martı ´nez et al., 2005). Halliday et al. (2000) came to the conclusion that there could be a relationship between the state of the carrier of the mu- tation both in the products and in their mothers which pre- disposes the infant to thrombophilia and a cerebral vascular accident. The prevalence of Leiden mutation is very variable in dif- ferent populations and goes from 5% (Zahed et al., 2006) up to 1 Genetics Department, National Institute of Rehabilitation (INR), Mexico City, Me ´xico. 2 Clinical Laboratory Department, INR, Mexico City, Me ´xico. 3 National School of Biological Science, IPN, Mexico City, Me ´xico. 4 Neurochemical Department, INNN, Mexico City, Me ´xico. 5 Rehabilitation Board, Sistema Nacional, DIF, Mexico City, Me ´xico. 6 Gastroenterology Department, INNSZ, Mexico City, Me ´xico. GENETIC TESTING AND MOLECULAR BIOMARKERS Volume 16, Number 8, 2012 ª Mary Ann Liebert, Inc. Pp. 978–980 DOI: 10.1089/gtmb.2012.0017 978