A Legido1, C D Katsetos. 1. Departamento de Pediatría Sección de Neurología, St. Christopher s Hospital for Children, College of Pennsylvania, Hahnemann University, Philadelphia, PA 19134-1095, USA. agustin.legido@drexel.edu
Abstract
OBJECTIVE: To review the current knowledge pertaining to the new pathogenetic aspects of cerebral palsy (CP). DEVELOPMENT: CP is a group of static, heterogeneous clinical syndromes, characterized by abnormal postural mechanisms and motor activities. Its prevalence in industrialized countries is 2 2.5/1000 newborns. CP should be differentiated from certain genetic or metabolic conditions with which it can be mistaken. Some cases of CP have a genetic basis and they are inherited following a mendelian pattern or are determined by specific isolated genes. Recently, the elevation of certain coagulation factors (i.e., Leiden factor V mutation) and cytokines (i.e. interleukins, a tumor necrosis factor) and interferons have been related to CP pathogenesis. Hypocapnia with PaCO2< 35 mmHg represents a risk for periventricular leukomalacia (PVL) in premature infants. PVL pathogenesis is complex and includes a series of mechanisms that interact among them: fetal/maternal infection, immuneinflammatory reaction, prematurity, intraventricular hemorrhage/iron, ischemia/reperfusion, free radical production, maturational sensitivity of oligodendrocytes, and glutamate effect. Neuroradiological and neuropathological data have demonstrated a cortical anatomical substrate for the intellectual deficits associated with PVL in premature infants. CONCLUSIONS: Current knowledge about CP pathogenesis opens the possibility of early diagnosis and development of new treatments, both therapeutic and preventive.
OBJECTIVE: To review the current knowledge pertaining to the new pathogenetic aspects of cerebral palsy (CP). DEVELOPMENT: CP is a group of static, heterogeneous clinical syndromes, characterized by abnormal postural mechanisms and motor activities. Its prevalence in industrialized countries is 2 2.5/1000 newborns. CP should be differentiated from certain genetic or metabolic conditions with which it can be mistaken. Some cases of CP have a genetic basis and they are inherited following a mendelian pattern or are determined by specific isolated genes. Recently, the elevation of certain coagulation factors (i.e., Leiden factor V mutation) and cytokines (i.e. interleukins, a tumor necrosis factor) and interferons have been related to CP pathogenesis. Hypocapnia with PaCO2< 35 mmHg represents a risk for periventricular leukomalacia (PVL) in premature infants. PVL pathogenesis is complex and includes a series of mechanisms that interact among them: fetal/maternal infection, immuneinflammatory reaction, prematurity, intraventricular hemorrhage/iron, ischemia/reperfusion, free radical production, maturational sensitivity of oligodendrocytes, and glutamate effect. Neuroradiological and neuropathological data have demonstrated a cortical anatomical substrate for the intellectual deficits associated with PVL in premature infants. CONCLUSIONS: Current knowledge about CP pathogenesis opens the possibility of early diagnosis and development of new treatments, both therapeutic and preventive.
Authors: María Inés Herrera; Matilde Otero-Losada; Lucas Daniel Udovin; Carlos Kusnier; Rodolfo Kölliker-Frers; Wanderley de Souza; Francisco Capani Journal: Neural Plast Date: 2017-02-23 Impact factor: 3.599