Revista de neurologia · 2003
[Cerebral palsy: new pathogenetic concepts].
Аннотация на английскомСтатьяОбзорНазвание и аннотация: Перевод в очереди
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Legido A, Katsetos C D
Аннотация
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.
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.