Language impairment associated with arachnoid cysts: recovery after surgical treatment.

Supporting data from the literature, we observe that large arachnoid cysts may affect cognitive function. Neuropsychologic assessment plus magnetic resonance imaging allowed for documentation of associations between left temporal arachnoid cysts, language impairment, and other cognitive dysfunctions. Significant cognitive improvements were evident soon after cysto-peritoneal shunting. These observations reinforce the rationale for neuropsychologic assessments of patients with developmental delay and arachnoid cysts, and support the potential benefit of surgical decompression for arachnoid cysts associated with neurologic deficits, even if surgery is performed well after the occurrence of neurologic deficits.

Early bifrontal brain injury: disturbances in cognitive function development.

We describe six psychomotor, language, and neuropsychological sequential developmental evaluations in a boy who sustained a severe bifrontal traumatic brain injury (TBI) at 19 months of age. Visuospatial, drawing, and writing skills failed to develop normally. Gradually increasing difficulties were noted in language leading to reading and spontaneous speech difficulties. The last two evaluations showed executive deficits in inhibition, flexibility, and working memory. Those executive abnormalities seemed to be involved in the other impairments. In conclusion, early frontal brain injury disorganizes the development of cognitive functions, and interactions exist between executive function and other cognitive functions during development.

Evaluation of early stimulation programs for enhancing brain development.

UNLABELLED: The term 'early intervention' designates educational and neuroprotection strategies aimed at enhancing brain development. Early educational strategies seek to take advantage of cerebral plasticity. Neuroprotection, a term initially used to characterize substances capable of preventing cell death, now encompasses all interventions that promote normal development and prevent disabilities, including organisational, therapeutic and environment-modifying measures, such as early stimulation programs. Early stimulation programs were first devised in the United States for vulnerable children in low-income families; positive effects were recorded regarding school failure rates and social problems. Programs have also been implemented in several countries for premature infants and low-birth-weight infants, who are at high risk for neurodevelopmental abnormalities. The programs target the child, the parents or both. The best evaluated programs are the NIDCAP (Newborn Individualized Developmental Care and Assessment Program) in Sweden for babies<1500 g in neonatal intensive care units and the longitudinal multisite program IHDP (Infant Health and Development Program) created in the United States for infants<37 weeks or <2500 g. CONCLUSION: Although the NIDCAP and the IHDP targeted different populations, they produced similar effects in several regards: efficacy was greatest with programs involving both the parents and the child; long-term stimulation improved cognitive outcomes and child-parent interactions; cognition showed greater improvements than motor skills and larger benefits were obtained in families that combined several risk factors including low education attainment by the mothers.

Neurodevelopmental outcome after severe traumatic brain injury in very young children: role for subcortical lesions.

Traumatic brain injury is a major cause of mortality and morbidity in children younger than 15 years of age. To evaluate the role of subcortical lesions on neurodevelopmental outcomes, long-term outcomes of 50 children with severe traumatic brain injury before 4 years of age (accidental injury, n = 21, nonaccidental injury, n = 29) were reviewed retrospectively and compared with late magnetic resonance imaging (MRI) findings: no visible lesions, cortical lesions, or subcortical lesions. Subcortical lesions occurred in both accidental and nonaccidental traumatic brain injuries. Traumatic brain injury severity (initial Glasgow Coma Scale or coma duration) was significantly associated with subcortical lesions. Long-term motor or visual deficiencies occurred in one third of patients and cognitive deficiencies in 52.1%. Although deficiencies occurred without visible MRI lesions, global outcome scores, motor delay, visual impairment, head growth slowing, global intellectual quotients, and planning performances were significantly worse in patients with subcortical lesions. An alarming deterioration in intellectual quotient over time was noted. It was concluded that neurodevelopmental outcomes are worrisome after severe traumatic brain injury in young children, and subcortical lesions affect the prognosis.

Levetiracetam in a neonate with malignant migrating partial seizures.

This report describes the first neonatal case of "malignant migrating partial seizures in infancy" with a positive therapeutic response to levetiracetam. This patient is the youngest reported infant with this rare syndrome, and the report provides the first documentation on levetiracetam treatment in a neonatal patient. Treatment with levetiracetam improved both ictal and interictal status. This observation also highlights the need to consider and include malignant migrating partial seizures in the differential diagnosis of early neonatal seizure disorders, even during the first hours of life.

Animal models of shaken baby syndrome: revisiting the pathophysiology of this devastating injury.

To better understand outcomes after early brain injuries, studies must address multiple variables including age at injury, the mechanisms and severity of injury, environmental factors (before and after injury) and developmental factors. Animal models are helpful for elucidating these different aspects. First, this paper describes a new model of shaken baby syndrome (SBS) in mice, without impact or hypoxia. Mortality was 27%; 75% of survivors had focal brain lesions consisting of haemorrhagic or cystic lesions of the white matter, corpus callosum and cerebellum. All shaken animals, with and without focal lesions, showed delayed white matter atrophy. White matter damage and atrophy were reduced by pre-treatment with an NMDA receptor antagonist, indicating that excess glutamate release contributed to the pathophysiology of the lesions. Secondly, it discusses data on neuroprotection after early brain injuries; drugs targeting the NMDA receptors cannot be used in clinical practice but indirect neuroprotection strategies including anti-NO, anti-free radicals and trophic factors hold promise for limiting the excitotoxic white matter damage induced by early injury, in particular caused by shaking, during brain development. Thirdly, it describes two experimental models in which SBS outcomes are determined when the trauma is combined with environmental influences, namely medications during the acute phase, most notably anti-epileptic drugs and rearing conditions.

Does in utero exposure to heavy maternal smoking induce nicotine withdrawal symptoms in neonates?

Maternal drug use during pregnancy is associated with fetal passive addiction and neonatal withdrawal syndrome. Cigarette smoking-highly prevalent during pregnancy-is associated with addiction and withdrawal syndrome in adults. We conducted a prospective, two-group parallel study on 17 consecutive newborns of heavy-smoking mothers and 16 newborns of nonsmoking, unexposed mothers (controls). Neurologic examinations were repeated at days 1, 2, and 5. Finnegan withdrawal score was assessed every 3 h during their first 4 d. Newborns of smoking mothers had significant levels of cotinine in the cord blood (85.8 +/- 3.4 ng/mL), whereas none of the controls had detectable levels. Similar findings were observed with urinary cotinine concentrations in the newborns (483.1 +/- 2.5 microg/g creatinine versus 43.6 +/- 1.5 microg/g creatinine; p = 0.0001). Neurologic scores were significantly lower in newborns of smokers than in control infants at days 1 (22.3 +/- 2.3 versus 26.5 +/- 1.1; p = 0.0001), 2 (22.4 +/- 3.3 versus 26.3 +/- 1.6; p = 0.0002), and 5 (24.3 +/- 2.1 versus 26.5 +/- 1.5; p = 0.002). Neurologic scores improved significantly from day 1 to 5 in newborns of smokers (p = 0.05), reaching values closer to control infants. Withdrawal scores were higher in newborns of smokers than in control infants at days 1 (4.5 +/- 1.1 versus 3.2 +/- 1.4; p = 0.05), 2 (4.7 +/- 1.7 versus 3.1 +/- 1.1; p = 0.002), and 4 (4.7 +/- 2.1 versus 2.9 +/- 1.4; p = 0.007). Significant correlations were observed between markers of nicotine exposure and neurologic-and withdrawal scores. We conclude that withdrawal symptoms occur in newborns exposed to heavy maternal smoking during pregnancy.

Neuroimaging of intraparenchymal lesions predicts outcome in shaken baby syndrome.

OBJECTIVE: Studies of long-term outcome on nonaccidental head injury (NAHI) in young children have shown severe neurodevelopmental sequelae in most cases. For improving the knowledge of outcome and for identifying prognostic factors, additional clinical and cerebral imaging data are needed. The aim of this study was to describe clinical and imaging features over time and to consider their value for predicting neurodevelopmental outcome. METHODS: A retrospective medical record review was conducted of 23 children with confirmed NAHI, for whom an extended follow-up of 2.5 to 13 years (mean: 6 years) was contemplated. Glasgow Coma Scale scores, severity of retinal hemorrhages, presence of skull fractures, cranial growth deceleration, and sequential neuroimaging data (computed tomography and/or magnetic resonance imaging) were compared with patterns of clinical evolution assessed by the Glasgow Outcome Scale. RESULTS: Clinical outcome showed that 14 (61%) children had severe disabilities, 8 (35%) had moderate disabilities, and 1 (4%) was normal. A low initial Glasgow Coma Scale score, severe retinal hemorrhages, presence of skull fracture, and cranial growth deceleration were significantly associated with poor developmental outcome. Eighteen of the 23 patients had abnormal magnetic resonance imaging scans. This examination disclosed atrophy when performed beyond 15 days of injury. Atrophy seemingly resulted from various brain lesions, namely, contusions, infarcts, and other lesions within the white matter. Presence of intraparenchymal brain lesions within the first 3 months was significantly associated with neurodevelopmental impairment. Severity of motor and cognitive dysfunctions was related to the extent of intraparenchymal lesions. CONCLUSIONS: Early clinical and radiologic findings in NAHI are of prognostic value for neurodevelopmental outcome.

Fructose-1,6-biphosphate prevents excitotoxic neuronal cell death in the neonatal mouse brain.

The excitotoxic cascade may represent an important pathway leading to brain damage and cerebral palsy. Brain lesions induced in newborn mice by ibotenate (acting on N-methyl-D-aspartate receptors) and by S-bromowillardiine (acting on alpha-3-amino-hydroxy-5-methyl-4-isoxazole propionic acid and kainate receptors) mimic some aspects of white matter cysts and transcortical necrosis observed in human perinatal brain damage. Fructose 1,6-biphosphate (FBP) is a high-energy glycolytic pathway intermediate which, in therapeutic doses, is non-toxic and neuroprotective in hypoxic-ischemic models of brain injury. Mechanisms of action include modulation of intracellular calcium through phospholipase C (PLC) activation. The goal of this study was to determine the neuroprotective effects of FBP in a mouse model of neonatal excitotoxic brain injury. Mice that received intraperitoneal FBP had a significant reduction in size of ibotenate-induced (80% reduction) or S-bromowillardiine-induced (40% reduction) cortical plate lesions when compared with control animals. Studies of fragmented DNA and cleaved caspase 3 confirmed the survival promoting effects of FBP. FBP had no detectable effect on excitotoxic white matter lesions. The effects of FBP were antagonized by co-administration of PLC, protein kinase C or mitogen-associated protein kinase inhibitors but not by protein kinase A inhibitor. A moderate, transient cooling of pups immediately after the insult extended the therapeutic window for FBP, as FBP administered 24 h after ibotenate was still significantly neuroprotective in these pups. This data extends the neuroprotective profile of FBP in neonatal brain injury and identifies gray matter lesions involving N-methyl-D-aspartate receptors as a major target for this promising drug.