Neurological Morbidity (neurological + morbidity)

Distribution by Scientific Domains


Selected Abstracts


Acute encephalopathy with biphasic seizures and late restricted diffusion on MRI in a Japanese child living in the USA

DEVELOPMENTAL MEDICINE & CHILD NEUROLOGY, Issue 9 2008
David E Traul MD PhD
We report an 18-month-old Japanese female living in the USA whose clinical course and radiographic findings were consistent with acute encephalopathy with biphasic seizures and late reduced diffusion (AESD). She was initially diagnosed with complex febrile seizures. However, on day 3 of admission, she had a cluster of complex partial seizures and the onset of a global developmental regression. In contrast to the normal magnetic resonance image of the brain obtained on admission, subsequent imaging demonstrated transient subcortical diffusion-weighted abnormalities in the white matter of the bilateral posterosuperior frontal, parietal, temporal, and occipital regions, with sparing of the perirolandic area. One year later, her developmental delay, although improved, persisted and she continued to experience sporadic seizures while being treated with topiramate monotherapy. Repeat imaging showed diffuse, poorly defined, increased T2 signals in the white matter of the posterosuperior frontal, parietal, temporal and occipital regions and diffuse cerebral volume loss. Previous reports of AESD have been limited to children aged under 4 years living in Japan. With the identification of this case, it is important that all physicians, not only those in Japan, who care for children with febrile seizures be aware of AESD and its associated neurological morbidity. [source]


Immediate Clinical Outcome after Prolonged Periods of Brain Protection: Retrospective Comparison of Hypothermic Circulatory Arrest, Retrograde, and Antegrade Perfusion

JOURNAL OF CARDIAC SURGERY, Issue 5 2009
Anil Z. Apaydin M.D.
Methods: Between 1993 and 2006, 339 patients underwent proximal aortic operations using a period of cerebral protection. Among these, 161 patients (mean age of 55 12 years) who required cerebral protection longer than 25 minutes were included in the analysis. Ascending aorta with or without root was replaced in all patients. In addition, total arch replacement was performed in 36 patients. All patients were cooled to rectal temperature of 16 C. Hypothermic circulatory arrest without adjunctive perfusion was used in 48 patients. Retrograde or antegrade cerebral perfusion was added in 94 and 19 patients, respectively. The mean duration of total cerebral protection was 42 17 minutes. Results: Overall mortality was 15.5% (25/161) and did not differ among the perfusion groups. There was no difference in the incidence of overall neurological events, temporary neurological dysfunction, or major stroke among the groups. Multivariate analysis revealed that transfusion of >3 units of blood (p < 0.03) was an incremental risk factor for mortality. History of hypertension (p < 0.03), coexisting systemic diseases (p < 0.005), and transfusion of >3 units of blood (p < 0.04) were predictors of temporary neurological dysfunction. Conclusion: In proximal aortic operations requiring prolonged periods of cerebral protection, the mortality and neurological morbidity are not determined by the type of cerebral protection method only. Factors like hypertension and diabetes may play a role in the development of temporary neurological dysfunction. [source]


Soluble endoglin modulates aberrant cerebral vascular remodeling,

ANNALS OF NEUROLOGY, Issue 1 2009
Yongmei Chen MD
Objective Brain arteriovenous malformations (AVMs) are an important cause of neurological morbidity in young adults. The pathophysiology of these lesions is poorly understood. A soluble form of endoglin (sEng) has been shown to cause endothelial dysfunction and induce preeclampsia. We tested if sEng would be elevated in brain AVM tissues relative to epilepsy brain tissues, and also investigated whether sEng overexpression via gene transfer in the mouse brain would induce vascular dysplasia and associated changes in downstream signaling pathways. Methods Expression levels of sEng in surgical specimens were determined by Western blot assay and enzyme-linked immunosorbent assay. Vascular dysplasia, levels of matrix metalloproteinase (MMP), and oxidative stress were determined by immunohistochemistry and gelatin zymography. Results Brain AVMs (n = 33) had higher mean sEng levels (245 175 vs 100 60, % of control, p = 0.04) compared with controls (n = 8), as determined by Western blot. In contrast, membrane-bound Eng was not significantly different (108 79 vs 100 63, % of control, p = 0.95). sEng gene transduction in the mouse brain induced abnormal vascular structures. It also increased MMP activity by 490 30% (MMP-9) and 220 30% (MMP-2), and oxidants by 260 20% (4-hydroxy-2-nonenal) at 2 weeks after injection, suggesting that MMPs and oxidative radicals may mediate sEng-induced pathological vascular remodeling. Interpretation The results suggest that elevated sEng may play a role in the generation of sporadic brain AVMs. Our findings may provide new targets for therapeutic intervention for patients with brain AVMs. Ann Neurol 2009;66:19,27 [source]


Presumed perinatal ischemic stroke: Vascular classification predicts outcomes

ANNALS OF NEUROLOGY, Issue 4 2008
Adam Kirton MD, FRCPC
Objective Perinatal stroke commonly causes childhood neurological morbidity. Presumed perinatal ischemic stroke (PPIS) defines children presenting outside a normal perinatal period with chronic, focal infarction on neuroimaging. Infarcts are assumed to represent arterial strokes, but recent evidence suggests the periventricular venous infarction (PVI) of infants born preterm may also occur in utero and present as PPIS. Using the largest published cohort, we aimed to define arterial and PVI PPIS syndromes and their outcomes. Methods A PPIS consecutive cohort was identified (SickKids Children's Stroke Program, 1992,2006). Systematic neuroradiological scoring executed by blinded investigators included previously defined arterial stroke syndromes. PVI criteria included unilateral injury with at least four of the following conditions: (1) focal periventricular encephalomalacia, (2) internal capsule T2 prolongation, (3) cortical and (4) relative basal ganglia sparing, and (5) remote hemorrhage. Arterial and PVI classifications were validated and correlated with neurological outcomes (Pediatric Stroke Outcome Measure). Results In 59 PPISs (64% male), 94% of lesions fell within potential middle cerebral artery territories. Although arterial proximal M1 infarction was most common (n = 19; 35%), venous PVI was second (n = 12; 22%) and accounted for 75% of subcortical injuries. Motor outcomes (mean follow-up, 5.3 years) were predicted by basal ganglia involvement including leg hemiparesis, spasticity, and need for assistive devices (p < 0.01). Nonmotor outcomes were associated with cortical involvement, including cognitive/behavioral outcomes, visual deficits, and epilepsy (p < 0.01). Classification interrater reliability was excellent (correlation coefficients > 0.975). Interpretation Recognizable PPIS patterns predict long-term morbidity and may guide surveillance, therapy, and counseling. PVI is an underrecognized cause of PPIS and congenital hemiplegia. Ann Neurol 2008 [source]


HIV-1 Persistence, Viral Reservoir, and the Central Nervous System in the HAART Era

BRAIN PATHOLOGY, Issue 1 2003
Olivier Lambotte
HAART therapy has led to a significant reduction of general and neurological morbidity, and mortality among HIV-1 infected patients. It can also decrease HIV-1 RNA titres in plasma and CSF towards undetectable level. However, the initial hope of achieving total eradication of the virus from the body has vanished. Even in patients who do not develop viral resistance or treatment intolerance, two kinds of viral persistence have been demonstrated both in lymphoid and central nervous system. The first one is a smoldering infection that persists, despite prolonged and apparently efficient HAART, in monocytes, tissue macrophages and most probably microglia. The second one is an integration of proviral DNA in the genome of subpopulations of CD4 lymphocytes of patients receiving efficient HAART. A similar viral integration in astrocytes and less likely in resting microglia is suggested by several studies, although it has yet to be demonstrated conclusively [source]