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Cortical Involvement (cortical + involvement)

Distribution by Scientific Domains

Medical Sciences	100%

Selected Abstracts

Different Electroclinical Manifestations of the Epilepsy Associated with Hamartomas Connecting to the Middle or Posterior Hypothalamus

EPILEPSIA, Issue 9 2003
Alberto J. R. Leal
Summary:,Purpose: The epilepsy associated with hypothalamic hamartomas (HHs) has typical clinical, electrophysiologic, and behavioral manifestations refractory to drug therapy and with unfavorable evolution. It is well known that only sessile lesions produce epilepsy, but no correlation has been established between the different types of sessile hamartomas and the diverse manifestations of the epilepsy. We correlate anatomic details of the hamartoma and the clinical and neurophysiologic manifestations of the associated epilepsy. Methods: HHs of seven patients with epilepsy (ages 2, 25 years) were classified as to lateralization and connection to the anteroposterior axis of the hypothalamus by using high-resolution brain magnetic resonance imaging. We correlated the anatomic classification with the clinical and neurophysiologic manifestations of the epilepsy as evaluated in long-term (24 h) video-EEG recordings. Results: HHs ranged in size from 0.4 to 2.6 cc, with complete lateralization in six of seven patients. Ictal manifestations showed good correlation with the lobar involvement of ictal/interictal EEGs. These manifestations suggest the existence of two types of cortical involvement, one associated with the temporal lobe, produced by hamartomas connected to the posterior hypothalamus (mamillary bodies), and the other associated with the frontal lobe, seen in lesions connecting to the middle hypothalamus. Conclusions: A consistent clinical and neurophysiologic pattern of either temporal or frontal lobe cortical secondary involvement was found in the patients of our series. It depends on whether the hamartoma connects to the mamillary bodies (temporal lobe cases) or whether it connects to the medial hypothalamus (frontal lobe cases). [source]

Cognitive disturbances in primary blepharospasm,

MOVEMENT DISORDERS, Issue 14 2009
Gabriela Gonzalez Alemán PhD
Abstract The common belief that primary dystonia is a purely motor disorder with no anatomical substrate and no other accompanying neurological dysfunction has recently been challenged. In addition, there is increasing evidence that the basal ganglia besides motor control, plays a role in cognitive functioning. However, no systematic cognitive performance evaluation has been carried out in patients with primary blepharospasm (BS), one of the most common forms of adult dystonia. We evaluated a series of 20 patients with primary BS and a group of 17 controls matched by severity of mood symptoms, age, and sex. BS patients performed significantly worse on the Luria sequencing test, Purdue pegboard test, reciprocal coordination, tactile denomination, and reverse visuospatial span and the differences persisted after correction for age, duration of disease, severity of BS, and degree of depression. The Wisconsin card sorting test showed no statistical difference, but BS patients made more errors and more perseverative answers than expected according to population means, whereas the control group performed poorly but within normal parameters. Our findings suggest broad cortical involvement in focal dystonia that is not correlated with the severity or duration of dystonia. © 2009 Movement Disorder Society [source]

Propagation of spreading depression inversely correlates with cortical myelin content,

ANNALS OF NEUROLOGY, Issue 3 2009
Doron Merkler MD
Objective Cortical myelin can be severely affected in patients with demyelinating disorders of the central nervous system. However, the functional implication of cortical demyelination remains elusive. In this study, we investigated whether cortical myelin influences cortical spreading depression (CSD). Methods CSD measurements were performed in rodent models of toxic and autoimmune induced cortical demyelination, in neuregulin-1 type I transgenic mice displaying cortical hypermyelination, and in glial fibrillary acidic protein,transgenic mice exhibiting pronounced astrogliosis. Results Cortical demyelination, but not astrogliosis or inflammation per se, was associated with accelerated CSD. In contrast, hypermyelinated neuregulin-1 type I transgenic mice displayed a decelerated CSD propagation. Interpretation Cortical myelin may be crucially involved in the stabilization and buffering of extracellular ion content that is decisive for CSD propagation velocity and cortical excitability, respectively. Our data thus indicate that cortical involvement in human demyelinating diseases may lead to relevant alterations of cortical function. Ann Neurol 2009;66:355,365 [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]

Imaging patterns of brain injury in term-birth asphyxia

ACTA PAEDIATRICA, Issue 3 2009
Renate Swarte
Abstract Aim: To develop an extended asphyxia-score based on cerebral ultrasound (US) and MRI in order to gain further insight into the pathophysiology of asphyxia. Patients and Methods: First week cerebral US and MRI of 80 asphyxiated term infants were scored according to a new scoring system based on separate grading of injury to deep grey matter and to (sub)cortical/white matter. Our findings were compared with published scoring systems. Results: Six patterns of brain injury were derived: deep grey matter injury with either limited or extensive cortical involvement, damage to deep grey matter with watershed injury, isolated watershed injury, isolated white matter injury (leukomalacia) and isolated cortical necrosis. The mortality rate was considerable in patterns with extensive cortical injury. Conclusion: Six patterns of brain injury, following term-birth asphyxia were found using a new imaging score. [source]