Intracranial Pressure Dysfunction Following Severe Intracerebral Hemorrhage in Middle-Aged Rats.

Rising intracranial pressure (ICP) aggravates secondary injury and heightens risk of death following intracerebral hemorrhage (ICH). Long-recognized compensatory mechanisms that lower ICP include reduced cerebrospinal fluid and venous blood volumes. Recently, we identified another compensatory mechanism in severe stroke, a decrease in cerebral parenchymal volume via widespread reductions in cell volume and extracellular space (tissue compliance). Here, we examined how age affects tissue compliance and ICP dynamics after severe ICH in rats (collagenase model). A planned comparison to historical young animal data revealed that aged SHAMs (no stroke) had significant cerebral atrophy (9% reduction, p ≤ 0.05), ventricular enlargement (9% increase, p ≤ 0.05), and smaller CA1 neuron volumes (21%, p ≤ 0.05). After ICH in aged animals, contralateral striatal neuron density and CA1 astrocyte density significantly increased (12% for neurons, 7% for astrocytes, p ≤ 0.05 vs. aged SHAMs). Unlike young animals, other regions in aged animals did not display significantly reduced cell soma volume despite a few trends. Nonetheless, overall contralateral hemisphere volume was 10% smaller in aged ICH animals compared to aged SHAMs (p ≤ 0.05). This age-dependent pattern of tissue compliance is not due to absent ICH-associated mass effect (83.2 mm3 avg. bleed volume) as aged ICH animals had significantly elevated mean and peak ICP (p ≤ 0.01), occurrence of ICP spiking events, as well as bilateral evidence of edema (e.g., 3% in injured brain, p ≤ 0.05 vs. aged SHAMs). Therefore, intracranial compliance reserve changes with age; after ICH, these and other age-related changes may cause greater fluctuation from baseline, increasing the chance of adverse outcomes like mortality.

An update to the Monro-Kellie doctrine to reflect tissue compliance after severe ischemic and hemorrhagic stroke.

High intracranial pressure (ICP) can impede cerebral blood flow resulting in secondary injury or death following severe stroke. Compensatory mechanisms include reduced cerebral blood and cerebrospinal fluid volumes, but these often fail to prevent raised ICP. Serendipitous observations in intracerebral hemorrhage (ICH) suggest that neurons far removed from a hematoma may shrink as an ICP compliance mechanism. Here, we sought to critically test this observation. We tracked the timing of distal tissue shrinkage (e.g. CA1) after collagenase-induced striatal ICH in rat; cell volume and density alterations (42% volume reduction, 34% density increase; p < 0.0001) were highest day one post-stroke, and rebounded over a week across brain regions. Similar effects were seen in the filament model of middle cerebral artery occlusion (22% volume reduction, 22% density increase; p ≤ 0.007), but not with the Vannucci-Rice model of hypoxic-ischemic encephalopathy (2.5% volume increase, 14% density increase; p ≥ 0.05). Concerningly, this 'tissue compliance' appears to cause sub-lethal damage, as revealed by electron microscopy after ICH. Our data challenge the long-held assumption that 'healthy' brain tissue outside the injured area maintains its volume. Given the magnitude of these effects, we posit that 'tissue compliance' is an important mechanism invoked after severe strokes.

An Unusual Cause of Frequent, Sudden, Transient, Unexplained Falls and New-Onset Status Epilepticus: Case Report and Mini-Review.

We report a 14-year old adolescent Caucasian female, who presented with frequent, sudden, transient, and unexplained falls leading to multiple serious injuries to her head and extremities requiring several visits to the emergency department. She was evaluated numerous times and imaging studies, echocardiogram, electrocardiogram, and electroencephalogram studies were all normal. She eventually presented to outside emergency department with dystonic posturing and status epilepticus and was transferred to our pediatric intensive care unit for further management. She was diagnosed with an uncommon, underrecognized and underdiagnosed condition. To our knowledge there is no such previous report in a pediatric patient.

Ganglion cell layer-inner plexiform layer thickness and vision loss in young children with optic pathway gliomas.

PURPOSE: To determine if measures of macular ganglion cell layer-inner plexiform layer (GCL-IPL) thickness can discriminate between children with and without vision loss (visual acuity or field) from their optic pathway glioma (OPG) using spectral-domain optical coherence tomography (SD-OCT). METHODS: Children with OPGs (sporadic or secondary to neurofibromatosis type 1) enrolled in a prospective study of SD-OCT were included if they were cooperative for vision testing and macular SD-OCT images were acquired. Manual segmentation of the macular GCL-IPL and macular retinal nerve fiber layer (RNFL) was performed using elliptical annuli with diameters of 1.5, 3.0, and 4.5 mm. Logistic regression assessed the ability of GCL-IPL and RNFL thickness measures (micrometers) to differentiate between the normal and abnormal vision groups. RESULTS: Forty-seven study eyes (normal vision = 31, abnormal vision = 16) from 26 children with OPGs were included. Median age was 5.3 years (range, 2.5-12.8). Thickness of all GCL-IPL and RNFL quadrants differed between the normal and abnormal vision groups (P < 0.01). All GCL-IPL measures demonstrated excellent discrimination between groups (area under the curve [AUC] > 0.90 for all diameters). Using the lower fifth percentile threshold, the number of abnormal GCL-IPL inner macula (3.0 mm) quadrants achieved the highest AUC (0.989) and was greater than the macula RNFL AUCs (P < 0.05). CONCLUSIONS: Decreased GCL-IPL thickness (