A Girl from Qatar with Post-Infantile Acquired Cerebral Palsy Caused By Submersion Injury: A Rare Etiology and a Therapeutic-Challenge.

Background: Cerebral palsy is a heterogeneous disorder that can cause a lifelong disability that is associated with a non-progressive damage in the brain. It is commonly caused by antenatal, perinatal, early postnatal and neonatal conditions. However, post-neonatal cases of acquired cerebral palsy have also been reported, and were commonly caused by infection. Patients and Methods: The family of a girl from Qatar, who developed severe cerebral palsy caused by submersion injury, consulted us about the possible therapies for her condition. Clinical picture and brain imaging abnormalities are described, and the relevant literatures were reviewed with the aim of suggesting possible evidence-based therapies. Results: At the age of 23 months, a previously healthy girl developed anoxic encephalopathy after experiencing submersion injury. MRI showed evidence of significant hypoxic ischemic injury primarily affecting the deep grey matter, hippocami, mid-brain and the posterior cortex. EEG showed diffuse slowness of cerebral activity and diffuse attenuation of the background without no epileptic abnormalities suggesting diffuse encephalopathy resulting from diffuse cortical injury. At the about age of three and half years, her family consulted us about her condition as she was still showing no awareness to the environment, showing no significant spontaneous movements. She had poor head control. Unable to sit or stand alone, and had a flexed posture. She was on levetiracetam (Keppra), diazepam, and baclofen 30 mg daily. She was still having tracheotomy, and was fed through gastrostomy tube. Conclusion: In this paper, the rare occurrence of severe post-infantile cerebral palsy is described. Emphasis is made on the possibility of using evidence-based multi-factorial therapies in cerebral palsy.

A Girl from Qatar with Post-Infantile Acquired Cerebral Palsy Caused By Submersion Injury: A Rare Etiology and a Therapeutic Challenge

Background: Cerebral palsy is a heterogeneous disorder that can cause a lifelong disability that is associated with a non-progressive damage in the brain. It is commonly caused by antenatal, perinatal, early postnatal and neonatal conditions. However, post-neonatal cases of acquired cerebral palsy have also been reported, and were commonly caused by infection. Patients and methods: The family of a girl from Qatar, who developed severe cerebral palsy caused by submersion injury, consulted us about the possible therapies for her condition. Clinical picture and brain imaging abnormalities are described, and the relevant literatures were reviewed with the aim of suggesting possible evidence-based therapies. Results: At the age of 23 months, a previously healthy girl developed anoxic encephalopathy after experiencing submersion injury. MRI showed evidence of significant hypoxic ischemic injury primarily affecting the deep grey matter, hippocami, mid-brain and the posterior cortex. EEG showed diffuse slowness of cerebral activity and diffuse attenuation of the background without no epileptic abnormalities suggesting diffuse encephalopathy resulting from diffuse cortical injury. At the about age of three and half years, her family consulted us about her condition as she was still showing no awareness to the environment, showing no significant spontaneous movements. She had poor head control. Unable to sit or stand alone, and had a flexed posture. She was on levetiracetam (Keppra), diazepam, and baclofen 30 mg daily. She was still having tracheotomy, and was fed through gastrostomy tube. Conclusion: In this paper, the rare occurrence of severe post-infantile cerebral palsy is described. Emphasis is made on the possibility of using evidence-based multi-factorial therapies in cerebral palsy.

An Anatomically Placed Tibial Tunnel does not Completely Surround a Simulated PCL Reconstruction Graft in the Proximal Tibia

Introduction It is hypothesized that anatomic tunnel placement will create tunnels with violation of the posterior cortex and subsequently an oblique aperture that is not circumferentially surrounded by bone. In this article, we aimed to characterize posterior cruciate ligament (PCL) tibial tunnel using a three-dimensional (3D) computed tomography (CT) model. Methods Ten normal knee CTs with the patella, femur, and fibula removed were used. Simulated 11 mm PCL tibial tunnels were created at 55, 50, 45, and 40 degrees. The morphology of the posterior proximal tibial exit was examined with 3D modeling software. The length of tunnel not circumferentially covered (cortex violation) was measured to where the tibial tunnel became circumferential. The surface area and volume of the cylinder both in contact with the tibial bone and that not in contact with the tibia were determined. The percentages of the stick-out length surface area and volume not in contact with bone were calculated. Results The mean stick-out length of uncovered graft at 55, 50, 45, and 40 degrees were 26.3, 20.5, 17.3, and 12.7 mm, respectively. The mean volume of exposed graft at 55, 50, 45, and 40 degrees were 840.8, 596.2, 425.6, and 302.9 mm3, respectively. The mean percent of volume of exposed graft at 55, 50, 45, and 40 degrees were 32, 29, 25, and 24%, respectively. The mean surface of exposed graft at 55, 50, 45, and 40 degrees were 372.2, 280.4, 208.8, and 153.3 mm2, respectively. The mean percent of surface area of exposed graft at 55, 50, 45, and 40 degrees were 40, 39, 34, and 34%, respectively. Conclusion Anatomic tibial tunnel creation using standard transtibial PCL reconstruction techniques consistently risks posterior tibial cortex violation and creation of an oblique aperture posteriorly. This risk is decreased with decreasing the angle of the tibial tunnel, though the posterior cortex is still compromised with angles as low as 40 degrees. With posterior cortex violation, a surgeon should be aware that a graft within the tunnel or socket posteriorly may not be fully in contact with bone. This is especially relevant with inlay and socket techniques.

Transcranial photoacoustic characterization of neurovascular physiology during early-stage photothrombotic stroke in neonatal piglets in vivo

Perinatal ischemic stroke is estimated to occur in 1/2300–1/5000 live births, but early differential diagnosis from global hypoxia-ischemia is often difficult. In this study, we tested the ability of a hand-held transcranial photoacoustic (PA) imaging probe to non-invasively detect a focal photothrombotic stroke (PTS) within 2 hours of stroke onset in a gyrencephalic piglet brain. 17 stroke lesions of approximately 1-cm2 area were introduced randomly in anterior or posterior cortex via the light/dye PTS technique in anesthetized neonatal piglets (n = 11). The contralateral non-ischemic region served as control tissue for discrimination contrast for the PA hemoglobin metrics: oxygen saturation, total hemoglobin (tHb), and individual quantities of oxygenated and deoxygenated hemoglobin (HbO2 and HbR). The PA-derived tissue oxygen saturation at 2 hours yielded a significant separation between control and affected regions-of-interest (p < 0.0001), which were well matched with 24-hr post-stroke cerebral infarction confirmed in the triphenyltetrazolium chloride-stained image. The quantity of HbO2 also displayed a significant contrast (p = 0.021), whereas tHb and HbR did not. The analysis on receiver operating characteristic curves and multivariate data analysis also agreed with the results above. This study shows that a hand-held transcranial PA neuroimaging device can detect a regional thrombotic stroke in the cerebral cortex of a neonatal piglet. In particular, we conclude that the oxygen saturation metric can be used alone to identify regional stroke lesions. The lack of change in tHb may be related to arbitrary hand-held imaging configuration and/or entrapment of red blood cells within the thrombotic stroke.

Advancement of PD Is Reflected by White Matter Changes in Olfactory Areas: A Pilot Study

Loss of sense of smell is a well-known non-motor symptom of Parkinson’s disease (PD). Here, we present insight into the association between PD advancement and equivalents of smell loss in olfactory-eloquent brain areas, such as the posterior cortex and orbitofrontal cortex. Twelve PD patients in different Hoehn and Yahr stages and 12 healthy normosmic individuals were examined with diffusion tensor imaging. Tract-based spatial statistics were used to analyze microstructural changes in white matter adjacent to the bilateral posterior and orbitofrontal cortex. Axial diffusivity, mean diffusivity, and radial diffusivity were significantly higher in olfactory ROIs in advanced PD patients. The results of this preliminary study indicate that PD advancement is associated with progressive neurodegeneration in olfactory-related brain areas.

Distributed context-dependent choice information in mouse posterior cortex

Choice information appears in multi-area brain networks mixed with sensory, motor, and cognitive variables. In the posterior cortex—traditionally implicated in decision computations—the presence, strength, and area specificity of choice signals are highly variable, limiting a cohesive understanding of their computational significance. Examining the mesoscale activity in the mouse posterior cortex during a visual task, we found that choice signals defined a decision variable in a low-dimensional embedding space with a prominent contribution along the ventral visual stream. Their subspace was near-orthogonal to concurrently represented sensory and motor-related activations, with modulations by task difficulty and by the animals’ attention state. A recurrent neural network trained with animals’ choices revealed an equivalent decision variable whose context-dependent dynamics agreed with that of the neural data. Our results demonstrated an independent, multi-area decision variable in the posterior cortex, controlled by task features and cognitive demands, possibly linked to contextual inference computations in dynamic animal–environment interactions.

Human spindle variability

In humans, sleep spindles are 10-16 Hz oscillations lasting approximately 0.5-2 s. Spindles, along with cortical slow oscillations, facilitate memory consolidation by enabling synaptic plasticity. Early recordings of spindles at the scalp found anterior channels had overall slower frequency than central-posterior channels. This robust, topographical finding led to dichotomizing spindles as slow versus fast, modeled as two distinct spindle generators in frontal versus posterior cortex. Using a large dataset of intracranial sEEG recordings (n=20, 365 bipolar recordings), we show that the difference in spindle frequency between frontal and parietal channels is comparable to the variability in spindle frequency within the course of individual spindles, across different spindles recorded by a given site, and across sites within a given region. Thus, fast and slow spindles only capture average differences that obscure a much larger underlying overlap in frequency. Furthermore, differences in mean frequency are only one of several ways that spindles differ. For example, compared to parietal, frontal spindles are smaller, tend to occur after parietal when both are engaged, and show a larger decrease in frequency within-spindles. However, frontal and parietal spindles are similar in being longer, less variable, and more widespread than occipital, temporal, and Rolandic spindles. These characteristics are accentuated in spindles which are highly phase-locked to posterior hippocampal spindles. We propose that rather than a strict parietal-fast/frontal-slow dichotomy, spindles differ continuously and quasi-independently in multiple dimensions, with variability due about equally to within-spindle, within-region and between-region factors.

De Novo PS1 Mutation (Pro436Gln) in a Very Early-Onset Posterior Variant of Alzheimer’s Disease Associated with Spasticity: A Case Report

We report a patient with sporadic Alzheimer’s disease with onset in his twenties found to carry the de novo Pro436Gln mutation in the presenilin 1 gene (PS1). Clinical phenotype featured a posterior cortical syndrome with severe visual agnosia and mild limb spasticity with brisk reflexes. Brain MRI and FDG-PET scans revealed severe parieto-occipital atrophy/hypometabolism. Cerebrospinal fluid biomarkers showed a decrease in Aβ 42 level and Aβ 42/40 ratio, increased phospho-tau, and normal total tau. Amyloid PET identified a very high burden of amyloid-β neuritic plaques in the posterior cortex. Similarities between this and two previously reported cases with this variant support that this mutation has a very strong impact on the clinical phenotype and is consistently associated with spasticity.

Transcranial photoacoustic characterization of neurovascular physiology during early-stage photothrombotic stroke in neonatal piglets in vivo

Perinatal ischemic stroke is estimated to occur in 1/2300-1/5000 live births, but early differential diagnosis from global hypoxia-ischemia is often difficult. In this study, we tested the ability of a hand-held transcranial photoacoustic (PA) imaging to non-invasively detect a focal photothrombotic stroke (PTS) within 2 hours of stroke onset in a gyrencephalic piglet brain. 17 stroke lesions of approximately 1-cm2 area were introduced randomly in anterior or posterior cortex via the light/dye PTS technique in anesthetized neonatal piglets (n = 11). The contralateral non-ischemic region served as control tissue for discrimination contrast for the PA hemoglobin metrics: HbO2 saturation, total hemoglobin (tHb), and individual quantities of oxygenated and deoxygenated hemoglobin (HbO2 and HbR). The PA-derived tissue HbO2 saturation at 2 hours yielded a significant separation between control and affected regions-of-interest (p < 0.0001), which were well matched with 24-hr post-stroke cerebral infarction confirmed in the triphenyltetrazolium chloride (TTC)-stained image. The quantity of HbO2 also displayed a significant contrast (p = 0.021), whereas tHb and HbR did not. The analysis on receiver operating characteristic curves and multivariate data analysis also agreed with the results above. This study shows that a hand-held transcranial PA neuroimaging can detect a regional thrombotic stroke in cerebral cortex of a neonatal piglet. In particular, we conclude that the HbO2 saturation metric can be used alone to identify regional stroke lesions. The lack of change in tHb may be related to arbitrary hand-held imaging configuration and/or entrapment of red blood cells within the thrombotic stroke.