In situ clearance of a proximal shunt malfunction in a child with hydrocephalus post cerebral arteriovenous malformation rupture noted intraoperatively.

BACKGROUND: Hydrocephalus shunt malfunctions remain treated with surgical intervention only. Despite efforts at identifying or preventing CSF shunt obstruction, no evidence currently exists to restore CSF flow following proximal occlusion, non-invasively. CASE DESCRIPTION: We present direct intraoperative evidence in the case of a 5-year-old male who developed hydrocephalus subsequent to hemorrhagic presentation post cerebral arteriovenous malformation rupture. After weeks of externalized CSF diversion for clearance of CSF red blood cells, he was taken to the operating room for removal of the external ventricular drain and placement of a ventriculoperitoneal shunt for hydrocephalus. At conclusion of placing his ventriculoperitoneal shunt with ReFlow flusher assist device, his shunt valve reservoir was noted to not refill. Following manual depression of the ReFlow flusher, we identified clearance of debris from the obstructed ventricular catheter allowing reestablished CSF flow through the shunt system under live intraoperative ultrasonography. Subsequently, there was return of brisk refill to the shunt valve reservoir. CONCLUSION: Observations here demonstrate a potentially useful technical strategy toward clearance of proximal shunt obstructions, in situ.

Sacral Rheumatoid Nodule: An Unusual Indication for Coccygectomy.

Here, we present a case report of a woman who presented with a large sacral rheumatoid nodule. This patient failed conservative treatment and presented in search of a surgical solution. We successfully removed her rheumatoid nodule using a surgical approach typically reserved for traumatic coccydynia. We show how coccygectomy, although a rare surgical procedure, was effective in treatment of a large rheumatoid nodule.

Implantation of Neuronal Stem Cells Enhances Object Recognition without Increasing Neurogenesis after Lateral Fluid Percussion Injury in Mice.

Cognitive deficits after traumatic brain injury (TBI) are debilitating and contribute to the morbidity and loss of productivity of over 10 million people worldwide. Cell transplantation has been linked to enhanced cognitive function after experimental traumatic brain injury, yet the mechanism of recovery is poorly understood. Since the hippocampus is a critical structure for learning and memory, supports adult neurogenesis, and is particularly vulnerable after TBI, we hypothesized that stem cell transplantation after TBI enhances cognitive recovery by modulation of endogenous hippocampal neurogenesis. We performed lateral fluid percussion injury (LFPI) in adult mice and transplanted embryonic stem cell-derived neural progenitor cells (NPC). Our data confirm an injury-induced cognitive deficit in novel object recognition, a hippocampal-dependent learning task, which is reversed one week after NPC transplantation. While LFPI alone promotes hippocampal neurogenesis, as revealed by doublecortin immunolabeling of immature neurons, subsequent NPC transplantation prevents increased neurogenesis and is not associated with morphological maturation of endogenous injury-induced immature neurons. Thus, NPC transplantation enhances cognitive recovery early after LFPI without a concomitant increase in neuron numbers or maturation.