Acute spontaneous intracranial epidural haematoma and disseminated intravascular coagulation in a paediatric sickle cell patient.

An African American teenage boy during an acute sickle cell crisis spontaneously developed acute bifrontal epidural haematomas (EDHs) in addition to disseminated intravascular coagulation (DIC). The successfully evacuated EDH reaccumulated postoperatively. After multiple transfusions, the patient underwent repeat surgery.

Transection of Omohyoid Muscle as an Aid During Vagus Nerve Stimulator Implantation.

Background: Exposure of the carotid sheath during vagus nerve stimulator (VNS) implantation is usually straightforward but can be difficult for patients with a large body habitus. In addition, the exposure must be done with care if the surgeon wants to keep the vagus nerve in situ without using retractors that might impair access.

Objective: We describe the use of the omohyoid muscle as a landmark for the jugular vein and report how transection of the omohyoid can facilitate rapid and wide exposure of the carotid sheath.

Intracranial calcified pseudocyst reaction to a shunt catheter.

A 9-year-old boy with spina bifida, Chiari II malformation, and hydrocephalus presented with signs of increased intracranial pressure consistent with a shunt malfunction. Radiological investigations revealed an intracranial calcified lesion along the ventricular catheter. A shunt tap revealed a translucent milky white fluid.

Effect of antioxidant treatment on spinal GABA neurons in a neuropathic pain model in the mouse.

One feature of neuropathic pain is a reduced spinal gamma-aminobutyric acid (GABA)-ergic inhibitory function. However, the mechanisms behind this attenuation remain to be elucidated. This study investigated the involvement of reactive oxygen species in the spinal GABA neuron loss and reduced GABA neuron excitability in spinal nerve ligation (SNL) model of neuropathic pain in mice.

Indium 111 diethylenetriamine pentaacetic acid scintigraphy in the identification and management of intrathecal pump malfunction.

Background: Intrathecal drug-delivery systems have become widely used tools in the management of refractory chronic pain and spasticity. Because increasing numbers of patients are using these systems, rehabilitation specialists frequently are the initial care providers who identify clinical signs and symptoms indicating possible complications relating to the implanted system. Identification of a pump malfunction often presents a diagnostic challenge.

Reactive oxygen species contribute to neuropathic pain by reducing spinal GABA release.

Although both a loss of spinal inhibitory neurotransmission and the involvement of oxidative stress have been regarded as important mechanisms in the pathogenesis of pain, the relationship between these 2 mechanisms has not been studied. To determine whether reactive oxygen species (ROS) involvement in pain mechanisms is related to the diminished inhibitory transmission in the substantia gelatinosa (SG) of the spinal dorsal horn, behavioral studies and whole-cell recordings were performed in FVB/NJ mice. Neuropathic pain was induced by a tight ligation of the L5 spinal nerve (SNL).

Protein misfolding disorders and rational design of antimisfolding agents.

Compelling evidence strongly suggests that the conversion of a normal soluble protein into a beta-sheet-rich oligomeric structure and further fibril formation is the critical step in the pathogenesis of several human diseases, termed protein misfolding disorders. Therefore, a promising therapeutic strategy consists of the design of molecules that prevent the misfolding and aggregation of these proteins. In this chapter, we survey the mechanism of protein misfolding and some strategies to rationally produce inhibitors of this process.