Spinal metastases compressing the spinal cord are a medical emergency and should be operated on if possible; however, patients' medical condition is often poor and surgical complications are common. Minimizing surgical extant, operative time, and blood loss can potentially reduce postoperative complications. This is a retrospective study describing the patients operated on in our department utilizing a minimally invasive surgery (MIS) approach to decompress and instrument the spine from November 2013 to November 2014. Five patients were operated on for thoracic or lumbar metastases. In all cases a unilateral decompression with expandable tubular retractor was followed by instrumentation of one level above and below the index level and additional screw at the index level contralateral to the decompression side. Cannulated fenestrated screws were used (Longitude FNS) and cement was injected to increase pullout resistance. Mean operative time was 134 minutes and estimated blood loss was minimal in all cases. Improvement was noticeable in neurological status, function, and pain scores. No complications were observed. Technological improvements in spinal instruments facilitate shorter and safer surgeries in oncologic patient population and thus reduce the complication rate. These technologies improve patients' quality of life and enable the treatment of patients with comorbidities.

Background Previous models of intracranial pressure (ICP) dynamics have not included flow of cerebral interstitial fluid (ISF) and changes in resistance to its flow when brain swelling occurs. We sought to develop a mathematical model that incorporates resistance to the bulk flow of cerebral ISF to better simulate the physiological changes that occur in pathologies in which brain swelling predominates and to assess the model’s ability to depict changes in cerebral physiology associated with cerebral edema. Methods We developed a lumped parameter model which includes a representation of cerebral ISF flow within brain tissue and its interactions with CSF flow and cerebral blood flow (CBF). The model is based on an electrical analog circuit with four intracranial compartments: the (1) subarachnoid space, (2) brain, (3) ventricles, (4) cerebral vasculature and the extracranial spinal thecal sac. We determined changes in pressure and volume within cerebral compartments at steady-state and simulated physiological perturbations including rapid injection of fluid into the intracranial space, hyperventilation, and hypoventilation. We simulated changes in resistance to flow or absorption of CSF and cerebral ISF to model hydrocephalus, cerebral edema, and to simulate disruption of the blood–brain barrier (BBB). Results The model accurately replicates well-accepted features of intracranial physiology including the exponential-like pressure–volume curve with rapid fluid injection, increased ICP pulse pressure with rising ICP, hydrocephalus resulting from increased resistance to CSF outflow, and changes associated with hyperventilation and hypoventilation. Importantly, modeling cerebral edema with increased resistance to cerebral ISF flow mimics key features of brain swelling including elevated ICP, increased brain volume, markedly reduced ventricular volume, and a contracted subarachnoid space. Similarly, a decreased resistance to flow of fluid across the BBB leads to an exponential-like rise in ICP and ventricular collapse. Conclusions The model accurately depicts the complex interactions that occur between pressure, volume, and resistances to flow in the different intracranial compartments under specific pathophysiological conditions. In modelling resistance to bulk flow of cerebral ISF, it may serve as a platform for improved modelling of cerebral edema and blood–brain barrier disruption that occur following brain injury.

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Chronic subdural hematoma (cSDH) is a common pathology that typically affects the elderly. It is believed to occur due to injury to the dural border cells, which creates an inflammation/proliferation reaction. Ineffective repair leads to the formation of a new external layer of cells and fragile capillaries, which damage easily and can worsen the condition. Conventionally, asymptomatic cSDH is managed by observation, and symptomatic cases are treated by surgical evacuation. Unfortunately, recurrence rates of the SDH following surgical evacuation can be high. One treatment option for SDH involves embolization of the middle meningeal artery (MMA). The MMA provides blood supply to the dura mater and feeds the membrane capillaries covering the SDH. MMA embolization blocks the blood flow to this system and can promote hematoma resolution. In this paper, we review the existing literature on MMA embolization and discuss the underlying pathophysiology of cSDH.