An anatomy-based lumped parameter model of cerebrospinal venous circulation: can an extracranial anatomical change impact intracranial hemodynamics?

Background The relationship between extracranial venous system abnormalities and central nervous system disorders has been recently theorized. In this paper we delve into this hypothesis by modeling the venous drainage in brain and spinal column areas and simulating the intracranial flow changes due to extracranial morphological stenoses. Methods A lumped parameter model of the cerebro-spinal venous drainage was created based on anatomical knowledge and vessels diameters and lengths taken from literature. Each vein was modeled as a hydraulic resistance, calculated through Poiseuille’s law. The inputs of the model were arterial flow rates of the intracranial, vertebral and lumbar districts. The effects of the obstruction of the main venous outflows were simulated. A database comprising 112 Multiple Sclerosis patients (Male/Female = 42/70; median age ± standard deviation = 43.7 ± 10.5 years) was retrospectively analyzed. Results The flow rate of the main veins estimated with the model was similar to the measures of 21 healthy controls (Male/Female = 10/11; mean age ± standard deviation = 31 ± 11 years), obtained with a 1.5 T Magnetic Resonance scanner. The intracranial reflux topography predicted with the model in cases of internal jugular vein diameter reduction was similar to those observed in the patients with internal jugular vein obstacles. Conclusions The proposed model can predict physiological and pathological behaviors with good fidelity. Despite the simplifications introduced in cerebrospinal venous circulation modeling, the key anatomical feature of the lumped parameter model allowed for a detailed analysis of the consequences of extracranial venous impairments on intracranial pressure and hemodynamics

The treatment for multilevel noncontiguous spinal fractures

We report the outcome of 30 patients with multilevel noncontiguous spinal fractures treated between 2000 and 2005. Ten cases were treated conservatively (group A), eight cases were operated on at only one level (group B), and 12 cases were treated surgically at both levels (group C). All cases were followed up for 14–60 months (mean 32 months). Initial mobilisation with a wheelchair or crutches in group A was 9.2±1.1 weeks, which was significantly longer than groups B and C with 6.8±0.7 weeks and 3.1±0.4 weeks, respectively. Operative time and blood loss in group C were significantly more than group B. The neurological deficit improved in six cases in group A (60%), six in group B (75%) and eight in group C (80%). Correction of kyphotic deformity was significantly superior in groups C and B at the operated level, and increasing deformity occurred in groups A and B at the non-operated level. From the results we believe that three treatment strategies were suitable for multilevel noncontiguous spinal fractures, and individualised treatment should be used in these patients. In the patients treated surgically, the clinical and radiographic outcomes are much better

Diagnosis and Treatment of the Intracranial Compartment Syndrome

The intracranial compartment syndrome is a condition characterized by a set of clinical symptoms and signs due to a rise in intracranial pressure (ICP). Intracranial hypertension is a life-treating condition that requires quick diagnosis and treatment; otherwise, it may progress in herniation syndrome and death. Consequently, timely recognition and management of elevated ICP is the first goal in order to maintain good cerebral perfusion pressure and to prevent irreversible secondary cerebral insult. Several pathologies may cause raised ICP, and it is fundamental to treat the specific underlying disease. Therefore, neuromonitoring assumes paramount significance for the rapid detection of harmful events and for a quick evaluation of the efficacy of medical treatment. In this chapter, we aimed to provide an overview of the current knowledge regarding the diagnosis and treatment of intracranial compartment syndrome

Disorders of Consciousness

The concept of consciousness has fascinated philosophers, psychologists and neurophysiologists for a long time; however, it remains difficult to give its univocal and universally accepted definition. Consciousness is defined as “the state of full awareness of the self and one’s relationship to the environment”; consequently, a distinction must be made between consciousness (or awareness) and vigilance/alertness (wakefulness). In fact, it is possible for a patient to be conscious, but unresponsive to the examiner, for lack of sensory inputs or for psychiatric reasons. Conversely, a subject can be alert and awake with open eyes, but not conscious and not aware (in part or at all) of itself and of the environment. From a neurophysiological point of view, it has been demonstrated that the brainstem Reticular Activating System (RAS) is responsible for the state of alertness, through its projections to the thalamus and cortex. The integrity of the upper cortical centres, which are closely related to each other and receive the reticular activating stimuli, is also essential for the maintenance of consciousness level. Therefore, Disorders Of Consciousness (DOC) and vigilance may depend on damage to one or both of these neurofunctional systems, acute or chronic, reversible or irreversible. Serious damage to the reticular system, with or without concomitant widespread cortical damage, can produce a state of coma. Coma is then a pathological condition in which the subject lies with eyes closed and he is neither conscious nor alert, with altered - or completely absent - responsiveness to stimuli. In case of widespread damage to the cerebral cortex without involvement of the RAS, a particular condition - named Vegetative State (VS) - may occur: the consciousness of self and of the environment is impaired, but a certain level of vigilance is still preserved. Moreover, there also exist several neurological conditions that can be defined as “borderline”, such as the Minimally Conscious State. Finally, brain death is the irreversible definitive impairment of both the cortical and brainstem functions. Electroencephalography is an important diagnostic and prognostic tool, useful to better characterise the evolution of a coma state, to recognise any kind of epileptiform activity - that could be clinically hidden - and to monitor the effects of antiepileptic drugs, level of sedation, and treatment of intracranial hypertension

Src Family Kinases in Brain Edema After Acute Brain Injury

Brain edema, the first stage of intracranial hypertension, has been associated with poor prognosis and increased mortality after acute brain injury, such as ischemic stroke, intracranial hemorrhage (ICH), and traumatic brain injury (TBI). The acute brain injury often initiates release of many molecules, including glutamate, adenosine, thrombin, oxyhemoglobin, cytokines, reactive oxygen species (ROS), damage associated molecular pattern molecules (DAMPs), and others. Most of those molecules activate Src family kinases (SFKs), a family of proto-oncogenic non-receptor tyrosine kinases, resulting in blood-brain barrier (BBB) disruption and brain edema at the acute stage after brain injury. However, SFKs also contributes to BBB self-repair and brain edema resolution in the chronic stage that follows brain injury. In this review we summarize possible pathways through which SFKs are implicated in both brain edema formation and its eventual resolution