Influence of Myelography and Postmyelographic CT on Therapeutic Decisions in Degenerative Diseases of the Cervical Spine.

Study Design: A retrospective analysis of clinical records and radiologic imaging by 3 independent reviewers to assess the indication for surgical treatment with and without myelography and postmyelographic computed tomography (MCT).

Objective: To evaluate whether myelography and MCT obtained in addition to magnetic resonance imaging (MRI) influence therapeutic decisions in degenerative diseases of the cervical spine.

Summary Of Background Data: MRI has become the standard examination in spinal diseases.

The temporal profile of cerebral blood flow and tissue metabolites indicates sustained metabolic depression after experimental subarachnoid hemorrhage in rats.

Background: Derangement of cerebral metabolism occurs after various insults such as ischemia, traumatic brain injury, and subarachnoid hemorrhage (SAH).

Objective: To investigate the course of cerebral blood flow and metabolic parameters in the first hours after experimental SAH.

Methods: Sixteen Sprague-Dawley rats were subjected to SAH using the endovascular filament model or served as controls (8 rats in each group).

Prophylactic intravenous magnesium sulfate for treatment of aneurysmal subarachnoid hemorrhage: a randomized, placebo-controlled, clinical study.

Objective: To examine whether the maintenance of elevated magnesium serum concentrations by intravenous administration of magnesium sulfate can reduce the occurrence of cerebral ischemic events after aneurysmal subarachnoid hemorrhage.

Design: Prospective, randomized, placebo-controlled study.

Setting: Neurosurgical intensive care unit of a University hospital.

Time-course of cerebral perfusion and tissue oxygenation in the first 6 h after experimental subarachnoid hemorrhage in rats.

Present knowledge about hemodynamic and metabolic changes after subarachnoid hemorrhage (SAH) originates from neuromonitoring usually starting with aneurysm surgery and animal studies that have been focusing on the first 1 to 3 h after SAH. Most patients, however, are referred to treatment several hours after the insult. We examined the course of hemodynamic parameters, cerebral blood flow, and tissue oxygenation (ptiO2) in the first 6 h after experimental SAH.

Acute vasoconstriction: decrease and recovery of cerebral blood flow after various intensities of experimental subarachnoid hemorrhage in rats.

Object: Immediate vasoconstriction after subarachnoid hemorrhage (SAH) has been observed in a number of experimental studies. However, it has not yet been examined which pattern this acute-type vascular reaction follows and whether it correlates with the intensity of SAH. It was the purpose of the present study to vary the extent of SAH using the endovascular filament model of SAH with increasing filament sizes and to compare the course of intracranial pressure (ICP), cerebral perfusion pressure (CPP), and regional cerebral blood flow (rCBF).

Clinical features, treatment, and prognosis of patients with acute subdural hematomas presenting in critical condition.

Objective: Spontaneous acute subdural hematoma (aSDH) may be caused by aneurysm rupture. Patients can present in very poor clinical condition with anisocoria or even bilaterally dilated pupils, absent brainstem reflexes, and cardiac insufficiency. For the clinician, the question is how should these patients be treated? Large series on this subject do not exist because aSDH is a rare event.

Special aspects of severe head injury: recent developments.

Trauma in general, and head injury in particular, is the most frequent cause of mortality and morbidity in those aged up to 45 years. Outcome from severe head injury depends on the nature and severity of the primary lesion, and the manifestations of secondary brain damage of extra- and intracranial origin. The most important sequela is cerebral ischaemia resulting from intracranial hypertension caused by, for example, traumatic brain swelling or intracranial haemorrhage and/or systemic complications, of which arterial hypotension is the most significant.

Arterial hypotension triggers perifocal depolarizations and aggravates secondary damage in focal brain injury.

Perifocal depolarizations (PFD) have been observed after traumatic brain injury, are known to disturb cerebrovascular reactivity and thus may contribute to the morphological consequences of brain injury. In this investigation, the role of PFD was studied in focal brain lesions with/without induction of delayed hypotension. Cerebral freeze lesions were induced in anesthetized normotensive rats that underwent perfusion fixation of brains 5 min, 4 h or 24 h after lesioning, respectively, to obtain quantitative histopathology.

Hyperoxic ventilation at the critical hematocrit: effects on myocardial perfusion and function.

Background: Hemodilution reduces hematocrit (Hct) and blood oxygen content. Tissue oxygenation is mainly preserved by increased cardiac output. As myocardial O2-demands increase, coronary vasodilatation becomes necessary to increase myocardial blood flow.

Correlation of lesion volume and brain swelling from a focal brain trauma.

Brain edema and secondary growth of a traumatic brain tissue necrosis are important manifestations of secondary brain damage and of prognostic significance in severe head injury. Aim of the current study was to analyze the interdependency of the resulting brain swelling from the size of the focal traumatic lesion. Male Sprague-Dawley rats were intubated and mechanically ventilated.

Relative cerebral blood flow during the secondary expansion of a cortical lesion in rats.

The size of a cerebral contusion is not finite at the moment of trauma, but liable to secondary increase during the following hours and days. In the present study we investigated whether this phenomenon may be related to changes in cortical blood flow (cCBF). In rats a cortical lesion grew to 140% of its initial volume during the first 24 h after injury.

Release of excitatory amino acids in the penumbra of a focal cortical necrosis.

A cortical tissue necrosis from focal trauma expands between 30% and 300% from its initial size within 24 h, depending on the species studied. To shed light on the pathophysiological processes in the penumbra 1 zone after a focal cortical lesion, the release of excitatory amino acids into the traumatic penumbra zone 1 was measured throughout the entire period of necrosis expansion. A microdialysis probe was inserted at an oblique angle into the cortex of Sprague-Dawley rats 2 mm below the brain surface.

Role of bradykinin B2 receptors in the formation of vasogenic brain edema in rats.

Bradykinin is a mediator of brain edema acting through B2 receptors. However, it is not known if bradykinin mediates the formation of cytotoxic or vasogenic brain swelling. To investigate this question we subjected rats to a cryogenic brain lesion over the left parietal cortex, a model well known to produce predominantly vasogenic brain edema.

Attenuation of secondary lesion growth in the brain after trauma by selective inhibition of the inducible NO-synthase.

In previous studies we have demonstrate that aminoguanidine pretreatment attenuates the secondary necrosis growth after focal brain trauma. Purpose of the present investigation was to elucidate the therapeutic potential of this iNOS-inhibitor when administered post lesion. Sprague-Dawley rats were subjected to a highly standardized cortical freezing lesion and administered with aminoguanidine (100 mg/kg i.

Interstitial lactate in the peritraumatic penumbra of rat brain.

A traumatic brain tissue necrosis is expanding to approximately 150% within 24 h after lesion. This process is accompanied by marked reduction of the perifocal cerebral blood flow likely to activate anaerobic glycolysis from a reduced O2-supply leading to an accumulation of lactic acid. The current study was carried out to assess the interstitial levels of lactic acid as a potential factor of secondary brain damage.

Cerebral blood flow and the secondary growth of brain tissue necrosis after trauma.

A local brain tissue necrosis from trauma progresses during the following 24 hours or longer. A decrease in cerebral blood flow has been observed both in the necrotic as well as adjacent cortical region, which may influence expansion of the lesion into the perifocal brain tissue. Currently the regional cortical blood flow (rCBF) was assessed by using scanning laser Doppler fluxmetry.

LF16-0687 a novel non-peptide bradykinin B2 receptor antagonist reduces vasogenic brain edema from a focal lesion in rats.

Head injury world wide is still the most frequent cause of morbidity and mortality among the population under 45 years. Approximately 50% of patients dying from severe head injury have a therapy refractory intracranial pressure rise (Baethmann 1998). Traumatic brain edema, e.

Role of nitric oxide in the secondary expansion of a cortical brain lesion from cold injury.

We have investigated the role of nitric oxide (NO) as mediator of the secondary growth of a traumatic cortical necrosis. For this purpose, a highly standardized focal lesion of the brain was induced in 46 Sprague-Dawley rats by cold injury. Twenty-four hours later--the timepoint of maximal lesion spread--the animals were sacrificed and brains were removed for histomorphometry of the maximal necrosis area and volume.

The effect of dietary alpha-tocopherol on the experimental vasogenic brain edema.

It has become increasingly obvious that free radicals and lipid peroxidation contribute to brain damage from trauma by mediating edema formation and ischemia. It should, therefore, be expected that the actual level of endogenous antioxidants, as for example, vitamin C and E in plasma, has an influence on the extent of free radical-induced injury. In this communication we investigate the effect of dietary changes in the free radical scavenger alpha-tocopherol on posttraumatic cerebral swelling in Sprague-Dawley rats.

Assessment of regional cortical blood flow following traumatic lesion of the brain.

A brain tissue necrosis from trauma gradually expands during the subsequent 24 h. Among others, deterioration of perifocal blood flow could be involved in the secondary extinction of initially viable brain tissue. A highly standardized freezing lesion was made in cerebral cortex of rats for frequent measurements of regional cortical blood flow with high spatial resolution by laser Doppler scanning flowmetry.

The penumbra zone of a traumatic cortical lesion: a microdialysis study of excitatory amino acid release.

A cortical tissue necrosis from focal trauma expands to 150% of its initial volume within 24 hrs. It is currently unknown, whether this phenomenon is part of the primary traumatic lesion or if it involves secondary mechanisms such as the release of excitatory amino acids into the traumatic penumbra zone. A microdialysis probe was inserted for that purpose in an oblique angle into the cortex of Sprague-Dawley rats, approximately 2 mm below the brain surface.

Treatment of vasogenic brain edema with the novel Cl- transport inhibitor torasemide.

The efficacy of the diuretic agent torasemide, which antagonizes the Na+/K+/Cl- cotransport and Cl- channels, was investigated to determine its inhibition of brain edema from a focal cerebral lesion. For this purpose, cold injury of the brain was induced in 50 Sprague-Dawley rats while monitoring arterial blood pressure. The brain was removed for gravimetric assessment of swelling of the traumatized hemisphere 24 h after trauma.

Therapeutical efficacy of a novel chloride transport blocker and an IP3-analogue in vasogenic brain edema.

The efficacy of torasemide, a novel chloride-channel blocker, and of PP56, an IP3 analogue, was currently examined in experimental brain edema. Following trephination in anesthesia rats were subjected to a focal cold injury of the left cerebral hemisphere. Animals of 4 experimental groups receiving either torasemide (i.

Growth kinetics of a primary brain tissue necrosis from a focal lesion.

Secondary brain damage, such as brain edema or impairment of the cerebral microcirculation may evolve from tissue necrosis of the brain induced by trauma or ischemia. This laboratory has provided novel information on the secondary increase of a primary brain tissue necrosis resulting from a focal lesion. We have presently investigated more closely the growth kinetics of this process during 24 h after trauma.