Spinal cord blood flow changes following systemic hypothermia and spinal cord compression injury: an experimental study in the rat using Laser-Doppler flowmetry.

STUDY DESIGN: It is well known that changes of the body temperature as well as trauma influence the blood flow in the brain and spinal cord. However, there is still a lack of knowledge concerning the levels of blood flow changes, especially during hypothermia. OBJECTIVES: This investigation was carried out to examine the effects of systemic hypothermia and trauma on spinal cord blood flow (SCBF). METHODS: Twenty-four rats were randomized either to thoracic laminectomy only (Th VII-IX) or to 35 g spinal cord compression trauma. The animals were further randomized to either constant normothermia (38 degrees C) or to a systemic cooling procedure, ie reduction of the esophageal temperature from 38 to 30 degrees C. SCBF was recorded 5 mm caudal to the injury zone using Laser-Doppler flowmetry which allows a non-invasive continuous recording of local changes in the blood flow. The autoregulation ability was tested at the end of the experiments by inducing a 30-50 mmHg blood-pressure fall, using blood-withdrawal from the carotid artery. RESULTS: The mean SCBF decreased 2.8% and 3.5% per centigrade reduction of esophageal temperature in the animals sustained to hypothermia with and without trauma, respectively. This could be compared to a decrease of 0.2%/min when only trauma was applied. No significant differences were seen between the groups concerning auto regulatory ability. CONCLUSIONS: Our results indicate that the core temperature has a high impact on the SCBF independent of previous trauma recorded by Laser-Doppler flowmetry. This influence exceeds the response mediated by moderate compression trauma alone.

Systemic hypothermia following spinal cord compression injury in the rat: an immunohistochemical study on MAP 2 with special reference to dendrite changes.

Systemic hypothermia has been shown to exert neuroprotective effects in experimental ischemic CNS models caused by vascular occlusions. The present study addresses the question as to whether systemic hypothermia has similar neuroprotective qualities following severe spinal cord compression trauma using microtubule-associated protein 2 (MAP2) immunohistochemistry combined with the avidin-biotin-peroxidase complex method as marker to identify neuronal and dendritic lesions. Fifteen rats were randomized into three equally sized groups. One group sustained thoracic laminectomy, the others severe spinal cord compression trauma of the T8-9 segment. The control group contained laminectomized animals submitted to a hypothermic procedure in which the esophageal temperature was reduced from 38 degrees C to 30 degrees C. The two trauma groups were either submitted to the same hypothermic procedure or kept normothermic during the corresponding time. All animals were sacrificed 24 h following the surgical procedure. The MAP2 immunostaining in the normothermic trauma group indicated marked reductions in MAP2 antigen in the cranial and caudal peri-injury zones (T7 and T10, respectively). This reduction was much less pronounced in the hypothermic trauma group. In fact, the MAP2 antigen was present in almost equally sized areas in both the hypothermic groups independent of previous laminectomy alone or the addition of trauma. Our study thus indicates that hypothermia has a neuroprotective effect on dendrites of rat spinal cords subjected to compression trauma.

Motor function changes in the rat following severe spinal cord injury. Does treatment with moderate systemic hypothermia improve functional outcome?

Systemic hypothermia exerts neuroprotective effects following trauma and ischemia caused by vascular occlusion in the brain. In the spinal cord similar effects have been demonstrated following ischemia after aortic occlusion. We have previously presented protective effects on several morphological parameters in the early period after the injury, using an established spinal cord compression injury model and systemic hypothermia. In the present study we have evaluated the effects on motor function following severe spinal cord compression trauma and treatment with moderate systemic hypothermia. Thirty Sprague Dawley rats were randomized into three groups: In group 1 (n = 4), the animals underwent a hypothermic procedure, including a 2 h hypothermic period with a body temperature of 30 degrees C, following the initial laminectomy. In group 2 (n = 12) a 50 g compression was applied to the spinal cords for 5 min, after which the animals were kept under normothermic anesthesia for 3 h. In group 3 (n = 14), the animals underwent the same trauma procedure as in group 2 and the same hypothermic procedure as in group 1. The animals were allowed to survive for 14 days, during which the motor function was recorded. This degree of trauma results in a non-reversible paraplegia, and the addition of systemic hypothermia as described above did not alter the neurological recovery as measured by two different methods of recording the motor function up to two weeks after injury. All animals survived in group 1. However, the mortality rates in group 2 were 25% and in group 3, 50%, respectively, which mirrors the severity of the trauma. The application of systemic hypothermia and the lack of experimental therapeutic success highlight the difficulties of transferring experimental beneficial neuroprotective effects to a clinically useful treatment method. In this experimental set-up the effects of the severe primary injury may overshadow the effects of the secondary injury mechanisms, which limits the therapeutic possibilities of systemic hypothermic treatment.

Systemic hypothermia following spinal cord compression injury in the rat: axonal changes studied by beta-APP, ubiquitin, and PGP 9.5 immunohistochemistry.

STUDY DESIGN: Systemic hypothermia exerts neuroprotective effects in experimental ischemic CNS models caused by vascular occlusions. Recent experimental and clinical studies have also demonstrated beneficial effects of hypothermic treatment following brain trauma. OBJECTIVES: The present study addresses the question as to whether systemic hypothermia has similar protective qualities following severe spinal cord compression trauma using beta-APP-, ubiquitin-, and PGP-9.5-immunohistochemistry combined with the ABC complex method as markers to identify axonal changes. METHODS: Fifteen rats were randomized into three equally large groups and sustained to either thoracic laminectomy or to severe spinal cord compression trauma of the Th 8 - 9 segments. The non-trauma group contained laminectomized animals submitted to a hypothermic procedure in which the core temperature was reduced from 38 to 30 degrees C. The two trauma groups were either submitted to the same hypothermic procedure or kept normothermic during the corresponding time. All animals were sacrificed 24 h following the surgical procedure. RESULTS: In the hypothermic non-trauma group no axonal changes were seen. The number of abnormal axons, as indicated by accumulation of immunoreactive material in enlarged axons, was lower in the peri-injury zones of the hypothermic trauma group than in the normothermic trauma group. This difference was most obvious in the cranial peri-injury zones. No differences were seen between the groups in the trauma zones. CONCLUSIONS: This study demonstrates reduced axonal swelling in the peri-injury zones of spinal cord injured rats treated with systemic hypothermia. These changes could either indicate neuroprotective effects of the hypothermic treatment, or be results of reduced axonal transport or protein synthesis. To evaluate the clinical importance of our findings, further studies including reliable outcome measures of the animals must be performed.

Systemic hypothermia following compression injury of rat spinal cord: reduction of plasma protein extravasation demonstrated by immunohistochemistry.

Systemic hypothermia has neuroprotective effects in experimental models of central nervous system ischemia caused by vascular occlusions. The present study addresses the question as to whether systemic hypothermia can influence the extravasation of plasma proteins following severe spinal cord compression trauma using immunohistochemistry to identify the plasma proteins albumin, fibrinogen and fibronectin. Fifteen rats were assigned to one of three groups and received either thoracic (T) laminectomy or severe spinal cord compression trauma of the T8-9 segment. One group comprised laminectomized animals without compression trauma submitted to a hypothermic procedure in which the core temperature was reduced from 38 degrees to 30 degrees C. The two trauma groups were either submitted to the same hypothermic procedure or kept normothermic during the corresponding time. All animals were killed 24 h following the surgical procedure. The normothermic and hypothermic trauma groups had indications of marked extravasation of albumin, fibrinogen and fibronectin at the site of the injury (T8-9). There was also pronounced extravasation in the cranial and caudal peri-injury zones (T7 and T10) of normothermic injured rats but, with few exceptions, not in the hypothermic ones with the same degree of compression. By measuring the cross-sectional area of the peri-injury zones we found in the hypothermic trauma group a significant reduction of the expansion compared with that present in normothermic injured rats. Our study thus indicates that hypothermia reduces the extravasation of the plasma proteins albumin, fibrinogen and fibronectin following spinal cord compression in the rat. Such a reduction may contribute to neuroprotective effects exerted by hypothermia.

Gender identity: affected by social change?

To determine whether social changes in attitudes toward the role of men and women have influenced gender identity measures, 60 male and female college students were assessed using both a Thematic Apperception Test measure (May's, 1966, Deprivation/Enhancement measure) and a self-report measure (Bem's, 1974, Sex Role Identity [BSRI]), both of which were developed more than 20 years ago. Although some recent research has found the BSRI to no longer differentiate between men and women (Twenge, 1997; Wilcox & Francis, 1997), this study found significant gender differences for both gender identity measures.1

Systemic hypothermia after spinal cord compression injury in the rat: does recorded temperature in accessible organs reflect the intramedullary temperature in the spinal cord?

This article addresses one basic issue regarding the use of systemic hypothermia in the acute management of spinal cord injury, namely, how to interpret temperature recordings in accessible organs such as the rectum or esophagus with reference to the spinal cord temperature. Thirty-six rats, divided into six groups, were randomized to laminectomy or to severe spinal cord compression trauma, and were further randomized to either a cooling/rewarming procedure or continuous normothermia (esophageal temperature 38 degrees C) for 90 min. The first procedure comprised normothermia during the surgical procedure, followed by lowering of the esophageal temperature from 38 degrees C to 30 degrees C (the hypothermic level), a 20-min steady-state period at 30 degrees C, rewarming to 38 degrees C, and finally a 20-min steady-state period at 38 degrees C. The esophageal, rectal, and epidural temperatures were recorded in all animals. The intramedullary temperature was also recorded invasively in four of the six groups. We conclude that the esophageal temperature is safe and easy to record and, in our setting, reflects the epidural temperature. The differences registrated may reflect a true deviation of the intramedullary temperature due to initial environmental exposure and secondary injury processes. Our results indicate that the esophageal temperature exceeds the intramedullary temperature during the initial recording and final steady state following rewarming, but not during the most crucial part of the experiment, the hypothermic period. The core temperature measured in the esophagus can therefore be used to evaluate the intramedullary temperature during alterations of the systemic temperature and during hypothermic periods.

Propionebacterium acnes in cultures from ventriculo-peritoneal shunts: infection or contamination?

We have examined the accuracy of our present CSF sampling technique in 14 referred patients with suspect shunt dysfunction. The study was performed comparing culture results from shunt reservoir punctures and sham samples from skin tissue fluid close to the reservoirs. Propionebacterium acnes (P acnes) was found in five of fifteen cultures from reservoir punctures and in five of fifteen sham procedures. Positive cultures correlated in two cases. Thirteen of the fourteen patients included in the study were followed clinically and their symptoms disappeared without antibiotic or surgical treatment. One patient was treated surgically. We conclude that bacterial growth in cultures from shunt reservoirs in cases with P acnes should be interpreted with great caution, as our findings indicate that they may be skin contaminations.

Nimodipine evoked dilation of cerebral arteries early during the development of late vasospasm in subarachnoid hemorrhage.

In subarachnoid hemorrhage (SAH) late cerebral ischemia may develop without significant visible narrowing of arteries at angiography, but in severe ischemic conditions "vasospasm" invariably seems to be present. The majority of patients with aneurysm rupture develop some degree of vasospasm, whereas relatively few suffer from ultimate brain infarction. The prophylactic use of the calcium antagonist Nimodipine is linked to a beneficial anti-ischemic effect in SAH, although narrowing of large bore arteries still seems to develop despite administration of this drug. Attenuation of vascular spasm, mainly in the arterioles has been implicated as the major mechanism of action, although a neuronprotective effect of Nimodipine has been suggested as well. The present paper presents fragmentary evidence that Nimodipine does elicit a vasoactive response in the cerebral vasculature early during the development of late cerebral vasospasm, and that this response seems closely linked to reversal of attendant ischemic symptoms.

Face height and tooth eruption in adults--a 20-year follow-up investigation.

A longitudinal roentgen cephalometric investigation of vertical craniofacial and dentoalveolar changes during 20 years of adulthood, was performed in 15 men and 15 women. Two lateral cephalograms taken at the average ages 25 and 45 years, were available of each subject. Skeletal and dental changes were described by 13 linear and four angular cephalometric measurements. The analysis of the linear variables showed that total anterior face height increased by 1.60 mm on average. Approximately one-fifth of this increase occurred in the upper and four-fifths in the lower face. In the dentoalveolar region, significant increments of all dimensions except overjet and overbite were found, indicating an eruptive movement of the teeth and a vertical development of their investing tissues. The analysis of the angular measurements showed that posterior rotation of the mandible and uprighting of the upper incisors had occurred during the period of investigation.