Endogenous cells (neurons and microglia) in the human spinal cord, not the blood-borne leukocytes, contribute to the early production of interleukin-1beta, interleukin-6, and tumor necrosis factor-alpha in the post-traumatic inflammatory response, and microglia are involved the early response to traumatic axonal injury.

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In this animal model, noncommunicating syringes continue to enlarge even when there is evidence that they are under high pressure. There may be an increase in pulse pressure rostral to the block of subarachnoid CSF flow, causing an increase in perivascular flow and contributing to syrinx formation. The source of fluid in noncommunicating syringomyelia may be arterial pulsation-dependent CSF flow from perivascular spaces into the central canal.

Axonal injury (AI), one of the principal determinants of clinical outcome after head injury, may evolve over several hours after injury, raising the future possibility of therapeutic intervention during this period. A new head impact model of AI in sheep was developed to examine pathological and physiological changes in the brain resulting from a graded traumatic insult. In this preliminary study 10 anesthetized and ventilated Merino ewes were used. Head injury was produced by impact from a humane stunner to the temporal region of an unrestrained head. Eight sheep were studied for 1, 2, 4, or 6 h after impact. Two sham animals (no impact, 6 h survival) were also examined. Arterial blood pressure, intracranial pressure, and cerebral blood flow were monitored continuously. A physiological index of injury severity was calculated by weighting the percentage shift from preinjury values for each monitored parameter over the first hour after injury. Immunostaining with amyloid precursor protein (APP) was used as a marker of axonal damage and the distribution of APP positive axons was recorded according to a sector scoring method (APPS). Widespread AI was identified in 7 of the 8 impacted animals, around cerebral contusions and in hemispheric white matter, central gray matter, brain stem, and cerebellum, and was detected as early as 1 h after injury. The degree of axonal injury (APPS) correlated well with an index of physiological response to injury (r = 0.83, p = 0.005).

The impetus for the enlargement of syringes is unknown. The authors hypothesize that there is a flow of cerebrospinal fluid (CSF) from perivascular spaces into the central canal and that the flow is driven by arterial pulsations. Using horseradish peroxidase as a tracer, the CSF flow was studied in normal sheep, in sheep with damped arterial pulsations, and in sheep with lowered spinal subarachnoid pressure. The CSF flow from perivascular spaces into the central canal was demonstrated in the normal sheep, and two patterns of flow were identified: 1) from perivascular spaces in the central gray matter; and 2) from perivascular spaces in the ventral white commissure. Flow into the central canal was also observed in the sheep with lowered spinal subarachnoid pressure, but not in those with reduced arterial pulse pressure. This study provides evidence that CSF flow from perivascular spaces into the central canal is dependent on arterial pulsations. Arterial pulsation-driven CSF flow may be the impetus for the expansion of syringes.

The authors describe two patients with traumatic cerebral edema and intracranial hypertension in whom the continued use of mannitol and furosemide resulted in a progressive lessening of the effect of these agents on the intracranial pressure (ICP) and caused prerenal failure. Intravenous administration of hypertonic saline (50 ml and 20 ml of a 5-mmol/ml saline solution over 10 minutes in Cases 1 and 2, respectively) produced a prolonged reduction in the ICP and improved renal function in both cases. It is suggested that if a reduction in ICP without diuresis is required in patients with traumatic cerebral edema, treatment with intravenous hypertonic saline should be considered.

This paper describes a biomechanical study of axonal injury due to a blunt impact to the head. The aim of the experimental model was to produce axonal injury analogous to that seen in human trauma while measuring the dynamics of the impact and the subsequent kinematics of the head. These measurements were made in a way to facilitate the simulation of these experiments using the finite element method. Sheep were anaesthetised and ventilated, and subjected to a single impact to the lateral aspect of their skull. The impact force was measured throughout the duration of the impact and the kinematics of the head was measured using a novel implementation of a nine-accelerometer array. The axonal injury was identified using amyloid precursor protein (APP) as a marker, intensified using antigen retrieval techniques. Axonal injury was consistently produced in all animals. Commonly injured regions included the sub-cortical and deep white matter, and the periventricular white matter surrounding the lateral ventricles. The observed axonal injury was mapped and quantified on three coronal sections of each brain. The measure used to describe the injury severity correlated with the peak magnitude of the impact force and with peak values of kinematic parameters, particularly the peak change of linear and angular velocity.