Experimental spinal cord injuries were induced in dogs by dropping calibrated weights through a vented tube onto a small impounder resting on the surgically exposed cord. The motion of the impounder and the drop-mass were recorded by high-speed photography and the resulting data were compared to those obtained from a computer simulation of the dynamics of the injury mechanism. It is concluded that this method of induced spinal cord injuries may yield markedly different degrees of cord compression depending upon the parameters of the animal material and apparatus even when the gm-cm of impact energy is maintained at a constant value. Some approaches to standardization of this injury model are suggested.

The fluorescent tracer Evans blue (EB) was studied after circulation time ranging from 30 seconds to 5 minutes following blood-brain barrier (BBB) injuries in 42 dogs. Selective neuronal stainings (sns), associated with BBB injuries, occurred to a high degree. This phenomenon was examined by modifications in existing fluorescence techniques. The mechanism of SNS was seen to lie in an almost imperceptible transport of EB along astrocytic processes connecting SNS with the adjacent vasculature. This report presents visual evidence under pathological conditions, and supports the concept of astrocytic processes as the normal route of transport between blood vessels and neurons. This requires long exposure photomicrographs since the fluorescing material is subtle within the neuroglial processes.

Two patients with bursting fractures of the atlas vertebra are presented. The use of a halo apparatus as an effective alternative to bedrest and cervical traction in these patients is discussed. Polytomography was helpful in establishing an accurate diagnosis.

✓ Vascularity and blood-brain barrier (BBB) function within spinal cord were studied with fluorescent microscopy at 14 intervals following 300 gm-cm injuries to the thoracolumbar spinal cord in 32 dogs. Histochemical staining with formaldehyde brought out a yellow-green fluorescence of vascular origin that was unrelated to tracer dye. This fluorescence accumulated in perivascular sites and is possibly related to catecholamine elevation within damaged spinal cord. Intrinsic CNS mechanisms for catecholamine build-up (increased transport, increased synthesis, increased release) are reviewed as well as the pharmacological action of alpha methyl tyrosine. It is hypothesized that an intrinsic CNS source of norepinephrine build-up is unlikely and that elevation of circulating catecholamine levels following stress and trauma leads to the extravasation of this material across injured BBBs within contused spinal cord.

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