Biomedical subjects

Y Olsson

Publications and source records attributed to Y Olsson.

At least 19 recordsLinked to original sources

PubMed1995

Changes of beta-amyloid precursor protein after compression trauma to the spinal cord: an experimental study in the rat using immunohistochemistry.

We evaluated by immunohistochemistry the changes of beta-amyloid precursor protein (beta APP) and beta-amyloid peptide (beta A) in the spinal cord of rats with compression injury at Th8-9 of mild, moderate, and severe degrees. The spinal cord of normal rats and animals with laminectomy revealed immunoreactivity to beta APP in nerve cell bodies, the initial part of a few axons of the gray matter, and in scattered glial cells. At 4 h after compression, beta APP-immunoreactivity occurred in a few swollen axons of the longitudinal tracts; such beta APP-immunoreactive axons remained throughout the experimental period of 9 days. The number of immunoreactive axons and the intensity of their immunoreactivity were increased in rats with moderate and severe compression. The caudal Th10 segment exhibited more pronounced accumulation of beta APP immunoreactivity than the cranial Th segment. There was no evidence of beta A accumulation after compression injury. In conclusion, there is a rapidly occurring, long-lasting accumulation of immunoreactive beta-amyloid precursor protein after compression injury of rat spinal cord. This accumulation is related to the degree of impact to the cord.

Amyloid beta-Peptides↗

PubMed1995

Astrocytic reaction after graded spinal cord compression in rats: immunohistochemical studies on glial fibrillary acidic protein and vimentin.

The relation between the degree of spinal cord compression and the extent of early posttraumatic reaction of astrocytes was investigated in rats using the blocking-weight technique to induce a spinal cord compression at the level of the Th8-9. Immunohistochemistry was used to detect changes in the expression of glial fibrillary acidic protein (GFAP) and vimentin up to 24 h after injury. A mild compression, which did not cause any measurable neurological deterioration, induced a mild increase of GFAP immunoreactivity at 4 h and a more marked and widespread immunoreactivity at 24 h. The greatest increase of GFAP immunoreactive astrocytes occurred in rats with moderate compression of the cord causing reversible paraparesis and in animals with severe compression leading to paraplegia. The increase of GFAP immunoreactivity was present already 4 h after injury in virtually all the segments investigated (Th5-6-Th11-12) and was most marked at 24 h. Vimentin immunoreactivity of control rats was present in the ependymal cells of the central canal, the leptomeninges, and walls of a few intramedullary vessels. Occasional astrocytes were stained. In rats surviving 24 h after moderate and severe compression vimentin immunoreactivity was increased in the walls of intramedullary blood vessels including capillaries of one rostral and one caudal segment. Many macrophages with immunoreactivity appeared and occasional glial cells with astrocyte shape were stained. This investigation shows that within 24 h after compression of the spinal cord a widespread astrocyte reaction occurs. Even a mild compression that does not produce any signs of motor dysfunction can induce widespread astrocyte alterations in the spinal cord. This astrocyte response is more marked in rats with more severe compression leading to more pronounced neurological deterioration. The increase in vimentin immunoreactivity of blood vessels is more localized and occurs in moderate and severe compression of the cord.

Animals↗

PubMed1994

Reactive astrocytes in viral infections of the human brain express endothelin-like immunoreactivity.

In order to investigate the expression of endothelin-like immunoreactivity in astrocytes of viral infections of the human brain the avidin-biotin peroxidase complex method and a polyclonal antiserum were used. Autopsy material was obtained from 5 cases of herpes simplex encephalitis, two of progressive multifocal leukoencephalopathy (PML) and two of subacute sclerosing panencephalitis (SSPE). All the 5 herpes simplex encephalitis cases presented groups of immunoreactive astrocytes around necrotic, inflammatory lesions. The PML cases exhibited a large number of immunoreactive astrocytes in and around lesions of the white matter. The cases of SSPE disclosed numerous, markedly stained fibrillary immunoreactive astrocytes; they were most abundant in degenerated regions of the white matter. The processes and peripheral cytoplasm of giant astrocytes in the PML cases contained immunoreactive material but the perinuclear region was devoid of such material. In the herpes simplex and the SSPE cases immunoreactivity was present throughout the cytoplasm and processes of reactive fibrillary astrocytes. Many nerve cells in the cerebral cortex, hippocampus, cerebellum and pons of control cases exhibited endothelin-like immunoreactivity but this occurred in only exceptional astrocytes of control cases. Endothelin-like immunoreactivity was not present in the oligodendrocytes and vascular endothelial cells of controls and cases of virus infection. The expression of endothelin-like immunoreactivity in astrocytes in human viral diseases reflects probably an increased intracellular content of endothelin. If this peptide is released from such astrocytes, it may act as a mitogen and by inducing constriction of arterioles it may influence the microcirculation.

Adolescent↗

PubMed1992

Immunohistochemical evidence of endothelin-1 in human choroid plexus.

An immunohistochemical investigation was carried out on 17 specimens of human choroid plexus obtained post mortem, 1 biopsy of normal choroid plexus including part of the lateral ventricle and 1 papilloma of the choroid plexus removed surgically. The material was fixed in formalin. Paraffin and cryostat sections were used. A polyclonal antiserum to endothelin-1 served as a primary antibody. The avidin-biotin-peroxidase method was applied to demonstrate the immunoreaction. The epithelial cells of the choroid plexuses, the choroid papilloma and most ependymal cells of the lateral ventricle showed a distinct brown reaction product in their cytoplasm indicating antigenic sites to endothelin-1. The reaction was of lesser intensity in the ependymal cells. The connective tissue in choroid plexus was unstained. A positive immunoreaction was present in the walls of some vessels in the choroid plexus in cryostat sections. This is the first report on the presence of antigenic sites to endothelin-1 in the epithelial cells of the human choroid plexus. The role of endothelin in these cells should be investigated to ascertain if the cells synthesize this biologically active peptide or if it is merely bound to receptors in them.

Adult↗

PubMed1992

Exudation of fibronectin and albumin after spinal cord injury in rats.

Spinal cord of the rat was investigated immunohistochemically to detect signs of extravasation of fibronectin in animals in which the cord was subjected to different degrees of compression trauma. Immunohistochemistry was performed after survival periods of 4 and 24 h and parallel sections were incubated for albumin immunoreactivity to detect signs of breakdown of the blood-spinal cord barrier. Extravascular reaction products indicating the presence of fibronectin were found within and in the vicinity of the compression provided that bleeding had occurred in the spinal cord, i.e., in rats with severe trauma. Immunoreactive material indicating extravascular albumin was present in the traumatized region and in many segments of the cord located away from the compressed part. Such material was seen both proximal and distal to the primary injury and even in rats with a low magnitude of compression. Generally, with more severe trauma and longer survival periods extravascular albumin was more extensively distributed along the cord. No signs of fibronectin antigen were detected in spinal cord segments away from the compression even though such regions showed albumin immunoreactivity outside the vessels. The results indicate that within and close to the primary injury of compressed spinal cord exudation of fibronectin may occur from the plasma of microvessels provided that the impact is severe enough to cause intramedullary hemorrhages.

Albumins↗

PubMed1992

Binswanger's disease in the absence of chronic arterial hypertension. A case report with clinical, radiological and immunohistochemical observations on intracerebral blood vessels.

The cerebral changes are described in a woman of 54 who suffered from Binswanger's encephalopathy: there were no signs or symptoms of chronic arterial hypertension. The disease presented as dementia of about 3 years duration. Computed tomography of the brain 2.5 years before her death showed bilateral widespread hypodense lesions in the cerebral white matter. She died of an asthmatic attack. Autopsy disclosed extensive bilateral degeneration of the central white matter, lacunes and gliosis. Severe obliterative arteriolosclerosis occurred in the meningeal vessels and those supplying the affected parts of the brain. Light microscopy showed that the most severe lesions occurred in the arterioles. Immunohistochemistry demonstrated profound extravasation of plasma proteins chiefly albumin, indicating dysfunction of the blood-brain barrier. Thus, the lesions characteristic of Binswanger's encephalopathy may develop in the absence of chronic arterial hypertension. Additional pathogenic factors, possibly genetic predisposition to vascular injury may play a role in the development of this condition.

Blood Proteins↗

PubMed1992

Dynorphin A content in the rat brain and spinal cord after a localized trauma to the spinal cord and its modification with p-chlorophenylalanine. An experimental study using radioimmunoassay technique.

The distribution of dynorphin A in the spinal cord and brain of normal rats and of rats subjected to a focal injury of the spinal cord was examined in a rat model using a radioimmunoassay (RIA) technique. The validity of RIA was checked by high performance liquid chromatography (HPLC). Furthermore, the possibility that the peptide is somehow functionally related with endogenous 5-hydroxytryptamine (5-HT, serotonin), was also evaluated using a pharmacological approach. In normal animals, the peptide content was very similar in the spinal cord segments (T9, T10-11, and T12) examined whereas, the dynorphin content of the whole brain was about two-fold higher compared with that in the spinal cord. A focal injury to the spinal cord in the right dorsal horn (about 1.5 mm deep, 2.5 mm long and 1.5 mm to the right of the midline) of the lower thoracic cord (T10-11) in urethane anaesthetised animals significantly altered the peptide content in the whole brain as well as in the spinal cord. Thus, a decrease in the peptide level in whole brain, T10-11 and in the T12 segments of the spinal cord was observed 1 and 2 h after trauma. At 5 h, the peptide had accumulated markedly in the T9 segment (about a two-fold increase) as compared with the controls. At this time, the peptide content had been restored in the T10-11 and T12 segments. On the other hand, the whole brain dynorphin level continued to remain low (by 55%) as compared to the control group.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1992

Release of endogenous neurochemicals may increase vascular permeability, induce edema and influence cell changes in trauma to the spinal cord.

Trauma to the spinal cord induces a series of electrophysiological, immunological and biochemical events, but it is still unclear how such reactions are initiated and maintained. Most likely release of neurochemicals, breakdown of microvascular permeability and the formation of vasogenic edema play important roles in the pathophysiology of spinal cord trauma. In an animal model we have focused the attention to the possible involvement of endogenous serotonin, prostaglandins and opioid peptides in the formation of edema and associated disturbances of vascular permeability. The trauma was produced in anesthetized rats by making a focal lesion in the right dorsal horn at the T10-11 segments. This injury resulted in a profound increase in the microvascular permeability to 131I-sodium and an elevation of water content in the rostral T9 and caudal T12 segments as measured 5 h after the onset of the injury. Light microscopy of the perifocal changes in the T9-T12 segments using Nissl stain and immunohistochemistry to glial fibrillary acidic protein (GFAP) and myelin basic protein (MBP) showed profound cellular changes which were most severe in the ipsilateral ventral horn. Many nerve cell bodies were shrunken and the tissue had a spongy edematous appearance. There was a marked increase of GFAP immunoreactivity as well as a significant diminution of MBP staining. Pre-treatment with p-chlorophenylalanine (p-CPA, an endogenous serotonin depletor and synthesis inhibitor) or indomethacin (an endogenous prostaglandin synthesis inhibitor) or naloxone (an opioid receptor antagonist) significantly reduced the permeability changes and the edema formation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1992

Characterization of prolactin receptors in human choroid plexus.

The specific binding of 125I-human prolactin (hPRL) was studied in different areas of the human brain. Particularly high binding affinity of the hormone was found in the choroid plexus and this tissue was therefore selected for further studies. The hippocampus, the hypothalamus and the pituitary were among other regions containing prolactin-binding sites. In the choroid plexus the amount of PRL receptors was significantly higher in females than in males and was also found in both sexes to decrease with age. The binding affinity of 125I-hPRL to choroid plexus was 3.0 x 10(9) M-1 and the binding capacity was 10.3 pmol per mg protein. Following solubilization with Triton X-100 the PRL receptor fraction retained its hormone-binding properties and upon molecular sieve chromatography it behaved as a protein with a molecular mass of approximately 250,000. Cross-linking of 125I-hPRL to receptors from choroid plexus and subsequent sodium dodecyl sulfate (SDS) polyacrylamide gel electrophoresis indicated a major hormone-binding unit of M(r) 44,000. This value is about 7,000 smaller than that reported earlier by us for the growth hormone receptors from the same tissue, following cross-linking to 125I-human growth hormone (hGH). By affinity column chromatography a complete separation of the hPRL and hGH binding units was achieved. It was thus shown that in choroid plexus the binding sites for GH and PRL occur as discrete entities.

Aging↗

PubMed1991

Evaluation of traumatic spinal cord edema using evoked potentials recorded from the spinal epidural space. An experimental study in the rat.

Spinal cord evoked potentials (SCEP) elicited by simultaneous distal tibial and sural nerve stimulation were continuously recorded from the epidural space at the T9 and T12 levels of urethane anaesthetized rats before and after a unilateral incision (about 3 mm deep and 5 mm long) in the right dorsal horn of the T10-11 segments. The changes in SCEP were correlated with the increase in spinal cord water content measured 5 h after injury. In addition, the influence of serotonin (5-HT) in mediating such changes was explored using a pharmacological approach. The changes in SCEP immediately after injury correlated well with development of spinal cord edema measured 5 h after injury. Thus, the maximal negative peak (MNP) amplitude of SCEP decreased by an average of 64.0% immediately after injury and the water content of the spinal cord was increased from 71.6% (controls) to 77.6% 5 h after injury. Pretreatment with p-CPA (a serotonin synthesis inhibitor) prevented the initial decrease of the MNP amplitude and also the increase of water content (72.5%). On the other hand, pretreatment with cyproheptadine (a 5-HT2 receptor antagonist) enhanced both the initial decrease of the MNP amplitude as well as the increase of water content (81.3%). The results show a good correlation between changes of SCEP immediately after injury and the magnitude of spinal cord edema (r = 0.9) measured 5 h after injury. The findings reveal a major role of serotonin in mediating early changes of SCEP and later development of spinal cord edema and demonstrate a prognostic value of early SCEP recordings in predicting the final outcome of traumatic spinal cord injuries.

Animals↗

PubMed1990

Changes in blood-brain barrier and cerebral blood flow following elevation of circulating serotonin level in anesthetized rats.

Plasma serotonin (5-HT) was elevated by an intravenous infusion of this amine into urethane-anaesthetized rats and the concentration approximated that present in various neurological diseases and mental abnormalities. An infusion of 10 micrograms per kg body weight for 10 min significantly increased blood-brain barrier (BBB) permeability to Evans blue and 131I-sodium measured in whole brain. Regional BBB determinations with labelled 131I-sodium showed that the permeability to this compound was increased in the cerebral cortex, hippocampus, caudate nucleus, hypothalamus, colliculus and the cerebellum but not in the pons and the medulla oblongata. Regional blood flow was reduced in the same parts which showed BBB abnormality tested with 125I-labeled microspheres. Pretreatment with cyproheptadine, a 5-HT2 receptor antagonist, prevented the BBB increase and the regional blood flow was near normal values. Similar effects were obtained with indomethacin, a prostaglandin synthesis inhibitor. Vinblastine, known to influence vesicular transport, eliminated extravasation of the tracers but the regional blood flow remained depressed. A hypothesis is put forward that serotonin after binding to its receptor in the cerebral vessels stimulates prostaglandin which either directly or by means of cyclic adenosine monophosphate causes an increased vesicular transport across the endothelial cells and thus an extravasation of tracer substances in the brain. Obviously, this form of exudation can be influenced by pharmacological means.

Animals↗

PubMed1990

Increased 5-hydroxytryptamine immunoreactivity in traumatized spinal cord. An experimental study in the rat.

The possibility that serotonin (5-hydroxytryptamine, 5-HT) is involved in the early tissue reactions occurring in spinal cord trauma was examined in a rat model using an immunocytochemical technique. The injury was made in the form of a 5-mm long and 2.5-mm wide lesion of the right dorsal horn at the level of T10-11. Injured rats, pretreated with the 5-HT synthesis blocking agent, p-chlorophenyl alanine (p-CPA) were compared with untreated injured controls and the animals were allowed to survive for 5 h. The distribution of 5-HT was examined in proximal and distal cross- sections of the cord, located 2 and 5 mm away from the injury. Normal rats showed immunoreactive material in nerve cell processes and in a few nerve cell bodies of the ventral horns. The trauma to the spinal cord caused a marked increase in 5-HT immunoreactivity in the segments located 2 mm proximal and distal to the injury, particularly in the ipsilateral ventral horn. The segment located 5 mm distal to the lesion showed a similar increase in immunoreactivity but it was apparently less pronounced in the corresponding proximal segment. Treatment with p-CPA markedly reduced the trauma-induced increase in 5-HT immunoreactivity in all the segments. These immunohistochemical findings were in line with the changes in the contents of 5-HT measured biochemically in corresponding spinal cord segments. At the onset of the trauma to the spinal cord 5-HT is thus present in the tissue, mainly in the form of 5-HT-containing nerve cell processes.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1990

Effects of p-chlorophenylalanine on microvascular permeability changes in spinal cord trauma. An experimental study in the rat using 131I-sodium and lanthanum tracers.

The possibility that serotonin can take part in the initiation of the increased microvascular permeability occurring in a spinal cord trauma was investigated in a rat model with 131I-sodium and lanthanum as tracers. We influenced the serotonin content in the tissue pharmacologically by treating animals with a serotonin synthesis inhibitor, p-chlorophenylalanine (p-CPA), before the production of the injury and compared the results with injured, untreated controls. A small incision was made in the dorsal horn of the lower thoracic cord. It caused a progressive extravasation of 131I-sodium in the damaged segment, measured after 1, 2 and 5 h. Rostral and caudal segments also showed a significant but lower accumulation of 131I-sodium. Lanthanum added to the fixative was used as an ionic tracer detectable by electron microscopy. The endothelial cells of microvessels removed from the perifocal region after 5 h showed a marked increase in the number of lanthanum-filled vesicles. Many endothelial cells had a diffuse penetration of the tracer into the cytoplasm and the basement membrane. However, the tight junctions usually remained closed to lanthanum. Pretreatment with p-CPA markedly reduced the extravasation of 131I-sodium measured at 5 h in the traumatized cord. At the cellular level, the endothelial vesicles filled with lanthanum approached the condition of uninjured animals. The diffuse infiltration of lanthanum into endothelial cells and its spread into the basement membrane of the vascular wall were usually absent. Our results indicate that serotonin plays a role in the initiation of the increased microvascular permeability which occurs in spinal cord injuries.

Animals↗

PubMed1990

Edema formation and cellular alterations following spinal cord injury in the rat and their modification with p-chlorophenylalanine.

The possibility that serotonin can modify the early pathological sequences occurring in spinal cord trauma was investigated in a rat model. To that end we took advantage of the possibility of influencing serotonin pharmacologically by treating animals with a serotonin synthesis inhibitor, p-chlorophenylalanine (p-CPA) before the production of the injury and compared the results with injured, untreated controls. A unilateral incision was made into the dorsal horn of the lower thoracic cord (about 2.5 mm deep, 4.5 mm long) and the rats were allowed to survive up to 5 h after the trauma. The injured region from untreated animals showed macroscopically at that time a pronounced swelling and the water content had increased by 3.5% as compared to intact controls. The segments rostral and caudal to the lesion also exhibited a profound increase in water content. Light microscopy revealed a significant expansion of the spinal cord as compared to controls. The swelling was most pronounced in the gray matter on the injured side. Electron microscopy showed distorted neurons, swollen astrocytes and extracellular edema in the gray matter in and around the primary lesion. There was also a sponginess in the surrounding white matter with disruption of myelin, collapsed axons and widened periaxonal spaces. Pretreatment of the rats with p-CPA significantly reduced the swelling of the injured spinal cord and there was no visible expansion. The ipsilateral edema in the central gray matter was considerable less pronounced as compared to that in untreated animals. The increase in water content was less than 1% in these animals.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1990

Vascular permeability of spinal nerve roots. A study in the rat with Evans blue and lanthanum as tracers.

The permeability of blood vessels in rat spinal nerve roots was investigated with Evans blue-albumin as an in vivo macromolecular tracer and lanthanum nitrate as an electron microscopic ionic marker added to a fixative. Rats injected intravenously with Evans blue, showed macroscopic distinct staining of dorsal root ganglia, whereas spinal nerve roots remained unstained. Fluorescence microscopy, however, revealed clear extravascular fluorescence both in ventral and dorsal roots 2 or 18 h after tracer administration. Two different types of blood vessels exists in spinal nerve roots; large extrinsic (radicular) in the root sheath and minute intrinsic vessels in the parenchyma. Lanthanum added to a fixative, perfused through the vessels was detected in the lumen of both types of vessels, usually adhering to the luminal plasma membrane and in many invaginations from that membrane. Lanthanum also entered the clefts between endothelial cells but was always stopped at the junctions which are, thus, of the tight type. Diffuse penetration of the compound into the cytoplasm was seen in one endothelial cell, but no fenestrations were detected. Junctions between the endothelial cells of vessels in rat spinal nerve roots are impermeable to lanthanum and most likely also to other large molecular substances like albumin. Thus, probable routes for serum albumin to enter the nerve roots, where it normally is present, must be either by centripetal extracellular diffusion from the ganglia and the peripheral nerve or by vascular leakage in the roots, caused by for instance pinocytosis across endothelial cells.

Animals↗

PubMed1990

Early accumulation of serotonin in rat spinal cord subjected to traumatic injury. Relation to edema and blood flow changes.

Changes in the concentration of serotonin (5-hydroxytryptamine) in the early period after a focal traumatic injury to rat spinal cord were determined and related to the formation of edema and alterations in blood flow. A unilateral, 5-mm-long and 3-mm-deep traumatic injury located 2 mm from the midline was created in the T10-11 segment of the cord. Five hours after the injury the serotonin concentration in the traumatized segment had increased more than 100% compared with controls. There was also a progressive increase in water content of the traumatized segment measured 1-5 h after the injury. On the other hand, the spinal cord blood flow showed a progressive decrease to about 35% of its initial value at 5 h. Pretreatment with p-chlorophenylalanine, a serotonin synthesis inhibitor, impeded the elevation in water content measured 5 h after the trauma. The spinal cord blood flow remained close to normal values and the increase in serotonin was absent. Our results show that trauma to the rat spinal cord will induce changes in the serotonin concentration of the tissue and that the associated formation of edema and blood flow alterations can be alleviated in serotonin depleted rats. Obviously, serotonin plays a significant role in the pathophysiology of traumatic injury of rat spinal cord.

Animals↗

PubMed1990

Alteration of substance P after trauma to the spinal cord: an experimental study in the rat.

The distribution of substance P was determined in the rat spinal cord and brain after a focal traumatic injury to the thoracic region (T10-11) of the spinal cord. There was at 1 and 2 h after the injury a statistically significant increase of the substance P content not only in the injured segment but also in samples removed 5 mm proximal (T9) and distal (T12) to the lesion. At 5 h the substance P content of the injured segment of the cord was reduced by 30% compared with controls. However, there was a significant increase in the concentration of this peptide in segments located 5 mm cranial and caudal to the injury (65% and 22%, respectively). Interestingly, the whole brain content of substance P showed a statistically significant 22% increase from control values at 5 h after the injury. At 1 and 2 h after the spinal cord injury there was a significant decrease in whole brain substance P concentration by 25% and 65%, respectively. Pretreatment with p-chlorophenylalanine (a serotonin synthesis inhibitor) markedly reduced the endogenous content of substance P in whole brain of normal animals. In these animals, the spinal cord content of the peptide was elevated by 83-123% as compared to untreated control animals. Spinal cord trauma inflicted on p-chlorophenylalanine-treated animals did not affect the brain peptide level at all. However, a profound decrease was noted in all the spinal cord segments at 5 h as compared to the untreated traumatized group. The decrease in this peptide was more pronounced in the cranial and the injured segments as compared to the caudal one.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1990

Neuropathological changes and neurological function after spinal cord compression in the rat.

As part of a series of experimental investigations of the effects of various pharmacological agents on the outcome of compressive spinal cord trauma in the rat, the time course of the cell changes in the cord at the site of and distal to the compression was studied at the light microscopic level. The degree of compression used with the present model results in a transient paraparesis that recovers almost completely over a period of 3 weeks as judged by the inclined plane technique. The most significant morphological findings were as follows. Initially (1 and 24 h after the impact) there was pronounced swelling and hemorrhage at the compression site, chiefly in the gray matter of the cord. On day 4 there was severe necrosis in the same region, with numerous macrophages and leukocytes. Rats killed after 21 days showed either minor residual signs of necrosis or essentially normal tissue architecture. Surprisingly, necrosis with delayed onset also developed in the dorsal columns, involving the pyramidal tracts. This necrosis was detected in animals killed after 9 and 21 days but not in those observed after 4 days or earlier. The longitudinal tracts of the white matter showed reduced staining in paraffin sections of the compression site. Epon sections revealed splits in the myelin sheaths and enlarged periaxonal spaces as early as 1 h after the impact. The alterations in the longitudinal tracts persisted throughout the 21-day observation period and extended down to L2-L4. There was gradual functional recovery, documented by the inclined plane test. Preinjury values were almost reached on day 21, although the cord still showed some morphological damage. In individual animals, no relation was found between degree of function as tested by inclined plane and extent of morphologic injury. Additional functional and morphological methods obviously are needed in future investigations of the effects of treatments on the outcome of compressive spinal cord injury.

Animals↗