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Contusion: an Ultrastructural Study

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Contusion: an Ultrastructural Study Journal ofNeurology, Neurosurgery, and Psychiatry 1991;54:427-434 427 Glial swelling following human cerebral J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.54.5.427 on 1 May 1991. Downloaded from contusion: an ultrastructural study R Bullock, W L Maxwell, D I Graham, G M Teasdale, J H Adams Abstract contusion, zones of profoundly reduced The ultrastructural features of cerebral regional blood flow (rCBF) have been found contusion seen three hours to 11 days adjacent to contusions, and this may be a after head injury were studied in 18 factor in the ischaemic neuronal necrosis patients undergoing surgery. Massive which is a prominent finding in pathological astrocytic swelling ("cytotoxic" oedema) studies. Alterations to the microvascular bed was seen three hours to three days after adjacent to cerebral contusion may therefore injury, maximal in perivascular foot be an important determinant of such changes.8 processes, and compressing some of the The purpose of this study was to determine underlying capillaries. The tight junc- ultrastructurally the changes in neuronal, glial tions were not disrupted. Neuronal and microvascular morphology which occur damage was most marked three to 11 with time following human cerebral con- days after ijury. The patho- tusion, and to determine their role in the physiological mechanisms leading to pathogenic processes which are known to oedema formation and neuronal degen- damage the brain after severe head injury. eration are discussed. Patients and methods Cerebral cortical contusions are generally Eighteen patients with severe cerebral con- regarded as the pathological hallmark of head tusion were studied. Clinical details are shown injury and are clinically important for several in table lB. In each patient, contusions were reasons.`5 Extensive swelling of the cortical shown on CT scan, and in seven patients, ribbon and underlying white matter may mass effect, acute clinical deterioration and occur acutely after cerebral contusions and associated haematomas necessitated urgent may cause mass effect, brain shift and raised operation, at which the contusion was resec- intracranial pressure, and these events may ted, and biopsy taken from the margins of the cause secondary ischaemic brain damage or resected tissue. In a further four patients, ICP death.6 When widespread, contusions cause monitoring was initially performed to ascer- extensive destruction of the cortical ribbon tain the need to remove the contusion, and particularly at the tips of the temporal and ICP rose necessitating surgery. In the remain- frontal lobes and the orbital surface of ing seven patients, delayed neurological the frontal lobes, and this may lead to deterioration occurred up to 11 days after http://jnnp.bmj.com/ post traumatic epilepsy, and to the neuro- injury, precipitating the operation. Specimens psychological and behavioural sequelae, of resected cerebral contusion from these typical of severe head patients were compared with specimens Institute of injury.7 Neurological Sciences, Although previous studies have focused processed in an identical manner, from four Glasgow upon the pathogenesis,45 histopathology,1 dis- control patients, with macroscopically and R Bullock tribution' 3 and quantification of cerebral con- radiologically normal brain tissue at the site of D IGraham tusion, many aspects remain unresolved.3 biopsy, who had either temporal lobectomy G M Teasdale Why do some cerebral contusions swell and for epilepsy or resection of deep temporal on September 30, 2021 by guest. Protected copyright. J H Adams generate raised intracranial pressure, while glioma. Clinical details of these patients are Correspondence to: others do not? What proportion of the shown in table 1A. Rongeur specimens Mr R Bullock, Department neuronal necrosis which is seen adjacent to around 2 cubic mm in size were taken from of Neurosurgery, Institute of Neurological Sciences, cerebral contusions is due to primary contact contused grey and white matter and Southemn GReer Hospitw, and how much of it is due to secon- immediately immersed in buffered glutaralde- Govan Road, Glasgow G51 damage, 4TF, UK dary factors, such as delayed reduction in hyde (350 m osm). Specimens were then Received 31 January 1990 blood flow to the contused area? stored at 4°C for two to seven days until and in final revised form In studies in which we have mapped processing for electronmicroscopy. The site 30 July 1990. Accepted 18 September 1990 cerebral blood flow following human cerebral from which the biopsy was taken was recorded by the surgeon and related as closely as possi- ble to the CT appearance on the pre-operative Table IA Controlpatients-clinical data scan. The study was approved by the Ethics Committee of the Institute of Neurological Age Case (years) Tissue biopsied Indicationfor surgery Sciences, Glasgow. 1 65 Cortex and white matter right Deep temporal glioma, seizures temporal tip 2 56 Left frontal cortex Partial left frontal lobectomy for Processingfor electronmicroscopy glioma After immersion fixation, specimens were cut 3 36 Posterior right temporal cortex and Right temporal lobectomy for glioma white matter into 200 p thick sections using a vibrotome, 4 22 Right temporal cortex Right temporal lobectomy for severe and ultrasonicated to dislodge non-adherent epilepsy blood components from the vessel lumina. 428 Bullock, Maxwell, Graham, Teasdale, Adams Table lB Patients with cerebral contusion-clinical data interest selected for transmission electron- J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.54.5.427 on 1 May 1991. Downloaded from microscopy. Thin sections were cut for the Age Interval between Case (years) injury and biopsy CT diagnosis and clinical details transmission EM and routinely stained with lead citrate and uranyl acetate and examined 67 3 hours Fall. Right temporal contusion, small acute subdural haematoma, hemispheric swelling, high ICP (died) in a JEOL 100 S transmission electronmicros- 2 33 6 hours Fall. Right frontal lobectomy for massive brain swelling cope. when acute subdural haematoma removed. (Alcoholic with clotting defect-died) 3 68 13 hours RTA. Right temporal contusion with deterioration of consciousness. Good recovery 4 18 16 hours RTA. Large traumatic, right frontal intracerebral Results haematoma and overlying contusion, deterioration of Biopsies were obtained at time points ranging consciousness. Good recovery 5 52 17 hours Found unconscious and drunk. Left temporal contusion from three hours to 11 days after injury. In all ("Burst lobe") and acute subdural haematoma. Disabled the specimens the quality of fixation as judged 6 18 23 hours RTA. Bifrontal contusions. Left frontal intracerebral haematoma, deteriorating consciousness. Disabled by preservation of intracellular organelles was 7 29 27 hours Assault. Focal right parietal contusion and depressed acceptable. fracture. Good recovery 8 17 28 hours RTA. Left hemispheric swelling and temporal contusions-ICP monitoring -+ high ICP. Disabled 9 59 31 hours RTA. Acute right extradural, subdural haematomas and right frontal contusion. Deteriorating consciousness. Control patients Disabled Normal glial, neuronal and vascular ultra- 10 55 33 hours Fell while drunk. Delayed deterioration. Coma. Bifrontal contusions. Thin left acute subdural haematoma. Good structure was present in all control patients, recovery and the neuropil and white matter density was 11 68 37hours RTA. Right temporal contusion, small acute subdural. normal (fig 1). Scanning electronmicroscopy ICP monitoring -+ high ICP. Good recovery 12 42 42 hours Found unconscious. Delayed deterioration. Bitemporal demonstrated pit-vesicle activity on the contusions. This left acute subdural. Good recovery 13 46 44 hours Fall. Delayed confusion. Right temporal contusion. ICP endothelial surface of the lumen of all vessels monitoring -. high ICP. Good recovery in the control patients (table 2). 14 59 49 hours Alcoholic epileptic. ? Fall. Delayed confusion. Bifrontal contusions, mass effect. Disabled 15 40 72 hours Fall. Right parietal acute subdural. Delayed ICP rise new low density. Right temporal -* re-opening craniotomy and right temporal lobectomy. Disabled Transmission EM findings in patients with 16 64 77 hours Fall. Multiple contusions. Left hemisphere, small cerebral contusion extradural haematoma. Right parietal. Delayed deterioration. Partial left temporal lobectomy. Disabled A) GROSS DISRUPTION OF TISSUE 17 44 5 days Hydrocephalic with shunt. Fell out of bed -. bifrontal In five specimens taken from three patients the contusions. Delayed coma. ICP high. Right frontal contusion evacuated. Disabled architecture of the cortical neuropil was dis- 18 72 11 days Fall. Persistently confused. Right frontal subacute rupted by red blood cells and plasma. When- subdural, small temporal contusion. (Burst lobe at surgery). Disabled ever this was seen, the adjacent neuropil was grossly abnormal, demonstrating marked vacuolation and lucency of astrocyte cyto- plasm (fig 2). Specimens were then fixed in 2% osmium tetroxide in phosphate buffer, and the slices were critical-point dried, mounted on scan- B) GLIAL CELL SWELLING ning electronmicroscopy stubs with silver The most consistent finding in both grey and paint and sputter-coated before viewing in a white matter in patients with cerebral con- JEOL 300 TS scanning electronmicroscope. tusions was severe swelling affecting par- http://jnnp.bmj.com/ Blood vessels were selected for particular ticularly astrocytes. This
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