OBJECTIVETo investigate the role of matrix metalloproteinase (MMP) in the transformation of subdural effusion into chronic subdural hematoma.

METHODSThe clinical data of 8 patients with subdural effusion that transformed into chronic subdural hematoma were collected and MMP-2 and MMP-9 levels were detected in the sudural effusion, chronic subdural hematoma and capsules of hematoma using gelatin-zymography.

RESULTSMMP-2 and MMP-9 increased significantly in chronic subdural hematoma as compared with those in subdural effusion (P<0.01), and their levels were also significantly higher in the outer membrane than in the inner membrane of hematoma.

CONCLUSIONSubdural effusion is a risk factor for the occurrence of chronic subdural hematoma, in which process MMP plays a role as the promoting factor acting primarily in the outer membrane of the hematoma.

Adult ; Aged ; Chronic Disease ; Female ; Hematoma, Subdural ; enzymology ; etiology ; Humans ; Male ; Matrix Metalloproteinase 2 ; metabolism ; Matrix Metalloproteinase 9 ; metabolism ; Middle Aged ; Subdural Effusion ; complications ; enzymology

The present study was performed to investigate the relationship between the concentrations of tissue-type plasminogen activator (t-PA) and plasminogen activator inhibitor (PAI) and the CT images in 23 cases of chronic subdural hematomas (SDHs). The concentrations of t-PA and PAI-1 were quantified by enzyme-linked immunosorbent assay (ELISA). Chronic SDHs were divided into five groups according to their appearance on computed tomography: high-density (n = 4), isodensity (n = 8), low-density (n = 5), mixed-density (n = 3), layering (n = 3) types. The volume of hematoma was measured with an image analyzing software program. The concentrations of t-PA were higher in layering (41.2 +/- 0.3 ng/ml, mean +/- standard error of the mean) and high-density (40.0 +/- 1.1 ng/ml) types compared to those of low-density (23.3 +/- 4.1 ng/ml) and iso-density (25.1 +/- 3.7 ng/ml) types. The concentrations of PAI-1 were lower in layering (95.9 +/- 1.0 ng/ml) and high-density (103.4 +/- 34.5 ng/ml) types compared to that of low-density (192.5 +/- 2.6 ng/ml) type. So the ratio between t-PA and PAI-1 (t-PA/PAI) was greater in layering and high-density types. The volume of hematoma was larger in mixed-density and layering types but statistically insignificant. These results presumably suggest that the ratio between t-PA and PAI concentration may contribute to the pathogenesis of the chronic SDH.
Adult ; Aged ; Enzyme-Linked Immunosorbent Assay ; Female ; Hematoma, Subdural/*metabolism ; Human ; Male ; Middle Age ; Plasminogen Activator Inhibitor 1/*analysis ; Tissue Plasminogen Activator/*analysis ; Tomography, X-Ray Computed

OBJECTIVETo investigate the risk factors of progressive brain contusion and to evaluate their impact on patients' outcome.

METHODSOne hundred and thirty two patients with traumatic brain contusion were enrolled in the study, including 70 cases with progressive contusion and 62 cases with non-progressive contusion. The risk factors were investigated with univariate and multivariate Logistic regression analysis.

RESULTSThe univariate analysis showed that Glasgow Coma Score (GCS) at admission, contusion volume at the first brain CT scans, midline shift, combined with skull fracture, subarachnoid hemorrhage, epidural hematoma, subdural hematoma, location of brain contusion, D-dimer levels, combined with type 2 diabetes were associated with progressive brain contusion. Multivariate Logistic regression analysis showed that GCS at admission, contusion volume at the first CT scans, combined with subarachnoid hemorrhage, combined with type 2 diabetes were the independent risk factors for disease progression. The outcome in the progressive group was more aggravated than that in non-progressive group (P = 0.001).

CONCLUSIONPatients with disturbance of consciousness, the larger contusion volume, combined with subarachnoid hemorrhage and diabetes are at risk for progressive brain contusion and unfavorable outcome.

Brain Injuries ; complications ; pathology ; Diabetes Mellitus, Type 2 ; complications ; Disease Progression ; Fibrin Fibrinogen Degradation Products ; metabolism ; Glasgow Coma Scale ; Hematoma, Epidural, Cranial ; complications ; Hematoma, Subdural ; complications ; Humans ; Risk Factors ; Subarachnoid Hemorrhage ; complications ; Tomography, X-Ray Computed

OBJECTIVETo observe the effect of Panax notoginseng (PN) on pathological features in chronic subdural hematoma (CSDH) rabbits and its mechanisms.

METHODSA stable pathological animal model similar to CSDH in humans could be established using subdural injections of small number of blood through a subdural pre-catheter in rabbits. After successful modeling, 18 rabbits were randomly divided into the model group, the low dose PN group (0.125 g/kg), and the high dose PN group (0.250 g/kg), 6 in each group. Normal saline was given to rabbits in the model group, while PN power was given to those in the PN groups by gastrogavage for 6 successive days. Pathologic features of the hematoma outer membrane were observed by HE staining. The activity of SOD and the content of MDA in the hematoma outer membrane were examined by the colorimetric method. Expressions of CD31, CD34, and VEGF in the hematoma outer membrane were observed by immunohistochemical assay. Expressions of VEGF in the peripheral blood and the subdural hematoma were detected by enzyme-linked immunosorbent assay (ELISA). Expressions of VEGFR-1 and VEGFR-2 in the hematoma outer membrane were detected by Western blot.

RESULTSCompared with the model group, the inflammatory reaction was comparatively lessen and the proliferation of the fibrous tissue was relatively mature in the low and high dose PN groups. The activity of SOD increased (P < 0.05); expressions of CD31 and CD34 were reduced (P < 0.01); VEGF expression in the residual hematoma fluid decreased (P < 0.05) in the high dose PN group. Expressions of VEGF and VEGFR-2 were all reduced in the high and low dose PN groups (P < 0. 05, P < 0.01). Compared with the low dose PN group, expressions of CD31 and CD34 were reduced (P < 0.01), and the VEGFR-2 expression was also reduced (P < 0.05) in the high dose PN group.

CONCLUSIONSPN could promote the fibrous repairing of subdural hematoma in CSDH rabbits. It also lessened inflammation and oxidative injury of the hematoma outer membrane and reduced expressions of VEGF. The pathological angiogenesis could be reduced through influencing VEGFR-2 receptor pathways, which might be an important mechanism.

Animals ; Disease Models, Animal ; Drugs, Chinese Herbal ; pharmacology ; Hematoma, Subdural, Chronic ; metabolism ; pathology ; Panax notoginseng ; chemistry ; Rabbits ; Vascular Endothelial Growth Factor A ; metabolism ; Vascular Endothelial Growth Factor Receptor-1 ; metabolism ; Vascular Endothelial Growth Factor Receptor-2 ; metabolism

Menkes disease is an X-linked recessively inherited neurodegenerative disorder of copper metabolism leading to death in early childhood. This disease is characterized by low serum, liver and brain Cu levels, whereas the Cu content in nearly all other organs is increased. The main clinical features are irregular kinky hair, characteristic face, progresssive degeneration of the central nervous system, bone changes, arterial rupture and thrombosis, and instability of temperature. We have experienced a case of Menkes disease in a eight months old male patient, who manifested by seizure, developmental delay, hypotonia, characteristic hair and face along with low levels of serum copper and ceruloplasmin. We report the characteristic findings of cranial MRI and MR angiography in this Menke's patient. In cranial MRI, he showed progressive brain atrophy with subdural hemorrhage and effusion. MR angiography revealed tortuosity of vessels clearly obviating necessity of more invasive conventional arteriography in diagnosis of this disease. This study suggested that cranial MRI and especially MR angiography might be helpful in making early diagnosis of this disease.
Angiography ; Atrophy ; Brain ; Central Nervous System ; Ceruloplasmin ; Copper ; Diagnosis ; Early Diagnosis ; Hair ; Hematoma, Subdural ; Humans ; Liver ; Magnetic Resonance Imaging ; Male ; Menkes Kinky Hair Syndrome ; Metabolism ; Muscle Hypotonia ; Neurodegenerative Diseases ; Rupture ; Seizures ; Thrombosis

We performed experiments to study the effects of acutely increased inracranial pressure on cereral gas metabolism. The results and findings were reported to The Journal of Catholic Medical College,(Vol. 24) 1973. We thereafter evaluated cerebral gas metabolism of fifty patients with acute cerebral lesions. Cerebral gas metabolism was measured by determining the pO2, pCO2, and pH values of arterial and venous blood and of the cerebrospinal fluid. Samplings of venous blood were obtained from the internal jugular vein. In the determination of the pH, pO2 and pCO2 of arterial and venous blood and cerebro-spinal fluid, the "Radiometer BMS 3 with Digital Acid-Base Analyser PHM 72" was used. These 50 patients had their gas metabolism measured at interval of 2 or 3 days, from the time of their admission to the time of either their recovery or death. The following observations were made 1. The 50 patients studied and observed included. a) Brain contusion 13 cases. b) Epidural or subdural hematoma 11 cases. c) Skull fracture 10 cases. d) Intracerebral hemorrhage 5 cases. e) Scalp laceration 1 cases. f) Arteriovenous malformation or cerebral rete 5 cases. g) Traumatic subarachnoid hemorrhage 1 cases. h) Intracranial aneurysm 4 cases. 2. There 50 patients have been subdivided according to level of consciousness as follows: a) Group A-Those who were alert with no neurological deficit. b) Group B-Those who were drowsy with mild neurological deficit. c) Group C-Those who were stuporous with severe neurological deficit. d) Group D-Those who were in coma. 3. It was observed that the pH, pO2, and pCO2 content of the arterial and venous blood and cerebrospinal fluid of those in Group A were within normal ranges. 4. Many cases classified under Group B had respiratory alkalosis of the arterial blood. However those who recovered or became worse revealed no noticeable changes in the cerebral gas metabolism studies. 5. Many cases classified under Group C had respiratory alkalosis in their arterial blood but only a few showed metabolic acidosis in the cerebrospinal fluid. However the patients who became worse manifested a marked metabolic acidosis in the cerebrospinal fluid. 6. Several patients in Group D had severe respiratory alkalosis as well as metabolic alkalosis in their arterial blood and marked metabolic acidosis in the their cerebrospinal fluid. 7. "Luxury perfusion syndrome" was not seen in any of the fifty cases studied. 8. Only a few cases manifested arterial hypoxemia in the all group. We believe this was due to the fact that tracheostomy and hyperventilation were done in the early stages with the aim of reducing the raised intracranial pressure.
Acidosis ; Alkalosis ; Alkalosis, Respiratory ; Anoxia ; Arteriovenous Malformations ; Brain Injuries ; Brain* ; Cerebral Hemorrhage ; Cerebrospinal Fluid ; Coma ; Consciousness ; Hematoma, Subdural ; Humans ; Hydrogen-Ion Concentration ; Hyperventilation ; Intracranial Aneurysm ; Intracranial Pressure ; Jugular Veins ; Lacerations ; Metabolism ; Perfusion ; Reference Values ; Scalp ; Skull Fractures ; Stupor ; Subarachnoid Hemorrhage, Traumatic ; Tracheostomy