Production of clinical form of chronic subdural hematoma in experimental animals

1972 ◽  
Vol 37 (5) ◽  
pp. 552-561 ◽  
Author(s):  
Satoru Watanabe ◽  
Hironobu Shimada ◽  
Shozo Ishii

✓ A method for producing a clinical form of experimental chronic subdural hematoma is reported. When blood is mixed with cerebrospinal fluid and incubated, a peculiar clot is formed which, when inoculated into the subdural space of dogs or monkeys, grows gradually. Histologically the capsule of the hematoma is comparable to that seen in human chronic subdural hematoma. In some animals progressive hemiparesis develops.

2000 ◽  
Vol 93 (5) ◽  
pp. 791-795 ◽  
Author(s):  
Hiroshi Nakaguchi ◽  
Takeo Tanishima ◽  
Norio Yoshimasu

Object. This study was conducted to determine the best position for the subdural drainage catheter to achieve a low recurrence rate after burr-hole irrigation and closed-system drainage of chronic subdural hematoma (CSDH).Methods. The authors studied 63 patients with CSDH in whom the drainage catheter tip was randomly placed and precisely determined on postoperative computerized tomography (CT) scans and 104 patients with CSDH in whom CT scans were obtained 7 days postsurgery. The location of the subdural drainage catheter, the maximum postoperative width of the subdural space, and the percentage of the ipsilateral subdural space occupied by air postoperatively were determined and compared with the postoperative recurrence and reoperation rates.Patients with parietal or occipital drainage had a higher rate of CSDH recurrence and much more subdural air than those with frontal drainage. In addition, patients with residual subdural air demonstrated on CT scans obtained 7 days postsurgery also had a higher recurrence rate than those without subdural air collections. Furthermore, patients with a subdural space wider than 10 mm on CT scans obtained 7 days postsurgery had a higher recurrence rate than those with a space measuring 10 mm or less.Conclusions. The incidence of postoperative fluid reaccumulation seems to be reduced by placing the tip of the drainage catheter in the frontal convexity and by removing subdural air during or after surgery.


1976 ◽  
Vol 45 (1) ◽  
pp. 26-31 ◽  
Author(s):  
Haruhide Ito ◽  
Shinjiro Yamamoto ◽  
Toshio Komai ◽  
Hidetaka Mizukoshi

✓ The authors describe studies performed on material aspirated from chronic subdural hematomas. Patients were given 51Cr-labeled red cells prior to aspiration, and it was possible to demonstrate that the mean daily hemorrhage into the hematoma space amounted to 10.2% of its volume. Immunoelectrophoresis of the aspirated hematoma fluid by monospecific anti-human fibrinogen revealed the presence of fibrin and fibrinogen degradation products that, measured by hemagglutination-inhibition immunoassay techniques, varied between 5.0 and 10,500 µg/ml with an average of 2604 µg/ml in 18 cases. The tissue activator was demonstrated by Todd's histological localization in the outer membrane of the chronic subdural hematoma in 11 cases, but not in the inner membrane. These results indicate that if a clot in the subdural space causes the formation of neomembrane, and excessive fibrinolysis occurs, the subdural clot would not only liquefy, but also enlarge by continuous hemorrhage from the neomembrane. Therefore, local hyperfibrinolysis and continuous bleeding are important in the etiology of the chronic subdural hematoma.


2000 ◽  
Vol 93 (4) ◽  
pp. 686-688 ◽  
Author(s):  
Shinya Mandai ◽  
Masaru Sakurai ◽  
Yuzo Matsumoto

✓ The authors present a case of refractory chronic subdural hematoma (CSH) in a 59-year-old man with coagulopathy due to liver cirrhosis. The patient was successfully treated by embolization of the middle meningeal artery after several drainage procedures. This new therapeutic approach to recurrent CSH is discussed.


2008 ◽  
Vol 108 (2) ◽  
pp. 275-280 ◽  
Author(s):  
Rudolf A. Kristof ◽  
Jochen M. Grimm ◽  
Birgit Stoffel-Wagner

Object The purpose of this study was to clarify whether cerebrospinal fluid (CSF) leakage into the subdural space is involved in the genesis of chronic subdural hematoma (CSDH) and subdural hygroma (SH) and to clarify whether this leakage of CSF into the subdural space influences the postoperative recurrence rate of CSDH and SH. Methods In this prospective observational study, 75 cases involving patients treated surgically for CSDH (67 patients) or SH (8 patients) were evaluated with respect to clinical and radiological findings at presentation, the content of β -trace protein (β TP) in the subdural fluid (βTPSF) and serum (βTPSER), and the CSDH/SH recurrence rate. The βTPSF was considered to indicate an admixture of CSF to the subdural fluid if βTPSF/βTPSER > 2. Results The median β TPSF level for the whole patient group was 4.29 mg/L (range 0.33–51 mg/L). Cerebrospinal fluid leakage, as indicated by βTPSF/βTPSER > 2, was found to be present in 93% of the patients with CSDH and in 100% of the patients with SH (p = 0.724). In patients who later had to undergo repeated surgery for recurrence of CSDH/SH, the βTPSF concentrations (median 6.69 mg/L, range 0.59–51 mg/L) were significantly higher (p = 0.04) than in patients not requiring reoperation (median 4.12 mg/L, range 0.33–26.8 mg/L). Conclusions As indicated by the presence of βTP in the subdural fluid, CSF leakage into the subdural space is present in the vast majority of patients with CSDH and SH. This leakage could be involved in the pathogenesis of CSDH and SH. Patients who experience recurrences of CSDH and SH have significantly higher concentrations of βTPSF at initial presentation than patients not requiring reoperation for recurrence. These findings are presented in the literature for the first time and have to be confirmed and expanded upon by further studies.


1975 ◽  
Vol 42 (1) ◽  
pp. 101-103 ◽  
Author(s):  
Eldad Melamed ◽  
Slvan Law ◽  
Avinoam Reches ◽  
Abraham Sahar

✓ A patient is presented in whom chronic subdural hematoma simulated transient ischemic attacks. The neurological manifestations were those of recurrent, transient episodes of expressive dysphasia preceded by focal sensory deficit. Various pathophysiological mechanisms which could have caused the unusual clinical picture are briefly considered.


1990 ◽  
Vol 73 (2) ◽  
pp. 201-205 ◽  
Author(s):  
Nobuhiko Aoki

✓ The cases of 30 infants with chronic subdural hematoma treated surgically between 1978 and 1987 (after the introduction of computerized tomography) were reviewed. This series was limited to infants presenting with increased intracranial pressure, neurological deficits, or developmental retardation. Nineteen patients were male and 11 were female, ranging in age from 1 to 14 months (average 6.1 months). The surgical treatment was initiated with percutaneous subdural tapping which was repeated periodically, if indicated, for 2 weeks. If the patients failed to respond to subdural tapping, subdural-peritoneal shunting was installed. The follow-up periods were from 3 months to 9 years 8 months (average 4 years 10 months). Computerized tomography at that time disclosed disappearance or minimal collection of subdural fluid in 28 cases (93%) and a significant collection (> 5 mm) in two (7%). Neurological examination revealed that the patients were “normal” in 17 cases (57%), “mildly or moderately disabled” in nine (30%), and “severely disabled” in four (13%). The majority of disabled patients had lesions secondary to infantile acute subdural hematoma, child abuse, or hemorrhagic diathesis. These results indicate that the treatment protocol in the present series is acceptable for the elimination of subdural hematoma. Together, early diagnosis and treatment of the etiological conditions causing the lesion are indispensable for obtaining a satisfactory neurological outcome.


1974 ◽  
Vol 40 (3) ◽  
pp. 347-350 ◽  
Author(s):  
Sheldon R. Hurwitz ◽  
Samuel E. Halpern ◽  
George Leopold

✓ Eighteen patients with chronic subdural hematomas were studied by both brain scans and echoencephalography. All cases were verified by cerebral angiography. Brain scanning was accurate in predicting hematomas in 93% of the cases, and echoencephalography in 44%. When hematomas were bilateral or when frontal clots caused no shift in the diencephalic midline, the routine echoencephalogram often was negative. The two procedures are complementary, and serial studies may be helpful in the study of changing clinical situations.


1985 ◽  
Vol 63 (5) ◽  
pp. 691-692 ◽  
Author(s):  
Zbigniew Kotwica ◽  
Jerzy Brzeziński

✓ Six cases of chronic subdural hematoma presenting with the clinical findings of acute subarachnoid hemorrhage are reported. No systemic or focal cause for the bleeding was found, and possible mechanisms are discussed.


1987 ◽  
Vol 67 (5) ◽  
pp. 710-716 ◽  
Author(s):  
Hisashi Aikawa ◽  
Kinuko Suzuki

✓ A new experimental model of chronic subdural hematoma in mice is described. A single intraperitoneal injection of 6-aminonicotinamide (25 mg/kg body weight) on the 5th postnatal day induced hydrocephalus in mice with almost 100% success. Approximately 60% of the mice spontaneously developed intracranial hemorrhage 20 days after the injection. About 1 week after the hemorrhage, a lens-shaped or spherical subdural hematoma was observed, accompanied by marked dilatation of the lateral ventricles and intraventricular hemorrhage. Histological examination revealed that the hematoma contained well-organized outer and inner membranes. Fresh hemorrhage surrounded by many hemosiderin-laden macrophages was seen at the margin of the hematoma adjacent to the organizing outer membrane, in which many fibroblasts and blood vessels were noted. The inner membrane of the hematoma was made up of several tiers of flattened cells with thin-walled blood vessels. The gross morphology and histology of these hematomas closely resembled those of human chronic subdural hematoma.


2004 ◽  
Vol 100 (4) ◽  
pp. 372-374 ◽  
Author(s):  
Carlo Bortolotti ◽  
Huan Wang ◽  
Kenneth Fraser ◽  
Giuseppe Lanzino

✓ The etiopathogenesis of traumatic spinal subdural hematoma (SSH) is uncertain. Unlike the supratentorial subdural space, no bridging veins traverse the spinal subdural space. The authors describe a case of subacute SSH that occurred after spontaneous resolution of traumatic intracranial SDH and suggest a causal relationship between the two. A 23-year-old woman suffered an acute intracranial SDH after a snowboarding accident. There was no clinical or radiological evidence of spine injury. Conservative management of the supratentorial SDH resulted in spontaneous radiologically documented resolution with redistribution of blood in the subdural space. Four days after the injury, the patient started noticing new onset of mild low-back pain. The pain progressively worsened. Magnetic resonance imaging of the lumbosacral spine 10 days after the original injury revealed a large L4—S2 SDH. Ten days after the original injury, bilateral L5—S1 laminotomy and drainage of the subacute spinal SDH were performed. The patient experienced immediate pain relief. The authors hypothesize that in some cases spinal SDH may be related to redistribution of blood from the supratentorial subdural space.


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