Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Subdural Space”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 361 records · Page 20Linked to original sources
PubMedDate not supplied

[Physiopathology of adult onset external hydrocephalus].

AIMS: In this paper we report on a new disorder known as adult onset external hydrocephalus. DEVELOPMENT: There is sufficient evidence to be able to establish the pathogenic hypotheses proposed here. Adult onset external hydrocephalus is related with traumatic injuries, surgery, subarachnoid haemorrhages and neurosurgical treatment of aneurysms. This disorder is produced by an expansion of the subarachnoid and subdural space due to the rupture of some part of the arachnoid membrane, which then allows fluid to flow into this compartment. In all cases there are three essential factors: the presence of some kind of intracranial bleeding, tearing of the arachnoid membrane and an excessive quantity of cerebrospinal fluid (CSF), probably because of reduced reabsorption by the arachnoid granulations. The degree to which reabsorption of CSF is affected is what conditions the prognosis in these patients rather than the accumulation within the subarachnoid or subdural cavity. Once this type of hydrocephalus is confirmed the patient requires a ventricular CSF shunt. We offer a classification of the different types of presentation. It is not very clear exactly when this shunt should be inserted or how to treat the isolated extra axial collection in absence of ventricular dilatation. CONCLUSIONS: The physiopathology of adult onset external hydrocephalus is a scientific challenge that will lay down the foundations for treatment with ventriculoperitoneal shunts

Adult↗
PubMed1997

An overview of chronic subdural hematoma: experience with 2300 cases.

BACKGROUND: Over a period of 30 years since 1966, 2300 cases of chronic subdural hematoma have been seen and treated. DESCRIPTION: A male preponderance among the cases was seen, in a ratio of 5:1. The condition presented with various manifestations. Nine hundred were seen in the pre-CT period (before 1980), compared to 1400 cases encountered after 1980. Since 1968, these cases have been managed by a small temporal craniotomy, with the dura left open and the subdural space communicating with the subtemporalis area. CONCLUSION: This procedure has resulted in marked reduction of recurrence, and membranectomy has not been required. There have been 11 deaths in this group of patients; the mortality rate is only 0.5%.

Adolescent↗
PubMed1981

[Cerebrovascular disorders in alcoholics (clinico-morphologic study)].

Under examination there were alcoholics aged 25 to 45 years, 44 of whom later died. At lifetime the addicts showed various clinical syndromes of acute vascular disorders, such as, hemorrhages to the brain matter, subarachnoidal hemorrhages, subdural hematomas, general disturbances of the cerebral circulation, as well as alcoholic cardiopathies. On postmortem examination both acute and chronic vascular disorders were revealed. The acute disorders manifested themselves in a pronounced plethora of the brain, the meninges and the internal organs; disturbances of the vascular wall permeability, and hemorrhages (large and small) to the brain, the subarachnoidal and subdural space and to the internal organs. In chronic vascular disorders, cerebrovascular fibrosis and atherosclerosis of the cerebral vessels, the aorta and the coronary arteries as well as residua of large and small hemorrhages sustained were recorded.

Adult↗
PubMed1982

Hypotension during surgery for subdural hematoma and effusion in infants.

A retrospective study of subdural hematoma was conducted in 36 patients ranging in age from 2 months to 9 years. Hypotension occurred in 41% of the children during the evacuation of the subdural hematoma. This study suggests that hypovolemia was caused, in part, by the blood loss into the subdural hematoma. In patients with hematoma larger than 8% of the intravascular volume, the frequency of the hypotension was high (88%). Infants, in particular, had larger hematomas, ranging in size from 8-27% of intravascular blood volume and, therefore, were at high risk to develop hypotension. These larger hematomas may be due to the infants' higher ratio of subdural space to the body weight. The study also suggests that the preoperative infusion of adequate fluid and blood is a significant factor in preventing hypotension during the hematoma evacuation.

Age Factors↗
PubMed1975

Junctions in the meninges and marginal glia.

The meninges of various mammals were prepared for examination with the electronmicroscope by thin sectioning or freeze-fracturing. Particular attention was given to the distribution of tight junctions in order to determine the basis for the meningeal barrier between the blood circulating in dural vessels and the cerebrospinal fluid in the subarachnoid space. While some dural blood vessels are fenestrated, those in the subarachnoid space are not and their component endothelial cells are joined by an extensive system of tight junctions. An extensive and continuous system of tight junctions was also found in a layer of specialized cells at the border of the arachnoid with the dura. This arachnoid barrier layer is apparently the only basis of the meningeal barrier because often cellular layers in the dura and arachnoid lack tight junctions although they are linked by gap junctions and desmosomes. In particular, tight junctions are lacking at the border of the "subdural space" which is actually a fascial plane within the dura. Tight junctions are also lacking between astrocytes at the surface of the brain but these cells are linked by gap junctions and a new type of intercellular junction. The distribution of these junctions, as well as assemblies of intramembranous particles at the astrocytic border, raises the question whether this layer might have a role in the exchange of certain substances between the brain and cerebrospinal fluid.

Animals↗
PubMed2004

Second-trimester diagnosis of intracranial vascular anomalies in a fetus with subdural hemorrhage.

OBJECTIVES: Risk factors for intracranial hemorrhage occurring in prenatal life are imperfectly known. A case of prenatal diagnosis of subdural hemorrhage associated with multiple intracranial vascular aneurysms is described. METHODS: Sonography and magnetic resonance imaging of the fetal head were obtained at 21 weeks' gestation and compared with pathologic findings. RESULTS: Sonography showed a large transonic mass displacing the normal intracranial structures. Magnetic resonance imaging demonstrated the hemorrhagic origin of the mass and showed multiple vascular anomalies. Postmortem examination confirmed the compression of the cerebral hemisphere by a blood collection, probably because of bleeding from one of the multiple vascular aneurysms into the subdural space. CONCLUSION: Magnetic resonance imaging with the use of single-shot ultrafast sequences may be useful not only in the differential diagnosis of fetal intracranial hemorrhage but also in identifying vascular risk factors.

Abnormalities, Multiple↗
PubMed2001

[Chronic subdural hematoma in patients over 80 years of age].

INTRODUCTION: Chronic subdural hematoma (CSH) represents one of the most frequent types of intracranial hemorrhage. Most occur in elderly patients causing a variety of therapeutic problems associated to systemic diseases. PATIENTS AND METHODS: A retrospective study of 90 patients older than 80 years of age with chronic subdural hematoma treated in the last 15 years was undertaken. For clinical evaluation on admission and at discharge we used the classification of Markwalder. Surgical treatment was performed in all patients and a burr hole craniostomy with closed drainage system was used. RESULTS: On admission, 73 patients (80%) were in satisfactory condition (grades 0-2); 17 (20%) were grade 3 or 4. Seven (7.7%) patients died but none due to surgery. In 6 (6.6%) of the patients, surgical reintervention was required to remove a recurring CSH. In 76.6% of the patients, the results achieved were graded 0 or 1. CONCLUSIONS: In our experience CSH in elderly patients should be treated with minimal surgery with a simple drainage of the subdural space. The good results suggest that the procedure could be considered as a first procedure in these patients and that age or concomitant diseases do not appear to be poor prognostic factors.

Aged↗
PubMed1995

Fatal clival subdural hematoma in a hemophiliac.

We report the case of a hemophiliac in whom developed an unusual site of intracranial bleeding, a subdural hematoma that extended in the posterior fossa anteriorly from the clivus into the upper spinal subdural space. The hematoma was delayed in onset and was fatal. We review the current management recommendations for hemophiliac patients with head injury and the clinical presentation of intracranial bleeding in hemophiliacs. The necessity for Factor VIII replacement and serial computed tomography scans is emphasized.

Adolescent↗
PubMed1983

[Postoperative regression speed of chronic subdural hematoma, with special reference to the subsequent study by CT xray].

Thirty-one adult patients with chronic subdural hematoma were treated surgically and followed Up by CT. In these cases, the postoperative regression of the hematoma cavity on CT was analysed in relation to patient's age, timing of operation, operative method, preoperative CT findings and postoperative clinical courses. In patients with older age and/or low density type of hematoma, slow reduction of subdural space was observed after operation. In five of these cases, the follow-up CT scans revealed reaccumulation of hematoma. Patients with high density type of hematoma and/or early operation from the onset showed a rapid reduction of hematoma cavity and clinical improvement.

Adult↗
PubMed1993

Diagnosis and results of different treatment regimens in patients with spinal abscesses.

Bacterial abscesses involving the spinal canal are associated with a high morbidity and mortality. Most frequently, these lesions are found in the epidural, rarely in the subdural space. In this report, our clinical material consists of a series of 16 patients treated during the last seven years. The clinical presentation included local neurological signs (back pain, para-/tetraparesis, bladder dysfunction), disturbances of consciousness (ranging from drowsiness to deep coma) and general inflammatory signs (meningism, fever). All patients presented with risk factors (septic foci, chronic diseases, and iatrogenic causes). Laboratory investigations revealed typically pathological blood sedimentation rate, leucocytosis and CSF-pleocytosis. Radiologically, the diagnosis was confirmed by myelography, CT and preferably MRI. The abscesses were located epidurally in 14 and subdurally in 2 cases. The surgical treatment included laminectomy, or multiple flavectomies in extensive lesions. Drainage systems (either simple silicon outflow drains or suction-/irrigation systems) were installed in all cases, as well as antibiotic treatment. Results of treatment: Following an observation period of 0.5-6 years, we found complete recovery in six (38%) cases, six (38%) others were mildly disabled and four (25%) patients died. Focussing on the results of the two different drainage systems, we found a statistically significant superiority of the inflow-/outflow system. Complications included mandatory re-exploration, post-inflammatory hydrocephalus, syringomyelia, spinal instability, surgical treatment of peripheral septic foci and therapy resistant septicaemia. In conclusion, we propose that spinal epi- or subdural abscesses require surgical evacuation, using a suction-/irrigation drainage system, as well as antibiotic and intensive care treatment.

Abscess↗
PubMed1993

Intracranial subdural empyema: burr hole exploration for diagnosis and treatment.

An analysis of 19 confirmed cases of subdural empyema treated in our unit during a 29-month period ending in May 1990 revealed that this was a disease of young males (mean age 19.6 yrs: male:female ratio 5:1) that was frequently associated with paranasal sinusitis. We have identified a characteristic symptom complex which when present together with focal neurological deficits makes the diagnosis highly probable. This consists of fever, headache, altered level of consciousness and frontal scalp swelling. In a practice setting where neuroradiological confirmation of the diagnosis is not always practicable, this clinical syndrome is helpful and should prompt early burr hole exploration of the subdural space. The only deaths (2 patients; 11%) occurred in patients who presented in coma. The remaining were either normal (6 patients) or continued to improve after treatment, which consisted of multiple burr hole drainage, broad spectrum antimicrobial treatment and eradication of the source of infection.

Adolescent↗
PubMed1990

Ischemic brain damage in a model of acute subdural hematoma.

Ischemic brain damage is the most important neuropathological finding in humans who die after acute subdural hematoma; however, its causes are poorly understood. We have produced acute subdural hematoma in the rat by injecting 400 microliters of autologous blood (approximately 20% of intracranial volume) into the subdural space. Extensive areas of ischemic damage, involving 14 to 16% of the volume of the hemisphere, developed in this model at 4 and 24 hours after the lesion. The hematomas were associated with a brief peak in intracranial pressure (51 mm Hg), which remained at three times normal levels (14 mm Hg) for 3 hours. In this model, therefore, ischemic damage appears to be due to the local effects of blood overlying the cortex at 4 hours after the ictus, rather than to globally raised intracranial pressure. The implications for the pathophysiology of acute subdural hematomas in humans are discussed.

Animals↗
PubMed1990

[Chronic subdural hematoma with a markedly fibrous hypertrophic membrane. Case report].

A 40-year-old female, who had taken low-dose oral contraceptives for 2 months before onset, developed transient dysarthria, left hemiparesis, and left hemihypesthesia. One month later, a computed tomography (CT) scan revealed a uniformly enhanced, convex-shaped, hypertrophic membrane with a lobulated lumen in the subdural space of the right parietal region. A right parietal craniotomy was performed. The membrane, consisting of elastic-hard, hypertrophic granulation tissue and yellowish, sticky fluid in the lumen, was readily freed and totally extirpated. Subsequently, the patient recovered without persistent symptoms. Light microscopic examination detected the sinusoidal channel layer and the fibrous layer in an alternating configuration, along with intramembranous hemorrhagic foci. Such hypertrophy must have been caused by repeated intramembranous hemorrhages and reactive granulation. Such findings of hematoma membrane have never previously been reported. Thus, this is an interesting case, clearly distinguished from typical chronic subdural hematoma.

Adult↗
PubMed2002

Ischemic preconditioning reduces infarct volume after subdural hematoma in the rat.

The aim of the present study was to investigate the effects of ischemic preconditioning on infarct volume in a rat model of subdural hematoma (SDH). Ischemic preconditioning was induced by 15 min transient middle cerebral artery (MCA) occlusion followed 3 days later by the injection of 300 microl of autologous venous blood into the subdural space. Preconditioning significantly reduced the volume of cortical infarction (by 26%, P<0.001) 24 h after SDH induction, but not brain swelling (P>0.05) relative to sham-operated non-preconditioned animals. These data support the view that ischemic preconditioning reduces ischemic brain damage in this rat model of SDH.

Animals↗
PubMed1987

Arachnoid cyst of the middle cranial fossa--aplasia of temporal lobe?

In 11 cases of intracranial, temporal arachnoid cysts the etiology, clinical and radiographic findings, surgical treatment, and outcome are reviewed in respect of post-traumatic subdural hematoma. Cysts of the middle cranial fossa are susceptible to trauma, which may cause bleeding either into the cyst or into the subdural space. Signs and symptoms of increasing intracranial pressure (ICP), local neurological deficits, and sometimes epileptic seizures may lead to hospitalization. CT or MRI scans are diagnostic in these cases. In cases of intracranial mass lesion with displacement of the midline structures and increasing ICP, osteoplastic craniotomy is performed and the lateral wall of the cyst is resected down to the tentorial notch by a microsurgical procedure, with opening into the basal cisterns. There were no operative or postoperative complications in 11 consecutive cases. However, one boy required a cystoperitoneal shunt 3 months later as a result of hydrocephalus following subdural hematoma. Asymptomatic arachnoid cysts are discussed with respect to brain function and social behavior.

Arachnoid↗
PubMed1984

Management of acute subdural hematomas from aneurysmal rupture.

Subdural hematomas (SDH) from ruptured aneurysm (RA) are much less common than intracerebral (ICH) hematomas or subarachnoid (SAH) or intraventricular hemorrhage (IVH). With computerized tomography, preoperative diagnosis is now made more often. The authors have collected 18 such cases from a review of 897 cases of RA admitted to eleven medical centers in 1980 and 1981. Nine (50%) of these patients died prior to discharge from hospital. Four (22%) had surgery and died postoperatively and 9 (50%) were operated upon and survived. Thirteen (72%) of the patients showed anisocoria, decreased consciousness and unilateral weakness prior to surgery. Eight (89%) of the fatalities had shown preoperative herniation as opposed to only 5 (56%) of the survivors. The overall incidence of delayed ischemia due to vasospasm was 11% (2 cases). Those who died had greater midline shift and larger SDH on the admission CT scan. Sixteen (89%) of these patients were female. Thirteen (72%) had ruptured aneurysms on the internal carotid artery. All of these hematomas were unilateral and uniformly hyperdense, and the convexity hematomas were crescentic in shape. Seventeen (94%) had evidence of blood in locations other than the subdural space. If the patient is potentially salvageable and has a midline shift, the SDH should probably be evacuated immediately and the aneurysm clipped at the same operation since the development of a tentorial herniation has such an adverse effect on outcome.

Acute Disease↗
PubMed2004

[Clinical analysis of 31 cases of traumatic interhemispheric subdural hematomas].

OBJECTIVE: To analyze the clinical characteristics, pathogenesis and management of traumatic interhemispheric subdural hematomas (ISH). METHODS: Thirty-one traumatic ISH cases were reviewed and analyzed retrospectively. RESULTS: Of the 31 patients, 29 were cured and 2 died of multi-system organ failure (MSOF) and cerebral hernia respectively. Typically, ISH manifested hemiplegia or paralysis of the counterlateral lower limb known as falx syndrome. CONCLUSIONS: CT scans showing hematocele in the interhemispheric subdural space in excess of 20 ml, or with a thickness of hematocele over 1cm, may serve as a diagnostic criteria for ISH. For the treatment of ISH, surgery and conservative management are suggested on the basis of functional disturbance or the stability of the disease.

Adolescent↗
PubMed1991

[A case of anti-phospholipid antibody syndrome associated with subdural hematoma].

We report a case of a 47-year-old man with anti-phospholipid antibody syndrome associated with subdural hematoma. The patient had several episodes of arthritis during his thirties. He developed venous thrombosis in his right lower leg at the age of 35, when laboratory studies demonstrated prolongation of activated partial thromboplastin time (APTT) and a biological false-positive result occurred on a syphilis test. When bulbar palsy and Horner's syndrome in the right eye suddenly appeared at the age of 42, he was diagnosed as having brain stem infarction. At the age of 47, he developed constructional apraxia, dyscalculia, skilled movement disturbances and generalized convulsions. Subdural hematoma and multiple lacunes in the cerebral white matter were demonstrated with brain MRI. Furthermore, the patient was positive for Rumpel-Leede phenomenon. Laboratory studies revealed mild thrombocytopenia, prolonged bleeding time and APTT, positive antinuclear antibody and positive test results for both lupus anticoagulant and an anti-cardiolipin antibody, namely anti-phospholipid antibodies. Based on these findings, we consider that the tendency of this patient to bleed may have been due to antiphospholipid antibodies, attacking the platelet membranes and that the bridging veins in the subdural space may be the site at which the bleeding tendency easily appears. Anti-phospholipid antibody syndrome accompanied by hemorrhagic complications had rarely been reported. We suggest that special attention should be given to hemorrhagic complications in patients with anti-phospholipid antibody syndrome associated with fragility of the vessels and/or platelet dysfunction.

Antiphospholipid Syndrome↗