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PubMed1991

Pathogenesis and biomechanics of traumatic intracranial haemorrhages.

Intracranial haemorrhage is frequently seen by the general pathologist in the context of neural trauma. Thus, the differential diagnosis, pathogenesis and biomechanics are of practical interest in the routine work. Extradural haematomas are produced when branches of the middle meningeal vessels are lacerated. They are commonly located in the temporal fossa, and other intracranial haematomas may be present. Skull fractures occur in a high percentage of cases and play a key role in the pathogenesis of this type of bleeding. Acute subdural haematomas commonly arise from tearing of the bridging veins. They are often located in the temporal and frontal regions, and the morbidity and mortality are related to the extent of the underlying brain damage. The visco-elastic behaviour of the bridging veins and their lack of reinforcement by arachnoid trabecula in the subdural space explains why they tear under high rates of acceleration during trauma. Subacute and chronic subdural haematomas are weakly correlated with trauma. The less striking onset of symptoms may be related to the rate of blood accumulation and the capacity of the brain to accommodate the mass effect of the bleeding. Intracerebral haematomas are probably due to the direct rupture of the intrinsic cerebral vessels. The mortality rate shows no correlation with location, but those located in the basal ganglia are compatible with a good recovery when occurring in isolation. Traumatic subarachnoid haemorrhage, when in isolation, is usually associated with evidence of injury elsewhere, such as the neck muscles or the ligamentary system of the cervical spinal column. It may be secondary to intraventricular bleeding due to tearing of the tela choroidea, or associated with contusions.

Biomechanical Phenomena↗
PubMed1977

Congenital brain defect masked by subdural fluid collection.

Two rare cases of subdural fluid collection are reported. In these cases, the subdural space was in direct communication with the lateral ventricle through the congenital brain defects. The subdural fluid was formed by the cerebrospinal fluid which passed from the lateral ventricle through the brain defects. The difficulty to diagnose these cases from the usual subdural hygroma is emphasized.

Brain↗
PubMed1986

[A case of posttraumatic vascular abnormality similar to dural arteriovenous malformation].

A case of posttraumatic vascular abnormality similar to dural arteriovenous malformation is reported. A 21-year-old man was injured in the traffic accident and admitted to our hospital with comatose state. Bilateral carotid angiograms revealed no abnormal findings. Then, he was treated conservatively as a diagnosis of cerebral contusion. Nine years after the initial admission, he was fallen into comatose state suddenly and admitted to a local hospital. On the next day, he was transferred to our hospital. Neurological examination disclosed comatose state, right oculomotor palsy, and left hemiparesis. CT scan showed a crescent shaped high density area in the right subdural space, right temporal intracerebral high density area, and left frontal low density area, suggesting right acute subdural hematoma, right temporal intracerebral hematoma, and left frontal old cerebral contusion respectively. Right carotid angiogram revealed an abnormal vascularity in the right middle fossa, which was fed by the middle meningeal artery and drained into the superior sagittal sinus and the transverse sinus. Surgical treatment was performed immediately. Following the evacuation of intracerebral hematoma, the abnormal vascular mass suggesting a nidus of arteriovenous malformation was removed totally, that was attached to the dura mater. Pathological specimen showed large veins and arteries with thrombus, however, no characteristic feature of arteriovenous malformation. Then, this was thought to be an arteriovenous fistula between the branches of middle meningeal artery and the veins of fibroglial scar following by the cerebral contusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1998

External hydrocephalus after aneurysm surgery: paradoxical response to ventricular shunting.

OBJECT: The authors sought to investigate the mechanisms and pathophysiological effects of subdural fluid collection after surgery for aneurysmal subarachnoid hemorrhage (SAH). METHODS: The authors retrospectively analyzed the medical records of 76 patients who had undergone craniotomy. The patients included 55 with aneurysmal SAH (SAH group) and 21 with unruptured aneurysms (non-SAH group) who were used as controls. Subdural fluid collection was more common in the SAH than in the non-SAH group (38% compared with 14%, p < 0.05). Although older patients appeared to be at greater risk for subdural fluid collection in both groups (p < 0.05), this condition developed even in relatively young patients with SAH. In the SAH group most subdural fluid collection was associated with ventricular dilation (81%), and a significant correlation was seen between fluid collection and the need for subsequent shunt placement (48% compared with 21%, p < 0.05). These results point to an association between hydrodynamic dysfunction and subdural fluid collection. The course of patients with subdural fluid collection varied from spontaneous resolution to normal-pressure hydrocephalus. Seven patients with persistent subdural collections underwent shunt placement (ventriculoperitoneal [VP] shunt in six and lumboperitoneal in one), which resulted in resolution of fluid collection in all seven. CONCLUSIONS: The results indicate that for most patients in the SAH group, subdural fluid collection represented "external hydrocephalus" rather than simple "subdural hygroma." Decreased absorption of cerebrospinal fluid because of SAH and surgically created tears in the arachnoid membrane communicating with the subdural space were factors in the development of external hydrocephalus. The authors believe that differentiating external hydrocephalus from subdural hygroma is extremely important, because VP shunt placement can be used to treat the former but could worsen the latter.

Absorption↗
PubMed1997

[Local immune defects--products of free oxygen radicals].

The discussion about the supporting task of four main active oxygen dependent mechanisms mediating and modulating immune signals was included in the work, along with the discussion on antioxidants influencing these mechanisms. The former include xanthine-oxidase, cyclooxygenase, lipoxygenase, aldehyde oxygenase metabolic chains. Currently, we are just beginning to realize that active oxygen and antioxidants can modulate the induction of physiological signals, and that these effects are not limited to the immune system. The effects of antioxidant treatment could represent neutralization of harmful radicals, albeit they can simply represent modulation of complex biochemical events which are essential parts of normal metabolism. Some natural antioxidants, e.g. alfa-to-copherol, ascorbic acid and beta-carotens are very good means of the primary prevention, but with acute failure of local antioxidants, they do not prevent the excessive production of proliferative inflammatory tissue. Tirilazad-mesylate has threefold beneficial influences: first as an inhibitor of the creation of oxygen radicals, second as a scavenger or quencher of free oxygen radicals, and finally in the arrangement of the defects in the phospholipid bilayer and possible receptors of macrophages, as well as T cells. The drug is suitable for active modulation of locally changed immune reactions and thus it rejects harmful proliferative inflammation in the subdural space. Until recently it has been eliminated by surgical procedure. The authors expel the thick (0.8 cm) subdural collection of the proliferative inflammatory product by tandem treatment which includes methylprednisolon+tirilazad-mesylate for three days, followed by fourteen days of methylprednisolon, which was gradually decreased in daily oral doses. This is a revolutionary change in the treatment of similar intracranial processes. (Fig. 4, Ref. 21.)

Anti-Inflammatory Agents↗
PubMed1981

[An anterior communicating artery aneurysm complicated by chronic subdural hematoma--a case report (author's transl)].

A 53-year-old housewife was admitted to the Department of Neurosurgery, Toyama Medical and Pharmaceutical University on June 6, 1980, because of disorientation, urinary incontinence and left hemiparesis. She had experienced "a fit of severe headache" many times for five years. On May 12, 1980, she experienced an abrupt, severe headache in a lavatory and was immediately brought to a nearby hospital. Her symptom was recovered gradually for a week but she experienced sudden onset of severe headache again on May 20. Subsequently, her state of consciousness gradually worsened and left sided hemiparesis arose. On admission, cerebral angiograms revealed an aneurysm of an anterior communicating artery and a subdural hematoma over the right hemisphere. On the third hospital day, radical operation was performed by bifrontal craniotomy. Neck of aneurysm was ligated and clipped successfully and dark brownish semiliquid contents of chronic subdural hematoma was evacuated. The lacerated portion of arachnoid with some distance from the aneurysm was observed and subarachnoid hemorrhage was thought to enter subdural space through this portion. Post-operative course was uneventful. Nine cases of intracranial aneurysms complicated by chronic subdural hematoma were reported previously, but an anterior communicating artery aneurysm case was not in these cases. We have some discussion about cerebral aneurysms complicated by chronic subdural hematoma, especially about the pathogenesis of chronic subdural hematoma.

Chronic Disease↗
PubMed2004

Traumatic acute subdural hygroma mimicking acute subdural hematoma.

Subdural hygroma is a frequent delayed complication of head trauma. Most hygromas are clinically 'silent' and a few cases have shown slow deterioration in the chronic stage. We report a case of subdural hygroma showing unique radiological findings and rapid deterioration. A 74-years-old female presented with a mild headache and consciousness disturbance after head injury. Computed tomography showed a midline shift as a result of two components piling up in the subdural space; the outer components showed low density, the inner components high density. Magnetic resonance imaging demonstrated that these two subdural components were subdural hygroma and subarachnoid hematoma. Simple burr hole irrigation, rather than large craniotomy, was thought to be more appropriate treatment to reduce the mass effect. Simple burr hole irrigation was performed to remove the subdural hygroma and the patient showed an excellent recovery. Careful examination of the radiological findings prevented an unnecessary procedure in this case. A possible mechanism of this phenomenon is discussed.

Acute Disease↗
PubMed1984

The sheath of the optic nerve.

The sheath of the optic nerve was studied in rhesus monkeys, humans, and rabbits. The sheath (i.e., dura mater and arachnoid mater) was normally found to be loose near the eyeball, with a much bigger space between the optic nerve and the sheath than anywhere else in its course, consequently presenting bulbous appearance just behind the eyeball. The space was narrowest in the region of the optic canal, with thick fibrous bands stretching from the dura mater to the pia mater of the optic nerve-so that the space assumed the character of a trabecular meshwork of closely knit fibers in the canal, with the subarachnoid and subdural spaces reduced to almost a capillary size in this region. Communication between the subarachnoid spaces of the cranial cavity and of the sheath was almost always seen; however, the extent of communication in the optic canal showed wide variation from one specimen to another. The significance of our findings in the interpretation of some clinical and pathological findings and processes is discussed.

Animals↗
PubMed2001

A modified technique to treat subdural hematomas: the subdural evacuating port system.

BACKGROUND: The Subdural Evacuating Port System (SEPS) is intended for drainage of subdural fluid collections such as hygromas and hematomas. Unlike other subdural fluid drainage systems, no drain is placed in the subdural space. This paper describes the technique and reports our experience thus far. METHODS: We treated 20 patients for 22 subdural hematomas. One or two ports were inserted for drainage of each subdural collection. Follow-up ranged from six to 24 months. RESULTS: Follow-up CT obtained at approximately one month postprocedure showed complete or near complete resolution of 18 of the subdural collections. Failure of the SEPS was noted in four patients and was related to plugging of the drainage system by clots secondary to the presence of fresh blood in the subdural collection. CONCLUSIONS: The Subdural Evacuating Port System (SEPS) permits the neurosurgeon to drain subacute or chronic hematomas by a method which is minimally invasive, simple and safe.

Aged↗
PubMed1993

[A rare case of middle fossa neuroepithelial cyst accompanied by chronic subdural hematoma].

We reported a rare case of middle fossa neuroepithelial cyst accompanied by chronic subdural hematoma. An eight-year-old boy was admitted to our hospital due to headache, disturbed consciousness and right hemiparesis. CT disclosed a left marginal high density in the left subdural space and remarkable midline shift. MRI showed a hematoma in the left to temporal tip extending to the chronic subdural hematoma. Radiological examinations revealed a cystic lesion with chronic subdural hematoma. An operation was performed to remove the hematoma. Intraoperatively, the hematoma in the cyst and the chronic subdural hematoma were observed. Histopathological diagnosis of the cyst wall was neuroepithelial cyst. The relationship between the neuroepithelial cyst and chronic subdural hematoma was discussed.

Brain Diseases↗
PubMed1979

Subdural hematomas: an unusual appearance on computed tomography.

It may at times be difficult to separate supra- from infratentorial and intra- from extraaxial pathology on the basis of axial transverse computed tomography (CT) scans. Coronal CT scans may be quite useful in more accurate localization of compartments. Three head injured patients with subdural hematomas were studied with axial transverse CT scans. In addition to the typical appearance of subdural hematomas, unusually shaped areas of increased attenuation were noted in the region of the tentorium cerebelli separate from the mass of the subdural collection. Coronal scans confirmed the supratentorial, extraaxial collection as an extension of the subdural hematoma into the supratentorial subdural space.

Cerebral Ventriculography↗
PubMedDate not supplied

[Brain glioma complicated by subdural hematoma].

A case is reported in which chronic subdural haematoma developed in association with a glioma of the left temporal lobe. The stroke-like onset of symptoms one month before surgical intervention, encapsulated liquid subdural haematoma, necrotic cerebral cortex over the tumour and easily bleeding peripheral parts of the tumour suggested a primary haemorrhage into the peripheral part of the tumour followed by penetration of the haematoma into the subdural space.

Astrocytoma↗
PubMedDate not supplied

Subdural hematomas and isolated transient aphasia.

Chronic subdural hematoma (CSDH) is particularly common in the older patient. Chronic subdural hematoma can present with atypical, and sometimes unusual, manifestations. It has an insidious onset and can, at times, be very difficult to diagnose. The most frequent presenting symptoms are headache, changes in mental status, and hemiparesis. Chronic subdural hematoma might also present as a transient ischemic attack. Here we report a case of CSDH that presented with intermittent aphasia and no other neurological deficit. Chronic subdural hematoma usually begins with a hemorrhage into the subdural space, which then becomes encapsulated by a membrane with abundant abnormal vessels in the outer portion of the membrane. Chronic subdural hematoma is a distinct and interesting clinical entity with diverse and insidious onset. A high index of suspicions is needed to make the early diagnosis and to start appropriate treatment to avoid morbidity and mortality.

Journal Article↗
PubMed1996

[Spontaneous intracranial hypotension syndrome].

Spontaneous intracranial hypotension is a rare but well known entity first described by the German neurosurgeon Schaltenbrand. We report the clinical and radiological findings of four patients (2 males, 2 females, mean age 55 years) presenting with this clinical entity and peculiar constant MRI findings. Intense postural headache was present in all patients together with a very low CSF pressure at lumbar tap although none of the patients had any history of recent lumbar puncture, spinal or cerebral surgery or cranio-cervical trauma. MRI revealed in all patients an intense meningeal enhancement and thickening which was most prominent on the dural side of the subdural space. The ventricular system was thin, presenting almost like slit ventricules. A downward shift of the cerebellar tonsils and hemorrhagic subdural collections were also observed in two patients. Biopsy of meninges performed in two patients showed fibrosis of the leptomeninges together with signs of old hemorrhage in one case. We postulate that histologic and radiologic changes are due to chronic subdural bleeding in relation with abnormal displacement of the nervous structures due to intracranial hypotension. The underlying cause of spontaneous intracranial hypotension is rarely established and the course of the disease is benign. Some authors have advocated to perform isotopic cysternography in search for a CSF leak, particularly in the spine, that could be surgically corrected. No such investigation has been conducted yet in our patients because the spontaneous evolution has been mostly favorable.

Cerebrovascular Disorders↗
PubMed2004

[A case of organized chronic subdural hematoma presented with transient neurologic deficits].

A 59-year-old diabetic male presented with transient motor aphasia and monoparesis of the right upper limb. Brain CT scan showed a low density area in the left subdural space with a mild midline shift. Magnetic resonance (MR) T2-weighted and fluid-attenuated inversion recovery (FLAIR) imagings revealed homogenous hyperintensity with a hypointense web-like structure in the subdural hematoma. Cervical MR angiography showed no abnormal lesion at the bifurcation of the bilateral common carotid arteries. Conventional cerebral angiography showed an avascular, crescent, space-occupying mass over the left hemisphere without an etiologic lesion of cerebral ischemia. CT perfusion imagings indicated reduced cerebral blood flow (CBF) and prolonged mean transit time (MTT) in the left middle cerebral artery territory underneath the subdural hematoma. No epileptic discharge was found in electroencephalogram. Operative findings indicated that the hematoma was encapsulated with thickened outer and inner membranes including paste-like materials, and the brain surface was intact. Postoperative CT perfusion imagings revealed normal CBF and MTT. The pathophysiological mechanism which the chronic subdural hematoma produces the transient neurological deficit is still uncertain. The mechanical pressure of the hematoma on the neighboring cerebral vessels may cause impairment of blood flow leading to cerebral ischemia and paralysis of function. Our case indicated the transient neurological deficits attributed to a decreased CBF around the subdural hematoma and a change in pressure exerted by the hematoma during changes of head position and increased blood viscosity.

Cerebrovascular Circulation↗
PubMed1982

Posterior fossa subdural hemorrhage in the newborn as a result of birth trauma.

During the past 19 years, 229 autopsies of intracranial hemmorrhages were performed at the Department of Pathology, and 23 cases of posterior fossa subdural hemorrhages were discovered (10.0%). 25 cases of posterior fossa subdural hemorrhages (2 of our own treated surgically and 23 untreated found at autopsy) are described in detail. 2 cases treated surgically responded favorably to surgical treatment. The mechanism of hemorrhage into posterior fossa subdural spaces is investigated and reconsidered following a review of the literature. The necessity for CT is emphasized for early diagnosis of posterior fossa subdural hemorrhage.

Birth Injuries↗
PubMed1994

A unifying theory for the definition and classification of hydrocephalus.

If the cerebrospinal fluid (CSF) is considered to be all the fluid (liquid), other than blood or the derivatives of its breakdown, that is normally contained within the brain, its cavities, and its spaces, this could be regarded as "brain fluid" in its most elemental form. "Pathological increases in intracranial CSF volume, independent of hydrostatic or barometric pressure", then, could be considered a definition of hydrocephalus. The observation of significant episodic variation in intracranial pressure (ICP) suggests the necessity of substituting the concept of "time-related pressure variations" for the older one of "level of pressure" in patients with defective ICP control mechanisms. It has been assumed that the subarachnoid channels are the first CSF compartment to dilate in response to the hydrocephalic process, reducing the CSF pressure and thereby establishing an equilibrium. When the equilibrium is disturbed, with progressive dilation of the subarachnoid channels, the increase in CSF pressure is transmitted to the ventricular system, resulting in its dilation (extraprenchymal hydrocephalus). Progressive ventricular dilation causes cerebral edema (intraparenchymal hydrocephalus) and obliterates the subarachnoid spaces as the hemispheres are compressed against the dura, resulting in apparent "internal hydrocephalus" in the absence of "external hydrocephalus". Thus, subarachnoid space or ventricular dilation occur as a result of intermittent increases in extraparenchymal CSF volume: the primary pressure force emanating from the subarachnoid and subdural spaces and from the intraventricular compartment. Hydrocephalus, therefore, may be present in a child who does not yet have dilated ventricles but in whom both CSF volume and pressure are increased. Thus, it becomes obvious that the term internal hydrocephalus is of little significance, since increases in intraparenchymal fluid--cerebral edema--cause the same volumetric changes as increases in intraventricular fluid volume. I suggest that hydrocephalus is a pathologic increase in intracranial CSF ("brain fluid") volume, whether intra- or extraparenchymal, independent of hydrostatic or barometric pressure. It may be classified as (1) intraparenchymal (cerebral edema) and (2) extraparenchymal, with the extraparenchymal types subclassified into subarachnoid, cisternal, and intraventricular forms.

Adult↗