Does the subdural space exist?

A potential space between the dura mater and the arachnoides is thought to exist, occupied by a serous fluid and called the subdural space. Recent studies may change this classical concept, however. The dura-arachnoid complex from the epidural to the arachnoid space is formed by morphologically distinct layers: the dura mater, the subdural compartment and the arachnoid mater, which are made up of different cell types. The dura mater consists of greater and lesser laminae formed mainly of collagen fibers aligned differently. The subdural compartment is formed by a number of so-called "neurothelial cells", which are in close contact with the inner dural layers. These cells are flat and have long interlaced branches. The arachnoides are made of cells grouped in three different layers. The outer layer is the "barrier arachnoid layer". Located just inside the anterior cell plane, this layer is made of less flattened cells that form an epithelial-type tissue, with complex cell-cell junctures surrounded by collagen fibers. The middle layer is the reticular arachnoid, composed of irregularly interlaced cells alternating with collagen fibers and intercellular gaps of varying sizes. The innermost layer, the trabecular arachnoid, is in direct contact with the subarachnoid space. The cells of this layer form strands that contribute to the weblike pattern found in the subarachnoid space. Recently, special techniques for fixing and preparing samples, preserving in situ the anatomical relations between the arachnoides and the dura mater, have allowed us to examine the normal configuration of the subdural space. All samples examined revealed the presence of a cellular plane between the dura mater and the arachnoides, with no evidence of the classically described space. The zone of least resistance in the dura-arachnoid complex was the subdural compartment, which could be torn mainly along intercellular spaces, though cell rupture was also observed, affecting the cytoplasmic membranes of adjacent cells. The subdural space is opened by tearing the subdural compartment between neurothelial cells alongside the collagen fibers of the dura mater. Such a tear can be caused mechanically by injecting air or contrast media, which exert pressure on a laminar structure that tends to separate because it is weaker than neighboring ones.     

Supratentorial arachnoid cyst and associated subdural hematoma: neuroradiologic studies

CT and MR images of 8 patients with supratentorial arachnoid cyst complicated by subdural hematoma were studied and compared with those of 8 patients who developed nontraumatic subdural hematoma without arachnoid cyst. Of the 8 patients with supratentorial arachnoid cyst, CT and MR disclosed temporal bulging and/or thinning of the temporal squama in all 6 patients with middle fossa arachnoid cysts, and the thinning of the calvaria was evident in another patient with a convexity cyst. Calvarial thinning at the site corresponding to interhemispheric arachnoid cyst was clearly depicted on coronal MR images. In contrast, none of the 8 young patients with nontraumatic subdural hematoma without arachnoid cyst had abnormal calvaria. Temporal bulging and thinning of the overlying calvaria were identified as diagnostic CT and MR features of arachnoid cyst with complicating intracystic and subdural hemorrhage. Radiologists should be aware of this association and should evaluate the bony structure carefully.     

Arachnoid cyst rupture producing subdural hygroma and intracranial hypertension: case reports

OBJECTIVE: To analyze the association between arachnoid cysts and subdural hygromas. METHODS: We reviewed five cases of arachnoid cysts that ruptured, producing acute subdural hygromas. The surgical management and diagnostic methods used are assessed. RESULTS: Five male patients ranging in age from 6 to 25 years sustained the rupture of arachnoid cysts, which produced acute subdural hygromas. Four of the patients had incurred blunt head trauma. All patients presented with symptoms referable to intracranial hypertension. The pathognomonic features of a middle fossa arachnoid cyst (MFAC) were noted on the computed tomographic scans and/or magnetic resonance images of each patient. The hygroma exerted mass effect on the ipsilateral hemisphere and was noted to be under significant pressure at the time of surgical intervention in each case. Two of the five cases are unique in the literature. In one, a coexisting quadrigeminal cyst ruptured, producing a subdural hygroma ipsilateral to the MFAC and dilating the basal cisterns. In the other, the MFAC ruptured into the basal cisterns as well as into the subdural space. The MFAC in each of the remaining three patients ruptured into the subdural space alone. All patients were treated with drainage of the subdural space. In the two patients in whom the basal cisterns were involved, both the hygromas and the MFACs failed to change significantly in size. The hygromas resolved completely and the MFACs decreased in size considerably in the three patients without cisternal involvement. CONCLUSION: The rupture of an arachnoid cyst can produce a subdural hygroma and intracranial hypertension. The latter mandates emergent drainage of the subdural space. In patients in whom the basal cisterns are not dilated by cyst rupture, both the MFACs and hygromas resolve after subdural drainage.     

Quantitative kinetic analysis of blood vessels in the outer membranes of chronic subdural hematomas

Dynamic biologic modeling was used to calculate the transfer rate constant for gadolinium-diethylenetriaminepenta-acetic acid (Gd-DTPA) and capillary permeability in the outer membrane of chronic subdural hematomas and effusions. Following intravenous Gd-DTPA injection, Gd concentrations in the subdural fluid and in timed arterial blood samples were measured by ion-coupled plasma emission spectrometry in 53 chronic subdural hematomas and 18 chronic subdural effusions. The capillary surface area in outer membrane was assessed morphometrically. Transfer rate constants for subdural hematomas and subdural effusions were 12.4 +/- 1.0 and 20.6 +/- 1.7 (x 10(-4)min-1, respectively. Capillary permeabilities for subdural hematomas and subdural effusions were 16 +/- 1.2 and 19 +/- 3.7 ml.min-1(mm2/mm3)-1, respectively. The capillary surface areas for subdural hematomas and subdural effusions were 48 +/- 3 and 77 +/- 10 mm2/mm3, respectively. The high degree of infiltration of Gd into subdural effusions reflects the high capillary surface area in the outer membrane rather than greater permeability of individual capillaries. The value of transfer rate constant was correlated inversely with the duration of the chronic subdural fluid collection. Immature outer membrane has a high transfer rate constant which allows extravasation of plasma components into the subdural space, resulting in increasing volume of the subdural effusion. Delayed magnetic resonance imaging following Gd administration may be clinically useful for estimating the age of chronic subdural fluid accumulations.     

Three-dimensional and ultrastructural ICAM-1 distribution in the choroid plexus, arachnoid membrane and dural sinus of inflammatory rats induced by LPS injection in the lateral ventricles

To investigate immunological environment in the cerebrospinal fluid (CSF) system, ultrastructural and three-dimensional localization of intercellular adhesion molecule-1 (ICAM-1) was studied in the choroid plexus, arachnoid membrane and dural sinus of LPS-stimulated rats with immuno-SEM and TEM. The choroid plexus epithelial cells expressed rich ICAM-1 along the microvilli. The arachnoid trabeculae fibroblast-like cells demonstrated ICAM-1 expression on both sides facing the subarachnoid space moderately. The dural sinus endothelial cells, however, showed only few ICAM-1 expression and no specific localization. These results suggest that the choroid plexus and arachnoid membrane may play an important mutual role for leukocyte migration in the CSF system, and that the CSF system may function in immunoreaction independently of the vascular system with the aid of up-regulated ICAM-1 expression.     

Arachnoid cysts: histologic, embryologic and physiopathologic review

Arachnoid cysts form a cavity containing a cerebrospinal-like fluid, the wall of which is composed of arachnoidal cells. Other types of intracranial cysts have been described, they differ from arachnoid cysts by the histological characteristics of their wall. To analyze homogeneous series, it is thus necessary to differentiate arachnoid cysts from the other types of cysts. Several localizations of these lesions have been described: the most frequent being the temporo-sylvian area. Arachnoid cysts are considered as resulting from congenital malformations that can change during postnatal life. They can no longer be considered as resulting from cerebral atrophy. This arachnoid malformation could be the primary event or be explained by an impairment of the cerebrospinal fluid drainage generated by venous agenesis. Several mechanisms could account for the inflation of these cysts: secretion by the cells forming the cyst walls, unidirectional valve, liquid movements secondary to pulsations of the veins.     

Experimental vasospasm produced without blood cell components--hypothesis for the development of cerebral vasospasm

A canine model of cerebral vasospasm using noncellular blood material (fibrin glue) was designed to investigate the effect of cerebrospinal fluid obstruction. The arachnoid membrane covering the cerebral arteries in the basal cistern was dissected and fibrin glue was applied to the adventitial surface of the arteries in three groups of animals. In Group 1, the arachnoid membrane was extensively dissected and fibrin glue was widely applied to the cerebral arteries. In Group 2, the dissection and coating was less extensive. Group 3 was a control group in which the arachnoid membrane was dissected but fibrin glue was not applied. Cerebral angiography 1 week later clearly demonstrated vasospasm in all six dogs in Group 1 and in four of six dogs in Group 2. Vasospasm did not occur in Group 3. The dogs were sacrificed and the arteries in the basal cistern were removed. Histological investigation showed typical findings of vasospasm and inertness of fibrin glue to the tissue. Cerebral vasospasm can be induced by a noncellular material from the blood densely applied to the arterial surface suggesting that obstruction of cerebrospinal fluid circulation around the artery may be important in the development of cerebral vasospasm.     

Cerebrospinal fluid bearing channels of the pia meter

The pia mater of the human brain hemispheres has liquor canals which form a continuous network communicating with the cisterns of the brain base. The wall of the liquor canals is formed by a fibro-collagenous framework covered from two sides with the arachnoidendothelium. In the canal walls there are openings, through which the lumens of the canals communicate with the lumens of alveoli. The liquor canals are divided into the circulatory and excretory ones. The circulatory canals are disposed in the depth of the cerebral sulci, the secretory canals--on the surface of the convolutions. The liquor moves along the circulatory canals from the cisterns of the brain base onto the surface of cerebral hemispheres. Excretory canals adjoin the arachnoid membrane which is part of its wall (the "roof"). In the "roof" of the liquor canals the fibrocollagenous basis and the number of layers of the arachnoid--endothelium are reduced, the intercellular spaces between the cells of the arachnoidendothelium are dilated. Through the roofs of the liquor canals the liquor is excreted from the subarachnoid space into the subdural space. Inside the liquor canals there are arteries of the pia mater hung up to the canal walls by trabeculae (cords) of a dense connective tissue.     

Chromatographic support to remove solvent/detergent mixture utilized as viral attenuation agent

BACKGROUND: Extracerebral fluid collections in infancy are a common diagnostic problem, because by noninvasive imaging studies (including cranial ultrasonography, CT and NMR), no definite differentiation between two distinct pathological conditions can be found until today: An enlargement of the subarachnoid spaces in children with macrocephaly is a frequent observation of mostly unknown etiology but is known to be associated with a good prognosis. If surgery is necessary in these patients, ventricular shunting is required. On the other hand subdural effusions are often of traumatic origin and require frequently neurosurgical intervention (subdural shunting). Most reports on extracerebral fluid collections in infancy have not differentiated between both pathological conditions and therefore reveal confusing results. Recent studies using magnetic resonance imaging have shown that vascular flow phenomena in the arachnoid space can be used to a reliable diagnosis, whereas previous noninvasive neuroimaging attempts including high resolution computerized tomography (CT) have been useless. PATIENTS AND METHODS: We investigated a cohort of 20 patients aged 4 mths to 30 mths (mean 10.5 +/- 6.6 months) 16 with the history of macrocephaly and normal neurological development and 4 patients after head trauma and symptoms of an elevated intracranial pressure. RESULTS: In all 16 patients with the clinical diagnosis of benign subarachnoid space enlargement colour coded Doppler sonography detected archnoid vessels within the fluid collection, furthermore high resolution ultrasound demonstrated the dural border of of the arachnoidea as an echogenic membrane, an observation useful as a further sign of the subarachnoid location of the fluid collection. In the 4 patients with subdural hematoma the fluid collection showed an increased echogenity, no vascular structures and no surrounding border. CONCLUSION: Out of these observations we conclude that high resolution ultrasound and colour-Doppler sonography are able to reliably differentiate between a subdural and a subarachnoid fluid collection. An NMR investigation with its higher risks (sedation, anesthesia) focused on this target only seems therefore to be not necessary in these patients.     

Subdural or sub-arachnoid pericerebral effusions in the infant with subdural or subarachnoid localisation (author's transl)

Twenty-seven "subdural" effusions in infants were treated, according to our previously suggested method: a simple external drainage, followed ater one week by an internal peritoneal shunt, if the effusion did not dry up by this time. Daily electrophoresis of the fluid obtained by external drainage has been performed in 20 cases, either until the disappearance of the effusion or until the peritoneal shunting after 7 days. In 8 persistent and in 5 rapidly disappearing effusions, cerebro-spinal fluid was immediately present or appeared during the first week, simultaneously with a lowering of the total protein content. In the other 7 rapidly disappearing effusions, the protein content remained high and a conspicuous plasmatic transsudation was disclosed; the possibility that cerebro-spinal fluid could be present even in some of those last cases is discussed. The fact that some effusions display, from the onset, the characteristics of cerebro-spinal fluid, leads to the question of their subarachnoid rather than subdural localisation. For this reason, we prefer to use the less committed denomination of pericerebral effusions, in which we may distinguish subdural effusions, with or without cerebro-spinal fluid, and subarachnoid effusions. Nevertheless, it is not always easy to establish the pathogenic character of an effusion revealed by CT-scan. Pressure measurements by fontanometry appear to be a useful examination for that purpose.     

Dental health amongst 11-15-year-old children in Sevagram, Maharashtra

Although most subdural hematomas are considered to be venous in origin, they may also be of arterial origin. When subdural bleeding is due to the rupture of an intracranial aneurysm, most commonly at the middle cerebral or internal carotid arteries, the amount of subdural blood is usually small and of no clinical importance. We describe two patients with subdural hematomas secondary to rupture of an intracranial aneurysm, who needed prompt surgical treatment. The first patient had a left internal carotid artery aneurysm at the origin of the ophthalmic artery. In the second patient the aneurysm was at the anterior communicating artery and rebled into the subdural space directly through a right intraparenchymatous frontobasal hematoma. The most probable mechanism of subdural bleeding in our two patients was the existence of adhesions between the aneurysm and the arachnoid due to previous minor hemorrhages. The indication of cerebral angiography in a patient with subdural hematoma is based mainly upon the existence of meningeal signs, the presence of blood in more than one intracranial compartment or the rapid progression of bleeding.     

Paramesencephalic arachnoid cysts

The term "paramesencephalic" is proposed to describe the location of a general class of arachnoid cysts observed in four patients. These cysts, which appear to arise within the subarachnoid space, are characterized by a lack of communication with the ventricular system. Usually, the arachnoid tissue is normal, and the cyst fluid resembles cerebrospinal fluid both macroscopically and microscopically. Hydrocephalus is variably accompanied by localizing signs. Problems may be encountered in the diagnosis of suprasellar (case 4), parapineal (case 3), incisural (case 1), and interpeduncular (cases 2 and 4) arachnoid cysts. Early surgical exploration is strongly recommended.     

Social anxiety in children with anxiety disorders: relation with social and emotional functioning

BACKGROUND: Oxygen radicals have been implicated as important mediators in the early pathogenesis of acute pancreatitis, but the mechanism by which they produce pancreatic tissue injury remains unclear. We have, therefore, investigated the effects of oxygen radicals on isolated rat pancreatic acinar cells as to the ultrastructure, cytosolic Ca2+ concentration and energy metabolism. METHODS: Acinar cells were exposed to an oxygen radical-generating system consisting of xanthine oxidase, hypoxanthine and chelated iron ions. Cell injury was assessed by LDH release and electron microscopy. Cytosolic Ca2+ levels and mitochondrial membrane potential were determined by flow cytometry; adenine nucleotide concentrations by HPLC. Mitochondrial dehydrogenase activity was measured by spectrophotometric assay. RESULTS: Oxygen radicals damaged the plasma membrane as shown by a 6-fold LDH increase in the incubation medium within 180 min. At the ultrastructural level, mitochondria were the most susceptible to oxidative stress. In correlation to the pronounced mitochondrial damage, the mitochondrial dehydrogenase activity declined by 70%, whereas the mitochondrial membrane potential was enhanced by 27% after 120 min. Together this may cause the 85% decrease in the ATP concentration and the corresponding increase in ADP/AMP observed in parallel. In addition, an immediate 26% increase in cytosolic Ca2+ was found, a change which could be inhibited by BAPTA, reducing cellular damage. CONCLUSION: Cytosolic Ca2+ synergizes with oxygen radicals causing alterations of the ultrastructure and energy metabolism of acinar cells which might contribute to the cellular changes found in early stages of acute pancreatitis.     

Unco-parahippocampectomy for direct surgical treatment of downward transtentorial herniation

Downward transtentorial herniation is a major cause of death and disability caused by acute supratentorial mass lesions. Thirteen patients, 7 men and 6 women aged from 23 to 75 years old, with progressive transtentorial herniation caused by cerebral contusion with acute subdural haematoma, acute brain swelling after aneurysmal subarachnoid haemorrhage, or massive cerebral infarction were treated by direct surgery using selective removal of the uncus and parahippocampal gyrus (unco-parahippocampectomy). All patients showed progressive deterioration of transtentorial herniation (late third nerve stage or midbrain stage) with unilateral pupillary dilation and absent light reflex. Preoperative Glasgow Coma Scale scores ranged from 4 to 8. Unco-parahippocampectomy was performed via the middle temporal gyrus under the operating microscope. The oculomotor nerve, posterior cerebral artery, and midbrain were directly decompressed. Incision of the arachnoid membrane in the tentorial incisura allowed free communication of the cerebrospinal fluid between the supra- and finfra-cranial fossae to reduce the pressure gradient. Two of the 13 patients died (15%). Two of the 11 survivors (18%) were functionally independent and 1 (9%) required minimal assistance but was independent at home. This series suggests the lifesaving nature of unco-parahippocampectomy in patients with deteriorating clinical condition because of transtentorial herniation.     

CT and MR in infants with pericerebral collections and macrocephaly: benign enlargement of the subarachnoid spaces versus subdural collections

PURPOSE: To compare CT and MR in the differentiation of benign enlargement of the subarachnoid spaces and subdural collections in infants with macrocephaly. METHODS: MR was performed in 19 infants with macrocephaly, showing bifrontal enlargement of the subarachnoid spaces on CT. RESULTS: In 11 patients, a single fluid layer could be distinguished on MR of the pericerebral collections, suggesting benign enlargement of the subarachnoid spaces. In eight patients, two separate layers were clearly differentiated, an outer layer that was hyperintense on all sequences and an inner layer with the same intensity as the cerebrospinal fluid. This indicated the presence of subdural collections. These collections were mainly frontal in six and extended over the entire hemisphere in two patients. On CT, these separate lesions were seen only in three patients and missed in three others. In two final patients, CT findings were equivocal with evidence of membrane formation within the hypodense collections. In seven patients with a subdural collection, subdural-external drainage was performed. In three patients, the collection was hemorrhagic. The protein content of the fluid showed a mean of 1381.7 +/- 785.6 mg/dL. The MR and surgical findings of a subdural collection correlated with the absence of a family history of macrocrania, an age under 5 months, and acute clinical signs of vomiting, somnolence, and hypotonia. CONCLUSION: MR appears essential in the differential diagnosis between benign enlargement of the subarachnoid spaces and subdural collections in infants.     

A resolving sign of acute subdural hematoma: from report of two cases

A 7-year-old-boy (Case 1) and a 60-year-old-man (Case 2) presented with rare spontaneous resolution of acute subdural hematoma (ASDH). They were admitted with consciousness disturbance, drowsy in Case 1 and sleepy in Case 2. Initial CT showed ASDH associated with a low density band between the hematoma and the inner wall of the skull base, combined with right parietal contusion in Case 2. Repeat CT showed that the hematoma had resolved spontaneously after a few hours, and the patients regained clear consciousness next day in Case 1 within a few days in Case 2 without surgical treatment. The mechanism of spontaneous resolution of ASDH was thought to involve pulsatile flow of cerebrospinal fluid (CSF) through the tear in the arachnoid membrane, resulting in redistribution and dispersal of the hematoma, and retrograde flow into the subarachnoid space. The characteristic feature of the CT findings, the low density band between the hematoma and the inner wall of the skull bone, probably shows this process. Spontaneous resolution of ASDH requires that the brain compensatory function maintains the normal outflow of CSF, and controls the intracranial pressure by CSF buffering, blood outflow via the venous system, and brain elasticity. The low density band may be a useful finding to distinguish cases with good and bad prognosis.     

A case of idiopathic spinal cord herniation

The authors experienced a case of idiopathic spinal cord herniation with duplicated dura mater. A 63-year-old woman presented right dominant slowly progressive spastic paraplegia and dissociated sensory disturbance. Magnetic resonance imaging (MRI) demonstrated an enlarged dorsal arachnoid space associated with an apparently focally narrowed thoracic cord. The cord was kinked towards the anterior and closely applied to vertebral body at the level of Th3-4. Computed tomographic myelography (CTM) revealed homogeneous filling at dorsal arachnoid space immediately after injection and no defects. At operation multilocular arachnoid cyst and duplicated dura mater was respectively observed dorsally, and ventrally. From defected area of the inner layer, a ventral part of the spinal cord was incarcerated between the two dural layers. After rejection of arachnoid cyst and inner layer was performed, the patient recovered neurologically. Idiopathic spinal cord herniation is a rare disease that shows slowly progressive myelopathy at middle age. The herniations were observed at ventral thoracic cord in all reported cases. The mechanism of this disease is still uncertain. But at least three successive factors seem to be necessary for formation of herniation, 1) abnormal structure of the dura mater such as defect, diverticulum and duplication; 2) adhesion between the cord and the destructive dura mater, and 3) continuous cerebrospinal fluid (CSF) pressure pushing the cord outward from subdural space. In the thoracic spine, mobility is limited compared with the cervical and lumbar spine, and because of physiological curvature the cord situates rather ventrally. For these reasons the incidence of adhesion might be higher at ventral thoracic spine. Although neuroradiological imagings especially MRI and CTM were useful, operative findings were necessary for definitive diagnosis in many reported cases. Considering the effectiveness of surgical treatment, study of the ventral side of the cord should be important to avoid misdiagnosis.     

Effect of vagotomy on the ultrastructural organization of the enterochromaffin cells of the rat duodenal mucosa

Detailed investigation of the ultrastructure of the enterochromaffine cells of the duodenal mucous membrane was conducted by electron microscopy. These cells were studied 7, 14, 28, and 56 days after bilateral subphrenic vagotomy. Vagotomy resulted in the alteration of the ultrastructural orgainzation of the enterochromaffine cells. These changes were due to disturbances of 5-hydroxytryptamine (serotonine) secretion. The changes in the ultrastructure of the enterochromaffine cells were most expressed 7 and 56 days after the operation. Temporary and relative normalization of the ultrastructure was observed in 28 days.     

Cytotoxic monocytes in the blood of HIV type 1-infected subjects destroy targeted T cells in a CD95-dependent fashion

HIV-1 infection changes the functional balance of macrophages in the body; it inhibits the development of macrophages capable of costimulating T cell responses and it favors the development of macrophages that kill T cells with which they form cellular conjugates. Cytotoxic macrophages destroy CD4 T cells, which they target through CD4-reactive immune-complexed HIV-1 envelope molecules on a large scale. They also destroy T cells that they target through presented antigen or mitogen. We show here that cytotoxic macrophages destroy their cellular targets at least partially in a CD95-dependent process in which T cells first modulate expression of most of their membrane receptors and subsequently die.     

Ultrastructure of collagen fibers in the outer membrane of recurrent chronic subdural hematoma

The three-dimensional structure of the collagen fibers in the outer membrane of recurrent chronic subdural hematoma was studied by scanning electron microscopy (SEM). Specimens obtained at surgery were treated with NaOH at room temperature to digest away all cellular components and expose the collagen fibers. SEM observation of the dural side of the outer membrane showed the collagen fibers were woven into a compact feltwork with a dense arrangement. The fiber bundles had a honeycomb structure framed by the collagen fibers. Observation of the hematoma side found the collagen bundles had a sparse wavy appearance. The arrangement of the collagen fibers on the dural side is different from that on the hematoma side. The thick outer membrane may be formed by granulation resulting from inflammatory reaction. Collagen fibrillar networks are not fragile, and may reinforce the outer membrane of the recurrent hematoma.