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The "subdural" space: a new look at an outdated concept.

This review considers the structure of the meninges, as seen at the electron microscopic level, with particular emphasis on the dura-arachnoid junction and whether a naturally occurring space is found at this interface. The classic view has been that a so-called subdural space is located between the arachnoid and dura and that subdural hematomas or hygromas are the result of blood or cerebrospinal fluid accumulating in this (preexisting) space. The dura is composed of elongated, flattened fibroblasts and copious amounts of extracellular collagen. A specialized layer of fibroblasts, the dural border cell layer, is found at the dura-arachnoid junction and is characterized by flattened fibroblasts, no extracellular collagen, extracellular spaces, and few cell junctions. These features combine to create a layer of the inner dura that is structurally weak when compared with external portions of the dura and the internally located arachnoid. The arachnoid layer is composed of larger cells with numerous cell junctions, no extracellular space, and no extracellular collagen. The occurrence of many tight junctions in this layer also serves as a barrier to the movement of fluids and ions. Fibroblasts specialized to form the arachnoid trabeculae attach to the inner surface of the arachnoid layer, bridge the subarachnoid space, and surround vessels in the subarachnoid space as well as attach to pia on the surface of the brain. Under normal conditions, there is no evidence of a naturally occurring space being extant at the dura-arachnoid junction. A space may appear at this point subsequent to pathological/traumatic processes that result in tissue damage with a cleaving opening of the structurally weakest plane in the meninges--through the dural border cell layer. Furthermore, when a space does appear, it is not "subdural" in location but rather within a morphologically distinct cell layer.

Animals↗

Migration of an extradural catheter into the subdural space. A case report.

After repeated, successful extradural injections in a parturient, the extradural catheter migrated into the subdural space. The injection of 3% chloroprocaine 10 ml resulted in an extensive block, which extended to the cranial nerves and paralysed the respiratory muscles. The position of the catheter tip was confirmed by fluoroscopy. Subdural injection should always be suspected when tests for subarachnoid injection are negative, but an extensive block occurs gradually within 15-20 min. Respiration and circulation should be supported until the block regresses.

Adult↗

[Primary malignant lymphoma in the dura and subdural space along the superior sagittal sinus. Case report].

A 56-year-old male with a 11-month history of late-onset epilepsy was hospitalized because of status epilepticus. The physical examination and laboratory data were normal. Neurological examination revealed weakness of the right leg. Coronal computed tomography showed a mass of slightly high density in the bilateral parietal convexity, with homogeneous enhancement by contrast medium. Magnetic resonance imaging disclosed an en-plaque epidural tumor in the parietal region along the superior sagittal sinus, which was normointense on T1- and T2-weighted images. Conventional and digital subtraction angiography showed an avascular mass between the superior sagittal sinus and the inner table of the skull at the parietal region. The mass was thought to be situated in the parietal epidural space. On surgery, however, the tumor was found to be located mainly in the dura and subdural space. The histological diagnosis was malignant lymphoma of the B cell type. Ga-scintigraphy, physical examination, and bone marrow and peripheral blood examinations disclosed no systemic abnormalities. Therefore, the tumor was interpreted as a primary intracranial malignant lymphoma. Reports of primary intracranial malignant lymphoma have been increasing, but most have been located in the cerebrum. The dural-subdural location in this case is evidently rare.

Angiography↗

Migration of a subduroperitoneal shunt catheter into the subdural space--case report.

An 82-year-old male with intractable bilateral chronic subdural hematomas was treated by emplacement of bilateral subduroperitoneal shunts on the left in 1990 and on the right in 1991. Chronic subdural hematoma recurred in 1992 due to an unusual migration of a shunt catheter into the subdural space. This migration was probably due to inadequate fixation of the shunt. Shunt replacement and fixation with an anchoring wing has resulted in no further complications for 2 years.

Aged↗

Arachnoid cyst with rupture into the subdural space.

Arachnoid cysts which develop in relation to the cerebral hemispheres are usually found in the middle cranial fossa. These cysts are usually asymptomatic but can produce symptoms if there is haemorrhage into the cyst or the development of an associated subdural hematoma. Recent publications have emphasised the association of arachnoid cysts of the middle fossa with subdural haematomas. This report describes a case of an asymptomatic arachnoid cyst which ruptured into the subdural space. This event was followed by the development of symptoms despite the lack of haemorrhage.

Arachnoid Cysts↗

Tension pneumocephalus of the cranial subdural space: a case report.

A case of subdural tension pneumocephalus is presented. Computerized cranial tomography permitted rapid diagnosis including localization of the air, thus facilitating prompt treatment. Tension pneumocephalus should be considered in a patient with a cerebrospinal fluid drainage device who deteriorates after craniotomy.

Aged↗

A new method of inducing selective brain hypothermia with saline perfusion into the subdural space: effects on transient cerebral ischemia in cats.

In this study, we tested brain surface cooling as a new method of inducing selective brain hypothermia, and evaluated its effects on focal cerebral ischemia using a cat model of transient middle cerebral artery (MCA) occlusion. Cats underwent 1 h of MCA occlusion followed by 5 h of reperfusion. Brain surface cooling was induced for 4 h during and after MCA occlusion in the hypothermia group, but not in the normothermia group. Brain surface cooling was performed using saline perfusion into the subdural space. Rectal temperature, brain surface temperature, and deep brain temperature were monitored, and regional cerebral blood flow (rCBF) and somatosensory evoked potential (SEP) were serially measured. After 5 h of reperfusion, water content was also measured. Although the rectal temperature was maintained at about 37 degrees C, the brain surface temperature decreased rapidly to 33 degrees C and was maintained at that temperature. For 3 h following reperfusion, the rCBF was lower in the hypothermia group than in the normothermia group. At 4 and 5 h after reperfusion, the recovery of SEP amplitude was significantly more enhanced in the hypothermia group than in the normothermia group. In the gray matter, the water content was significantly more diminished in the hypothermia group than in the normothermia group. These results demonstrate that our method is useful for protecting the ischemic brain from a transient MCA occlusion. This method may be adapted for neurological surgery.

Animals↗

[Simultaneous cephalic migration of a ventriculoperitoneal shunt into the intraventricular and subdural spaces. A case report].

INTRODUCTION: Hydrocephaly is defined as a hemodynamic disorder in which the production, circulation or reabsorption of cerebrospinal fluid is involved. Migration, in a cephalic direction, into the subdural and intraventricular spaces of the proximal ends (shunt malfunction), is very unusual and perhaps not yet reported. It probably involves movement of the craniospinal region of the patient which leads to a follow on effect due to an underlying disorder. CLINICAL CASE: We report the case of a polytraumatized baby (non hospital birth, subarachnoid hemorrhage, porencephaly and subsequent hydrocephaly), who had had multiple shunts inserted. On her most recent admission the shunt was not working properly, as confirmed on plain radiological examination. This showed migration of the catheter, in cephalic direction, into the intraventricular and subdural space. CONCLUSIONS: In order that such migration could occur, conditioning factors would be necessary: such as detachment of the shunt at the distal end (technical fault), underlying disease (porencephaly), dynamic factors causing expulsion (abdominal peristaltic movements) dynamic translocation factor (neck movements), dynamic attraction factor (increased CSF reabsorption) and unishunt catheter (offering no resistance to passage through the trepanation orifice).

Cerebral Ventricles↗

[Accidental catheterization of the subdural space. Confirmation by radiological study].

We report two cases of accidental subdural blockade after peridural anesthesia. The blockade was detected postoperatively in both cases, two hours after start of continuous perfusion in one patient and eight hours afterwards in the other. Subdural diffusion was confirmed after injection of a radiopaque contrast medium. Subdural blockade usually manifests as an extensive neural block that is disproportionate to the amount of anesthetic injected. We discuss the need for frequent monitoring of metameric, sensory and motor levels to detect possible catheter misplacement, in addition to routine monitoring of heart rate, arterial pressure and oxygen saturation. When subdural blockade is suspected, epidural perfusion should be discontinued in order to prevent extensive sensory and motor blocks. A firm diagnosis can only be made by X-ray. A simple radiograph may adequately demonstrate subdural placement in some cases, although computed axial tomography should be performed when doubt arises.

Adult↗

[Accidental catheterization of the subdural space: a complication of continuous spinal anesthesia and continuous peridural anesthesia].

Two cases of subdural catheter placement following continuous spinal and continuous epidural anaesthesia are presented. In the first, despite an easy reflux of clear cerebrospinal fluid through the catheter, the injection of 4 ml bupivacaine 0.5 per cent with epinephrine 1:200,000 followed by 3 ml tetracaine 0.5 per cent showed a failure of spinal anesthesia. In the second, the administration through the catheter of 20 ml lidocaine 2.0 per cent CO2 plus epinephrine 1:200,000 and of ten ml bupivacaine 0.5 per cent lead to an insufficient, patchy and asymmetrical analgesia. The clinical signs observed in these two cases are compared with previous publications. The importance of an x-ray contrast study to confirm the diagnosis of subdural catheter insertion is stressed.

Adolescent↗