Traumatic pneumocephalus.
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This study describes the seemingly rare occurrence of bone formation within the proximal superior aspect of Meckel's cave thus forming a bony foramen for the proximal trigeminal nerve to traverse. The anatomy of Meckel's cave is reviewed and the clinical potential for nerve compression from this bony anomaly discussed.
We describe an experimental model to produce closed traumatic injuries to the spinal cord of adult rats. This model uses an inflatable balloon that is introduced in the dorsal subdural space and moved to a location rostral to the laminectomy site. The spinal cord trauma can be graded by varying either the duration of compression or the volume of saline used to inflate the balloon. The locomotor deficit of animals with various degrees of injury has been assessed at increasing delays after trauma. The parameters generating transient or definitive deficits of varying intensity were defined. Some injured animals underwent nuclear magnetic resonance imaging. Detailed histopathological studies demonstrated that the extent of the spinal lesion was significantly correlated with the physical parameters of compression and with the severity of the behavioral deficit.
In the bullfrog, the meninges surrounding the central nervous system include an arachnoid mater that contains layers of cells with abundant intermediate filaments (IFs) having unique organizational characteristics. This membrane contains an inner lamina of cells that resemble fibroblasts and an outer lamina of flattened cells that are almost filled with IFs. The IFs of the outer arachnoid are arranged in compact, arching bundles that lie parallel to the outer surface of the central nervous system. Thus, sections cut tangentially to the membrane reveal bending of filament bundles, whereas transverse sections do not. In some cells bordering the subdural space, bundles of filaments are organized into highly-ordered spiral arrays. Attachments to the numerous desmosomes and, apparently, to the nuclear envelope suggest anchoring of cytoplasmic structures by the IF system. Microtubules occur primarily near the plasma membrane and the nucleus. Numerous caveolae also are associated with the plasma membrane. The unusual abundance, organization, and cytoplasmic relations of IFs in the bullfrog arachnoid suggest that this membrane may serve as an important model for study of fundamental cytoskeletal relations and function.
The dura mater encephali of the rat is richly supplied by myelinated (A-axons) and unmyelinated (C-axons) nerve fibres. For the supratentorial part the main nerve supply stems from all three branches of the trigeminal nerve. Finally, 250 myelinated and 800 unmyelinated nerve fibres innervate one side of the supratentorial part. The vascular bed of the dura mater exhibits long postcapillary venules up to 200 micron in length with segments of endothelial fenestration. Lymphatic vessels occur within the dura mater. They leave the cranial cavity through the openings of the cribriform plate, rostral to the bulla tympani together with the transverse sinus, and the middle meningeal artery. The perineural sheath builds up a tube-like net containing the A- and C-axons. It is spacious in the parietal dura mater and dense at the sagittal sinus along its extension from rostral to caudal and at the confluence of sinuses. Terminals of both the A- and C-axons are of the unencapsulated type. Unencapsulated Ruffini-like receptors stemming from A-axons are found in the dural connective tissue at sites where superficial cerebral veins enter the sagittal sinus and at the confluence of sinuses. The terminations of single A-axons together with C-fibre bundles mix up in their final course in one Schwann cell to build up multiaxonal units or terminations (up to 15 axonal profiles). A morphological differentiation is made due to the topography of these terminations; firstly, in different segments of the vascular bed: postcapillary venule, venule, the sinus wall, lymphatic vessel wall, and secondly, within the dura mater: inner periosteal layer, collagenous fibre bundles of the meningeal layer and at the mesothelial cell layer of the subdural space.
The spatial situation of the cervical spine has been studied under endoscopic and CT-scanning conditions. The effects of ventro- and dorsoflexial movements upon the width of the epidural and subdural space have been noted, and their significance concerning the positioning of the injureds cervical spine has been discussed. The most spacegiving position of the cervical spine is a slight ventroflexion, which is therefore considered the best cervical spine position in case of space requiring alterations of the cervical spine.
Intracranial hemorrhage in neonates is often found in either the subependymal area or the subdural space. The former is observed particularly in premature infants and is attributable to damage of the germinal matrix layer. The latter usually occurs in the vicinity of the falx and tentorium cerebri of full-term neonates and is thought to be caused by birth injury. Two cases of intracerebral hemorrhage in full-term newborn babies are reported. In both the hematoma was located at the left frontal area under the coronal suture. Angiograms revealed no causative signs, such as arteriovenous malformation, aneurysm or angioma. Observations on CT scans and during surgery led to the conclusion that the hemorrhages were caused by the moulding which forced the frontal bone to slip under the parietal bone at the coronal suture and then press on the fragile cerebral vasculature of the neonates, thus causing contusion.
A man with adult T-cell leukaemia (ATL) underwent massive spinal cord necrosis caused by Aspergillus infection. Leukopenia due to anti-cancer chemotherapy resulted in pulmonary Aspergillus infection. The aspergilloma was reduced in size by anti-fungal chemotherapy, but paraplegia occurred. At autopsy, the pulmonary aspergilloma was encapsulated and showed no contiguous extension of the infection to the epidural or subdural spaces or spinal cord. However, at the T5 level of the spinal cord, there was marked necrosis with haemorrhage caused by Aspergillus infection, but without leukaemic cell infiltration of the spinal cord. Dichotomously branching Aspergillus hyphae filled the blood vessels of the T5 level of the spinal cord.
Thanks to the wider use of sonography to examine the spinal content in the neonate, normal anatomy and anomalies may be detected easily. Yet, unusual sonographic patterns are also observed. These must be differentiated from true pathologies. During a prospective study of 103 neurologically asymptomatic neonates, atypical sonographic patterns were found in 16 patients, corresponding to normal variants in 13. Nine of these 13 patients presented with a widening of the distal part of the central echo complex (one had a dilated ventriculus terminalis). Nerve roots of the cauda equina were disposed asymmetrically in three patients; the spinal cord movements were still present. In two of these babies, this distribution was associated with thin arachnoid pseudocysts. One patient presented with transitorily hyperechoic and narrow subdural spaces, probably related to neonatal dehydration. None of the 13 patients showing normal variants required any treatment. The other 3 patients (of 16) presented with equivocal entities of unknown evolution: sonographic tethered cord, fibrolipoma of the filum terminale and epidural varices. Sonography is highly accurate in evaluating the spinal cord content and aids differentiation of normal and normal variants from equivocal or pathological entities.
Arrays of platinum (faradaic) and anodized, sintered tantalum pentoxide (capacitor) electrodes were implanted bilaterally in the subdural space of the parietal cortex of the cat. Two weeks after implantation both types of electrodes were pulsed for seven hours with identical waveforms consisting of controlled-current, charge-balanced, symmetric, anodic-first pulse pairs, 400 microseconds/phase and a charge density of 80-100 microC/cm2 (microcoulombs per square cm) at 50 pps (pulses per second). One group of animals was sacrificed immediately following stimulation and a second smaller group one week after stimulation. Tissues beneath both types of pulsed electrodes were damaged, but the difference in damage for the two electrode types was not statistically significant. Tissue beneath unpulsed electrodes was normal. At the ultrastructural level, in animals killed immediately after stimulation, shrunken and hyperchromic neurons were intermixed with neurons showing early intracellular edema. Glial cells appeared essentially normal. In animals killed one week after stimulation most of the damaged neurons had recovered, but the presence of shrunken, vacuolated and degenerating neurons showed that some of the cells were damaged irreversibly. It is concluded that most of the neural damage from stimulations of the brain surface at the level used in this study derives from processes associated with passage of the stimulus current through tissue, such as neuronal hyperactivity rather than electrochemical reactions associated with current injection across the electrode-tissue interface, since such reactions occur only with the faradaic electrodes.
We describe a case of postoperative subdural dislocation (between dura and arachnoidea spinalis) of an epidural catheter. After 24 h of normal functioning of the catheter, the injection of 5 ml lidocaine caused an extensive unilateral sensory block including the cranial nerves. X-ray control excluded an epidural or intrathecal position of the catheter. A delayed dislocation of the epidural catheter into the subdural space can occur but this complication only usually becomes evident after injection of a normal dose of local anaesthetic into the catheter and can have catastrophic consequences. The safety of patients can only be guaranteed if epidural catheters are managed solely by professional anaesthesiological personnel. Anatomy, mechanisms of complications and clinical differential diagnosis are discussed.
Non-communicating hydrocephalus can cause rupture of the lateral or third ventricle, generally in the medial wall of the trigone or the posterior wall of the third ventricle, resulting in a cystic lesion known as ventricular diverticulum. In this paper, we describe a rare case of ventricular diverticulum located in the posterior horn of the lateral ventricle and expanding to bulge with a convexity reaching into the subdural space in a neonate. Aplasia cutis congenita and a bone defect were also present in the same neonate. Early surgical repair of the scalp defect and ventriculoperitoneal shunting were performed. In addition to illustrating the rare co-existence of a ventricular diverticulum at the posterior horn of the lateral ventricle and aplasia cutis congenita in a neonate, this case also offers new insights into the pathogenesis of these congenital anomalies.
The purpose of the study was to identify extracranial locations in which temperature changes in humans reflect those of intracranial temperature in a reliable and repeatable way. This was achieved by subjecting 14 non-anaesthetized patients after neurosurgery to face fanning while intracranial and extracranial temperatures were continuously measured. In all patients the cranium was closed and the group included both febrile and non-febrile as well as hyperthermic and normothermic patients. The patients' faces were fanned for 20-30 min, with a small fan at an air speed of 3.25 m s(-1). This gave intracranial temperature changes measured in the subdural space ( T(sd)) that were highly and significantly correlated ( r=0.91, P<0.05, n=14) with changes in tympanic temperatures ( T(ty)). A low, statistically insignificant correlation ( r=0.40, P>0.05, n=12) was found between T(sd) and oesophageal temperatures. In conclusion, intracranial temperature changes, induced by face fanning, were reliably reflected by the changes in T(ty).
INTRODUCTION: In patients undergoing decompressive craniectomy, the bone flap is temporarily preserved either in the subcutaneous tissue of the patient or frozen. However, there are some drawbacks related to these methods. MATERIAL AND METHODS: In 16 patients in whom the bone flap was removed for decompressive craniectomy, the bone was firstly washed in hydrogen peroxide and then placed in hermetically-sealed bags and sterilized using ethylene oxide. The bone was repositioned after an average period of 4.3 months. RESULTS: One patient sustained an infection of the surgical wound which required permanent exclusion of the bone flap. In all the others, esthetic and functional results were good after an average follow-up of 20 months. Control CT-scan of the bone flap demonstrated preservation of its structural features with fusion of the bone margins and revitalization of the flap. On MRI a subdural space was again visible. CONCLUSIONS: Sterilization of the bone flap with ethylene oxide in patients undergoing decompressive craniectomy avoids some of the drawbacks related to the techniques currently used. The easiness, low cost, good aesthetic and functional results of this procedure make it a valid alternative to other techniques for preservation of autologous bone in decompressive craniectomies.
Serial computed tomography (CT) scanning was performed on 138 patients suffering from severe head injuries (i.e., with scores of 8 or less on Glasgow Coma Scale). Standard practice called for scans to be done upon admission (within hours of the injury) and after 1, 3, and 7 days and 1 month. Subsequent CT scans depended on the patient's condition. Clinical results at the time of discharge were graded according to the Glasgow Outcome Scale. During the serial CT scan, there were new findings (not visualized on the initial CT scan but appearing on subsequent scans) in 91 of the 138 patients. These new findings were classified into seven types: (1) decreased density collection in the subdural space; (2) ventricular dilatation; (3) intracerebral hematoma; (4) intraventricular hemorrhage; (5) extracerebral hematoma; (6) edema; and (7) infarction. We defined intracerebral hematoma, intraventricular hemorrhage, extracerebral hematoma, edema, and infarction as new lesions. Of the 60 patients with new lesions, 12 had a good outcome and 48 had a poor outcome. Of 78 patients who did not have any new lesions, 60 had a good outcome and 18 had a poor outcome. A significant correlation was found between good outcome and the absence of new lesions and between bad outcome and the development of new lesions (p less than 0.001; X2 = 44.038). We conclude that serial CT scanning can help predict the outcome of patients with severe head injuries and may be very important in their examination and care.
The ability of MK-801, a non-competitive N-methyl-D-aspartate receptor antagonist, to protect neurons in the cerebral cortex from injury induced by prolonged electrical stimulation was assessed in cats. Platinum disc electrodes 8.0 mm in diameter and with a surface area of 0.5 cm2 were implanted in the subdural space over the parietal cortex. Ten days after implantation of the electrodes, all animals received continuous stimulation for 7 h using charge-balanced, cathodic-first, controlled current pulses with a charge density of 20 microC/cm2 and a charge/phase of 10 microC/phase. They received either no MK-801, or 0.33 or 5.0 mg/kg (i.v.) administered intravenously, just before the start of the stimulation. Immediately following the stimulation, the animals were perfused and the cerebral cortex examined by light microscopy at eight sites beneath the electrodes. Neuronal damage in the form of shrunken, hyperchromic neurons and perineuronal halos was present only beneath the stimulating electrodes; damage was moderate to severe in stimulated animals that had not received MK-801, slight in animals receiving 0.33 mg/kg, and none to slight in animals receiving 5.0 mg/kg. These results indicate that MK-801, in an apparently dose-dependent fashion, provides substantial but not complete protection against neuronal injury induced by prolonged electrical stimulation. Thus prolonged electrical stimulation can be added to the list of neuropathologic conditions which involve glutamate-induced excitotoxic damage via the N-methyl-D-aspartate receptor. The results also support the hypothesis of neuronal hyperactivity as a principal cause of electrically-induced injury in the central nervous system. The implications for design of protocols for functional electrical stimulation are discussed.
The mechanical accuracy of several available stereotactic instruments is extremely high as measured in tests with rigid phantoms. The author's experience with stereotactic-guided resection by craniotomy using both "frameless" and framed methods simultaneously is that neither the image accuracy nor the mechanical accuracy of the instrument is the limiting factor in the usefulness of the guidance. Rather, it appears that the errors encountered in actual use have to do with tissue position changes which occur during the procedure. The accuracy may be better for extrinsic lesions rigidly attached to the skull, but for intrinsic lesions, tissue position changes occur following the release of cerebrospinal fluid, air entry into the subdural spaces, tumor debulking, or cyst drainage. The potential error appears to be worse with hydrocephalus, intraoperative dehydration, collapse of larger cysts, and debulking of large tumors. Even with very small intrinsic tumors in young, not atrophic patients, the error may be 5 mm. The need for intraoperative update of the guidance image is obvious if greater accuracy is required. The advantages of such "imaging-interactive" stereotactic surgery have long been apparent from stereotactic biopsy procedures performed in the CT scanner where errors such as needle deflection or hemorrhage can be appreciated and corrected promptly. With intraoperative scanning it is also possible to monitor the progress of a cyst aspiration and confirm the site of a biopsy to avoid unnecessary sampling in cases where the pathology is inherently equivocal.