TL;DR: Old age, pre-existing cerebral infarction, and persistence of subdural air after surgery were significantly correlated with poor brain re-expansion (p < 0.001), which will further improve the surgical outcome for patients with CSDH.
Abstract: Chronic subdural hematoma (CSDH) is one of the most common clinical entities in daily neurosurgical practice. The diagnosis and treatment are well established, but recurrence, complications, and factors related to these problems, especially in the elderly, are not completely understood. This study evaluated the clinical features, radiological findings, and surgical results in a large series of the patients treated at the same institution. 500 consecutive patients (359 men and 141 women) with CSDH were treated by burr hole craniostomy with closed system drainage from January 1987 through February 1999. Causes, clinical and computed tomographic findings, surgical results, re-expansion of brain after surgery, and hematoma recurrence were statistically analyzed to elucidate the potential risks of CSDH. Most patients (89.4%) had good recovery, 8.4% showed no change, and 2.2% worsened. Six patients (1.2%) died, three due to disseminated intravascular coagulation. Recurrence of hematoma was recognized in 49 patients (9.8%), at 1 to 8 weeks (3.5 +/- 1.9 weeks) after the first operation. The brain re-expansion rate at one week after operation was 45.0 +/- 21.4% in patients with hematoma recurrence and significantly lower than 55.3 +/- 19.1% in patients without recurrence (p < 0.001). Old age, pre-existing cerebral infarction, and persistence of subdural air after surgery were significantly correlated with poor brain re-expansion (p < 0.001). Twenty-seven patients (5.4%) suffered postoperative complications, of which 13 cases were acute subdural hematoma caused by incomplete hemostasis of the scalp wound and four cases were tension pneumocephalus. Careful hemostasis and complete replacement of subdural hematoma by normal saline to prevent influx of air into the subdural space will further improve the surgical outcome for patients with CSDH.
TL;DR: In this paper, a detailed neuropathological study of non-accidental head injury in children was conducted, which included immunocytochemistry for microscopic damage, and statistically significant patterns of age-related damage emerged.
Abstract: Fifty-three cases of non-accidental head injury in children were subjected to detailed neuropathological study, which included immunocytochemistry for microscopic damage. Clinical details were available for all the cases. There were 37 infants, age at head injury ranging from 20 days to 9 months, and 16 children (range 13 months to 8 years). The most common injuries were skull fractures (36% of cases), acute subdural bleeding (72%) and retinal haemorrhages (71%); the most usual cause of death was raised intracranial pressure secondary to brain swelling (82%). On microscopy, severe hypoxic brain damage was present in 77% of cases. While vascular axonal damage was found in 21 out of 53 cases, diffuse traumatic axonal injury was present in only three. Eleven additional cases, all of them infants, showed evidence of localized axonal injury to the craniocervical junction or the cervical cord. When the data were analysed by median age at head injury, statistically significant patterns of age-related damage emerged. Our study shows that infants of 2-3 months typically present with a history of apnoea or other breathing abnormalities, show axonal damage at the craniocervical junction, and tend also to have a skull fracture, a thin film of subdural haemorrhage, but lack extracranial injury. Children over 1 year are more likely to suffer severe extracranial, particularly abdominal, injuries. They tend to have larger subdural haemorrhages, and where traumatic axonal injury is present, show patterns of hemispheric white matter damage more akin to those reported in adults. Diffuse axonal injury is an uncommon sequel of inflicted head injury in children.
TL;DR: The meninges of various mammals were prepared for examination with the electronmicroscope by thin sectioning or freeze‐fracturing to determine the basis for the meningeal barrier between the blood circulating in dural vessels and the cerebrospinal fluid in the subarachnoid space.
Abstract: 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.
TL;DR: Dural haemorrhage in non‐traumatic infant deaths: does it explain the bleeding in ‘shaken baby syndrome’?
Abstract: A histological review of dura mater taken from a post-mortem series of 50 paediatric cases aged up to 5 months revealed fresh bleeding in the dura in 36/50, the bleeding ranging from small perivascular haemorrhages to extensive haemorrhage which had ruptured onto the surface of the dura Severe hypoxia had been documented clinically in 27 of the 36 cases (75%) In a similar review of three infants presenting with classical 'shaken baby syndrome', intradural haemorrhage was also found, in addition to subdural bleeding, and we believe that our findings may have relevance to the pathogenesis of some infantile subdural haemorrhage Recent work has shown that, in a proportion of infants with fatal head injury, there is little traumatic brain damage and that the significant finding is craniocervical injury, which causes respiratory abnormalities, severe global hypoxia and brain swelling, with raised intracranial pressure We propose that, in such infants, a combination of severe hypoxia, brain swelling and raised central venous pressure causes blood to leak from intracranial veins into the subdural space, and that the cause of the subdural bleeding in some cases of infant head injury is therefore not traumatic rupture of bridging veins, but a phenomenon of immaturity Hypoxia with brain swelling would also account for retinal haemorrhages, and so provide a unified hypothesis for the clinical and neuropathological findings in cases of infant head injury, without impact or considerable force being necessary
TL;DR: This procedure has resulted in marked reduction of recurrence, and membranectomy has not been required, in a group of patients with chronic subdural hematoma.