The effect of haematoma, brain injury, and secondary insult on brain swelling in traumatic acute subdural haemorrhage.

OBJECTIVE: The high mortality of acute subdural haematoma (ASDH) is largely explained by its frequent association with primary brain damage consisting of contusion and brain swelling. However, the nature and causes of brain swelling after traumatic brain injury are multifactorial and poorly understood. The purpose of this study was to investigate the pathophysiology of brain swelling associated with ASDH in traumatic brain injury. METHODS: We examined whether the thickness of the haematoma, parenchymal injury, or presence of a secondary insult had an effect on traumatic brain swelling. The variables that might affect the pathophysiology of ASDH were examined, including: (1) age and mechanism of injury, (2) neurological findings, (3) secondary insult and extracranial injuries, (4) pre-operative computed tomography (CT) scan results, and (5) outcome. RESULTS: A total of 212 patients were included in this study. On CT scan, 159 patients (75.0%) did not have brain swelling, 29 (13.7%) had hemispheric brain swelling, and 24 (11.3%) had diffuse brain swelling. Brain swelling associated with ASDH is caused by secondary insult in addition to parenchymal injury. In the present study, the outcome of ASDH associated with brain swelling was poor, even when treated with early surgical evacuation; the mortality rate of such patients was over 75%. CONCLUSIONS: Given our findings, it is possible that the poor outcome of ASDH patients depends not only on the characteristics of the haematoma itself, but also on the presence of additional cerebral parenchymal injury and secondary insult.

Diffuse brain injury complicated by acute subdural hematoma and secondary insults in the rodents: the effect of surgical evacuation.

Head Trauma associated with acute sudural hematoma (SDH) and complicated by secondary insult is a grave clinical combination with complex pathophysiology. The aim of this study was to develop a clinically relevant injury model, which can be used to study the interaction between injury mechanisms. We present a novel model of SDH combined with diffuse brain injury (DBI) and a hypoxic secondary insult, and investigate the effects of surgical evacuation. Adult Sprague-Dawley rats were given a 300 microliters SDH and 20 minute-hypoxia following Impact Acceleration DBI. Hematoma was evacuated at one hour post-injury. Physiological parameters were measured for 5 hours, together with assessment of brain water content. Secondary insult after traumatic SDH was associated with significant brain swelling and stimulated refractory rise in ICP. In traumatic SDH complicated by secondary insult, brain swelling is exacerbated by surgical evacuation.

Diffuse brain injury complicated by acute subdural hematoma in the rodents: the effect of early or delayed surgical evacuation.

Of all the possible clinical factors affecting the outcome of patients suffering acute subdural hematomas (SDH), timing of surgical evacuation is certainly the most debated. The purpose of this study was to develop an experimental model able to reproduce the clinical behavior of post-traumatic SDH as observed in head injured patients. We present a novel model of SDH combined with diffuse brain injury (DBI), and investigate the effects of early and delayed surgical evacuation. Following Impact Acceleration DBI, adult Sprague-Dawley rats were given a 400 microliters SDH. Hematoma was then evacuated at one (rapid evacuation) or four hours (delayed evacuation) post-injury. Physiological parameters were measured for 5 hours, followed by the assessment of brain water content. In this experimental model, there is strong evidence that trauma acts synergistically with SDH enhancing brain edema formation and increasing ICP. In absence of secondary insult, rapid evacuation of traumatic SDH limits exposure to high ICP, reduces brain edema and is beneficial.

Application of chemical shift imaging for measurement of NAA in head injured patients.

Neurochemical damage following brain injury can be assessed non-invasively by measurement of N-Acetyl-Aspartate (NAA) using Proton Magnetic Resonance Spectroscopy (1HMRS). This report documents results of applying Chemical Shift Imaging (CSI) postprocessing for measuring NAA in traumatically injured brain. Following stabilization, severely head-injured patients (GCS 8 or less) were transported to the MRI suite. Semi-quantitative measurement of NAA, creatine (Cr/PCr) and choline (Cho) were obtained from single voxels (8 cm3) and CSI for acquisition of smaller voxels (2 cm3) throughout areas of the brain. Studies were completed with no complication. In focal injury, SVS positioned at the site of lesion demonstrated reduced NAA, compared to contralateral hemisphere. In diffuse injury, CSI demonstrated uniform reduction of NAA throughout the brain. NAA/Cho showed normal levels within 24 hours of injury averaging 2.4 and decreased over the next 10 days reaching a plateau of 0.75. At 30 days, NAA showed no recovery in poor outcome patients. In patients with good outcome, NAA initially low recovered near baseline levels. CSI provides a comprehensive neurochemical assessment of neuronal damage. NAA decreases and remains low in patients with poor outcome. NAA recovers in patients with favorable outcome, suggesting marginal metabolic impairment and possible re-synthesis of the NAA pool.

[A case of spontaneous rupture of a suprasellar cystic mass].

The author reported a case of a spontaneous rupture of a suprasellar cystic tumor. A 67-year-old man complained of bitemporal homonymous hemianopsia. His visual acuity was 0.02 on the right side and 0.04 on the left side. Skull XP revealed no abnormal findings, but brain CT scan showed a cystic mass without calcification in the suprasellar region. Brain MRI at the same lesion site depicted a low-intensity mass on T1-weighted image without gadolinium enhancement, and a high-intensity mass on T2-weighted image. The patient was treated conservatively because of complications such as diabetes mellitus, cerebral infarction and old myocardiac infarction. MRI taken 5 years after the initial MRI revealed disappearance of the suprasellar cystic mass. However, the patient's neurological findings, including visual signs, revealed no deterioration. His physical and radiological findings had remained uneventful. In this report, we reviewed the literatures about spontaneous rupture of suprasellar cystic tumors. It was considered that in this case, according to the neurological, radiological and CSF findings, the suprasellar cystic mass might be a Rathke's cleft cyst or arachnoid cyst.

[The relationship between delayed traumatic intracerebral hematoma and coagulopathy in patients diagnosed with a traumatic subarachnoid hemorrhage].

It has long been recognized that a traumatic insult to brain tissue may result in substantive coagulation abnormalities. The present study was carried out in an attempt to find out the association of coagulopathy and the development of delayed traumatic intracerebral hematoma (DTICH) in patients diagnosed with a traumatic subarachnoid hemorrhage (TSAH). Sixty-three patients were diagnosed as having TSAH from the initial CT scans obtained within 2 hours after trauma. On admission, peripheral blood samples for coagulation studies were taken within 6 hours after injury. All patients had subsequent CT scans performed within 24 hours of admission. Thirty (47.6%) of 63 patients exhibited radiological evidence of DTICH on their subsequent CT scans. There was a significant correlation between the increased value of serum fibrinogen degradation product (FDP > 40 micrograms/ml) and the development of DTICH. We observed that the origin of the hematoma might be caused by those radiographically unidentifiable parenchymal lesions often found with TSAH on the initial CT scan. We conclude that a clotting study at the time of admission is of value in predicting the occurrence of DTICH associated with TSAH.

The synergistic effect of acute subdural hematoma combined with diffuse traumatic brain injury on brain edema.

It is well-documented that acute subdural hematoma (ASDH) following diffuse traumatic brain injury (dTBI) contributes to severe disability and high mortality. The objective of this study was to characterize edema formation in a model of ASDH and ASDH following dTBI. Eighteen Sprague-Dawley rats were separated into three groups: Sham operated (n = 6), ASDH (n = 6), ASDH following dTBI (n = 6). Diffuse TBI was produced via the Impact-Acceleration Model [10]. ASDH was induced in the left hemisphere using the well-described method [11]. Total tissue water content was determined 4 hours after TBI utilizing wet-weight/dry-weight assessment. Our results show that ASDH causes a significant increase in tissue water content in the left hemisphere (79.2 +/- 0.7%) compared with the contralateral hemisphere (78.5 +/- 0.5%, p = 0.009). Animals exposed to ASDH following dTBI had significantly greater edema formation than those with ASDH (right: 80.9 +/- 0.4%, left: 80.5 +/- 0.7, p = 0.008). There was no significant difference between the left and right hemisphere. We conclude that edema formation in ASDH is worsened by the combination of dTBI and ASDH. Furthermore a diffuse and focal injury in combination retain the features of the diffuse injury, but with increased severity. Further studies are required to elucidate the synergistic mechanisms involved in these pathological processes.

[A ruptured aneurysm of the anterior and posterior inferior cerebellar artery: a case report].

We report a case of an anterior and posterior-inferior cerebellar artery (AICA-PICA) aneurysm. The patient was a 62-year-old woman who suffered from sudden onset of severe headache and nuchalgia. Computed tomography (CT) scan revealed subarachnoid hemorrhage in the ambient cistern and blood clots in the 3rd and 4th ventricles. Vertebral angiography demonstrated an aneurysm located at the distal segment of the left AICA-PICA. Three demensional CT scan was very useful for the decision concerning surgical strategy. The patient underwent bilateral occipital craniectomy and the aneurysm was clipped successfully via the midline suboccipital approach. Her postoperative course was uneventful. Postoperative angiography showed successful clipping of the aneurysm. Distal AICA-PICA aneurysm is a very rare disease and only one case has been reported in the literature. The clinical features, CT findings, and surgical approach of distal AICA-PICA aneurysms are briefly discussed while reviewing the literature.

[Crushing head injuries: report of six cases].

We report 6 cases of crushing head injuries produced by static loading forces, which are defined as those that occur over a longer period of time (> 200 ms) and are applied over a large area. Patients ranged in age from 4 to 53 years. There were five male and one female. The causes of injuries in 5 cases were industrial accidents. In one case, the patient's head was run over by a motor vehicle in a parking lot. Glasgow Coma Scale scores ranged from 3 to 12. Three patients had cerebrospinal fluid otorrhea and rhinorrhea. Computed tomograms showed multiple calvarial and basilar cranial fractures, as well as intracranial hematomas, pneumocephalus and diffuse cerebral swelling. In 4 cases, fatal compressive brain damage occurred. Compression of the skull beyond a certain degree causes damages to the brain itself and the great vessels through cerebral compression. We consider that this damage may contribute to mortality in such injuries.

Traumatic middle cerebral artery occlusion from boxing.

A case of a traumatic middle cerebral artery occlusion resulting from a boxing injury is presented. A 22-year-old man, an amateur boxer, was admitted because of difficulty in speaking, that had appeared a day after a sparring fight. A computed tomographic scan showed low-density areas in the left globus pallidus and corona radiata. A carotid angiogram indicated complete occlusion of the left middle cerebral artery at its origin and an irregularity and narrowing of the left internal carotid artery in its supraclinoid portion. The patient was discharged 4 weeks after the admission with some persistent expressive dysphasia that diminished during the next month. The clinical features and mechanisms of the traumatic middle cerebral artery occlusion are discussed.

Infected subdural hematoma.

A case is presented in which Escherichia coli seeded a pre-existing chronic subdural hematoma. A 77-year-old woman was admitted to our hospital because of lethargy, left hemiparesis and fever. Drainage through a burr hole was performed with the diagnosis of bilateral chronic subdural hematoma. Operative findings revealed the infected subdural hematoma on the right side and non-infected subdural hematoma on the left side. Cultures of the subdural hematoma grew Escherichia coli. In view of the pyuria, the etiology of the infected subdural hematoma was postulated to be a urinary tract infection. In the majority of 14 reported cases, the causative organisms were Escherichia coli, Salmonella, and the systemic sources of infection included the urinary tract, gastrointestinal disease, or were unknown. The possibility of infected subdural hematoma should be considered when computed tomography findings suggestive of chronic subdural hematoma exist in a patient with signs of infection.

[A case of hearing loss caused by overdrainage of cerebrospinal fluid after ventriculo-peritoneal shunting procedure].

We describe a case of intracranial hypotension syndrome due to overdrainage of cerebrospinal fluid presented with hearing loss after ventriculoperitoneal shunting procedure. A 69-year-old man suffering from subarachnoid hemorrhage presented with an angiogram showing two aneurysms, one of the right internal carotid and one of the middle cerebral artery. Neck clipping was performed. One month later, he developed normal pressure hydrocephalus (NPH), which was treated by ventriculoperitoneal (NPH), which was treated by ventriculoperitoneal shunting procedure using low pressure Pudenz system. Trias of NPH were improved by insertion of shunt system. However, he complained of hearing loss which was worsened by upright position and improved by lying down. Such kinds of phenomenon were demonstrated by audiogram showing that the transitory decrease of hearing and electrocochleography showing the elongation of N1 latency at upright position. These data suggested that his hearing loss was caused by inner ear or auditory nerve lesion. After the shunt system was replaced into the antisiphon device, his hearing disturbance improved. Axial computed tomography of bone window at the level of orbitomeatal line demonstrated widely perilymphatic duct on both sides. This finding suggested that the fluctuation of intracranial pressure was easily transmitted into the cochlear through the widened perilymphatic duct, resulting in hearing disturbance.

[Acute subdural hematoma caused by professional boxing].

Knockout in boxing entails deliberate production of the state of unconsciousness. Acute subdural hematoma which is the most common acute brain injury in boxing, accounts for 75% of all acute brain injuries and is the leading cause of boxing fatalities. The aim of this study is to evaluate acute subdural hematoma caused by professional boxing by analyzing the content of bouts, the level of consciousness on admission, CT scan, therapy and outcome 3 months after admission. Fifteen boxers who had suffered from acute subdural hematoma were classified into three groups according to the pattern of loss of consciousness. Transient unconsciousness type (Transient type): boxers who had returned to alertness within an hour from the time of injury. Lucid interval type: neurological deterioration appeared with a lucid interval from ten minutes to an hour after knockout. Deterioration of consciousness type (Deterioration type): A state of unconsciousness appeared and worsened from a few minutes after knockout. Analyzing the number of rounds in bouts indicated that the hematoma occurred most frequently in bouts of 10 rounds. All of our subjects presented subdural hematomas without cerebral contusions on CT scan. With regard to the location of the hematomas, 9 hematomas involved the left side, 3 the right, 2 the suboccipit and 1 the interhemisphere. Transient type was found in 7 patients who had GCS scores of 14, 15 on admission. Since CT scan revealed thin subdural hematoma with or without mild midline shift, conservative therapy was carried out in all patients. All patients had a good recovery. Five patients of lucid interval type with an admission GCS score of 4, 6 and 7 demonstrated thicker hematoma compared to that presented by the transient type with significant midline shift on CT scan. All patients required surgery. Outcome of this type was good recovery (n = 2), moderate disability (n = 1), persistent vegetative state (n = 1), death (n = 1). Three patients of deterioration type had GCS scores of 5, 6. Because of subdural hematoma with remarkable midline shift on CT scan, all patients underwent surgery. Outcome was good recovery (n = 1), moderate disability (n = 1), persistent vegetative state (n = 1). Overall outcome was good recovery 66.7%, moderate disability 13.3%, persistent vegetative state 13.3%, death 6.7%. Furthermore, 8 patients who underwent surgery with a GCS score of less than 8 exhibited good recovery 37.5%, moderate disability 25%, persistent vegetative state 25%, death 12.5%. CT scan of lucid interval and deterioration type showed a tendency to show thick subdural hematoma and remarkable midline shift compared to transient type. Outcomes of lucid interval and deterioration type were worse than those of transient type. This result suggests that the influence of repeated head injury and diffuse brain injury might make a difference between these groups. Repeated head injury means that further impacts repeatedly damaged the injured brain after bleeding in the bouts. Overall outcome was better than that published in previous reports and also than that observed in other head injuries, for example, traffic accident and fall. The reasons for this could be that the patients were younger, that there was immediate surgical treatment, and that brain injury without cerebral contusion had contributed to better outcome. Finally, the best medical management intervention seems to be to diagnose and treat the lesions as early as possible after occurrence of subdural hematoma.

[A case of unilateral atypical moyamoya disease of adult onset with stenosis of the basilar artery].

A 29-year-old, 39-week-pregnant female who had headache and nausea was admitted to our hospital. She bore a baby son by natural delivery after several hours. After labor, her headache was continuous. Brain CT scan demonstrated intracerebral and intraventricular hemorrhage. After conservative treatment for two weeks, her only neurological deficiency was visual field defect. Angiography demonstrated that her left internal carotid artery had partial stenosis at the C2 portion. Her right internal carotid artery had stenosis at the C2 portion. Her right middle cerebral artery was occluded at the M1 portion, and abnormal vascular networks had developed in the ganglionic region. Stenosis was also found in the basilar artery. We diagnosed her as being a case of adult-onset, unilateral, atypical Moyamoya disease with basilar artery stenosis. As our case was of adult-onset, and as she showed no ischemic signs, we did not think that reconstructive surgery was indicated. About the posterior circulation of Moyamoya or atypical Moyamoya disease, it was reported that in cases of juvenile onset the vertebral, basilar or posterior cerebral artery was sometimes stenosed or occluded, but, in adult-onset cases, stenosis or occlusion of the posterior cerebral artery would be an abnormality. Our case is a very rare example of unilateral atypical Moyamoya disease of adult onset with basilar artery stenosis.