The influence of apolipoprotein E genotype on outcome after spontaneous subarachnoid hemorrhage: a preliminary study

OBJECTIVE: Possession of an apolipoprotein E (APOE)epsilon4 allele has been shown to be associated with a poor outcome after closed head injury and spontaneous intracerebral hemorrhage but not after ischemic stroke. This study assessed the influence of the APOE genotype on outcome in patients admitted to a neurosurgical unit with spontaneous subarachnoid hemorrhage. METHODS: A total of 100 patients with spontaneous subarachnoid hemorrhage were studied. Four patients were excluded because the diagnosis of subarachnoid hemorrhage was not confirmed. The incidence of rehemorrhage and delayed ischemia and the outcome at 6 months were determined using the Glasgow Outcome Scale. APOE genotypes were determined by polymerase chain reaction and restriction enzyme digestion. RESULTS: Allele frequencies in this patient group were 0.04 for epsilon2, 0.86 for epsilon3, and 0.1 for epsilon4. Of 96 patients, 72 had an aneurysmal hemorrhage and 1 had a hemorrhage from an arteriovenous malformation. In 14 patients, the results of angiography were negative, and in 9, no angiogram was performed. Of the 96 patients, 20 had one or more epsilon4 allele. Outcome at 6 months was no worse in patients with one or more epsilon4 allele than in those with no epsilon4 allele (odds ratio, 0.98; 95% confidence interval, 0.35-2.74). None of the 12 patients who experienced delayed ischemic deterioration had an epsilon4 allele. Of the 20 patients with an epsilon4 allele, 3 had a rehemorrhage, as compared with 6 of 76 patients without an epsilon4 allele. CONCLUSION: There was underrepresentation of the epsilon4 allele in this group when compared with previously studied cases of subarachnoid hemorrhage with a fatal outcome and with the general population. This suggests that patients with the epsilon4 allele who have a subarachnoid hemorrhage are less likely to be admitted to a neurosurgical unit. This study does not support an association between possession of an epsilon4 allele and poor outcome in patients admitted to a neurosurgical unit with spontaneous subarachnoid hemorrhage, although the wide confidence interval does not preclude a clinically relevant association between APOE genotype and outcome. The findings indicate that an association between genotype and the development of delayed ischemic complications after subarachnoid hemorrhage may be possible.     

How we die: the impact of nonneurologic organ dysfunction after severe traumatic brain injury

Although nonneurologic organ dysfunction (NNOD) has been shown to significantly affect mortality in subarachnoid hemorrhage, the contribution of NNOD to mortality after severe traumatic brain injury (TBI) has yet to be defined. We hypothesized that NNOD has a significant impact on mortality after severe TBI. The trauma registry was queried for all patients admitted between January 2004 and December 2004 who died during their initial hospitalization after severe TBI (head Abbreviated Injury Score 3 or greater). Cause of death and contributing factors to mortality were determined by an attending trauma surgeon from the medical record. The data were analyzed using both Fisher's exact and Wilcoxon rank sum. One hundred thirty-five patients met inclusion criteria. Sixty-seven per cent were males, 83 per cent were white, and the mean age was 38.5 years. Mean length of stay was 2.9 days. Fifty-four patients (40%) had isolated TBI (chest Abbreviated Injury Score = 0, abdominal Abbreviated Injury Score = 0). Of the 81 deaths attributed to a single cause, 48 (60%) patients died from nonsurvivable TBI or brain death, whereas 33 (40%) died of a nonneurologic cause. Cardiovascular and respiratory dysfunction (excluding pneumonia) contributed to mortality in 51.1 per cent and 34.1 per cent of patients, respectively. NNOD contributes to approximately two-thirds of all deaths after severe TBI. These complications occur early and are seen even among those with isolated head injuries. These findings demonstrate the impact of the extracranial manifestations of severe TBI on overall mortality and highlight potential areas for future intervention and research.     

On-the-field management of athletic head injuries

Head injuries are prevalent in collision sports. Concussions represent the relatively benign end of the spectrum of injuries. Severe closed head injuries include epidural hematomas, acute subdural hematomas, intracerebral hematomas, intraventricular hematomas, subarachnoid hemorrhages, and diffuse axonal injuries. Second impact syndrome represents a severe cerebral autoregulatory dysfunction that can lead to death in an athlete who sustains a second (often minor) closed head trauma while still symptomatic from a previous head injury. Generally, athletes who have suffered a severe closed head injury should not return to play. Exceptions include athletes asymptomatic for 1 year who return to a noncontact sport and those who recover completely from an epidural hematoma without underlying brain injury. Several guidelines for returning athletes to play have been proposed and are commonly used. The team physician has the responsibility of on-the-field evaluation and management of athletes with head injuries, as well as of advising them when it is safe to return to play.     

Echocardiographic evaluation of left ventricular wall motion before and after heart transplantation.

Forty transplanted hearts were retrospectively investigated before, immediately after, and 15 +/- 12 months after heart transplantation by two-dimensional echocardiography for the presence and course of left ventricular myocardial wall motion abnormalities. Fourteen heart donors who were brain dead because of subarachnoid hemorrhage formed group 1 (mean age, 35 years); 21 heart donors who were brain dead because of head injury formed group 2 (mean age, 29 years), and five heart donors who were brain dead because of head injury with an additional chest trauma formed group 3 (mean age, 28 years). Myocardial wall motion was examined in six different myocardial segments (inferior, septal, anterior, posterior, posterolateral, apical) and was quantitatively assessed by a modified score index system (score index 0 = normal wall motion; score index 1 = diffuse hypokinesia). Overall, 27 of the 40 heart donors showed mild to severe (9 of the 40) wall motion abnormalities, which improved shortly after heart transplantation (score index: 0.36 vs 0.18, p < 0.01), and remained improved 15 months after heart transplantation (score index: 0.15). Among the different study groups, a significant improvement occurred in the myocardial wall motion score index on a short-term and long-term basis in all the groups, except for group 2, regarding the long-term follow-up. This study concluded that brain-dead, potential heart donors often reveal mild-to-severe left ventricular wall motion abnormalities, which are readily detected and semiquantitated by two-dimensional echocardiography.(ABSTRACT TRUNCATED AT 250 WORDS)     

Reversible myocardial dysfunction after traumatic brain injury: mechanisms and implications for heart transplantation

Reversible myocardial dysfunction is known to occur in patients with cerebrovascular accidents and brain death. Several mechanisms for transient myocardial dysfunction have been proposed, including increased sympathetic activity, hormone depletion, and a reduction in coronary perfusion pressure. The relative importance of each of these mechanisms remains controversial. We report the case of a 19-year-old man who suffered traumatic brain death associated with reversible myocardial dysfunction despite elevated cardiac enzymes. Myocardial recovery occurred after correcting his hemodynamic instability and hypothermia emphasizing the importance of normalization of coronary perfusion pressure and core body temperature. The mechanisms for reversible myocardial dysfunction and their implications for heart transplantation following traumatic brain death are reviewed. A diagnostic strategy is proposed that would allow early recognition of reversible myocardial dysfunction in brain-dead patients.     

Early seizures after mild closed head injury.

The authors review the seizure incidence in 4232 adult patients with mild closed head injury who did not receive prophylactic anticonvulsant agents. One hundred patients (2.36%) experienced seizures within 1 week after head injury; 43 of these (1.02% of the series) had seizures within 24 hours after trauma. Most of the seizures (84%) that developed during the 1st week after injury were of the generalized tonic-clonic type. The incidence of generalized tonic-clonic seizures was higher than that of partial seizures with motor symptoms both within 24 hours (91% vs. 9%) and during the Day 2 to 7 period (79% vs. 21%). No definite intracranial pathological findings were detected by computerized tomography (CT) in 53% of patients with early posttraumatic seizures; six patients had intracranial hemorrhage without intracranial parenchymal damage (three with epidural hematoma and three with subarachnoid hemorrhage). The most common positive CT findings in the early posttraumatic-seizure group were intracerebral hemorrhage (24%), followed by acute subdural hematoma with intracerebral hemorrhage (17%). Intracerebral parenchymal damage could be identified on CT scans in 41 (48.8%) of 84 patients with generalized tonic-clonic seizures and five (31%) of 16 patients with partial seizures with motor symptoms. The intracerebral parenchymal damage was most commonly detected in the frontal lobe (21%) and the temporal lobe (19%). Seven patients with early posttraumatic seizures received emergency craniotomy to remove an intracranial hematoma (epidural in three, subdural and intracerebral in four) because the mass effect resulted in significant midline shift as seen on CT scans. This review suggests that early posttraumatic seizures after mild closed head injury have a high incidence (53%) in patients with normal CT scan findings. Although the possibility of surgically correctable intracranial hemorrhage is low (7%), the condition may be devastating if not treated properly.     

Delayed traumatic intracerebral hemorrhage.

Delayed traumatic intracerebral hemorrhage refers to the appearance of hemorrhage (usually within 48 hours of head trauma) in areas of the brain that were normal in appearance or nearly so on the CT scan taken shortly after injury. Neurologic deterioration is common but is not universally the rule. The frequency of delayed traumatic intracerebral hemorrhage is variable but is reported to occur in 1% to 8% of patients with severe head injury. The pathogenesis is multifactorial and may result from one or more of the following: coagulation abnormalities, necrosis of blood vessels in areas of brain injury, dysautoregulation, and release of tamponade effect with evacuation of extra-axial hematomas. Outcome is poor, and most series report a mortality of 50% or higher.     

Spontaneous intracerebral hemorrhage: epidemiology and clinical presentation

The advent of widespread CT availability has dramatically changed our understanding of the incidence and risk factors regarding intracerebral hemorrhage (ICH). In the pre-CT era, many patients with a small ICH were misclassified having had ischemic strokes and patients with massive ICH or subarachnoid hemorrhage (SAH) were often difficult to classify correctly. The fact that the precise mechanism of spontaneous ICH is often difficult to ascertain without pathologic evidence continues to hamper epidemiologic studies. This article reviews the incidence rates, natural history, epidemiology, and clinical presentations of nontraumatic ICH.     

Results of the surgical treatment of patients with brain cavernoma that manifested by intracerebral hemorrhage

Although, for a long time, they have been known as a kind of vascular lesion, cavernomas have mostly been incidental or causative autopsy finding or have subsequently been histologically confirmed after surgical interventions undertaken due to intracerebral and spinal spontaneous hematoma of various localization. The aim of this study was to establish on the basis of the outcome of the operative treatment, whether the surgical interventions were justified and to systematize indications for surgical treatment of the cerebral cavernoma that initially manifested by hemorrhage. The subject of the study was a group of 38 patients who had been operated at the Institute for Neurosurgery during a ten-year period, from 1990 until 2000. The study group consisted of 16 male and 22 female patients. All operated patients had cyst intraparenchymal lesions. In our group of surgically treated patients three had been treated urgently due to spontaneous intracerebral hematoma, and intraoperatively taken material after inspection of the cavum pointed to the fact that cavernoma had been the cause of hemorrhage. All the others, after postoperatively done MRI of the brain, in some even DSA, were completely evaluated, and histologically confirmed. Not one hemorrhaging cavernoma showed signs of subarachnoid hemorrhage, although 60% of operated patients had cortically localized lesion. Most of the operated patients, except for the three mentioned because of urgent intervention did not give massive intraparenchymal lesion that, in the clinical picture, would lead to the change of the state of consciousness. Focal neurologic deficit was a dominant clinical presentation. On the basis of the analysis of the clinically pathologic correlations and direct and longstanding operative results of the surgical treatment of cavernoma, operative treatment is indicated in all superficial lobar lesions as well as in those that are localized in the brain chambers and pineal region regardless of the type of the clinical presentation.     

Penetration of intravenous hydroxyethyl starch into the cerebrospinal fluid in patients with impaired blood-brain barrier function

Hypovolemic patients with impairment of the blood-brain barrier may receive IV hydroxyethyl starch (HES) to stabilize cardiovascular function and to increase cerebral perfusion pressure. It is not known whether HES can penetrate into the cerebrospinal fluid (CSF) under those conditions. We investigated plasma and CSF levels of HES after IV infusion in patients with suspected disturbance of the blood-brain barrier. Eight adult patients were studied who were being treated for head trauma or subarachnoid hemorrhage, with an external CSF drain in place. All patients exhibited radiographic signs of blood-brain barrier impairment diagnosed by cerebral computed tomography. After IV infusion of 500 to 1000 mL of HES 200,000/0.5, plasma HES levels were measured. Additionally, all CSF that was drained within 8 h after the HES infusion was collected, and HES concentrations were measured. All patients had detectable HES plasma concentrations (3.41 to 9.95 mg/mL). In contrast, no HES could be detected in the CSF of any patient. These data indicate that IV HES 200,000/0.5 does not penetrate into the CSF in patients with disturbed blood-brain barrier function after subarachnoid hemorrhage or head trauma. Further study is required to determine whether HES penetrates into the intracranial interstitium, despite the absence of HES in the CSF. IMPLICATIONS: Patients may receive IV hydroxyethyl starch (HES) after head trauma or subarachnoid hemorrhage. The results of the present study indicate that in patients with suspected blood-brain barrier impairment, HES does not penetrate from the plasma into the cerebrospinal fluid.     

Clinical evaluation of patients with isolated,traumatic, localized subarachnoid hemorrhage

Three hundred and fifty cases of patients with head injury were admitted to our hospital from 1998 to 2000. Among these cases, 10 cases manifested isolated, localized subarachnoid hemorrhage on the first computed tomographic image after the trauma. Traumatic subarachnoid hemorrhage was found in the ambient, suprasellar, and sylvian fissure, Bleeding was seen in the ambient cistern or suprasellar cistern at the site of the blow on the frontal or occipital area of the head. The bleeding was seen in the sylvian fissure at the site of the temporal head blow. The bleeding was washed out after one day. None of the patients had symptomatic spasms, and all of the patients had a good prognosis. The mechanism of isolated, traumatic, localized subarachnoid hemorrhage was considered as shear strain or coup and contre-coup injury.     

Does routine serial computed tomography of the head influence management of traumatic brain injury? A prospective evaluation

BACKGROUND: Computed tomography (CT) of the head is the current standard for diagnosing intracranial pathology following blunt head trauma. It is common practice to repeat the head CT to evaluate any progression of injury. Recent retrospective reviews have challenged the need for serial head CT after traumatic brain injury (TBI). This study intends to prospectively examine the value of routine serial head CT after TBI. METHODS: Consecutive adult blunt trauma patients with an abnormal head CT admitted to an urban, Level I trauma center from January 2003 to September 2003 were prospectively studied. Variables collected included: initial head CT results, indication for repeat head CT (routine versus neurologic change), number and results of repeat head CT scans, and clinical interventions following repeat head CT. RESULTS: Over the 9-month period, there were 128 patients admitted with an abnormal head CT after sustaining blunt trauma. The 16 patients who died within 24 hours and the 12 patients who went directly to craniotomy were excluded. The remaining 100 patients make up the study population. Abnormal head CT findings were subarachnoid hemorrhage (47%), intraparenchymal hemorrhage (37%), subdural hematoma (28%), contusion (14%), epidural hematoma (11%), intraventricular hemorrhage (3%), and diffuse axonal injury (2%). Overall, 32 patients (32%) had only the admission head CT, while 68 patients (68%) underwent 90 repeat CT scans. Of the repeat head CT scans, 81 (90%) were performed on a routine basis without neurologic change. The remaining 9 (10%) were performed for a change in Glasgow Coma Scale (n = 5), change in intracranial pressure (n = 1), change in Glasgow Coma Scale and intracranial pressure (n = 1), change in pupil size (n = 1), or sudden appearance of a headache (n = 1). Three patients had their care altered after repeat head CT: two underwent craniotomy and one was started on barbiturate therapy. All three patients had their repeat head CT after neurologic change (decrease in Glasgow Coma Scale in 2 and increase in intracranial pressure in 1). CONCLUSIONS: Serial head CT is common after TBI. Most repeat head CT scans are performed on a routine basis without neurologic change. Few patients with TBI have their management altered after repeat head CT, and these patients have neurologic deterioration before the repeat head CT. The use of routine serial head CT in patients without neurologic deterioration is not supported by the findings of this study.     

Acute subdural hematoma caused by mild head trauma in the aged]

We encountered 8 cases of acute subdural hematoma caused by mild head trauma in the aged. In this report, these cases were analyzed, taking into consideration clinical symptoms, CT scan, operative findings and outcome. The age ranged from 70 to 92 years (mean age of 79.7 years). 4 patients were male and 4 female. Head trauma was caused by falls in 4 patients, but in the other 4 patients the causes were unknown. Initial symptoms were headache, nausea and vomiting in 5 patients and mild disturbance of consciousness with lucid intervals in 3 patients. Seven patients had more than 100 on JCS and less than 9 on GCS on admission. Small craniotomy (HITT) was performed in 4 patients. Large craniotomy was performed in 2 patients, and decompressive craniectomy was carried out in 2 patients. The bleeding focus came from the cortical artery of the middle cerebral artery in 4 patients, cerebral contusion in 2 patients, and was unknown in 2 patients for HITT. CT scan on admission showed mixed density area of acute subdural hematoma in all of the patients, and intraventricular hemorrhage, intracerebral hemorrhage and subarachnoid hemorrhage in 3 patients. CT scan after operation revealed a new area of cerebral contusion in 3 patients, delayed traumatic intracerebral hematoma (DTICH) in 2 patients, and hypertensive intracerebral hemorrhage in 1 patient. Two patients recovered to good and fair without general complication. But the outcome in 5 patients with general complication was poor for 3 patients and fatal for 2 patients. In conclusion, large craniotomy is recommended because of bleeding from the cortical artery of the middle cerebral artery.(ABSTRACT TRUNCATED AT 250 WORDS)     

Sympathetic nervous activation following subarachnoid hemorrhage: Influence of intravenous clonidine

BACKGROUND: Subarachnoid hemorrhage is often accompanied by systemic complications and cerebral vasospasm. Elevated levels of circulating catecholamines may be involved in the pathophysiology behind these events. The alpha-2-agonist clonidine inhibits sympathetic outflow by a central mechanism. Unrestricted sympathoexcitation may be detrimental and administration of clonidine may be beneficial in these patients. METHODS: Using isotope dilution methodology, norepinephrine kinetic determinations, comprising determination of arterial norepinephrine concentration and rates of norepinephrine spillover to and removal, or clearance, from plasma, were performed on three occasions during the first week after subarachnoid hemorrhage in 25 patients. Eleven of these patients received clonidine (continuous i.v. infusion 5.8 +/- 0.7 microg x kg(-1) x 24 h(-1)) and the remainder, standard therapy. Initial results were compared with 17 healthy age-matched subjects and eight patients suffering from severe traumatic brain injury without traumatic subarachnoid hemorrhage. RESULTS: Subarachnoid hemorrhage patients exhibited markedly elevated arterial plasma norepinephrine concentrations [3.74 +/- 0.48, P < 0.001 vs. healthy subjects (1.59 +/- 0.11 nmol/L) and P < 0.05 vs. head trauma patients (1.94 +/- 0.29 nmol/L)]. The rate of clearance of norepinephrine from plasma in the subarachnoid patients was also significantly greater than that observed in the healthy subjects (2.66 +/- 0.15 vs. 2.14 +/- 0.15 L/min, P < 0.05) and the head trauma patients (2.00 +/- 0.12 L/min, P < 0.05). Compared with both control groups, on admission the rate of spillover of norepinephrine to plasma following subarachnoid hemorrhage was markedly elevated (9.11 +/- 1.12, P < 0.001). Clonidine treatment (continuous i.v. infusion 5.8 +/- 0.7 microg x kg(-1) x 24 h(-1)) did not reduce the increased rate of spillover of norepinephrine to plasma following subarachnoid hemorrhage. CONCLUSION: Sympathetic nervous activity is markedly elevated following subarachnoid bleeding. Clonidine had no effect on the rate of norepinephrine spillover to, or clearance from, plasma in these patients. Clearly, further studies are required to elucidate the mechanisms responsible for generating sympathetic nervous activation following subarachnoid hemorrhage.     

Traumatic intraventricular hemorrhage: report of twenty-six cases and consideration of the pathogenic mechanism

A series of 26 patients suffering traumatic intraventricular hemorrhage (IVH) after closed head injury is reviewed, and the pathogenic mechanism of the traumatic IVH is discussed considering the site of origin of the IVH. Computed tomographic detection of the origin of the IVH was possible in 15 patients (Group 1): 6 had frontal or temporal contusional intracerebral hemorrhage spreading into the ventricle (Subgroup A), 5 had the original hemorrhage in the caudate nucleus (Subgroup B), and 4 originally bled in the thalamus (Subgroup C). The origin of the IVH was not determined in 11 patients (Group 2): 6 had concomitant hemorrhage around the brain stem (Subgroup D), and 5 had small IVH with or without small intracerebral hemorrhage (Subgroup E). The site of impact was not uniform in Subgroup A, whereas the other four subgroups usually had frontal or occipital impact. In Subgroup A, the IVH was discovered more than several hours after trauma. In the other four subgroups, however, the IVH was detected in as short a time as 0.5 to 1.5 hours after trauma. In Subgroups B and C, the impact along the long axis of the skull and the early occurrence of hemorrhage in the basal ganglia suggest that shear injury between the perforating vessels and the basal ganglia may be the responsible mechanism. The several other possible mechanisms in Subgroups D and E are reviewed and discussed in relation to diffuse brain injury.     

Serum levels of Hsp 72 measured early after trauma correlate with survival

BACKGROUND: Experimental studies have shown that hemorrhagic shock is associated with the expression of inducible heat proteins, especially heat shock protein (Hsp) 72, in liver, brain, heart, and kidney. Moreover, induction of Hsp 72 by various stressors before the onset of shock has been associated with the attenuation of organ injury caused by hemorrhage. However, it is not known whether Hsp 72 is expressed after severe trauma in humans. The purpose of this study was therefore to determine whether Hsp 72 could be detected in the serum of patients early after severe trauma and whether serum levels of Hsp 72 might correlate with survival of trauma patients or the severity of the postinjury inflammatory response. METHODS: Clinical data were collected prospectively over a 3-year period for trauma patients mechanically ventilated for more than 2 days who met the following inclusion criteria: Injury Severity Score > or = 16, and age > 18 years. Physiologic data for quantitative assessment of organ dysfunction were collected for each patient. Hsp 72 and nitrate and nitrite levels were measured in the serum of trauma patients collected at or 12 to 48 hours after the admission to the emergency department. RESULTS: Sixty-seven patients with severe trauma were enrolled in the study. Hsp 72 was detected in the serum of all trauma patients. All patients with high initial serum levels of Hsp 72 (serum levels > 15 ng/mL) survived, whereas 29% of the patients with low Hsp 72 serum levels died from their traumatic injuries (p = 0.01). The overall mortality was 21%, occurring within 5 to 7 days. Patients who died were older (mean age, 54 +/- 15 years) than those who survived (mean age, 36 +/- 15 years) (p < 0.0.05). The cause of death was attributable to head injury in 79%, although the severity of head injury (Abbreviated Injury Scale score) was not statistically different between survivors with high serum values of Hsp 72 and patients who died. There was no correlation between the initial serum Hsp 72 values and the severity of organ dysfunction or clinical indicators of the inflammatory response. CONCLUSION: Hsp 72 can be detected in the serum of severely traumatized patients within 30 minutes after injury. Elevated initial serum levels of Hsp 72 (serum levels > 15 ng/mL) are associated with survival after severe trauma, but are not related to the incidence or severity of the postinjury inflammatory response or organ dysfunction.     

Spontaneous regression of an aneurysm at a nonbranching site of the supraclinoid internal carotid artery. Case report

The authors report on a patient who had presented with a subarachnoid hemorrhage whose bleeding source was not revealed on initial angiography, although subsequent studies disclosed a saccular aneurysm at a nonbranching site of the left internal carotid artery (ICA). The aneurysm could have been caused spontaneously or after blunt head trauma. The patient was supportively observed given the considerable risks associated with aggressive treatments. The present case represents the first involving spontaneous complete regression of an aneurysm at a nonbranching site of the supraclinoid ICA.     

Association of head trauma with cervical spine injury, spinal cord injury, or both

BACKGROUND: Links between cervical spine and/or spinal cord injuries and head trauma have not been reported in detail. METHODS: 188 patients with cervical spine and/or spinal cord injury were divided into two groups, i.e., with upper cervical and mid-lower cervical injury, and compared for head injury. RESULTS: Associated head trauma was investigated in 188 patients with cervical spine and/or spinal cord injuries; 35% had moderate or severe injuries. Brain damage was more frequently observed in patients with upper cervical injury than in those with mid to lower cervical injury. Those patients with upper cervical injury appeared to have an elevated risk of suffering skull base fractures, traumatic subarachnoid hemorrhage, and contusional hemotoma. CONCLUSIONS: Approximately one third of patients with cervical spine and/or spinal cord injuries had moderate or severe head injuries. Brain damage was more frequently associated with upper cervical injury. Those patients with upper cervical injury are at greater risk of suffering from skull base fractures and severe intracranial hematomas than those with mid to lower cervical injury.     

Acute subdural hematoma in patients who underwent aneurysm clipping--four case reports

Four patients presented with intracranial hemorrhage mainly consisting of acute subdural hematoma (ASDH), who had all undergone aneurysm clipping 2-20 years earlier. Whether the clips had slipped or new trauma had caused the bleeding was difficult to determine, since the initial computed tomography showed that the subarachnoid hemorrhage or the intracerebral hematoma developed near the clips. Angiography in three patients showed that the clips had not slipped off. Three of four ASDHs appeared in the same side as the craniotomy used for the previous aneurysm surgery. Anti-platelet agents and ventriculoperitoneal shunting had been previously used in two patients with no causal signs of trauma. The outcomes were poor in three patients and one patient died. Weakening of the extra- or intracranial structure after aneurysm surgery might have been involved together with the postoperative anti-platelet agent and shunt treatment in the etiology of the present ASDH.     

Metastatic cerebral choriocarcinoma without pelvic or pulmonary metastases

A unique case of chorionic carcinoma of the right frontal lobe of the brain with extensive subarachnoid and intracerebral hemorrhage is presented. No pelvic or pulmonary findings by physical or X-ray examination were present. The craniotomy, irradiation and chemotherapy effected a cure. A nephrectomy was necessary during the postoperative period.