Traumatic aneurysm of the supraclinoid internal carotid artery-case report-.

A 23-year-old male was admitted after a motor vehicle accident with acute epidural hematoma, diffuse subarachnoid hemorrhage (SAH) in the basal cistern, and fractures at the anterior cranial base. Angiography revealed an aneurysm of the right supraclinoid internal carotid artery (ICA). His consciousness suddenly worsened on the 23rd day. Expansion of the SAH in the basal cistern and two hump aneurysms were detected. He underwent endovascular embolization of these aneurysms and the right ICA with Guglielmi detachable coil. Traumatic aneurysms are difficult to diagnose in the early period after injury and are associated with a high mortality. Endovascular treatments for traumatic aneurysms have lower mortality rate, and can be performed under local anesthesia.

Therapeutic hypothermia for severely head-injured patients with acute subdural haematoma.

The benefit of hypothermia therapy for severely head-injured patients has been a matter of controversy, and the appropriate indications have yet to be clarified. The authors have employed mild hypothermia to treat severe acute subdural haematoma (ASDH) patients postoperatively as a means of controlling intracranial pressure. The potential roles of hypothermia in the treatment of severe ASDH patients are discussed. Between 1997 and 2000, 18 ASDH patients with a GCS on admission of 6 or less were treated by haematoma evacuation with postoperative mild hypothermia. The efficacy of hypothermia was evaluated retrospectively by comparing the outcome of these 18 patients with that of 15 ASDH patients who underwent surgery without postoperative hypothermia between 1993 and 1996. Hypothermia significantly increased both the survival and favorable outcome rates of the 18 ASDH patients, compared with the historic controls. However, the benefit of hypothermia was seen only in ASDH patients without associated cerebral contusion, and no significant protective effect of hypothermia was seen in ASDH patients with contusion. Hypothermia may be a useful postoperative therapeutic modality for severe ASDH without concomitant cerebral contusion. A future prospective study is warranted to support the conclusions of this retrospective study.

Rebleeding from a primary brain tumor manifesting as intracerebral hemorrhage (CNN 04/077, revised version).

Symptomatic spontaneous intratumoral hemorrhage is a rare event in a patient with a brain tumor (BT). Although the treatment of choice in such a case is surgical removal of both the tumor and the hemorrhage, the optimal timing for surgical intervention has not been clearly established, particularly in those who present with minimal neurological deficits and a small hemorrhage volume. Two cases of primary BTs manifesting as an intracerebral hemorrhage (ICH) are described, in which rebleeding from the tumor occurred shortly after the initial hemorrhage. The patients each presented with the sudden onset of a headache and minimal neurological deficits, and the neuroradiological workup was consistent with a diagnosis of hemorrhagic BT. Each patient remained neurologically stable, and elective surgery had been planned within 7 days of their admission, but rebleeding occurred 5 and 6 days, respectively, after admission. A BT manifesting as an ICH may rebleed shortly after the initial bleeding, and should be treated on an emergency basis instead of an elective basis regardless of the patient's neurological status on admission or hematoma volume on the initial CT scans.

Treatment of spontaneous intracranial hypotension secondary to C-2 meningeal cyst by surgical packing--case report.

A 41-year-old man presented with progressive worsening of postural headache. Computed tomography (CT) showed bilateral subdural hematomas without prior history of trauma. The diagnosis was spontaneous intracranial hypotension (SIH). Conservative treatment with oral steroids failed to prevent gradual deterioration of the patient's consciousness. CT myelography revealed massive cerebrospinal fluid (CSF) leakage between the C-1 and C-2 levels. The leak was repaired surgically via a laminectomy. A cyst, thought to be a meningeal cyst, was discovered adjacent to the right C-2 nerve root, and CSF was seen seeping out from around the cyst after a Valsalva maneuver. The presumed dural defect of the cyst was sealed by packing with muscle fragments and fibrin glue. The symptoms disappeared soon after surgery. He was discharged 1 month after surgery without deficits. Most SIH cases are benign and can be managed conservatively, or by the epidural blood patch method. Surgery is more invasive than the epidural blood patch method, but should be performed in patients with a high cervical lesion and massive CSF leakage.

Cerebellar hemorrhage secondary to cranial metastasis of prostate cancer--case report.

A 77-year-old man with a 9-year history of prostate cancer presented with high fever and dysphagia. The initial diagnosis was aspiration pneumonia, but the patient became comatose 2 days after admission, and neuroradiological workup revealed cerebellar hemorrhage, obstructive hydrocephalus, and extensive destruction of the occipital bone secondary to cranial metastasis. The diagnosis was cerebellar hemorrhage secondary to cranial metastasis of prostate cancer. Tumor resection was abandoned because of the patient's poor health. Shunt surgery and palliative radiotherapy were temporarily effective in restoring his consciousness, but he died of systemic infection 3 weeks after surgery. Metastasis of prostate cancer to the cranium, particularly to the skull base, rarely causes lower cranial nerve paresis, and awareness of this sign may lead to earlier detection of the cranial metastasis and prevention of cerebellar hemorrhage.

Malignant peripheral nerve sheath tumor in the anterior skull base associated with neurofibromatosis type 1--case report.

A 36-year-old man presented with a tumor in the anterior skull base manifesting as headache and visual disturbance. Neurofibromatosis type 1 (NF-1) was identified in early childhood in the patient, and also in his father. Subtotal excision of the tumor was performed, leaving the portion extending outside of the cranium. The histological diagnosis was malignant peripheral nerve sheath tumor. Local radiotherapy was instituted postoperatively. Facial paralysis and dysphagia appeared 7 months after the first operation. Magnetic resonance imaging revealed new lesions in the lateral ventricle and around the brainstem. These tumors were also subtotally excised, but the patient died 10 months after the first operation. The tumor very likely originated from the meningeal branch of the trigeminal nerve. Treatment of such tumors developing inside the cranium should include the widest resection possible, followed by irradiation of the entire neuraxis including the spinal cord to inhibit dissemination through the cerebrospinal fluid. Treatment should be started as quickly as possible if the tumor is associated with NF-1, because of the poor prognosis associated with this condition.

Postoperative communicating hydrocephalus in patients with supratentorial malignant glioma.

Postoperative communicating hydrocephalus in adult patients with supratentorial malignant glioma is a relatively uncommon condition that occurs months after the initial operation of tumor excision. It occurred in only five of 50 consecutive cases treated in our department during the past 10 years. The hydrocephalus appeared to be attributable to leptomeningeal dissemination of tumor cells and subsequent impairment in cerebrospinal fluid (CSF) absorption. The tumors were located adjacent to the lateral ventricles in all five patients, and the proximity of the tumor to the cerebral ventricles may have facilitated dissemination of the tumor cells into the CSF space, resulting in hydrocephalus. The hydrocephalus was treated by a shunt surgery in all five cases, and the symptoms temporarily improved. None of the five patients experienced shunt malfunction or abdominal symptoms attributable to metastasis to the peritoneal cavity, and all five patients died of regrowth of the intracranial tumor or of pneumonia.

"Occult" ruptured cerebral aneurysms revealed by repeat angiography: result from a large retrospective study.

Not infrequently, cerebral angiography performed immediately after the onset of subarachnoid hemorrhage (SAH) fails to reveal any causative lesion. Although the cause of the SAH in most of these cases remains unknown, repeat angiography sometimes discloses a lesion not detected by the initial angiography. The frequency of finding a ruptured aneurysm by repeat angiography and the angiographic characteristics of such aneurysms have been investigated retrospectively. Nineteen among 316 non-traumatic SAH patients (6%) showed initially negative angiogram, and 7 of 19 patients (36%) were identified as harboring an "initially occult" aneurysm. It was possible to identify the expected cause of these initial false-negative angiograms in four of those seven patients. The aneurysm was located in the anterior communicating artery (ACoA) complex in four of the seven patients. When interpreting the angiograms of patients with SAH, neurologists and neurosurgeons should bear in mind the finding that the ACoA complex is the most frequent site of "initially occult" aneurysms. One patient had a dissecting aneurysm of the internal carotid artery, and although such lesions have been considered rare, they should be included in the differential diagnosis of SAH of unknown origin.

Induced hypothermia in experimental traumatic spinal cord injury: an update.

The use of induced hypothermia in the treatment of traumatic spinal cord injury (SCI) has been studied extensively between the 1960s and 1970s. Although the treatment showed some promise, it became less popular by the 1980s, mainly because of its adverse effects. However, a revival of hypothermia in the treatment of traumatic brain injury (TBI) in the last decade has encouraged neuroscientists to conduct experiments to reevaluate the potential benefits of hypothermia in traumatic SCI. All laboratory investigations studying the mechanisms of action and/or the efficacy of induced hypothermia in treating experimental traumatic SCI published in the last decade were reviewed. Although efficacy of hypothermia in improving functional outcome of mild to moderate traumatic SCI has been demonstrated, hypothermia may not be protective against severe traumatic SCI. At present, induced hypothermia has yet to be recognized or approved as a potential treatment having therapeutic value for traumatic SCI in humans. The continued search for a possible synergistic effect of induced hypothermia and pharmacological therapy may yield some promise. It has also been deduced from these laboratory studies that hyperthermia is deleterious and rigorous measures to prevent hyperthermia should be taken to minimize the propagation of secondary neuronal damage after traumatic SCI.

Subcortical hemorrhage caused by methamphetamine abuse: efficacy of the triage system in the differential diagnosis--case report.

A 32-year-old woman was brought to the emergency room with hemiplegia on the left and consciousness disturbance. Her prior medical history and the circumstances of the onset were unknown. Brain computed tomography showed intracerebral hemorrhage (ICH) with a midline shift of more than 10 mm in the right parietal lobe. Cerebral angiography failed to show any vascular anomalies. Urine analysis with the triage system, a qualitative screening test for psychotropic drug abuse, showed positive reaction for amphetamines. Subsequent laboratory examination confirmed a highly elevated serum concentration of methamphetamine. The patient underwent evacuation of the hemorrhage via a craniotomy, and was discharged 40 days after admission. Abuse of illegal drugs including amphetamines among young adults is increasing in many developed countries, and the suspicion of possible drug abuse should always be raised in young patients with angiographically negative ICH. A urinalysis screening test for psychotropic agents should be a part of routine emergency room diagnostic procedures for such patients.

Ring-enhanced mass in the brain of a woman with systemic lupus erythematosus and elevated serum CA19-9 level: brain abscess or metastatic tumor?--case report.

A 70-year-old woman with systemic lupus erythematosus presented with a brain abscess manifesting as progressive monoparesis of the right lower extremity over 4 days. She had had no episodes of fever, and did not complain of headache or exhibit any signs of meningeal irritability. Computed tomography of the brain showed a round, low-density mass with strong ring enhancement in the left frontal lobe. Laboratory examination found a moderately elevated serum level of CA19-9, a marker of some digestive organ cancers. Together with the absence of febrile episodes, headache, and a rise in leukocyte count, the initial suspicion was metastatic brain tumor rather than brain abscess. However, diffusion-weighted magnetic resonance imaging depicted the mass as a very hyperintense area. The neuroimaging diagnosis was brain abscess. After conservative treatment with intravenous antibiotics for 6 weeks, the brain abscess completely resolved, and the patient was discharged without neurological deficits.

Normokalemia and hyperglycemia in subarachnoid hemorrhage patients resuscitated from prehospital cardiopulmonary arrest.

Severe metabolic acidosis develops following prolonged periods of cardiopulmonary arrest (CPA), and excessive hydrogen ions derived from lactate and other noxious acids cause marked hyperkalemia in most CPA patients. This study investigated whether the serum electrolyte imbalance in resuscitated CPA patients is affected by the etiology of the CPA. Between 1999 and 2000, return of spontaneous circulation (ROSC) was achieved and serum electrolyte concentration measurements and blood gas analysis (BGA) were performed in 65 of 270 CPA patients treated. Of the 65 patients, subarachnoid hemorrhage (SAH) was the cause of the CPA in ten, cardiac attack was the cause in 16 and asphyxia was the cause in nine patients. The clinical and laboratory data of these 35 patients were retrospectively compared among the three groups. The SAH group had significantly lower serum potassium concentrations than the other two groups and significantly higher glucose concentrations than the asphyxia group. Massive amounts of catecholamines are released into the systemic circulation of SAH patients and our results may indicate that the amount of catecholamines released in resuscitated SAH patients is greater than in heart attack or asphyxia patients, resulting in a lower serum potassium concentration despite the presence of severe metabolic acidosis. It should be clarified in a prospective study whether the presence of normokalemia and hyperglycemia in resuscitated CPA patients reliably predicts the presence of SAH.

Mild hypothermia in neurologic emergency: an update.

Induced hypothermia to treat various neurologic emergencies, which had initially been introduced into clinical practice in the 1940s and 1950s, had become obsolete by the 1980s. In the early 1990s, however, it made a comeback in the treatment of severe traumatic brain injury. The success of mild hypothermia led to the broadening of its application to many other neurologic emergencies. We sought to summarize recent developments in mild hypothermia, as well as its therapeutic potential and limitations. Mild hypothermia has been applied with varying degrees of success in many neurologic emergencies, including traumatic brain injury, spinal cord injury, ischemic stroke, subarachnoid hemorrhage, out-of-hospital cardiopulmonary arrest, hepatic encephalopathy, perinatal asphyxia (hypoxic-anoxic encephalopathy), and infantile viral encephalopathy. At present, the efficacy and safety of mild hypothermia remain unproved. Although the preliminary clinical studies have shown that mild hypothermia can be a feasible and relatively safe treatment, multicenter randomized, controlled trials are warranted to define the indications for induced hypothermia in an evidence-based fashion.

Mild hypothermia for hemispheric cerebral infarction after evacuation of an acute subdural hematoma in an infant.

The use of mild hypothermia to treat hemispheric infarction after evacuation of an acute subdural hematoma in an infant is reported. The patient, a 2-year-old boy, presented with a deteriorating level of consciousness after a fall from a tree. Computed tomography (CT) scan revealed an acute subdural hematoma on the right side with marked midline shift, and emergency evacuation of the hematoma was performed. The postoperative course was uneventful until the patient's intracranial pressure (ICP) rose and his condition deteriorated 3 days after surgery. CT scan revealed a hemispheric infarction on the injured side. Mild hypothermia was induced to control the ICP and protect the brain. While the hypothermia was effective in lowering the elevated ICP, it failed to arrest progression of the infarction. The patient was discharged with mild disability 2 months after the injury. No serious complications occurred during or after the hypothermia. Our experience indicates that hypothermia can be a useful procedure for controlling the ICP in children with severe traumatic brain injury including acute subdural hematoma, although its capability to protect the brain from severe, progressive ischemia appears to be limited.

Endovascular treatment for poorest-grade subarachnoid hemorrhage in the acute stage: has the outcome been improved?

OBJECTIVE: Patients with poor-grade subarachnoid hemorrhage (SAH) have been considered good candidates for endovascular treatment. The results of treatment of Grade V SAH, the poorest grade, however, have not been fully elucidated. METHODS: The clinical characteristics and outcome parameters of 22 World Federation of Neurosurgical Societies Grade V SAH patients treated endovascularly in the acute stage between 1998 and 2000 are summarized and compared with those of 18 Grade V SAH patients treated conservatively between 1995 and 1997. RESULTS: Among the 22 patients treated endovascularly, 8 patients (36.4%) survived. The rate was significantly higher than that of the 18 patients treated conservatively (5.6%), only one of whom survived. The favorable outcome rate, however, was not significantly different between the two groups (4.5% versus 6.0%). Subdivision of both treatment groups according to Glasgow Coma Scale (GCS) score showed that the improved survival among those treated endovascularly was attributable to the improved survival in those with a preprocedural GCS score of 6 but not of 4 or 5. CONCLUSION: Endovascular treatment of the 22 World Federation of Neurosurgical Societies Grade V SAH patients improved their survival rate but not their favorable outcome rate in comparison with conservative treatment. Further accumulation of clinical data is essential to determine whether endovascular treatment can improve the functional outcome of those with GCS scores of 6 and whether there is no role for endovascular treatment in those with GCS scores of 4 or 5.

Prolonged unilateral vasodilatation and brain edema in fulminant hepatic failure, associated with symptomatic seizure.

We report prolonged unilateral vasodilatation and hemispheric brain edema in a 49-year-old man with fulminant hepatic failure (FHF). The patient presented with a tonic-clonic seizure caused by a hypertensive subcortical hemorrhage in the left parietal lobe. Serial computed tomography (CT) scans showed progressive darkening of the ipsilateral hemisphere, suggesting hemispheric cerebral infarction, but the patient did not show clinical signs of deterioration. Brain magnetic resonance angiography showed dilation of the large arteries of the left hemisphere. Evaluation of cerebral blood flow 7 days postictus with single photon emission CT revealed marked ipsilateral hyperperfusion. The darkening of the hemisphere was brain edema elicited by hyperperfusion. Brain edema was reversible, disappearing 14 days postictus. Hemispheric brain edema was caused by unilateral cerebral vasodilatation and resultant hyperperfusion. Although brain edema is a major complication in FHF patients and cerebral hyperperfusion is responsible for edema formation, CT findings of these patients almost invariably show a bilateral lesion. Unilateral vasodilatation and subsequent hemispheric hyperperfusion may be due to overproduction of vasodilators, already abundant in the brains of patients with severe hepatic failure, by seizure activity.

Early resolution of third nerve palsy following endovascular treatment of a posterior communicating artery aneurysm.

A 69-year-old man underwent successful endovascular treatment of a posterior communicating artery aneurysm that had caused a third nerve palsy. Pupil size became normal within 10 days and ptosis and ocular ductions became normal within 3 weeks of the procedure. Based on the reported recovery rates of third nerve palsy after aneurysmal clipping, recovery may occur more rapidly in patients who undergo endovascular treatment. Further data are necessary to substantiate this hypothesis.