Multiple intracerebral hemorrhages due to cerebral amyloid angiopathy after head trauma

Cerebral amyloid angiopathy (CAA) is an important cause of intracerebral hemorrhage and ischemic cerebrovascular disease in some normotensive elderly patients. The diagnosis is made by proof of amyloid deposition in the vessel wall. A case of recurrent and multiple intracerebral hemorrhages due to cerebral amyloid angiopathy after head injury is reported. A 74-year-old female was referred to our hospital because of head injury. CT scan showed traumatic subarachnoid hemorrhage and intraventricular hematoma. Her consciousness was clear but slight disorientation was recognized. Conservative therapy was performed. During the course subcortical hemorrhages occurred five times and during the second one, right frontal and right parietal hemorrhages occurred simultaneously. Her consciousness deteriorated. The second subcortical hemorrhage was especially complicated by a ventriculoperitoneal shunt operation. A biopsy of the cortex was performed and pathological examination revealed amyloid deposition in the walls of small pial and cortical vessels. Occasional duplicated wall, obliterative intimal proliferation and disappearance of elastic lamina were recognized. The patient sank into a vegetative state due to recurrent and multiple hemorrhages. CAA results in two possibilities, hemorrhage and ischemic cerebrovascular disease. When lobar or subcortical hemorrhage is encountered in a normotensive elderly patient, the possibility of a CAA-related hemorrhage should be considered. The author carefully emphasizes that there is indication for neurosurgical treatment in CAA patients and proposes that therapy for ischemic cerebrovascular disease should be given special attention.     

Postoperative intracerebral hemorrhages: A survey of computed tomographic findings after 1074 intracranial operations

We surveyed computed tomographic findings after 1074 intracranial operations to determine the incidence and etiology of postoperative intracerebral hemorrhages. Medium or large hemorrhages occurred after 42 operations (3.9%). Larger hemorrhages, hemorrhages in the suprasellar region, and hemorrhages associated with other types often preceded a poor outcome. Major etiologies underlying postoperative intracerebral hemorrhages were uncontrolled bleeding from a blind area, difficult dissection of a tumor from the brain, retraction injury, vessel injury from a needle, bleeding from a residual tumor, local hemodynamic changes after removal of a tumor, premature rupture of an aneurysm, and hypertensive putaminal hemorrhage. Hypertension during recovery from anesthesia was another important factor.     

Relationship between stroke and asymptomatic minute hemorrhages in hypertensive patients

Asymptomatic small hemorrhages were identified in hypertensive patients by T2*-weighted gradient echo magnetic resonance (MR) imaging to investigate the relationship between hypertensive intracerebral hemorrhage and asymptomatic minute hemorrhages. Forty-eight patients with hypertensive intracerebral hemorrhage or cerebral infarction with hypertension (these diseases were defined as stroke) were treated in National Defense Medical College from April 1998 to February 2000. All patients had no past history of stroke or head injury, underwent MR imaging within 6 months of the stroke attack, were aged from 40 to 80 years, and had no diagnosis of aneurysm, angioma, or moyamoya disease. Patients were divided into the infarction group and hemorrhage group. All foci over 2 mm in size appearing as hypointense on T2*-weighted MR imaging and unrelated to stroke areas were defined as minute hemorrhages. There were no significant differences between the two groups with respect to sex, age, and history of diabetes mellitus. The incidence of minute hemorrhages in the hemorrhage group (21/26) was greater than in the infarction group (9/22, p < 0.01). The incidence of minute hemorrhages in the basal ganglia (18/26) was greater in the hemorrhage group than in the infarction group (4/22, p < 0.001). Symptomatic intracerebral hemorrhage may be preceded by asymptomatic minute hemorrhage.     

A clinico-pathological study on subarachnoid hemorrhage in autopsied cases: the significance of iron containing granule cells seen in autopsied brain with subarachnoid hemorrhage (author's transl)]

Cerebral infarction and petechial hemorrhage are seen in autopsied brains with subarachnoid hemorrhage as most important findings. However, the pathogenesis for the development of these lesions are still obscure. We have been doing clinico-pathological study on the cerebral petechial hemorrhages following subarachnoid hemorrhage. In this report, the findings of these hemorrhagic lesions were presented in detail by means of Perls-Stieda's iron staining. The results are as follows. Cerebral petechial hemorrhages were seen in 3 out of 13 autopsied cases with subarachnoid hemorrhage and almost all hemarrhagic lesions were perivascular. These hemorrhagic lesions were dominantly seen in the regions, thalamus, hypothalamus, midbrain which were close to the accumulated blood clot in the basal cistern, and in the cerebral cortex beneath the accumulated blood clot. Iron containing granular cells were seen not only in the brain surrounding the petechial hemorrhages but also around the vessels which did not show any hemorrhages. On the other hand, it is well known that it needs more than 7 days after hemorrhage in tissue to demonstrate iron containing granular cells by Perls-Stieda' iron staining. So, it might be estimated that the patients survived more than 7 days after the occurance of intracerebral hemorrhages when iron containing granular cells were demonstrated in the autopsied brains. It could be presumed in this study that the petechial hemorrhages following subarachnoid hemorrhage occurred at an early stage of their clinical courses.     

Use of intraoperative ultrasonography to improve the diagnostic accuracy of exploratory burr holes in patients with traumatic tentorial herniation

Seventeen head-injured patients with signs of brain stem compression at admission underwent emergency bilateral burr-hole exploration before computerized tomographic (CT) scanning. After exploration of the epidural and subdural spaces, real-time ultrasonography was performed intraoperatively to identify intraaxial hematomas. Epidural or subdural hematomas were identified surgically in 11 patients (65%) and immediately evacuated through a craniotomy; in 2 patients, bilateral subdural hematomas were removed. Ultrasonography showed no evidence of intracerebral mass lesions in 14 (82%) of the 17 patients, demonstrated extensive contusions of the temporal lobe in 2 patients (prompting partial lobectomy in both cases), and revealed a small intraparenchymal hematoma deep within the dominant hemisphere, which was not removed, in 1 patient. The sensitivity of ultrasound images for identifying intraparenchymal lesions was evaluated postoperatively by CT or autopsy. In 15 patients (88%), the results of ultrasonography were confirmed. In 2 (12%), CT scans showed small but significant lesions at the frontal pole missed by ultrasonography; one patient had a residual subdural hematoma, and the other a small intraparenchymal hemorrhage. These results confirm that patients with clinical evidence of brain stem compression soon after head injury often have extraaxial hematomas that can be readily identified by burr-hole exploration. Although intraparenchymal hematomas are rare immediately after head injury, they can usually be identified by intraoperative ultrasonography. This simple technique can reduce the risk of missing intracranial hematomas during emergency burr-hole exploration and improve intraoperative decision making in this population of severely head-injured patients.     

A study of plasma atrial natriuretic peptide, antidiuretic hormone and aldosterone levels in a series of patients with intracranial disease and hyponatremia]

For intracranial diseases, plasma atrial natriuretic peptide (ANP), antidiuretic hormone (ADH) and aldosterone were determined and their effects on the development of hyponatremia with central origin were studied. The subjects were 71 cases of intracranial diseases which were admitted to our hospital during a period of 1 year from March, 1989 to March, 1990. The diseases were broken down to subarachnoid hemorrhage 26 cases, hypertensive intracerebral hemorrhage 19 cases, head injury 12 cases, cerebral infarction 11 cases and 3 other cases. Serum-urine electrolytes, plasma ANP and ADH were determined in the acute stage on Day 1 to 4, in the hyponatremia stage on Day 5 to 14 and in the chronic stage on Day 15 downward. Hyponatremia was defined as the serum sodium level of 130 mEq/l or less. Cases evidently having other causes such as heart failure and renal insufficiency were excluded. In the normal control group of persons who were admitted to our hospital for a close checkup (n = 20), plasma ANP was 26.5 +/- 11.6 pg/ml (10-50); levels of 50 pg/ml or more were regarded as abnormally high. 1) Hyponatremia was found in 18 cases (25.4%), subarachnoid hemorrhage in 7 cases, hypertensive intracerebral hemorrhage in 4 cases, head injury in 5 cases and others in 2 cases. 2) The time of onset of hyponatremia was on the 8.3 hospital day. The duration was 7.2 days. The minimum serum sodium level was 124.6 mEq/l. 3) There was no significant change in the plasma aldosterone level at each stage.2+ Predicting development of hyponatremia from plasma ADH and ANP levels in the acute stage is difficult. Inadequate secretion of ANP rather than ADH appeared to be an important factor for the development of hyponatremia, but the plasma ANP level was not always abnormally high, so involvement of other sodium diuretic factors should also be kept in mind.     

CSF withdrawal for the treatment of intracranial hypertension in acute head injuries

Summary Long-term ICP recording was carried out in 151 acute head injury patients—131 comatose patients admitted to ICU, and 20 non-comatose patients harbouring intracerebral mass lesions (lacerations or haematomas) in whom a decision to operate was doubtful. CSF withdrawal was used in 39 cases: by intermittent subtraction in 23 patients, and by continuous ventricular drainage (VD) in the remainder. In the acute stage, within 72 hours of injury, CSF subtraction proved of little use in influencing ICP or clinical time course. Conversely, at a latter stage, CSF withdrawal either by repeated intermittent subtraction or by continuous VD could very often control raised ICP. However, some patients had to undergo permanent shunting eventually. Elevated ICP was also safely controlled in four out of eight patients with intracerebral mass lesions and stationary symptoms. Such patients recovered quickly, and operation was avoided.     

Simultaneous, bilateral hypertensive intracranial hematomas

The reported incidences of bilateral intracerebral hemorrhages due to systemic arterial hypertension are exceptionally rare in Japan. Unilateral hemorrhages, on the other hand, are less uncommon. Recently, we have examined two patients with bilateral intracerebral hemorrhages due to hypertension. The first case involved bilateral thalamic hemorrhages; and in the other, a contralateral hemorrhage developed postoperatively, subsequent to the evacuation of a primary hematoma. The characteristic neurological manifestation of bilateral intracerebral hemorrhages include quadriparesis, bilateral Babinski's signs, stupor, and coma. Published information regarding the anatomy of intracerebral hemorrhages due to hypertension is inconclusive, but the bilateral basal ganglias are believed to be most frequently involved. One school of thought explains the pathomechanism of bilateral hemorrhages as a symmetrical rupture of cerebral microaneurysm. However, it is possible that an unilateral hematoma was formed by a ruptured microaneurysm, and subsequently, a contralateral hemorrhage developed in relatively short time due to circulatory disturbance. As in the case of general cerebral hemorrhage, a craniotomy is also indicated for hypertensive bilateral intracerebral hemorrhage.     

Risk factors for the development of post-traumatic cerebral vasospasm

BACKGROUND: Post-traumatic vasospasm is a well-recognized sequela of head injury. The risk factors associated with post-traumatic vasospasm have not been well defined. We studied 119 consecutive patients with head injury to determine the risk factors for post-traumatic vasospasm. METHODS: Twenty-nine (27.1%) patients were excluded from the study because of poor insonation (n = 12) or a hospital stay of less than 72 hours (n = 17). Seventy (77.8%) of 90 patients suffered severe head injury. Sixteen (17.8%) patients sustained moderate head injury and four (4.4%) patients sustained mild head injury. All patients were monitored with transcranial Doppler (TCD) ultrasonography daily. RESULTS: Post-traumatic vasospasm was detected in 32 (35.6%) of 90 patients. Among these patients, 29 (90.6%) had severe head injury, and three (9.4%) had moderate head injury. None of the patients with mild head injury suffered post-traumatic vasospasm. In most cases, the onset of post-traumatic vasospasm began on the fifth day and lasted 1 to 9 days. In 8 (25%) patients, post-traumatic vasospasm began within the first three days of the head injury. Among 32 patients with post-traumatic vasospasm, 10 (31.2%) patients had mild vasospasm, 20 (65.5%) had moderate vasospasm, and 2 (6.3%) had severe post-traumatic vasospasm. Clinical deterioration was documented in two (2.5%) patients. CONCLUSIONS: Development of post-traumatic vasospasm correlated only with severe subarachnoid hemorrhage on initial computed tomographic scan. There was an increased incidence of post-traumatic vasospasm in patients with epidural hematomas, subdural hematomas, and intracerebral hemorrhages. The Glasgow Coma Scale (GCS) score on admission was inversely related to the development of post-traumatic vasospasm. In most cases, the period of vasospasm was short and clinical deterioration was rare. Probably, two varieties of post-traumatic vasospasm exist, one that lasts a shorter time and does not correlate with the presence of SAH, and a second that correlates with the presence of SAH, lasts longer, and resembles aneurysmal vasospasm.     

Progression of traumatic intracerebral hemorrhage: a prospective observational study

ABSTRACT Preliminary evidence has shown that intracerebral hemorrhages, either spontaneous (sICH) or traumatic (tICH) often expand over time. An association between hemorrhage expansion and clinical outcomes has been described for sICH. The intent of this prospective, observational study was to characterize the temporal profile of hemorrhage progression, as measured by serial computed tomography (CT) scanning, with the aim of better understanding the natural course of hemorrhage progression in tICH. There was also a desire to document the baseline adverse event (AE) profile in this patient group. An important motive for performing this study was to set the stage for subsequent studies that will examine the role of a new systemic hemostatic agent in tICH. Subjects were enrolled if they had tICH lesions of at least 2 mL on a baseline CT scan obtained within 6 h of a head injury. CT scans were repeated at 24 and 72 h. Clinical outcomes and pre-defined AEs were documented. The data showed that 51% of the subjects demonstrated an increase in tICH volume, and that most of the increase occurred early. In addition, larger hematomas exhibited the greatest expansion. Thromboembolic complications were identified in 13% of subjects. This study demonstrates that tICH expansion between the baseline and 24-h CT scans occurred in approximately half of the subjects. The earlier after injury that the initial CT scan is obtained, the greater is the likelihood that the hematoma will expand on subsequent scans. The time frame during which hemorrhagic expansion occurs provides an opportunity for early intervention to limit a process with adverse prognostic implications.     

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.     

The incidence of delayed traumatic intracerebral hematoma with extradural hemorrhages

After introduction of computerized tomography (CT), we experienced 22 patients with traumatic extradural and intracerebral combined hematomas, of whom 15 underwent sequential CT scans. In 14 of the 22 patients or 13 of the 15 patients whose initial CT scans were performed early, within 6 hours after injury, intracerebral hematomas developed more slowly than extradural hematomas. In ten of the 13 patients, development of intracerebral hematomas was demonstrated only after removal of extradural hematomas, and in four patients acute brain swelling was observed during surgery. Therefore it is emphasized that the incidence of post-surgical intracerebral hematoma with extradural hemorrhages is high and that acute brain swelling during surgery for extradural hematomas is largely caused by the delayed intracerebral hematomas.     

Outcome of patients with diffuse axonal injury: the significance and prognostic value of MRI in the acute phase

BACKGROUND: To compare the magnetic resonance imaging (MRI) findings in the acute phase with outcome in patients with diffuse axonal injury (DAI). METHODS: A group of 33 patients with closed head injury and discrepancy between the apparently normal computed tomographic scan findings and their neurologic statuses were studied with MRI during the first 48 hours. Among them, 24 were found to suffer from DAI-type lesions. According to the Glasgow Coma Scale (GCS), 19 patients suffered from severe head injury (GCS score <8) and 5 patients had moderate head injury (GCS score of 9-12). Four MRI sequences in various planes were applied. Patients were divided into three groups, according to staging described in the literature. RESULTS: In five patients, MRI demonstrated nonhemorrhagic DAI lesions stage 1. In 11 patients, findings were consistent with DAI lesions stage 2, eight nonhemorrhagic and three hemorrhagic. Eight patients showed DAI lesions stage 3, six of which were nonhemorrhagic. CONCLUSIONS: MRI is more sensitive compared with computed tomography in the detection of traumatic brain lesions, especially the nonhemorrhagic DAI. The presence of hemorrhage in DAI-type lesions and the association with traumatic space-occupying lesions is a poor prognostic sign. Isolated nonhemorrhagic DAI-type lesions are not associated with poor clinical outcome.     

Recurrent intracerebral hemorrhage due to hypertension

We report a series of 14 patients who had recurrent intracerebral hemorrhage due to hypertension. These patients comprise 2.7% of all those admitted to the Soonchunhyang University Chonan Hospital for hypertensive intracerebral hemorrhage from 1985 to 1988. Women outnumbered men by 13 to 1. The mean age of the patients was 54.5 years at the time of the first hemorrhage and 55.4 years at the time of the second hemorrhage. The mean interval between attacks was 13.1 months. All patients were hypertensive on admission, and in 10 patients hypertension had been diagnosed previously. None of the patients had received regular antihypertensive therapy, even after the first hemorrhage. Hemiplegia was the most common deficit seen after both the first and second attacks. The site of the first hemorrhage was ganglionic in 9 patients, cerebellar in 3 patients, and lobar in 2 patients. The site of the second hemorrhage was ganglionic in 9 patients and lobar in 5. The site of recurrent hemorrhage was different from the initial site in all patients except one. The most common pattern of recurrence was "ganglionic-ganglionic." The "lobar-lobar" pattern was noted in only 1 patient. The hypertensive changes of the cerebral arteries are considered to be the major cause of these recurrent hemorrhages. We believe that recurrent intracerebral hemorrhages in hypertensive patients are not rare as previously thought. Possible reasons for the increased frequency of recurrent intracerebral hemorrhage are discussed.     

A case of multiple metastatic brain tumors with repeated intracerebral hemorrhages

We report a case of multiple metastatic brain tumors with repeated intracerebral hemorrhages. A 73-year-old man suffered from a cerebellar hemorrhage. Subsequent hemorrhages repeatedly occurred in the right temporal lobe, the 4th ventricle, the midbrain, and the septum pellucidum. Three months after admission, CT revealed enhanced masses with surrounding edema in the cerebellar vermis and midbrain, suggesting brain tumors. We eventually diagnosed these masses in an autopsy as metastatic brain tumors of lung adenocarcinoma. Intravascular embolization with tumor cells was a probable cause of the multiple repeated intracerebral hemorrhages.     

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.     

Rodent model of direct cranial blast injury

Traumatic brain injury resulting from an explosive blast is one of the most serious wounds suffered by warfighters, yet the effects of explosive blast overpressure directly impacting the head are poorly understood. We developed a rodent model of direct cranial blast injury (dcBI), in which a blast overpressure could be delivered exclusively to the head, precluding indirect brain injury via thoracic transmission of the blast wave. We constructed and validated a Cranium Only Blast Injury Apparatus (COBIA) to deliver blast overpressures generated by detonating .22 caliber cartridges of smokeless powder. Blast waveforms generated by COBIA replicated those recorded within armored vehicles penetrated by munitions. Lethal dcBI (LD(50) ～ 515?kPa) was associated with: (1) apparent brainstem failure, characterized by immediate opisthotonus and apnea leading to cardiac arrest that could not be overcome by cardiopulmonary resuscitation; (2) widespread subarachnoid hemorrhages without cortical contusions or intracerebral or intraventricular hemorrhages; and (3) no pulmonary abnormalities. Sub-lethal dcBI was associated with: (1) apnea lasting up to 15?sec, with transient abnormalities in oxygen saturation; (2) very few delayed deaths; (3) subarachnoid hemorrhages, especially in the path of the blast wave; (4) abnormal immunolabeling for IgG, cleaved caspase-3, and β-amyloid precursor protein (β-APP), and staining for Fluoro-Jade C, all in deep brain regions away from the subarachnoid hemorrhages, but in the path of the blast wave; and (5) abnormalities on the accelerating Rotarod that persisted for the 1 week period of observation. We conclude that exposure of the head alone to severe explosive blast predisposes to significant neurological dysfunction.     

Intraoperative use of real time ultrasonography applied to aneurysm surgery

The intraoperative application of real time ultrasonography during 13 neurosurgical operations for intracranial aneurysms is reported. In 2 cases, the aneurysms themselves could be detected clearly by real time ultrasonic imaging. In the case of a large aneurysm, information about the nature of the aneurysmal wall was obtained. Other lesions coexisting with the aneurysm (namely, intracerebral hematoma, massive subarachnoid hemorrhage, and hydrocephalus) could be recognized clearly. Real time intraoperative ultrasonography is considered to be useful in aneurysm surgery.     

Current updates in perioperative management of intracerebral hemorrhage

Spontaneous intracerebral hemorrhages (ICH) account for 10% to 30% of all strokes and are a result of acute bleeding into the brain by rupturing of small penetrating arteries. Despite major advancements during the past several decades in the management of ischemic strokes and other causes of hemorrhagic strokes, such as ruptured aneurysm, arteriovenous malformations (AVMs), or cavernous angioma, there has been limited progress made in the treatment of ICH. The prognosis for patients who suffer intracerebral hemorrhage remains poor. The societal impact of these hemorrhagic strokes is magnified by the fact that affected patients typically are a decade younger than those afflicted with ischemic strokes.     

Traumatic intracerebral lesions without extracerebral haematoma in 218 patients

Summary 218 of the 852 patients in the HIT-2 study of head injury had intracerebral lesions only. They were analysed to get more information on the optimal treatment of these severely injured patients. The initial CT scans were reviewed to exclude patients with extracerebral lesions, and to make a radiological diagnosis of contusion, contusion under a depressed fracture, diffuse axonal injury, or intracerebral haematoma. Deterioration after admission to hospital was seen in 71% of patients. Patients with contusions, and contusions from depressed fractures in particular showed a worse outcome than expected, while patients with diffuse injury had a tendency to improve rather than to deteriorate. Patients with intracerebral haematoma seemed to improve if the mass was evacuated. Nimodipine had an impact only in patients with contusions. Our findings mandate surgical evacuation of contusions and intracerebral haematomas in patients with lesions larger than 20 ml who also have radiological signs of a mass effect. Regardless of an apparently good clinical state in the early phase, intracerebral lesions larger than 50 ml seemed to benefit from surgery as compared to nonsurgical treatment.The findings indicated that a further refinement of diagnostic criteria may enable individually tailored head injury treatment to interfere with most important pathogenic mechanisms. More accurate diagnoses will improve head injury treatment and outcome, and are a prerequisite for making successful pharmaceutical trials of head injury in the future.