Acute brain edema in fatal head injury: analysis by dynamic CT scanning

1985 ◽  
Vol 63 (6) ◽  
pp. 830-839 ◽  
Author(s):  
Eiji Yoshino ◽  
Tarumi Yamaki ◽  
Toshihiro Higuchi ◽  
Yoshiharu Horikawa ◽  
Kimiyoshi Hirakawa
Keyword(s):  
Head Injury ◽  
Brain Edema ◽  
Subdural Hematoma ◽  
Ct Scans ◽  
Acute Subdural Hematoma ◽  
Dynamic Ct ◽  
Content Type ◽  
Injured Patients ◽  
Fine Print ◽  
Diffuse Brain

✓ Dynamic computerized tomography (CT) was performed on 42 patients with acute head injury to evaluate the hemodynamics and to elucidate the nature of fatal diffuse brain bulk enlargement. Patients were divided into two groups according to the outcome: Group A included 17 nonfatally injured patients, eight with acute epidural hematomas and nine with acute subdural hematomas; Group B included 25 fatally injured patients, 16 with acute subdural hematomas and nine with bilateral brain bulk enlargement. Remarkable brain bulk enlargement could be seen in all fatally injured patients with acute subdural hematoma. In 29 (69%) of 42 patients, dynamic CT was performed within 2 hours after the impact. In the nonfatally injured patients with brain bulk enlargement, dynamic CT scans suggested a hyperemic state. On the other hand, in 17 (68%) of the 25 fatally injured patients, dynamic CT scans revealed a severely ischemic state. In the fatally injured patients with acute subdural hematoma, CT Hounsfield numbers in the enlarged hemisphere (hematoma side) were significantly lower than those of the opposite side (p < 0.001). Severe diffuse brain damage confirmed by follow-up CT scans and uncontrollable high intracranial pressure were noted in the fatally injured patients. Brain bulk enlargement following head injury originates from acute brain edema and an increase of cerebral blood volume. In cases of fatal head injury, acute brain edema is the more common cause of brain bulk enlargement and occurs more rapidly than is usually thought.

Acute subdural hematoma

1982 ◽  
Vol 57 (2) ◽  
pp. 254-257 ◽  
Author(s):  
Henry A. Shenkin
Keyword(s):  
Computerized Tomography ◽  
Subdural Hematoma ◽  
Neurological Status ◽  
Neurological Dysfunction ◽  
Acute Subdural Hematoma ◽  
Consecutive Series ◽  
Content Type ◽  
Subdural Hematomas ◽  
Fine Print

✓ In a consecutive series of 39 cases of acute subdural hematoma (SDH), encountered since computerized tomography diagnosis became available, 61.5% were found to be the result of bleeding from a small cortical artery, 25.6% were of venous origin, 7.7% resulted from cerebral contusions, and 5% were acute bleeds into chronic subdural hematomas. Craniotomy was performed promptly on admission, but there was no difference in survival (overall 51.3%) between patients with arterial and venous bleeds. The only apparent factor affecting survival in this series was the preoperative neurological status: 67% of patients who were decerebrate and had fixed pupils prior to operation died. Of patients with less severe neurological dysfunction, only 20% failed to survive.

Clinicopathological investigation of gyral high density on computerized tomography following severe head injury in children

1995 ◽  
Vol 82 (6) ◽  
pp. 995-1001 ◽  
Author(s):  
Takehide Onuma ◽  
Yasuko Shimosegawa ◽  
Motonobu Kameyama ◽  
Hiroaki Arai ◽  
Kiyoshi Ishii
Keyword(s):  
Computerized Tomography ◽  
Head Trauma ◽  
Brain Atrophy ◽  
High Density ◽  
Ct Scans ◽  
Severe Head Trauma ◽  
Content Type ◽  
Subacute Stage ◽  
Fine Print ◽  
Diffuse Brain

✓ The authors have treated five cases of severe head trauma in children in which abnormally high density along gyri, “gyral high density,” was seen on plain computerized tomography (CT) scans in the subacute stage of the injury. The prognosis in all cases was poor, with either severe disability or a vegetative state as the outcome due to significant brain atrophy following gyral high density. This pathology was classified into three clinical stages: 1) acute stage, cerebral ischemia in which there is diffuse low density of the cerebrum on CT scans (most marked on the 3rd and 4th days); 2) subacute stage, hemorrhagic infarction showing gyral high density on plain CT scans (between 1 and 4 weeks); and 3) chronic stage, brain atrophy (beginning 4 weeks after the trauma). In their consecutive series of head-injured patients (516 children, 1459 adults), the authors did not find gyral high density on CT scan in adults. This is probably due to the fact that adults who suffer the severe head trauma associated with diffuse brain swelling or diffuse brain edema cannot survive, thus making this gyral high density unique to children.

Impairment of helper T-cell function and lymphokineactivated killer cytotoxicity following severe head injury

1991 ◽  
Vol 75 (5) ◽  
pp. 766-773 ◽  
Author(s):  
Keith B. Quattrocchi ◽  
Edmund H. Frank ◽  
Claramae H. Miller ◽  
Asim Amin ◽  
Bernardo W. Issel ◽  
...  
Keyword(s):  
T Cell ◽  
Head Injury ◽  
Severe Head Injury ◽  
Cell Cytotoxicity ◽  
Content Type ◽  
Lak Cell ◽  
Head Injured ◽  
Injured Patients ◽  
Fine Print

✓ Infection is a major complication of severe head injury, occurring in 50% to 75% of patients who survive to hospitalization. Previous investigations of immune activity following head injury have demonstrated suppression of helper T-cell activation. In this study, the in vitro production of interferon-gamma (INF-γ), interleukin-1 (IL-1), and interleukin-2 (IL-2) was determined in 25 head-injured patients following incubation of peripheral blood lymphocytes (PBL's) with the lymphocyte mitogen phytohemagglutinin (PHA). In order to elucidate the functional status of cellular cytotoxicity, lymphokine-activated killer (LAK) cell cytotoxicity assays were performed both prior to and following incubation of PBL's with IL-2 in five patients with severe head injury. The production of INF-γ and IL-2 by PHA-stimulated PBL's was maximally depressed within 24 hours of injury (p < 0.001 for INF-γ, p = 0.035 for IL-2) and partially normalized within 21 days of injury. There was no change in the production of IL-1. When comparing the in vitro LAK cell cytotoxicity of PBL's from head-injured patients and normal subjects, there was a significant depression in LAK cell cytotoxicity both prior to (p = 0.010) and following (p < 0.001) incubation of PBL's with IL-2. The results of this study indicate that IL-2 and INF-γ production, normally required for inducing cell-mediated immunity, is suppressed following severe head injury. The failure of IL-2 to enhance LAK cell cytotoxicity suggests that factors other than decreased IL-2 production, such as inhibitory soluble mediators or suppressor lymphocytes, may be responsible for the reduction in cellular immune activity following severe head injury. These findings may have significant implications in designing clinical studies aimed at reducing the incidence of infection following severe head injury.

Diagnosis of an “isodense” pituitary microadenoma by dynamic CT scanning

1984 ◽  
Vol 60 (2) ◽  
pp. 424-427 ◽  
Author(s):  
Takeshi Hasegawa ◽  
Haruhide Ito ◽  
Katsuo Shoin ◽  
Yuzaburo Kogure ◽  
Toshihiko Kubota ◽  
...  
Keyword(s):  
Pituitary Gland ◽  
Adrenocorticotropic Hormone ◽  
Ct Scanning ◽  
Ct Scans ◽  
Dynamic Ct ◽  
Content Type ◽  
Pituitary Microadenoma ◽  
Enhanced Ct ◽  
Dynamic Ct Scanning ◽  
Fine Print

✓ A case of Nelson's syndrome with an adrenocorticotropic hormone-secreting pituitary chromophobe microadenoma is presented to demonstrate the potential capability of rapid sequential (dynamic) computerized tomography (CT) scanning for the diagnosis of a pituitary microadenoma that was isodense with the adjacent pituitary gland on conventional enhanced CT scanning. The dynamic CT scans showed transient high density in this microadenoma contrasting with the pituitary gland in the early-enhancement phase, and thereafter the contrast density was indistinguishable from that of the pituitary gland in the delayed-enhancement phase. For the detection of pituitary microadenoma, dynamic CT combined with subsequent delayed CT scanning can provide diagnostic and localizing information.

Chronic subdural hematoma in infancy

1990 ◽  
Vol 73 (2) ◽  
pp. 201-205 ◽  
Author(s):  
Nobuhiko Aoki
Keyword(s):  
Computerized Tomography ◽  
Subdural Hematoma ◽  
Treatment Protocol ◽  
Chronic Subdural Hematoma ◽  
Neurological Deficits ◽  
Acute Subdural Hematoma ◽  
Hemorrhagic Diathesis ◽  
Content Type ◽  
Fine Print ◽  
Subdural Tapping

✓ The cases of 30 infants with chronic subdural hematoma treated surgically between 1978 and 1987 (after the introduction of computerized tomography) were reviewed. This series was limited to infants presenting with increased intracranial pressure, neurological deficits, or developmental retardation. Nineteen patients were male and 11 were female, ranging in age from 1 to 14 months (average 6.1 months). The surgical treatment was initiated with percutaneous subdural tapping which was repeated periodically, if indicated, for 2 weeks. If the patients failed to respond to subdural tapping, subdural-peritoneal shunting was installed. The follow-up periods were from 3 months to 9 years 8 months (average 4 years 10 months). Computerized tomography at that time disclosed disappearance or minimal collection of subdural fluid in 28 cases (93%) and a significant collection (> 5 mm) in two (7%). Neurological examination revealed that the patients were “normal” in 17 cases (57%), “mildly or moderately disabled” in nine (30%), and “severely disabled” in four (13%). The majority of disabled patients had lesions secondary to infantile acute subdural hematoma, child abuse, or hemorrhagic diathesis. These results indicate that the treatment protocol in the present series is acceptable for the elimination of subdural hematoma. Together, early diagnosis and treatment of the etiological conditions causing the lesion are indispensable for obtaining a satisfactory neurological outcome.

High-risk mild head injury

1997 ◽  
Vol 87 (2) ◽  
pp. 234-238 ◽  
Author(s):  
John N. K. Hsiang ◽  
Theresa Yeung ◽  
Ashley L. M. Yu ◽  
Wai S. Poon
Keyword(s):  
Head Injury ◽  
High Risk ◽  
Mild Head Injury ◽  
Radiographic Findings ◽  
Content Type ◽  
Head Injured ◽  
Definition Of ◽  
Gcs Score ◽  
Injured Patients ◽  
Fine Print

✓ The generally accepted definition of mild head injury includes Glasgow Coma Scale (GCS) scores of 13 to 15. However, many studies have shown that there is a heterogeneous pathophysiology among patients with GCS scores in this range. The current definition of mild head injury is misleading because patients classified in this category can have severe sequelae. Therefore, a prospective study of 1360 head-injured patients with GCS scores ranging from 13 to 15 who were admitted to the neurosurgery service during 1994 and 1995 was undertaken to modify the current definition of mild head injury. Data regarding patients' age, sex, GCS score, radiographic findings, neurosurgical intervention, and 6-month outcome were collected and analyzed. The results of this study showed that patients with lower GCS scores tended to have suffered more serious injury. There was a statistically significant trend across GCS scores for percentage of patients with positive acute radiographic findings, percentage receiving neurosurgical interventions, and percentage with poor outcome. The presence of postinjury vomiting did not correlate with findings of acute radiographic abnormalities. Based on the results of this study, the authors divided all head-injured patients with GCS scores ranging from 13 to 15 into mild head injury and high-risk mild head injury groups. Mild head injury is defined as a GCS score of 15 without acute radiographic abnormalities, whereas high-risk mild head injury is defined as GCS scores of 13 or 14, or a GCS score of 15 with acute radiographic abnormalities. This more precise definition of mild head injury is simple to use and may help avoid the confusion caused by the current classification.

Acute subdural hematoma and death following lateral cervical spinal puncture

1983 ◽  
Vol 58 (2) ◽  
pp. 284-286 ◽  
Author(s):  
Larry A. Rogers
Keyword(s):  
Vertebral Artery ◽  
Subdural Hematoma ◽  
Posterior Cranial Fossa ◽  
Acute Subdural Hematoma ◽  
Content Type ◽  
Spinal Puncture ◽  
Cranial Fossa ◽  
Fine Print

✓ An acute subdural hematoma dissecting into the posterior cranial fossa and resulting in death is reported. The patient had undergone spinal puncture by the lateral cervical technique prior to development of the hematoma. Autopsy demonstrated that the source of hemorrhage was an anomalous intraspinal vertebral artery.

Infantile acute subdural hematoma

1984 ◽  
Vol 61 (2) ◽  
pp. 273-280 ◽  
Author(s):  
Nobuhiko Aoki ◽  
Hideaki Masuzawa
Keyword(s):  
Head Trauma ◽  
Subdural Hematoma ◽  
Acute Subdural Hematoma ◽  
Minor Head Trauma ◽  
Cerebral Contusion ◽  
Content Type ◽  
Male Predominance ◽  
Funduscopic Examination ◽  
Fine Print ◽  
Subdural Tapping

✓ Twenty-six cases of infantile acute subdural hematoma treated between 1972 and 1983 were reviewed. The series was limited to infants with acute subdural hematoma apparently due to minor head trauma without loss of consciousness, and not associated with cerebral contusion. Twenty-three of the patients were boys, and three were girls, showing a clear male predominance. The patients ranged in age between 3 and 13 months, with an average age of 8.1 months, the majority of patients being between 7 and 10 months old. Most of the patients were brought to the hospital because of generalized tonic convulsion which developed soon after minor head trauma, and all patients had retinal and preretinal hemorrhage. The cases were graded into mild, intermediate, and fulminant types, mainly on the basis of the level of consciousness and motor weakness. Treatment for fulminant cases was emergency craniotomy, and that for mild cases was subdural tapping alone. For intermediate cases, craniotomy or subdural tapping was selected according to the contents of the hematoma. The follow-up results included death in two cases, mild physical retardation in one case, and epilepsy in one case. The remaining 23 patients showed normal development. The relationship between computerized tomography (CT) findings and clinical grading was analyzed. Because some mild and intermediate cases could be missed on CT, the importance of noting the characteristic clinical course and of funduscopic examination is stressed.

A use-dependent sodium channel antagonist, 619C89, in reduction of ischemic brain damage and glutamate release after acute subdural hematoma in the rat

1996 ◽  
Vol 85 (1) ◽  
pp. 104-111 ◽  
Author(s):  
Eiji Tsuchida ◽  
John F. Harms ◽  
John J. Woodward ◽  
Ross Bullock
Keyword(s):  
Sodium Channel ◽  
Subdural Hematoma ◽  
Neuronal Damage ◽  
Glutamate Release ◽  
Acute Subdural Hematoma ◽  
Extracellular Glutamate ◽  
Ischemic Brain ◽  
Content Type ◽  
Glutamate Concentration ◽  
Fine Print

✓ Acute subdural hematoma kills or disables more severely head injured patients than any other complication of cranial trauma. The main pathological factor involved is ischemic neuronal damage, which is caused by raised intracranial pressure and local effect. The authors have evaluated the hypothesis that a novel use-dependent sodium channel antagonist, 619C89, could reduce ischemic brain damage in the rat subdural hematoma model. Because previous studies have shown that focal neuronal damage may be mediated by “excitotoxic” mechanisms, and because excitatory amino acid levels have been shown to be markedly elevated after brain trauma in humans, the authors have measured levels of glutamate, aspartate, and threonine within the cortex underneath the hematoma, using in vivo microdialysis before and after induction of hematoma, in both vehicle- and drug-treated rats. Postinjury treatment with 619C89 (30 mg/kg) significantly reduced the volume of hemispheric ischemic damage produced by subdural hematoma, from 99.77 ± 7.51 mm3 in vehicle-treated control rats to 46.07 ± 11.06 mm3 (p = 0.0007) in drug-treated animals. In the vehicle-treated animals, induction of subdural hematoma led to a fourfold increase in glutamate in the first 30 minutes after subdural hematoma occurred. The mean extracellular glutamate concentration in these animals remained 2- to 2.6-fold increased over the following 2.5 hours. In the 619C89-treated animals, the release of glutamate from the cortex underneath the hematoma was significantly attenuated. In these rats, induction of subdural hematoma led to a 2.7-fold increase in the first 30-minute sample, but extracellular glutamate concentration returned to near-basal levels thereafter, compared with vehicle-treated animals (p < 0.05). These results show that 619C89 is highly neuroprotective in this model and that its effects may, in part, be mediated by the inhibiton of glutamate release from the ischemic cortex underneath the hematoma.

Cell-mediated immunity in severely head-injured patients: the role of suppressor lymphocytes and serum factors

1992 ◽  
Vol 77 (5) ◽  
pp. 694-699 ◽  
Author(s):  
Keith B. Quattrocchi ◽  
Claramae H. Miller ◽  
Franklin C. Wagner ◽  
Sally J. DeNardo ◽  
Gerald L. DeNardo ◽  
...  
Keyword(s):  
Head Injury ◽  
Cellular Immunity ◽  
Severe Head Injury ◽  
Normal Subjects ◽  
Lymphocyte Function ◽  
Serum Factors ◽  
Content Type ◽  
Head Injured ◽  
Injured Patients ◽  
Fine Print

✓ Severe head injury results in suppression of cellular immunity associated with defective in vitro functioning of effector lymphocytes, such as helper T cells and cytotoxic T cells. It is not known whether this suppression in effector lymphocyte function is due to intrinsic lymphocyte dysfunction, to suppressor peripheral blood mononuclear cells (PBMC's) such as suppressor lymphocytes or suppressor monocytes, or to serum factors capable of inhibiting effector lymphocyte function. The purpose of this study was to determine whether a subpopulation of PBMC's and/or serum factors) are responsible for this observed suppression in cell-mediated immunity. Cell-mediated immune activity was determined measuring in vitro lymphokine-activated killer (LAK) cytotoxicity following incubation of PBMC's from 15 head-injured patients with those from 15 heterologous normal subjects. The PBMC's were separated into lymphocyte-enriched and monocyte-enriched subpopulations by plastic adherence techniques, and the effect of each population on LAK cytotoxicity was determined. Additionally, the effect on cytotoxicity of serum from the head-injured patients was determined in a dose-response fashion. There was significant depression in LAK cytotoxicity when: 1) PBMC's from normal subjects were incubated with PBMC's from head-injured patients (p < 0.001); 2) lymphocytes (PBMC's depleted of monocytes) from head-injured patients were incubated with PBMC's from normal subjects (p < 0.001); and 3) PBMC's from normal subjects were incubated with serum from head-injured patients (p < 0.001). No suppression in cellular immunity was noted when lymphocytes from normal subjects were incubated with monocytes from head-injured patients. The results indicate that lymphocytes rather than monocytes actively inhibit cellular immunity following severe head injury. The detection of immmunosuppressive serum factors suggests a mechanism by which lymphocytes might be modulated by severe head injury.

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