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.     

Traumatic brain damage: serum S-100 protein measurements related to neuroradiological findings

This study was designed to investigate the correlation between S-100 protein serum measurements and neuroradiological findings in patients with head injury. We studied 278 patients with minor, moderate, and severe head injuries and 110 controls with no history of neurological disease. The study recruited patients from three Scandinavian neurotrauma centers. Serum levels of S-100 protein were measured at admittance, and computed tomographic scans of the brain were obtained within 24 h postinjury in all patients. In a subgroup of 45 patients with minor head injuries, magnetic resonance imaging was also performed. Increased serum level of S-100 protein was detected in 108 (39%) patients, and CT scan demonstrated intracranial pathology in 25 (9%) (brain contusion n = 13, subdural hematoma n = 6, epidural hematoma n = 2, traumatic subarachnoid hemorrhage n = 2, and brain edema n = 2). The proportion of patients with detectable serum level was significantly (p < 0.01) higher among those with intracranial pathology (92%) compared to those without (34%). The negative predictive value of an undetectable S-100 serum level was 0.99. Undetectable serum level of S-100 protein predicts normal intracranial findings on CT scan. Determination of S-100 protein in serum may be used to select patients for CT scanning.     

Basal cisternostomy for traumatic brain injury: A case report of unexpected good recovery

In subarachnoid hemorrhage following traumatic brain injury (TBI), the high intracisternal pressure drives the cerebrospinal fluid into the brain parenchyma, causing cerebral edema. Basal cisternostomy involves opening the basal cisterns to atmospheric pressure and draining cerebrospinal fluid in an attempt to reverse the edema. We describe a case of basal cisternostomy combined with decompressive craniectomy. A 35-year-old man with severe TBI following a road vehicle accident presented with acute subdural hematoma, Glasgow coma scale score of 6, fixed pupils and no corneal response. Opening of the basal cisterns and placement of a temporary cisternal drain led to immediate relaxation of the brain. The patient had a Glasgow coma scale score of 15 on postoperative day 6 and was discharged on day 10. We think basal cisternostomy is a feasible and effective procedure that should be considered in the management of TBI.     

急性颅脑损伤后进展性出血性损伤危险因素分析

目的探讨急性颅脑损伤后发生进展性出血性损伤危险因素。方法分析274例你和性颅脑外伤患者临床资料,分为进展组86例和非进展组188例,对照分析两组相关因素。结果两组除首次头颅CT时间外,年龄、性别、GCS评分、瞳孔扩大、平均动脉压、合并颅骨折、合并硬膜外血肿、合并脑挫伤、合并蛛网膜下腔出血、双侧伤、首次CT血肿量、两次CT血肿量差之间差异,均有统计学意义(P均<0.05)。GCS<12分、瞳孔扩大、合并脑挫伤、合并蛛网膜下腔出血及首次CT血肿量>10ml为发生进展性出血性损伤的独立危险因素(P均<0.05)。结论急性颅脑损伤患者及时进行头颅CT检查,对血肿量>10ml,GCS评分1<12分、瞳孔扩大及合并脑挫伤和蛛网膜下腔出血患者,应密切观察病情进展,尽早复查头颅CT以及时发现进展性出血性损伤。     

Computerized tomography (CT), EMI scanner, in the diagnosis of acute traumatic intracranial hematomas (author's transl)

Eighteen examinations of acute head trauma have been performed using computerized tomography (CT), EMI scanner, before and after operation in our department since September, 1975. Diagnostic findings in CT before emergency operations of 5 cases including epidural hematoma (1), subdural hematoma (2), intracerebral hematoma (1), and combined hematoma (1) were presented and the diagnostic value of this new method was compared with that of cerebral angiography. CT was proved to be highly valuable in the diagnosis of not only intracranial hematomas but also cerebral edema, cerebral contusion and other abnormalities of the brain structures in head injury.     

Diffuse axonal injury and early intracranial sequelae in severe head injury.

The importance of diffuse axonal injury (DAI) and early intracranial sequelae was studied in 107 patients with diffuse and focal brain injuries. Comprehensive neuropathological study was also undertaken in 24 fatal patients. The mortality rate was clearly the highest in traumatic subarachnoid hemorrhage, followed by acute subdural hematoma, cerebral contusion with delayed hematoma formation, traumatic intracerebral hematoma, diffuse cerebral swelling, DAI with classical features, and finally nearly normal on computed tomographic scans. The mean flow velocities in the middle cerebral artery recorded by transcranial Doppler ultrasound were variable in diffuse brain injury, but commonly decreased on the hematoma side depending on increased intracranial pressure and decreased cerebral perfusion pressure in focal brain injury. Deep-seated hemorrhagic lesions did not expand in diffuse brain injury, but sizable hematoma developed within 24 hours in focal brain injury. The platelet count was significantly lower in patients with poor outcomes in focal brain injury. Histological evidence of classical DAI was found in eight (50%) of 16 cases with focal brain injury. DAI of varying severity is the common subjacent lesion in patients with severe head injury, but the final outcome varies greatly with different lesion types.     

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.     

Progressive brain injury

The aim of this study was to evaluate the clinical manifestations and prognostic factors of progressive brain injury following trauma. We reviewed the records of 779 patients with head injury who had an admission Glasgow Coma Scale of 9 or more; 70 (7.0%) developed progressive brain injury as evidenced on serial CT scans. Of these 70 patients, 19 (27.1%) had a subdural hematoma, 19 (27.1%) an epidural hematoma, 16 (22.9%) a cerebral contusion, 13 (18.6%) an intracerebral hematoma, and 3 (4.3%) a diffuse brain swelling. Three months after injury, 36 (51.4%) patients died, 2 (2.9%) were left in a vegetative state and 23 (32.9%) had a favorable outcome. The appearance of progressive brain injury was associated with patient age, admission Glasgow Coma Scale, injury mechanisms, skull fracture and hemorrhagic lesions on the initial CT scan. Patients with the extracerebral lesions deteriorated 4 hours after injury, whereas those with intracerebral lesions deteriorated 8 hours after injury. The outcome based on Glasgow Outcome Scale was significantly associated with age, type of intracranial lesion, Glasgow Coma Scale following deterioration, the mechanism of injury and surgical treatment. It is concluded that early repeated CT scan is indicated in patients with risk factors of developing progressive brain injury.     

Computer-aided assessment of head computed tomography (CT) studies in patients with suspected traumatic brain injury

In this study, we sought to determine the accuracy of a computer algorithm that automatically assesses head computed tomography (CT) studies in patients with suspected traumatic brain injury (TBI) for features of intracranial hemorrhage and mass effect, employing a neuroradiologist's interpretation as the gold standard. To this end, we designed a suite of computer algorithms that evaluates in a fully automated fashion the presence of intracranial blood and/or mass effect based on the following CT findings: (1) presence or absence of a subdural or epidural hematoma, (2) presence or absence of subarachnoid hemorrhage, (3) presence or absence of an intraparenchymal hematoma, (4) presence or absence of clinically significant midline shift (>or=5 mm), and (5) normal, partly effaced, or completely effaced basal cisterns. The algorithm displays abnormal findings as color overlays on the original head CT images, and calculates the volume of each type of blood collection, the midline shift, and the volume of the basal cisterns, based on the above-described features. Thresholds and parameters yielding optimal accuracy of the computer algorithm were determined using a development sample of 33 selected, nonconsecutive patients. The software was then applied to a validation sample of 250 consecutive patients evaluated for suspicion of acute TBI at our institution in 2006-2007. Software detection of the presence of at least one noncontrast CT (NCT) feature of acute TBI demonstrated high sensitivity of 98% and high negative predictive value (NPV) of 99%. There was actually only one false negative case, where a very subtle subdural hematoma, extending exclusively along the falx, was diagnosed by the neuroradiologist, while the case was considered as normal by the computer algorithm. The software was excellent at detecting the presence of mass effect and intracranial hemorrhage, but showed some disagreements with the neuroradiologist in quantifying the degree of mass effect and characterizing the type of intracranial hemorrhage. In summary, we have developed a fully automated computer algorithm that demonstrated excellent sensitivity for acute intracranial hemorrhage and clinically significant midline shift, while maintaining intermediate specificity. Further studies are required to evaluate the potential favorable impact of this software on facilitating workflow and improving diagnostic accuracy when used as a screening aid by physicians with different levels of experience.     

Efficacy of standard trauma craniectomy for refractory intracranial hypertension with severe traumatic brain injury: a multicenter, prospective, randomized controlled study

To compare the effect of standard trauma craniectomy (STC) versus limited craniectomy (LC) on the outcome of severe traumatic brain injury (TBI) with refractory intracranial hypertension, we conducted a study at five medical centers of 486 patients with severe TBI (Glasgow Coma Scale score 0.05). The results of the study indicate that STC significantly improves outcome in severe TBI with refractory intracranial hypertension resulting from unilateral frontotemporoparietal contusion with or without intracerebral or subdural hematoma. This suggests that STC, rather than LC, be recommended for such patients.     

Temporal profile of release of neurobiochemical markers of brain damage after traumatic brain injury is associated with intracranial pathology as demonstrated in cranial computerized tomography

This study aimed at the investigation of release patterns of neuron specific enolase (NSE) and protein S-100B after traumatic brain injury (TBI) and their association with intracranial pathologic changes as demonstrated in computerized tomography (CT). We analyzed NSE and S-100B concentrations in serial venous blood samples taken one to three days after TBI in 66 patients by the use of immunoluminometric assays. These markers are considered to be specific neurobiochemical indicators of damage to glial (S-100B) or neuronal (NSE) brain tissue. Standardized neurological examination and plani- and volumetric evaluation of computerized tomography scans were performed in all patients. Patients with medium severe to severe TBI [Glasgow Coma Scale (GCS) score at the site of accident < or =12] exhibited significantly higher NSE and S-100B concentrations and a significantly longer release compared to patients with minor head injury (GCS: 13-15). Both, patients with and without visible intracerebral pathology in CT scans exhibited elevated concentrations of NSE and S-100B after TBI and a significant decrease in the follow-up blood samples. Release patterns of S-100B and NSE differed in patients with primary cortical contusions, diffuse axonal injury (DAI), and signs of cerebral edema (ICP) without focal mass lesions. All serum concentrations of NSE and S-100B were significantly correlated with the volume of contusions. The data of the present study indicate that the early release patterns of NSE and S-100 may mirror different pathophysiological consequences of traumatic brain injury.     

Delayed traumatic intracerebral hematomas after surgical decompression

Delayed traumatic intracerebral hematomas found after an initially unrevealing computerized tomographic scan have been reported occasionally. Such hemorrhage may occur in an area of brain contusion with cerebral vessel injury. Four cases of intracerebral hematoma appearing after evacuation of a different traumatic intracranial mass lesion are reported. This suggests that an intracranial mass lesion may tamponade cerebral venous oozing in an area of brain contusion and delay the accumulation of intracerebral blood, accounting for the late discovery of a parenchymal hematoma. (Neurosurgery, 5: 653--655, 1979).     

Incidence of intracranial injury in orbital wall fracture patients not classified as traumatic brain injury

ObjectiveThe detection of intracranial injury in patients with facial injury rather than traumatic brain injury (TBI) remains a challenge for emergency physicians. This study aimed to evaluate the incidence and risk factors of intracranial injury in patients with orbital wall fracture (OWF), who were classified with a chief complaint of facial injury rather than TBI.MethodsThis retrospective case-control study enrolled adult OWF patients (age ≥18 years) who presented at the hospital between January 2004 and March 2016. Patients with definite TBI were excluded because non-contrast head computed tomography (CT) is recommended for such patients.ResultsA total of 1220 patients with OWF were finally enrolled. CT of the head was performed on 677 patients, and the incidence of concomitant intracranial injury was found to be 9% (62/677). Patients with definite TBI were excluded. Symptoms raising a suspicion of TBI, such as loss of consciousness, alcohol intoxication, or vomiting, were present in 347 of the patients, with 44 of these patients (13%) showing a concomitant intracranial injury. Of the 330 patients without such symptoms, 18 (6%) demonstrated a concomitant intracranial injury. In OWF patients, superior wall fracture (odds ratio [OR], 4.15; 95% confidence interval [CI], 2.06–8.34; P < 0.001), associated frontal bone fracture (OR, 4.38; 95% CI, 2.08–9.23; P < 0.001), and older age (decades) (OR, 1.03; 95% CI, 1.01–1.04; P = 0.002) were independent risk factors for concomitant intracranial injury.ConclusionsEmergency physicians should maintain a high degree of suspicion of TBI, even when their primary concern is facial trauma with OWF. Head CT is recommended for OWF patients with a superior OWF, frontal bone fracture, or increased age.     

Computerized transverse axial tomography in intracerebral, intracerebellar and intraventricular hemorrhage (author's transl)

Computerized transverse axial tomography (CT) of the brain is a recently developed method which allows non-invasive roentgenologic evaluation of intracranial diseases. The advent of CT represents a great advance in the diagnosis of a very wide variety of intracranial lesions, including cerebrovascular diseases. Especially, CT was found to be extremely informative in evaluating intracerebral, intracerebellar and intraventricular hemorrhage. The purpose of this report is to evaluate the clinical usefulness of CT in the diagnosis of intracranial hemorrhage. From the seven hundreds cases of various intracranial diseases hitherto examined by the EMI-scanner (160 X 160 matrix), twenty-three cases of nontraumatic intracranial hemorrhage were selected for the present study. Fifteen cases of fresh hemorrhage consisted of hypertensive cerebrovascular disease, arterio-venous malformation, aneurysm and unknown etiology, number of cases being six, three, four and two, respectively. All cases were examined within fifteen days after the ictus and the positive findings were obtained in all cases. The characteristic feature of the hematoma is the circumscribed and increased density area surrounded by the decreased density zone probably representing the accompanied brain edema. The sequential CT studies revealed that the hematoma area was gradually decreased in its density and finally transformed into the rather low density one in four weeks or so after the ictus. The smallest hematoma detected by CT was the cerebellar hematoma about five grams in weight, which was failed to be recognized by the angiography. In cases of the old hemorrhage, besides the decreased density area of the hematoma, such findings were obtained as cerebral atrophy, ventricular dilatation and porencephalic change. It would be concluded that CT study is the most useful aid at present available in the diagnosis of intracranial hemorrhage. The precise anatomic extent of the hematoma, associated brain edema, ventricular deformity and displacement and hydrocephalus are all readily assessed by CT.     

Atorvastatin reduction of intracranial hematoma volume in rats subjected to controlled cortical impact

OBJECT: Atorvastatin, a beta-hydroxy-beta-methylglutaryl coenzyme A reductase inhibitor, has pleiotropic effects such as improving thrombogenic profile, promoting angiogenesis, and reducing inflammatory responses and has shown promise in enhancing neurological functional improvement and promoting neuroplasticity in animal models of traumatic brain injury (TBI), stroke, and intracranial hemorrhage. The authors tested the effect of atorvastatin on intracranial hematoma after TBI. METHODS: Male Wistar rats were subjected to controlled cortical impact, and atorvastatin (1 mg/kg) was orally administered 1 day after TBI and daily for 7 days thereafter. Rats were killed at 1, 8, and 15 days post-TBI. The temporal profile of intraparenchymal hematoma was measured on brain tissue sections by using a MicroComputer Imaging Device and light microscopy. CONCLUSIONS: Data in this study showed that intraparenchymal and intraventricular hemorrhages are present 1 day after TBI and are absorbed at 15 days after TBI. Furthermore, atorvastatin reduces the volume of intracranial hematoma 8 days after TBI.     

The effect of tranexamic acid in traumatic brain injury: A randomized controlled trial

Purpose: Traumatic brain injury (TBI) is a leading cause of death and disability. Intracranial hemorrhage (ICH) secondary to TBI is associated with a high risk of coagulopathy which leads to increasing risk of hemorrhage growth and higher mortality rate. Therefore, antifibrinolytic agents such as tranexamic acid (TA) might reduce traumatic ICH. The aim of the present study was to investigate the extent of ICH growth after TA administration in TBI patients. Methods: This single-blind randomized controlled trial was conducted on patients with traumatic ICH (with less than 30 ml) referring to the emergency department of Vali-Asr Hospital, Arak, Iran in 2014. Patients, based on the inclusion and exclusion criteria, were divided into intervention and control groups (40 patients each). All patients received a conservative treatment for ICH, as well as either intravenous TA or placebo. The extent of ICH growth as the primary outcome was measured by brain CT scan after 48 h. Results: Although brain CT scan showed a significant increase in hemorrhage volume in both groups after 48 h, it was significantly less in the TA group than in the control group (p ¼ 0.04). The mean total hemorrhage expansion was (1.7 ± 9.7) ml and (4.3 ± 12.9) ml in TA and placebo groups, respectively (p < 0.001). Conclusion: It has been established that TA, as an effective hospital-based treatment for acute TBI, could reduce ICH growth. Larger studies are needed to compare the effectiveness of different doses.     

Traumatic intracerebral hematoma--which patients should undergo surgical evacuation? CT scan features and ICP monitoring as a basis for decision making

When a patient presents to the neurosurgeon with a traumatic intracerebral hematoma and has not deteriorated or developed new neurological deficit since the injury, the decision to remove the hematoma may be difficult. Of 244 patients with traumatic intracerebral hematomas, 85 were selected for intracranial pressure monitoring to assist in deciding whether surgical evacuation was indicated. None had deteriorated in conscious level or developed new neurological deficit since injury. Fifty-five patients (65%) demonstrated high intracranial pressure and underwent craniotomy. In 30 patients, intracranial pressure remained under 30 mm Hg, and their hematomas were not initially removed. Five of these 30 patients suddenly deteriorated or died 6 to 11 days after injury, with features of high intracranial pressure clinically or at postmortem. Intracranial pressure monitoring therefore failed to predict a late rise in intracranial pressure in 16.6% of those with low intracranial pressure initially. An analysis of computed tomography scanning and clinical features was therefore carried out to search for better predictors of the need for surgery. Our data suggest that basal cistern status, coma score, and the severity of edema surrounding the intracerebral hematoma should be used, in addition to intracranial pressure monitoring, to improve management of patients with traumatic intracerebral hematoma.     

神经激肽1受体拮抗剂对大鼠创伤性脑损伤的影响

目的 研究大鼠创伤性脑损伤(Traumatic brain injury,TBI)后血P物质(Substance P,SP)的表达和神经激肽1受体拮抗剂对TBI的作用,探讨抑制神经源性炎症反应对创伤性脑损伤的影响.方法 建立大鼠自由落体创伤模型,药物组于创伤后立即尾静脉给予n-乙酰左旋色氨酸(n-acetyl-L-tryptophan,NAT)(25 μmol/kg).大鼠TBI后30分钟和6小时利用酶联免疫吸附法检测血SP的含量,TBI后24小时采用rotarod试验评估大鼠神经行为功能及干湿称重法检测脑组织含水量.结果 大鼠TBI后30分钟时血SP浓度出现明显升高(P＜0.01),6小时时血SP浓度降低.大鼠TBI后24小时脑组织含水量明显升高,其神经行为功能下降,NAT可减少TBI后24h脑组织含水量并改善神经功能损伤(P＜0.05).结论 大鼠TBI早期血SP浓度增高,NAT通过抑制神经源性炎症可减轻脑水肿及神经功能损伤.     

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.     

Bilateral traumatic hemorrhage in the basal ganglia: report of two cases

Hematomas of the basal ganglia in head injury have long been recognized by pathologists with an interest in head injury but their mechanism has not been revealed clearly. We report two cases of bilateral traumatic hemorrhage in the basal ganglia. Case #1, a 17-year-old male was admitted to our hospital immediately after a traffic accident. Neurological examination revealed that the patient was comatose and had right hemiparesis. CT scan showed bilateral hemorrhage of the basal ganglia and subarachnoid hemorrhage in the perimesencephalic cistern. MRI showed high signal intensity areas in the bilateral basal ganglia, perimesencephalic cistern, cerebral white matter and corpus callosum. The patient was diagnosed as having diffuse axonal injury coinciding with bilateral hemorrhage of the basal ganglia. Stereotactic aspiration for the hematoma of the left basal ganglia was carried out. Case #2, a 75-year-old male was admitted immediately after falling from the roof of his house. Neurological examination revealed no neurological deficit except for headache and nausea. CT scan on the day of injury revealed no abnormality. But CT scan 12 hours following the injury showed bilateral hemorrhage of the basal ganglia. Blood pressure of the patient was within normal range and he was diagnosed as having traumatic bilateral intracerebral hematoma. Conservative treatment was carried out and the patient was discharged 7 days after injury with no neurological deficit. The mechanism of traumatic hemorrhage of the basal ganglia has not been clear. In case #1, diffuse axonal injury (DAI) may have played an important role in the bilateral hemorrhage. But in case #2, non-DAI factor such as vasoparalysis syndrome may have existed.(ABSTRACT TRUNCATED AT 250 WORDS)