Objective: Traumatic brain injury (TBI) by traffic accident in young children is not so often reported. Those patients were examined to clarify the status for further medical care.
Methods: Twenty five patients with TBI by traffic accident in recent 20 years whose age was under 6 years at injury were examined. We retrospectively investigated age at injury and present, causes, treatments during acute stage, outcome (physical disability, intellectual disability, higher brain dysfunction, epilepsy) and representative rehabilitation. We compared the degree of disability at infancy and at school age.
Results: The average age was 3 years 7 months at onset and 12 years 1 month at present. Accidents during walking were in 16 patients (64%), in the car were in 9 patients (36%). Glasgow coma scale under 8 in 18 patients (72%) was prominent. Types of brain damage were diffuse brain injury in 10 patients (40%), subduralhematoma in 8 patients (32%), contusion in 6 cases (24%), etc. Treatments at acute stage were coservative in 12 patients (48%), hematoma evacuation in 7 patients (14%), hypothermia in 6 patients (12%), etc. Outcome was physical disability in 10 patients (40%), intellectual disability in 20 patients (80%), higher brain dysfunction in 20 patients (80%), and epilepsy in 6 patients (24%). The degree of disability evaluated at school age was worse compared to that at infancy in 6 of 20 patients. The characteristics of those patients were as follows; no physical disability, no or mild intellectual disability, and higher brain dysfunction which became prominent after school age. Rehabilitation for memory disturbance and attention disturbance was presented.
Conclusion: The degree of disability should be evaluated after school attendance, especially with patients whose physical and intellectual disability was mild, and higher brain dysfunction was prominent.
Background: There is an argument for the benefit of the helmet wearing at the time on a bicycle ride. We discuss the usefulness for head injury in traffic accident.
Methods: We reviewed 13 cases, admitted to PICU in our hospital from April 2011 to April 2015, by traffic accident on a bicycle ride. We compared sex, age, conscious level and imaging findings between the cases with (A group) and without bicycle helmet (B group).
Results: There was no significant difference in two groups about sex, age, and conscious level. However, more cases exist in B group as for skull fracture, brain contusion, and subcutaneous hematoma. On the other hand, A group had more cases suffered from the diffuse axon injury and subarachnoid hemorrhage.
Conclusion: Helmet is effective to the direct injury of head, but might be little effective to the rotational injury.
Background: Several pathological and epidemiological studies have demonstrated a possible relationship between traumatic brain injury (TBI) and Alzheimer’s disease (AD). However, how TBI contributes to the onset and progression of AD is unknown. We examined AD-related histopathological changes and cognitive impairment after TBI in the triple transgenic-AD model mice. We also examined amyloid β (Aβ) deposition in the brain using positron emission tomography (PET) in patients with chronic neuropsychological impairment after TBI.
Basic study: AD model mice and wild type (WT) mice were subjected to diffuse TBI using the weight-drop method or sham treatment. Spatial learning ability was evaluated using Morris water maze test in acute phase (4–7 days) and chronic phase (25–28 days) after TBI. Animals were sacrificed 7 or 28 days after TBI and expressions of amyloid precursor protein (APP) and Aβ in the hippocampus were examined using immunohistochemistry. In WT mice, TBI induced significant spatial learning deficit compared to sham-treated mice with increased Aβ deposition over the first 7 days, however, spatial learning ability was recovered to the control level with decreased Aβ deposition 4 weeks after TBI. In AD mice, compared to sham-treated mice, TBI mice demonstrated significant deficits in the spatial learning ability 4 weeks after TBI accompanied with increased Aβ depositions in the hippocampus.
Clinical study: Twelve patients (11 men and 1 woman, mean age 47.6 ± 6.2 years) were examined Aβ deposition in the brain using Pittsburgh Compound B (PIB) PET. PIB was positive in 1 patient (age 78), equivocal in 2 patients and negative in the other 9 patients. There were no relationships between the severity of injury, initial CT findings, elapsed time from the injury to examination, and the scores of neuropsychological tests and PIB deposition in the brain.
Conclusion: The profile of TBI-induced cognitive impairment and Aβ pathology was different between the WT and AD mice. TBI induces a significant increase in Aβ deposition in the hippocampus compared to control animals 28 days after TBI and this is associated with worse spatial learning ability only in AD mice. Moreover, the absence of Aβ deposition in most patients with chronic neuropsychological impairment after TBI does not support the premise that Aβ pathology progresses over time uniformly in the traumatized brain. TBI-induced cognitive impairment concomitant by progressive Aβ pathology may be occurred only in aged brain with reduced cognitive reserve with silent Aβ burden.
It is reported that arachnoid cyst (AC) is ruptured due to head injury. There are also several reports on acute subdural hematoma (ASDH) with AC by sport-related head injury. However, their relationship is not clear. We present a case of ASDH associated with AC by sport-related head injury.
A 16-year-old-male suffered head injury in rugby game, and he had a headache. It was pointed that he had AC in right middle cranial fossa and posterior cranial fossa by previous CT scan. Initial CT showed the volume loss AC. The density of AC was changed to slightly higher. A subdural space of middle fossa and inter-hemispheric fissure was larger. The MRI showed that AC was continued to subdural space. So, we diagnosed that ASDH associated with ruptured AC by head injury.
We found two major points. 1; There is a possibility of ASDH with ruptured AC by contact sports. 2; Previous CT is very important in diagnosis about this case. A medical check before contact sports is useful and recommended to compare radiological changes pre and post head injury. Especially, MRI is convenient to a prolonged case and return-to-play.
We here in report a case of diffuse idiopathic skeletal hyperostosis (DISH) presenting delayed neurological deterioration following multiple vertebral body fractures. A 71-year-old man fell on his buttocks. The patient was treated conservatively as a diagnosis of simple vertebral body compression fracture. One month later, he developed progressive motor weakness on his lower extremities and was transferred to our hospital. Neuroimaging studies revealed multiple vertebral body fractures (reverse Chance fracture on T11, old compression fracture on T12, and Chance fracture on L1 vertebral body respectively) associated with extensive hyperostotic findings suggesting DISH. Because his neurological deterioration appeared to be caused by the spinal instability, posterior fixation underwent using pedicle screws and hooks combined with vertebroplasty. The patient was recovered to be ambulatory 10 months after the surgery.
DISH may cause rigid mobility of the vertebral column leading unexpected vertebral body fractures and instabilities allowing delayed neurological deterioration. DISH is not rare even in Asian elderly people. If the vertebral fracture is found in elderly patients, CT and MRI recommend for diagnosing DISH.
Although chronic subdural hematomas usually affect elderly individuals, they sometimes affect young individuals. We present a case of 19-year-old male with a chronic subdural hematoma that occurred because of previous headbanging. During a rock concert, the patient was intensely headbanging, after which he experienced persisting headache, and his symptoms gradually deteriorated. He visited our hospital for a chief complaint of a headache. Brain CT revealed a right subdural hematoma, and he was urgently admitted. He was treated with emergency surgical drainage with a mass of hematoma. His postoperative status was pretty fair, and he was discharged on hospital day 8. Follow-up brain MRI showed an arachnoid cyst in the right frontal lobe, and the cyst was considered to be the cause of hematoma. To date, only two cases of headbanging-associated chronic subdural hematoma have been reported in western countries. To our knowledge, our patient is the first Japanese case.
18-year-old man had a motorcycle accident and lay bleeding at the site of the accident. The witness called a local surgeon in the nearby clinic and the surgeon performed hemostasis on the site. After ambulance crew arrived, the surgeon continued to perform hemostasis in answer to demands and rode on an ambulance together to hospital. Following the arrival at our hospital, Emergency Room (ER) physicians, cardiovascular surgeon and neurosurgeon started to treat the patient as soon as possible. Because of continuous bleeding and unstable circulation dynamics, we couldn’t transport him to the operation room and decided to repair the injured artery in ER. Finally, we could suture the injured artery successfully. On the day of operation and 8th day after admission, we performed Digital Subtraction Angiography and confirm no complications like carotid artery stenosis and pseudoaneurysm. On the 15th day, he was discharged from hospital without any neurological deficits.
Blunt common carotid artery injury with hypovolemic shock is associated with a high mortality rate and extremely low survival rate. We experienced a case of common carotid artery laceration due to the direct application of force to the neck. In this case, early therapeutic intervention by local surgeon and resourceful surgical assessment contributed to successful resuscitation without no neurological complications. In addition, common carotid artery was easy to approach surgically in ER. This report suggested that challenging surgical interventions in ER were necessary to treat a case of fatal carotid artery injury occasionally.
Background: Children with minor head injury have a low, but serious risk of traumatic intracranial haemorrhage. Medical research on criteria for head computerized tomography (CT) examinations for children is still inconclusive, because CT scanning is required to identify severe traumatic head injury, including acute epidural haematoma. However, radiation exposure is also an important problem.
From the medical perspective the decision to take neuro-imaging, including CT examination, for children with minor head injury must be made carefully, because of the possibility of negative impact on cognitive abilities or an increased risk of cancer from ionizing radiation.
From the legal perspective, when a pediatric patient with a minor head injury who did not have a CT head examination performed at the discretion of a doctor, but died several hours later from a traumatic intracranial haemorrhage, the doctor who had failed to order the head CT examination could be sued for medical malpractice. On the other hand, even if decreased cognitive abilities or an increased cancer risk occur more than a decade after that radiation exposure in a patient who had a head CT examination during childhood because of minor head trauma, a doctor who ordered the CT examination is not at risk of being sued for medical malpractice.
Conclusion: A balanced judgment between medical and legal problems of medical care must be made. In other words, medical issues related to society, like the criteria for the CT scanning of children with a minor head injury, must be considered carefully.