Non-fatal Bihemispheric Penetrating Brain Injury from a Crossbow Arrow with Good Clinical Outcome: Case Report

Crossbow injuries to the head have seldom been reported in the literature, and they represent a unique type of penetrating brain injury (PBI) in which a low-velocity arrow results in an intracranial fragment larger than most high-velocity projectiles, usually with a lethal outcome.We present the case of a 34-year-oldman who attempted suicide with a self-inflicted cranial injury from a crossbow arrow, with a right parietal point of entry and a palpable subcutaneous tip in the left parietal region. The emergency team reported a Glasgow coma scale (GCS) score of 15, and the patient was brought sedated and intubated. Computed tomography (CT) imaging scans showed that the arrow crossed both parietal lobes, with mild subarachnoid hemorrhage and small cerebral contusions adjacent to its intracranial path. Careful retrograde removal of the penetrating arrow was performed in the CT suite, followed by an immediate CT scan, which excluded procedure-related complications. The patient woke up easily and was discharged 3 days later withmild left hand apraxia and no other neurologic deficits. To the best of our knowledge, there are no similar case reports describing both good clinical outcome and rapid discharge after a bihemispheric PBI. Individualizing the management of each patient is therefore crucial to achieve the best possible outcome as PBI cases still represent a major challenge to practicing neurosurgeons worldwide.

NRG1-ErbB4 signaling promotes functional recovery in a murine model of traumatic brain injury via regulation of GABA release.

Traumatic brain injury (TBI) is a serious health problem in the world. However, little is known about the pathogenesis and molecular mechanisms of TBI. Here, we show that TBI activates neuregulin 1 (NRG1)-ErbB4 signaling, with an increased expression of NRG1 and ErbB4 in the traumatic region. Specifically knocking out ErbB4 in parvalbumin-positive (PV+) interneurons exacerbates motor function deficits in mice after TBI. Consistently, PV-ErbB4-/- mice showed larger necrotic area and more edema when compared with PV-ErbB4+/+ mice. Replenishment of NRG1 through intranasal application of the recombinant protein in PV-ErbB4+/+ mice enhanced neurological function. Moreover, using an in vitro neuronal culture system, we found that NRG1-ErbB4 signaling protects neurons from glutamate-induced death, and such protective effects could be diminished by GABA receptor antagonist. These results indicate that NRG-ErbB4 signaling protects cortical neurons from TBI-induced damage, and such effect is probably mediated by promoting GABA activity. Taken together, these findings unveil a previously unappreciated role for NRG1-ErB4 signaling in preventing neuronal cell death during functional recovery after TBI.

Management of Penetrating Brain Injury Caused by a Nail Gun: Three Case Reports and Literature Review.

BACKGROUND: Penetrating brain injury (PBI) caused by a nail gun is an extremely rare neurosurgical emergency that poses a challenge for neurosurgeons because of its rarity and complexity. CASE DESCRIPTION: Here we present 3 cases of PBI caused by a nail gun. In the first case, the nail entered through the right parietal bone and lodged in the right parietal lobe and basal ganglia. In the second case, the nail entered through the right occipital bone and lodged in the right occipital lobe. In the third case, the nail entered through the right parietal bone and lodged in the right frontal and parietal lobes. All patients underwent surgical removal of the nail. The first patient presented with reduced left-side strength, whereas the second and third patients were neurologically intact on presentation. CONCLUSIONS: PBI caused by a nail gun can present with differing clinical manifestations, and most cases require immediate surgery. A rational management strategy should provide a good postoperative prognosis with minimal neurologic deficits in these patients.

Giant intracranial arteriovenous malformation as the focus of epileptic seizures.

A man in his late thirties was found in a supine position in the hallway of his house. He had been diagnosed with epilepsy at approximately 20 years old. Since stopping treatment, epileptic events occurred more frequently and his condition deteriorated in the past 2 years. Autopsy revealed that head injuries were found on the left side of his head. A fracture from the left parietal bone to the anterior cranial fossa was also detected. A subdural hemorrhage (hematoma) spanned a wide range. A subarachnoid hemorrhage was also identified in the left parietal region. His brain weighed 1603 g, was edematous, and showed right uncal herniation. In the right cerebral hemisphere, a thick, enlarged blood vessel ran from the sagittal sinus. An egg-sized tumorous lesion of blood vessels was found on the bottom of the frontal lobe. This vascular lesion had formed between the sagittal sinus and right anterior cerebral artery. Pathologically, veins and arteries were found together, and, thus, this case was diagnosed as an arteriovenous malformation (AVM). No other pathological and toxicological findings were observed. Subdural hematoma, the cause of death, occurred from the fall to the floor. An epileptic seizure may have been the cause of the fall. AVM on his brain was considered to be the focal lesion of epileptic seizures.

Ideomotor Apraxia Due to Injury of the Superior Longitudinal Fasciculus.

We report on a patient who showed ideomotor apraxia due to injury of the superior longitudinal fasciculus following brain tumor and tumor bleeding, which was demonstrated by diffusion tensor tractography (DTT). A 60-yr-old, right-handed male patient underwent removal of brain meningioma and drainage of intraventricular hemorrhage and intracerebral hemorrhage in the left fronto-parietal lobe. At the time of DTT scanning (5 wk after onset), he was able to move the right upper extremity against gravity. The patient exhibited an intact ideational plan for motor performance. In addition, he was able to use actual objects (scissors, eraser) using his right wrist and hand. However, he had difficulty in using his right upper extremity for pantomime of object use, imitating gestures (meaningless or meaningful), and movement of his right upper extremity proximal. Score on the ideomotor apraxia test for the right side was 4 (cut-off score < 32). DTTs for the left superior longitudinal fasciculus to the left premotor cortex and left inferior parietal lobule showed partial injury, compared with the right superior longitudinal fasciculus. These injuries appeared to be the reason for ideomotor apraxia in this patient.

Traumatic brain injury precipitates cognitive impairment and extracellular Aß aggregation in Alzheimer's disease transgenic mice.

Traumatic brain injury (TBI) has become a signature wound of the wars in Iraq and Afghanistan. Many American soldiers, even those undiagnosed but likely suffering from mild TBI, display Alzheimer's disease (AD)-like cognitive impairments, suggesting a pathological overlap between TBI and AD. This study examined the cognitive and neurohistological effects of TBI in presymptomatic APP/PS1 AD-transgenic mice. AD mice and non-transgenic (NT) mice received an experimental TBI on the right parietal cortex using the controlled cortical impact model. Animals were trained in a water maze task for spatial memory before TBI, and then reevaluated in the same task at two and six weeks post-TBI. The results showed that AD mice with TBI made significantly more errors in the task than AD mice without TBI and NT mice regardless of TBI. A separate group of AD mice and NT mice were evaluated neurohistologically at six weeks after TBI. The number of extracellular beta-amyloid (Aß)-deposits significantly increased by at least one fold in the cortex of AD mice that received TBI compared to the NT mice that received TBI or the AD and NT mice that underwent sham surgery. A significant decrease in MAP2 positive cells, indicating neuronal loss, was observed in the cortex of both the AD and NT mice that received TBI compared to the AD and NT mice subjected to sham surgery. Similar changes in extracellular Aß deposits and MAP2 positive cells were also seen in the hippocampus. These results demonstrate for the first time that TBI precipitates cognitive impairment in presymptomatic AD mice, while also confirming extracellular Aß deposits following TBI. The recognition of this pathological link between TBI and AD should aid in developing novel treatments directed at abrogating cellular injury and extracellular Aß deposition in the brain.

Spontaneous migration of a retained bullet within the brain: a case report.

Gunshot injury to the head is usually mortal, and spontaneous migration of a retained bullet is rare. We report the case of a 23-year-old man with a spontaneously migrated bullet within the brain. Cranial computerized tomography (CT) indicated that the bullet was lodged deeply in the left parietal region. The patient was conscious and had right homonymous hemianopsia. The bullet was close to the vital structures and deep-seated; therefore, surgical intervention was not considered. Two months after the injury, repeat CT revealed that the bullet had migrated posteriorly and caudally due to gravitational factors. Management of the retained bullet was controversial. Removal of a deep-seated bullet may cause additional neurological deficit, but migration of a retained bullet may cause damage to vital structures, producing significant neurological damage. We proposed that the bullet in the brain should be removed if it could be reasonably accessed without causing additional neurological damage.

Overheated and melted intracranial pressure transducer as cause of thermal brain injury during magnetic resonance imaging: case report.

Magnetic resonance imaging is used with increasing frequency to provide accurate clinical information in cases of acute brain injury, and it is important to ensure that intracranial pressure (ICP) monitoring devices are both safe and accurate inside the MRI suite. A rare case of thermal brain injury during MRI associated with an overheated ICP transducer is reported. This 20-year-old man had sustained a severe contusion of the right temporal and parietal lobes during a motor vehicle accident. An MR-compatible ICP transducer was placed in the left frontal lobe. The patient was treated with therapeutic hypothermia, barbiturate therapy, partial right temporal lobectomy, and decompressive craniectomy. Immediately after MRI examination on hospital Day 6, the ICP monitor was found to have stopped working, and the transducer was subsequently removed. The patient developed meningitis after this event, and repeat MRI revealed additional brain injury deep in the white matter on the left side, at the location of the ICP transducer. It is suspected that this new injury was caused by heating due to the radiofrequency radiation used in MRI because it was ascertained that the tip of the transducer had been melted and scorched. Scanning conditions--including configuration of the transducer, MRI parameters such as the type of radiofrequency coil, and the specific absorption rate limit--deviated from the manufacturer's recommendations. In cooperation with the manufacturer, the authors developed a precautionary tag describing guidelines for safe MR scanning to attach to the display unit of the product. Strict adherence to the manufacturer's guidelines is very important for preventing serious complications in patients with ICP monitors undergoing MRI examinations.

Metástasis coroideas: clarinada hacia la nada: presentación de casos icónicos / Choroid metastasis: clarion call toward nothing: presentation of two iconic cases

La metástasis intraoculares de tumores sólidos o hematológicos, son un problema clínico para el oftalmólogo práctico y el oncólogo. La localización más frecuente es la coroides, constituyendo el tumor intraocular más frecuente. Suelen diagnósticarsé en pacientes en estadios tumorales muy avanzados, por lo que en el pasado la mayoría de las series publicadas eran descripciones de necropsias. Su diagnóstico generalmente puede hacerse mediante cuidadoso examen. Se estima que la frecuencia general en pacientes que fallecen por cáncer es de aproximadamente 12%, pero puede elevarse en 37% en aquellos con carcinoma mamario, muy superior a la de los tumores primarios, fundamentalmente los melanomas. No obstante, sin compresión ha aumentado en años recientes ofreciendose nuevas formas de tratamiento siendo todavía la radioterapia la que permite a los pacientes mantener una visión.

Intraocular metastases of solid and hematological tumors are clinical problem for the practicing ophthalmologist and oncologist. Its diagnosis can usually be made through careful examination. The most common intraocular tumor. They are often diagnosed in patients in very advanced tumor stages, which is why in the past most of the published series were descriptions of necropsies. The overall frequency of ocular metastases in patients dying of cancer is approximately 12%, but it can be as high as 37% in patients with breast cancer, highly superior to primary tumors, mainly melanomas. Hawever, our understanding of them has increased in recent years, offering new forms of treatment. Radiation therapy is still the cornerstone of treatment, allowing nost patients to maintain usefull vision. Clinical cases with photographic support of an iconic patient are presented to illustrate the problem.

Re-formation of acute parietal epidural hematoma following rapid spontaneous resolution in a multitraumatic child: a case report.

Acute epidural hematomas resulting from traumatic brain injury remain among the most common causes of mortality and disability. In the literature, there are cases about the resolution and recurrence of spinal epidural hematomas. This case is characterized by the rapid disappearance and re-formation of an acute cranial epidural hematoma (EDH) associated with no overlying skull fracture. Various authors have reported resolution of EDHs managed conservatively, but rapid resolution and recurrence of cranial EDH was not reported before.

Post-traumatic frontal and parieto-occipital extradural haematomas: a retrospective analysis of 41 patients and review of the literature.

BACKGROUND: The purpose of this study was to analyse the differences between patients with frontal (FEDH) or parieto-occipital (POEDH) epidural haematomas and evaluate possible statistically significant prognostic factors. MATERIAL AND METHODS: In this retrospective study of a group of 41 patients with a FEDH (17) or POEDH (24 individuals), the authors analysed the influence of gender, age, type of injury, clinical presentation, Glasgow coma scale (GCS) score on admission, radiological findings, and time interval from trauma to surgery on outcomes. A good recovery and moderate disability were considered a "good" or "favourable outcome", whereas severe disability, a vegetative state or death was a "poor outcome". RESULTS: In the POEDH subgroup, a higher GCS score on admission and a younger age were statistically significant prognostic factors for a better outcome (p=0.006, rs=0.702). In the subgroup of patients with FEDHs, the results were not significant. However, patients with FEDHs more frequently had "good outcomes" than members of the POEDH subgroup (88.2 vs. 70.9%). Children (≤ 18 years old) constituted a smaller portion of the POEDH subgroup (12.5%) than those in the FEDH subgroup (41.2%). The evaluation of time intervals between the accident and surgery (≤ 24 h vs. > 24 h) showed no significant influence on outcomes in any of the studied subgroups. However, patients undergoing surgery within 24 h of their injury had a less favourable GCS score on admission than those operated on more than 24 h after their injury. Subacute and chronic clinical courses predominated in patients with a FEDH (10/17 FEDH vs. 11/22 POEDH). Different accompanying intradural lesions occurred in 12 patients of the POEDH subgroup, but only in 2 of the FEDH subgroup (50 vs. 11.8%). However, the presence of such lesions did not significantly deteriorate surgical outcomes in either of the subgroups.

Stem cell survival and functional outcome after traumatic brain injury is dependent on transplant timing and location.

PURPOSE: Recent work indicates that transplanted neural stem cells (NSCs) can survive, migrate to the injury site, and facilitate recovery from traumatic brain injury (TBI). The present study manipulated timing and location of NSC transplants following controlled cortical impact injury (CCI) in mice to determine optimal transplant conditions. METHODS: In Experiment 1 (timing), NSCs (E14.5 mouse) were injected into the host striatum, ipsilateral to the injury, at 2, 7, or 14 days. In Experiment 2 (location), NSCs or vehicle were injected into the mouse striatum (7 days post-CCI) either ipsilateral or contralateral to the injury and cognitive and motor abilities were assessed from weeks 1-8 post-transplant. Histological measures of NSC survival, migration, and differentiation were taken at 6 and 8 weeks post-transplant. RESULTS: The results demonstrate that: (1) 2-7 days post-injury is the optimal time-range for delivering NSCs; (2) time of transplantation does not affect short-term phenotypic differentiation; (3) transplant location affects survival, migration, phenotype, and functional efficacy; and (4) NSC-mediated functional recovery is not contingent upon NSC migration or phenotypic differentiation. CONCLUSIONS: These findings provide further support for the idea that mechanisms other than the replacement of damaged neurons or glia, such as NSC-induced increases in protective neurotrophic factors, may be responsible for the functional recovery observed in this model of TBI.

Intracranial impalement with entrance site in the mandibular region: postmortem elucidation of an accidental fall on a wooden plant stick.

A 78-year-old woman with a history of transient ischemic attacks was found in the doorway of her house in a somnolent and unresponsive condition. In the right mandibular region, a small skin wound was localized, which was surgically treated. Six days after admission to the hospital, an exploratory craniotomy was performed because of abnormal CT findings. Apart from tissue lesions and hemorrhages a small bone fragment was detected in the right cerebral cortex, which was removed. After 11 days in hospital, the patient died from failure of central regulatory functions. At the forensic autopsy, a 15 cm long wound track running upward from the skin wound in the right mandibular region through the bony skull base to the right parietal lobe of the brain was noted. Apparently, the surgically removed bone fragment had been displaced from the right middle cranial fossa. The site of the incident in the deceased's house was inspected again and a bamboo pole used to stabilize a potted plant standing on the floor was found and sent to the trace evidence laboratory. Analysis showed blood and tissue deposits from the victim. On the basis of all the findings and the circumstances of the case, a fatal impalement injury caused by an accidental fall could be assumed.

Injury severity differentially alters sensitivity to dexamethasone after traumatic brain injury.

We have reported differential short- and long-term dysregulation of the neuroendocrine stress response after traumatic brain injury (TBI) produced by controlled cortical impact (CCI). We have now investigated three possible mechanisms for this TBI-induced dysregulation: (1) effects on the sensitivity of negative-feedback systems to glucocorticoids; (2) effects on the sensitivity of pituitary corticotrophs to corticotropin-releasing hormone (CRH); and (3) effects on neuronal loss in the hilar region of the dentate gyrus and in the CA3b layer of the dorsal hippocampus. TBI was induced to the left parietal cortex in adult male rats with a pneumatic piston, at two different impact velocities and compression depths, to produce either moderate or mild CCI. At 7 and 35 days after surgery, the rats were injected SC with the synthetic glucocorticoid analog dexamethasone (DEX; 0.01, 0.10, or 1.00 mg/kg) or saline, and 2 h later were subjected to 30 min of restraint stress and tail vein blood collection. Whereas all doses of DEX suppressed corticosterone (CORT) and adrenocorticotropic hormone (ACTH) responses to stress on both days, CORT and ACTH were significantly more suppressed after 0.01 mg/kg DEX in the moderate TBI group than in the mild TBI or sham groups. At both 7 and 35 days post-TBI, CRH (1.0 and 10.0 microg/kg IP) stimulated CORT and ACTH in all rats, regardless of injury condition. Hippocampal cell loss was greatest at 48 days after moderate TBI. Enhanced sensitivity to glucocorticoid negative feedback and greater hippocampal cell loss, but not altered pituitary responses to CRH, contribute to the short- and long-term attenuation of the neuroendocrine stress response following moderate TBI. The role of TBI-induced alterations in glucocorticoid receptors in limbic system sites in enhanced glucocorticoid feedback sensitivity requires further investigation.

Erythropoietin inhibits the increase of intestinal labile zinc and the expression of inflammatory mediators after traumatic brain injury in rats.

BACKGROUND: The objective of this study was to determine the effect of erythropoietin (Epo) on the intestinal labile zinc and the inflammatory factor in rats after traumatic brain injury (TBI). METHODS: Male Sprague-Dawley rats were randomly divided into nine groups: (a) normal group; (b) sham-operation group; (c, d, e, f, and g) TBI group, killed at 1 hour, 6 hour, 24 hour, and 72 hour and 7 days postinjury, respectively; (h and i) TBI + saline and TBI + Epo, killed at 24 hour or 72 hour postinjury. Parietal brain contusion was produced by a free-falling weight on the exposed dura of the right parietal lobe. Intestinal labile zinc, the tumor necrosis factor-alpha, interleukin (IL)-8, and wet/dry weight ratio were investigated in different groups. RESULTS: The gut contains a certain amount of labile zinc in normal animals and TBI caused obviously gradual increment of intestinal liabled zinc. The levels of inflammatory mediators and the gut wet/dry weight ratio were also found to increase in the trauma group (p < 0.05). There was a highly positive correlation between the abundance of zinc fluorescence and these proinflammation factors. Epo significantly reduced the intestinal labile zinc, the inflammatory mediators, and the gut wet/dry weight ratio compared with TBI group (p < 0.05). CONCLUSIONS: Epo can protect intestine from TBI-induced injury by attenuating intestinal inflammation and labile zinc accumulation in vivo.

Contributions of the retrosplenial and posterior parietal cortices to cue-specific and contextual fear conditioning.

The retrosplenial cortex (RSP) and the posterior parietal cortex (PPC) are the primary sources of cortical sensory input to the postrhinal cortex (POR) in rodents. Together, these areas compose a major corticohippocampal circuit that is involved in processing visuospatial information. The POR has been implicated in contextual learning and memory, consistent with the type of information presumably being processed by this region. By comparison, little is known about the role of the RSP or the PPC in contextual learning. In the present study, rats were trained either before or after surgery in a standard signaled fear conditioning task in which an auditory cue was paired with foot shock. Contextual fear and tone-specific fear were assessed in subsequent test sessions. In Experiment 1, electrolytic damage to the RSP either before or immediately after training impaired the expression of contextual fear but not tone-specific fear. In contrast, electrolytic damage to the PPC had no effect on conditional fear to the context or the tone in Experiment 2. These findings indicate that the RSP, but not the PPC, contributes to the processing of contextual information by the POR corticohippocampal processing stream.

Effects of post-training lesions in the hippocampus and the parietal cortex on idiothetic information processing in the rat.

Dead reckoning can be defined as the ability to navigate using idiothetic information based on self-movement cues without using allothetic information such as environmental cues. In the present study, we investigated the effects of hippocampal and parietal cortex lesions on homing behavior using dead reckoning in rats. Experimentally naive Wistar rats were trained with a homing task in which rats were required to take a food pellet from a cup in the arena and to return home with the pellet. After training, rats were divided into a control (CONT) group (n = 16), hippocampal lesioned (HIPP) group (n = 16), and parietal cortex lesioned (PARC) group (n = 16), and rats in the lesioned groups underwent surgery. After surgery, Test 1 (with four cups) and Test 2 (with one cup but the outgoing path was diverted by a barrier) were conducted. The HIPP group showed severe impairment in homing, but the performance of the PARC group did not differ from that of the CONT group. HIPP rats either approached wrong doors or ate the pellet in the arena. Circular statistics showed that homing directions of CONT and PARC rats showed concentration towards home, whereas those of HIPP rats did not. Our results exhibiting HIPP rats' failure in homing agree with many previous studies, but the results obtained from PARC rats were different from previous studies. These results indicate that the intact hippocampus is important for dead reckoning, but the role of the parietal cortex in dead reckoning is still not clear.

Successful repair of an intracranial nail-gun injury involving the parietal region and the superior sagittal sinus. Case report.

Intracranial nail injuries to the brain are rare. Various techniques for the removal of penetrating nails have been reported, but to date successful nail extraction following an injury involving the superior sagittal sinus (SSS) has not been reported. The authors report the case of a nail-gun injury to the midline parietal region with penetration of the SSS. They describe an original surgical technique involving the use of a graft patch of temporal fascia and muscle to repair the SSS following extraction of the nail. The procedure resulted in preservation of distal flow across the sinus and a good neurological outcome. Technical considerations in the repair of penetrating posterior SSS injuries are discussed. Penetrating nail injuries to the brain involving the SSS can be successfully repaired with maintenance of sinus patency.

Proliferation, migration, and differentiation of human neural stem/progenitor cells after transplantation into a rat model of traumatic brain injury.

OBJECT: Cultures containing human neural stem and progenitor cells (neurospheres) have the capacity to proliferate and differentiate into the major phenotypes of the adult brain. These properties make them candidates for therapeutic transplantation in cases of neurological diseases that involve cell loss. In this study, long-term cultured and cryopreserved cells were transplanted into the traumatically injured rat brain to evaluate the potential for human neural stem/progenitor cells to survive and differentiate following traumatic injury. METHODS: Neural stem/progenitor cell cultures were established from 10-week-old human forebrain. Immunosuppressed adult rats received a unilateral parietal cortical contusion injury, which was delivered using the weight-drop method. Immediately following the injury, these animals received transplants of neural stem/progenitor cells, which were placed close to the site of injury. Two or 6 weeks after the procedure, these animals were killed and their brains were examined by immunohistochemical analysis. At both 2 and 6 weeks postoperatively, the transplanted human cells were found in the perilesional zone, hippocampus, corpus callosum, and ipsilateral subependymal zone of the rats. Compared with the 2-week time point, an increased number of HuN-positive cells was observed at 6 weeks. In addition, at 6 weeks post-injury/transplantation, the cells were noted to cross the midline to the contralateral corpus callosum and into the contralateral cortex. Double labeling demonstrated neuronal and astrocytic, but not oligodendrocytic differentiation. Moreover, the cortex appeared to provide an environment that was less hospitable to neuronal differentiation than the hippocampus. CONCLUSIONS: This study shows that expandable human neural stem/progenitor cells survive transplantation, and migrate, differentiate, and proliferate in the injured brain. These cells could potentially be developed for transplantation therapy in cases of traumatic brain injury.