Subarachnoid hemorrhage misdiagnosed as acute coronary syndrome leading to catastrophic neurologic injury: A case report

BACKGROUND Elevated levels of cardiac troponin and abnormal electrocardiogram changes are the primary basis for clinical diagnosis of acute coronary syndrome(ACS).Troponin levels in ACS patients can often be more than 50 times the upper reference limit.Some patients with subarachnoid hemorrhage(SAH)also show electrocardiogram abnormalities,myocardial damage,and elevated cardiac biomarkers.Unlike ACS patients,patients with SAH only have a slight increase in troponin,and the use of anticoagulants or antiplatelet drugs is prohibited.Because of the opposite treatment modalities,it is essential for clinicians to distinguish between SAH and ACS.CASE SUMMARY A 56-year-old female patient was admitted to the emergency department at night with a sudden onset of severe back pain.The final diagnosis was intraspinal hematoma in the thoracic spine.We performed an emergency thoracic spinal canal hematoma evacuation procedure with the assistance of a microscope.Intraoperatively,diffuse hematoma formation was found in the T7-T10 spinal canal,and no obvious spinal vascular malformation changes were observed.Postoperative head and spinal magnetic resonance imaging(MRI)showed a small amount of SAH in the skull,no obvious abnormalities in the cervical and thoracic spinal canals,and no abnormal signals in the lumbar spinal canal.Thoracoab-dominal aorta computed tomography angiography showed no vascular malfor-mation.Postoperative motor system examination showed Medical Research Council Scale grade 1/5 strength in both lower extremities,and the patient experienced decreased sensation below the T12 rib margin and reported a Visual Analog Scale score of 3.CONCLUSION Extremely elevated troponin levels(more than 50 times the normal range)are not unique to coronary artery disease.SAH can also result in extremely high troponin levels,and antiplatelet drugs are contraindicated in such cases.Emergency MRI can help in the early differential diagnosis,as a misdiagnosis of ACS can lead to catastrophic neurological damage in patients with spontaneous spinal SAH.

Gait analysis in swine,sheep,and goats after neurologic injury:a literature review

Medical research on neurologic ailments requires representative animal models to validate treatments before they are translated to human clinical trials.Rodents are the predominant animal model used in neurological research despite limited anatomic and physiologic similarities to humans.As a result,functional testing designed to assess locomotor recovery after neurologic impairment is well established in rodent models.Comparatively,large r,more clinically relevant models have not been as well studied.To achieve similar locomotor testing standardization in larger animals,the models must be accessible to a wide array of researchers.Non-human primates are the most relevant animal model fo r translational research,however ethical and financial barriers limit their accessibility.This review focuses on swine,sheep,and goats as large animal alternatives for transitional studies between rodents and non-human primates.The objective of this review is to compare motor testing and data collection methods used in swine,sheep,and goats to encourage testing standardization in these larger animal models.The PubMed database was analyzed by searching combinations of swine,sheep,and goats,neurologic injuries,and functional assessments.Findings were categorized by animal model,data collection method,and assessment design.Swine and sheep were used in the majority of the studies,while only two studies were found using goats.The functional assessments included open pen analysis,treadmill walking,and guided free walking.Data collection methods included subjective behavioral rating scales and objective tools such as pressure-sensitive mats and image-based analysis software.Overall,swine and sheep were well-suited for a variety of assessment designs,with treadmill walking and guided free walking offering the most consistency across multiple trials.Data collection methods varied,but image-based gait analysis software provided the most robust analysis.Future studies should be conducted to standardize functional testing methods after neurologic impairment in large animals.

A mouse model of weight-drop closed head injury:emphasis on cognitive and neurological deficiency

Traumatic brain injury（TBI） is a leading cause of death and disability in individuals worldwide.Producing a clinically relevant TBI model in small-sized animals remains fairly challenging.For good screening of potential therapeutics,which are effective in the treatment of TBI,animal models of TBI should be established and standardized.In this study,we established mouse models of closed head injury using the Shohami weight-drop method with some modifications concerning cognitive deficiency assessment and provided a detailed description of the severe TBI animal model.We found that 250 g falling weight from 2 cm height produced severe closed head injury in C57BL/6 male mice.Cognitive disorders in mice with severe closed head injury could be detected using passive avoidance test on day 7 after injury.Findings from this study indicate that weight-drop injury animal models are suitable for further screening of brain neuroprotectants and potentially are similar to those seen in human TBI.

Improvement of neurological function in rats with spinal cord injury after the transplantation of neural stem cells directly differentiated from bone marrow mesenchymal stem cells

Objective To study the effect and mechanism of neurological function recovery in rats with spinal cord injury ( SCI) rats after transplantation of neural stem cells which are directly differentiated from bone marrow mesenchymal stem cells ( BMSC ) ,and to investigate the suitable engraftment time. Methods BMSC at 3rd passage were differentiated into neural stem cells ( NSC) , and immunofluorescence staining was used to

Ischemia and reperfusion injury of the spinal cord:experimental strategies to examine postischemic paraplegia

Thoracoabdominal aortic replacement,necessary in case of injuries,aneurysms and dissections,shows a high complication rate as a consequence of the perioperative ischemia/reperfusion-sequence（I/R）.Clamping above and below the lesion leads to the spinal cord suffering from ischemia.Clamping times of less than 30 minutes show only a small risk of neurological deficit,

Neuronal apoptosis after hypothermia circulatory arrest and intermittent antegrade cerebral perfusion

Objective To observe the influence of hypotherrnic circulatory arrest （HCA） on the apoptotic processes of neurons in the hippocampus and the expression of the related genes Bcl-2 and Bax, and compare to the intermittent antegrade cerebral perfusion. Methods Eighteen dogs were randomly divided into three groups： control group （6 animals, underwent normal temperature cardiopulmonary bypass, NCPB）, HCA group （6 animals, underwent HCA for 1 h）, and HCA ＋ IACP group （6 animals, underwent HCA for 1 h, combined with intermittent antegrade cerebral perfusion （IACP） every 15 min）. The hippocampus tissue was retrieved 2h after the CPB discontinued The expression of Bcl-2 and Bax were examined with immunohistochemistry method. The cytomorphologic changes of the hippocampus tissue were investigated with transmission electron microscopy （TEM）. Results The immunohistochemical staining showed that Bax protein levels were significantly higher in HCA group than in the other two groups （P〈0.01）, while Bcl-2 protein levels were significantly higher in HCA ＋ IACP group than that of the other two groups （P〈0.01）. Meanwhile, the TEM results showed that there was no apoptosis of neurons in control group, but neuronal apoptotic changes could be clearly observed in HCA group, and only a small amount of apoptotic neurons were seen in HCA ＋ IACP group. Conclusions HCA alone can induce neuronal apoptosis in the hippocampus. IACP during the HCA period has a protective effect on the cerebral tissue through suppressing apoptosis by decreasing Bax expression and increasing Bcl-2 expression.

Increase of beta-amyloid and C-reactive protein in liver transplant recipients with postoperative cognitive dysfunction

BACKGROUND: Postoperative cognitive dysfunction (POCD) is an adverse condition characterized by declined cognitive functions following surgeries and anesthesia. POCD has been associated with increased hospital stay and mortality. There are histological similarities to Alzheimer’s disease. Most early studies were conducted in patients receiving cardiac surgery. Since there is no information about POCD in liver transplant recipients, we measured the incidence of POCD in patients after liver transplantation and examined the correlation between neurological dysfunction and biological markers of dementia- based diseases. METHODS: We studied 25 patients who had a liver transplan- tation between July 2008 and February 2009. Patients with prior encephalopathy or risk factors associated with the development of POCD were excluded from the study. Five validated neuropsychiatric tests were used for diagnosis. The diagnosis was based on one standard deviation decline in two of the five neuropsychiatric tests. The correlation between patient variables and the development of POCD was examined. Serum levels of beta-amyloid and C-reactive protein were measured by standard ELISA and compared between patients with and without POCD. RESULTS: POCD was present in 11 (44%) of the 25 patients. Patients with POCD had significantly higher MELD scores, were more often Child-Pugh class C and received more blood transfusion during surgery. The serum beta-amyloid protein and C-reactive protein concentrations were significantly increased at 24 hours after surgery in the POCD group.CONCLUSIONS: The incidence of POCD in our group of liver transplant patients was greater than that reported in other surgical patients. The increase in the serum biomarkers of dementia in the POCD patients supports the hypothesis that chronic cognitive defects are due to a process similar to that seen in Alzheimer’s disease.

Synergetic protective effects of combined blockade by two kinds of autolesion mediator receptor on neurological function after cervical cord injury

Abstract Objective To investigate the effects of combined blockade by platelet activating factor (PAF) receptor antagonist BN 52021 in combination with opiate receptor antagonist naloxone on neurological function and neurological tissue damage after cervical cord injury. Methods Spinal cord contusion at C 6 segment was made with Allen method in cats, which were randomly divided into four groups: saline control group; BN 52021 group; naloxone group; and combined treatment group with BN 52021 and naloxone. Alteration of cervical cord blood flow, blood barrier permeability of the spinal cord, cervical cord tissue pathology and neurological functional scores were studied after experimental cervical cord injury. Results The animals treated with BN 52021 or naloxone had significantly better functional scores than saline controls 6 weeks after injury (P<0.05). Moreover, the combined treatment showed significantly better neurologic recovery than either naloxone or BN 52021 treated animals (P<0.05). The other indexes in combined treatment animals were also superior to those in naloxone or BN 52021 treated animals. Conclusions Combined blockade by two kinds of autolesion mediator receptor can more effectively inhibit secondary damage production and development after cervical cord injury and improve neurologic function.

The concentration game: differential effects of bioactive signaling in 2D and3D culture

Traumatic injuries to the central nervous system,such as traumatic brain injury,spinal cord injury and stroke,have a high prevalence,enormous financial costs and lack clinical treatments that restore neurological function（Ma et al.,2014）These injuries trigger a series of secondary biochemical and cellular responses that ultimately lead to cellular death and themaintenance of an unsupportive extracellular matrix （ECM） for tissue regeneration （Silva et al., 2014）. Artificial ECM or scaf- folds represent a way to alter this unsupportive environment to improve the efficacy of stem cell therapies and enhance neural tissue regeneration （Figure 1）.

Neuroelectrophysiological characteristics of Hirayama disease： report of 14 cases

Background Hirayama disease is a juvenile muscular atrophy of the distal upper extremities and affects mainly young males. The present study aimed to investigate the neuroelectrophysiological characteristics of Hirayama disease. Methods We retrospectively analyzed the neural conduction velocity （NCV） parameters and needle-electrode electromyograms （EMG） of 14 patients with Hirayama disease. According to the clinical features of the patients, NCV was performed on affected upper-limb including median nerves and ulnar nerves, while EMG was selectively performed on upper and lower extremities, sternocleidomast and thoracic paraspinal muscles. Results The median nerves of all affected upper limbs of patients with Hirayama disease had normal conduction velocities and compound motor action potentials （CMAPs）. The ulnar nerves of all affected upper limbs also had normal conduction velocities. Of the 16 measured ulnar nerves of the affected upper limbs, eight had normal CMAPS, while the other eight showed CMAPs below the normal value by 〉20%. All patients had neurogenic injury on the affected side in muscles innervated by anterior horn cells at the lower cervical region （C7-8, T1）. Four patients had unilateral upper-limb muscle neurogenic injury on the affected side. Seven patients had bilateral upper-limb muscle neurogenic injury, while only two patients experienced bilateral upper-limb muscle atrophy / weakness. The other three patients showed extensive neurogenic injury （unilateral upper-limb muscle atrophy/weakness in one patient, bilateral symptoms in the other two patients）. Conclusions Electromyographic examination showed that the majority of Hirayama disease patients exhibited characteristic segmental injury in the anterior horn of the lower cervical region, while a few patients exhibited extensive neurogenic injury. These data suggest that the actual influence of Hirayama disease may be more extensive than indicated by the clinical presentations.