Extent Of Neurological Deficit Research Articles

MicroRNA miR-188-5p enhances SUMO2/3 conjugation by targeting SENP3 and alleviates focal cerebral ischemia/reperfusion injury in rats.

Expression of miR-188-5p changes upon experiencing cerebral I/R injury. SENP3 is a predicted target of miR-188-5p. The study aimed to examine the potential mechanism underlying the miR-188-5p mediated enhancement of SUMO2/3 conjugation via targeting SENP3 and alleviation against cerebral I/R injury. Focal cerebral I/R was established in Sprague-Dawley rats using the MCAO model. The expression of miR-188-5p was modulated through intracerebroventricular (ICV) administration of its mimics or inhibitors. The expression of miR-188-5p, SENP3, and SUMO2/3 was detected using RT-qPCR or western blot analysis. Dual luciferase reporter assays were conducted to demonstrate the targeting effect of miR-188-5p on SENP3 in N2a cells. HE staining and TUNEL staining were performed to evaluate neurocellular morphological changes and detect neurocellular apoptosis, respectively. The extent of neurological deficits was evaluated using mNSS. TTC staining was used to evaluate the infarct area. In the cerebral ischemic penumbra, the expression of miR-188-5p declined and SENP3 levels increased following I/R. Dual luciferase reporter assays confirmed that miR-188-5p directly acted on SENP3 in N2a cells. As a self-protective mechanism, SUMO2/3 conjugation increased after reperfusion. After ICV administration of miR-188-5p inhibitor, the expression of miR-188-5p was down-regulated, the expression of SENP3 was up-regulated, the SUMO2/3 conjugation decreased, and cerebral I/R injury was exacerbated. However, ICV administration of small hairpin RNA targeting SENP3 partially reversed the effects of the miR-188-5p inhibitor. MiR-188-5p mitigated cerebral I/R injury by down-regulating SENP3 expression and consequently enhancing SUMO2/3 conjugation in rats.

Early presentation of traumatic cervical disc herniation with neurologic deficit and without an adjacent bone lesion

The purpose of this study was to explore clinical features and the operational opportunity of traumatic cervical disc herniation. Patients with cervical spine injury (413) were retrospectively reviewed. Six patients with neurological deficits were identified to have disc herniation without adjacent bone lesion. The diagnosis was confirmed by MRI. The Japanese Orthopedic Association (JOA) score was used to assess the severity of clinical symptoms. Different grading systems have been used in analyzing various stages of herniated cervical discs. All patients underwent anterior cervical decompression, insertion of autologous iliac crest graft, and fixation with cervical plate. The causes of injury were road traffic accidents in four patients and sport and domestic accidents in one patient each. There were five patients with single intervertebral disc herniation and one patient with double. Pre-operative JOA score was 14 for three patients, the remaining three patients scored 10, 6, and 3 respectively. At final follow-up, the score was 17 for four patients and 14 for two patients. Traumatic cervical disc herniation with neurologic deficit and without adjacent bone lesion is a rare condition. MRI is the golden examination to confirm diagnosis. Early recognition is essential for appropriate therapy and to minimize the extent of neurological deficit. The MRI is mandatory in diagnosing different types of traumatic herniated cervical disc. Discectomy and anterior cervical interbody fusion using autologous iliac crest graft are the treatment options.

Evaluation of relationship between timing of surgery and functional outcome considering the extent of neurological deficit in patients with cauda equina syndrome secondary to lumbar disc herniation

<p class="abstract"><strong>Background:</strong> Cauda equina syndrome (CES) is a rare but severe neurological disorder most commonly due to lumbar disc herniation. The role of urgent surgery in improving the outcome of patients with CES remains controversial.</p><p class="abstract"><strong>Methods:</strong> In the present study retrospective evaluation of 44 patients with CES secondary to lumbar disc herniation treated at our hospital between 2009 and 2017 has been done. The patients were categorized into complete (CES-R) and incomplete (CES-I) types of CES and the relationship between timing of surgery and outcome were evaluated.<strong></strong></p><p class="abstract"><strong>Results:</strong> Out of 44 patients, 28 patients presented with CES-I and 16 patients presented with CES-R. In patients with CES-I there was statistically significant difference (p=0.0001) in all observed surgical outcome between the patients operated within 48 hrs and those operated after 48 hrs. In patients with CES-R, no correlation was found between onset of symptoms and timing of surgery as recovery was partial in all the patients except 3 who completely recovered, irrespective of their operative times. (p=0.494).</p><p><strong>Conclusions:</strong> Early diagnosis and treatment in form of emergency decompressive surgery done within 48 hours of onset of autonomic symptoms in CES-I patients can prevent further neurological damage and deterioration to CES-R. For CES-R patients operating within 48 hours made no difference to their outcome. However, necessary investigations and planned surgery by skilful surgeon should be arranged as soon as is reasonably possible for patients with CES-R. </p>

Connexin40 correlates with oxidative stress in brains of traumatic brain injury rats.

Oxidative stress is an important factor in the pathophysiologic changes after traumatic brain injury (TBI). Connexin43 (Cx43) was reported to contribute to cerebral damage. However, the impacts of Cx40 have not been investigated in detail. In the present study, we hypothesized that Cx40 was involved in oxidative stress-induced brain injury after TBI. The controlled cortical impact (CCI) model was introduced to Wistar rats as a TBI model. Neurological deficits, oxidative stress and Cx40 were evaluated in TBI rats and N-acetylcysteine (NAC)-treated TBI rats. Neurological severity score (NSS) was used to assess neurological deficits. Brain infarction was measured by histo-staining. Brain edema was evaluated by measuring the brain water content. Cortex samples were collected to measure the tissue levels of malonyldialdehyde (MDA), nitric oxide (NO) and glutathione (GSH) and NADPH oxidase activity. Cx40 expression was determined by Western-blot. TBI-induced brain injuries gradually increased from 6 h to 24 h post CCI, and the severity remained till 72 h. The level of oxidative stress was consistent with the extent of neurological deficits. Cx40 was upregulated after TBI in a linear correlated manner with increased oxidative stress. With NAC intervention, both neurological deficits and oxidative stress were significantly attenuated. Meanwhile, elevated Cx40 expression in cortex was also prevented by NAC treatment. These studies revealed the relationship between levels of Cx40 and oxidative stress after TBI. The cortex Cx40 expression was positively correlated with the cerebral oxidative stress, indicating the involvement of Cx40 in the progress of brain damage.

Early Sacral Neuromodulation in Spinal Cord Injury—Can It Regenerate Nerves?

The extent of neurologic deficit in spinal cord injury (SCI) is dependent on the primary injury, biologic responses to injury, including inflammation, edema, and scar formation, and neural restructuring. During the recovery phase of SCI, which follows a period of spinal shock lasting weeks to up to 2 years, uninhibited spinal reflexes result in detrusor overactivity with dyssynergia of the urethral sphincter, associated with progressive lower urinary tract dysfunction and potentially upper tract deterioration. Minimization of secondary injury following acute SCI and optimization of nerve regeneration may maximize functional recovery and limit end organ dysfunction, including of the lower urinary tract. Early administration of neuromodulation via electrical or electromagnetic stimulation has been shown to limit secondary injury and potentially restore function. Low-frequency electrical stimulation accelerates axonal growth in the peripheral nervous system and may have a similar benefit in the central nervous system. Limited evidence suggests that sacral neuromodulation has the potential to limit or even prevent maladaptive neural restructuring of the lower urinary tract when administered during the spinal shock phase, when the bladder is areflexic. Herein, we review the pathophysiology of voiding dysfunction following acute injury, existing evidence for the benefit of early SNM in SCI, and possible mechanisms of action, including neural regeneration.

Demographic pattern, clinical profile and outcome of traumatic spinal cord injuries at a tertiary care hospital

Abstract Background: Traumatic spinal cord injury (SCI) is recognized as a serious public health problem resulting in significant morbidity, mortality and permanent disability. The present study is aimed to describe the epidemiological characteristics and outcome of patients with traumatic spinal cord injury in rural tertiary referral care center form South India. Material and methods: The present study was conducted at Narayana Medical College and Hospital, Nellore. All patients admitted and managed for traumatic spinal cord injury were retrieved and data collected in a pre-designed proforma. Patient characteristics, details of etiology, mechanism of injury, level of injury, extent of neurological deficits, details of investigations, details of management and immediate outcome were recorded. Results: A total 152 patients were included in the present study. The mean age was 38.45 years and majority the patients were young adult males. The mean hospital stay was 19.12 days. 71.7% percent patients were non-agriculture workers (mainly involved in construction work) and 28.3% patients were farmers. 61.2% of the patients sustained injuries due to fall from height and 34.2% patients sustained injuries due road traffic accidents. Cervical spine injuries were most common (44.1%), followed by thoraco-lumbar region (36.8%) and dorsal spinal region (19.1%). 9 patients expired in post-injury during hospital stay and all of them had complete cervical spinal cord injury. All patients received aggressive rehabilitation care. Conclusion: In accordance with the literature our results reflect that traumatic spinal cord injuries affect young population and can leave these persons with significant functional and physical morbidity. The major limitation of the study is that it is a single institution based and may not reflect the true spectrum of traumatic spinal cord injuries in the population.

The clinical outcome after occipitocervical fusion due to metastases of the upper cervical spine: a consecutive case series and a systematic review of the literature

Increasing incidences of osseous metastatic malignancies and higher life expectancy in patients are resulting in a raise of occipitocervical metastases. Those patients with infaust prognosis have a significantly reduced quality of life. In Germany, between 800 and 1680 new cases per year are expected. Treatment algorithms include the evaluation of the general condition, the operability of visceral metastases, the tumor localization, the sensitivity to chemo-/radiotherapy, the fracture risk and the extent of neurological deficits and myelopathies. A systematic review on clinical studies or case series in posterior occipitocervical fusions due to metastases to the craniocervical transition yielded nine publications with 48 patients without neurological deficit. The mean survival time in the given follow-up was 6.44 months (n = 26; SD: 5,28; 95 % CI: 4.3-8.57). When measured, the clinical outcome was improved towards the VAS, the DENIS Pain Scale and the quality of life through the activities of daily living (ADL). We searched our clinical database for occipitocervical stabilizations in patients with craniocervical metastases. The prospectively collected data included the preoperative Tokuhashi score, SIN score, neurological status, length of hospitalization, perioperative course/loss of blood/complication rate, as well as the Karnofsky- index and pain measured by VAS preoperatively and in follow-up. Six patients were treated in this consecutive case series. The median age was 72 years (min./max.: 65/82), the average BMI 31.75 (min./max.: 19.3/38.1). The mean preoperative Karnofsky-index was 35 % (min./max.: 23.99/46.01; 95 % CI: 8.39) the mean preoperative Tokuhashi-score 7 (min./max.: 4/10), the mean preoperative VAS7 (min./max.: 4.8/9.2; 95 % CI: 1.68). There were no perioperative complications. In the follow-up, one patient showed a loosening of the screws in the osteolytic massae laterales and one patient suffered from a construct failure after fall. Metastases of the craniocervical transition are rare. The initial treatment of instability includes the application of a rigid Miami-J-collar or a Halo fixator. The decision for an operative procedure must accurately assess the individual patient characteristics to provide him a balanced concept between operational risk and clinical benefit. The assessment should be based on the life expectation and the expected quality of life in dependency of the respective therapeutic concept and its risks. The sole posterior stabilization of craniocervical instability through occipitocervical fusion leads to a reduction of pain, has a low perioperative risk, and may prevent a hospitalization. It is justified for selected patients to receive this treatment to help alleviate pain and to improve their quality of life. From our experience, rare cases of pain without instability should undergo conservative treatment in the first line. Due to the low availability of data on the manifestation and the clinical course of craniocervical metastases, there is a need for the collection of both the descriptive patient data include the radiographic findings as well as the clinical outcome and socio-economic factors using appropriate scoring systems.

Therapy of Spine Metastasis Causing Paralysis Symptoms – Operation and Rehabilitation

Most common manifestation of tumor metastasis after lungs and liver is the skeletal system with 60-80% of spine metastasis. In 30% of all cancer patients with metastatic spinal complaints are initial presentation of malignant primary disease while the primary paraplegia occurs in 5-10% of all spinal metastases. Thus a further operational metastases treatment is dependent on the entire metastasis status, the type and Tomita score as well as the risk of surgery considering general patient status. From 01.01.11 to 31.12.12 we included 16 patients with tumors. In 27% of the cases the first symptoms were paraplegia, but the primary tumor was determined in only one of these cases. 73% of patients underwent surgical treatment within the first 24 hours after admission. The hospital stay was 22 days. 56.3% of patients had incomplete paralysis at admission and 71% of these patients had postoperative improvement in neurological outcomes. All patients benefited as part of operational and rehabilitative treatment of a significant reduction in pain and 50% of patients were able to be discharged home. At the onset of paralytic symptoms we recommend immediate operation. In a multidisciplinary case conference the oncological treatment regimens should be defined also for the necessary paralysis treatment. Decision guidance is the height of paralysis, tumorgenesis, ASA classification and the pain symptoms of the patient. The treatment must adjusted and individualized according to the patient's general health, life expectancy, the primary tumor, the grading of metastasis and extent of neurological deficit.

Acute symptomatic hypoglycaemia mimicking ischaemic stroke on imaging: a systemic review.

BackgroundAcute symptomatic hypoglycaemia is a differential diagnosis in patients presenting with stroke-like neurological impairment, but few textbooks describe the full brain imaging appearances. We systematically reviewed the literature to identify how often hypoglycaemia may mimic ischaemic stroke on imaging, common patterns and relationships with hypoglycaemia severity, duration, clinical outcome and add two new cases.MethodsWe searched EMBASE and Medline databases for papers reporting imaging in adults with symptomatic hypoglycaemia. We analysed the clinical presentation, outcome, brain imaging findings, duration and severity of hypoglycaemia, time course of lesion appearance, including two new cases.ResultsWe found 42 papers describing computed tomography or magnetic resonance imaging in 65 patients, plus our two cases with symptomatic hypoglycaemia. Imaging abnormalities on computed tomography and magnetic resonance were uni or bilateral, cortical or sub-cortical. Thirteen (20%) mimicked cortical or lacunar stroke. Acute lesions had restricted diffusion on magnetic resonance or low attenuation on computed tomography, plus swelling; older lesions showed focal atrophy or disappeared, as with ischaemic stroke. The association between the depth or duration of hypoglycaemia, the severity or extent of neurological deficit, and the imaging abnormalities, was weak.ConclusionImaging abnormalities in patients with hypoglycaemia are uncommon but very variable, weakly associated with neurological deficit, and about a fifth mimic acute ischaemic stroke. Blood glucose testing should be routine in all patients with acute neurological impairment and hypoglycaemia should be included in the differential diagnosis of imaging appearances in patients presenting with acute stroke.

Amenorrhea, Pregnancy, and Pregnancy Outcomes in Women Following Spinal Cord Injury: A Retrospective Cross-Sectional Study

ObjectiveTo assess the prevalence of amenorrhea and pregnancy as well as pregnancy outcomes following spinal cord injury (SCI) in women. MethodsIn this retrospective cross-sectional study, women with SCI were interviewed regarding demographic data, details about the timing and type of SCI they sustained, whether the neurologic deficit was complete or incomplete, and reproductive history. The study was initiated in September 2001 and lasted 3 years. Measures were compared for significance with the level of injury and extent of neurologic deficit using descriptive statistics, analysis of variance, and 2-tailed t tests. ResultsOf 128 women, 53 (41.4%) had postinjury amenorrhea. The amenorrhea was transient in 50 of 53 women. SCI occurred at the mean (± SD) age of 27 ± 9 years. In this group the lesions were at thoracic spine in 35 (66%), cervical spine in 16 (30%), and lumbar spine in 2 (4%). Neurologic deficit was complete in 31 women (58%) and incomplete in 22 (42%). The occurrence of amenorrhea was not influenced by the extent of neurologic deficit. Of 50 women who experienced transient amenorrhea, 10 (20%) became pregnant (6 livebirths, 4 elective terminations). Mean duration of amenorrhea was 7.96 ± 10.9 months; there was no significant difference between mean duration of amenorrhea in women who got pregnant vs those who did not (6.4 ± 3.8 months vs 15.8 ± 30.8 months; P = .34). Pregnancy rate was significantly higher among those who sustained injury at a younger age (21.6 ± 5.3 years vs 28.3 ± 9.3 years;P = .033). ConclusionsLevel of injury did not influence duration of amenorrhea or occurrence of pregnancy. Women who experience transient amenorrhea after SCI may achieve successful pregnancies. (Endocr Pract. 2008; 14: 437-441)

Purine Metabolism in Acute Cerebral Ischemia

Objective: to study the specific features of purine metabolism in clinically significant acute cerebral ischemia. Subjects and materials. Three hundred and fifty patients with the acutest cerebral ischemic stroke were examined. The parameters of gas and electrolyte composition, acid-base balance, the levels of malonic dialdehyde, adenine, guanine, hypox-anthine, xanthine, and uric acid, and the activity of xanthine oxidase were determined in arterial and venous bloods and spinal fluid. Results. In ischemic stroke, hyperuricemia reflects the severity of cerebral metabolic disturbances, hemodynamic instability, hypercoagulation susceptiility, and the extent of neurological deficit. In ischemic stroke, hyperuri-corachia is accompanied by the higher spinal fluid levels of adenine, guanine, hypoxanthine, and xanthine and it is an indirect indicator of respiratory disorders of central genesis, systemic acidosis, hypercoagulation susceptibility, free radical oxidation activation, the intensity of a stressor response to cerebral ischemia, cerebral metabolic disturbances, the depth of reduced consciousness, and the severity of neurological deficit. Conclusion. The high venous blood activity of xanthine oxidase in ischemic stroke is associated with the better neurological parameters in all follow-up periods, the better early functional outcome, and lower mortality rates. Key words: hyperuricemia, stroke, xanthine oxidase, uric acid, cerebral ischemia.

Neurological and psychosocial outcome after subarachnoid haemorrhage, and the Hunt & Hess scale as a predictor of clinical outcome

In a retrospective study, the outcome of 87 patients with ruptured intracranial aneurysm was assessed. Follow-up included neurological examination, grading of the Glasgow Outcome Scale (GOS) of each patient, and answering a psycho-social questionnaire. This questionnaire was answered by the patients themselves or by a relative when the patient was not able to answer. The follow-up was performed more than 12 months after the occurrence of subarachnoid hemorrhage (SAH) in each patient. The psycho-social questionnaire pertained to the degree of independence in everyday activities, household management, stress endurance, memory and concentration, social and leisure activities, social contacts, occupational status, and marital relationships. By summarizing the results of these domains, the quality of life was then determined using the method described by McKenna et al. Neurological deficits in the form of an incomplete paresis of the third cranial nerve and subjective reduction of memory and concentration were identified in 3.5% and 34.5-39% of the patients, respectively. Of the 87 study participants, 58.2% were fully independent, 22.4% were able to live at home with the support of their relatives, and 5 patients were fully dependent. The occupational status of 21 patients who were fully employed before SAH was unaffected, whereas 3 patients were placed in positions with less responsibility, and 21 patients were either unable to continue working, unemployed, or retired. The quality of life was not reduced in 57.2%, while a mild reduction in the quality of life was reported by 23.8% and a severe reduction by 19.0% of the participants. The ability of the initial Hunt & Hess grade, the initial Fisher grade, the extent of neurological deficits, and the occupational status after SAH to predict the patient's outcome was also evaluated. For statistical analysis, the Kendall-Tau-b-test for non-parametric correlations was applied. Significant correlations were found between the initial Hunt & Hess grade and the initial Fisher grade, between neurological deficits and GOS, between quality of life and occupational outcome, as well as between the GOS and quality of life assessment, but not between initial Hunt & Hess grade and GOS or quality of life, between neurological deficits and quality of life, between initial Hunt & Hess grade and occupational outcome, between initial Fisher grade and occupational outcome, and also not between initial Fisher grade and GOS or quality of life. Our results suggest that neither the initial Hunt & Hess grade nor the initial Fisher grade are suitable parameters for predicting the outcome of patients with ruptured intracranial aneurysms. The fact that GOS and quality of life correlated significantly confirms the use of GOS as a simple method for evaluating patient outcome, although it is not a grading system for evaluating functional disorders such as memory or subtle cognitive impairments.

Neurological and Psychosocial Outcome after Subarachnoid Haemorrhage, and the Hunt & Hess Scale as a Predictor of Clinical Outcome

In a retrospective study, the outcome of 87 patients with ruptured intracranial aneurysm was assessed. Follow-up included neurological examination, grading of the Glasgow Outcome Scale (GOS) of each patient, and answering a psycho-social questionnaire. This questionnaire was answered by the patients themselves or by a relative when the patient was not able to answer. The follow-up was performed more than 12 months after the occurrence of subarachnoid hemorrhage (SAH) in each patient. The psycho-social questionnaire pertained to the degree of independence in everyday activities, household management, stress endurance, memory and concentration, social and leisure activities, social contacts, occupational status, and marital relationships. By summarizing the results of these domains, the quality of life was then determined using the method described by McKenna et al. Neurological deficits in the form of an incomplete paresis of the third cranial nerve and subjective reduction of memory and concentration were identified in 3.5 % and 34.5-39 % of the patients, respectively. Of the 87 study participants, 58.2 % were fully independent, 22.4 % were able to live at home with the support of their relatives, and 5 patients were fully dependent. The occupational status of 21 patients who were fully employed before SAH was unaffected, whereas 3 patients were placed in positions with less responsibility, and 21 patients were either unable to continue working, unemployed, or retired. The quality of life was not reduced in 57.2 %, while a mild reduction in the quality of life was reported by 23.8 % and a severe reduction by 19.0 % of the participants. The ability of the initial Hunt and Hess grade, the initial Fisher grade, the extent of neurological deficits, and the occupational status after SAH to predict the patient's outcome was also evaluated. For statistical analysis, the Kendall-Tau-b-test for non-parametric correlations was applied. Significant correlations were found between the initial Hunt and Hess grade and the initial Fisher grade, between neurological deficits and GOS, between quality of life and occupational outcome, as well as between the GOS and quality of life assessment, but not between initial Hunt and Hess grade and GOS or quality of life, between neurological deficits and quality of life, between initial Hunt and Hess grade and occupational outcome, between initial Fisher grade and occupational outcome, and also not between initial Fisher grade and GOS or quality of life. Our results suggest that neither the initial Hunt & Hess grade nor the initial Fisher grade are suitable parameters for predicting the outcome of patients with ruptured intracranial aneurysms. The fact that GOS and quality of life correlated significantly confirms the use of GOS as a simple method for evaluating patient outcome, although it is not a grading system for evaluating functional disorders such as memory or subtle cognitive impairments.

Neuroprotective efficacy and therapeutic time window of peroxynitrite decomposition catalysts in focal cerebral ischemia in rats.

Free radicals have been implicated in cerebral ischemia reperfusion (IR) injury. Massive production of nitric oxide and superoxide results in continuous formation of peroxynitrite even several hours after IR insult. This can produce DNA strand nicks, hydroxylation and/or nitration of cytosolic components of neuron, leading to neuronal death. Peroxynitrite decomposition catalysts 5,10,15,20-tetrakis(N-methyl-4'-pyridyl)porphyrinato iron (III) (FeTMPyP) and 5,10,15,20-tetrakis(4-sulfonatophenyl)porphyrinato iron (III) (FeTPPS) have been demonstrated to protect neurons in in vitro cultures; however, their neuroprotective efficacy in cerebral IR injury has not been explored. In the present study, we investigated the efficacy and the therapeutic time window of FeTMPyP and FeTPPS in focal cerebral ischemia (FCI). FCI was induced according to the middle cerebral artery occlusion (MCAO) method. After 2 h of MCAO and 70 h of reperfusion, the extent of neurological deficits, infarct and edema volume were measured in Sprague-Dawley rats. FeTMPyP and FeTPPS were administered at different time points 2, 6, 9 and 12 h post MCAO. FeTMPyP and FeTPPS (3 mg kg(-1), i.v.) treatment at 2 and 6 h post MCAO produced significant reduction in infarct volume, edema volume and neurological deficits. However, treatment at latter time points did not produce significant neuroprotection. Significant reduction of peroxynitrite in blood and nitrotyrosine in brain sections was observed on FeTMPyP and FeTPPS treatment. As delayed treatment of FeTMPyP and FeTPPS produced neuroprotection, we tested whether treatment had any influence over the apoptotic neuronal death. DNA fragmentation and in situ nick end-labeling assays showed that FeTMPyP and FeTPPS treatment reduced IR injury-induced DNA fragmentation. In conclusion, peroxynitrite decomposition catalysts (FeTMPyP and FeTPPS) produced prominent neuroprotection even if administered 6 h post MCAO and the neuroprotective effect is at least in part due to the reduction of peroxynitrite and apoptosis.

Upregulation of ICAM-1 and MCP-1 but not of MIP-2 and sensorimotor deficit in response to traumatic axonal injury in rats.

The pathophysiology of traumatic axonal injury (TAI) is only partially understood. In this study, we investigated the inflammatory response as well as the extent of neurological deficit in a rat model of traumatic brain injury (TBI). Forty-two adult rats were subjected to moderate impact-acceleration brain injury and their brains were analyzed immunohistochemically for ICAM-1 expression and neutrophil infiltration from 1 hr up to 14 days after trauma. In addition, the chemotactic factors MIP-2 and MCP-1 were measured in brain homogenates by ELISA. For evaluating the neurological deficit, three sensorimotor tests were applied for the first time in this model. In the first 24 hr after trauma, the number of ICAM-1 positive vessels increased up to 4-fold in cortical and subcortical regions compared with sham operated controls (P < 0.05). Maximal ICAM-1 expression (up to 8-fold increase) was detected after 4 days (P < 0.001 vs. 24 hr), returning to control levels in all brain regions by 7 days after trauma. MCP-1 was elevated between 4 hr and 16 hr post-injury as compared with controls. In contrast, neither neutrophil infiltration nor elevation of MIP-2, both events relevant in focal brain injury, could be detected. In all neurological tests, a significant deficit was observed in traumatized rats as compared with sham operated animals from Day 1 post-injury (grasping reflex of the hindpaws: P < 0.001, vibrissae-evoked forelimb placing: P = 0.002, lateral stepping: P = 0.037). In conclusion, after moderate impact acceleration brain injury ICAM-1 upregulation has been demonstrated in the absence of neutrophil infiltration and is paralleled by a selective induction of chemokines, pointing out that individual and distinct inflammatory events occur after diffuse vs. focal TBI.

Prognosis and recovery in ischaemic and traumatic spinal cord injury: clinical and electrophysiological evaluation

OBJECTIVESTo compare prognostic factors and functional recovery between paraplegic patients with either ischaemic (28 patients) or traumatic (39 patients) spinal cord injury (SCI).METHODSOn admission to the spinal injury centre and...

A longitudinal prospective study of soluble adhesion molecules in acute stroke.

Activation of endothelial cells is a consequence of cerebral ischemia and leads to the expression of adhesion molecules such as intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1), and E-selectin, which can be released into the blood. This study aimed to define the kinetics of soluble adhesion molecule serum levels after cerebral ischemia and their correlation with the extent of neurological deficits, clinical outcome, and infarct volume as measured on CT scans. Methods-Plasma levels of soluble (s) ICAM-1, sVCAM-1, and sE-selectin were repeatedly determined by ELISA in 38 patients during a period of 14 days after acute cerebral ischemia. Soluble adhesion molecule levels demonstrated considerable variability. Overall, concentrations revealed characteristic and significant changes after completed strokes but not after transient ischemic attacks. In patients with completed stroke (n=26) but not in patients with transient ischemic attacks (n=12), sICAM-1 peaked within 24 hours (P=0.04), sVCAM-1 reached a maximum after 5 days (P=0.02), and sE-selectin levels decreased after 5 days (P=0.002). There was no clear-cut correlation of soluble adhesion molecule levels with infarct volume or clinical disability. The initial increase of sE-selectin levels was higher in more disabled patients (P=0.02). sICAM-1 levels were higher in patients with signs of infection (n=9; P=0.03). As a result of large interindividual variability influenced by ischemia-independent factors, soluble adhesion molecules are not reliable candidates as surrogate markers in acute cerebral ischemia. The characteristic profile of individual soluble adhesion molecules after completed stroke supports prior hypotheses of their involvement in the pathogenesis of acute cerebral ischemia, but this needs to be clarified in detail.

Higher cortical function deficits among acute stroke patients: The stroke data bank experience

Objectives. Both the number and type of higher cortical function deficits (HCFD) in acute stroke patients are important diagnostically and for gauging the extent of neurological deficits. Methods. The Stroke Data Bank (SDB) provided a large prospective data base for such evaluation. Thirty-one different HCFDs, each defined in the SDB manual, were considered. Results. Of 1,805 patients in the SDB, 641 instances of HCFD in 422 patients were recorded in alert patients at initial examination (within the first 7 to 10 days of ictus). Aphasia (41%) was the most commonly found HCFD, followed by neglect syndrome (27.2%), apraxia (11.7%), and anosognosia (11.1%). Agnosia (3.9%), alexia (3.3%), and aprosodia (1.5%) were less frequently found HCFDs. Cardioembolic infarct was most likely to have associated HCFDs (66%), and lacunar infarction was least likely to be accompanied by HCFDs (6%), with infarction caused by large artery thrombosis (50%) and infarct of undetermined cause (47%) having similar frequencies. The co-occurrence of sensory and motor deficits among the eight major subgroups of HCFD showed that neglect syndrome, apraxia, and anosognosia were most likely to be associated with long tract signs, whereas alexia, aprosodia, and agnosia invariably were not associated with sensorimotor impairment. Approximately half of aphasic patients had associated sensorimotor impairment. Conclusion. Our findings show that higher cortical function deficits are prevalent in the acute phase of stroke, particularly aphasia and neglect syndromes. They are more often associated with nonlacunar stroke and some are less likely to be associated with any sensorimotor deficits.

The problems of L-dopa therapy in the course of Parkinson syndrome

101 patients with Parkinson's disease were analyzed in a retrospective study to evaluate the influence of L-Dopa monotherapy, duration of the disease and age at onset on the clinical course of the syndrome. The effects of L-Dopa dosage adjustments after hospitalization were particularly considered. patients with late onset of symptoms showed a more accelerated deterioration as compared to those with early manifestation of the disease who also were less severely affected. Patients treated with L-Dopa for more than five years had a greater neurological deficit score than patients who had not received L-Dopa. Besides a more severe course, these patients also exhibited significantly more dyskinesias and on-off-phenomena. It should be emphasized that in our study, 73% of the 101 patients had been treated inadequately prior to admission to our clinic. The extent of neurological deficit could be improved by L-Dopa dose adjustments in those cases. Only in 11% of cases, an augmentation of the dopa medication was found to be effective in improving the clinical syndrome, whereas in 43%, a substantial reduction of dosage was necessary and resulted in a marked improvement of the clinical syndrome.

Improved short-term neurological recovery with flunarizine in a canine model of cardiac arrest

A 10-minute cardiac arrest was produced in dogs by electrical fibrillation of the heart. Recovery of cerebral function was monitored by estimating the cerebral metabolic rate of oxygen consumption (CMRO 2), cerebral blood flow (CBF), electroencephalograph (EEG) and extent of neurological deficit. The study group received flunarizine (0.1 mg/kg intravenously) at the beginning of resuscitation, while control animals were given the drug vehicle. By four hours after resuscitation, CMRO 2 in flunarizine-treated dogs was 121 ± 43% of pre-arrest baseline, as compared with 37 ± 9% in control animals ( P < 0.02). In the flunarizine group, CBF was 83 ± 21% of baseline, while it was only 31 ± 8% in controls ( P < 0.01). As compared with the control group, no other significant changes were detected in electrocardiographic, hemodynamic, or biochemical parameters in the flunarizine-treated dogs. A significant improvement in the visual EEG score ( P < 0.001) and neurological deficit ( P < 0.05) was seen in flunarizine-treated dogs six hours after ischemic insult.