NDS Scores Research Articles

Influence of gabapentin on the degree of sedation, physiological variables and propofol dosage in cats premedicated with acepromazine and methadone: a randomized, prospective, blinded, clinical study.

This study evaluated the influence of gabapentin on sedation, propofol dosage, and physiological variables in cats premedicated with acepromazine and methadone. Thirty-four cats were randomly assigned to receive 100mg of oral gabapentin (Gabapentin group) or placebo (Control group) 100min before intramuscular premedication with acepromazine (0.05mg/kg) plus methadone (0.3mg/kg). Variables recorded included sedation, using the Dynamic Interactive Visual Analog Scale (DIVAS, range 0-100mm) and a Numeric Descriptive Scale (NDS, range 0-14), heart rate, respiratory rate and Doppler systolic arterial pressure (SAP). All variables were measured before (T0), 100min after administration of gabapentin or placebo (T1), and 30min after premedication (T2). Physiological variables were also recorded after anesthetic induction with propofol (T3). At T2, NDS scores were higher in Gabapentin than the Control group [median (interquartile range): 4 (2-5) versus 2 (1-4), p = 0.028], whereas DIVAS scores were not significantly different [Control: 9 (4-13); Gabapentin: 12 (5-32)]. Despite the significant difference between groups in NDS scores, overall sedation scores were mild at T1 and T2 regardless of gabapentin administration. The propofol dosage did not differ between groups. The most concerning adverse effect was arterial hypotension (SAP < 90 mmHg), recorded only at T3 in 71% of cats in the Control group and 100% in the Gabapentin group, without significant difference between groups. Administration of gabapentin before premedication with acepromazine and methadone in healthy cats did not result in a clinically significant influence on sedation levels, physiological variables, or propofol dosage required for anesthesia induction.

Prevalence and Predictors of Diabetic Peripheral Neuropathy in Newly Diagnosed Type 2 Diabetes Mellitus Patients.

The present study aimed to determine the prevalence and predictors of DPN in newly diagnosed T2DM patients. Diabetic Peripheral Neuropathy (DPN) is the most common and debilitating complication of Type 2 Diabetes Mellitus (T2DM). Newly diagnosed T2DM patients visiting the outpatient department were recruited. Detailed demographic parameters, histories, physical examinations, and biochemical investigations were carried out. Patients were screened for DPN using the Diabetic Neuropathy Symptom (DNS) score, the revised Disability Neuropathy Score (NDS), Vibration Perception Threshold (VPT) using a biosthesiometer, and the 10g SW Monofilament Test (MFT). A total of 350 newly diagnosed T2DM patients (mean age 46.4±13.6 years) were included. The prevalence of DPN was found to be 34% using the combined DNS and NDS scores. VPT was moderately impaired in 18.3% and severely impaired in 12% patients, while MFT revealed a loss of protective sensation in 35.4% patients. After logistic regression analysis, DPN was significantly associated with increasing age (OR 1.08, 95%CI 1.06-1.11), increasing HbA1C levels (OR 1.23, 95%CI 1.05-1.42), increasing TSH levels (OR 1.23, 95%CI 1.05-1.44), presence of hypertension (OR 2.78, 95%CI 1.51-5.11), and reduced BMI (OR 0.9, 95%CI 0.84- 0.99). The sensitivity and specificity of detecting DPN by combining VPT and MFT were 91.6% and 84.2%, respectively. The prevalence of DPN was high even in newly diagnosed T2DM and associated significantly with increasing age, HbA1C levels, TSH levels, hypertension, and reduced BMI. Earlier screening for DPN, along with aggressive control of glycemia, blood pressure, and hypothyroidism, may be beneficial.

Abstract TMP118: Aged Maternal Gut Microbiome Impairs Offspring Behavior and Exacerbates Stroke Outcome

The microbiome plays a significant role in influencing general health. A disruption of the gut biome homeostasis, dysbiosis, can be both the effect of disease or a precondition. The maternal biome has been shown to play a vital role in offspring brain and immune development by shaping the metabolic environment for the embryo. Therefore, an aged dysbiotic maternal biome may increase stroke risk factors among offspring and additionally, worsen stroke outcome. Young female C57B6 mice 3-month (M) of age had their host gut bacteria cleared via antibiotic treatment prior to recolonization via fecal microbiome transplants from 3M control, and 14M middle aged female mice. After breeding, the subsequent offspring was aged to 14 months, followed by behavioral tests, glucose tolerance, prior to a transient 60-minute middle cerebral artery occlusion (MCAO or sham surgery). The maternal biome had a significant effect on offspring biome at 2M, 6M and 9M of age, shifting the beta-diversity of females significantly (p=&lt;0.01), and males to a lesser extent (p=0.241), extending into adulthood. Additional sex specific changes were observed in adult mouse behavior with decreased motor function and increased anxiety being prevalent in male offspring at 2 months of age (p=0.0338 and 0.0261 respectively) but not in females. At 6 months of age female offspring from dysbiotic mothers exhibited significantly impaired object recognition abilities compared to control (p=&gt;0.01). Once the offspring had been subjected to a 60 min MCAO, a spontaneous recovery was observed in NDS scores in all females and in the control males, but not in males from dysbiotic mothers, suggesting that male stroke outcome is negatively affected by dysbiotic mothers. The maternal microbiome has a significant impact on offspring biome composition and health. Mice from mothers with aged microbiome exhibited sex specific early life motor function and cognitive impairment. Additionally, male offspring from dysbiotic mothers have a worsened stroke outcome.

Identification and Validation of Novel Potential Pathogenesis and Biomarkers to Predict the Neurological Outcome after Cardiac Arrest.

Predicting neurological outcomes after cardiac arrest remains a major issue. This study aimed to identify novel biomarkers capable of predicting neurological prognosis after cardiac arrest. Expression profiles of GSE29540 and GSE92696 were downloaded from the Gene Expression Omnibus (GEO) database to obtain differentially expressed genes (DEGs) between high and low brain performance category (CPC) scoring subgroups. Weighted gene co-expression network analysis (WGCNA) was used to screen key gene modules and crossover genes in these datasets. The protein-protein interaction (PPI) network of crossover genes was constructed from the STRING database. Based on the PPI network, the most important hub genes were identified by the cytoHubba plugin of Cytoscape software. Eight hub genes (RPL27, EEF1B2, PFDN5, RBX1, PSMD14, HINT1, SNRPD2, and RPL26) were finally screened and validated, which were downregulated in the group with poor neurological prognosis. In addition, GSEA identified critical pathways associated with these genes. Finally, a Pearson correlation analysis showed that the mRNA expression of hub genes EEF1B2, PSMD14, RPFDN5, RBX1, and SNRPD2 were significantly and positively correlated with NDS scores in rats. Our work could provide comprehensive insights into understanding pathogenesis and potential new biomarkers for predicting neurological outcomes after cardiac arrest.

High-Dose Vitamin D Supplementation Improves Microcirculation and Reduces Inflammation in Diabetic Neuropathy Patients.

We assessed the effect of different doses of vitamin D supplementation on microcirculation, signs and symptoms of peripheral neuropathy and inflammatory markers in patients with type 2 diabetes (T2DM). Sixty-seven patients with T2DM and peripheral neuropathy (34 females) were randomized into two treatment groups: Cholecalciferol 5000 IU and 40,000 IU once/week orally for 24 weeks. Severity of neuropathy (NSS, NDS scores, visual analogue scale), cutaneous microcirculation (MC) parameters and inflammatory markers (ILs, CRP, TNFα) were assessed before and after treatment. Vitamin D deficiency/insufficiency was detected in 78% of the 62 completed subjects. Following treatment with cholecalciferol 40,000 IU/week, a significant decrease in neuropathy severity (NSS, p = 0.001; NDS, p = 0.001; VAS, p = 0.001) and improvement of cutaneous MC were observed (p < 0.05). Also, we found a decrease in IL-6 level (2.5 pg/mL vs. 0.6 pg/mL, p < 0.001) and an increase in IL-10 level (2.5 pg/mL vs. 4.5 pg/mL, p < 0.001) after 24 weeks of vitamin D supplementation in this group. No changes were detected in the cholecalciferol 5000 IU/week group. High-dose cholecalciferol supplementation of 40,000 IU/week for 24 weeks was associated with improvement in clinical manifestation, cutaneous microcirculation and inflammatory markers in patients with T2DM and peripheral neuropathy.

Biomarkers of the development and progression of diabetic polyneuropathy

To study the diagnostic potential of brain-derived neurotrophic factor (BDNF) and vascular endothelial growth factor (VEGFA) and their high affinity receptors (TrkB, VEGFR2) in the development and progression of diabetic polyneuropathy. The main group consisted of 65 patients with diabetes mellitus and confirmed DPN. The comparison group included 14 people with diabetes mellitus without DPN. The control group consisted of 15 healthy individuals. Clinical characteristics of DPN were evaluated with VAS, PainDetect, TSS, NSS, NDS scores. The degree of polyneuropathy was verified by electroneuromyography. Serum levels of the growth factors and their receptors were studied using enzyme-linked immunosorbent assay. Elevated expression of serum BDNF, VEGFA and TrkB was found in patients with DPN, regardless of the presence of symptoms. The severe stage of DPN is characterized by painless form of polyneuropathy, the deficiency of serum BDNF, VEGFA and VEGFR2 and the high serum level of TrkB. The high expression of BDNF affects the intensity of neuropathic pain, the severity of the clinical signs of DPN and is associated with the severity of axonal damage to sensory nerve fibers. The increase in the TrkB level is associated with the painless form of neuropathy and the degree of nerve fiber demyelination. Enhanced serum expression of BDNF and VEGFA is proposed as a biomarker for the development of DPN, while different concentrations of TrkB and VEGFR2 receptors can be considered as predictors of DPN severity.

Influence of improved pterion approach on nerve function and prognosis of craniocerebral trauma patients

Objective To explore the effects of improved pterion approach on neurological function and prognosis of patients with craniocerebral trauma. Methods From July 2014 to July 2016, 100 patients with craniocerebral trauma admitted to Hangzhou Dajiang East Hospital were selected in this study, and they were divided into two groups according to different surgical methods, with 50 cases in each group.The control group was given traditional surgical approach, and the observation group was given improved pterion approach surgery.The neurological function, safety and prognosis of the two groups were observed. Results The NDS scores and GCS scores had no statistically significant differences between the two groups before treatment(t=1.03, 0.98, all P>0.05). After treatment, the NDS scores of the two groups were significantly reduced(t=5.62, 7.23, all P<0.05), the GCS scores of the two groups were significantly improved(t=3.46, 4.75, all P<0.05). The NDS score of the observation group was (13.72±5.42)points, which was significantly lower than that of the control group[(20.72±6.51)points](t=4.32, P<0.05). The GCS score of the observation group was (11.25±2.63)points, which was significantly higher than that of the control group[(8.42±1.35)points](t=3.27, P<0.05). The incidence rate of complications of the control group was significantly higher than that of the observation group[48%(24/50) vs.18%(9/50), χ2=7.36, P<0.05]. The mortality rate of the control group was significantly higher than that of the observation group[32%(15/50) vs.16%(8/50), χ2=3.17, P<0.05], and the recovery rate of the control group was significantly lower than that of the observation group[14%(7/50) vs.28%(14/50), χ2=6.35, P<0.05]. Before treatment, there were no statistically significant differences in the Spitzer index between the two groups(t=1.01, 0.98, 0.92, 0.98, 0.87, all P<0.05). After treatment, the Spitzer index of the two groups were significantly higher than those before treatment(t=2.72, 3.64, 2.83, 3.45, 3.52, 3.67, 3.84, 4.61, 4.53, 5.27, all P<0.05), which of the observation group were significantly higher than those of the control group(t=2.56, 2.73, 4.26, 4.43, 3.95, all P<0.05). Conclusion The improved pterion approach in the treatment of patients with craniocerebral trauma has better neural functional recovery than traditional surgery, and it has lower mortality rate and complication rate, better security, and can encourage patients to improve the quality of life, and it has better prognosis. Key words: Craniocerebral trauma; Surgical procedures, operativ; Glasgow coma scale; Postoperative complications; Prognosis; Comparative effectivehess research

Abstract 255: Dendrimer-Based N-Acetyl-l-Cysteine Therapy Improves 7 Days Outcomes After Cardiac Arrest in a Rat Model

Cardiac arrest (CA) entails significant risks of coma resulting in poor neurological and behavioral outcomes after resuscitation. Morbidity and mortality in post-CA patients are due largely to the cerebral dysfunction that accompanies prolonged whole-body ischemia called as post-CA syndrome (PCAS). PCAS involves strong inflammatory responses including neuroinflammation. Currently, there are no proven neuroprotective therapies to improve post-CA outcomes apart from therapeutic hypothermia. Furthermore, there are no acceptable approaches which can target neuroinflammation and lead to good neurological outcome post-CA. Moreover, delivering drugs across the blood-brain barrier to the target injured cells for treating diffuse brain injury is a major challenge. We hypothesize that dendrimer-based N-acetyl-L-cysteine (D-NAC) therapy ameliorates Neuroinflammation by specifically targeting activated glial cells and leads to a marked improvement in post-CA neurological outcome. we used an asphyxial CA rat model to determine the effects of D-NAC treatment. D-NAC was administered 30-minute post return of spontaneous circulation after cardiopulmonary resuscitation (ROSC). The behavioral neurologic deficit score (NDS score) was evaluated at 4, 24 and 48 hrs post-CA. CA resulted in a 50% decrease in survival and a dramatic decrease in NDS score acutely. D-NAC improved survival to 75% and led to a more rapid improvement in NDS scores when compared to the saline group in the short term while free NAC was not effective. We also tested long term (7 days) behavioral outcomes (novel object and fear conditioning) post-CA. Administration of D-NAC significantly improved novel object recognition and decreases freezing behavior in a novel context suggesting an improvement in cognitive deficits following CA in this model. In summary, acute administration of D-NAC following CA results in physiological and behavioral improvements both acutely and long term.

Therapeutic effect of vascular interventional therapy and aspirin combined with defibrase on cerebral ischemia in rats.

Therapeutic effect of vascular interventional therapy and aspirin combined with defibrase in the treatment of cerebral ischemia in rat model were investigated. Ninety rats were selected to establish cerebral ischemia model. Animal models were randomly divided into observation group and control group, with 45 rats in each group. Rats in observation group were treated with vascular intervention, and control group was treated with aspirin combined with defibrase. Peak systolic velocity (Vs) and end-diastolic velocity (Vd) were compared between two groups before and after 12 months of treatment. Therapeutic effects were compared before and after 6 months, and before and after 12 months of treatment. Vs and Vd of vascular lesions in observation group at 12 months were reduced after treatment, and were significantly lower than those in control group (p<0.05). After treatment, Vs and Vd in observation group were significantly reduced (p<0.05). There was no significant difference in Vs and Vd values between the groups before treatment (p>0.05). NDS scores in observation group were significantly lower than those in control group at 6 months and 1 year after treatment (p<0.05). There were no significant changes in NDS score at 6 and 12 months after treatment in control group compared with pretreatment group (p>0.05). NDS in observation group was significantly reduced at 6 and 12 months after treatment compared with pretreatment level (p<0.05). One year after treatment, incidence of cerebral infarction and transient ischemic attack and mortality in observation group were significantly lower than those in the control group (p<0.05). Intracranial vascular interventional therapy can achieve satisfactory outcomes in the treatment of cerebral ischemia, and can effectively promote nerve function recovery, and reduce the incidence of cerebrovascular diseases and mortality.

Therapeutic hypothermia promotes cerebral blood flow recovery and brain homeostasis after resuscitation from cardiac arrest in a rat model

Laboratory and clinical studies have demonstrated that therapeutic hypothermia (TH), when applied as soon as possible after resuscitation from cardiac arrest (CA), results in better neurological outcome. This study tested the hypothesis that TH would promote cerebral blood flow (CBF) restoration and its maintenance after return of spontaneous circulation (ROSC) from CA. Twelve Wistar rats resuscitated from 7-min asphyxial CA were randomized into two groups: hypothermia group (7 H, n = 6), treated with mild TH (33–34℃) immediately after ROSC and normothermia group (7 N, n = 6,37.0 ± 0.5℃). Multiple parameters including mean arterial pressure, CBF, electroencephalogram (EEG) were recorded. The neurological outcomes were evaluated using electrophysiological (information quantity, IQ, of EEG) methods and a comprehensive behavior examination (neurological deficit score, NDS). TH consistently promoted better CBF restoration approaching the baseline levels in the 7 H group as compared with the 7 N group. CBF during the first 5–30 min post ROSC of the two groups was 7 H:90.5% ± 3.4% versus 7 N:76.7% ± 3.5% (P < 0.01). Subjects in the 7 H group showed significantly better IQ scores after ROSC and better NDS scores at 4 and 24 h. Early application of TH facilitates restoration of CBF back to baseline levels after CA, which in turn results in the restoration of brain electrical activity and improved neurological outcome.

Curative efficacy of penehyclidine combined with edaravone on acute cerebral infarction and their effects on serum TNF-α and NDS score in rats.

To investigate the effects of penehyclidine combined with edaravone on acute cerebral infarction (ACI) in rats. A rat model of middle cerebral artery infarction was created. The rats were randomly divided into sham, model and treatment group. After grouping, rats in the treatment groups were treated with edaravone combined with phenecyclidine. The rats in the sham and model group were given an equal volume of phosphate-buffered saline (PBS). The therapeutic effects on rats at 3 d and 7 d after treatment were observed, the levels of serum TNF-α, interleukin-6 (IL-6) and high-mobility group box 1 protein (HMGB1) before and after treatment were compared, and the NDS scores were recorded. After treatment, the effective rate in treatment groups was higher than that in control group. The expression levels of serum TNF-α, HMGB1 and IL-6 in treatment groups showed gradually decreasing trends after treatment, and there were significant differences in the levels before and after treatment (p<0.05). At 3 d, the decrease ranges of expression levels of TNF-α, HMGB1, and IL-6 in model and treatment groups were larger than those in control group; there were statistically significant differences in the expression levels between the two groups (p<0.05). The NDS score was gradually decreased after treatment, while the activities of daily living (ADL) score were gradually increased after treatment. There were significant differences in the scores between the two groups at each time point (p<0.05). There were positive correlations of the expression levels of serum IL-6 and HMGB1 with the expression level of TNF-α (correlation coefficient=0.8731 and 0.9084, p<0.01), and there was also a positive correlation between the TNF-α level and the NDS score (correlation coefficient=0.8331, p<0.01). Penehyclidine combined with edaravone has a better clinical treatment effect on ACI rats, which can significantly reduce the levels of serum TNF-α, IL-6 and HMGB1 and the NDS score, so it is worthy of popularization in clinical application.

Effects of Three Acepromazine Doses on the Incidence of Morphine-Induced Vomiting, Sedation and Some Physiological Variables in Dogs

Background: Acepromazine was found to reduce the incidence of vomiting induced by opioids such as morphine, hydromorphone and oxymorphone in dogs. Despite the effectiveness of the phenothiazine in preventing opioid-induced vomiting in this species, a single dose of acepromazine (0.05 mg/kg) was tested and the influence of dose on the antiemetic effect of the drug is unknown. The primary objective of this study was to evaluate the effect of three acepromazine doses on the incidence of vomiting induced by morphine in dogs. A secondary aim was to assess the degree of sedation and effects on physiological variables following administration of the combinations tested.Materials, Methods &amp; Results: All dogs received 0.5 mg/kg morphine (IM). Fifteen min before morphine, dogs in the Control, ACPLD, ACPMD and ACPHD groups were administered (IM) physiological saline or acepromazine at doses of 0.025, 0.05 and 0.1 mg/kg, respectively. In Phase 1, purpose-bred dogs (n = 8) underwent each of the four treatments in a randomized, crossover design; the incidence of vomiting, sedation, pulse rate (PR), systolic, mean and diastolic blood pressures (SAP, MAP and DAP) were investigated for 60 min. Sedation was assessed by a numeric descriptive scale (NDS, range 0-3) and a simple numerical scale (SNS, range 1-10). In Phase 2, client-owned dogs (n = 50) received a single treatment and only the incidence of vomiting was assessed. There was no significant difference between groups on the incidence of vomiting recorded in Phase 1, Phase 2 and the average of Phases 1 and 2. A significant decrease in PR was observed in most groups but no significant difference was detected between groups. Blood pressure decreased in all groups; during most of the evaluation period, SAP, MAP and DAP were significantly higher in the Control than in other treatments. Dogs in this study presented mild to intense sedation. A significant difference in NDS scores was observed between the Control and ACPMD groups whereas for SNS scores, significant differences were detected between the ACPMD and ACPHD groups compared with the Control group. The number of dogs presenting intense sedation as judged by the NDS (NDS score = 3) were: 1/8, 3/8, 3/8 and 4/8 dogs in the Control, ACPLD, ACPMD and ACPHD groups, respectively.Discussion: The hypothesis of the study was rejected. The acepromazine dose did not influence the frequency of morphineinduced vomiting, the degree of sedation or cardiovascular variables after administration of either treatment. The frequency of vomiting was high (≥ 75%) in dogs of the present study regardless of the treatment administered. There was no significant difference in the frequency of vomiting in ACPLD, ACPMD and ACPHD as compared to the Control group. This finding was unexpected because it has been reported in a previous study that acepromazine reduced the incidence of opioid-induced vomiting in dogs. ACPLD, ACPMD and ACPHD improved the quality of sedation compared to the Control treatment but no significant difference in sedation scores was observed among these groups. These findings suggest that, when combined to morphine, there is no improvement in sedation when the acepromazine dose is increased above 0.025 mg/kg in dogs. Despite a significant decrease, mean values of PR, SAP, MAP and DAP remained within the physiological range for conscious dogs. In summary, none of the acepromazine doses was effective in preventing morphine-induced vomiting in dogs. Sedation is greater after acepromazine-morphine combinations than after morphine alone and is not influenced by the acepromazine dose. Cardiovascular effects induced by combinations administered in this study were well tolerated and of little clinical relevance to healthy conscious dogs.

Clinical characteristics and risk factors of diabetic peripheral neuropathy of type 1 diabetes mellitus patients.

Small nerve fibers are more easily injured than large ones for diabetic peripheral neuropathy (DPN). The study investigated the characteristics and related risk factors of DPN of T1DM patients using nerve conduction velocity and CPT values, which provided evidences for its early diagnosis. 70 T1DM patients and 48 healthy volunteers were included. All subjects accepted nerve conduction velocity and CPT examinations for four limbs. Detailed clinical indicators were recorded. CPT values were compared between TIDM group and control group. The risk factors affecting DPN were further explored. Compared with the control group, CPT values under three frequencies were decreased in T1DM group. The abnormality rate of sural nerves was higher than that of median nerves (P<0.001). Median nerve dysfunction mainly presented as hypoesthesia under 250Hz and 5Hz current stimulus. And sural nerve dysfunction mainly presented as hyperesthesia under three frequencies. Compared with left median nerve, abnormal rate of right median nerve was higher under 2000Hz current stimulus (P=0.035). However, abnormal rate of left sural nerve was higher than that of right side under 250Hz and 5Hz current stimulus (P=0.001, <0.001). Duration, NDS scores and CPT values of right median nerve under 2000Hz current stimulus were independent risk factors of abnormal nerve conduction velocity. The study proved that DPN of T1DM are mainly lower limb-injured., amyelinated and thin myelinated nerve fiber-involved. CPT can be combined with traditional nerve conduction velocity examination, which will help the diagnosis of DPN of T1DM earlier and more comprehensively.

Effects of three methadone doses combined with acepromazine on sedation and some cardiopulmonary variables in dogs

ObjectiveTo evaluate the sedative and cardiopulmonary effects of three methadone doses, combined with acepromazine, in dogs. Study designProspective, randomized, complete block study. AnimalsSix healthy, adult, cross-bred dogs weighing 17.2±4.4 kg (mean±standard deviation). MethodsEach dog was administered four treatments: acepromazine (0.05 mg kg−1) alone or acepromazine (same dose) in combination with methadone (0.25, 0.50 or 0.75 mg kg−1). All drugs were administered intramuscularly. Sedation was scored by a numeric descriptive scale (NDS, range 0–3) and a simple numerical scale (SNS, range 0–10). Heart rate, invasive blood pressure, arterial blood gases and rectal temperature were measured at 15 to 30 minute intervals for 120 minutes. ResultsAccording to NDS scores, mild to moderate sedation (NDS=1–2) was observed in most dogs in the acepromazine treatment, with only one out of six dogs scored as exhibiting intense sedation (NDS=3). All treatments with methadone resulted in significantly higher SNS scores compared with acepromazine alone. In these treatments, most dogs exhibited intense sedation (NDS=3). Increasing the dose of methadone from 0.25 to 0.50 or 0.75 mg kg−1 prolonged sedation in a dose-related manner, but did not influence the degree of sedation. The main adverse effects following administration of acepromazine–methadone treatments were decreased blood pressure, mild respiratory acidosis and decreased rectal temperature. These effects were well tolerated and resolved without treatment. Conclusions and clinical relevanceIn this study in six dogs, acepromazine–methadone administration resulted in intense sedation in most dogs. The results are interpreted to indicate that a low dose of methadone (0.25 mg kg−1) administered in combination with acepromazine (0.05 mg kg−1) will induce short-term sedation in dogs, whereas higher doses of methadone should be administered when prolonged sedation is desired.

Quantitative EEG markers in severe post-resuscitation brain injury with therapeutic hypothermia.

Therapeutic hypothermia has been regarded as one of the most effective post-cardiac arrest (CA) treatments to improve survival and functional recovery. However, many clinical prognostic markers after resuscitation have become less reliable under hypothermia. In this study, we applied and compared two developed quantitative measures - information quantity (IQ) and sub-band IQ (SIQ) - to evaluate the accuracy of EEG markers on predicting cortical recovery under therapeutic hypothermia. A total of 14 rats under 9-min asphyxial-CA, leading to severe brain injury, were randomly divided into two groups: hypothermia (32°C-34°C) and normothermia (36.5-37.5°C) (n=7 per group). For each rat, EEG and temperature were continuously recorded for the first 15 hrs. EEG was then recorded for serial 30 mins at 24, 48 and 72 hrs. The neurologic deficit score was evaluated daily to assess the neurologic recovery. Early SIQ and IQ were both significantly correlated with the 72-hr NDS, when the rats remained comatose. Both IQ and SIQ were able to discriminate the animals with good and bad functional outcomes starting from 1 hr after resuscitation. There was no significant difference in 72-hr NDS results (hypothermia (median (25th, 75th), 65 (52, 67)) versus normothermia (53.5 (52.25, 66.75))) (p>0.05) due to the high mortality rate (5/14) with severe brain injury. Contrary to IQ recovery but similarly to NDS scores, the SIQ recovery was not significantly different between the hypothermia (0.66±0.04) and normothermia (0.64±0.04) groups (p>0.05). IQ could identify the presence of high-frequency oscillations during the recovery from severe brain injury. We demonstrated that while SIQ was able to provide additional sub-band EEG information related to the recovery of different brain functions, both early IQ and SIQ markers are able to accurately predict neurologic outcome after CA.

Effects of different degrees and duration of hypothermia on traumatic brain injury in dogs

Objective To investigate the effects of different degrees and duration of hypothermia on severe traumatic brain injury in dogs. Methods Thirty-six one-year-old healthy dogs weighing 13-15 kg were used in this study. Traumatic brain injury model was estabhshed according to the method described by Feeney. Orthogonal design was used in this experiment. Two empirical factors: temperature (factor A) and duration (factor B) were used. Body temperature was maintained at 38 ℃ (A1), 31 ℃ (A2) or35 ℃ (A3) for 6 h (B1) or 12 h (B2).The dogs were divided into 6 groups: group A1B1 , A1B2, A2B1, A2B2, A3B1 and A3B2. Blood gas analysis was performed after the target temperature was maintained for the target duration. Neurological deficit was assessed and scored (0 = no deficit, 500 = severe neurological deficit) and blood samples were obtained at 24, 48 and 72 h after brain injury for determination of serum concentrations of neuron-specific enolase (NSE) and myelin basic protein (MBP) and plasma S-100β protein concentration. Brains were removed at the 72 h after brain injury for determination of Bcl-2 and Bax expression and detection of apoptosis in the brain. Results Hypothermia significantly decreased serum NSE, MBP and plasma S-100β concentrations, neuronal apoptosis and NDS scores;up-regulated Bcl-2 expression and down-regulated Bax expression in brain tissue in the 4 hypothermia groups (group A2B1, A2B2, A3B1 and A3B2) as compared with the control groups (group A1 B1, A1 B2). Best neuroprotective effects were observed in group A3 B1 (35 ℃ for 6 h) in terms of serum NSE, NBP and plasma S-100β concentrations, neuronal apoptosis and cerebral Bax and Bcl-2 expression, but there was no significant difference in the NDS scores among the 4 hypothermia groups. Conclusion Hypothermia can provide neuroprotection in a dog model of traumatic brain injury but the neuroprotective effect is independent of the degree and duration of hypothermia. Key words: Hypothermia, induced; Brain injuries

Postoperative analgesic effects of epidural administration of neostigmine alone or in combination with morphine in ovariohysterectomized dogs

To evaluate analgesic effects of epidurally administered neostigmine alone or in combination with morphine in dogs after ovariohysterectomy. Animals-40 healthy bitches. After acepromazine premedication, anesthesia was induced. Dogs randomly received 1 of the following 4 epidural treatments 30 minutes before ovariohysterectomy (n = 10/group): saline (0.9% NaCl) solution (control), morphine (0.1 mg/kg), neostigmine (10 microg/kg), or morphine-neostigmine (0.1 mg/kg and 10 microg/kg, respectively). Analgesia was assessed for 24 hours after surgery by use of a visual analogue scale (VAS; scale of 0 to 10) or numeric descriptive scale (NDS; scale of 0 to 24) and by the need for supplemental analgesia (morphine [0.5 mg/kg, IM] administered when VAS was > or = 4 or NDS was > or = 8). Significantly more control dogs (n = 8) received supplemental analgesia, compared with the number of neostigmine-treated dogs (1); no dogs in the remaining groups received supplemental analgesia. Compared with values for the control dogs, the NDS scores were lower for morphine-neostigmine-treated dogs (from 2 to 6 hours and at 12 hours) and for morphine-treated dogs (all time points). The NDS scores were lower for morphine-treated dogs at 3, 12, and 24 hours, compared with values for neostigmine-treated dogs. The VAS was less sensitive than the NDS for detecting differences among groups. Epidurally administered neostigmine reduced the use of supplemental analgesia after ovariohysterectomy in dogs. However, analgesic effects were less pronounced than for epidurally administered morphine or morphine-neostigmine. Adding neostigmine to epidurally administered morphine did not potentiate opioid-induced analgesia.

Metamotivational dominance, states and injuries in risk and safe sports

Male risk sport participants (36 snowboarders) were compared with male safe sport participants (26 badminton players) using the Telic Dominance Scale [Murgatroyd, S., Rushton, C., Apter, M.J., and Ray, C. (1978) The development of the telic dominance scale. Journal of Personality Assessment, 42, 519–527] and the Negativistic Dominance Scale [McDermott, M.R., and Apter, M. J. (1988). The Negativism Dominance Scale. In M. J. Apter, J.H. Kerr, and M.P. Cowles (Eds.), Progress in reversal theory. Amsterdam: North-Holland] and the Telic/Paratelic State Instrument. Subjects also completed an Injury Behaviour Checklist giving information on the objective risk of the sports pursued. Risk sportsmen scored significantly lower than safe sportsmen on the TDS total score and on the Serious-Mindedness and Arousal Avoidance subscales, but there were no significant differences in Planning Orientation. Risk sportsmen scored significantly higher than safe on total NDS and on the Proactive subscale but not on the Reactive subscale. Analysis of T/PSI scores showed that both groups remained in their dominant state throughout the time course of the investigation. Risk sportsmen received more frequent and more serious injuries throughout the period of study and both TDS and NDS scores were significantly correlated with number of injuries. Discussion of high-risk sport as a way of meeting arousal, escape and control needs, and as expressing rebellion is related to values and stereotypes involved in risky sports and to implications in identifying possible addictions and preventing injuries.

Neurodevelopmental screening of in utero growth-retarded prematurely born children before school age.

As part of a prospective follow-up study of two premature cohorts (gestational age less than or equal to 36 weeks) born between 1976 and 1977, designed to evaluate the effects of IUGR on morbidity, mortality and neurological development in prematurely born children, 71 prematurely born children (48 AGA, 23 IUGR) without major neurological handicaps were subjected to detailed assessment of their neurological and psychological status at the age of 4 years. Thirty-six healthy full-term children formed a control group. The socioeconomic status of the families of the premature groups was similar to that of the families of the control group. The assessment consisted of a neurodevelopmental screening test and four psychological tests. Validation of the NDS test in relation to proven cognitive problems (sensitivity 96%, specificity 64%, relative risk 16.74) and determination of normal ranges were based on findings in the control group. There were significantly more children with moderate to high risk scores (greater than or equal to 10) among the IUGR group than among the AGA group. The neurodevelopmental profile of the preterm IUGR group was characterized by complex deviations of motor, visual and perceptual functions from normal. Preterm AGA children had only slightly higher risk scores in relation to fine motor, upper motor and perceptive functions than control children. Of the various perinatal factors studied, IUGR (especially in relation to boys who needed respirator therapy) was the most likely to be associated with abnormal NDS scores before school age.