Characterization of basal forebrain glutamate neurons suggests a role in control of arousal and avoidance behavior.

The basal forebrain (BF) is involved in arousal, attention, and reward processing but the role of individual BF neuronal subtypes is still being uncovered. Glutamatergic neurons are the least well-understood of the three main BF neurotransmitter phenotypes. Here we analyzed the distribution, size, calcium-binding protein content and projections of the major group of BF glutamatergic neurons expressing the vesicular glutamate transporter subtype 2 (vGluT2) and tested the functional effect of activating them. Mice expressing Cre recombinase under the control of the vGluT2 promoter were crossed with a reporter strain expressing the red fluorescent protein, tdTomato, to generate vGluT2-cre-tdTomato mice. Immunohistochemical staining for choline acetyltransferase and a cross with mice expressing green fluorescent protein selectively in GABAergic neurons confirmed that cholinergic, GABAergic and vGluT2+ neurons represent distinct BF subpopulations. Subsets of BF vGluT2+ neurons expressed the calcium-binding proteins calbindin or calretinin, suggesting that multiple subtypes of BF vGluT2+ neurons exist. Anterograde tracing using adeno-associated viral vectors expressing channelrhodopsin2-enhanced yellow fluorescent fusion proteins revealed major projections of BF vGluT2+ neurons to neighboring BF cholinergic and parvalbumin neurons, as well as to extra-BF areas involved in the control of arousal or aversive/rewarding behavior such as the lateral habenula and ventral tegmental area. Optogenetic activation of BF vGluT2+ neurons elicited a striking avoidance of the area where stimulation was given, whereas stimulation of BF parvalbumin or cholinergic neurons did not. Together with previous optogenetic findings suggesting an arousal-promoting role, our findings suggest that BF vGluT2 neurons play a dual role in promoting wakefulness and avoidance behavior.

Historic cohort: outcome of chronic exertional compartment syndrome-suspected patients.

INTRODUCTION: Exercise-related leg pain (ERLP) may be caused by chronic exertional compartment syndrome (CECS), occurring mainly in athletes and military recruits. In military populations, the effectiveness of surgical treatment in CECS is debated. The purpose of this study is to assess the outcome of surgical treatment for CECS in Alrijne Hospital (the Netherlands), a civilian hospital with supraregional referral function. METHODS: A historic cohort study was performed on patients with ERLP who were suspected for CECS and were referred for intracompartmental pressure measurement (ICPM) from 2013 to 2017 (n=160). Patient demographics, ICPM and survey response were analysed. RESULTS: The mean delay before visitation was 29.0±30.3 months. When comparing surgical-treated patients with CECS with conservative-treated patients with ERLP, surgical-treated patients were more satisfied, reported better recovery towards former level of performance (2.8±2.0 vs 3.9±1.7 and 2.5±1.6 vs 3.2±1.4 on a 7-point Likert scale, respectively) and better subjective injury status (79.3±22.6 vs 63.5±27.4 using the Single Assessment Numeric Evaluation score). Treatment satisfaction was 75.0% in surgical-treated CECS versus 51.4% in conservative-treated ERLP. CONCLUSION: Civilian patients report improved functional outcomes after fasciotomy for CECS. Future research should focus on non-invasive diagnostic options and methods to determine which treatment is the most appropriate for each individual patient.

Activation of basal forebrain purinergic P2 receptors promotes wakefulness in mice.

The functions of purinergic P2 receptors (P2Rs) for extracellular adenosine triphosphate (ATP) are poorly understood. Here, for the first time, we show that activation of P2Rs in an important arousal region, the basal forebrain (BF), promotes wakefulness, whereas inhibition of P2Rs promotes sleep. Infusion of a non-hydrolysable P2R agonist, ATP-γ-S, into mouse BF increased wakefulness following sleep deprivation. ATP-γ-S depolarized BF cholinergic and cortically-projecting GABAergic neurons in vitro, an effect blocked by antagonists of ionotropic P2Rs (P2XRs) or glutamate receptors. In vivo, ATP-γ-S infusion increased BF glutamate release. Thus, activation of BF P2XRs promotes glutamate release and excitation of wake-active neurons. Conversely, pharmacological antagonism of BF P2XRs decreased spontaneous wakefulness during the dark (active) period. Together with previous findings, our results suggest sleep-wake regulation by BF extracellular ATP involves a balance between excitatory, wakefulness-promoting effects mediated by direct activation of P2XRs and inhibitory, sleep-promoting effects mediated by degradation to adenosine.

The menagerie of the basal forebrain: how many (neural) species are there, what do they look like, how do they behave and who talks to whom?

The diverse cell-types of the basal forebrain control sleep-wake states, cortical activity and reward processing. Large, slow-firing, cholinergic neurons suppress cortical delta activity and promote cortical plasticity in response to reinforcers. Large, fast-firing, cortically-projecting GABAergic neurons promote wakefulness and fast cortical activity. In particular, parvalbumin/GABAergic neurons promote neocortical gamma band activity. Conversely, excitation of slower-firing somatostatin/GABAergic neurons promotes sleep through inhibition of cortically-projecting neurons. Activation of glutamatergic neurons promotes wakefulness, likely by exciting other cortically-projecting neurons. Similarly, cholinergic neurons indirectly promote wakefulness by excitation of wake-promoting, cortically-projecting GABAergic neurons and/or inhibition of sleep-promoting somatostatin/GABAergic neurons. Both glia and neurons increase the levels of adenosine during prolonged wakefulness. Adenosine presynaptically inhibits glutamatergic inputs to wake-promoting cholinergic and GABAergic/parvalbumin neurons, promoting sleep.

A phase I, open-label, dose-escalation, multicenter study of the JAK2 inhibitor NS-018 in patients with myelofibrosis.

NS-018 is a Janus-activated kinase 2 (JAK2)-selective inhibitor, targeting the JAK-signal transducer and activator of transcription (STAT) pathway that is deregulated in myelofibrosis. In this phase I, dose-escalation portion of a phase I/II study, patients with myelofibrosis received oral NS-018 in continuous 28-day cycles. The primary study objective was to evaluate safety, tolerability and clinically active dose of NS-018. Forty-eight patients were treated; 23 (48%) had previously received a JAK inhibitor (JAKi). The most common drug-related adverse events were thrombocytopenia (27%)/anemia (15%) for hematologic events, and dizziness (23%)/nausea (19%) for non-hematologic events. Once daily NS-018 at 300 mg was chosen as the phase II study dose based on improved tolerability compared with higher doses. A ⩾50% reduction in palpable spleen size was achieved in 56% of patients (47% of patients with prior JAKi treatment), and improvements were observed in myelofibrosis-associated symptoms. Bone marrow fibrosis grade (local assessment) improved from baseline in 11/30 evaluable patients (37%) after 3 cycles of NS-018. JAK2 allele burden was largely unchanged. Changes in cytokine/protein levels were noted after 4 weeks of treatment. NS-018 reached peak plasma concentration in 1-2 h and did not accumulate with multiple dosing. NS-018 will be assessed in patients with previous JAKi exposure in the phase II portion.

Home-based vs inpatient education for children newly diagnosed with type 1 diabetes.

BACKGROUND: Initial management of children diagnosed with type 1 diabetes (T1D) varies worldwide with sparse high quality evidence regarding the impact of different models of care. AIM: To compare the inpatient model of care with a hybrid home-based alternative, examining metabolic and psychosocial outcomes, diabetes knowledge, length of stay, and patient satisfaction. SUBJECTS AND METHODS: The study design was a randomized-controlled trial. Inclusion criteria were: newly diagnosed T1D, aged 3 to 16 years, living within approximately 1 hour of the hospital, English-speaking, access to transport, absence of significant medical or psychosocial comorbidity. Patients were randomized to standard care with a 5 to 6 day initial inpatient stay or discharge after 2 days for home-based management. All patients received practical skills training in the first 48 hours. The intervention group was visited twice/day by a nurse for 2 days to assist with injections, then a multi-disciplinary team made 3 home visits over 2 weeks to complete education. Patients were followed up for 12 months. Clinical outcomes included HbA1c, hypoglycemia, and diabetes-related readmissions. Surveys measured patient satisfaction, diabetes knowledge, family impact, and quality of life. RESULTS: Fifty patients were recruited, 25 to each group. There were no differences in medical or psychosocial outcomes or diabetes knowledge. Average length of admission was 1.9 days shorter for the intervention group. Families indicated that with hindsight, most would choose home- over hospital-based management. CONCLUSIONS: With adequate support, children newly diagnosed with T1D can be safely managed at home following practical skills training.

Necrotising fasciitis due to an infected sebaceous cyst.

The current case presents a patient who was admitted to our hospital with the diagnosis of cellulitis of the right groin. In the following days, the patient's condition deteriorated and developed a septic shock. Exploration in the operating room showed a necrotising fasciitis of the adductor muscles, with an infected sebaceous cyst in the inguinal crest as port d'entrée. After extensive surgical debridement, antibiotic therapy, haemodynamic and respiratory support, the patient recovered. Necrotising fasciitis is a rare but very lethal condition, which necessitates aggressive surgical therapy and antibiotic support. The current case report is the first report to show a necrotising fasciitis due to an infected sebaceous cyst.

Adenosine inhibits the excitatory synaptic inputs to Basal forebrain cholinergic, GABAergic, and parvalbumin neurons in mice.

Coffee and tea contain the stimulants caffeine and theophylline. These compounds act as antagonists of adenosine receptors. Adenosine promotes sleep and its extracellular concentration rises in association with prolonged wakefulness, particularly in the basal forebrain (BF) region involved in activating the cerebral cortex. However, the effect of adenosine on identified BF neurons, especially non-cholinergic neurons, is incompletely understood. Here we used whole-cell patch-clamp recordings in mouse brain slices prepared from two validated transgenic mouse lines with fluorescent proteins expressed in GABAergic or parvalbumin (PV) neurons to determine the effect of adenosine. Whole-cell recordings were made from BF cholinergic neurons and from BF GABAergic and PV neurons with the size (>20 µm) and intrinsic membrane properties (prominent H-currents) corresponding to cortically projecting neurons. A brief (2 min) bath application of adenosine (100 µM) decreased the frequency but not the amplitude of spontaneous excitatory postsynaptic currents (EPSCs) in all groups of BF cholinergic, GABAergic, and PV neurons we recorded. In addition, adenosine decreased the frequency of miniature EPSCs in BF cholinergic neurons. Adenosine had no effect on the frequency of spontaneous inhibitory postsynaptic currents in cholinergic neurons or GABAergic neurons with large H-currents but reduced them in a group of GABAergic neurons with smaller H-currents. All effects of adenosine were blocked by a selective, adenosine A1 receptor antagonist, cyclopentyltheophylline (CPT, 1 µM). Adenosine had no postsynaptic effects. Taken together, our work suggests that adenosine promotes sleep by an A1 receptor-mediated inhibition of glutamatergic inputs to cortically projecting cholinergic and GABA/PV neurons. Conversely, caffeine and theophylline promote attentive wakefulness by inhibiting these A1 receptors in BF thereby promoting the high-frequency oscillations in the cortex required for attention and cognition.

Control of sleep and wakefulness.

This review summarizes the brain mechanisms controlling sleep and wakefulness. Wakefulness promoting systems cause low-voltage, fast activity in the electroencephalogram (EEG). Multiple interacting neurotransmitter systems in the brain stem, hypothalamus, and basal forebrain converge onto common effector systems in the thalamus and cortex. Sleep results from the inhibition of wake-promoting systems by homeostatic sleep factors such as adenosine and nitric oxide and GABAergic neurons in the preoptic area of the hypothalamus, resulting in large-amplitude, slow EEG oscillations. Local, activity-dependent factors modulate the amplitude and frequency of cortical slow oscillations. Non-rapid-eye-movement (NREM) sleep results in conservation of brain energy and facilitates memory consolidation through the modulation of synaptic weights. Rapid-eye-movement (REM) sleep results from the interaction of brain stem cholinergic, aminergic, and GABAergic neurons which control the activity of glutamatergic reticular formation neurons leading to REM sleep phenomena such as muscle atonia, REMs, dreaming, and cortical activation. Strong activation of limbic regions during REM sleep suggests a role in regulation of emotion. Genetic studies suggest that brain mechanisms controlling waking and NREM sleep are strongly conserved throughout evolution, underscoring their enormous importance for brain function. Sleep disruption interferes with the normal restorative functions of NREM and REM sleep, resulting in disruptions of breathing and cardiovascular function, changes in emotional reactivity, and cognitive impairments in attention, memory, and decision making.

Sleep fragmentation reduces hippocampal CA1 pyramidal cell excitability and response to adenosine.

Sleep fragmentation (SF) impairs the restorative/cognitive benefits of sleep via as yet unidentified alterations in neural physiology. Previously, we found that hippocampal synaptic plasticity and spatial learning are impaired in a rat model of SF which utilizes a treadmill to awaken the animals every 2 min, mimicking the frequency of awakenings observed in human sleep apnea patients. Here, we investigated the cellular mechanisms responsible for these effects, using whole-cell patch-clamp recordings. 24h of SF decreased the excitability of hippocampal CA1 pyramidal neurons via decreased input resistance, without alterations in other intrinsic membrane or action potential properties (when compared to cage controls, or to exercise controls that experienced the same total amount of treadmill movement as SF rats). Contrary to our initial prediction, the hyperpolarizing response to bath applied adenosine (30 microM) was reduced in the CA1 neurons of SF treated rats. Our initial prediction was based on the evidence that sleep loss upregulates cortical adenosine A1 receptors; however, the present findings are consistent with a very recent report that hippocampal A1 receptors are not elevated by sleep loss. Thus, increased adenosinergic inhibition is unlikely to be responsible for reduced hippocampal long-term potentiation in SF rats. Instead, the reduced excitability of CA1 pyramidal neurons observed here may contribute to the loss of hippocampal long-term potentiation and hippocampus-dependent cognitive impairments associated with sleep disruption.

Efficacy and safety of dasatinib in imatinib-resistant or -intolerant patients with chronic myeloid leukemia in blast phase.

Dasatinib is an inhibitor of BCR-ABL and SRC-family kinases for patients with imatinib-resistant or -intolerant chronic myelogenous leukemia (CML). In this international phase II trial, dasatinib was administered orally (70 mg twice daily) to patients with myeloid blast phase (MBP, n=109) or lymphoid blast phase (LBP, n=48) CML. After a minimum follow-up of 12 months (range 0.03-20.7 months), major hematologic responses were induced in 34% (MBP-CML) and 35% (LBP-CML) of patients. Major cytogenetic responses were attained in 33% (MBP-CML) and 52% (LBP-CML) of patients and complete cytogenetic responses were attained in 26 and 46%, respectively. Median progression-free survival was 6.7 (MBP-CML) and 3.0 (LBP-CML) months. Median overall survival was 11.8 (MBP-CML) and 5.3 (LBP-CML) months. Overall, dasatinib had acceptable tolerability. Fluid retention events were more frequent in the MBP-CML than the LBP-CML cohort: pleural effusion occurred in 36 and 13% (all grades) and 15 and 6% (grades 3/4), respectively. Other non-hematologic side effects were primarily grade 1/2; grade 3/4 events were recorded in

Cytokine upregulation of proteinase-activated-receptors 2 and 4 expression mediated by p38 MAP kinase and inhibitory kappa B kinase beta in human endothelial cells.

BACKGROUND AND PURPOSE: Up-regulation of proteinase-activated receptor-2 (PAR2) is a factor in a number of disease states and we have therefore examined the signalling pathways involved in the expression of the receptor. EXPERIMENTAL APPROACH: We investigated the effects of tumour necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), trypsin and the PAR2 activating peptide, 2-furoyl(2f)-LIGKV-OH on both mRNA and functional expression of PAR2 in human umbilical vein endothelial cells (HUVECs). The effect of specific chemical inhibitors and dominant negative adenovirus constructs of the mitogen-activated protein kinase (MAPK) cascade and the nuclear factor kappa B (NF-kappaB) signalling pathway was assessed. Methods included semi-quantitative and quantitative RT-PCR, [(3)H]inositol phosphate (IP) accumulation and Ca(2+)-dependent fluorescence. KEY RESULTS: The above agonists induced both mRNA and functional expression of PAR2; PAR4 mRNA, but not that for PAR1 or PAR-3, also increased following TNFalpha treatment. Inhibition of p38 MAP kinase reduced PAR2 and PAR4 expression, whilst inhibition of MEK1/ERK/JNK was without effect. A similar dependency upon p38 MAP kinase was observed for the expression of PAR4. TNFalpha -induced enhancement of PAR2 stimulated [(3)H]-inositol phosphate accumulation (IP) and Ca(2+) signalling was abolished following SB203580 pre-treatment. Infection with adenovirus encoding dominant-negative IKKbeta (Ad.IKKbeta(+/-)) and to a lesser extent dominant-negative IKKalpha (Ad.IKKalpha(+/-)), substantially reduced both control and IL-1beta- induced expression of both PAR2 and PAR4 mRNA and enhancement of PAR2-stimulated IP accumulation and Ca(2+) mobilisation. CONCLUSIONS AND IMPLICATIONS: These data reveal for the first time the signalling events involved in the upregulation of both PAR2 and PAR4 during pro-inflammatory challenge.

Mechanisms of resistance to imatinib in CML patients: a paradigm for the advantages and pitfalls of molecularly targeted therapy.

One of the challenges of cancer therapeutics is to discover targets unique to the tumor cell population. Constitutively activated tyrosine kinases play a role in the malignant phenotype in a number of different cancers. While the kinases may be present in the normal cell, the cancer cell is often dependent upon the activation of the kinase for the maintenance of malignant growth. Inhibition of kinase activation may therefore selectively inhibit malignant proliferation. In the case of chronic myelogenous leukemia (CML), the activated tyrosine kinase (BCR-ABL) is due to a chromosomal translocation that defines this disease, and is necessary for malignant transformation. Imatinib mesylate (Gleevec, Novartis) is a small molecule tyrosine kinase inhibitor, developed through the chemical modification to be selected for a small number of tyrosine kinases present in human cells. This agent is also orally bioavailable and has been found to be effective in clinical trials. We have learned much through the clinical use of this agent. 1) Specific targeting of activated signal transduction pathways may be effective in inhibiting cancer cells. 2) Cancer cells may not only be inherently resistant to small molecule inhibitors, but may also develop resistance after exposure to the inhibitor. 3) Increased knowledge regarding critical signal transduction pathways, the structure of the molecules that are being targeted and the inhibitors themselves, will allow us to understand resistance as it develops and create new molecules to bypass resistance. We will discuss imatinib as an important example of the success and pitfalls of targeted therapeutics for cancer.

Issues for military women in deployment: an overview.

The stresses of deployment affect both sexes, but some are either mildly or markedly different for women. These include certain female health and gynecological issues, nursing, and pregnancy. Separation from small children, isolation, the possibility of sexual assault, and risks of combat or being taken hostage are concerns for both genders. All of these issues should be addressed before and during deployment to ensure optimal individual and unit functioning and improve retention. Gynecological infections, redeployment for abnormal Papanicolaou smears, and pregnancy while on deployment can be avoided with proper hygiene and planning. There are resources available in pamphlet form, electronically, and on CD-ROM to help prepare service members, leaders, and health care personnel. Improvements in the ability to maintain personal hygiene and to communicate home should benefit both sexes.

Intraoperative vs postoperative morphine improves analgesia without increasing PONV on emergence from ambulatory surgery.

PURPOSE: To compare the timing of administration of morphine in patients undergoing painful ambulatory surgical procedures to determine whether there was a difference in postoperative nausea or vomiting (PONV), quality of analgesia, and recovery profile. METHODS: In a double-blinded, placebo-controlled, prospective study, 70 ASA I-II patients were randomized to receive 0.1 mg x kg(-1) morphine intraoperatively (lop) (n=35), or postoperatively (Pop) (n=35). The severity of nausea and pain were measured using visual analog scales (VAS). RESULTS: There was no difference between the groups in postoperative nausea scores or the incidence of PONV. Upon awakening, patients who received Pop morphine had higher pain VAS scores with movement (7.6 +/- 2 vs 5.4 +/- 3, P < 0.003) and at rest (6.9 +/- 3 vs 5.1 +/- 3, P < 0.013) than the lop morphine group. The total number of PCA attempts and analgesic requirements were similar. Patients who received Pop morphine were able to drink sooner than the lop group (90 +/- 34 vs 111 +/- 38 min, P < 0.05). All other recovery milestones were similar. Times to discharge from hospital were similar. CONCLUSIONS: Administration of 0.1 mg x kg(-1) morphine iv intraoperatively improves postoperative analgesia upon emergence from painful ambulatory surgical procedures without increasing the incidence of PONV There was no increase in PONV when morphine was administered intraoperatively rather than postoperatively.

Continuous administration of angiostatin inhibits accelerated growth of colorectal liver metastases after partial hepatectomy.

Human plasminogen-derived angiostatin is one of the most potent antiangiogenic agents currently known. However, it is unclear whether angiostatin is also effective against accelerated tumor growth induced by local up-regulation of growth factors, including angiogenesis stimulators, such as in regenerating liver. Prior to addressing this question, we tested, in mice, whether continuous administration of angiostatin could improve its biological effects. This assumption was based on the relatively short half-life of angiostatin in mice, as well as on the theoretical necessity to suppress tumor-induced angiogenesis continually. The findings presented here clearly indicate continuous administration to be superior to the conventional twice-daily bolus injections. Using the maximally effective regimen of 100 mg/kg/day via s.c. pump infusion, we found angiostatin to not only suppress s.c. primary tumors but also to significantly inhibit the outgrowth of colorectal hepatic metastases in resting liver and even to inhibit accelerated tumor growth in regenerating liver after 70% partial hepatectomy. In conclusion, angiostatin could play an important role in patients subjected to partial hepatectomy to prevent outgrowth of residual micrometastases, provided it is administered continuously to obtain maximal biological effects.

Postoperative pain in ambulatory surgery.

UNLABELLED: Postoperative pain is a common reason for the delayed discharge and unanticipated hospital admission of out-patients. In this study, we examined the pattern of pain in ambulatory surgical patients and determined those factors that predict postoperative pain. Ten thousand eight consecutive ambulatory surgical patients were prospectively studied. Preoperative patient characteristics, intraoperative variables, and pain in the postanesthesia care unit (PACU) and the ambulatory surgical unit (ASU) and 24 h postoperatively were documented. The incidence of severe pain was 5.3% in the PACU, 1.7% in the ASU, and 5.3% 24 h postoperatively. In the PACU, younger male adults (36 +/- 13 vs 47 +/- 22 yr), ASA physical status I patients, and patients with a higher body mass index (26 +/- 5 vs 25 +/- 5 kg) had a higher incidence of severe pain. In the group with severe pain, the duration of anesthesia, the duration of stay in the PACU and the ASU, and the time to discharge was longer than in the group without severe pain. In the PACU, orthopedic patients had the highest incidence of pain (16.1%), followed by urologic (13.4%), general surgery (11.5%), and plastic surgery (10.0%) patients. In patients who had general anesthesia, the intraoperative dose of fentanyl was significantly smaller in the group with severe pain than in the group without severe pain when body mass index and duration of anesthesia were taken into consideration. Body mass index, duration of anesthesia, and certain types of surgery were significant predictors of severe pain in the PACU. This knowledge will allow us to identify those patients at risk of severe postoperative pain and manage them prophylactically. IMPLICATIONS: The pattern of pain was examined in 10,008 consecutive ambulatory surgical patients. The incidence of severe pain was 5.3% in the postanesthesia care unit, 1.7% in the ambulatory surgical unit, and 5.3% 24 h postoperatively. Body mass, duration of anesthesia, and certain types of surgery were significant predictors of pain in the postanesthesia care unit. These data will allow us to better predict those patients who need intense prophylactic analgesic therapy.

Suprascapular nerve block for postoperative pain relief in arthroscopic shoulder surgery: a new modality?

Arthroscopic shoulder surgery has a 45% incidence of severe postoperative pain. Opiates and interscalene nerve blocks have a high incidence of side effects, and intraarticular local anesthetic has been shown to be ineffective when used for postoperative pain relief. The suprascapular nerve supplies 70% of the sensory nerve supply to the shoulder joint, and local anesthetic block of this nerve is effective in certain shoulder pain disorders. To determine the efficacy of a suprascapular nerve block, subcutaneous saline was compared with a suprascapular nerve block using 10mL of 0.5% bupivacaine with 1:200,000 epinephrine before general anesthesia was induced. In the immediate postoperative period, a 51% reduction in demand and a 31% reduction in consumption of morphine delivered by a patient-controlled analgesic system was demonstrated. There was more than fivefold reduction in the incidence of nausea, as well as reduced visual analog and verbal pain scores for patients who received a suprascapular nerve block. The duration of hospital stay was reduced by 24% in the suprascapular nerve block group. A 24-h phone call interview revealed a 40% reduction in analgesic consumption and a reduction in verbal pain scores at rest and on abduction. There were no complications from the suprascapular nerve block. This study demonstrates that a suprascapular nerve block for pain relief in arthroscopic shoulder surgery is an effective and safe modality of postoperative pain relief.