[Acute Psychosis after Consumption of Synthetic Cannabinoids]. / Akute Psychose nach Konsum von synthetischen Cannabinoiden.

INTRODUCTION: Mocarz is a Legal high that consists of dried parts of plants mixed with synthetic cannabinoids. There is currently limited information on its acute toxicity. CASE REPORT: We describe a 35-year-old patient with no previous medical and psychiatric history who was admitted to the psychiatric clinic after developing agitation and paranoid psychotic symptoms following the use of Mocarz purchased over the internet. CONCLUSION: Legal highs are a challenge in psychiatric acute care, because they provoke unpredictable mental states endangering self and others.

[Optimising pain therapy for neurological inpatients]. / Optimierung der Schmerztherapie an neurologischen Stationen.

BACKGROUND: The Department of Neurology at the Medical University Graz has implemented a multiprofessional pain management concept and evaluated the outcome by means of a patient survey. METHODS: Standard operating procedures for standardised pain measurement, documentation and therapy were developed. All engaged professional participants were trained before implementation. RESULTS: 88.7 % of the surveyed 63 patients reported pain during the hospitalisation. During the night and in the morning, the occurrence of severe pain was most likely. The position or activity most likely triggering severe pain was mobilisation (19 %). Patients with degenerative diseases of the spine without radiculopathy reported the highest levels of pain. CONCLUSIONS: Pain is an important problem for neurological inpatients. Nocturnal pain, pain induced by mobilisation, and pain therapy for patients with degenerative diseases of the spine without radiculopathy require particular attention.

[Poststroke-bipolar affective disorder]. / Poststroke-Bipolar affektive Erkrankung.

A few weeks after suffering from a basal ganglia infarction (globus pallidus) with left-sided hemiplegia, a 23-year-old woman exhibited for the first time a pronounced mania with self-endangerment. The use of oral contraceptives was the only determinable risk factor. During the further course, the mother also developed a depressive disorder. Thus a certain genetic predisposition for affective disorders may be relevant, although this would not explain the outbreak by itself. An association between the right-sided basal ganglia infarction and the occurrence of a bipolar affective disorder has been described in the literature. Vascular or, respectively, inflammatory risk factors in synopsis with the aetiopathogenesis of bipolar affective disorders are also discussed in depth in this case report.

Preoperative interscalene block for elective shoulder surgery: loss of benefit over early postoperative block after patient discharge to home.

UNLABELLED: We performed a randomized, prospective, parallel-group, open-label, multicenter trial to compare the effects of pre- versus postoperative interscalene block using levobupivacaine on postoperative pain and analgesic requirements. One-hundred-two outpatients scheduled for elective shoulder surgery were randomized to receive 30 mL of 0.5% levobupivacaine either preoperatively (PRE group) or postoperatively (POST group). Analgesic outcome measures during the postoperative period were: (a). time to first request for analgesic medication after surgery, (b). pain intensity using the visual analog scale at rest and during arm movement, and (c). total analgesic consumption of nonsteroidal antiinflammatory drugs and opioids. The time to first analgesic request did not differ between treatment groups. However, mean maximum pain intensity scores during the day of surgery were significantly less for the PRE group than the POST group, both at rest (P = 0.001) and after movement (P = 0.004). The mean opioid administered during surgery was lower in the PRE than the POST group (P < 0.001). Levobupivacaine was well tolerated in both treatment groups, and no adverse reactions were related to this local anesthetic. In conclusion, preoperative interscalene block with levobupivacaine provided superior pain control for the first 12 h after surgery, but this benefit was not maintained during the week after discharge because the subjects assumed control of their own pain relief as outpatients. IMPLICATIONS: Preoperative interscalene block with levobupivacaine provides safe and effective analgesia for same-day elective shoulder surgery, but the benefit of this one-time intervention does not persist.

Tratamiento del dolor agudo postoperatorio: protocolos y procedimientos del New England Medical Center de Boston / Management of postoperative acute pain: protocols and procedures at the New England Center of Boston

El dolor agudo postoperatorio puede ser tratado de diversas maneras. El New England Medical Center de Boston, Massachussetts, ha optado por un modelo basado en las recomendaciones de la Asociación Internacional para el Estudio del Dolor, la Sociedad Americana del Dolor y la Agencia para la política y la investigación en Salud del departamento de Salud de los Estados Unidos. Este manual es, en primer lugar, una guía para orientar a los residentes que rotan por primera vez por el área de Dolor Agudo; y, en segundo lugar, un resumen de los protocolos y procedimientos específicos del Servicio (AU)

Alterations in neuropeptide Y, tyrosine hydroxylase, and Y-receptor subtype distribution following spinal nerve injury to rats.

Recent animal models of experimental nerve injury have proven useful in evaluating potential sympathetic involvement in neuropathic pain syndromes. We have employed a widely adopted unilateral L5/L6 spinal nerve ligation model to compare the development of mechanical allodynia with neurochemical changes both at the site of peripheral nerve injury and in the dorsal root ganglia (DRG). We have focused on the expression of neuropeptide Y (NPY), a well-studied regulatory peptide and phenotypic marker of sympathetic neurons, and functionally related Y-receptor binding sites following nerve injury. In sympathetic neurons, NPY is colocalized and coreleased with norepinephrine (NE) at peripheral sites of action. Furthermore, NPY gene expression is induced within the population of medium- and large-diameter DRG neurons of the A beta-fiber class after experimental nerve injury. We therefore hypothesized that concurrent alterations in NPY and NE expression by sympathetic and sensory neurons may be a contributing factor to sympathetically-maintained neuropathic conditions. Animals with unilateral L5/L6 spinal nerve ligation developed mechanical allodynia of the hind paw ipsilateral to the site of injury that persisted until sacrifice at postoperative day 10. A significant induction of preproneuropeptide Y-encoding (PPNPY) mRNA, as detected by in situ hybridization histochemistry (ISHH), occurred in populations of medium- and large-diameter DRG neurons ipsilateral to the site of injury. Immunohistochemical analysis indicated a marked decline in the number of labeled sympathetic axons positive for tyrosine hydroxylase-like and NPY-like immunoreactivities (TH-LI and NPY-LI, respectively) proximal to the site of nerve injury and almost complete elimination of immunopositive fibers distal to the site of ligation. Whereas, the extent of colocalization of NPY-LI to TH-LI-positive sympathetic axons in unaffected L4 or L5 nerve segments exceeded 80%, this figure declined to approximately 50% in regenerating axons of ligated spinal nerve L5. The portion of NPY-LI that was not colocalized to sympathetic TH-LI-positive fibers was most likely contributed by regenerating sensory axons, consistent with marked de novo synthesis of NPY by DRG neurons. In end bulb axon terminals, i.e. morphological profiles characteristic of neuromas, NPY-LI-positive elements that were not colocalized to TH-LI-positive sympathetic elements appeared to be spatially segregated from those of sympathetic origin with colocalized TH-LI and NPY-LI. Receptor autoradiography indicated that small- and medium-diameter DRG somata of the C-fiber class normally express both Y1 and Y2 receptor subtypes. The pattern of the distribution of Y-receptor binding sites appeared to be relatively unaffected by spinal nerve ligation. In contrast, there was a marked increase in the density of Y2 receptor binding sites in the proximal segment of ligated spinal nerve L5, consistent with previously published data indicating differential transport of the Y2 autoregulatory receptor subtype to nerve terminals. Induction of NPY gene expression in injured DRG neurons is consistent with appearance of NPY-LI-positive end bulbs derived from regenerating sensory axons that are found in developing neuromas containing a relatively high density of transported prejunctional Y2 receptors. Newly established functional interactions of spatially segregated sensory- and sympathetically-derived end bulbs in developing neuromas may enhance neuronal hyperexcitability engendered by aberrant electrical activity at the site of injury. Injury-related alterations in the regulatory activities of NPY released within the DRG at somally-distributed Y-receptors may also contribute to the development and/or persistence of symptoms characteristic of sympathetically-maintained pain. Finally, at later times NPY-mediated modulation of NE release from invading sympathetic axon terminals within the DRG may affect the extent of alpha2 rece

Jet ventilation in upper airway obstruction: description and model lung testing of a new jetting device.

UNLABELLED: Patients with critical upper airway stenosis require a tracheotomy for corrective surgery. We describe a new transtracheal device that permits safe ventilation of these patients without tracheotomy. It is based on a coaxial bicannular design that allows "push-pull" ventilation by jetting gas through the inner cannula and applying suction through the outer cannula. It further allows monitoring of airway pressure, tidal volume, and end-tidal CO2. The device was placed in the "trachea" of an artificial lung, and the preparation was made airtight by sealing the proximal end of the trachea. Tidal volumes and their associated pressures were measured simultaneously at different parts of the airway at several lung compliances and airway resistance settings while varying the jet and suction pressures. A large range of tidal volumes was achieved at safe airway pressures using clinically relevant airway resistance and lung compliance settings. Airway pressures measured through the device correlated well with pressures measured directly in the airways at the same time. Tidal volumes, measured through a Wright respirometer in the suction line, exceeded actual values at high suction settings and decreased below actual values at low suction settings. This new form of jet ventilation allowed efficient ventilation of the artificial lung with a totally occluded upper airway. IMPLICATIONS: Tracheotomy is required for surgery to relieve stridor because gas forced into the trachea at high pressures through a percutaneously placed needle (jetting) cannot be exhaled quickly enough for respiration. We describe a device that allows jetting in the stridorous patient by actively assisting expiration, thereby eliminating the tracheotomy requirement.

Differential effect of central versus parenteral administration of morphine sulfate on regional concentrations of reduced glutathione in rat brain.

Prior studies in rodents have shown significant depletion of reduced glutathione (GSH) in peripheral organs following acute systemic or central administration of opioids. However, little information exists on whether opioid administration affects concentrations of brain GSH. Recently, clinical observations have indicated acute declines of GSH concentrations in the cerebrospinal fluid of cancer patients after acute intracerebroventricular (ICV) morphine which may contribute to the development of organic behavioral brain syndromes associated with central opioid analgesia. Collectively these data led us to investigate the affect of acute systemic and central morphine on regional concentrations of GSH in rat brain. Systemic morphine had no effect on GSH concentrations in selected brain areas. In contrast, ICV morphine resulted in selective GSH depletion in the caudate nucleus, consistent with concurrent excitatory locomotive behavior. This change may have reflected morphine-induced oxidative stress together with increased metabolic activity within the extrapyramidal system.

Dextromethorphan inhibits ischemia-induced c-fos expression and delayed neuronal death in hippocampal neurons.

BACKGROUND: Dextromethorphan (DM), a widely used antitussive agent, has been shown to possess both anticonvulsant and neuroprotective properties functionally related to its inhibitory effects on glutamate-induced neurotoxicity. The current study was designed to determine whether DM administration prevents delayed neuronal degeneration in central nervous system areas after global forebrain ischemia and whether this correlates with inhibition of induction of the immediate early gene c-fos. METHODS: Mongolian gerbils, anesthetized with 2% halothane in air at 37 degrees C, received either 0.9% sodium chloride (vehicle, n = 9) or 50 mg/kg DM in vehicle (n = 9) by intraperitoneal injection before bilateral carotid artery occlusion. After 1 h of reperfusion under anesthesia, the animals were killed and the brains removed. Immunohistochemistry was used to detect neurons expressing Fos protein. Computer-assisted image analysis quantified changes in the number of labeled neurons as a function of drug treatment. To determine the extent of delayed neuronal degeneration within the hippocampus, other animals were treated with either DM (n = 7) or vehicle (n = 6) before carotid artery occlusion and allowed to survive for 1 week. RESULTS: Global forebrain ischemia produced consistent patterns of Fos-like immunoreactivity in the hippocampus and neocortex of vehicle-treated animals. DM inhibited the induction of c-fos from 65% to 91%. DM also protected against delayed neuronal degeneration in the CA1 region of the hippocampus (P < 0.001). CONCLUSIONS: The induction of nuclear-associated Fos protein represents a sensitive marker of cellular responses to ischemia and a method to assay the effectiveness of pharmacologic interventions. DM markedly inhibited ischemia-induced Fos expression and prevented cell death in CA1. DM given before conditions of ischemia or decreased central nervous system perfusion may be highly beneficial.

Intraoperative reinfusion of whole blood using a new autoinfusion device.

Aortic aneurysm resection is frequently associated with considerable blood loss and requires transfusion. To minimize complications and cost many institutions use a "cell saving" method that allows reinfusion of the washed red cell fraction of blood suctioned from the operative field. The disadvantages of this technique are that homologous transfusion is regularly required to replace platelets and coagulation factors. Red cell transfusion may also be required when there is rapid major blood loss as the wash cycle may be too long to subject a patient, in a high-risk group for coronary artery disease, to anaemia. A new autoinfusion device anticoagulates blood as it is suctioned from the operative field then filters, defoams, and returns it whole to the patient without a processing time lapse. We successfully used the device in a patient for aortic aneurysm resection to reinfuse two-thirds of his blood volume shed over 80 min. Neither banked red cells nor plasma were used. His haematocrit and coagulation profile remained stable throughout surgery and recovery. The potential complications and cost of homologous transfusion were avoided.

Substance P markedly potentiates the antinociceptive effects of morphine sulfate administered at the spinal level.

The undecapeptide substance P and the alkaloid morphine sulfate are two agents previously thought to have opposite roles in the mediation of spinal nociceptive processes. The present report, however, demonstrates that low doses of substance P when coadministered with marginally effective doses of morphine sulfate into the rat subarachnoid space produce a markedly enhanced analgesic response, as monitored by the tail-flick test. This pharmacological effect is blocked by prior treatment with the opioid antagonist naloxone, indicating that the potentiated analgesic response is mediated by opioid-responsive neurons. In addition, the putative immediate precursor form of substance P (i.e., substance P-glycine) may substitute for the mature compound in the potentiated pharmacological effect. Moreover, the described synergism is unaffected by transection of the spinal cord, demonstrating the lack of supraspinal modulation of the observed phenomenon. Based on these observations, we are now able to dissociate opioid-potentiating and analgesic properties of substance P from traditional hyperalgesic effects realized at significantly higher concentrations. Consistent with previous biochemical data, a likely mechanism underlying the peptide-mediated enhancement of opioid analgesia may center on the ability of substance P to release endogenous opioid peptides within the local spinal cord environment. Finally, the pharmacological relationship of coadministered substance P and morphine sulfate established here supports the hypothesis that spinal tachykinin and opioid systems have a direct functional interaction in the modulation of local nociceptive responses.

Ibuprofen pretreatment inhibits prostacyclin release during abdominal exploration in aortic surgery.

Mesenteric traction during aortic surgery produces facial flushing, reduced mean arterial pressure (MAP), and systemic vascular resistance (SVR) with increased heart rate (HR) and cardiac index (CI). Elevated 6-keto-prostaglandin-F1 alpha (6-keto-PGF1 alpha) suggests prostacyclin is the mediator. To test this hypothesis, the cyclooxygenase inhibitor, ibuprofen (n = 14), or placebo (n = 13) was administered to patients electively scheduled for aortic reconstruction. The hemodynamic measurements and plasma concentrations of prostanoids between groups were compared immediately before (0), and 5, 10, 15, 30, and 45 min following mesenteric traction. Following mesenteric traction significant differences (P less than 0.05) were observed between the ibuprofen pretreatment and placebo group over time in SVR, MAP, HR, CI, 6-keto-PGF1 alpha, and thromboxane B2 (TXB2). Significant differences between groups at individual times were found in SVR, HR, CI, 6-keto-PGF1 alpha, and TXB2. In the placebo group flushing was accompanied by reduced SVR and MAP and increased HR and CI. The greatest effect was seen at 10 min and resolved over 30 min. Plasma concentration of 6-keto-PGF1 alpha increased from 159 +/- 103 (mean +/- SEM) pg/ml to a peak value of 3,765 +/- 803 at 10 min. A late increase in TXB2 occurred with a peak value of 1,970 +/- 891 (mean +/- SEM) pg/ml at 30 min. In the ibuprofen pretreated group no significant changes occurred in hemodynamic measurements or concentrations of prostanoids. The inhibition of 6-keto-PGF1 alpha and its associated hemodynamic changes in the treatment group, but not in the placebo group, confirms the hypothesis that prostacyclin is the mediator of the mesenteric traction response in abdominal aortic surgery.

Hemodynamics and prostacyclin release in the early phases of aortic surgery: comparison of transabdominal and retroperitoneal approaches.

Although the retroperitoneal aortic approach (RP) is advocated to reduce myocardial ischemia and cardiac-related death, inadequate physiologic data exist to support this contention. As the aorta is exposed via the transabdominal approach (TA) we noted some patients have manifested reduced systemic vascular resistance (SVR) associated with tachycardia, reduced blood pressure, and facial flushing. To determine whether RP offered physiologic advantages over TA we compared cardiac dynamics and blood levels of 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha), the stable metabolite of prostacyclin, during exposure of the aorta in 52 patients (33 with TA and 19 with RP), comparable in age, cardiac history, medications, and body surface area. Serial measurements of mean arterial pressure, heart rate, wedge pressure, pulmonary artery pressure, cardiac index, and 6-keto-PGF1 alpha were obtained. Results revealed decreased mean arterial pressure and systemic vascular resistance, increased cardiac index and heart rate, and facial flush occurring 10 minutes after the bowel was explored in TA. This was not observed in RP. These hemodynamic alterations correlated in time and magnitude with a fourteen fold increase in 6-keto-PGF1 alpha. These changes in cardiac indexes can produce increased myocardial oxygen consumption with the risk for myocardial ischemia, particularly in patients with coronary artery disease. The absence of this response to bowel exploration in RP may account for some of the observed advantages in "high-risk" aortic reconstruction.

Physiological aspects of the role of human albumin in the treatment of chronic and acute blood loss.

Human albumin is the most important oncotic-active protein (1 g albumin attaches 18 g water). It is essential for the water exchange between intra- and extracellular space and for homeostasis. The physiological distribution of albumin, its daily exchange and degradation are being discussed. At the example of normo- and hypovolaemic patients and acute blood-loss the stabilising effect on the blood-volume and the hemodynamic efficacy of human albumin are shown. Human albumin was infused into patients with hypoproteinemia and hypovolaemia as well as to surgical patients with normovolaemia. Volunteers received albumin after an acute blood-loss. Under and after the albumin-infusion the albumin disappeared partly from the blood-stream. The loss to the extravascular compartments was greatest among patients with hypoproteinemia. Among volunteers with experimental blood-loss the infused volume disappeared in an amount of 45 to 106 ml per hour. When human albumin is given over a longer period the synthesis of endogenous albumin and of globulins may be inhibited or at least depressed. Albumin has a positive effect on the hemodynamic. The cardiac-output and the stroke volume increased. The peripheral resistance fell in the same time. Renal filtration rate and the urine volume increased, in contrast renal resistance was lowered.

[Haemodynamic effects of dextran 6% in the treatment of haemorrhage (author's transl)]. / Einfluss von makromolekularem Dextran auf die Hämodynamik des menschlichen Blutkreislaufes bei kontrollierter Hypovolämie.

An isovolaemic infusion of dextran 6% after 1000 ml haemorrhage produced an increase in blood volume. This response persisted over a 4 h period, during which time a marked increase of venous return, stroke volume and cardiac output was be demonstrated. Improvement in the central circulation was produced through a significant drop in total peripheral resistance. The administration of the plasma expander was associated with an acute renal hyperperfusion.