Superficial temporal artery injury and delayed post-cranioplasty infection.

OBJECTIVE: Complications after cranioplasty after decompressive craniectomy (DC) have been reported to be as high as 40%. The superficial temporal artery (STA) is at substantial risk for injury in standard reverse question-mark incisions that are typically used for unilateral DC. The authors hypothesize that STA injury during craniectomy predisposes patients to post-cranioplasty surgical site infection (SSI) and/or wound complication. METHODS: A retrospective study of all patients at a single institution who underwent cranioplasty after decompressive craniectomy and who underwent imaging of the head (computed tomography angiogram, magnetic resonance imaging with intravenous contrast, or diagnostic cerebral angiography) for any indication between the two procedures was undertaken. The degree of STA injury was classified and univariate statistics were used to compare groups. RESULTS: Fifty-four patients met inclusion criteria. Thirty-three patients (61%) had evidence of complete or partial STA injury on pre-cranioplasty imaging. Nine patients (16.7%) developed either an SSI or wound complication after cranioplasty and, among these, four (7.4%) experienced delayed (>2 weeks from cranioplasty) complications. Seven of 9 patients required surgical debridement and cranioplasty explant. There was a stepwise but non-significant increase in post-cranioplasty SSI (STA present: 10%, STA partial injury: 17%, STA complete injury: 24%, P=0.53) and delayed post-cranioplasty SSI (STA present: 0%, STA partial injury: 8%, STA complete injury: 14%, P=0.26). CONCLUSIONS: There is a notable but statistically non-significant trend toward increased rates of SSI in patients with complete or partial STA injury during craniectomy.

Banded vs. non-banded Roux-en-Y gastric bypass for morbid obesity: a systematic review and meta-analysis.

We aim to review the available literature on patients with morbid obesity treated with banded (BRYGB) or non-banded Roux-en-Y gastric bypass (NBRYGB), in order to compare the clinical outcomes and intraoperative parameters of the two methods. A systematic literature search was performed in PubMed, Cochrane library and Scopus databases, in accordance with the PRISMA guidelines. Eight studies met the inclusion criteria incorporating 3899 patients. This study reveals similar rates of complications, mortality, remission of type 2 diabetes, hypertension, dyslipidaemia, gastroesophageal reflux and obstructive sleep apnoea, along with similar % excess weight loss (%EWL) at 1 and 2 years postoperatively. In contrast, according to an analysis of two eligible studies the BRYGB procedure was associated with increased %EWL at 5 years postoperatively. These results should be interpreted with caution due to the small number of statistical arms and randomized controlled studies. However, the present article represents the best available evidence in the field. Well-designed, randomized controlled studies, comparing BRYGB to NBRYGB, are necessary to further assess their clinical outcomes.

Absence of 5-HT3 and cholinergic mechanisms in improgan antinociception.

Improgan, an analgesic derived from histamine antagonists, acts in the brain stem to activate descending non-opioid, pain-relieving circuits, but the mechanism of action of this drug remains elusive. Because improgan has a moderate affinity for 5-HT(3) receptors, and, since cholinergic and serotonergic drugs can modulate descending analgesic circuits, roles for 5-HT(3), nicotinic and muscarinic receptors in improgan antinociception were presently investigated in rats. Improgan (80 microg, icv) induced nearly maximal inhibition of hot plate and tail flick nociceptive responses, and these actions we unaffected by antagonists of muscarinic (atropine, 5.9 mg/kg, i.p.) and nicotinic (mecamylamine, 2 mg/kg, i.p.) receptors. Control experiments verified that these antagonist treatments were maximally effective against muscarinic and nicotinic antinociception in both tests. In addition, improgan antinociception was unaffected by icv pretreatment with a 5-HT(3) antagonist (ondansetron, 20 microg). When given alone, icv treatment with neither this antagonist nor a 5-HT(3) agonist (m-chlorophenylbiguanide, 1000 nmol, icv) modified thermal nociceptive latencies. These results show no role for supraspinal cholinergic and 5-HT(3) receptors in improgan antinociception. The findings help to narrow the search for the relevant mediators of the action of this novel analgesic agent.

Activation of brain stem nuclei by improgan, a non-opioid analgesic.

Improgan is a compound developed from histamine antagonists which shows the pre-clinical profile of a highly effective, non-opioid analgesic when administered into the rodent CNS. Pharmacological studies suggest that improgan activates descending pain-relieving circuits, but the brain and spinal sites of action of this drug have not been previously studied. Presently, the effects of intracerebral and intrathecal microinjections of improgan were evaluated on thermal nociceptive responses in rats. Improgan produced large, dose- and time-related reductions in nociceptive responses following administration into the ventrolateral periaqueductal gray (PAG), the dorsal PAG, and the rostral ventromedial medulla (RVM). The drug had no measurable effects after injections into the caudate nucleus, basolateral amygdala, hippocampus, ventromedial hypothalamus, superior colliculi, ventrolateral medulla, or the spinal subarachnoid space. Inactivation of the RVM by muscimol microinjections completely attenuated antincociceptive responses produced by intraventricular improgan. These findings, taken with earlier results, show that, like opioids and cannabinoids, improgan acts in the PAG and RVM to activate descending analgesic systems. Unlike these other analgesics, improgan does not act in the spinal cord or in CNS areas outside of the brain stem.

A role for spinal, but not supraspinal, alpha(2) adrenergic receptors in the actions of improgan, a powerful, non-opioid analgesic.

Improgan is a derivative of cimetidine that induces non-opioid antinociception after intracerebroventricular (i.c.v.) administration, but the mechanism of action of this compound remains unknown. Since activation of either supraspinal or spinal alpha(2) adrenergic receptors can induce antinociception, and since improgan showed affinity for these receptors in vitro, the effects of the alpha(2) antagonist yohimbine on improgan antinociception were presently studied in rats on the hot plate and tail flick tests. Systemic yohimbine pretreatment (4 mg/kg, i.p.) completely blocked improgan antinociception (80 microg, i.c.v.), suggesting a mediator role for alpha(2) receptors. However, i.c.v. pretreatment with yohimbine (30 microg) had no effect on improgan antinociception. Since this treatment completely antagonized clonidine antinociception (40 microg, i.c.v.), supraspinal alpha(2) receptors seem to mediate the antinociceptive effects of clonidine, but not that produced by improgan. In contrast, intrathecal (i.t.) yohimbine pretreatment (30 microg) completely blocked the antinociception elicited by i.c.v. improgan and i.c.v. morphine. These results suggest that spinal (but not supraspinal) alpha(2) adrenergic receptors play a significant role in the pain-relieving actions of improgan. Furthermore, although improgan shows some affinity at alpha(2) receptors, this drug does not act directly at these receptors to induce antinociceptive responses. Like several other classes of analgesics, improgan-like drugs seem to activate non-opioid, descending pain-relieving circuits.