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PubMed2006

A phenotypic-genetic study of a group of Polish patients with spinal and bulbar muscular atrophy.

We studied phenotype-genotype correlation in a group of Polish males with spinal and bulbar muscular atrophy (SBMA) and in female carriers. Eleven males with suspected SBMA phenotype and three suspected female carriers were examined. Male patients presented with the predominant signs of progressive, symmetrical distal limb weakness with amyotrophy, facial muscular weakness with orofacial fasciculations, nasal voice and slight dysphagia, gynaecomastia, decreased potency, as well as hand tremor and distal peripheral sensory disturbances in a few cases. One of the carriers presented with a 30-year history of fasciculations and minimal distal weakness and cramps in the legs, while the other two were asymptomatic. DNA analysis revealed expanded size of CAG repeats in Xq11-12 in the AR gene in 10 out of 11 men (range 45-52 CAG repeats) and in the women (range 46-48 CAG repeats). There was no correlation between CAG repeat size and the age of disease onset and duration of the disease. A rare, predominantly distal distribution of weakness and amyotrophy was found in our group of the SBMA patients (8 out of 11 cases) from three unrelated kindreds and also in the remaining two sporadic cases. The extended CAG repeats within families were stable.

Adult↗
PubMed2002

Pharmacological antagonism of lethal effects induced by O-isobutyl S-[2-(diethylamino)ethyl]methylphosphonothioate.

O-Isobutyl S-[2-(diethylamino)ethyl]methylphosphonothioate (VR) is a structural isomer of a more widely known chemical warfare agent O-ethyl S-[2(diisopropylamino)ethyl]methylphosphonothioate (VX). VR has the potential of being used as military threat/sabotage/terrorist agent. The development of a sound medical countermeasure will undoubtedly enhance not only our medical readiness and ability in VR casualty management, but also our defense posture against the deployment of VR in both combat and politically volatile environments. Acute exposure to a lethal dose of VR has been shown to cause cholinergic hyperfunction, incapacitation, seizures, convulsions, cardiorespiratory depression and death. In this study, pharmacological antagonism of VR-induced cardiorespiratory failure and lethality was investigated in guinea pigs chronically instrumented for concurrent recordings of electrocorticogram, diaphragmatic EMG, Lead II ECG, heart rate and neck skeletal muscle EMG. Thirty (30) min prior to intoxication with a 2 x LD50 dose of VR (22.6 micrograms/kg, s.c.), animals were pretreated with pyridostigmine (0.026 mg/kg, i.m.). Immediately after VR intoxication, animals were given pralidoxime chloride (2-PAM; 25 mg/kg, i.m.) and atropine sulfate (2, 8 or 16 mg/kg, i.m.). In animals that displayed seizures and convulsions, diazepam (5 mg/kg, i.m.) was administered 10 min following the onset of epileptiform activities. Responses to pretreatment/therapy modality were evaluated at 24 h post-VR. All animals survived the 2 x LD50 VR challenge. With the exception of an increased heart rate in response to atropine, the myocardial and diaphragmatic (respiratory) activity profiles appeared normal throughout the course of intoxication and recovery. Animals receiving 2 mg/kg atropine all developed fasciculations, seizures, signs of excessive mucoid/salivary secretion, and needed diazepam adjunct therapy. One-half (50%) of the animals receiving 8 mg/kg atropine developed seizure activities and were given diazepam, whereas the other half only showed a brief period of increase in CNS excitability. No fasciculations, seizures or convulsions were noted in animals receiving 16 mg/kg atropine. In summary, although lethality can be prevented with the pretreatment/therapy modality containing 2 mg/kg atropine and diazepam adjunct, a complete CNS and cardiorespiratory recovery from 2 x LD50 of VR requires a minimum of 8 mg/kg atropine.

Animals↗
PubMed1986

Differential contributions of Ng-CAM and N-CAM to cell adhesion in different neural regions.

Individual neurons can express both the neural cell adhesion molecule (N-CAM) and the neuron-glia cell adhesion molecule (Ng-CAM) at their cell surfaces. To determine how the functions of the two molecules may be differentially controlled, we have used specific antibodies to each cell adhesion molecule (CAM) to perturb its function, first in brain membrane vesicle aggregation and then in tissue culture assays testing the fasciculation of neurite outgrowths from cultured dorsal root ganglia, the migration of granule cells in cerebellar explants, and the formation of histological layers in the developing retina. Our strategy was initially to delineate further the binding mechanisms for each CAM. Antibodies to Ng-CAM and N-CAM each inhibited brain membrane vesicle aggregation but the binding mechanisms of the two CAMs differed. As expected from the known homophilic binding mechanism of N-CAM, anti-N-CAM-coated vesicles did not co-aggregate with uncoated vesicles. Anti-Ng-CAM-coated vesicles readily co-aggregated with uncoated vesicles in accord with a postulated heterophilic binding mechanism. It was also shown that N-CAM was not a ligand for Ng-CAM. In contrast to assays with brain membrane vesicles, cellular systems can reveal functional differences for each CAM reflecting its relative amount (prevalence modulation) and location (polarity modulation). Consistent with this, each of the three cellular processes examined in vitro was preferentially inhibited only by anti-N-CAM or by anti-Ng-CAM antibodies. Both neurite fasciculation and the migration of cerebellar granule cells were preferentially inhibited by anti-Ng-CAM antibodies. Anti-N-CAM antibodies inhibited the formation of histological layers in the retina. The data on perturbation by antibodies were correlated with the relative levels of expression of Ng-CAM and N-CAM in each of these different neural regions. Quantitative immunoblotting experiments indicated that the relative Ng-CAM/N-CAM ratios in comparable extracts of brain, dorsal root ganglia, and retina were respectively 0.32, 0.81, and 0.04. During culture of dorsal root ganglia in the presence of nerve growth factor, the Ng-CAM/N-CAM ratio rose to 4.95 in neurite outgrowths and 1.99 in the ganglion proper, reflecting both polarity and prevalence modulation. These results suggest that the relative ability of anti-Ng-CAM and anti-N-CAM antibodies to inhibit cell-cell interactions in different neural tissues is strongly correlated with the local Ng-CAM/N-CAM ratio.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1986

Immunoelectron microscopic localization of neural cell adhesion molecules (L1, N-CAM, and MAG) and their shared carbohydrate epitope and myelin basic protein in developing sciatic nerve.

The cellular and subcellular localization of the neural cell adhesion molecules L1, N-CAM, and myelin-associated glycoprotein (MAG), their shared carbohydrate epitope L2/HNK-1, and the myelin basic protein (MBP) were studied by pre- and post-embedding immunoelectron microscopic labeling procedures in developing mouse sciatic nerve. L1 and N-CAM showed a similar staining pattern. Both were localized on small, non-myelinated, fasciculating axons and axons ensheathed by non-myelinating Schwann cells. Schwann cells were also positive for L1 and N-CAM in their non-myelinating state and at the onset of myelination, when the Schwann cell processes had turned approximately 1.5 loops. Thereafter, neither axon nor Schwann cell could be detected to express the L1 antigen, whereas N-CAM was found in the periaxonal area and, more weakly, in compact myelin of myelinated fibers. Compact myelin, Schmidt-Lanterman incisures, paranodal loops, and finger-like processes of Schwann cells at nodes of Ranvier were L1-negative. At the nodes of Ranvier, the axolemma was also always L1- and N-CAM-negative. The L2/HNK-1 carbohydrate epitope coincided in its cellular and subcellular localization most closely to that observed for L1. MAG appeared on Schwann cells at the time L1 expression ceased. MAG was then expressed at sites of axon-myelinating Schwann cell apposition and non-compacted loops of developing myelin. When compaction of myelin occurred, MAG remained present only at the axon-Schwann cell interface; Schmidt-Lanterman incisures, inner and outer mesaxons, and paranodal loops, but not at finger-like processes of Schwann cells at nodes of Ranvier or compacted myelin. All three adhesion molecules and the L2/HNK-1 epitope could be detected in a non-uniform staining pattern in basement membrane of Schwann cells and collagen fibrils of the endoneurium. MBP was detectable in compacted myelin, but not in Schmidt-Lanterman incisures, inner and outer mesaxon, paranodal loops, and finger-like processes at nodes of Ranvier, nor in the periaxonal regions of myelinated fibers, thus showing a complementary distribution to MAG. These studies show that axon-Schwann cell interactions are characterized by the sequential appearance of cell adhesion molecules and MBP apparently coordinated in time and space. From this sequence it may be deduced that L1 and N-CAM are involved in fasciculation, initial axon-Schwann cell interaction, and onset of myelination, with MAG to follow and MBP to appear only in compacted myelin. In contrast to L1, N-CAM may be further involved in the maintenance of compact myelin and axon-myelin apposition of larger diameter axons.

Aging↗
PubMed1999

Mammalian homologue of the Caenorhabditis elegans UNC-76 protein involved in axonal outgrowth is a protein kinase C zeta-interacting protein.

By the yeast two-hybrid screening of a rat brain cDNA library with the regulatory domain of protein kinase C zeta (PKCzeta) as a bait, we have cloned a gene coding for a novel PKCzeta-interacting protein homologous to the Caenorhabditis elegans UNC-76 protein involved in axonal outgrowth and fasciculation. The protein designated FEZ1 (fasciculation and elongation protein zeta-1) consisting of 393 amino acid residues shows a high Asp/Glu content and contains several regions predicted to form amphipathic helices. Northern blot analysis has revealed that FEZ1 mRNA is abundantly expressed in adult rat brain and throughout the developmental stages of mouse embryo. By the yeast two-hybrid assay with various deletion mutants of PKC, FEZ1 was shown to interact with the NH2-terminal variable region (V1) of PKCzeta and weakly with that of PKCepsilon. In the COS-7 cells coexpressing FEZ1 and PKCzeta, FEZ1 was present mainly in the plasma membrane, associating with PKCzeta and being phosphorylated. These results indicate that FEZ1 is a novel substrate of PKCzeta. When the constitutively active mutant of PKCzeta was used, FEZ1 was found in the cytoplasm of COS-7 cells. Upon treatment of the cells with a PKC inhibitor, staurosporin, FEZ1 was translocated from the cytoplasm to the plasma membrane, suggesting that the cytoplasmic translocation of FEZ1 is directly regulated by the PKCzeta activity. Although expression of FEZ1 alone had no effect on PC12 cells, coexpression of FEZ1 and constitutively active PKCzeta stimulated the neuronal differentiation of PC12 cells. Combined with the recent finding that a human FEZ1 protein is able to complement the function of UNC-76 necessary for normal axonal bundling and elongation within axon bundles in the nematode, these results suggest that FEZ1 plays a crucial role in the axon guidance machinery in mammals by interacting with PKCzeta.

Adaptor Proteins, Signal Transducing↗
PubMed1999

Neurotractin, a novel neurite outgrowth-promoting Ig-like protein that interacts with CEPU-1 and LAMP.

The formation of axon tracts in nervous system histogenesis is the result of selective axon fasciculation and specific growth cone guidance in embryonic development. One group of proteins implicated in neurite outgrowth, fasciculation, and guidance is the neural members of the Ig superfamily (IgSF). In an attempt to identify and characterize new proteins of this superfamily in the developing nervous system, we used a PCR-based strategy with degenerated primers that represent conserved sequences around the characteristic cysteine residues of Ig-like domains. Using this approach, we identified a novel neural IgSF member, termed neurotractin. This GPI-linked cell surface glycoprotein is composed of three Ig-like domains and belongs to the IgLON subgroup of neural IgSF members. It is expressed in two isoforms with apparent molecular masses of 50 and 37 kD, termed L-form and S-form, respectively. Monoclonal antibodies were used to analyze its biochemical features and histological distribution. Neurotractin is restricted to subsets of developing commissural and longitudinal axon tracts in the chick central nervous system. Recombinant neurotractin promotes neurite outgrowth of telencephalic neurons and interacts with the IgSF members CEPU-1 (KD = 3 x 10(-8) M) and LAMP. Our data suggest that neurotractin participates in the regulation of neurite outgrowth in the developing brain.

Amino Acid Sequence↗
PubMed1978

Suxamethonium-induced muscle contracture following traumatic denervation in man.

The effects of the systemic and of the i.v. regional administration of suxamethonium were investigated in 23 patients with traumatic nerve injury. Following the systemic administration of suxamethonium 100 mg, normally innervated muscles showed muscle fasciculations initially, followed by muscular relaxation. On the other hand, denervated muscles did not fasciculate and, in 21 patients, manifested suxamethonium-induced contractures. In the other two patients no response was observed. In 10 of the patients, the i.v. regional administration of suxamethonium 5 mg was followed by a contracture of the denervated muscle which was maintained until the tourniquet was deflated. No systemic reaction to suxamethonium, other than mild ptosis, followed the release of the tourniquet.

Humans↗
PubMed1990

Changes in resistance to mouth opening induced by depolarizing and non-depolarizing neuromuscular relaxants.

Mouth opening was measured in 43 children anaesthetized with isoflurane and paralysed with vecuronium or suxamethonium. Measurements of mouth opening were made for up to 10 min after loss of the adductor pollicis twitch and cessation of muscle fasciculations. In 22 patients receiving suxamethonium, a significant (P less than 0.001) reduction in mean mouth opening occurred in the 60 s after loss of twitch and cessation of fasciculations. Mouth opening reductions could last for up to 10 min after the loss of twitch, beyond the return of the twitch. One patient experienced "masseter spasm"; he did not develop malignant hyperpyrexia during 2.5 h of isoflurane anaesthesia. Patients receiving vecuronium showed a significant (P less than 0.0006) increase in mouth opening. In 20 subjects, mouth opening was generated with a small (1.67 N) and a larger (4.32 N) force. Proportionally equal reductions in mouth opening were obtained with either force after suxamethonium administration. Relatively equal increases with either force followed vecuronium administration. Isolated masseter spasm is not pathognomonic for malignant hyperpyrexia. If the diagnosis of malignant hyperpyrexia is contemplated, signs of hypermetabolism, such as increases in end-tidal carbon dioxide concentration during constant minute ventilation, should be sought.

Analysis of Variance↗
PubMed1994

Use of ketorolac in the prevention of suxamethonium myalgia.

We have evaluated the effect of ketorolac in the prevention of suxamethonium myalgia. Sixty ASA I patients who presented for extraction of wisdom teeth as day cases were allocated randomly to one of three equal groups. Patients received either 0.9% saline (placebo), atracurium 0.05 mg kg-1 i.v. or ketorolac 10 mg i.v., 3 min before induction of anaesthesia. Follow-up postal questionnaires (97% response rate) at 48 h showed no reduction in the incidence of myalgia after ketorolac pretreatment compared with saline. The use of atracurium reduced the incidence of myalgia by 60% (P < 0.001) and the severity of fasciculations (P < 0.001). There was no difference in the severity of fasciculations between the saline and ketorolac groups. Intubating conditions were comparable in the three groups.

Adolescent↗
PubMed1994

Differences in behaviour of sensory and motor axons following release of ischaemia.

The changes in excitability and supernormality of sensory and motor axons of the median (or ulnar) nerve were tracked during and following ischaemia at the wrist for periods of 5-20 min in normal human volunteers. Supernormality was defined as the fractional increase in excitability produced by a maximal conditioning stimulus, 10 ms before the test stimulus. With relatively brief periods of ischaemia (< 10 min), sensory and motor axons behaved similarly, with an increase in excitability (producing a decrease in threshold) and a decrease in supernormality during ischaemia and a long-lasting decrease in excitability (and increase in supernormality) following release of ischaemia. Most subjects reported paraesthesiae during brief periods of ischaemia but not after its release. No one experienced fasciculation. The threshold changes were generally similar during longer periods of ischaemia, but in the post-ischaemic phase the behaviour of sensory and motor axons diverged. After a rapid post-ischaemic increase, the threshold of sensory axons decreased, approaching the pre-ischaemic level, before rising again and then slowly returning to the control level. Sensory axons of different threshold behaved in a qualitatively similar manner, with no evidence of a bimodal distribution of thresholds in the post-ischaemic phase (as occurs with motor axons when the ischaemia is sufficient to produce fasciculation; see Bostock et al. J. Physiol (Lond) 1991; 441: 537-57). The 'notch' on the threshold plot for sensory axons lasted 20-40 min and was accompanied by a relatively small but appropriate change in supernormality. No such 'notch' was seen with motor axons. The changes in latency were generally similar for sensory and motor axons, largely paralleling the supernormality plots, except at the time of the 'notch'. To test the hypothesis that the differences in behaviour of sensory and motor axons resulted from differences in inward rectification activated by hyperpolarization, the changes in threshold produced by long-lasting (300 ms) depolarizing and hyperpolarizing current pulses were compared for sensory and motor axons. In seven of eight subjects, there was evidence of more inward rectification in sensory axons. In the eighth subject, motor axons behaved similarly to sensory axons. It is concluded that a difference in inward rectification contributes to but is insufficient by itself to account for the differences in behaviour of sensory and motor axons and that the greater propensity of sensor y axons to discharge ectopically cannot be attributed to a single factor.

Action Potentials↗
PubMed2005

Essential role for the Prader-Willi syndrome protein necdin in axonal outgrowth.

Necdin and Magel2 are related proteins inactivated in Prader-Willi syndrome (PWS), a sporadic chromosomal deletion disorder. We demonstrate that necdin and Magel2 bind to and prevent proteasomal degradation of Fez1, a fasciculation and elongation protein implicated in axonal outgrowth and kinesin-mediated transport, and also bind to the Bardet-Biedl syndrome (BBS) protein BBS4 in co-transfected cells. The interactions among necdin, Magel2, Fez1 and BBS4 occur at or near centrosomes. Centrosomal or pericentriolar dysfunction has previously been implicated in BBS and may also be important in the features of PWS that overlap with BBS, such as learning disabilities, hypogonadism and obesity. Morphological abnormalities in axonal outgrowth and fasciculation manifest in several regions of the nervous system in necdin null mouse embryos, including axons of sympathetic, retinal ganglion cell, serotonergic and catecholaminergic neurons. These data demonstrate that necdin mediates intracellular processes essential for neurite outgrowth and that loss of necdin impinges on axonal outgrowth. We further suggest that loss of necdin contributes to the neurological phenotype of PWS, and raise the possibility that co-deletion of necdin and the related protein Magel2 may explain the lack of single gene mutations in PWS.

Animals↗
PubMed1986

Cerebral stimulation following succinylcholine in dogs.

The effects of iv succinylcholine (SCh) on the electroencephalogram (EEG), cerebral blood flow (CBF), cerebral metabolic rate (CMRO2), intracranial pressure (ICP), central venous pressure (CVP), and mean arterial pressure (MAP) were tested in halothane-anesthetized dogs. Six dogs were maintained at 0.87 +/- 0.00% (mean +/- SE) expired halothane (1.0 MAC) and received both SCh 1.0 mg X kg-1 and lactated Ringer's solution placebo 0.05 ml X kg-1. Fasciculations began 24 +/- 4 s after iv SCh. Fasciculations were followed by immediate EEG arousal in five of six dogs and increases in CBF in all six. Average CBF was 151 +/- 14% of control for the 0-15 min measurement period and 127 +/- 7% of control for the 15-30 min period. Both were significantly greater than pre-SCh control values and placebo group values. Peak CBF of 177 +/- 19% of control occurred 3 min after iv SCh and was accompanied by a peak ICP of 435 +/- 131% of control. ICP values were significantly different between SCh and placebo treatments only during the periods of greatest CBF (1 to 5 min after iv SCh). Average PaCO2 values after iv SCh were significantly greater than pre-SCh control values and placebo values during each 15-min measurement interval. Average PaCO2 was 116 +/- 2% of control during the 0-15 min measurement period, 114 +/- 2% of control during the 15-30 min period, and 109 +/- 1% of control during the 30-45 min period. CVP, MAP, and CMRO2 did not significantly change after iv SCh.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia↗
PubMed1990

The effects of intravenous succinylcholine on cerebral function and muscle afferent activity following complete ischemia in halothane-anesthetized dogs.

The effects of iv succinylcholine (SCh) on cerebral blood flow (CBF), the electroencephalogram (EEG), muscle afferent activity (MAA), electromyographic activity (EMG), and PaCO2 were tested in six halothane-anesthetized dogs (1.0 MAC) more than 1 h after a 10-min period of complete cerebral ischemia. All dogs received treatments of both iv SCh (1.0 mg.kg-1) and saline placebo in a random sequence. Fasciculations and substantial increases in EMG activity were observed in all dogs following SCh administration. At the onset of fasciculations, there was an increase in MAA to a peak value of 353 +/- 74% of control (mean +/- SE; n = 5 for MAA; n = 6 for all other variables) at the 1-min measurement point. Thereafter, MAA gradually declined toward control values. There were delayed increases in PaCO2 throughout the 45-min study period, achieving values of 106 +/- 1% to 118 +/- 4% of control (an increase in PaCO2 of 2-7 mmHg). Despite the increases in MAA and PaCO2, there were no significant increases in CBF during the study. The control EEG 1-h after complete cerebral ischemia, but immediately before administering the drug treatments, consisted predominantly of a delta rhythm, denoting cerebral dysfunction. In one dog, SCh administration produced transient attenuation of the delta rhythm, a change consistent with cerebral stimulation. In the remaining five dogs, SCh had no effect on the EEG. Treatment with saline placebo did not affect any variable measured. The authors conclude that, in the electrically dysfunctioning brain (e.g., as occurs following resuscitation from complete cerebral ischemia), the cerebral (i.e., CBF and EEG) response to iv SCh is attenuated when compared to the previously reported response in normal brain.

Anesthesia, Inhalation↗
PubMed1994

Jaw relaxation after a halothane/succinylcholine sequence in children.

BACKGROUND: Lack of complete jaw relaxation after a halothane-succinylcholine sequence has been described in the literature. To date, however, most existing studies are retrospective, and lack agreement on the magnitude and incidence of this phenomenon. This prospective study examined the incidence and degree of incomplete jaw relaxation in 500 children who were given intravenous succinylcholine during halothane anesthesia. METHODS: Five hundred consecutive unmedicated children received a minimum dose of 2 mg/kg intravenous succinylcholine after induction of anesthesia with halothane. The degree of jaw relaxation was assessed 45-60 s later by the same observer using a standardized clinical scale. The degree of relaxation was correlated with the type of surgical procedure, and the presence and intensity of fasciculations. RESULTS: Complete relaxation (mouth opened easily and fully) occurred in 95.4% of study patients. Incomplete relaxation (firm manual separation required to open the mouth fully) was seen in 4.4% of the patients. One child (0.2%) had masseter muscle rigidity (mouth could not be fully opened but intubation possible). There were no incidents of trismus (teeth clamped shut and intubation via direct visualization impossible). The incidence of incomplete relaxation and masseter muscle rigidity did not correlate with the presence or degree of fasciculations or the type of surgical procedure. There were no clinical signs of a hypermetabolic state or myoglobinuria in any patient. CONCLUSIONS: Incomplete jaw relaxation after a halothane-succinylcholine sequence is not uncommon in children, and is considered a normal response.

Anesthesia↗
PubMed1999

Monitoring of anaesthesia in neurophysiological experiments.

Cortical activity can be substantially changed by the type of anaesthetic used, and by its dose level. For easy monitoring of depth of anaesthesia we describe the changes in electroencephalogram and electrocardiogram accompanying changes in depth of anaesthesia in the cat. Anaesthesia was induced by the volatile anaesthetic isoflurane. The high-frequency components (around 30 Hz) in the electroencephalogram disappear in deep anaesthesia. The electrocardiogram also shows substantial changes in contamination due to muscle fasciculations with anaesthesia level. Fasciculations appear as noise in the electrocardiogram. The amplitude of the electrical muscle activity contaminating the ECG can be easily used for the maintainance of a constant level of anaesthesia during a neurophysiological experiment.

Anesthesia↗
PubMed2005

Evaluation of conventional subciliary incision used in blepharoplasty: preoperative and postoperative videography and electromyography findings.

BACKGROUND: The purpose of this study was to evaluate the innervation and function of the orbicularis oculi area clinically, with video imaging, and electrically, with electromyography, before and after lower-eyelid blepharoplasty using a conventional subciliary incision. METHODS: Nine patients (18 eyes) were studied before and 4 to 12 weeks after lower-eyelid blepharoplasty. Video imaging documented clinical changes in involuntary (blink) and voluntary (squeeze and squint) eyelid function as well as resting lid position and tone. Electromyography was performed using concentric needle electrodes (25 mm in length, 0.03 mm in diameter) placed in the lateral and medial subciliary orbicularis oculi. A total of 36 sites in nine patients (four sites per patient) were studied. Acute denervation was identified by the presence of fasciculation; fibrillation potentials; insertional activity; sharp waves; and grade based on standard electromyography techniques. All patients underwent lower-eyelid blepharoplasty with a subciliary incision, skin-muscle flap and canthal anchoring with canthopexy or cantholysis, and canthoplasty. RESULTS: Video imaging of the lower eyelid before and after blepharoplasty showed evidence of eyelid malposition or abnormal voluntary or involuntary orbicularis oculi muscle function. There was no evidence of acute denervation in 34 of 36 sites (94 percent). Two patients had abnormal fasciculation in the left lateral position on two of 36 sites (6 percent). Thirty-three weeks postoperatively, one patient was retested and a normal electromyography result was obtained. CONCLUSIONS: This study demonstrated that lower-lid malposition or abnormal function after lower-lid blepharoplasty cannot be explained by denervation of the zygomatic branch of the facial nerve. Any acute or residual denervation seen in the subciliary orbicularis is not clinically significant. The importance of lower-lid support and canthal anchoring cannot be emphasized enough in preventing lower-lid malposition. Blepharoplasty is a challenging procedure that requires careful preoperative planning, intraoperative reassessment, and meticulous surgical technique to optimize facial rejuvenation and patient safety.

Adult↗
PubMed1982

Diazepam and suxamethonium muscle pain (a dose-response study).

Postoperative muscle pain occurred in 17.2% of patients given diazepam intravenously 5 minutes prior to suxamethonium. The incidence of muscle pain was 48% in those patients who were not given diazepam before suxamethonium. The difference is statistically significant (p less than 0.01). Five mg diazepam reduced the incidence of pain but not significantly (p = 0.30); 10 mg diazepam significantly reduced the incidence (p less than 0.05); while 15 and 20 mg diazepam showed better effects (p less than 0.01). Diazepam pretreatment also reduced the severity, frequency and duration of muscle pain. The incidence of fasciculations was significantly reduced but there was no correlation between the incidence of fasciculations and the occurrence of muscle pains.

Adult↗
PubMed1985

Failure of two benzodiazepines to prevent suxamethonium-induced muscle pain.

In a randomised double-blind trial carried out on fit, unpremedicated patients undergoing standard minor operations with early postoperative mobility, using a standard form of anaesthesia, pretreatment with diazepam 0.15 mg/kg or midazolam 0.1 mg/kg failed to reduce significantly the incidence of postoperative muscle pains following suxamethonium 1 mg/kg. By contrast, tubocurarine 0.05 mg/kg proved to be effective as a pretreatment. Neither benzodiazepine influenced the incidence or severity of fasciculations seen with suxamethonium or the duration of neuromuscular block. Tubocurarine virtually abolished visible fasciculation and, in the dose used, reduced the intensity and duration of the neuromuscular block. There were no clinically significant changes in serum potassium, creatinine phosphokinase or aldolase after suxamethonium, although 5 out of 47 showed an atypical rise in creatinine phosphokinase.

Adolescent↗