Brachial plexus injury as an unusual complication of coronary artery bypass graft surgery.
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Brachial plexus injury is an unusual and under-recognised complication of coronary artery bypass grafting especially when internal mammary artery harvesting takes place. It is believed to be due to sternal retraction resulting in compression of the brachial plexus. Although the majority of cases are transient, there are cases where the injury is permanent and may have severe implications as illustrated in the accompanying case history. (+info)
Scheuermann's disease as a model displaying the mechanism of venous obstruction in thoracic outlet syndrome and migraine patients: MRI and MRA.
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Kyphosis of the thoracic spine rotates the scapulae anterior laterally, clavicles and subclavius muscles anteriorly, displaces the manubrium posteriorly, which increases the slope of the first ribs. This increases tension on the anterior scalene muscles and the neurovascular bundles which causes brachial plexopathy (TOS). Scheuermann's disease (spinal osteochondrosis; juvenile kyphoscoliosis) is a disorder which consists of vertebral wedging endplate irregularity and narrowing of the intervertebral disk space causing kyphosis of the thoracic spine and may also involve the lumbar space. It occurs at puberty and involves both male and females. Abduction external rotation of the upper extremities (arms overhead) posterior inferiorly rotate the clavicles and the subclavius muscles which enhances tension on the venous drainage and neurovascular supply that diminishes venous return. This triggers complaints of thoracic outlet syndrome (TOS) and migraine headache. Bilateral magnetic resonance imaging (MRI) demonstrates compressing abnormalities of the brachial plexus. Five patients with Scheuermann's disease were imaged with the 1.5 Tesla magnet (Signa; General Electric Medical Systems, Milwaukee, WI) 3-D reconstruction MRI. T1W and T2W pulse sequences were performed in transverse, the coronal, transverse oblique, sagittal, and coronal abduction external rotation planes using 4 mm slice thickness and 512 x 256 matrix size. Water bags were used to enhance the signal to noise ratio. Magnetic resonance angiography (MRA) 2-D Time Of Flight (TOF) was obtained to compression for anatomic display evaluate perfusion of the brachial plexus. MRI and MRA captured sites of brachial plexus. One patient was selected for this presentation, which demonstrates the compression of the brachial plexus and venous obstruction which triggered complaints of thoracic outlet syndrome. (+info)
Prognosis and early management of birth injuries to the brachial plexus.
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Twenty-four cases of birth injury to the brachial plexus were seen in 21 infants over 15 years. Obstetric complications were common, and in 11 cases traction was needed to deliver the shoulders. Three out of every four arms fully recovered after exercises. Splints were not needed. Reconstructive procedures were performed on three permanently paralysed arms when the children were aged about 4. There was no way of predicting which patients would recover. The muscles supplied by the suprascapular nerve were paralysed in all patients, and this paralysis persisted in those whose arms failed to recover fully. (+info)
Ultrasonography for depiction of brachial plexus injury.
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Recent development of ultrasonographic equipment has allowed improved spatial resolution for visualizing normal and pathologic conditions of peripheral nerves. Regarding the brachial plexus, only ultrasonographic studies that have described the normal appearance have been reported. To the best of our knowledge, no case report regarding the ultrasonographic description of a brachial plexus lesion has been published. We report the ultrasonographic findings of a brachial plexus injury after extirpation of a suspected enlarged supraclavicular lymph node. (+info)
Similar motor block effects and disposition kinetics between lidocaine and (+/-)mepivacaine in patients undergoing axillary brachial plexus block during day case surgery.
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The aim of this investigation was to compare the clinical effects and pharmacokinetics of lidocaine (one metabolite) and mepivacaine (two metabolites) in 2 groups of 15 patients undergoing axillary brachial plexus anaesthesia. The study had a randomised design. The 30 patients were divided into 2 groups. The patients received either lidocaine (600 mg = 2.561 mMol + 5 mg ml(-1) adrenaline) or mepivacaine (600 mg = 2.436 mMol + 5 microg ml(-1) adrenaline), injected via the axilla near the brachial plexus over a period of 30 s. Onset of surgical analgesia was defined as the period from the end of the local anaesthetic injection to the loss of pinprick sensation in the distribution of the ulnar, radial, and median nerve. Motor block was measured. Onset of motor block was similar for both drugs. Lidocaine is eliminated biexponentially with a t1/2alpha of 9.95 +/- 14.3 min and a t1/2beta of 2.86 +/- 1.55 h. Lidocaine is metabolised into MEGX (tmax 2.31 +/- 0.84 h; Cmax 0.32 +/- 0.13 mg l(-1); t1/2beta 2.36 +/- 2.35 h; total body clearance was 67.9 +/- 28.9 l h(-1)). Mepivacaine is eliminated rapidly and monoexponentially with a t1/2 of 4.78 +/- 2.38 h, a Cmax of 3.89 +/- 0.83 mg l(-1), and a tmax of 0.41 +/- 0.19 h. The total body clearance of mepivacaine is 50% of that of lidocaine, 26.9 +/- 10.6 l h(-1) vs. 67.9 +/- 28.9 l h-1, respectively (p < 0.0001). (+/-)mepivacaine is metabolised into (+/-)4-OHmepivacaine (Cmax 0.45 +/- 0.25 mg l(-1); t1/2beta 6.48 +/- 6.57 h) and (+/-)2,6-pipecoloxylidide (Cmax 0.56 +/- 0.30 mg l(-1); t1/2beta 1.48 +/- 0.74 h). For the axillary brachial plexus block, lidocaine and mepivacaine show similar pharmacodynamic and pharmacokinetic behaviour, despite the number of metabolites, and can therefore be used to the clinical preference for this regional anaesthetic technique. (+info)
MR imaging in human rabies.
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BACKGROUND AND PURPOSE: Whether human rabies of different forms, encephalitic (furious) and paralytic (dumb), share similar MR imaging patterns is unknown. We assessed the diagnostic value of MR imaging in both forms of the disease and compared the clinical and neuroimaging findings. METHODS: Three patients with paralytic and two with encephalitic rabies were examined during preserved or deteriorated levels of consciousness. Six MR examinations of the brain, three of the spinal cord, and one of the brachial plexus were performed with a 1.5-T superconducting magnet. RESULTS: No difference was noted between the MR findings in both clinical forms of human rabies. Nonenhancing, ill-defined, mild hyperintensity changes in the brain stem, hippocampi, hypothalami, deep and subcortical white matter, and deep and cortical gray matter were demonstrated on T2-weighted images in the noncomatose patients with rabies. Enhancement along the brachial plexus of the bitten arm was noted in one patient with encephalitic rabies who at that time had only local neuropathic pain symptoms. Enhancement with gadolinium-based contrast material was seen at the hypothalami, brain stem nuclei, spinal cord gray matter, and intradural cervical nerve roots only when the patients became comatose. CONCLUSION: Both forms of human rabies share a similar MR imaging pattern. Such pattern and the lack of enhancement in a noncomatose patient with suspected encephalitis may differentiate rabies from other viral encephalitides. (+info)
Failure of activation of spinal motoneurones after muscle fatigue in healthy subjects studied by transcranial magnetic stimulation.
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During a sustained maximal effort a progressive decline in the ability to drive motoneurones (MNs) develops. We used the recently developed triple stimulation technique (TST) to study corticospinal conduction after fatiguing exercise in healthy subjects. This method employs a collision technique to estimate the proportion of motor units activated by a transcranial magnetic stimulus. Following a sustained contraction of the abductor digiti minimi muscle at 50 % maximal force maintained to exhaustion there was an immediate reduction of the TST response from > 95 % to about 60 %. This effect recovered to control levels within 1 min and implies that a decreased number of spinal MNs were excited. Additional TST experiments after maximal and submaximal efforts showed that the decrease in size of the TST response was related to duration and strength of exercise. Motor evoked potentials (MEPs) after conventional transcranial magnetic stimulation (TMS) and responses to peripheral nerve stimulation were recorded following the same fatigue protocol. The size of both the MEPs and the peripheral responses increased after the contraction and were in direct contrast to the decrease in size of the TST response. This points to increased probability of repetitive spinal MN activation during fatigue even if some MNs in the pool failed to discharge. Silent period duration following cortical stimulation lengthened by an average of 55 ms after the contraction and recovered within a time course similar to that of the TST response depression. Overall, the results suggest that the outflow from the motor cortex could become insufficient to drive all spinal MNs to discharge when the muscle is fatigued and that complex interactions between failure of activation and compensatory mechanisms to maintain motor unit activation occur during sustained voluntary activity. When inability to maintain force occurs during submaximal effort, failure of activation of motor units is predominant. (+info)
Systemically administered alpha2-agonist-induced peripheral vasoconstriction in humans.
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BACKGROUND: alpha(2)-Adrenoceptors mediate both sympatholytic and vasoconstrictive hemodynamic effects. The goal of this study was to profile the peripheral vasoconstrictive effects of a selective alpha(2)-adrenoceptor agonist in isolation from the sympatholytic effects it also induces. METHODS: The authors administered increasing plasma target concentrations of dexmedetomidine (0.075, 0.15, 0.3, and 0.6 ng/mL) or saline placebo to healthy young volunteers in whom the sympatholytic effects of the drug were attenuated in one of two ways: general anesthesia (propofol-alfentanil-nitrous oxide) or axillary brachial plexus block. Measurements were made of finger blood volume (an indicator of vasoconstriction) by photoplethysmographic determination of light transmitted through a finger (LTF) and hemodynamic variables. Measurements made before and during the four steps of infusion were compared by repeated-measures ANOVA. RESULTS: In anesthetized volunteers, all concentrations of dexmedetomidine increased LTF (vasoconstriction) and systolic blood pressure (P < 0.001 for both), whereas placebo did not. In awake volunteers, all concentrations decreased systolic blood pressure (P < 0.001). Concentrations of 0.15, 0.3, and 0.6 ng/mL decreased LTF (vasodilation) in the neurally intact hand; in contrast, the same concentrations increased LTF (vasoconstriction) in the sympathectomized hand (P < 0.001 for both). CONCLUSIONS: The results of this study are the first to characterize the lower end of the dose-response curve for vasoconstriction induced by dexmedetomidine. By denervating the vascular bed of interest or by decreasing sympathetic nervous system activity, the authors were able to observe vasoconstriction induced by a systemically administered alpha(2)-agonist with minimal interference from the sympatholytic effects of the drug. (+info)