Intraoperative radial nerve injury during coronary artery surgery – report of two cases

BACKGROUND: Peripheral nerve injury and brachial plexopathy are known, though rare complications of coronary artery surgery. The ulnar nerve is most frequently affected, whereas radial nerve lesions are much less common accounting for only 3% of such intraoperative injuries. CASE PRESENTATIONS: Two 52- and 50-year-old men underwent coronary artery surgery. On the first postoperative day they both complained of wrist drop on the left. Neurological examination revealed a paresis of the wrist and finger extensor muscles (0/5), and the brachioradialis (4/5) with hypoaesthesia on the radial aspect of the dorsum of the left hand. Both biceps and triceps reflexes were normoactive, whereas the brachioradialis reflex was diminished on the left. Muscles innervated from the median and ulnar nerve, as well as all muscles above the elbow were unaffected. Electrophysiological studies were performed 3 weeks later, when muscle power of the affected muscles had already begun to improve. Nerve conduction studies and needle electromyography revealed a partial conduction block of the radial nerve along the spiral groove, motor axonal loss distal to the site of the lesion and moderate impairment in recruitment with fibrillation potentials in radial innervated muscles below the elbow and normal findings in triceps and deltoid. Electrophysiology data pointed towards a radial nerve injury in the spiral groove. We assume external compression as the causative factor. The only apparatus attached to the patients' left upper arm was the sternal retractor, used for dissection of the internal mammary artery. Both patients were overweight and lying on the operating table for a considerable time might have caused the compression of their left upper arm on the self retractor's supporting column which was fixed to the table rail 5 cm above the left elbow joint, in the site where the radial nerve is directly apposed to the humerus. CONCLUSION: Although very uncommon, external compression due to the use of a self retractor during coronary artery surgery can affect – especially in obese subjects – the radial nerve within the spiral groove leading to paresis and should therefore be included in the list of possible mechanisms of radial nerve injury

Assessment of Impact Energy Harvesting in Composite Beams with Piezoelectric Transducers

Piezoelectric energy harvesting (PEH) is studied in the case of a low-velocity impact of a rigid mass on a composite beam. A methodology is outlined, encompassing modelling of the open-circuit impact response in a finite element (FE) package, formulation of a lumped parameter (LP) model for the piezoelectric transducer connected with the harvesting circuit, and experimental verification of the impact using a custom portable configuration with impactor motion control. The subcircuit capacitor charging effect, the impactor mass and velocity on the harvesting subcircuit response, and the obtained output power are quantified. The results indicate that the current methodology can be used as a design tool for the structure and the harvesting circuit to achieve power output from composite beams with piezoelectric patches under impact conditions

Rituximab therapy in monoclonal IgM-related neuropathies

Monoclonal IgM-related neuropathies constitute a heterogeneous group of disorders, which are generally poorly responsive to treatment. Rituximab, a chimeric monoclonal antibody against the CD20 molecule, has been used with success in patients with neuropathy and monoclonal IgM with anti-MAG or anti-GM1 ganglioside activity. Based on this observation, four patients were treated with IgM-related neuropathy with rituximab. Between January 1999 - December 2000, four patients with IgM-related neuropathy ( one with chronic inflammatory demyelinating polyneuropathy ( CIDP) and three with sensorimotor demyelinating neuropathy) were treated with rituximab. Rituximab was administered at a standard dose of 375 mg m(-2) iv weekly for a consecutive 4 weeks; 3 months later, four additional weekly courses were administered to patients who did not experience deterioration of their neuropathy symptoms. Neurological evaluation was performed before each rituximab infusion and at 1 week and 2 months after last infusion and every 6 months the following years; including motor (MRC in six muscle groups, 9-hole peg test, 10 m walk, hand grip strength), sensory neuropathy ( vibration threshold and sensory subjective score) assessment. Neurophysiological parameters were also assessed (MNCV, SNCV, CMAP, SNAP). Strength improved in three of four patients; including the patient with CIDP. This patient developed a significant worsening of her weakness 3 weeks after the initiation of rituximab. This phenomenon coincided with a serum monoclonal IgM flare and resolved spontaneously 1 week later. Her improvement is ongoing for more than 5 years. Considering neurophysiological parameters, two patients showed a slight improved regarding conduction velocities and CMAP (10%) and the patient with IgM flare had a transient worsening of conduction velocities followed by improvement. In conclusion, rituximab is a safe and well-tolerated treatment which may be effective in some patients with IgM-related neuropathy

Rituximab therapy in monoclonal IgM-related neuropathies

Monoclonal IgM-related neuropathies constitute a heterogeneous group of disorders, which are generally poorly responsive to treatment. Rituximab, a chimeric monoclonal antibody against the CD20 molecule, has been used with success in patients with neuropathy and monoclonal IgM with anti-MAG or anti-GM1 ganglioside activity. Based on this observation, four patients were treated with IgM-related neuropathy with rituximab. Between January 1999 - December 2000, four patients with IgM-related neuropathy ( one with chronic inflammatory demyelinating polyneuropathy ( CIDP) and three with sensorimotor demyelinating neuropathy) were treated with rituximab. Rituximab was administered at a standard dose of 375 mg m(-2) iv weekly for a consecutive 4 weeks; 3 months later, four additional weekly courses were administered to patients who did not experience deterioration of their neuropathy symptoms. Neurological evaluation was performed before each rituximab infusion and at 1 week and 2 months after last infusion and every 6 months the following years; including motor (MRC in six muscle groups, 9-hole peg test, 10 m walk, hand grip strength), sensory neuropathy ( vibration threshold and sensory subjective score) assessment. Neurophysiological parameters were also assessed (MNCV, SNCV, CMAP, SNAP). Strength improved in three of four patients; including the patient with CIDP. This patient developed a significant worsening of her weakness 3 weeks after the initiation of rituximab. This phenomenon coincided with a serum monoclonal IgM flare and resolved spontaneously 1 week later. Her improvement is ongoing for more than 5 years. Considering neurophysiological parameters, two patients showed a slight improved regarding conduction velocities and CMAP (10%) and the patient with IgM flare had a transient worsening of conduction velocities followed by improvement. In conclusion, rituximab is a safe and well-tolerated treatment which may be effective in some patients with IgM-related neuropathy

Oxaliplatin-induced neuropathy: a long-term clinical and neurophysiologic follow-up study

Acute oxaliplatin neurotoxicity and chronic sensory cumulative neuropathy were investigated in a long-term study of 31 consecutive patients with advanced colorectal cancer. Our results improve the knowledge of acute neurotoxicity and support the finding of the persistence of the sensory nerve deficits for years after the cessation of oxaliplatin therapy. Background Oxaliplatin is an effective drug used mainly for advanced colorectal cancer. Neurotoxicity is the major side effect of oxaliplatin. The present clinical and neurophysiologic study was conducted to evaluate patients receiving oxaliplatin therapy. Patients and Methods Thirty-one consecutive patients with colorectal cancer who received oxaliplatin therapy were followed up for more than 3 years. The patients underwent clinical and neurophysiologic tests for large and small fiber function at every visit. Results Most of the patients received oxaliplatin-based chemotherapy at the initial dose of 130 mg/m2 for 6 to 8 cycles, normally every 3 weeks. Acute neurotoxicity with cold and mechanical hyperalgesia was reported by the vast majority of patients after each cycle of therapy and was confirmed by the quantitative sensory, filament, and axon reflex test. Chronic sensory cumulative neuropathy developed in most of the patients after the middle of therapy with numbness and was assessed using clinical scales, nerve conduction studies, and the vibration threshold. Our results support the persistence of the sensory nerve deficits for years after cessation of oxaliplatin therapy. Conclusion Our study has confirmed the results of a few previous long-term studies concerning the persistence of chronic large sensory fiber neuropathy and the influence of the cumulative dose of oxaliplatin on the development and severity of the chronic neuropathy. Our findings have improved the knowledge about the acute oxaliplatin-induced neurotoxicity using the C-fiber axon reflex response. © 2016 Elsevier Inc

Differential sensitivity of thick and thin fibers to HIV and therapy-induced neuropathy

The study assessed HIV-related and anti-retroviral therapy-induced neuropathy in myelinated and unmyelinated nerve fibers. One hundred consecutive HIV patients were examined clinically and standard nerve conduction velocities were measured. In addition, electrically induced sympathetic skin response (SSR) was assessed in the palms and soles. The difference in delay of SSR in palms and soles (Delta SSR) was calculated as an indirect measure of C-fiber conduction velocity. Thick fiber conduction velocities significantly decreased with age and increasing stage of the disease, whereas no effect of stage was found for Delta SSR (p=0.6). In contrast, medication of at least one of the most known neurotoxic drugs zalcitabine, stavudine, or didanosine did not result in significantly lower conduction velocities in thick fibers (51.29 +/- 3.4 m/s vs. 50.86 +/- 3.5 m/s), but was related to an increased Delta SSR. Delta SSR allows an indirect measurement of C-fiber conduction velocity. In HIV this measure of unmyelinated sympathetic fibers was most sensitive to anti-viral treatment whereas conduction velocity of myelinated somatic fibers was more sensitive to disease-related neuropathy. The results suggest that HIV neuropathy preferably affects myelinated and anti-retroviral therapy unmyelinated fibers. (c) 2007 Elsevier B.V. All rights reserved

Presymptomatic neuromuscular disorders disclosed following statin treatment

It is well recognized that statins affect muscular tissue adversely and that their use is associated with clinically important myositis, rhabdomyolysis, mild elevation of serum creatine kinase (CK) levels, myalgias, muscle weakness, muscle cramps, and persistent myalgias or serum CK level elevations after statin treatment is discontinued. The association between statins and the disclosure of presymptomatic metabolic myopathy is another underrated phenomenon related to statin therapy that was recently recognized in rare cases. The purpose of this report is to provide additional support for this association and to report other neuromuscular disorders that have also been seen following statin intake. The present case series illustrates that statins may act as unmasking agents in asymptomatic patients with a latent neuromuscular disorder. Thus, it may be postulated that statin intake may be a sufficient insult to precipitate neuromuscular symptoms and substantially increase muscle enzymes in presymptomatic patients with an abnormal neuromuscular substrate. In conclusion, muscular symptoms or increased serum CK levels persisting after statin treatment discontinuation should alert the clinician to pursue further diagnostic evaluations for the detection of potential underlying neuromuscular diseases

Mutational analysis of Greek patients with suspected hereditary neuropathy with liability to pressure palsies (HNPP): a 15-year experience

There has been limited information from population studies regarding the overall frequency of the common 1.5-Mb 17p11.2 deletion and even scarcer data regarding the overall frequency of PMP22 micromutations in patients with a clinical suspicion of hereditary neuropathy with liability to pressure palsies (HNPP). We have analysed 100 consecutive Greek patients referred for HNPP genetic testing over a 15-year period to our Neurogenetics Unit in Athens, a reference centre for all regions of Greece. All patients were screened for the 1.5-Mb deletion and a selected subgroup of deletion-negative patients for PMP22 micromutations. Mutation-positive and mutation-negative patients were compared for various clinical parameters. In total, 54 mutation-positive patients were identified. In index cases, the deletion frequency was 47.8%, and the PMP22 micromutation frequency was 2.2%. Within mutation-positive patients, the common deletion represented 95.7% and PMP22 micromutations 4.3% of cases. Two previously reported PMP22 micromutations (c.364_365delCC and c.79-2A>G) were detected. HNPP index cases had a 2.8-1 male-to-female ratio, similar to mutation-negative patients. A typical phenotype (recurrent or isolated palsies) was present in 82.4% of symptomatic HNPP cases, significantly higher than mutation-negative patients. Sensitivity of proposed electrophysiological diagnostic criteria for HNPP was calculated at 95.7% and specificity at 80.5%. In conclusion, the common HNPP deletion accounts for approximate to 50% and PMP22 micromutations for approximate to 2% of cases in a large consecutive cohort of patients with suspected HNPP. The mutational and phenotypic spectrum of HNPP is similar in the Greek population compared with other populations. Proposed electrophysiological diagnostic criteria perform satisfactorily in everyday clinical practice