Left Abductor Pollicis Brevis Muscle Research Articles

Interhemispheric Inhibition Between Primary Sensory Cortices is not Influenced by Acute Muscle Pain

Bilateral deficits in sensorimotor function have been observed in unilateral musculoskeletal pain conditions. Altered interhemispheric inhibition (IHI) between primary sensory cortices (S1s) is one mechanism that could explain this phenomenon. However, IHI between S1s in response to acute muscle pain, and the relationship between IHI and pressure pain sensitivity in the unaffected limb have not been examined. In 21 healthy individuals, IHI was assessed using somatosensory evoked potentials in response to paired median nerve electrical stimulation at: 1) baseline; 2) immediately following pain resolution; and 3) at 30-minutes follow-up. Acute muscle pain was induced by injection of hypertonic saline into the right abductor pollicis brevis (APB) muscle. Pressure pain thresholds were assessed at the right and left APB muscles before and 30-minutes after pain resolution. Compared to baseline, IHI from the affected to unaffected S1 was unaltered in response to acute muscle pain immediately following pain resolution, or at 30-minutes follow-up. Pressure pain thresholds were reduced over the right (P = .001) and left (P = .001) APB muscles at 30-minutes follow-up. These findings suggest IHI between S1s is unaffected by acute, short-lasting muscle pain, despite the development of increased sensitivity to pressure in the unaffected APB muscle. PerspectiveIHI from the affected S1 (contralateral to the side of pain) to unaffected S1 is unaltered following the resolution of acute muscle pain. This finding suggests that IHI between S1s may not be relevant in the development of bilateral sensorimotor symptoms in unilateral pain conditions.

Convergent Associative Motor Cortical Plasticity Induced by Conditional Somatosensory and Motor Reaction Afferents.

Objective: Associative motor cortical plasticity can be non-invasively induced by paired median nerve electric stimulation and transcranial magnetic stimulation (TMS) of the primary motor cortex (M1). This study investigates whether a simultaneous motor reaction of the other hand advances the associative plasticity in M1.Methods: Twenty-four right-handed subjects received conventional paired associative stimulation (PAS) and PAS with simultaneous motor reaction (PASmr) with at least a 1-week interval. The PASmr protocol additionally included left abductor pollicis brevis muscle movement responding to a digital sound. The motor reaction time was individually measured. The M1 excitability was examined by the motor evoked potential (MEP), short-interval intracortical inhibition (SICI), and intracortical facilitation (ICF) before and after the PAS protocols.Results: The conventional PAS protocol significantly facilitated MEP and suppressed SICI. A negative correlation between the reaction time and the MEP change, and a positive correlation between the reaction time and the ICF change were found in the PASmr protocol. By subgrouping analysis, we further found significant facilitation of MEP and a reduction of ICF in the subjects with fast reaction times but not in those with slow reaction times.Conclusion: Synchronized motor reaction ipsilateral to the stimulated M1 induces associative M1 motor plasticity through the spike-timing dependent principle. MEP and ICF change could represent this kind of plasticity. The current findings provide a novel insight into designing rehabilitation programs concerning motor function.

Brain changes following four weeks of unimanual motor training: Evidence from behavior, neural stimulation, cortical thickness, and functional MRI.

Although different aspects of neuroplasticity can be quantified with behavioral probes, brain stimulation, and brain imaging assessments, no study to date has combined all these approaches into one comprehensive assessment of brain plasticity. Here, 24 healthy right-handed participants practiced a sequence of finger-thumb opposition movements for 10 min each day with their left hand. After 4weeks, performance for the practiced sequence improved significantly (P < 0.05 FWE) relative to a matched control sequence, with both the left (mean increase: 53.0% practiced, 6.5% control) and right (21.0%; 15.8%) hands. Training also induced significant (cluster p-FWE < 0.001) reductions in functional MRI activation for execution of the trained sequence, relative to the control sequence. These changes were observed as clusters in the premotor and supplementary motor cortices (right hemisphere, 301 voxel cluster; left hemisphere 700 voxel cluster), and sensorimotor cortices and superior parietal lobules (right hemisphere 864 voxel cluster; left hemisphere, 1947 voxel cluster). Transcranial magnetic stimulation over the right ("trained") primary motor cortex yielded a 58.6% mean increase in a measure of motor evoked potential amplitude, as recorded at the left abductor pollicis brevis muscle. Cortical thickness analyses based on structural MRI suggested changes in the right precentral gyrus, right post central gyrus, right dorsolateral prefrontal cortex, and potentially the right supplementary motor area. Such findings are consistent with LTP-like neuroplastic changes in areas that were already responsible for finger sequence execution, rather than improved recruitment of previously nonutilized tissue. Hum Brain Mapp 38:4773-4787, 2017. © 2017 Wiley Periodicals, Inc.

Recovery of an injured corticospinal tract during a critical period in a patient with intracerebral hemorrhage

Most of the motor recovery in stroke occurs within 3 months after stroke onset and this period has been regarded as critical for motor recovery. Little is known about the motor recovery process during the critical period of stroke. We report on a patient with intracerebral hemorrhage (ICH) who showed recovery of an injured corticospinal tract (CST) during the critical period for motor recovery. A 43-year-old woman underwent conservative management for a spontaneous ICH in the right corona radiata and basal ganglia. She presented with complete left hemiplegia at the onset of ICH. She showed continuous and slow recovery, and consequently, she was able to flex her left fingers without gravity at 6 weeks after onset and extend the left fingers without gravity at 12 weeks. The 3- and 6-week DTTs showed that the right CST was discontinued around the hematoma. However, the 12-week DTT revealed that the right CST was originated from the right primary motor cortex and descended along the CST pathway. No motor evoked potential (MEP) was evoked from the right hemisphere on the 3- and 6-week TMS study. However, on the 12-week TMS study, an MEP which had the characteristics of the CST was evoked from the right hemisphere to the left abductor pollicis brevis muscle. Our results indicate that the injured right CST had been recovered between 6 weeks and 12 weeks after ICH onset. Consequently, we believe that this case demonstrated the recovery process of a severely injured CST during the critical period for motor recovery after ICH.

Influence of current direction on short-interval intracortical facilitation probed with paired-pulse TMS

Background: Transcranial magnetic stimulation (TMS) of the human primary motor hand area (M1-HAND) can produce multiple descending volleys in fast-conducting corticospinal neurons, especially so-called I waves which result from trans-synaptic excitation. The facilitatory interaction between these I waves can be studied with paired-pulse TMS using a conditioning-test paradigm referred to as short interval intracortical facilitation (SICF). Here, we examined whether SICF depends on the current direction of the TMS pulses. Methods: In ten healthy volunteers aged 22–29, we applied paired-pulse TMS to right M1-HAND at intensity slightly above resting motor threshold to probe the impact of current direction on SICF. SICF was tested at inter-stimulus intervals (ISIs) ranging from 1.0 to 5.0 ms by recording the motor evoked potential (MEP) from the left abductor pollicis brevis muscle. In a first experiment, we probed SICF with monophasic stimuli evoking an anterior-posterior (AP-AP condition) or posterior-anterior (PA-PA condition) current in M1-HAND. In a separate experiment, the two TMS pulses had a half-sine wave configuration and evoked tissue currents with opposing directions (PA-AP condition and AP-PA condition). Results: For all four combinations of current directions, paired-pulse TMS yielded three facilitatory peaks at ISIs of 1.2, 2.6 and 4.8 ms separated by distinct troughs without facilitation. The SICF peaks were comparable with respect to magnitude and periodicity. Conclusion: The results indicate that, at slightly suprathreshold intensities, all types of sagittally oriented tissue currents induce a similar amount of facilitatory I wave interaction in human M1-HAND when using a conventional SICF paradigm.

Carpal Tunnel Syndrome After Ciprofloxacin-Induced Tendinitis

To the Editor: Different types of antibiotics can affect the peripheral nervous system and cause neuropathies, myopathies, and neuromuscular junction disorders by direct or indirect mechanisms.1 Fluoroquinolones may also cause seizures or encephalopathy, and a few cases of tendinitis have been reported as well.2-4 Tendinitis may occur as early as 2 hours after the first dose, and 50% of patients develop symptoms within 6 days of starting medication. Tenosynovitis has also been reported in association with recurrent carpal tunnel syndrome.5 We report a case of ciprofloxacin-related tendinitis leading to carpal tunnel syndrome A 77-year-old right-handed woman developed a urinary tract infection and was empirically treated with oral ciprofloxacin. Three days later, she developed bilateral hand pain and swelling, which improved after the medication was stopped and with a brief course of oral steroids and antihistamines. Symptoms were consistent with flexor tendinitis with focal tenderness and swelling. There was no history of diabetes, gout, rheumatoid arthritis, or of other autoimmune diseases. Because severe pain persisted waking her up, she was referred to a neurologist. At that time, 4 weeks after the onset and swelling resolved, the pain still involved the first three fingers, more severely on the left. She performed her daily activities independently, but pain got worse when these fingers were touched. She denied any neck or upper arm discomfort. On examination, she had slight atrophy and weakness of left thenar muscles (Medical Research Council 5-/5) with decreased sensation over distal aspects of the first three fingers on the left and left thenar allodynia. The remainder of the examination was normal. Electrodiagnostic testing was performed at 6 weeks after the onset and confirmed the diagnosis of bilateral distal median nerve entrapments (carpal tunnel syndrome) (Table 1), more severe on the left. Needle examination showed only few fibrillation potentials in the left abductor pollicis brevis muscle. The use of a wrist splint did not alleviate the symptoms. Repeat study 3 months later did not show significant improvement. Because symptoms persisted, she underwent bilateral sequential carpal tunnel releases resulting in resolution of her symptoms. Flexor tendinitis and inflammatory arthritis can precipitate median nerve entrapment in a confined space of carpal tunnel. Increased incidence of tendonitis has been described in elderly (older than 60 years of age) and with renal dysfunction or corticosteroid treatment.2-4 Most commonly, Achilles and patellar tendons are affected, but few cases of shoulder and hand tendinitis were reported. 2,3 Tendon rupture was reported in 5% of patients with quinolone-related tendinitis.2 Timely discontinuation of ciprofloxacin in our patient probably prevented tendon rupture and more significant nerve injury. Asymmetry of median nerve entrapments with more severe findings on the left in our case may be attributable to asymmetric tendinitis or possible pre-existing nerve entrapment aggravated by inflammation. Therefore, we should consider drug-induced tendinitis as a potential cause of musculoskeletal pain after institution of fluoroquinolone therapy. A recent report indicates that fluoroquinolones may also precipitate painful small fiber neuropathy expanding the spectrum of their toxicity.6 Early recognition of possible toxicity is crucial to stop the offending agent, avoid exercise, and hopefully reduce morbidity of fluoroquinolone-induced tendinitis.

Nitrous oxide can enhance the hypnotic effect, but not the suppression of spinal motor neuron excitability by propofol in humans

We investigated whether nitrous oxide can enhance the suppressive effect of propofol on spinal motor neuron excitability in humans. Sixteen adult patients were prospectively randomly assigned to be given either propofol alone (group P; n = 8) or a supplement of 66% nitrous oxide with propofol (group PN; n = 8) for intraoperative sedation. Propofol was administered by a target-controlled infusion system to maintain sequentially increasing plasma propofol concentrations (Cpt) of 0.5, 0.8, 1.0, 1.3, 1.5 and 1.8 microg x ml(-1) in all patients. Assessment of the patient's level of sedation in both groups was performed with the Wilson Sedation Scale (WSS). F-wave analysis on the left abductor pollicis brevis muscle was carried out for the assessment of spinal motor neuron excitability at each plasma propofol concentration. Significant differences in the WSS scores between group P and group PN were observed at 0.8, 1.0, 1.3, and 1.5 microg x ml(-1) of Cpt (group P < group PN; P < 0.01). Cpt greater than 1.0 microg x ml(-1) significantly reduced F-wave persistence in a concentration-dependent manner, and the ICpt 50 and ICpt 95 values for plasma propofol concentration (plasma propofol concentrations that produced 50% and 95% inhibition of the baseline, respectively) were 1.05 and 1.95 microg x ml(-1) in group P, and 1.07 and 2.14 microg x ml(-1) in group PN, respectively. These results suggest that nitrous oxide can enhance the hypnotic effect, but not the suppression of spinal motoneuron excitability by propofol in humans at clinical levels of Cpt.

Efficacy of a half dose of oral pyridostigmine in the treatment of chronic fatigue syndrome: three case reports

Chronic fatigue syndrome (CFS) is characterized by persistent mental and physical fatigue for at least 6 months. Its pathophysiology is unknown and there is no proven effective treatment. We describe three cases who fulfill the criteria of CFS, in whom a defect of neuromuscular transmission and dysautonomia are present and who respond to acetylcholine-esterase inhibition. Case 1: 18-year-old female with a 3-year history of CFS. Response of compound-muscle-action potential, recorded using surface recording electrode, over left abductor pollicis brevis muscle, to repetitive nerve stimulation (RNS) at a rate of 10 Hz showed a 42% incremental response. Composite autonomic scoring system (CASS) showed mild cholinergic impairment (cardiovagal score: 1; sudomotor score: 2). Serological tests for Epstein–Barr virus (EBV) revealed positive antiviral capsid antigens (anti-VCA) immunoglobulins G (IgG). Oral pyridostigmine therapy (30 mg) resulted in marked improvement in symptoms. Case 2: 28-year-old female with 10-year history of CFS. RNS, using identical protocol, showed a 60% incremental response over the same muscle. CASS showed mild cholinergic impairment (cardiovagal score: 1; sudomotor score: 2) and this patient was also positive for EBV. This patient responded dramatically to 10-mg pyridostigmine. Case 3: 29-year-old female with a history of CFS for longer than 15 years. Repetitive stimulation, using identical paradigm to left abductor pollicis brevis muscle, showed a 42% incremental response. CASS showed mildly cholinergic impairment (cardiovagal score: 2; sudomotor score: 1). EBV antibody titers were positive. Patient responded to 30-mg pyridostigmine with an improvement in her fatigue. These three cases generate the hypothesis that the fatigue in some patients with clinical CFS might be due to a combination of mild neuromuscular transmission defect combined with cholinergic dysautonomia. Support for this thesis derives from the improvement with cholinesterase inhibition.

Elevated 14-3-3 protein and axonal loss in immunoglobulin-responsive, idiopathic acute transverse myelitis

Objectives: To report the elevation of the 14-3-3 protein and the complete denervation of hand muscles in idiopathic acute transverse myelitis (IATM) of the cervical cord. Case description: In a 29-year-old woman with a 2-week history of neck pain and repeated attenuated flus, subacute quadriplegia, hypaesthesia of both arms, a T3 sensory level, and urinary dysfunction occurred. Based upon the clinical findings, the cervical MRIs, and an elevated 14-3-3 protein in the CSF, IATM C4–C7 was diagnosed. Ten, 17, 28 and 61 days after onset, nerve conduction studies revealed complete denervation of the right abductor pollicis brevis and abductor digiti minimi muscles but gradual improvement of the compound muscle action potential of the left abductor pollicis brevis muscle. F-waves of the right median nerve were absent. Tibial somatosensory evoked potentials showed a prolonged central conduction time. Transcranial magnetic stimulation evoked a response in the left but not the right abductor digiti minimi muscle. Conclusion: IATM may cause elevation of the 14-3-3 protein and loss of motor axons originating from affected anterior horn cells.

A noninvasive technique to assess completeness of spinal cord lesions in humans

The effect of scalp stimulation delivered through electrodes overlying the motor cortex was evaluated in five healthy subjects and six patients with traumatic spinal cord injury. The latency to the onset of the electromyographic response was measured in the biceps brachii and abductor pollicis brevis muscles. In all the patients, latencies to the muscle (biceps brachii) whose innervation originated above the lesion were in the normal range; whereas, latencies to the muscle (abductor pollicis brevis) whose innervation originated below the lesion were prolonged. Electromyographic signals were recorded in muscles which showed no voluntary motor activity. No lateral differences in latencies were found in healthy subjects; however, in the patients, significant differences were obtained between the right and left abductor pollicis brevis muscles. The results of this study demonstrate that the spinal cord of patients with a lesion deemed to be clinically complete, contains nerve fibers which descend through the lesion and are capable of conveying impulses leading to muscle contraction.