Little evidence for an epidemic of myopia in Australian primary school children over the last 30 years

BACKGROUND: Recently reported prevalences of myopia in primary school children vary greatly in different regions of the world. This study aimed to estimate the prevalence of refractive errors in an unselected urban population of young primary school children in eastern Sydney, Australia, between 1998 and 2004, for comparison with our previously published data gathered using the same protocols and other Australian studies over the last 30 years. METHODS: Right eye refractive data from non-cycloplegic retinoscopy was analysed for 1,936 children aged 4 to 12 years who underwent a full eye examination whilst on a vision science excursion to the Vision Education Centre Clinic at the University of New South Wales. Myopia was defined as spherical equivalents equal to or less than -0.50 D, and hyperopia as spherical equivalents greater than +0.50 D. RESULTS: The mean spherical equivalent decreased significantly (p < 0.0001) with age from +0.73 ± 0.1D (SE) at age 4 to +0.21 ± 0.11D at age 12 years. The proportion of children across all ages with myopia of -0.50D or more was 8.4%, ranging from 2.3% of 4 year olds to 14.7% of 12 year olds. Hyperopia greater than +0.50D was present in 38.4%. A 3-way ANOVA for cohort, age and gender of both the current and our previous data showed a significant main effect for age (p < 0.0001) but not for cohort (p = 0.134) or gender (p = 0.61). CONCLUSIONS: Comparison of our new data with our early 1990s data and that from studies of over 8,000 Australian non-clinical rural and urban children in the 1970's and 1980's provided no evidence for the rapidly increasing prevalence of myopia described elsewhere in the world. In fact, the prevalence of myopia in Australian children continues to be significantly lower than that reported in Asia and North America despite changing demographics. This raises the issue of whether these results are a reflection of Australia's stable educational system and lifestyle over the last 30 years

An Estimation of the Extent of Cropland Abandonment in Mountainous Regions of China

With the wages for migrant workers increasing dramatically in China since 2003, the size of the agricultural labour forces has been shrinking rapidly. Intensively substituting agricultural machinery for the shrinking farm labour force is hardly possible for croplands in the mountainous regions of China where mechanization is difficult to achieve due to small field size and rough terrain. This has eventually led to cropland abandonment in these regions. Considering the high pressure for food security in China, cropland abandonment in the mountainous regions should not be ignored. By employing a novel method, this study estimates the extent of recently abandoned croplands (period 2000–2010) and the changes that can be expected in the future in China's mountainous areas. The results show that the total extent of abandoned croplands in Chinese mountainous counties during the period 2000 to 2010 is estimated at 147 million mu (1 mu = 666.67 m2); in total, about 28% of croplands in mountainous counties was abandoned, including croplands converted in the Grain for Green Programme. With 3 scenario assumptions, a sizeable extent, 114 to 203 million mu, of croplands may be abandoned from 2010 to 2030 with the rapid decrease and ageing of projected farm labour forces. This could exacerbate the future challenges of maintaining China's food security. A substantial increase in agricultural project investments, including land consolidation and agricultural productive fixed assets, especially microtillage machines, could help mitigate the risk of cropland abandonment. Additionally, land‐use and environmental policymaking should take into account the expanding cropland abandonment in mountainous regions

Burning pain: Axonal dysfunction in erythromelalgia

Erythromelalgia (EM) is a rare neurovascular disorder characterized by intermittent severe burning pain, erythema, and warmth in the extremities on heat stimuli. To investigate the underlying pathophysiology, peripheral axonal excitability studies were performed and changes with heating and therapy explored. Multiple excitability indices (stimulus-response curve, strength-duration time constant (SDTC), threshold electrotonus, and recovery cycle) were investigated in 23 (9 EMSCN9A+ and 14 EMSCN9A-) genetically characterized patients with EM stimulating median motor and sensory axons at the wrist. At rest, patients with EM showed a higher threshold and rheobase (P < 0.001) compared with controls. Threshold electrotonus and current-voltage relationships demonstrated greater changes of thresholds in both depolarizing and hyperpolarizing preconditioning electrotonus in both EM cohorts compared with controls in sensory axons (P < 0.005). When average temperature was raised from 31.5°C to 36.3°C in EMSCN9A+ patients, excitability changes showed depolarization, specifically SDTC significantly increased, in contrast to the effects of temperature previously established in healthy subjects (P < 0.05). With treatment, 4 EMSCN9A+ patients (4/9) reported improvement with mexiletine, associated with reduction in SDTC in motor and sensory axons. This is the first study of primary EM using threshold tracking techniques to demonstrate alterations in peripheral axonal membrane function. Taken together, these changes may be attributed to systemic neurovascular abnormalities in EM, with chronic postischaemic resting membrane potential hyperpolarization due to Na + /K + pump overactivity. With heating, a trigger of acute symptoms, axonal depolarization developed, corresponding to acute axonal ischaemia. This study has provided novel insights into EM pathophysiology

Short-term peripheral nerve stimulation ameliorates axonal dysfunction after spinal cord injury

© 2015 the American Physiological Society. There is accumulating evidence that peripheral motor axons deteriorate following spinal cord injury (SCI). Secondary axonal dysfunction can exacerbate muscle atrophy, contribute to peripheral neuropathies and neuropathic pain, and lead to further functional impairment. In an attempt to ameliorate the adverse downstream effects that developed following SCI, we investigated the effects of a short-term peripheral nerve stimulation (PNS) program on motor axonal excitability in 22 SCI patients. Axonal excitability studies were undertaken in the median and common peroneal nerves (CPN) bilaterally before and after a 6-wk unilateral PNS program. PNS was delivered percutaneously over the median nerve at the wrist and CPN around the fibular head, and the compound muscle action potential (CMAP) from the abductor pollicis brevis and tibialis anterior was recorded. Stimulus intensity was above motor threshold, and pulses (450 µs) were delivered at 100 Hz with a 2-s on/off cycle for 30 min 5 days/wk. SCI patients had consistently high thresholds with a reduced CMAP consistent with axonal loss; in some patients the peripheral nerves were completely inexcitable. Nerve excitability studies revealed profound changes in membrane potential, with a “fanned-in” appearance in threshold electrotonus, consistent with membrane depolarization, and significantly reduced superexcitability during the recovery cycle. These membrane dysfunctions were ameliorated after 6 wk of PNS, which produced a significant hyperpolarizing effect. The contralateral, nonstimulated nerves remained depolarized. Short-term PNS reversed axonal dysfunction following SCI, may provide an opportunity to prevent chronic changes in axonal and muscular function, and may improve rehabilitation outcomes

Segmental motoneuronal dysfunction is a feature of amyotrophic lateral sclerosis

© 2014 International Federation of Clinical Neurophysiology. Objectives: There is accumulating evidence of dysfunction of spinal circuits in the pathogenesis of amyotrophic lateral sclerosis (ALS). Methods: The present study was undertaken to characterise the pathophysiological changes in segmental motoneuronal excitability in 28 ALS patients, using recruitment curves of the soleus H-reflex and M-wave, compared with clinical assessments of upper motor neuron (UMN) and lower motor neuron dysfunction. Results: H-reflex recruitment curves established that Hmax/Mmax and slope (Hθ/Mθ) ratios predicted clinical UMN dysfunction (p<0.001). Changes in Hθ/Mθ were driven by reduced Mθ. Assessment of Hmax/Mmax was similar in the ALS and control groups, and was affected by overlap of the H and M recruitment curves in ALS patients. Conclusion: Changes in the slope ratio (Hθ/Mθ) in ALS suggested that alterations in peripheral motor nerve excitability following UMN damage may affect the recorded H-reflex. Increased collision of reflex discharges with antidromically-conducted motor impulses may be exacerbated in ALS due to preferential loss of large-caliber α-motoneurones, which may explain the similarities in Hmax/Mmax between groups. Significance: Findings from the present study provide further insight into the pathophysiology of ALS, specifically the relative contributions of premotoneuronal and segmental motoneuronal dysfunction

Paclitaxel-induced neuropathy: Potential association of MAPT and GSK3B genotypes

Background: Paclitaxel treatment produces dose-limiting peripheral neurotoxicity, which adversely affects treatment and long-term outcomes. In the present study, the contribution of genetic polymorphisms to paclitaxel-induced neurotoxicity were assessed in 21 patients, focusing on polymorphisms involved in the tau-microtubule pathway, an important target of paclitaxel involved in neurotoxicity development. Methods: Polymorphisms in the microtubule-associated protein tau (MAPT) gene (haplotype 1 and rs242557 polymorphism) and the glycogen synthase kinase-3ß (GSK3ß) gene (rs6438552 polymorphism) were investigated. Neurotoxicity was assessed using neuropathy grading scales, neurophysiological studies and patient questionnaires. Results: A significant relationship between the GSK-3B rs6438552 polymorphism and paclitaxel-induced neurotoxicity was evident. Conclusions: Polymorphisms in tau-associated genes may contribute to the development of paclitaxel-induced neurotoxicity, although larger series will be necessary to confirm these findings

Motor unit changes in children with symptomatic spinal muscular atrophy treated with nusinersen

Objectives To elucidate the motor unit response to intrathecal nusinersen in children with symptomatic spinal muscular atrophy (SMA) using a novel motor unit number estimation technique. Methods MScanFit MUNE studies were sequentially undertaken from the abductor pollicis brevis muscle after stimulation of the median nerve in a prospective cohort of symptomatic children with SMA, undergoing intrathecal treatment with nusinersen at a single neuromuscular centre from June 2017 to August 2019. Electrophysiological measures included compound muscle action potential (CMAP), motor unit number estimation (MUNE), motor unit number contributing to 50%-100% of CMAP (N50) and measures of collateral reinnervation including largest single motor unit potential (LSMUP) and amplitude of the smallest unit contributing to N50 (A50). Results Twenty children (median age 99 months, range 4-193) were followed for a median of 13.8 (4-33.5) months. Therapeutic intervention was an independent and significant contributor to an increase in CMAP (p = 0.005), MUNE (p = 0.001) and N50 (p = 0.04). The magnitude of this electrophysiological response was increased in children with shorter disease durations (p<0.05). Electrophysiological changes delineated children who were functionally stable from those who attained clinically significant gains in motor function. Interpretation Nusinersen therapy facilitated functional innervation in SMA through recovery of smaller motor units. Delineation of biomechanisms of therapeutic response may be the first step in identifying potential novel targets for disease modification in this and other motor neuropathies. MScanFit MUNE techniques may have a broader role in establishing biomarkers of therapeutic response in similar adult-onset diseases