Leber’s Hereditary Optic Neuropathy Plus Causing Recurrent Myelopathy due to an MT-DN1 Mutation at G3635A

A 51-year-old man with known Leber’s hereditary optic neuropathy (LHON) presented with worsening lower extremity weakness and numbness. Following an episode of myelopathy two years before, he had been ambulating with a walker but over two weeks became wheelchair bound. He also developed a sensory level below the T4 dermatome to light touch, pinprick, and vibration. MRI of his cervical and thoracic spine showed a nonenhancing T2 hyperintense lesion extending from C2 to T12. At his presentation two years earlier, he was found to have a longitudinally extensive myelopathy attributed to his LHON. Genetic testing revealed a 3635 guanine to adenine mutation. MRI at that presentation demonstrated a C1-T10 lesion involving the central and posterior cord but, unlike the new lesion, did not involve the ventral and lateral horns. Given the similarity to his prior presentation and a negative evaluation for alternative etiologies, he was thought to have recurrent myelopathy secondary to Leber’s Plus. To our knowledge, recurrent myelopathy due specifically to the G3635A mutation in Leber’s Plus has not been reported previously.

Prevention of trigeminocardiac reflex-induced severe bradycardia during cerebral aneurysm clipping surgery by topical anesthesia of the dura surface and atropine administration: a case report

Background Trigeminocardiac reflex (TCR) by stimulation of the sensory branch of the trigeminal nerve induces transient bradycardia and hypotension. We report a case in which light mechanical stimulation to the dura mater during brain surgery induced severe bradycardia. Case presentation A 77-year-old woman with bradycardia-tachycardia syndrome was scheduled for clipping of an unruptured left middle cerebral artery aneurysm. General anesthesia was performed with propofol, remifentanil, and rocuronium. Before starting surgery, the function of the pyramidal tract was examined by motor evoked potential. Transcranial electric stimulation for motor evoked potential induced atrial fibrillation and tachycardia. Continuous administration of landiolol was started and verapamil was used for tachycardia. During detachment of the dura mater from the bone, an electrocardiogram suddenly showed sinus arrest for 6 s. Immediately after the manipulation was interrupted, a junctional rhythm appeared. However, light touch to the dura mater induced severe bradycardia again, and atropine was therefore administered. In addition, the dura surface was anesthetized with topical lidocaine infiltration. After that, light touch-induced bradycardia was prevented. Conclusions We experienced a case of severe bradycardia during surgery due to TCR caused by light mechanical stimulation to the dura mater. Topical anesthesia of the dura surface and atropine administration were effective for preventing TCR-induced bradycardia.

Spinal Cord Tissue Bridges Validation Study: Predictive Relationships With Sensory Scores Following Cervical Spinal Cord Injury

Background: Using magnetic resonance imaging (MRI), widths of ventral tissue bridges demonstrated significant predictive relationships with future pinprick sensory scores, and widths of dorsal tissue bridges demonstrated significant predictive relationships with future light touch sensory scores, following spinal cord injury (SCI). These studies involved smaller participant numbers, and external validation of their findings is warranted. Objectives: The purpose of this study was to validate these previous findings using a larger independent data set. Methods: Widths of ventral and dorsal tissue bridges were quantified using MRI in persons post cervical level SCI (average 3.7 weeks post injury), and pinprick and light touch sensory scores were acquired at discharge from inpatient rehabilitation (average 14.3 weeks post injury). Pearson product-moments were calculated and linear regression models were created from these data. Results: Wider ventral tissue bridges were significantly correlated with pinprick scores (r = 0.31, p < 0.001, N = 136) and wider dorsal tissue bridges were significantly correlated with light touch scores (r = 0.31, p < 0.001, N = 136) at discharge from inpatient rehabilitation. Conclusion: This retrospective study’s results provide external validation of previous findings, using a larger sample size. Following SCI, ventral tissue bridges hold significant predictive relationships with future pinprick sensory scores and dorsal tissue bridges hold significant predictive relationships with future light touch sensory scores.

Knismesis: the aversive facet of tickle

There are two different kinds of tickle, knismesis (feather-light tickle) and gargalesis (more intense tickle eliciting involuntary laughter). In this article we review earlier and recent advances in tickle psychophysics and in neurophysiology of touch afferents and hypothesize that knismesis is signaled by populations of rapidly adapted hair follicle afferents, can stimulate itch neurons via dorsal horn projections, and is heavily moderated by afferent inputs from other touch neurons. Finally, we suggest that pathological light touch intolerance observed in autism spectrum disorder may reflect knismesis hyper-responsiveness and attenuated knismesis inhibition stemming from impaired integration of sensory inputs from other touch submodalities.

Conclusion

This chapter reiterates the key arguments and findings of the book. The British state pursued financial liberalization in the 1970s and 1980s in an attempt to reconcile the demands of domestic civil society with the suffocating, impersonal pressures of the global economic crisis on Britain’s balances with the rest of the world. Financialization was an accidental result, not an intended outcome. In addition, this chapter explores how the four liberalizations examined here impacted upon the trajectory of financialization in the late twentieth and early twenty-first centuries. Britain’s liberalization of its financial sector boosted global capital mobility, and thus created powerful pressures on other states to follow suit, contributing to a dynamic of competitive deregulation that spread around the world. Further, the arm’s-length, depoliticized design of the 1986 FSA generated an institutional path dependency, whereby future British systems of financial governance would take a similarly light-touch form. This meant that London would incubate a series of banking scandals in the 1990s, as well as being home to some of the riskiest financial practices exposed by the 2008 crisis. Finally, the growing financial flows unleashed by the liberalizations of the 1970s and 1980s were increasingly channelled into the housing market, resulting in Britain’s particular dynamic of housing-centric financialization.