Hand surgery in a new“hand-brain” era:change the hand,rebuild the brain

Amputated hand,and paralyzed hand,are diseases not on the conventional list of the hand surgery world,but now have gradually become the new direction for hand surgeons.A good example is the advancements in treating amputations after traumatic injury of the upper limb.Targeted muscle reinnervation combined with a highly functional bionic arm can greatly compensate for the missing part of the amputated arm[1],which in general satisfies the need for strength and dexterity in daily life.According to the classic cortical homunculus first drawn by Penfield,the hand area occupied nearly-one-third of the sensorimotor cortex[2].Thus,interventions with the hands enable the modulation of brain function,providing a solution for brain disorders through skillful utilization of brain plasticity.With the recent advancements in neuroscience and biomedical engineering technology,hand surgeons find themselves entering an era with a bigger performance stage than ever before.For paralyzed hand,the most common cause is central neurological diseases such as stroke or cerebral palsy,or paraplegia.Although it is more challenging since surgeons should balance spasticity and motor function at the same time,efforts have been made by hand surgeons around the world,such as hyper selective neurectomy,tendon lengthening or transfer to reduce the spasticity and reconstruct the motor function[3].Considering the fact that the number of patients with paralyzed hands is over 10 million,which far exceeds the traditional nerve injury entity,this area is the potential further direction of hand surgery.In this article,we will discuss the opportunities and pitfalls in the combination of hand surgery techniques and brain-computer-interface(BCI)in treating paralyzed hands from the perspective of hand surgery development.

Restoring After Central Nervous System Injuries:Neural Mechanisms and Translational Applications of Motor Recovery

Central nervous system(CNS)injuries,including stroke,traumatic brain injury,and spinal cord injury,are leading causes of long-term disability.It is estimated that more than half of the survivors of severe unilateral injury are unable to use the denervated limb.Previous studies have focused on neuroprotective interventions in the affected hemisphere to limit brain lesions and neurorepair measures to promote recovery.However,the ability to increase plasticity in the injured brain is restricted and difficult to improve.Therefore,over several decades,researchers have been prompted to enhance the compensation by the unaffected hemisphere.Animal experiments have revealed that regrowth of ipsilateral descending fibers from the unaffected hemisphere to denervated motor neurons plays a significant role in the restoration of motor function.In addition,several clinical treatments have been designed to restore ipsilateral motor control,including brain stimulation,nerve transfer surgery,and brain–computer interface systems.Here,we comprehensively review the neural mechanisms as well as translational applications of ipsilateral motor control upon rehabilitation after CNS injuries.

Neuroinflammation Mediates Faster Brachial Plexus Regeneration in Subjects with Cerebral Injury

Our previous investigation suggested that faster seventh cervical nerve(C7)regeneration occurs in patients with cerebral injury undergoing contralateral C7 transfer.This finding needed further verification,and the mechanism remained largely unknown.Here,Tinel’s test revealed faster C7 regeneration in patients with cerebral injury,which was further confirmed in mice by electrophysiological recordings and histological analysis.Furthermore,we identified an altered systemic inflammatory response that led to the transformation of macrophage polarization as a mechanism underlying the increased nerve regeneration in patients with cerebral injury.In mice,we showed that,as a contributing factor,serum amyloid protein A1(SAA1)promoted C7 regeneration and interfered with macrophage polarization in vivo.Our results indicate that altered inflammation promotes the regenerative capacity of the C7 nerve by altering macrophage behavior.SAA1 may be a therapeutic target to improve the recovery of injured peripheral nerves.