In 1886, William Gowers for the first time clearly described the striking features of the spasticity that manifests after acute‐onset hemiplegia: “The late rigidity comes on in the course of a few weeks, … In the upper limb the position is that of adduction of the shoulder, flexion of the elbow, flexion and pronation of the wrist, and still greater flexion of the fingers…” (Fig. 1; Gowers & Barker, 1886). Several experimental studies tried to determine the reason why flexor muscles are affected in this way after stroke. The research group headed by Baker showed in monkeys that after a corticospinal tract lesion, inputs from reticular formation to forearm flexor and intrinsic hand muscles are strengthened whereas those to forearm extensor muscles are unaffected (Zaaimi et al. 2012). It is possible that a similar imbalance at the subcortical level occurs in humans after stroke, resulting in flexor spasticity and interference with recovery of hand function, although other factors could also be contributing.
Figure 1. Late rigidity in hemiplegia 5 months after onset.
Detail of original drawing from Gowers & Barker (1886, p. 76).
In this issue of Journal of Physiology the same group of researchers use a novel approach to determine whether specific characteristic of the intrinsic plasticity of human cortical circuits controlling flexor muscles might contribute to their propensity to develop spasticity after stroke (Riashad Foysal & Baker, 2019). To this end, they studied different forms of brain plasticity in healthy subjects using transcranial magnetic stimulation (TMS) techniques. They evaluated the effects of two different protocols that are known to induce long‐term potentiation (LTP)‐like changes. The first protocol, termed intermittent theta‐burst stimulation (iTBS), uses trains of low‐intensity and high‐frequency stimuli delivered to the motor cortex at the theta rhythm; the second one is called paired associative stimulation (PAS) and is based on coupling peripheral nerve stimulation with motor cortex stimulation. Although iTBS and PAS induce similar after‐effects on motor cortex excitability, their physiological bases are thought to have different mechanisms given that they are differentially affected in some pathological conditions (Dileone et al. 2016). Riashad Foysal & Baker (2019) compare the effects of PAS produced either by pairing motor cortex TMS with motor point stimulation of flexor digitorum superficialis or extensor digitorum communis muscles with those of iTBS in the same muscles. They find that while iTBS has similar effects on flexor and extensor muscles, the effects of PAS are present in the hand muscles and in flexor digitorum superficialis but absent in extensor digitorum communis. Because recovery in stroke is related to the level of inducible LTP‐like activity (Di Lazzaro et al. 2010), this implies that flexor muscles have a higher potential for recovery and therefore predispose to an imbalance between flexor and extensor muscles that progresses during recovery and finally results in an abnormal hand posture. Thus, a physiologically higher level of associative plasticity in brain areas controlling flexor muscles might predispose to the development of spasticity in pathological conditions such as stroke because of an altered association between sensorimotor inputs and outputs.
Interestingly, using a similar approach it has been previously shown that an abnormality in associative plasticity is also present in focal hand dystonia. In contrast to healthy controls, in dystonic patients PAS‐induced after‐effects are not confined to the muscles contiguous to the sensory territory supplied by the stimulated peripheral nerve but also involve distant muscles (Suppa et al. 2017). In dystonia, the abnormality of sensory‐motor plasticity might represent an endophenotypic trait that predisposes to the development of dystonia while in stroke patients it might be the structural brain lesion that results in a hand posture abnormality by interacting with an innate physiological asymmetry in the level of plasticity of cortical areas controlling different muscles. Of note is that the PAS protocol used by Riashad Foysal & Baker (2019), in which the motor point is stimulated instead of the peripheral nerve, seems not to have the same spatial specificity of the standard PAS described by Stefan et al. (2000) in that stimulation of the motor point of either flexor digitorum superficialis or extensor digitorum communis induced plastic changes in both forearm flexors, and intrinsic hand muscles.
The study by Riashad Foysal & Baker (2019) confirms that non‐invasive brain stimulation techniques can provide unique insights into the physiological basis of human brain plasticity. The assessment of sensory‐motor plasticity in stroke might be useful for the early detection of changes that might interfere with functional recovery and also for the development and implementation of strategies aimed at preventing the deleterious consequences of maladaptive plasticity.
Additional information
Competing interest
None.
Funding
No funding was received.
Edited by: Janet Taylor & Dario Farina
Linked articles: This Perspectives article highlights an article by Riashad Foysal & Baker. To read this article, visit https://doi.org/10.1113/JP277462.
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