[Intensity in the neurorehabilitation of spastic paresis]. / Intensité et rééducation motrice dans la parésie spastique.

Neurorestoration of motor command in spastic paresis requires a double action of stimulation and guidance of central nervous system plasticity. Beyond drug therapies, electrical stimulation and cell therapies, which may stimulate plasticity without precisely guiding it, two interventions seem capable of driving plasticity with a double stimulation and guidance component: the lesion itself (lesion-induced plasticity) and durable behavior modifications (behavior-induced plasticity). Modern literature makes it clear that the intensity of the neuronal and physical training is a primary condition to foster behavior-induced plasticity. When it comes to working on movement, intensity can be achieved by the combination of two key components, one is the difficulty of the trained movement, the other is the number of repetitions or the daily duration of the practice. A number of recent studies shed light on promising recovery prospects, particularly using the emergence of new technologies such as robot-assisted therapy and concepts such as guided self-rehabilitation contracts.

[Does upper limb robot-assisted rehabilitation contribute to improve the prognosis of post-stroke hemiparesis?]. / La rééducation du membre supérieur assistée par robot contribue-t-elle à améliorer le pronostic de l'hémiparésie vasculaire ?

INTRODUCTION: Upper limb robot-assisted rehabilitation is a novel physical treatment for neurological motor impairments. During the last decade, this rehabilitation option utilizing technological tools has been evaluated in hemiparetic patients, mostly after stroke. STATE OF ART: Studies at acute and chronic stages suggested good tolerance and a significant and persistent reduction of motor impairment; a real impact on disability has been shown in acute/sub acute patients. PERSPECTIVES: Improved access to rehabilitation robots and an optimal use will probably be associated with higher efficiency of rehabilitative work in the paretic upper limb. CONCLUSIONS: Even if this treatment is still confined to a narrow circle of users, the device's biomechanical properties and clinical suggestions from the literature may show promise for the future of rehabilitation.

[Neurorehabilitation in parkinsonian syndromes]. / Neurorééducation des syndromes parkinsoniens.

Parkinson's disease is a frequent and major source of motor disability, for which physical therapies currently involve less than a third of ambulatory patients and are thus underutilized when compared to chemical and surgical treatments. However, dopaminergic therapies alone prove unable to prevent worsening of motor disability after a number of years. There is rising interest about physical neurorehabilitative therapy for Parkinson's disease, for its symptomatic therapeutic properties, but also for its potential neuroprotective effects in the light of compelling, recent animal literature. The approach to therapy in an individual patient may be governed at the most basic level by the disease stage. For moderate stages of Parkinson's disease (ambulatory patients who have retained a certain degree of physical independence), therapy may focus on the teaching of exercises to the patient: strategies established in controlled studies when used over few weeks periods include motor strengthening programs in the lower limb, high intensity aerobic exercises, attentional strategies using in particular verbal instruction sets, sensory cueing, active axial rotation exercises and high-number repetition of specific tasks. A randomized protocol will soon evaluate the concept of asymmetric motor training, combining a strengthening program in extensor, abductor, external rotator and supinator muscles and a stretching program in their antagonists. For advanced stages (individuals with compromised sit-to-stand, ambulation and significant disability), the therapeutic focus may shift to the teaching of compensation strategies to the patient and the caregiver, both to lessen the effects of motor impairment and to optimize safety. A number of these compensatory strategies are reviewed, some being validated in controlled protocols. In idiopathic Parkinson's disease, clinicians must continue evaluating the symptomatic and perhaps neuroprotective value of physical treatment strategies used over the long term. In atypical parkinsonism, physical treatments often remain the only realistic methods to improve motor behavior and reduce functional deficiencies. The relatively short duration of the effects of physical therapies implies that such programs be pursued over long periods of time, or repeated frequently, for their benefits to be maintained over time.

Botulinum neurotoxin versus tizanidine in upper limb spasticity: a placebo-controlled study.

BACKGROUND: While spasticity is commonly treated with oral agents or botulinum neurotoxin (BoNT) injection, these treatments have not been systematically compared. METHODS: This study performed a randomised, double-blind, placebo-controlled trial to compare injection of BoNT-Type A into spastic upper limb muscles versus oral tizanidine (TZD), or placebo, in 60 subjects with upper-limb spasticity due to stroke or traumatic brain injury (TBI). Wrist flexors were systematically injected, while other upper limb muscles were injected as per investigator judgement. Participants were randomised into three groups: (1) intramuscular BoNT plus oral placebo; (2) oral TZD plus intramuscular placebo; (3) intramuscular placebo plus oral placebo. The primary outcome was the difference in change in wrist flexor modified Ashworth score (MAS) between groups. Other outcome measures included MAS at elbow and finger joints, Disability Assessment Scale (DAS) and adverse events (AE). RESULTS: BoNT produced greater tone reduction than TZD or placebo in finger and wrist flexors at week 3 (p<0.001 vs TZD; p<0.02 vs placebo) and 6 (p = 0.001 vs TZD; p = 0.08 vs placebo), and greater improvement in the cosmesis domain of the DAS at week 6 (p<0.01). TZD was not superior to placebo in tone reduction at either time point (p>or=0.09). The incidence of AE related to study treatment was higher with TZD than in the BoNT (p<0.01) or placebo groups (p = 0.001). CONCLUSIONS: BoNT is safer and more effective than TZD in reducing tone and disfigurement in upper-extremity spasticity, and may be considered as first-line therapy for this disorder.

Muscle Shortening and Spastic Cocontraction in Gastrocnemius Medialis and Peroneus Longus in Very Young Hemiparetic Children.

OBJECTIVES: Muscle shortening and spastic cocontraction in ankle plantar flexors may alter gait since early childhood in cerebral palsy (CP). We evaluated gastrosoleus complex (GSC) length, and gastrocnemius medialis (GM) and peroneus longus (PL) activity during swing phase, in very young hemiparetic children with equinovalgus. METHODS: This was an observational, retrospective, and monocentric outpatient study in a pediatric hospital. Ten very young hemiparetic children (age 3 ± 1 yrs) were enrolled. These CP children were assessed for muscle extensibility (Tardieu scale XV1) in GSC (angle of arrest during slow-speed passive ankle dorsiflexion with the knee extended) and monitored for GM and PL electromyography (EMG) during the swing phase of gait. The swing phase was divided into three periods (T1, T2, and T3), in which we measured a cocontraction index (CCI), ratio of the Root Mean Square EMG (RMS-EMG) from each muscle during that period to the peak 500 ms RMS-EMG obtained from voluntary plantar flexion during standing on tiptoes (from several 5-second series, the highest RMS value was computed over 500 ms around the peak). RESULTS: On the paretic side: (i) the mean XV1-GSC was 100° (8°) (median (SD)) versus 106° (3°) on the nonparetic side (p = 0.032, Mann-Whitney); (ii) XV1-GSC diminished with age between ages of 2 and 5 (Spearman, ρ = 0.019); (iii) CCIGM and CCIPL during swing phase were higher than on the nonparetic side (CCIGM, 0.32 (0.20) versus 0.15 (0.09), p < 0.01; CCIPL, 0.52 (0.30) versus 0.24 (0.17), p < 0.01), with an early difference significant for PL from T1 (p = 0.03). CONCLUSIONS: In very young hemiparetic children, the paretic GSC may rapidly shorten in the first years of life. GM and PL cocontraction during swing phase are excessive, which contributes to dynamic equinovalgus. Muscle extensibility (XV1) may have to be monitored and preserved in the first years of life in children with CP. Additional measurements of cocontraction may further help target treatments with botulinum toxin, especially in peroneus longus.

Coefficients of impairment in deforming spastic paresis.

This position paper introduces an assessment method using staged calculation of coefficients of impairment in spastic paresis, with its rationale and proposed use. The syndrome of deforming spastic paresis superimposes two disorders around each joint: a neural disorder comprising stretch-sensitive paresis in agonists and antagonist muscle overactivity, and a muscle disorder ("spastic myopathy") combining shortening and loss of extensibility in antagonists. Antagonist muscle overactivity includes spastic cocontraction (misdirected descending command), spastic dystonia (tonic involuntary muscle activation, at rest) and spasticity (increased velocity-dependent reflexes to phasic stretch, at rest). This understanding of various types of antagonist resistance as the key limiting factors in paretic movements prompts a stepwise, quantified, clinical assessment of antagonist resistances, elaborating on the previously developed Tardieu Scale. Step 1 quantifies limb function (e.g. ambulation speed in lower limb, Modified Frenchay Scale in upper limb). The following four steps evaluate various angles X of antagonist resistance, in degrees all measured from 0°, position of minimal stretch of the tested antagonist. Step 2 rates the functional muscle length, termed XV1 (V1, slowest stretch velocity possible), evaluated as the angle of arrest upon slow and strong passive muscle stretch. XV1 is appreciated with respect to the expected normal passive amplitude, XN, and reflects combined muscle contracture and residual spastic dystonia. Step 3 determines the angle of catch upon fast stretch, termed XV3 (V3, fastest stretch velocity possible), reflecting spasticity. Step 4 measures the maximal active range of motion against the antagonist, termed XA, reflecting agonist capacity to overcome passive (stiffness) and active (spastic cocontraction) antagonist resistances over a single movement. Finally, Step 5 rates the residual active amplitude after 15 seconds of maximal amplitude rapid alternating movements, XA15. Amplitude decrement from XA to XA15 reflects fatigability. Coefficients of shortening (XN-XV1)/XN, spasticity (XV1-XV3)/XV1, weakness (XV1-XA)/XV1 and fatigability (XA-XA15)/XA are derived. A high (e.g., >10%) coefficient of shortening prompts aggressive treatment of the muscle disorder--e.g., by stretch programs, such as prolonged stretch postures -, while high coefficients of weakness or fatigability prompt addressing the neural motor command disorder, e.g. using training programs such as repeated alternating movements of maximal amplitude.

Early morning off-medication dyskinesias, dystonia, and choreic subtypes.

BACKGROUND: Abnormal involuntary movements (dyskinesias) are common in patients with Parkinson disease (PD) as a consequence of the disease and dopaminergic replacement therapy. Early morning off-medication choreic dyskinesias have been recently reported after fetal dopaminergic cell transplantations in patients with advanced PD. OBJECTIVE: To determine the frequency and severity of the early morning off-medication dyskinesias in consecutive patients with advanced PD and an insufficient response to medical management before they undergo neurosurgery. METHODS: Consecutive patients with advanced idiopathic PD were examined and videotaped before undergoing neurosurgery that included pallidotomy, fetal transplantation, or deep brain stimulation. The examination took place in the morning in the practically defined off state, at least 12 hours after the last dose of dopaminergic drugs. Parkinson disease was characterized using the Unified Parkinson's Disease Rating Scale and the Hoehn and Yahr stage. Dyskinesias were rated with the Abnormal Involuntary Movements Scale and the Rush Dyskinesia Rating Scale. Patients' characteristics and medications were compared using the Wilcoxon rank sum and the Fisher exact tests. RESULTS: Of 68 consecutive patients (44 [65%] men and 24 [35%] women), 11 (16%) had early morning off-medication dyskinesia, with a 95% upper confidence limit of 24%. Focal dystonia was the most common off-medication dyskinesia, and occurred in 10 patients (15%), with a 95% upper confidence limit of 22%; and off-choreic dyskinesia occurred in 1 patient (1.5%), with a 95% upper confidence limit of 4%. There was no difference in PD medications between the patients with and those without dyskinesias. CONCLUSIONS: The most common form of off-medication dyskinesia seen in patients with advanced PD is dystonia. Early morning off-medication choreic dyskinesias are rare but do occur in patients with advanced PD before surgical intervention. The presence and type of off-medication dyskinesias should be monitored in clinical and surgical studies in patients with PD as part of the safety and evaluation of clinical benefits.

Bilateral optic disk pallor after unilateral internal carotid artery occlusion.

Bilateral pallor of the optic disks was observed in a 52-year-old man after dissection of an internal carotid artery. Diffuse pallor of the ipsilateral optic disk reflected infarction of the ipsilateral optic nerve and "bow-tie" atrophy of the contralateral optic disk reflected infarction of the ipsilateral optic tract. The findings were due to an occlusion of the internal carotid artery proximal to the origin of the ophthalmic artery, resulting also in insufficiency in the area of supply of the anterior choroidal artery.

Evidence for fusimotor drive in stroke patients based on muscle spindle thixotropy.

To study fusimotor function in stroke patients, we compared the amplitude of stretch reflexes elicited in flexor carpi radialis (FCR) after contraction of FCR with the wrist held flexed ('hold-short') or extended ('hold-long'). Seven subjects with impaired hand function and spasticity due to stroke, and seven healthy subjects were investigated. Surface electrodes recorded electromyographic activity of wrist flexors and extensors while subjects performed isometric wrist flexions with the wrist alternately in 15 degrees of flexion or extension. After contractions the wrist was moved passively to the mid-position, and stretch reflexes were elicited via controlled mechanical taps delivered over the FCR tendon. For both groups, the amplitude of the stretch reflex was greater after 'hold-short' than 'hold-long' contractions. This finding is consistent with the 'after-effects' of intrafusal fibre activation, and suggests that fusimotor neurones are activated during voluntary contractions of the paretic limb, just as in the limb of a healthy subject.

Pathophysiology of impairment in patients with spasticity and use of stretch as a treatment of spastic hypertonia.

Paralysis, muscle shortening, and muscle overactivity are the three main disabling factors in patients with spasticity. Occurring after most central lesions, muscle overactivity and shortening are not equally spread throughout all muscles of the body. In an agonist-antagonist couple, there is invariably "greater" overactivity and shortening of one versus the other. This is the rationale for the use of targeted local treatments that train the weaker agonist and stretch and partially block the more overactive and shorter antagonist. Central paralysis, muscle shortening, and muscle overactivity are intertwined, and the three corresponding therapies, motor training, stretch, and local partial blocks, should be implemented in combination. This triple treatment is the main condition for any functional recovery. Muscle shortening occurs acutely after a central nervous system lesion; therefore its treatment should be implemented as rapidly as possible.

Physical modalities other than stretch in spastic hypertonia.

This article reviews various physical modalities that have been used in spastic hypertonia, particularly superficial heat and cold, diathermies (ultrasound, microwave, and short-wave irradiation), electrical stimulation (transcutaneous electrical nerve stimulation), implanted spinal stimulation (rectal stimulation), and massage (deep friction, superficial contact). The duration of the effects of most physical therapies is relatively short (e.g., cooling, heating, and massage), which often may limit their application to immediate prestretch or pre-exercise periods. The potential capacity of ultrasound therapy to improve the efficacy of chronic stretch in lengthening muscle may be a promising option. The neurodestructive potential of high intensity microwave for the personnel involved and controlled evidence of its value is required before this modality can be recommended in spasticity. Overall, controlled, double-blind studies are mandated to evaluate the long-term impact of repeated use of these short-term modalities on function and recovery in patients with spasticity.

Neuromuscular blockers.

The use of corrosive, injectable neuromuscular blockers has been a treatment option for many years; however, the more recent advent of botulinum toxin (BTX) treatment has revived interest in localized treatments. This article reviews the use of local anesthetics, alcohol, phenol, and BTX treatment for localized muscular overactivity syndromes.

Estimating foot inertial parameters: a new regression approach.

BACKGROUND: Estimating the inertial parameters for the foot (mass, center of mass position and inertia tensor) is important for applications involving the ankle joint such as inverse dynamics or stiffness measurement techniques (e.g. Quick-release). Scaling equations relying on foot length and body mass are widely used. However, because of the complex foot geometry, such equations may represent an oversimplified solution. Our aim was to evaluate these approaches and propose a new method. METHODS: Thirty-four right feet (17 Males, mean age and weight 30 years, 75 kg; 17 Females, 32 years, 61.5 kg) were reconstructed using a 3D surface scanner and used as geometrical references. Associated inertial parameters were calculated directly on each reference assuming a uniform density distribution and were compared to corresponding scaling and multiple regression estimates. Finally, an alternative method, based on multiple non-linear regressions, was proposed considering both foot length (L) and ankle width (W). FINDINGS: Comparisons showed that reference mass and moments of inertia were greater than scaling predictions with mean difference up to 33 and 16% for mass and moments of inertia respectively. The maximum standard errors of estimate for scaled moments of inertia reached 26%. The alternative solution involving ankle width in the equations lowered the gap with reference data (8.7% max standard errors of estimate) for both genders. INTERPRETATION: This strategy, requiring two simple and accessible measurements, may offer a better practicality/relevance compromise for clinical routine use, in regards to existing scaling and regression equations.

Assessment: Botulinum neurotoxin for the treatment of spasticity (an evidence-based review): report of the Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology.

OBJECTIVE: To perform an evidence-based review of the safety and efficacy of botulinum neurotoxin (BoNT) in the treatment of adult and childhood spasticity. METHODS: A literature search was performed including MEDLINE and Current Contents for therapeutic articles relevant to BoNT and spasticity. Authors reviewed, abstracted, and classified articles based on American Academy of Neurology criteria (Class I-IV). RESULTS: The highest quality literature available for the respective indications was as follows: adult spasticity (14 Class I studies); spastic equinus and adductor spasticity in pediatric cerebral palsy (six Class I studies). RECOMMENDATIONS: Botulinum neurotoxin should be offered as a treatment option for the treatment of spasticity in adults and children (Level A).

Evidence for further recruitment of group I fibres with high stimulus intensities when using surface electrodes in man.

Changes in the firing probability of voluntarily activated motor units in the human lower limb were recorded in response to stimuli applied to peripheral nerves of the lower limb using surface electrodes. In each instance the monosynaptic Ia excitation produced by heteronymous afferent volleys was studied. This peak of excitation was found to increase with the intensity of the stimulation up to 2.5-4 x the motor threshold (MT), i.e., 4-7 x the threshold of Ia afferents. It is concluded that, when using surface electrodes in human subjects, group Ia effects may not be maximal with stimulus intensities below 4 x MT, and the effects evoked by different afferent populations (e.g., Ia and II) cannot be clearly separated solely on the basis of the electrical excitability of these fibres.

Evidence for corticospinal excitation of presumed propriospinal neurones in man.

1. The possibility that stimulation of the motor cortex facilitates transmission in the pathway mediating non-monosynaptic ('propriospinal') excitation from low-threshold afferents to upper limb motoneurones was investigated. 2. Convergence between peripheral afferent volleys (from the ulnar or musculo-cutaneous nerve) and corticospinal volleys (evoked by magnetic stimulation of the motor cortex) was investigated using the spatial facilitation technique. Thus the effects of these volleys on the flexor carpi radialis H reflex were compared when applied separately and together. When cortical stimulation was optimal for the muscle from which the conditioning volley originated the facilitation of the reflex on combined stimulation was significantly larger than the algebraic sum of the effects of separate stimuli. 3. The extra facilitation on combined stimulation had all the characteristics of 'propriospinal' excitation (low threshold, long central delay, brief duration and depression when the afferent input was increased), and it is suggested that this reflects corticospinal excitation of 'propriospinal' neurones. 4. When varying the time interval between cortical and test stimulations, it was shown that extra facilitation on combined stimulation began 1 ms later than the onset of the control reflex facilitation. Assuming that the latter onset reflects the arrival of the monosynaptic corticospinal volley at the motoneurone pool, this 1 ms delay suggests a disynaptic pathway for the cortical excitation of motoneurones through 'propriospinal' neurones. 5. As at the onset of voluntary movement, the pattern of the cortical excitation of 'propriospinal' neurones was quite specific: extra facilitation of the reflex on combined stimulation only occurred when the cortical volley was preferentially directed to motoneurones supplying the muscle from which the afferents used for the peripheral volley originated. 6. It is concluded that corticospinal axons activate human 'propriospinal' neurones and thereby produce disynaptic excitation of the motoneurone pool. Given temporal summation with the monosynaptic excitation, this 'propriospinally mediated' disynaptic excitation might make a significant contribution to the evoked EMG potential.

Convergence of descending and various peripheral inputs onto common propriospinal-like neurones in man.

1. The patterns of excitation and convergence by peripheral afferents on propriospinal-like neurones projecting to forearm flexor carpi radialis (FCR) motoneurones in human subjects were determined at rest and during various voluntary contractions, using H reflex testing. 2. At rest, the FCR H reflex could be facilitated by mixed nerve (ulnar, musculocutaneous) and cutaneous (afferents from both sides of the hand) inputs. The characteristics of this facilitation (low threshold, long central latency, short duration) were compatible with those of the propriospinal-like system. Quantitatively this facilitation was rare and weak. 3. Voluntary contraction increased the extent of the propriospinal-like facilitation of the FCR H reflex. It is shown in the companion paper (Burke, Gracies, Meunier & Pierrot-Deseilligny, 1992) that this increase results not from a decrease in presynaptic inhibition of afferents to propriospinal-like neurones, but from increased excitation of these neurones. It is argued that at the onset of contraction this excitation is purely descending in origin, whereas the contraction-induced afferent discharge is probably the major factor during weak tonic contraction. 4. The distribution of the increased facilitation of the FCR H reflex depended on the muscles involved in the contraction: ulnar nerve-evoked facilitation was increased much more at the onset of voluntary wrist flexion than voluntary elbow flexion, and vice versa for the musculo-cutaneous-induced facilitation. This finding is consistent with the view that there are subsets of propriospinal-like neurones, specialized with regard to afferent input, and indicates that descending excitation is directed preferentially to the subset of neurones which receives excitatory feedback from the contracting muscle. 5. To investigate the convergence of different afferent inputs onto common neurones the spatial facilitation technique was used. When present the convergence had a threshold and time course compatible with those of the propriospinal-like system. Convergence was found between the different mixed nerves and between ulnar and superficial radial nerves. 6. The wide convergence found between different inputs onto common neurones and the finding that, during contraction of a given muscle, descending excitation reaches subsets of neurones projecting to motor nuclei of muscles operating at other joints suggest that the propriospinal-like system would be operative during complex multi-joint movements.

Changes in presynaptic inhibition of afferents to propriospinal-like neurones in man during voluntary contractions.

1. The possibility was investigated that the facilitation of the transmission in the propriospinal-like system during voluntary contraction, documented in the companion paper (Burke, Gracies, Mazevet, Meunier & Pierrot-Deseilligny, 1992), is due to a decrease in presynaptic inhibition of afferents projecting to propriospinal-like neurones. 2. The radial nerve was stimulated to evoke presynaptic inhibition of the monosynaptic Ia projections to forearm flexor motoneurones (Berardelli, Day, Marsden & Rothwell, 1987) and, hopefully, of the afferent input to propriospinal-like neurones projecting to these motoneurones. 3. The propriospinal-like excitation of forearm motoneurones evoked from mixed afferent inputs was depressed by radial nerve stimulation, and this depression was long-lasting (200 ms). Despite the convergence of mixed nerve and cutaneous afferents onto common propriospinal-like neurones, the radial stimulation did not depress the cutaneous-induced excitation. This differential effect and the time course of the depression suggest that it results from presynaptic inhibition of mixed nerve afferents (presumably large muscle afferents) projecting to propriospinal-like neurones. 4. With voluntary contractions, phasic or tonic, the radial-induced depression of the propriospinal-like excitation evoked by mixed nerve afferents was much greater than at rest, but the cutaneous-evoked excitation was unchanged. Thus, with voluntary contractions, there was no evidence of decreased gating of the afferent input to propriospinal-like neurones whether the input was of muscle or cutaneous origin and it is concluded that changes in presynaptic inhibition cannot account for the facilitation of the transmission in the propriospinal-like system during voluntary contraction. 5. By contrast, presynaptic inhibition of the monosynaptic Ia projections to motoneurones was consistently reduced at the onset of contraction, and to a much lesser extent during a weak tonic contraction.

Excitability changes in human cutaneous afferents induced by prolonged repetitive axonal activity.

1. The present study was undertaken to document the excitability changes produced by prolonged high-frequency trains of impulses in cutaneous afferents of six human subjects. 2. Trains of supramaximal stimuli at 200 Hz for 2 min or less produced a prolonged depression in excitability, consistent with activation of the electrogenic Na+-K+ pump. Trains of longer duration resulted in an initial period of hyperexcitability which, with 10 min trains, was associated with the sensation of paraesthesiae in all subjects. This transient hyperexcitability gradually gave way to a long-lasting period of hypoexcitability. 3. The excitability changes were reproducible, and were accompanied by corresponding changes in supernormality, refractoriness, strength-duration time constant and rheobase current, suggesting that the changes in axonal excitability reflected a change in membrane potential. 4. The transient increase in excitability that follows tetanic trains of 10 min had qualitatively similar effects on cutaneous axons as ischaemia or application of a depolarizing current. The post-tetanic changes in the supernormal period of sensory axons were those expected from the changes in excitability, without evidence of a gross distortion in its time course, as has been previously demonstrated in a hyperstimulated human motor axon. 5. It is concluded that the post-tetanic hyperexcitability of human sensory axons is probably driven by increased K+ accumulation in the restricted diffusion space under the myelin sheath, much as in motor axons, the differences in behaviour of sensory and motor axons being explicable by greater inward rectification in sensory axons.