Posts Tagged passive movement

[ARTICLE] Strength of ~20-Hz Rebound and Motor Recovery After Stroke – Full Text


Background. Stroke is a major cause of disability worldwide, and effective rehabilitation is crucial to regain skills for independent living. Recently, novel therapeutic approaches manipulating the excitatory-inhibitory balance of the motor cortex have been introduced to boost recovery after stroke. However, stroke-induced neurophysiological changes of the motor cortex may vary despite of similar clinical symptoms. Therefore, better understanding of excitability changes after stroke is essential when developing and targeting novel therapeutic approaches.

Objective and Methods. We identified recovery-related alterations in motor cortex excitability after stroke using magnetoencephalography. Dynamics (suppression and rebound) of the ~20-Hz motor cortex rhythm were monitored during passive movement of the index finger in 23 stroke patients with upper limb paresis at acute phase, 1 month, and 1 year after stroke.

Results. After stroke, the strength of the ~20-Hz rebound to stimulation of both impaired and healthy hand was decreased with respect to the controls in the affected (AH) and unaffected (UH) hemispheres, and increased during recovery. Importantly, the rebound strength was lower than that of the controls in the AH and UH also to healthy-hand stimulation despite of intact afferent input. In the AH, the rebound strength to impaired-hand stimulation correlated with hand motor recovery.

Conclusions. Motor cortex excitability is increased bilaterally after stroke and decreases concomitantly with recovery. Motor cortex excitability changes are related to both alterations in local excitatory-inhibitory circuits and changes in afferent input. Fluent sensorimotor integration, which is closely coupled with excitability changes, seems to be a key factor for motor recovery.

Approximately 75% of stroke survivors suffer from permanent disability; thus, stroke causes significant human suffering and poses a major economic burden on the society.1 Recovery from stroke is based on brain’s plasticity. Studies in both animals and humans have shown that a period of enhanced plasticity occurs 1-4 weeks after stroke.25 After this sensitive period, the effectiveness of poststroke rehabilitation diminishes dramatically. Recently, there have been promising attempts to prolong or enhance the sensitive period with pharmacological manipulations68 or with noninvasive brain stimulation,9,10 both aiming at changing the cortical excitation-inhibition balance. However, patients with initially similar clinical symptoms may recover differently, possibly because the underlying neurophysiological changes vary between these patients. Thus, understanding and monitoring recovery-related neurophysiological mechanisms and their temporal evolution is crucial for developing efficient, personalized rehabilitation.

Fluent upper limb motor function is important for independency in daily life. Integration of proprioceptive and tactile input with motor plans forms the basis of smooth and precise movements.11 Afferent input mediates its effect on motor functions by modulating the motor cortex excitability.12 Accordingly, our previous study in healthy subjects indicated that proprioceptive input strongly modulates the ~20-Hz motor cortex rhythm, causing an initial suppression followed by a strong and robust rebound.13 Prior studies have suggested that the ~20-Hz rebound reflects deactivation or inhibition of the motor cortex.1417 Moreover, a combined magnetiencephalography (MEG) and magnetic resonance spectroscopy study showed that the ~20-Hz rebound strength is associated with the concentration of the inhibitory neurotransmitter GABA (γ-aminobutyric acid).18

To study alterations in motor cortex excitability after stroke and its association with motor recovery, we measured the dynamics of ~20-Hz motor cortex oscillations during passive movement of the index fingers in 23 stroke patients at the acute phase and during 1-year recovery. The motivation of this study was to understand the neurophysiological mechanisms underlying stroke recovery, which is instrumental for developing novel therapeutic interventions.

Continue —> Strength of ~20-Hz Rebound and Motor Recovery After Stroke – Feb 04, 2017


Figure 1. (A) Setup for passive movement. (B) Representative signals of 1 patient at T0 (1-7 days), T1 (1 month), and T2 (12 months) after stroke. Two upper rows: Magnetoencephalography signals from a single gradiometer channel (raw and filtered to 15-25 Hz over the primary sensorimotor cortex. The ~20-Hz modulation is observable even to a single movement. Third row: Magnitude of acceleration. Total duration of the movement highlighted in gray.

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[Abstract] Isokinetic muscular strengthening of upper limb versus passive movement in chronic stroke patients. Randomised controlled trial


The sensori-motor impairment of upper limb (UL) affects more than 50% of patients after stroke. The objective of this work was to study the efficiency of isokinetic muscle strengthening (IMS) in the chronic phase of stroke in this population.

Material/Patients and methods

The patients underwent 6 weeks of outpatient rehabilitation, 3 days per week, combining physiotherapy (twice/day) and occupational therapy every day. The program was completed by 30 minutes elbow and wrist concentric slow speed IMS of flexor and extensor muscles, in the study group versus 30 minutes passive mobilisation of the joints carried out by the same isokinetic dynamometer in the control group.

Inclusion criteria

Age > 18 years, post stroke period > 6 months, muscle strength > 2/5 manual testing, spasticity < 3/5 on the Ashworth scale. Lack of motion range limitations and cognitive disorders.

Principal judgement criteria

The UL Fugl Meyer (FM) score gain at the end of the program (6 weeks).

Secondary criteria

FM at 3 and 6 months, Box and Block test, Barthel Index and measures of muscle strength at 6 weeks, 3 and 6 months.


Twenty patients were included: 16 men, 13 left hemiplegia, 16 ischemic strokes, average age 63. The gain in the FM score at 6 weeks was comparable between the two groups: 3.5 point (±4.4) versus +6 (±4.5) in the control group (P = 0.224). We have not observed shoulder pain or increase spasticity. No significant differences between the two groups has been demonstrated on secondary endpoints.

All patients improved their FM score (4.7; P < 0.001) and Box and Block test (3 cubes; P = 0.013) at the end of the program. This benefit was maintained at 3 and 6 months.

Discussion – Conclusion

Combined with an intensive multidisciplinary rehabilitation program, IMS of UL is not more efficient than passive mobilisation of the wrist and elbow late after stroke.

Our study also suggests the value of an intensive, out-patient rehabilitation treatment program in chronic phase after stroke, in cases of mild to moderate motor deficit of UL, remains beneficial over 6 months post-program.

Source: Isokinetic muscular strengthening of upper limb versus passive movement in chronic stroke patients. Randomised controlled trial

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