Should We Care About Early Post-Stroke Rehabilitation? Not Yet, but Soon

Zeiler, Steven R.

doi:10.1007/s11910-019-0927-x

Cited by 40 publications

(41 citation statements)

References 85 publications

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“…The effect of a reduced sustained response was confirmed by optogenetically activating vM1. These results show how stroke impairs the function of connected cortical areas and suggest the effective usage of sensory electrical stimulation (SES) in the acute phase of stroke for recovery 29,30 .…”

Section: Discussionmentioning

confidence: 87%

“…1). These times are analogous to the acute (<30 days, corresponding to the inpatient rehabilitation period) and subacute (60-90 days, corresponding to the typical outpatient therapy delivery) phases in human 6,30,[43][44][45] . Each mouse was anesthetized with isoflurane (0.8-1.0% during recording) supplemented with an intraperitoneal injection of chlorprothixene hydrochloride (2 mg/kg) for sedation.…”

Section: Discussionmentioning

confidence: 98%

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Layer-specific sensory processing impairment in the primary somatosensory cortex after motor cortex infarction

Fukui

Osaki

Ueta

et al. 2020

Sci Rep

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Laminar patterns of projections from vM1 to vS1. The projection pattern from vM1 to vS1 is not uniform but varies between layers in vS1 9,21. To validate the layer dependency of the projection pattern from the vM1 infarction area, we injected an anterograde tracer, Biotinylated dextran amine (BDA), into vM1 (Fig. 1A) and identified vM1 axonal innervations in vS1. The signal intensity (green line in Fig. 1B) of the anterogradely labelled axons from vM1 was calculated. For this calculation, the signal of the soma, which is the result of a small amount of retrograde labelling by BDA 22 , was excluded. At the population level, the signal intensity was relatively stronger in L1 and L5b, but weaker in L4 compared to the mean intensity of all layers (N = 3) (Figs. 1C and S1). As summarised in Fig. 1D, vM1 axons projected densely to L1 and L5b.

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Section: Discussionmentioning

confidence: 87%

Section: Discussionmentioning

confidence: 98%

Layer-specific sensory processing impairment in the primary somatosensory cortex after motor cortex infarction

Fukui

Osaki

Ueta

et al. 2020

Sci Rep

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“…Animal models of stroke recovery demonstrate patterns of gene expression and injury responses in the first few days after injury that evolve with time [ 54 – 57 ]. In animals, these processes might constitute a time-limited “sensitive period” for enhanced recovery after stroke [ 58 , 59 ]. In this pilot study of motor behaviors during the first week after stroke, we characterized spontaneous motor behaviors in patients [ 60 , 61 ].…”

Section: Discussionmentioning

confidence: 99%

Characterizing upper extremity motor behavior in the first week after stroke

et al. 2020

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Background Animal models of brain recovery identify the first days after lesioning as a time of great flux in sensorimotor function and physiology. After rodent motor system lesioning, daily skill training in the less affected forelimb reduces skill acquisition in the more affected forelimb. We asked whether spontaneous human motor behaviors of the less affected upper extremity (UE) early after stroke resemble the animal training model, with the potential to suppress clinical recovery. Methods This prospective observational study used a convenience sample of patients (n = 25, mean 4.5 ±1.8) days after stroke with a wide severity range; Controls were hospitalized for nonneurological conditions (n = 12).

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“…In the present study, we tried to elucidate the relationship between serum BDNF levels and motor recovery in response to AR-based rehabilitation over a 60–90-day post-stroke period, which is still considered to belong to the plastic window for stroke recovery [ 35 , 36 ]. Our results show that AR-based rehabilitation is accompanied by a significant augmentation of serum BDNF levels as well as by a highly significant improvement of motor function.…”

Section: Discussionmentioning

confidence: 99%

Serum BDNF’s Role as a Biomarker for Motor Training in the Context of AR-Based Rehabilitation after Ischemic Stroke

et al. 2020

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Background: brain-derived neurotrophic factor (BDNF) may play a role during neurorehabilitation following ischemic stroke. This study aimed to elucidate the possible role of BDNF during early recovery from ischemic stroke assisted by motor training. Methods: fifty patients were included after acute recovery from ischemic stroke: 21 first received classical rehabilitation followed by ‘motor rehabilitation using motion sensors and augmented reality’ (AR-rehabilitation), 14 only received AR-rehabilitation, and 15 were only observed. Serum BDNF levels were measured on the first day of stroke, on the 14th day, before AR-based rehabilitation (median, 45th day), and after the AR-based rehabilitation (median, 82nd day). Motor impairment was quantified clinically using the Fugl–Meyer scale (FMA); functional disability and activities of daily living (ADL) were measured using the Modified Rankin Scale (mRS). For comparison, serum BDNF was measured in 50 healthy individuals. Results: BDNF levels were found to significantly increase during the phase with AR-based rehabilitation. The pattern of the sequentially measured BDNF levels was similar in the treated patients. Untreated patients had significantly lower BDNF levels at the endpoint. Conclusions: the fluctuations of BDNF levels are not consistently related to motor improvement but seem to react to active treatment. Without active rehabilitation treatment, BDNF tends to decrease.

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Should We Care About Early Post-Stroke Rehabilitation? Not Yet, but Soon

Cited by 40 publications

References 85 publications

Layer-specific sensory processing impairment in the primary somatosensory cortex after motor cortex infarction

Layer-specific sensory processing impairment in the primary somatosensory cortex after motor cortex infarction

Characterizing upper extremity motor behavior in the first week after stroke

Serum BDNF’s Role as a Biomarker for Motor Training in the Context of AR-Based Rehabilitation after Ischemic Stroke

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