Quantitative Assessment of Hand Spasticity After Stroke: Imaging Correlates and Impact on Motor Recovery

Survivors don't give a shit about 'assessment'. That does absolutely nothing to get them to 100% recovery. Useless, I would have you fired. 

Quantitative Assessment of Hand Spasticity After Stroke: Imaging Correlates and Impact on Motor Recovery

Jeanette Plantin^1*, Gaia V. Pennati¹, Pauline Roca^2,3, Jean-Claude Baron⁴, Evaldas Laurencikas^1,5, Karin Weber¹, Alison K. Godbolt¹, Jörgen Borg¹ and Påvel G. Lindberg^1,2

• ¹Division of Rehabilitation Medicine, Department of Clinical Sciences, Karolinska Institutet, Danderyd University Hospital, Stockholm, Sweden
• ²Institut de Psychiatrie et Neurosciences de Paris, Inserm U1266, Paris, France
• ³Department of Neuroimaging, Sainte-Anne Hospital Center, Université Paris Descartes Sorbonne Paris Cité, Paris, France
• ⁴Department of Neurology, Hôpital Sainte-Anne, Université de Paris, Paris, France
• ⁵Division of Radiology, Department of Clinical Sciences, Karolinska Institutet, Danderyd University Hospital, Stockholm, Sweden

Objective: This longitudinal observational study investigated how neural stretch-resistance in wrist and finger flexors develops after stroke and relates to motor recovery, secondary complications, and lesion location.

Methods: Sixty-one patients were assessed at 3 weeks (T1), three (T2), and 6 months (T3) after stroke using the NeuroFlexor method and clinical tests. Magnetic Resonance Imaging was used to calculate weighted corticospinal tract lesion load (wCST-LL) and to perform voxel-based lesion symptom mapping.

Results: NeuroFlexor assessment demonstrated spasticity (neural component [NC] >3.4N normative cut-off) in 33% of patients at T1 and in 51% at T3. Four subgroups were identified: early Severe spasticity (n = 10), early Moderate spasticity (n = 10), Late developing spasticity (n = 17) and No spasticity (n = 24). All except the Severe spasticity group improved significantly in Fugl-Meyer Assessment (FMA-HAND) to T3. The Severe and Late spasticity groups did not improve in Box and Blocks Test. The Severe spasticity group showed a 25° reduction in passive range of movement and more frequent arm pain at T3. wCST-LL correlated positively with NC at T1 and T3, even after controlling for FMA-HAND and lesion volume. Voxel-based lesion symptom mapping showed that lesioned white matter below cortical hand knob correlated positively with NC.

Conclusion: Severe hand spasticity early after stroke is negatively associated with hand motor recovery and positively associated with the development of secondary complications. Corticospinal tract damage predicts development of spasticity. Early quantitative hand spasticity measurement may have potential to predict motor recovery and could guide targeted rehabilitation interventions after stroke.

Introduction

Spasticity of the muscles contributing to hand function (hereafter “hand spasticity”) is a common sensorimotor disorder after stroke (1), can be disabling (2), and is related to development of contracture and pain (3, 4). However, longitudinal studies investigating how hand spasticity relates to hand motor recovery, are scarce (4). A better understanding of the relationship between spasticity severity early after stroke and motor recovery could inform about which patients could potentially benefit from different treatment paradigms. For example, spasticity, comprising a velocity dependent increase in tonic stretch reflexes (5), can be reduced by blocking neuromuscular transmission with botulinum toxin. In the upper limb, botulinum toxin has been shown to reduce spasticity and pain and improve limb positioning (6). Results in recent studies also suggest that botulinum toxin treatment has been associated with improvement in both passive and active range of movement post-stroke (7). Further, other non-neural factors (elasticity, viscosity) may also contribute to resistance to passive stretch (8), which may go undetected when using the most frequently applied measure of muscle tone, the modified Ashworth scale (9, 10) and potentially confound clinical trials.

The use of a validated biomechanical assessment (11) could improve diagnostic accuracy by separately measuring the neural component (NC) and non-neural components contributing to passive stretch-resistance (12). Further, improved diagnostic accuracy also opens new opportunities for longitudinal characterization (4, 11), and for charting the relation between severity and lesion location using modern imaging techniques (13). Given that reducing post-stroke spasticity may be associated with improved active range of movement (7) we hypothesized that hand spasticity early post-stroke would relate to poor hand motor recovery. More specifically, we predicted that severe early spasticity would be associated with less longitudinal improvement in clinical measures of sensorimotor hand function. We characterized longitudinal changes in hand spasticity, i.e., the neural component of passive stretch-resistance after stroke, using a validated biomechanical method with normative data, and studied the relation to hand motor recovery, muscle contracture, and pain. We also explored corticospinal tract (CST) lesion load and lesion location using voxel-based lesion symptom mapping (13) to gain insights into the neural correlates of hand spasticity.

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