OBJECTIVES: Intrathecal baclofen (ITB) is commonly used for reduction of spasticity in chronic spinal cord injury (SCI). Its clinical effect is well-known; however, exact mechanisms of long-term effect of continuous ITB administration (cITBa) on modulation of cortical processes have not been elucidated. The aim of this study was to evaluate changes in motor cortex activation for healthy upper limbs in comparison to impaired lower limbs by functional magnetic resonance imaging (fMRI). METHODS: Ten subjects (eight males, 20-69 years) with thoracic SCI presenting no voluntary movements of lower limbs (except one) were enrolled in the fMRI study. fMRI at 1.5T with a finger tapping paradigm and mental movement simulating foot flexion on the dominant side were performed before, 3 months, and 1 year after start of cITBa. fMRI data processing was carried out using FMRI Expert Analysis Tool (FEAT), part of FSL. A second-level analysis was carried out using FLAME stages 1 and 2. The level of spasticity was assessed with the Modified Ashworth scale (MAS). RESULTS: Continuous ITB significantly decreased limb spasticity in all the subjects (group MAS spasticity dropped from 3 to 0.3). The second-level analysis (Z > 1.6, cluster significance threshold p =0.05) revealed increased activation of the primary sensorimotor cortex of the foot between baseline and 3 months, and 3 months and 1 year. CONCLUSION: Increased sensorimotor cortex activation with spasticity reduction after cITBa may reflect distant functional reorganization because of long-term mediated neuroplastic changes in the sensorimotor cortex. Better understanding of modulation of brain function in SCI after cITBa may influence the field of neurorehabilitation.

• Keywords
• functional MRI, intrathecal baclofen, motor cortex activity, plasticity, spinal cord injury,
• Publication type
• Journal Article MeSH

In dystonic and spastic movement disorders, abnormalities of motor control and somatosensory processing as well as cortical modulations associated with clinical improvement after botulinum toxin A (BoNT-A) treatment have been reported, but electrophysiological evidence remains controversial. In the present observational study, we aimed to uncover central correlates of post-stroke spasticity (PSS) and BoNT-A-related changes in the sensorimotor cortex by investigating the cortical components of somatosensory evoked potentials (SEPs). Thirty-one chronic stroke patients with PSS of the upper limb were treated with BoNT-A application into the affected muscles and physiotherapy. Clinical and electrophysiological evaluations were performed just before BoNT-A application (W0), then 4 weeks (W4) and 11 weeks (W11) later. PSS was evaluated with the modified Ashworth scale (MAS). Median nerve SEPs were examined in both upper limbs with subsequent statistical analysis of the peak-to-peak amplitudes of precentral P22/N30 and postcentral N20/P23 components. At baseline (W0), postcentral SEPs were significantly lower over the affected cortex. At follow up, cortical SEPs did not show any significant changes attributable to BoNT-A and/or physiotherapy, despite clear clinical improvement. Our results imply that conventional SEPs are of limited value in evaluating cortical changes after BoNT-A treatment and further studies are needed to elucidate its central actions.

• MeSH
• Botulinum Toxins, Type A administration & dosage   MeSH
• Stroke complications   physiopathology   MeSH
• Adult MeSH
• Upper Extremity innervation   MeSH
• Middle Aged MeSH
• Humans MeSH
• Young Adult MeSH
• Follow-Up Studies MeSH
• Neuromuscular Agents administration & dosage   MeSH
• Median Nerve drug effects   physiopathology   MeSH
• Stroke Rehabilitation methods   MeSH
• Aged MeSH
• Evoked Potentials, Somatosensory drug effects   MeSH
• Somatosensory Cortex drug effects   physiopathology   MeSH
• Muscle Spasticity diagnosis   drug therapy   etiology   physiopathology   MeSH
• Exercise Therapy methods   MeSH
• Treatment Outcome MeSH
• Check Tag
• Adult MeSH
• Middle Aged MeSH
• Humans MeSH
• Young Adult MeSH
• Male MeSH
• Aged MeSH
• Female MeSH
• Publication type
• Journal Article MeSH
• Observational Study MeSH
• Names of Substances
• Botulinum Toxins, Type A MeSH
• Neuromuscular Agents MeSH

In dystonic and spastic movement disorders, however different in their pathophysiological mechanisms, a similar impairment of sensorimotor control with special emphasis on afferentation is assumed. Peripheral intervention on afferent inputs evokes plastic changes within the central sensorimotor system. Intramuscular application of botulinum toxin type A (BoNT-A) is a standard evidence-based treatment for both conditions. Apart from its peripheral action on muscle spindles, a growing body of evidence suggests that BoNT-A effects could also be mediated by changes at the central level including cerebral cortex. We review recent studies employing electrophysiology and neuroimaging to investigate how intramuscular application of BoNT-A influences cortical reorganization. Based on such data, BoNT-A becomes gradually accepted as a promising tool to correct the maladaptive plastic changes within the sensorimotor cortex. In summary, electrophysiology and especially neuroimaging studies with BoNT-A further our understanding of pathophysiology underlying dystonic and spastic movement disorders and may consequently help develop novel treatment strategies based on neural plasticity.

• Keywords
• botulinum toxin, dystonia, electrophysiology, functional magnetic resonance imaging, neural plasticity, spasticity,
• MeSH
• Botulinum Toxins, Type A adverse effects   therapeutic use   MeSH
• Dystonia diagnosis   drug therapy   physiopathology   MeSH
• Muscle, Skeletal innervation   MeSH
• Humans MeSH
• Magnetic Resonance Imaging MeSH
• Brain Mapping MeSH
• Cerebral Cortex diagnostic imaging   drug effects   physiopathology   MeSH
• Neuromuscular Agents adverse effects   therapeutic use   MeSH
• Neuronal Plasticity drug effects   MeSH
• Recovery of Function MeSH
• Motor Activity drug effects   MeSH
• Treatment Outcome MeSH
• Animals MeSH
• Check Tag
• Humans MeSH
• Animals MeSH
• Publication type
• Journal Article MeSH
• Research Support, Non-U.S. Gov't MeSH
• Review MeSH
• Names of Substances
• Botulinum Toxins, Type A MeSH
• Neuromuscular Agents MeSH