The majority of patients simultaneously develop motor dysfunction and spastic hypertonia after ischemic strokes, which can be associated with an increasing trend in motor impairments, seriously impeding the rehabilitation process. Evidence suggests that some deficits in the KCC2 expression in the spinal cord along with maladaptive endogenous plasticity via GABAA receptors are often involved in the pathology of spastic hypertonia after a stroke. In this respect, acupuncture has been commonly used in clinical settings for post-stroke patients\' rehabilitation. Nevertheless, the mechanism of the modulating activity of this alternative medicine in the spinal pathways to relieve spasticity and improve functional recovery after a stroke has still remained unclear. Utilizing laser speckle imaging, functional assessments (viz. neurologic function scale, muscular tension scale, foot balance test, and gait analysis), H-reflex recording, TTC, Western blotting, RT-qPCR, ELISA, and immunofluorescence molecular assay, the study results illustrated that acupuncture could significantly alleviate the spinal hyperreflexia, decrease muscle tone, and enhance locomotor function by elevating the GABA, KCC2, and GABAAγ2 expressions in the lumbar spine of a rat model of post-ischemic stroke with spastic hypertonia. Furthermore, the KCC2 antagonist DIOA abolished the benefits induced by this practice. Overall, the data revealed that acupuncture is a promising therapeutic approach for spastic hypertonia after a stroke, and the positive outcomes in this sense could be achieved via activating the KCC2-mediated spinal GABAA signaling pathway.

Spasticity is a motor disorder that manifests as a component of the upper motor neuron syndrome. It is associated with paralysis and can cause significant disability. The most common causes leading to spasticity include stroke, traumatic brain injury, multiple sclerosis, spinal cord injury, and cerebral palsy. This article discusses the pathophysiology and clinical findings associated with each of the most common etiologies of upper extremity spasticity.

To study the effects of single versus serial casting post-Botulinum toxin A (BoNT-A) injections on hypoextensibility of triceps surae in children, 2-7 years old, with cerebral palsy and equinus gait.
A randomized, stratified, parallel, two-group trial was conducted at a pediatric health center with assessments at baseline, precast, postcast and, 1-, 2-, and 6-month follow-ups. One week following BoNT-A injections into triceps surae muscle, a single below-knee cast (n = 10) or 3 serial casts (n = 10) were applied for 3 weeks. Primary outcome measure was the Modified Tardieu Scale (MTS), secondary outcome measures were Modified Ashworth Scale (MAS), GAITRite™, Gross Motor Function Measure-66 (GMFM-66), and Pediatric Evaluation of Disability Inventory (PEDI).
Significant effects of time, but not group-by-time, were found for MTS R1 (P < 0.001), MTS R2 (P < 0.001), MAS (P = 0.001), GMFM-66 (P = 0.002), and PEDI (P < 0.001-0.009). One participant who received a single cast did not complete the 6-month assessment.
Magnitudes of improvements were similar using single or serial casting. If these findings are corroborated in a larger scale study, the recommendation of a single cast may be appropriate due to its greater convenience for families and clinicians.

Aberrant vestibular nuclear function is proposed to be a principle driver of limb muscle spasticity after stroke. We sought to determine whether altered cortical modulation of descending vestibulospinal pathways post-stroke could impact the excitability of biceps brachii motoneurons. Twelve chronic hemispheric stroke survivors aged 46-68 years were enrolled. Sound evoked biceps myogenic potentials (SEBMPs) were recorded from the spastic and contralateral biceps muscles using surface EMG electrodes. We assessed the impact of descending vestibulospinal pathways on biceps muscle activity and evaluated the relationship between vestibular function and the severity of spasticity. Spastic SEBMP responses were recorded in 11/12 subjects. Almost 60% of stroke subjects showed evoked responses solely on the spastic side. These data strongly support the idea that vestibular drive is asymmetrically distributed to biceps motoneuron pools in hemiparetic spastic stroke survivors. This abnormal vestibular drive is very likely to be a factor mediating the striking differences in motoneuron excitability between the clinically affected and clinically spared sides. This study extends our previous observations on vestibular nuclear changes following hemispheric stroke and potentially sheds light on the underlying mechanisms of post-stroke spasticity.

OBJECTIVE: Baclofen is a zwitterion molecule where increased ions in the excipient increase the solubility. We developed baclofen in a stable solution similar to cerebrospinal fluid (CSF) without bicarbonate and proteins to improve the solubility of the baclofen and to reduce the potential toxicity to the central nervous system (CNS) and subarachnoid space. The objective is to develop a solution of baclofen wherein baclofen is solubilized in a multivalent physiological ion solution such as artificial cerebrospinal fluid (aCSF) at a concentration from 2 mg/cc to 10 mg/cc.
METHODS: First, to determine the solubility of Baclofen in aCSF, solubility was determined at six different pH levels at 37°C, by the addition of aCSF to a known amount of Baclofen. The final concentrations were confirmed by high performance liquid chromatography (HPLC) analysis. Second, the stability of Baclofen at 4 mg/cc investigated in a test manufacturing batch utilizing standard methods of production of 1500 20 cc vials inverted for 18 months at 25°C at 60% humidity. The stability and purity of the baclofen was verified at 18 months by HPLC analysis.
RESULTS: Baclofen was initially soluble between pH of 6-8 above 7 mg/cc but fell back to 6.3-5.8 mg/cc level with time. Baclofen produced in vials with inversion were noted to be stable at 4 mg/cc at 18 months with less than 2% breakdown of the baclofen in solution.
CONCLUSIONS: Baclofen is much more soluble in artificial CSF than normal saline. The artificial CSF may also be less toxic to the subarachnoid space than saline.