Cutaneous Silent Period and Spasticity

The cutaneous silent period (CSP) is a brief transient suppression of the voluntary muscle contraction that follows a noxious cutaneous nerve stimulation. Studies in patients with central disorders of motor control such as dystonia and Parkinson's disease have shown CSP abnormalities indicating that supraspinal pathways influence this inhibitory spinal reflex. The aim of this study is to investigate the association between CSP parameters (duration and latency) and spasticity in stroke.

The cutaneous silent period (CSP) is a brief transient suppression of the voluntary muscle contraction that follows a noxious cutaneous nerve stimulation. Studies in patients with central disorders of motor control such as dystonia and Parkinson's disease have shown CSP abnormalities indicating that supraspinal pathways influence this inhibitory spinal reflex. Spasticity is a serious problem that creates great difficulty for both patients and clinicians. The Support Programme for Assembly of a database for Spasticity Measurement (SPASM) group defined the spasticity as "disordered sensory-motor control, resulting from an upper motor neuron lesion, presenting as intermittent or sustained involuntary activation of muscles". Spasticity occurs in different types depending on the duration of the lesion present in the central nervous system (acute or slowly emerging), the size of the lesion and the location of the lesion such as cerebral cortex, brain stem or spinal cord. There are three major approaches, clinical, neurophysiological and biomechanical, for assessing spasticity. Stimulating the cutaneous nerve of the index finger at low-intensity, researchers have evoked an inhibition of the electromyographic (EMG) activity with a long latency and a short duration, namely the I2 inhibitory response of the cutaneo-muscular reflexes in the hand. ıt was suggested that the I2 inhibitory response, whose latency and duration overlap the CSP, was mediated by low-threshold, large-diameter fibers. Hence, because high-intensity electrical stimuli used to evoke the CSP activate large-diameter as well as small-diameter fibers, both fiber types may contribute in generating the CSP .

The central neural substrates producing the alpha-motor neuron inhibition after high-intensity stimulation differ from those after low-intensity stimulation. Low-intensity non-painful stimulation elicits a typical polysynaptic pattern of exteroceptive reflexes, whereas high-intensity electrical stimulation elicits an oligosynaptic pattern. Several studies investigated whether the CSP after high intensity finger stimulation arises from interruption of the excitatory drive to motor neurons (pre-synaptic inhibition) or inhibition of motor neurons themselves (post-synaptic inhibition). Studies using H-reflexes, F waves, and motor evoked potentials to assess motor neuron excitability showed that during the CSP motor neurons mainly receive post-synaptic inhibition transmitted through spinal inhibitory interneurons. Studies in patients with central disorders of motor control such as dystonia and Parkinson's disease have shown CSP abnormalities indicating that supraspinal pathways influence this inhibitory spinal reflex.

It was investigated whether the CSP parameters, F parameters are different between patients with stroke and amyotrophic lateral sclerosis (ALS) and healthy controls.

They found that CSP latency was higher in patients with stroke and ALS than healthy subjects. There was no difference in KSP duration and F-latency compared to healthy subjects. Contrary to these results, in another study did not show a relationship between spasticity and CSP parameters in twelve patients with stroke. The results of the existing studies on the relationship between spasticity and CSP parameters are conflicting. The influence of the descending suprasegmental pathways on the origin of the CSP is yet to be elucidated. Therefore; there is a need for a properly designed study investigating this relationship in a homogeneous sample. Given these results, we aimed to investigate the association between CSP parameters (duration and latency) and spasticity in patients with stroke. modified Ashworth scale, Modified Tardieu scale, Brunnstrom motor stage ve Fugl Meyer upper extremity score, Barthel index will be measured. Patients with stroke will underwent electromyographic assessments of F-wave latency, F-M ratio, CSP latency and duration, upper extremity nerve conduction studies. Association between clinical assessments and electrophysiological assessments will be investigated.

Eligibility Criteria:
Inclusion Criteria:

1. First ever time stroke
2. Time since stroke \>1 month
3. Being able to understand the instructions (mini mental test score\>24)

Exclusion Criteria:

1. Diseases which might affect CSP parameters (Parkinsonism, restless leg syndrome, carpal tunel syndrome etc.)
2. Autonomic nervous system disease
3. Antispasticity medication use
4. Hemiplegic shoulder pain
5. Botulinum toxin injection within 6 months