An observational study was conducted on individuals with Spinal cord injury at Physiotherapy OPD of the tertiary care hospital at Ahmednagar. A convenient sampling strategy was utilized to enroll subjects after obtaining the ethical clearance. Ten SCI subjects aged between 18 to 60 years participated in the study. Written informed consent was obtained in the regional language from all the participants. The demographic data including name, age, gender, address, level of injury, and dominance was noted. Participants were in a prone lying position and the area to be assessed was cleaned with spirit to avoid hair resistance. Unipolar stimulation, in which the cathode is placed over the nerve and the anode is positioned on the opposite side of the limb, is recommended in most situations to selectively activate Ia afferents at lower thresholds and to reduce the stimulus artifact. Electrode placement was done according to the standardized procedure to elicit the Soleus H reflex i.e. bipolar surface electrodes were placed approximately 2 cm apart over the corresponding muscle belly and an inactive electrode was placed on the TA tendon. Ten soleus H-reflex were elicited from the right leg at 3,6 and 9 months respectively. H reflex is a monosynaptic reflex elicited by submaximal stimulation of the tibial nerve and recorded from the calf muscle. It is interpreted by the latency which is measured from the stimulus artifact to the first deflection from the baseline and amplitude is measured from base to peak of the negative phase or can be measured from peak to peak. The Intraclass Correlation Coefficients obtained for latency, amplitude and duration of the H-wave were 0.46, 0.97, 0.99 respectively. The H max /M max and Hslp/Mslp showed very good reliability i.e. ICC – 0.87 and 0.92 respectively.

Descriptive statistics were obtained and the normality of the data was checked using the Kolmogorov-Smirnov Normality test. Within-group comparison was done by Freidman test and post hoc analysis was done using Dunn’s Multiple comparison test. Categorical variables were measured by graphs and tables.

When the spinal cord is injured all the functions of the spinal cord below the level of injury are depressed as the result of spinal shock. Spinal shock may last from days up to several weeks. After SCI there is also a secondary injury mechanism that takes place further affecting the neurons and glia, the major event for secondary injury is cell death which can be because of various mediators induced by the injury, apoptosis and necrosis are the two leading originally identified mechanisms to follow SCI.² The series of cellular, molecular, and biochemical phenomena that continues to harm the cord after SCI is still referred with the term secondary injury in the field. Within a few minutes after primary injury secondary injury starts and may continue for weeks or maybe months leading to a cascade of progressive damage to the spinal cord around the lesion. Immediately after the injury, there is an initiation of the acute phase in which there is damage to vasculature, imbalance of ions, accumulation of neurotransmitters, edema, influx of calcium, free radical formation, lipid peroxidation, inflammation and necrotic cell death.⁴ Due to the injury there in disruption in the blood supply and hypo-perfusion and this is the early consequence of primary injury. In SCI cases there can be hypovolemia and hemodynamic shock due to excess bleeding and because of the compromised perfusion and ischemia, there is neurogenic shock. Vessels like anterior spinal artery that are large remains intact while damage to small vessels and capillaries susceptible to traumatic damage leads to extravasation of leukocytes and red blood cells.² Further disruption of the blood flow is because of edema and hemorrhage-induced vasospasm in intact vessels.⁸ A study by Benito Penalva et al. analyzed the effect of 40 sessions of robotic treadmill gait training on TMS-mediated soleus H-reflex facilitation in a population of subjects with incomplete SCI. In that study, training improved a baseline deficit in the ‘direct’ (20 ms) facilitation time window, and this correlated with clinical improvement.⁹ During spinal shock many electrophysiological studies vindicate supraspinal segmental inhibition with results of presynaptic inhibition and block monosynaptic and polysynaptic reflex arcs. Nevertheless, the spinal neurons gradually regain their excitability.

Similarly, we aimed to observe the reflexive changes in the individual with spinal cord injury. The mean score of H-reflex Amplitude improved significantly at 3, 6, and 9 months of injury. A study found that patients with complete SCI had significantly increased H-reflex ratio at short ISI compared with healthy and incomplete SCI subjects, whereas no significant differences in H-reflex recovery were found between incomplete SCI and the control group at short ISIs. This study revealed alteration in spinal reflex activity in SCI individuals which depends on the severity of SCI,but not the level of SCI.¹⁰ These findings contribute to a better understanding of spinal reflex excitability regulation and could serve as electrophysiological measures of therapeutic interventions.

A study by Kumru et al aimed to evaluate the changes in the excitability of the Soleus H reflex circuit modifies according to severity and level of injury. And whether H-reflex and its prognosis depend on the level or the severity of the disease. The soleus H max and M max responses and the H reflex recovery curve at interstimulus intervals (ISIs) ranging from 50 to 1,000 ms were obtained in 38 individuals with Spinal Cord Injury and 18 healthy subjects. Comparison of complete and incomplete SCI was also analyzed. A smaller amplitude correlated with more severe SCI or more caudal lesion in the case of M_max. H-reflex recovery curve was increased significantly in complete SCI at ISIs < 500 ms and in incomplete SCI at ISIs>200 ms concerning healthy subjects. They concluded that the changes in spinal reflexes and its recovery curve after SCI depend on the severity, but not on the level of the lesion.¹¹ The resolution of spinal cord shock occurs over a period and it slowly transit showing the symptoms of spasticity. Meanwhile, the spinal neurons gradually regain their excitability by the mechanism of synaptic reorganization. The body is in a continuous process of repair and recovery after the injury.

The findings of the study revealed that there is a gradual increase in H-reflex amplitude in individuals post-injury. Therefore, the spinal neurons gradually regain their excitability and recovery takes place over a period of time.