Interaction of the Left–Right Somatosensory Pathways in Patients With Thalamic Hemorrhage: A Case Report

Abstract

Neural plasticity compensates for the loss of motor function after stroke. However, whether neural plasticity occurs in the somatosensory pathways after stroke is unknown. We investigated the left–right somatosensory interaction in two hemorrhagic patients using a paired somatosensory evoked potentials (p-SEPs) recorded at CP3 and CP4, which was defined as an amplitude difference between the SEPs of paired median nerve stimulations to both sides and that of single stimulation to the affected side. Patient 1 (61-year-old, left thalamic hemorrhage) has a moderate motor impairment, severe sensory deficit, and complained of pain in the affected right upper limb. Patient 2 (72-year-old, right thalamic hemorrhage) had slight motor and sensory impairments with no complaints of pain. Single SEPs (s-SEPs) were obtained by stimulation of the right and left median nerves, respectively. For paired stimulations, 1 ms after the first stimulation to the non-affected side, followed by a second stimulation to the affected side. In patient 1, a s-SEP with stimulation to the non-affected side and a p-SEP were observed in CP4. However, a s-SEP was not observed in either hemisphere with stimulation to the affected side. On the other hand, in patient 2, a s-SEP in CP3 with stimulation to the non-affected side and in CP4 with stimulation to the affected side were observed; however, a p-SEP was not observed. In addition, to investigate the mechanism by which ipsilateral median nerve stimulation enhances contralateral p-SEP in patient 1, we compared the SEP averaged over the first 250 epochs with the SEP averaged over the second 250 epochs (total number of epochs recorded: 500). The results showed that in the patient 1, when the bilateral median nerve was stimulated continuously, the habituation did not occur and the response was larger than that of the s-SEP with unilateral median nerve stimulation. In the current case report, the damage to the thalamus may cause neuroplasticity in terms of the left–right interaction (e.g., left and right S1). The somatosensory input from the affected side may interfere with the habituation of the contralateral somatosensory system and conversely increase the response.

Effects of mirror therapy on spasticity and sensory impairment after stroke: Systematic review and meta‐analysis

“…11 To achieve this, stimulation of neuroplasticity of the central nervous system plays an important role in creating new pathways to repair and reconnect motor areas and somatosensory inputs to regain functionality. 16 Several studies have analyzed the effectiveness of physiotherapy interventions on brain neuroplasticity and functional recovery. Some proposed exercise-based conventional therapies (eg, therapeutic exercise, 17 active/ passive mobilizations 18 ) and others were based on standard neurorestoration intervention protocols (eg, Bobath, 19 Proprioceptive Neuromuscular Facilitation, 20 Perfetti 21 ).…”

“…This functional interaction between somatosensory and motor systems has led to the development of rehabilitation approaches oriented to achieve functional improvements combining motor training with the integration of sensory information (eg, somatosensory, visual, auditory, multisensorial, and cortical information), increasing corticospinal excitability and enlarging motor cortex representation of the stimulated body areas 11 . To achieve this, stimulation of neuroplasticity of the central nervous system plays an important role in creating new pathways to repair and reconnect motor areas and somatosensory inputs to regain functionality 16 …”