gms | German Medical Science

Objective: The concept of "Cortico-spinal Reserve in patients suffering from degenerative cervical Myelopathy" (CReMe) has been recently introduced. In patients suffering from mild symptoms (JOA>12) and thus preserved reserve an enlarged motor area due to a higher recruitment of supplementary motor areas (M2) was observed. In contrast, severely symptomatic patients (JOA<12) with an exhausted reserve presented with a restricted motor area, reduced recruitment curve and increased inhibition. The current prospective multicentre trial has been designed to validate the new pathophysiological concept.

Methods: In our on-goingtrial, we have enrolled 120 patients with degenerative cervical myelopathy (DCM) from 4 spine centres in Germany and Switzerland. The study was sponsored by a DWG research grant. On the basis of the initial Japanese Orthopaedic Association (JOA) Score three patient groups were established (JOA≤12, 13-15, 15-17). Corticospinal excitability was determined by navigated transcranial magnetic stimulation (nTMS) with the following parameters: Resting motor threshold (RMT), Recruitment curve (RC), Cortical silent period (CSP) and Motor area.

Results: In patients with moderate symptoms (JOA 12-15) we encountered a compensatory increase of motor cortex activation (motor area: p<05; mean ± SD JOA 12-15: 308,5 ± 213,3 vs. JOA ≤ 12: 225,7 ± 159,5) and maintained corticospinal excitability (RC slope p=0.4; JOA 12-15: 10,6 ± 6 vs. JOA 15-17: 11,1 ± 5,2). In contrast patients with severe symptoms (JOA ≤12) presented a reduced excitability of cortico-cortical axons reflected by an elevated RMT (p<0.05; JOA ≤12: 43,8 ± 11,4 vs. JOA 15-17: 39,2 ± 8,4) and reduced corticospinal excitability expressed by a lower RC slope (p<0.05; JOA ≤12: 8,4 ± 4,8 vs. JOA 15-17: 11,1 ± 5,2). The diminished cortical motor area (p<0.05, see above) further revealed a functional restriction on the cortical level in this group.

Conclusion: In summary our prospective multicentre trial has confirmed our concept for functional reorganization in patients suffering from DCM i.e. the "corticospinal reserve capacity". It became apparent that the individual pattern of compensation is a sensitive marker to objectify the state of the disease and may indicate imminent non-reversible clinical deterioration. This innovative approach to describe the pathomechanisms in DCM might revise current concepts of clinical diagnostics and might have an impact on future treatment strategies.