Painless motor radiculopathy of the cervical spine: clinical and radiological characteristics and long-term outcomes after operative decompression

Abstract

<jats:sec><jats:title>OBJECTIVE</jats:title><jats:p>Various neurological diseases are known to cause progressive painless paresis of the upper limbs. In this study the authors describe the previously unspecified syndrome of compression-induced painless cervical radiculopathy with predominant motor deficit and muscular atrophy, and highlight the clinical and radiological characteristics and outcomes after surgery for this rare syndrome, along with its neurological differential diagnoses.</jats:p></jats:sec><jats:sec><jats:title>METHODS</jats:title><jats:p>Medical records of 788 patients undergoing surgical decompression due to degenerative cervical spine diseases between 2005 and 2014 were assessed. Among those patients, 31 (3.9%, male to female ratio 4.8 to 1, mean age 60 years) presented with painless compressive cervical motor radiculopathy due to neuroforaminal stenosis without signs of myelopathy; long-term evaluation was available in 23 patients with 49 symptomatic foraminal stenoses. Clinical, imaging, and operative findings as well as the long-term course of paresis and quality of life were analyzed.</jats:p></jats:sec><jats:sec><jats:title>RESULTS</jats:title><jats:p>Presenting symptoms (mean duration 13.3 months) included a defining progressive flaccid radicular paresis (median grade 3/5) without any history of radiating pain (100%) and a concomitant muscular atrophy (78%); 83% of the patients were smokers and 17% patients had diabetes. Imaging revealed a predominantly anterior nerve root compression at the neuroforaminal entrance in 98% of stenoses. Thirty stenoses (11 patients) were initially decompressed via an anterior surgical approach and 19 stenoses (12 patients) via a posterior surgical approach. Overall reoperation rate due to new or recurrent stenoses was 22%, with time to reoperation shorter in smokers (p = 0.033). Independently of the surgical procedure chosen, long-term follow-up (mean 3.9 years) revealed a stable or improved paresis in 87% of the patients (median grade 4/5) and an excellent general performance and quality of life.</jats:p></jats:sec><jats:sec><jats:title>CONCLUSIONS</jats:title><jats:p>Painless cervical motor radiculopathy predominantly occurs due to focal compression of the anterior nerve root at the neuroforaminal entrance. Surgical decompression is effective in stabilizing or improving motor function with a resulting favorable long-term outcome.</jats:p></jats:sec>

Amyotrophic lateral sclerosis mimics

“…146,148 4.9 | Radiculopathy Cervical and lumbosacral radiculopathy can mimic ALS in rare cases where pain and sensory loss is absent. [149][150][151][152] For example, a lumbosacral radiculopathy at the L4/5 or L5/S1 levels may conceivably be mistaken as ALS due to asymmetric distal weakness. [153][154][155] However, the relative lack of progression of weakness would distinguish radiculopathy from ALS.…”

“…Cervical and lumbosacral radiculopathy can mimic ALS in rare cases where pain and sensory loss is absent 149‐152 . For example, a lumbosacral radiculopathy at the L4/5 or L5/S1 levels may conceivably be mistaken as ALS due to asymmetric distal weakness 153‐155 .…”

Cervical spine radiculopathy epidemiology: A systematic review

“…It was anticipated that studies may use different CSR diagnostic criteria. CSR may not always be associated with pain (i.e., a painless radiculopathy) (Siller et al, 2018), and often, there is a combination of clinical findings or outcomes, which can be attributed to clinical examination techniques utilised (Thoomes et al, 2018). Our inclusion criteria reflected this anticipated variation.…”

“…Diagnosis is made by a detailed patient interview and physical assessment. Subjective complaints of paraesthesia, hyperaesthesia, dysaesthesia and/or allodynia, substantiated by neurological examination, quantitative sensory testing and/or electrodiagnostic testing are typical findings (Backonja et al, 2013; Dillingham, 2013; Siller, Kasem, Witt, Tonn, & Zausinger, 2018; Treede et al, 2008). Painful or restricted neck movements, diminished deep tendon reflex and/or upper limb weakness are characteristic examination outcomes (Iyer & Kim, 2016; Rubinstein, Pool, van Tulder, Riphagen, & de Vet, 2007).…”

Differential diagnoses of amyotrophic lateral sclerosis are more variegated than anticipated

“…Missing in this list of differentials of ALS are mitochondrial disorders, compression-induced painless cervical radiculopathy,[2] late-onset Hirayama disease,[3] Niemann–Pick disease type C,[4] Herpesvirus myelitis,[5] mitochondrial membrane protein-associated neurodegeneration,[6] spinocerebellar ataxia Type 3,[7] hexosaminidase A deficiency,[7] Parkinson's disease,[7] spinal muscular atrophy,[7] monomelic amyotrophy,[7] Morvan syndrome,[8] capecitabine-induced leukoencephalopathy,[9] tumor necrosis factor-alpha therapy of psoriatic arthritis,[10] GM2 gangliosidoses (Sandhoff disease, AB-variant, and Tay–Sachs disease), frontotemporal dementia, Huntington's disease, Alzheimer's disease, flail arm syndrome, Lyme disease, progressive muscular atrophy, cramp fasciculation syndrome, pure motor neuropathy with or without conduction block, Sjögren syndrome, aluminium intoxication, and lead intoxication.…”