Case Report: Critique of Neurological Examination Report (23.10.2020)

While UNMH (USA/NM) confirmed a diagnosis of myalgia on 5/25/2016, with follow-up scheduled on a PRN basis,

a subsequent neurology evaluation in Germany could not confirm the presence of muscle weakness.

The German report — documenting a neurophysiological assessment in Sept. 2020, of the now 71-year-old female — is methodologically sound but interpretatively lacking. Although the technical execution of repetitive nerve stimulation, nerve conduction studies, and EMG appears appropriate, the report fails to incorporate a crucial clinical finding: the patient’s marked pain sensitivity. This omission limits the diagnostic value of the evaluation and leaves a significant symptom unexplored within its clinical context.

1. Methodological Rigor vs. Interpretative Narrowness
The neurophysiological testing is competently performed, with results clearly indicating the absence of neuromuscular transmission disorders, polyneuropathy, or overt myopathic/neurogenic pathology. However, the interpretative section confines itself strictly to structural normality, effectively dismissing the most salient clinical finding: the disproportionate pain response during EMG.

2. Clinical Oversight
The report’s acknowledgment of the patient’s repeated crying out with each needle insertion is reduced to a passing remark, unaccompanied by exploration of differential diagnoses. This omission is not trivial. Hyperalgesia, whether central or peripheral, is well-established in chronic pain conditions, postoperative syndromes, and central nervous system disorders — all of which are relevant given the patient’s history of Chiari malformation with decompression surgery and prior lumbar spinal infection. Ignoring this symptom effectively divorces the physiological testing from the lived clinical reality.

3. Missed Opportunity for Biopsychosocial Integration
The exclusion of structural nerve or muscle injury should have been the starting point for further analysis, not the endpoint. The patient’s pain response warrants discussion of central sensitization, small fiber neuropathy, and non-structural mechanisms of pain amplification, none of which are detectable via standard conduction studies. Even in the absence of psychiatric comorbidity or needle phobia (both denied by the patient), psychosocial factors, prior medical trauma, and genetic low-threshold phenotypes remain plausible contributors — yet these are entirely unaddressed.

4. Implications for Clinical Practice
The failure to contextualize heightened pain sensitivity risks reinforcing a binary, “normal/abnormal” model of nerve function that is no longer supported by pain science. The report implicitly frames normal electrophysiology as synonymous with absence of pathology, an oversimplification that may lead to under-recognition of pain syndromes with functional or central origins. Such omissions can delay appropriate management, exacerbate disability, and undermine patient trust in medical assessment.

5. Overall Assessment
This report exemplifies a recurring limitation in clinical neurophysiology: the conflation of normal electrophysiological metrics with normal nervous system function. While the technical competence is unquestionable, the interpretative failure to engage with a conspicuous, atypical pain response renders the document incomplete. A more rigorous, patient-centered approach would require integrating the normal test findings into a broader pathophysiological discussion, considering both structural and functional mechanisms, and providing at least a preliminary hypothesis for the observed hyperalgesia.

Recommendation:
Future reports should move beyond a narrow electrophysiological focus to incorporate modern pain neuroscience principles, ensuring that significant patient-reported symptoms are neither minimized nor left unexplored.

© 2000-2025 Sieglinde W. Alexander. All writings by Sieglinde W. Alexander have a fife year copy right. Library of Congress Card Number: LCN 00-192742