Poliomyelitis was endemic among the children of mid-nineteenth century Paris, especially in crowded urban environments where public hygiene was limited. Although the communicable nature of the disease was gaining recognition, a mechanistic understanding of the cause of paralysis was lacking. It was commonly held that the paralysis in this disease was “essential” in nature, an obfuscational proposition that declared that the pathogenic process existed in a realm beyond the ken of contemporary medical science and hence, was indescribable and unknowable. Duchenne, thought to be somewhat of a contrarian among his colleagues, noted homologies in his observations of electrical muscle and nerve stimulation in patients with facial palsy, poliomyelitis and spinal cord injuries. He used electrostimulation of muscles and nerves to examine patients with spinal cord diseases, including those presumed to be poliomyelitis, to characterize patterns of affected muscles as excitable or not. He demonstrated that those atrophic muscle groups, which were unresponsive to direct electrical stimulation, generally did not recover while contiguous muscles, which exhibited a tangible response to supramaximal electrical stimulation, would exhibit the capacity to regain function. He was able to discern that this testing could be performed early in the disease and might provide important prognostic insights. Given the high incidence of poliomyelitis in urban centers of the period and the fact that most of the acutely affected were children since a majority of adults were rendered immune by prior infection, children constituted a large segment of Duchenne’s patients. He focused on this experience in his writings and in didactic sessions with his fellow neurologists in Paris. Imagine Duchenne explicating the fine points of the electrodiagnostic evaluation of a child with acute paralysis before Charcot and his contemporaries at the Hôpital Universitaire Pitié-Salpêtrière during the 1860s. Duchenne correctly inferred that the site of the primary lesion in poliomyelitis must be the anterior horn cells in the spinal cord. At the time, autopsy studies in individuals with poliomyelitis had been performed on patients with longstanding paralysis who died from unrelated causes. Visual inspection of post mortem pathological specimens of the spinal cord failed to demonstrate evidence of definite abnormality. Microscopic anatomy of the spinal cord, however, had not been studied in this disease. Duchenne argued that the key to understanding the pathogenesis lay in a more scrupulous examination of the spinal cord in these patients. Over the ensuing decade, Duchenne’s hypothesis was confirmed by several observers, including his younger colleague Dr. Jean-Martin Charcot in a paper published in 1870. Duchenne came to be highly regarded for his clinical and pathophysiological acumen and was referred to by Charcot as “mon maître en neurologie” or my mentor in neurology.

Duchenne first illustrated the superficial phenomenology of brachial plexus palsy in 1862 in association with a photograph of a 6 year old boy exhibiting the sequellae of a brachial plexus injury sustained at birth. Even before that publication, he had recognized a stereotypical constellation of features which he termed “obstetric palsy of the brachial plexus”. It required another decade to collect and publish his anatomical observations on three patients with that injury in 1872. Duchenne surmised that the injury was related to traction of the head against the after coming shoulder with concomitant injury to the plexus in the course of delivery of an infant with shoulder dystocia. It is fitting that the baton was metaphorically passed in this fashion as Dr. Wilhelm Heinrich Erb (1840–1921) published his findings on the physiological and anatomical substrates for this malady in 1874 [3]. Erb was familiar with Duchenne and his opinions regarding the disease along with his studies of anatomy and clinical electrophysiology. He freely acknowledged his colleague’s precedence in describing the nature of the injury. Erb’s singular contribution was the amalgamation of electrophysiology and neuroanatomy with the use of electrodiagnostic methods to localize the site of the anatomic lesion to the upper trunk of the brachial plexus. He employed a needle electrode inserted at the medial border of the supraclavicular fossa beneath the insertion of the sternocleidomastoid to stimulate the brachial plexus near the confluence of cervical nerve roots five and six at the origin of the upper trunk. Tetanic stimulation at that site in normal subjects elicited a constellation of simultaneous muscle contractions resulting in the assumption of what was described as a “fencer’s posture” with abduction of the shoulder, flexion of the biceps and supination of the forearm. The agonist muscles activated by electrical stimulation of the brachial plexus near “Erb’s point” predicted the pattern of weakness resulting from an injury to the upper trunk of the brachial plexus at that site. Anatomic studies confirmed Erb’s notion of the localization of the injury with evidence of consequent chronic denervation in muscles downstream from the injury.