Auguste Dejerine Klumpke

Augusta Marie Déjerine-Klumpke, MD (October 15, 1859 – November 5, 1927) was an extraordinary American-born French neurologist, neuroanatomist, and clinical pioneer whose discoveries transformed the understanding of the brachial plexus, peripheral nerve injuries, and neurorehabilitation. Breaking entrenched gender barriers as the very first female interne des hôpitaux de Paris in 1885 and later as the first female president of the Société de Neurologie de Paris, she achieved worldwide scientific acclaim while still a medical student by discovering and characterizing lower brachial plexus palsy (Klumpke’s palsy, involving the C8 and T1 ventral roots). Crucially, she demonstrated for the first time in medical history that avulsion or severe traction of the T1 anterior spinal root tears the preganglionic sympathetic fibers of the ramus communicans albus, producing ipsilateral miosis, partial ptosis, and enophthalmos—the pathognomonic oculosympathetic constellation known as Déjerine-Klumpke syndrome with Horner’s sign. In a legendary thirty-year intellectual and matrimonial partnership with Jules Déjerine at the Bicêtre and Salpêtrière hospitals, she co-authored the monumental two-volume neuroanatomical treatise Anatomie des centres nerveux (1895–1901) and Sémiologie des affections du système nerveux (1914). During the First World War, as director of the military neurotrauma center at the Hôtel des Invalides, she pioneered comprehensive spinal cord injury rehabilitation, rigorous decubitus ulcer prevention, and specialized bladder nursing, establishing the anatomical, diagnostic, and clinical foundations upon which modern peripheral nerve surgeons, brachial plexus reconstructive specialists, and paediatric orthopaedists stand today.

1. The Shoulders of Giants: Historical Context & Significance

In the late nineteenth century, clinical neurology and neuroanatomy were undergoing a golden age in Paris, anchored by the pioneering investigations of Jean-Martin Charcot, Alfred Vulpian, and Guillaume-Benjamin-Amand Duchenne de Boulogne. Across the Rhine, Wilhelm Erb in 1874 had delineated the clinical presentation of upper brachial plexus palsy (Erb’s palsy, involving the C5 and C6 nerve roots), recognized by the classic “waiter’s tip” posture resulting from paralysis of the deltoid, biceps brachii, brachialis, and supinator. However, injuries to the lower components of the brachial plexus remained an enigmatic diagnostic void. Clinicians routinely conflated lower plexus lesions with distal peripheral neuropathies of the ulnar and median nerves, progressive muscular atrophy, or obscure spinal cord myelopathies. More significantly, the physiological and anatomical relationship connecting the lower cervical and upper thoracic nerve roots to the sympathetic innervation of the eye remained completely unmapped in human clinical medicine.

“If I have seen further, it is by standing on the shoulders of giants.”

Sir Isaac Newton (1675) / Bernard of Chartres

Modern orthopaedic surgeons, peripheral nerve reconstructive specialists, and paediatric clinicians stand squarely upon the shoulders of Augusta Déjerine-Klumpke. While still an undergraduate medical student working in the laboratory of Professor Alfred Vulpian, Klumpke unraveled the anatomy, clinical symptomatology, and pathophysiology of lower brachial plexus trauma. Through rigorous clinical examinations of patients presenting with flaccid paralysis of the hand and painstaking experimental animal investigations, she proved that isolated disruption of the eighth cervical (C8) and first thoracic (T1) ventral roots produces paralysis of the intrinsic muscles of the hand and the long digital flexors, generating the characteristic “true claw hand” deformity (main en griffe) accompanied by sensory loss along the medial aspect of the forearm and hand. In an extraordinary biological insight published in 1885, Klumpke demonstrated that the anterior root of T1 carries preganglionic sympathetic fibers that traverse the ramus communicans albus to join the cervical sympathetic chain; consequently, avulsion or severe stretching of the T1 root produces ipsilateral pupillary miosis, partial ptosis, enophthalmos, and hemifacial anhidrosis, representing the classic oculosympathetic triad described by Claude Bernard and Johann Friedrich Horner. This historic discovery established the first direct anatomical link between a radicular brachial plexus lesion and the autonomic nervous system. Today, the presence of Klumpke’s oculosympathetic sign serves as the ultimate pathognomonic clinical marker of preganglionic T1 root avulsion, alerting reconstructive surgeons that spontaneous axonal regeneration is biologically impossible and guiding timely microvascular nerve transfers.

2. Early Life, Formative Education & Career Milestones

Education and Formative Surgical Training

Augusta Marie Klumpke was born in San Francisco, California, on October 15, 1859, into an exceptionally talented, cosmopolitan, and determined family. Her father, John Gerard Klumpke, was a successful real estate investor and California Forty-Niner pioneer of German extraction; her mother, Dorothea Mattilda Tolle, was an educated, forward-thinking matriarch who instilled in her daughters an uncompromising commitment to scholarship and professional self-determination. The Klumpke household produced an extraordinary assembly of pioneering women: Augusta’s elder sister Anna Klumpke became an acclaimed portrait artist and the companion and biographer of Rosa Bonheur; Dorothea Klumpke Roberts achieved international renown as a brilliant astronomer and head of the Bureau of Measurements at the Paris Observatory; Julia Klumpke became a virtuoso concert violinist and composer; and Mathilda Klumpke emerged as an accomplished concert pianist and pupil of Antoine François Marmontel.

Following her parents’ marital separation in 1871, Dorothea Klumpke took her daughters to Europe to ensure they received the most rigorous education available. After residing in Göttingen, Cannstatt, and Lausanne, the family settled permanently in Paris in 1877. Drawn to the natural sciences and deeply inspired by the pioneering example of Madeleine Brès (the first French woman to receive a medical degree, graduating in 1875), Augusta resolved to pursue a career in medicine. She gained admission to the Faculté de Médecine de Paris in October 1877, entering an institution where female scholars were viewed with intense skepticism and openly subjected to hostile verbal protests in lecture amphitheaters. Undeterred, Augusta distinguished herself through quiet dignity, meticulous dissection technique, and flawless academic performance, rapidly earning the admiration and mentorship of Professor Alfred Vulpian, then Chair of Pathological Anatomy and later Dean of the Faculty.

In 1880, Klumpke successfully sat the competitive examinations for the hospital externat, winning high ranking and securing clinical placements at the Hôtel-Dieu and the Charité. It was during her tenure as an extern in Vulpian’s wards that she encountered a young woman who had sustained a severe traction injury to the lower brachial plexus following an occupational accident, presenting with intrinsic hand paralysis and an unexplained constricted pupil. Vulpian encouraged the young student to pursue the problem. Conducting exhaustive anatomical dissections and experimental electrical stimulation and rhizotomies on the anterior cervical and thoracic roots in canine models, Klumpke mapped the precise origin of the oculosympathetic fibers emerging from the T1 ventral root. She presented her revolutionary findings to the Société de Biologie in 1885, publishing her masterwork in the Revue de Médecine at the age of twenty-six.

Despite her international scientific recognition, Klumpke encountered formidable institutional resistance when she sought to sit the competitive concours for the Internat des hôpitaux de Paris, the indispensable gateway to elite hospital residencies and clinical leadership in France. The municipal administration of the Assistance Publique strictly barred female candidates from the examination. A fierce academic and political struggle erupted across Paris, pitting conservative medical faculties against progressive reformers led by Dean Alfred Vulpian and the physiologist-politician Paul Bert, then Minister of Public Education. In 1885, under ministerial order, the Assistance Publique capitulated and opened the competition to women. Klumpke sat the grueling written and oral examinations alongside her male peers and triumphed, becoming the very first female interne des hôpitaux de Paris in history. In 1889, she completed her medical doctorate, defending an exhaustive clinicopathological thesis titled Des polynévrites en général et des paralysies et atrophies saturnines en particulier (On polyneuritis in general and lead-induced paralysis and atrophies in particular), for which she was awarded the prestigious Prix Godard by the Académie Nationale de Médecine.

Academic Appointments and Clinical Leadership

During her residency at the Hôpital Bicêtre and the Salpêtrière, Augusta met Jules Déjerine (1849–1917), a brilliant and relentless neurologist whose clinical acumen matched her own anatomical genius. United by a shared dedication to microscopic pathology and clinical-neurological correlation, they married in 1888, whereupon Augusta became a naturalized French citizen and assumed the name Augusta Déjerine-Klumpke. Together, they formed one of the most prolific intellectual partnerships in the history of medicine. In their private research facility, the celebrated Laboratoire Déjerine, Augusta served as chief microscopic histologist, master dissector, and scientific collaborator. In 1895 and 1901, they published the monumental two-volume atlas Anatomie des centres nerveux, encompassing more than 1,500 pages and hundreds of intricate, hand-drawn microscopic reconstructions illustrating human cerebral, cerebellar, and spinal tracts. In 1910, Jules Déjerine succeeded Fulgence Raymond to assume the prestigious Chair of Clinical Neurology at the Salpêtrière, previously held by Jean-Martin Charcot.

The outbreak of the First World War in August 1914 profoundly transformed Déjerine-Klumpke’s clinical focus. As devastating artillery bombardments and machine-gun fire produced unprecedented volumes of traumatic neurotrauma, the Déjerines converted the 6th military service at the Salpêtrière into a specialized neurological trauma hospital. In 1914, Augusta was elected the first female president of the Société de Neurologie de Paris, steering the French neurological community through the immense challenges of wartime neurotrauma. Simultaneously, she was appointed chief physician of the military neurological service at the Hôtel des Invalides (Centre Neurologique des Invalides), assuming clinical leadership over hundreds of French soldiers afflicted with complete traumatic paraplegia and severe peripheral nerve transections.

At Les Invalides, Déjerine-Klumpke revolutionized the care of spinal cord injury. Rejecting the fatalistic dogma of the era (which regarded traumatic spinal transection as an inevitable, rapid death sentence resulting from sepsis), she organized specialized nursing units dedicated to rigorous patient turning every two hours, impeccable skin hygiene on water and horsehair beds to prevent decubitus ulcers, and strict sterile intermittent catheterization to combat ascending pyelonephritis. She designed functional orthoses to counteract equinus contractures, introduced early bedside vocational rehabilitation, and published comprehensive monographs on wartime ballistic peripheral nerve lesions. In recognition of her heroic scientific and military medical service, the French Republic appointed her Chevalier de la Légion d’Honneur in 1913 and elevated her to Officier de la Légion d’Honneur in 1921.

Following the death of Jules Déjerine from chronic nephritis and physical exhaustion in February 1917, Augusta dedicated the remainder of her life to organizing and preserving their vast scientific collection. Aided by their daughter, Dr. Yvonne Déjerine (herself a distinguished physician who married the prominent orthopaedic surgeon and spine specialist Étienne Sorrel), Augusta established the Fondation Déjerine and endowed the Laboratoire Déjerine at the Faculté de Médecine de Paris, ensuring that their histological specimens, serial brain sections, and photographic archives remained permanently accessible to global neuroscience. She died in Paris on November 5, 1927, at the age of sixty-eight, and was laid to rest beside Jules Déjerine in the 28th division of Père Lachaise Cemetery.

3. Core Orthopaedic Breakthroughs, Eponymous Signs & Innovations

Augusta Déjerine-Klumpke’s scientific legacy spans fundamental neuroanatomy, peripheral nerve surgery, clinical semiology, and reconstructive physical medicine. Her discoveries provided the anatomical and functional blueprint for diagnostic evaluation and operative decision-making in brachial plexus pathology.

Hallmark Anatomical, Diagnostic and Operative Contributions

• Klumpke’s Palsy (Lower Brachial Plexus Palsy / Paralysie Radiculaire Inférieure): The definitive clinical characterization of inferior brachial plexus palsy resulting from traction or tearing of the C8 and T1 anterior spinal roots. The syndrome is clinically defined by flaccid paralysis of the intrinsic hand muscles and long digital flexors, producing an intrinsic-minus “true claw hand” deformity, accompanied by dermatomal sensory anesthesia along the ulnar border of the forearm, wrist, and hand.
• Déjerine-Klumpke Syndrome (C8-T1 Palsy with Associated Oculosympathetic Horner’s Sign): The pathognomonic co-occurrence of lower brachial plexus paralysis with ipsilateral partial ptosis, pupillary miosis, enophthalmos, and hemifacial anhidrosis. Klumpke proved that this oculosympathetic disruption signifies avulsion of the T1 ventral root proximal to or at the level of the white ramus communicans, serving as the gold standard clinical sign of an inoperable preganglionic root avulsion.
• Mapping of the Spinal Oculosympathetic Tract (Ciliospinal Center of Budge to T1 Ramus Communicans): The first definitive experimental and clinical localization of the preganglionic pupillodilator pathway in human anatomy. Klumpke demonstrated that autonomic preganglionic axons originating from the ciliospinal center in the spinal cord exit exclusively via the T1 ventral spinal root, entering the paravertebral sympathetic trunk via the ramus communicans albus before ascending to the superior cervical ganglion.
• Pioneering Wartime Spinal Cord Injury Rehabilitation & Paraplegia Nursing Protocols: Conceptualized and instituted the first systematic clinical protocols for long-term survival in traumatic spinal cord transection at the Hôtel des Invalides during World War I. Her regimen combined strict two-hour rotational positioning, continuous skin inspection, sterile intermittent urinary drainage, and restorative orthotic splinting, anticipating modern spinal injury unit doctrines by three decades.
• Co-authorship of Landmark Neuroanatomical Treatises (Anatomie des centres nerveux & Sémiologie): Co-architect, histological dissector, and author of the monumental two-volume atlas of human neuroanatomy (1895–1901) and the masterwork on clinical neurological semiotics (1914), which established modern clinical methods for evaluating motor tracts, sensory pathways, and peripheral reflex arcs.
• Historic Desegregation of European Hospital Training: Overcame entrenched systemic gender discrimination to become the first female interne des hôpitaux de Paris in 1885, establishing a historic precedent that opened formal hospital residency training, operative surgical exposure, and academic clinical appointments to women across Europe.

Biomechanical Principles, Operative Mechanics & Clinical Pathophysiology

The biomechanical vulnerability of the lower brachial plexus relates directly to its anatomical architecture and regional skeletal relationships. The eighth cervical (C8) and first thoracic (T1) ventral primary rami emerge from the neural foramina and converge to form the lower trunk (truncus inferior) of the brachial plexus. This large neural trunk rests directly upon the bony superior surface of the first rib, passing immediately posterior to the third portion of the subclavian artery before dividing into anterior and posterior divisions behind the clavicle. Because the lower trunk is tethered inferiorly as it arches over the osseous fulcrum of the first rib, force vectors applied to the upper extremity produce distinct patterns of strain along the plexus depending on the position of the arm.

The primary kinematic mechanism producing Klumpke’s palsy is extreme hyperabduction traction applied to the upper extremity. When the arm is forcefully pulled upward and laterally beyond ninety to one hundred and twenty degrees (such as when an individual falls from a height and instinctively clutches an overhead scaffold or branch, or when an unrestrained passenger is ejected from a motor vehicle with the arm trapped overhead), the lower trunk is stretched taut across the sharp edge of the first rib. In obstetric practice, neonatal Klumpke’s palsy (or the lower trunk component of global obstetric brachial plexus palsy) occurs during difficult breech deliveries when traction is exerted on an extended, abducted after-coming arm, or during cephalic deliveries with shoulder dystocia when excessive upward and lateral traction is applied to deliver the posterior shoulder. This mechanism stands in stark biomechanical contrast to Erb’s palsy (C5-C6 upper trunk), which is produced by traction in hyperadduction and lateral distraction of the neck away from the depressed shoulder.

The motor deficit in pure C8-T1 lesions generates a devastating loss of manual dexterity characterized by the “true claw hand” (main en griffe). The pathophysiological basis of this deformity resides in the complete paralysis of all intrinsic musculature of the hand, which receives its motor supply from C8 and T1 via the ulnar nerve (all interossei, hypothenar muscles, medial two lumbricals, and adductor pollicis) and the median nerve (thenar muscles and lateral two lumbricals). Under normal biomechanics, the intrinsic muscles act as dynamic stabilizers of the digital rays: the interossei and lumbricals pass volar to the transverse axes of the metacarpophalangeal (MCP) joints to produce flexion, while inserting dorsally into the lateral bands and central slip of the extensor apparatus to produce active extension of the proximal interphalangeal (PIP) and distal interphalangeal (DIP) joints (the “intrinsic-plus” posture).

When the C8 and T1 roots are disrupted, the hand collapses into an “intrinsic-minus” deformity. The extrinsic long finger extensors (the extensor digitorum communis, extensor indicis, and extensor digiti minimi, innervated by the radial nerve, predominantly C7) act without intrinsic opposition, pulling the MCP joints into rigid hyperextension. Simultaneously, the extrinsic long finger flexors (flexor digitorum superficialis and flexor digitorum profundus) maintain baseline passive tone or active tension. With the MCP joints locked in hyperextension, the extrinsic flexors exert an uncounteracted flexion moment across the PIP and DIP joints, forcing the fingers into severe flexion. This produces the classic multi-digit clawing, most pronounced in the ring and small fingers. Concurrently, sensory denervation manifests across the C8 and T1 dermatomes, producing profound cutaneous anesthesia along the medial (ulnar) border of the hand, little finger, ulnar half of the ring finger, and medial aspect of the forearm (via the medial antebrachial cutaneous nerve, originating from the medial cord). The hand is rendered functionally crippled, devoid of pinch, hook, or spherical grasp.

The neuroanatomical crowning achievement of Augusta Déjerine-Klumpke was demonstrating the autonomic circuit responsible for the oculosympathetic sign in lower plexus lesions. First-order sympathetic neurons originate in the posterolateral hypothalamus and descend through the brainstem and cervical spinal cord to synapse in the intermediolateral cell column at the C8–T2 spinal cord segments (the ciliospinal center of Budge). Second-order preganglionic sympathetic axons exit the spinal cord exclusively through the ventral root of T1. Immediately distal to the intervertebral foramen, these preganglionic myelinated fibers diverge from the T1 spinal nerve via the ramus communicans albus (white communicating ramus) to join the paravertebral sympathetic chain. They ascend through the inferior cervical (stellate) ganglion and middle cervical ganglion to synapse in the superior cervical ganglion at the C2–C3 level. Third-order postganglionic unmyelinated fibers then travel along the internal and external carotid arteries to innervate the pupillodilator smooth muscle (dilator pupillae), Müller’s superior tarsal muscle of the upper eyelid, the orbital smooth muscle of the eye, and the facial sweat glands.

This anatomical trajectory provides surgeons with an infallible prognostic tool to differentiate between preganglionic root avulsion and postganglionic nerve rupture. A preganglionic avulsion occurs when violent traction tears the delicate anterior and posterior rootlets directly out of the spinal cord substance proximal to the dorsal root ganglion (DRG). Because the sympathetic preganglionic fibers diverge through the white ramus communicans immediately adjacent to the intervertebral foramen, a traction force violent enough to avulse the T1 root invariably disrupts this sympathetic outflow, producing full ipsilateral Horner’s syndrome (ptosis, miosis, enophthalmos, and anhidrosis). In contrast, postganglionic ruptures occur distal to the DRG and distal to the white ramus communicans; in these lesions, the oculosympathetic pathway remains intact, and Horner’s syndrome is absent.

The clinical and surgical implications of Déjerine-Klumpke syndrome with Horner’s sign are definitive. A preganglionic root avulsion represents a central nervous system injury within the subarachnoid space; the avulsed rootlets undergo irreversible glial scarring, making direct nerve suture or proximal cable grafting from the spinal cord biologically impossible. Furthermore, electrodiagnostic testing in preganglionic avulsion demonstrates a classic diagnostic dissociation: sensory nerve action potentials (SNAPs) for the ulnar and medial antebrachial cutaneous nerves remain completely preserved despite dense clinical anesthesia, because the primary sensory pseudounipolar cell bodies within the dorsal root ganglion remain intact outside the spinal canal. Confirmation of Déjerine-Klumpke syndrome therefore alerts the reconstructive team that expectant observation is futile. Modern operative protocols dictate immediate surgical reconstruction bypassing the avulsed roots, utilizing distal intraplexal and extraplexal motor nerve transfers (such as transferring the anterior interosseous nerve to the ulnar motor branch or supinator motor branches to the posterior interosseous nerve) or free functional muscle transplantation (such as a microneurovascular gracilis muscle transfer innervated by the spinal accessory or intercostal nerves) before irreversible motor endplate fibrosis supervenes.

4. Master Class Pro-Tip

1. Pathognomonic Distinction via the Oculosympathetic Horner Sign: In every suspected lower brachial plexus injury (whether in a neonate following a difficult breech delivery or an adult after high-energy motorcycle traction trauma), the presence of an ipsilateral Horner’s syndrome (subtle partial ptosis, pupillary miosis, apparent enophthalmos, and hemifacial anhidrosis) is pathognomonic evidence of preganglionic T1 root avulsion proximal to the dorsal root ganglion. Because the sympathetic preganglionic fibers exit through the T1 anterior root to enter the white ramus communicans immediately adjacent to the intervertebral foramen, a positive Horner’s sign proves central rootlet disruption from the spinal cord substance. Expectant observation hoping for spontaneous root regeneration across a central avulsion is biologically futile; immediate multidisciplinary surgical consultation is mandatory.

2. Electrodiagnostic Concordance and the Intact SNAP Paradox: Reconcile clinical anesthesia with electrodiagnostic testing by recognizing the preganglionic sensory paradox. If a patient exhibits dense sensory loss in the C8–T1 dermatomes (ulnar border of the hand and medial forearm) but electrodiagnostic testing demonstrates preserved, normal sensory nerve action potentials (SNAPs) for the ulnar sensory and medial antebrachial cutaneous nerves, this confirms that the primary sensory pseudounipolar cell bodies in the dorsal root ganglion remain intact outside the spinal canal while the central sensory rootlets are avulsed from the spinal cord. In contrast, postganglionic ruptures distal to the DRG cause Wallerian degeneration of peripheral sensory fibers, resulting in completely absent SNAPs. Combine this finding with paraspinal cervical electromyography: fibrillations and positive sharp waves in the posterior cervical paraspinal musculature confirm disruption of the posterior primary rami, verifying root-level avulsion.

3. The Biological Clock and Strategic Distal Nerve Transfers: Do not waste valuable reconstructive time waiting for recovery in lower plexus root avulsions. Motor endplates in intrinsic hand muscles undergo irreversible, fibrotic degeneration within 12 to 18 months following denervation. Because the distance from the cervical spine to the intrinsic hand muscles exceeds 600 to 750 millimeters, even if a proximal root could be grafted, regenerating axons advancing at 1 mm per day would reach the hand far too late (over 20 to 25 months), resulting in total functional failure. Surgical management requires early distal nerve transfers (neurotizations) situated close to the target endplates: transfer of the anterior interosseous nerve (AIN) to the deep branch of the ulnar motor nerve restores intrinsic interosseous and adductor pollicis tone, while supinator or extensor carpi radialis brevis (ECRB) motor branches can be transferred to restore finger extension. In complete or delayed brachial plexus root avulsions, prioritize early free functional muscle transfer (e.g., gracilis transfer reinervated by the spinal accessory nerve or intercostal nerves) to restore definitive finger flexion and hand grasp.

Master Class Surgical Pearl: Differentiating Preganglionic Avulsion in Klumpke’s Palsy via the Oculosympathetic Horner Sign

5. Primary Landmark Publications & Bibliography

The foundational contributions of Augusta Déjerine-Klumpke to neuroanatomy, peripheral nerve surgery, and clinical neurology are preserved in these original landmark monographs and peer-reviewed historical literature:

• Dejerine-Klumpke A. Contribution à l’étude des paralysies radiculaires du plexus brachial. Paralysies radiculaires totales. Paralysies radiculaires inférieures. De la participation des filets sympathiques oculo-pupillaires dans ces paralysies. Rev Med (Paris). 1885;5:591-616, 739-790.
• Ulgen BO, Brumblay H, Yang LJ, Doyle TE, Chung KC. Augusta Déjerine-Klumpke (1859–1927) and her eponym. J Neurol Neurosurg Psychiatry. 2008;79(6):739. DOI | PubMed
• Shoja MM, Tubbs RS, Loukas M, Shokouhi G, Jerry Oakes W. Augusta Déjerine-Klumpke, M.D. (1859–1927): a historical perspective on Klumpke’s palsy. Neurosurgery. 2008;63(2):359-367. DOI | PubMed
• Loukas M, Blaak C, Tubbs RS. Augusta Déjerine-Klumpke: the first female neuroanatomist. Clin Anat. 2007;20(8):875-877. DOI | PubMed
• Bogousslavsky J. The Klumpke family – memories by Doctor Déjerine, born Augusta Klumpke. Eur Neurol. 2005;53(3):113-120. DOI | PubMed
• Déjerine J, Déjerine-Klumpke A. Anatomie des centres nerveux. Paris: Rueff et Cie; 1895–1901.
• Mostofi SB. Auguste Dejerine Klumpke 1859–1927. In: Mostofi SB, ed. Who’s Who in Orthopedics. London: Springer-Verlag; 2005:177. DOI

6. Biographical Provenance & Acknowledgments

This historical biography was synthesized for the OrthopaedicsOne Knowledge Network as part of A Who’s Who of Orthopaedics, adapted and expanded from the foundational biographical directory Who’s Who in Orthopedics (Springer-Verlag London) edited by Seyed B. Mostofi, BSc, MBBS, FRCS (Ed).