Trauma eponyms (1837–1950): a comprehensive historical review

Abstract

Trauma eponyms reflect historical advancements in trauma medicine across various organ systems, often honoring pioneering physicians. These terms trace the evolution of medical understanding, particularly during wartime, though some have been replaced by more precise terminology. A comprehensive literature review was performed using the PubMed database to identify trauma-related eponyms described from 1837 to 1950. Supplementary biographical sources were also consulted. Eponyms were analyzed regarding their geographic distribution, affected organ systems, and ongoing clinical relevance, emphasizing connections to advancements in imaging, surgical procedures, and trauma care. A total of 30 trauma-related eponyms were identified, predominantly originating from France and Germany, highlighting the European leadership in medical research during the 19th and early 20th centuries. The pre–World War I period (1837–1914) emphasized anatomical and pathological observations, exemplified by eponyms such as Ollivier syndrome (1837), Curling ulcer (1842), and Klumpke paralysis (1885). The World Wars and subsequent postwar era (1914–1950) prompted significant innovations in battlefield medicine and surgical techniques, resulting in eponyms such as Tinel sign (1915), Bywaters syndrome (1941), and Fegeler syndrome (1949). While some eponyms have become obsolete, others remain clinically relevant due to clearly defined pathophysiological characteristics. Developments in imaging modalities (x-rays, magnetic resonance imaging, and computed tomography) and surgical methods have reinforced the contemporary relevance of these terms. Trauma-related eponyms provide a historical framework for understanding the evolution of trauma care. Their continued use highlights their diagnostic value and the enduring influence of historical medical discoveries on contemporary clinical practice.

INTRODUCTION

The word “trauma” derives from the Greek τραῦμα, meaning “wound” or “injury,” with the suffix “-ma” indicating the result of an action or process [1]. In medical terminology, trauma refers to physical injuries caused by external forces, including mechanical, thermal, or chemical factors [2]. Trauma remains a leading cause of death and disability worldwide, particularly among individuals aged 1 to 44 years in the United States, where motor vehicle collisions, falls, burns, and gunshot wounds are among the primary contributors [3].

Historically, progress in trauma care has been closely linked to the exigencies of warfare and industrialization. During the Napoleonic Wars, Dominique Jean Larrey introduced key innovations in battlefield medicine, including triage systems and ambulances volantes (flying ambulances) for rapid evacuation [4]. In World War I, the widespread adoption of the Thomas splint drastically reduced mortality from femoral fractures, while Harold Gillies advanced facial reconstructive surgery for wounded soldiers [5]. By World War II, further developments such as blood plasma transfusions, infection control using penicillin, and the establishment of Mobile Army Surgical Hospitals revolutionized trauma care. These wartime innovations, which also included improvements in fracture management and wound care, laid the foundation for modern emergency medical systems and surgical practice [6].

As trauma medicine advanced, so did its terminology. Eponyms emerged to honor physicians who described specific trauma-related conditions, including clinical signs (e.g., the Hoffmann sign or the Tinel sign), syndromes (e.g., Bywaters syndrome or Klumpke paralysis), and trauma-induced pathologies (e.g., Morel-Lavallée syndrome or Purtscher syndrome) [7]. Although many of these terms have since been replaced by descriptive nomenclature, they persist as both historical and clinical markers, reflecting the evolution of diagnostic and therapeutic approaches.

Understanding the distinction between signs and symptoms is important in medical terminology. A syndrome represents a cluster of symptoms that collectively form a characteristic clinical picture, facilitating the classification of a condition. A syndrome may be reclassified as a disease once it is better understood and its symptoms have been more definitively characterized [8]. A symptom refers to an observable manifestation of a disease that lacks specific diagnostic significance on its own. In contrast, a sign is an objective clinical finding whose significance requires interpretation through reasoning and judgment [8]. Signs are particularly valuable in diagnosis because they provide physicians with insights into the underlying disease. A symptom may become a sign when it possesses the defining attributes of a sign—namely, when a conclusion can be drawn from its presence. If no inference can be made, it remains a symptom [8].

This study investigates trauma-related eponyms introduced between 1837 and 1950, situating them in the broader context of medical and surgical advancements. It provides a chronological overview of selected eponyms, accompanied by biographical profiles of the physicians associated with them, and analyzes their clinical relevance in light of developments in imaging, surgical innovations, and specialized trauma care.

METHODS

A comprehensive literature search was conducted using the PubMed database to identify trauma-related eponyms introduced between 1837 and 1950. The search terms included a combination of individual physician names and MeSH (Medical Subject Headings) terms such as disease, signs, symptoms, trauma, and specific eponym names. The search was limited to publications available up to February 2025.

To supplement the medical literature, biographical details were collected from academic biographies, journal articles, reference books, and historical reviews. Web-based searches were also employed to identify obituaries, awards, and notable achievements of physicians associated with these eponyms. Eponyms were included in the study only if they originated directly from trauma cases, as determined through clinical descriptions and historical documentation. Terms arising from experimental research (e.g., Brown-Séquard syndrome or Duret hemorrhage) or those associated solely with long-bone fractures were excluded.

Two independent reviewers screened titles, abstracts, and full texts for relevance. Disagreements were resolved through discussion, ensuring consistency in the selection process. Each eponym was categorized by geographic origin, affected organ system, and current clinical relevance. Particular attention was given to how technological and surgical advancements have influenced the persistence or obsolescence of these terms in modern practice.

RESULTS

A total of 30 trauma-related eponyms were identified from 12 countries, with the greatest number attributed to France (n=11) and Germany (n=4), followed by the United Kingdom (n=3)and the United States (n=3). Two additional contributions came from Switzerland, and one each from Austria, Estonia, Norway, Poland, South Africa, Spain, and Ukraine (Table 1) [9–39]. This geographic distribution underscores the prominence of European medical scholarship in trauma care during the 19th and early 20th centuries.

Table 1.

Trauma-related eponyms (1837–1950)

Eponym	Year	Birthplace country of namesake	Affected organ system	Description
Ollivier syndrome [9]	1837	France	Systemic	Traumatic asphyxia due to thoracic compression, causing facial and cervical cyanosis, petechial hemorrhage, and cerebral congestion.
Curling ulcer [10]	1842	UK	Gastrointestinal	Stress-induced duodenal ulcer in burn patients, caused by inflammation and ischemia, potentially leading to perforation and peritonitis.
Chassaignac disease [11]	1856	France	Musculoskeletal	Radial head subluxation in children from sudden traction, causing pain, limited movement, and a pronated arm posture.
Morel-Lavallée syndrome [12]	1863	France	Skin and subcutaneous tissues	Soft tissue degloving injury from trauma, causing hemolymphatic fluid accumulation and skin separation from underlying fascia.
Laugier sign [13]	1867	France	Musculoskeletal	Bloody ear discharge transitioning to clear fluid, indicating skull fracture with tympanic membrane penetration.
Duplay disease [14]	1872	France	Musculoskeletal	Chronic shoulder inflammation after trauma, causing pain, restricted movement, and stiffness due to adhesions, also known as adhesive capsulitis.
Berlin disease (edema) [15]	1873	Germany	Ocular	Posttraumatic retinal opacity due to blunt trauma, characterized by retinal swelling and potential subretinal hemorrhage.
Klumpke syndrome (paralysis) [16]	1885	USA	Nervous	Lower brachial plexus injury (C8, T1), causing intrinsic hand paralysis, claw hand deformity, sensory loss, and often Horner syndrome.
Kümmell disease (kyphosis/spondylitis) [17]	1895	Germany	Musculoskeletal	Delayed osteonecrosis following spinal fracture, leading to progressive back pain, kyphosis, and vertebral collapse.
Ehret syndrome (paralysis) [18]	1898	Germany	Musculoskeletal	Functional paralysis causing peroneal muscle atrophy, with pain and contractures affecting unaffected areas due to compensatory positioning.
Secrétan syndrome [19]	1901	Switzerland	Musculoskeletal	Posttraumatic edema and induration in the dorsal metacarpals, causing pain and resistance during finger flexion.
Hoffa disease (syndrome) [20]	1904	South Africa	Musculoskeletal	Inflammatory fibrous hyperplasia of the infrapatellar fat pad, leading to knee pain, quadriceps atrophy, and swelling.
Tapia syndrome [21]	1905	Spain	Nervous	Unilateral paralysis of the tongue and vocal cords due to vagus and hypoglossal nerve involvement from trauma or surgery.
Siegrist spots (streaks) [22]	1906	Switzerland	Ocular	Pigmented retinal lesions from traumatic rupture of posterior ciliary arteries, often after blunt ocular trauma.
Coats (white) ring [23]	1912	UK	Ocular	Circular corneal opacity with white dots, typically following foreign body injury and healing in the cornea.
Purtscher syndrome (disease/retinopathy) [24]	1912	Austria	Ocular	Retinal angiopathy from trauma, causing vision loss, cotton wool spots, hemorrhage, and optic disc swelling due to microvascular damage.
Hoffmann sign [25]	1915	Estonia	Nervous	Tapping is used to assess nerve viability after surgery by applying a moderate stimulus to the affected area, eliciting a tingling sensation indicating nerve regeneration.
Tinel sign [26]	1915	France	Nervous	A diagnostic method to assess nerve regeneration, applying light pressure to an injured nerve to elicit a tingling sensation, indicating nerve recovery.
Babinski-Froment syndrome [27]	1915, 1917	France	Nervous and musculoskeletal	Traumatic injuries may lead to contractures, paralysis, vasomotor symptoms, and tissue damage, sometimes affecting muscle and bone.
Collet-Sicard syndrome [28,29]	1915, 1917	France	Nervous	Unilateral palsy affecting cranial nerves IX–XII.
Villaret syndrome [30]	1916	France	Nervous	Injury to the posterior retroparotid space affects multiple cranial nerves, causing various symptoms including facial paralysis and dysphonia.
Frey syndrome [31]	1923	Ukraine	Nervous	Auriculotemporal nerve injury causing gustatory sweating, vasomotor changes, and trophic disturbances.
Lhermitte sign [32]	1924	France	Nervous	Electrical-type pain triggered by neck flexion, radiating from the head to limbs.
Meleney ulcer [33]	1924	USA	Skin and soft tissues	Rapid progression of swelling, redness, fever, and blisters following trauma, evolving to purple or blue discoloration.
Raeder (paratrigeminal) syndrome [34]	1924	Norway	Nervous	Involves oculopupillary sympathetic paresis and trigeminal nerve symptoms, affecting other cranial nerves.
Frenkel syndrome [35]	1931	Poland	Ocular	Traumatic contusion of the eye may cause pupil paralysis, progressing to iridoplegia and lens displacement.
Coleman syndrome [36]	1938	USA	Musculoskeletal	Cervical spine injuries associated with head or shoulder trauma, particularly in unconscious patients.
Mondor disease [37]	1939	France	Vascular	Subacute phlebitis of the saphenous vein, forming a hard cord beneath the skin, often with redness and nodules.
Bywaters syndrome [38]	1941	UK	Systemic	Crush injuries leading to shock, oliguria, and acute renal failure.
Fegeler syndrome [39]	1949	Germany	Nervous	Persistent pain and weakness in the left side of the body due to sympathetic nerve disruption following trauma.

The eponyms span two major historical periods. The pre–World War I era (1837–1914) includes 16 eponyms, most of which are grounded in anatomical and pathological observations foundational to early trauma medicine. Representative examples include Ollivier syndrome (1837), associated with traumatic asphyxia; Curling ulcer (1842), describing stress-induced gastrointestinal pathology in burn patients; and Klumpke paralysis (1885), referring to lower brachial plexus injuries. Contributions to musculoskeletal trauma, such as Chassaignac disease (1856) and Kümmell disease (1895), and ocular trauma, including Berlin edema (1873) and Purtscher syndrome (1912), reflect early interest in trauma-induced dysfunctions (Table 1) [9–39].

The World Wars and postwar period (1914–1950) yielded 14 eponyms, driven by rapid developments in battlefield medicine, surgery, and neurology. Noteworthy examples include the Hoffmann sign and Tinel sign (1915), used to evaluate nerve regeneration in World War I; Babinski-Froment syndrome (1917), relating to neuromuscular trauma; and Bywaters syndrome (1941), which emerged from studies of crush injuries during the London Blitz. Fegeler syndrome (1949), described in the aftermath of World War II, illustrates the continued refinement of neurological diagnostics (Table 1) [9–39].

These 30 eponyms can be broadly categorized into clinical signs, syndromes, diseases, and descriptive terms. Clinical signs include the Hoffmann sign, Laugier sign, Lhermitte sign, and Tinel sign. Syndromes encompass a wide range of trauma-related conditions, such as Babinski-Froment syndrome, Bywaters syndrome, Collet-Sicard syndrome, Ehret syndrome, Fegeler syndrome, Frenkel syndrome, Frey syndrome, Klumpke paralysis, Morel-Lavallée syndrome, Raeder syndrome, Secrétan syndrome, Tapia syndrome, Ollivier syndrome, Purtscher syndrome, and Villaret syndrome. Diseases include Chassaignac disease, Duplay disease, Hoffa disease, Kümmell disease, and Mondor disease. Descriptive terms include Berlin edema, Coats white ring, Curling ulcer, Meleney ulcer, and Siegrist spots.

In terms of affected organ systems, the nervous system accounted for the highest number, with 10 eponyms. This was followed by the musculoskeletal system with 8, the ocular system with 5, and systemic conditions with 2. The gastrointestinal and vascular systems each had one associated eponym, as did the skin and subcutaneous tissue. There was also one eponym involving both the nervous and musculoskeletal systems and another associated with soft tissue injuries.

This distribution reflects a historical emphasis on conditions that were accessible to direct clinical observation, particularly musculoskeletal injuries, nerve lesions, and ocular trauma, prior to the advent of advanced imaging. While earlier eponyms focused on anatomical findings, those coined during and after the World Wars increasingly emphasized clinical syndromes and surgical approaches, reflecting evolving diagnostic priorities in trauma care.

Ollivier syndrome

Charles-Prosper Ollivier (1796–1845) was a French physician recognized for his work on spinal cord pathology. His Traité des maladies de la moelle épinière (1827) was among the earliest systematic studies of spinal cord diseases [40,41]. In 1837, he documented trauma-induced asphyxiation following a crowd disaster at the Champs de Mars, presenting his findings to the Royal Academy of Medicine. He described postmortem signs such as facial and cervical cyanosis, petechial hemorrhages, and conjunctival vascular injection, attributing them to chest compression-induced asphyxia, sometimes accompanied by rib fractures and bruising [9]. His observations contributed to early forensic assessments of mechanical asphyxia.

Curling ulcer

Thomas Blizard Curling (1811–1888) was a British surgeon known for his contributions to burn-related gastrointestinal pathology [42]. His findings advanced the understanding of stress-induced gastrointestinal pathology in burn patients. Curling served as a surgeon at London Hospital and later became president of the Royal College of Surgeons [42,43]. In 1842, he documented duodenal ulceration in 12 burn patients, attributing it to acute inflammation following extensive skin injury, which led to localized ulceration of the duodenal mucosa [10]. He noted that these ulcers, now termed Curling ulcers, could progress to perforation and peritonitis, emphasizing their clinical significance [10].

Chassaignac disease

Édouard-Pierre-Marie Chassaignac (1804–1879) was a French surgeon noted for his contributions to surgical pathology and techniques. In 1856, he described a condition in children aged 2 to 4 years, characterized by sudden-onset pain and paralysis of the upper extremity, typically following a traumatic fall or excessive traction to the hand or forearm [11]. Affected children exhibited a limp arm with slight flexion and pronation, avoiding movement due to pain. Initially, Chassaignac suspected rupture of the annular ligament; however, the absence of bruising or deformity and rapid symptom resolution led him to reconsider [11]. This condition, now known as the nursemaid’s elbow or radial head subluxation, results from displacement of the radial head through the annular ligament.

Morel-Lavallée syndrome

Victor-Auguste-François Morel-Lavallée (1811–1865) was a French surgeon recognized for his studies on traumatic soft tissue injuries. He earned his medical degree with a thesis on clavicle dislocations and later became a professor of surgery [44]. In 1863, he described a condition caused by traumatic separation of the skin and underlying soft tissues due to tangential or oblique force [12]. He observed that these separations formed fluid-filled pockets, with their depth and extent varying by injury severity. In severe cases, detachment extended to the periosteum, resulting in complete disunion of tissue layers [12]. His findings laid the foundation for understanding closed degloving injuries, now known as Morel-Lavallée lesions.

Laugier sign

Stanislas Laugier (1799–1872) was a French surgeon renowned for his contributions to surgical pathology. He held various academic and hospital positions in Paris, including chair of the surgical clinic at Hôtel-Dieu and membership in the National Academy of Medicine [45]. In 1839, Laugier described a clinical sign associated with skull fractures penetrating the tympanic membrane. He observed that initial ear discharge was slightly bloody but soon became clear and colorless, with variations in quantity, indicating a minor fracture near the petrous bone fissure [13]. This finding distinguished it from more severe fractures causing significant hemorrhage, contributing to the early diagnostic understanding of cerebrospinal fluid otorrhea in basilar skull fractures.

Duplay disease

Simon-Emmanuel Duplay (1836–1924) was a French surgeon recognized for his contributions to surgical pathology. He held various academic positions in Paris and was elected to the Academy of Medicine in 1879 [46]. In 1872, Duplay described chronic scapulohumeral periarthritis, now known as frozen shoulder or adhesive capsulitis [46]. He noted significant shoulder movement impairment, particularly abduction, with pain triggered by pressure at anatomical points such as the acromion and deltoid insertion [14]. Chronic cases progressed to muscle atrophy and shoulder flattening due to disuse [14]. Duplay proposed that adhesions between the humerus, acromion-coracoid ligament, and inferior deltoid restricted motion and caused stiffness.

Berlin disease (edema)

Rudolf August Johann Ludwig Wilhelm Berlin (1833–1897) was a German ophthalmologist who made significant contributions to comparative ophthalmology, holding academic positions in Stuttgart and Rostock, where he later served as rector [47]. In 1873, he described retinal changes following blunt ocular trauma in eight patients; these changes initially presented as moderate visual impairment with gray, patchy retinal opacity that progressively spread and lightened [15]. He attributed this condition, now known as Berlin edema, to retinal swelling caused by hemorrhagic infiltration between the choroid and retina, leading to progressive opacity and vision disturbance [15]. His work laid the foundation for understanding traumatic retinal edema, now referred to as commotio retinae.

Klumpke syndrome (paralysis)

Augusta Déjerine-Klumpke (1859–1927) was a pioneering neurologist recognized for her work on brachial plexus injuries. She became the first woman admitted as both an interne and externe in the Hospitals of Paris and held prominent academic positions [48]. In 1885, she described a traumatic injury involving the lower brachial plexus roots (C8 and T1), resulting in motor and ocular symptoms in 14 patients with inferior root paralysis [16]. Sensory deficits affected the posterior and medial arm, with intrinsic hand muscle paralysis leading to claw hand deformity. She also observed oculopupillary phenomena, including miosis, palpebral fissure narrowing, and enophthalmos, due to sympathetic chain injury. These phenomena are now recognized as Horner syndrome [16].

Kümmell disease (kyphosis/spondylitis)

Hermann Kümmell (1852–1937) was a German surgeon known for his contributions to spinal surgery. He served as a professor of surgery at the University of Hamburg [49]. In 1895, Kümmell described a condition in which patients experienced localized pain and vertebral compression fractures following trauma, such as a heavy object falling on the shoulder or hyperextension [17]. The pain initially subsided but could reemerge weeks or months later, sometimes with neuralgia and an unsteady gait. In severe cases, kyphosis and gibbosity developed, resembling acute tuberculous spondylitis [17]. This condition, now known as Kümmell disease, involves delayed-onset pain and deformity following minor trauma [50].

Ehret syndrome (paralysis)

Heinrich Ehret (1870–1915) was a German physician who became an extraordinary professor at the University of Strasbourg in 1904 [51]. He described a painful form of functional paralysis, often after trauma, leading to contractures and atrophy of the peroneal muscles. This paralysis could extend to other areas as the body adopted the least painful position [18]. Ehret referred to this condition as “functional habituation paralysis” and emphasized the need for early physical therapy to improve prognosis [18]. Ehret syndrome, or Ehret paralysis, is considered a disuse syndrome resulting from prolonged immobility or abnormal positioning due to pain.

Secrétan syndrome

Henri-François Secrétan (1856–1916) was a Swiss physician recognized for his work on traumatic conditions. In 1901, he reported traumatic atrophy of the dorsal metacarpals and firm edema in the dorsal hand following violent contusion [19]. He observed swelling across the dorsal metacarpals and the base of the fingers, particularly affecting the proximal metacarpals. Patients experienced discomfort during finger flexion, with resistance at the dorsum of the hand where extensor tendons attach, along with persistent induration [19]. Secrétan’s findings contributed to the understanding of traumatic edema and hyperplasia in the hand following injury [52].

Hoffa syndrome (disease)

Albert Hoffa (1859–1907) was an orthopedic surgeon born in South Africa known for his contributions to orthopedics. He trained at the University of Marburg and the University of Freiburg, graduating in 1882 [53]. Hoffa described inflammatory fibrous hyperplasia of adipose tissue in the knee after trauma, such as a fall or blow to the knee [20]. Clinical features include severe knee pain, mild effusion, quadriceps atrophy, and doughy swelling beneath the patellar ligament [20]. This condition of fat pad impingement, known as Hoffa disease, affects the knee’s fatty tissue and is managed conservatively with rest, ice, and massage, although some patients may experience persistent symptoms while walking.

Tapia syndrome

Antonio García-Tapia Abad (1875–1950) was a Spanish physician recognized for his contributions to otolaryngology. He earned his medical degree from the Central University of Madrid in 1896 and later served as the president of the College of Physicians of Madrid [54]. Tapia described a case involving a bullfighter who sustained a neck injury, leading to hoarseness, swallowing difficulty, hemiplegia, and hemifacial paralysis. He attributed these symptoms to a thrombus from the internal carotid artery embolizing to the internal capsule, resulting in unilateral paralysis of the tongue and vocal cords [21]. Tapia syndrome is characterized by unilateral paralysis of the tongue and vocal cords, often accompanied by weakness in the sternocleidomastoid and trapezius muscles.

Siegrist spots (streaks)

August Siegrist (1865–1947) was a Swiss ophthalmologist known for his contributions to ocular pathology. He studied medicine at several universities and became a professor of ophthalmology at the University of Bern, where he directed the University Eye Clinic from 1903 to 1935 [55]. In 1896, Siegrist described ocular findings in patients with traumatic eye injuries. Ophthalmoscopic examination revealed yellowish discoloration that progressed to pigmentary infiltration, often extending from the optic papilla to the macula, resulting in white streaks from macular hemorrhage [22]. He attributed these lesions to the traumatic rupture of a posterior ciliary artery, contributing to retinal wrinkling [56]. These findings are now known as pigmented Siegrist spots or streaks, a form of posttraumatic chorioretinopathy.

Coats (white) ring

George Coats (1876–1915) was a Scottish ophthalmologist who earned his medical degree from the University of Glasgow in 1901. He worked at several hospitals, including the Royal London Ophthalmic Hospital (Moorfields) and St. Mary’s Hospital [23,57]. Coats described a condition involving a small, superficial, opaque white ring in the cornea, observed in two cases. The ring’s outline was circular, with fine lines and three-minute opaque white dots at the center, while the rest of the cornea remained clear [23]. This condition, known as Coats white ring, is also associated with Coats disease, a retinal exudative disorder [57].

Purtscher syndrome (disease/retinopathy)

Othmar Purtscher (1852–1927) was an Austrian ophthalmologist recognized for his work on traumatic retinal conditions. He earned his medical degree from the University of Innsbruck in 1876 and later founded the Ophthalmic Clinic in Klagenfurt [58]. In 1910, Purtscher presented two cases at the Heidelberg Ophthalmological Society, describing visual impairment following head trauma [24]. He identified white spots (cotton wool spots) in the retina and coined the term angiopathia retinae traumatica (traumatic retinal angiopathy) [24]. Purtscher theorized that increased intracranial pressure caused venous congestion, leading to blood leakage into the retina and perivascular spaces; this hypothesis was supported by animal studies [24].

Hoffmann sign

Paul Hoffmann (1884–1962) developed the “tapping test” in 1920 to assess nerve viability following trauma [59]. The technique involves applying a moderate tapping stimulus to a sutured nerve, which elicits a tingling sensation, indicating nerve regeneration [25]. As regeneration progresses, the affected area expands. The test can be performed using fingers, a percussion hammer, or thumb pressure. Hoffmann’s method enables an early evaluation of nerve recovery before motor or sensory function returns, making it highly useful for assessing nerve sutures after trauma. This technique emphasizes the need for accurate site location to prevent disturbing the entire extremity during assessment [25,59].

Tinel sign

Jules Tinel (1879–1952) expanded on Hoffmann’s work by describing the “tingling sign” in 1915 as a method to assess nerve regeneration [26,60]. This diagnostic technique involves applying light pressure to an injured nerve, triggering a tingling sensation, often described as electrical, in the skin region served by the affected nerve. The sensation is most noticeable 4 to 6 weeks after injury. The Tinel sign is essential for evaluating nerve recovery—persistent tingling after applied pressure at the suture site suggests poor regeneration, while tingling extending beyond the injury site indicates ongoing healing. This sign remains a cornerstone of clinical practice in nerve injury assessment [26,60].

Babinski-Froment syndrome

Joseph François Félix Babinski (1857–1932) and Jules Froment (1878–1946) were pioneering French neurologists. Babinski cofounded the Société de Neurologie de Paris and is best known for the Babinski sign, a major contribution to neurological reflex studies [61]. Froment, working with Babinski, helped define the Froment sign, which is associated with ulnar nerve palsy [62]. In 1917, they described a syndrome involving contractures, paralysis, vasomotor symptoms, and tissue damage following traumatic injury. These symptoms, which extend beyond the injury site and lead to muscle atrophy, hyperreflexia, and autonomic dysfunction, are now understood as complex regional pain syndrome [27].

Collet-Sicard syndrome

Frédéric Justin Collet (1870–1966) and Jean-Athanase Sicard (1872–1929) were French physicians recognized for their contributions to neurology. Collet cofounded the Bibliothèque de la Tuberculose and published works on auditory disorders [63]. Sicard developed a diagnostic technique for spinal conditions [64]. In 1915, Collet described a syndrome in a soldier with a bullet wound to the base of the skull, affecting cranial nerves IX–XII and causing symptoms such as tongue deviation and tachycardia [28]. Sicard reported a similar case in 1917 [29]. Collet-Sicard syndrome results from damage to cranial nerves IX–XII and is observed in conditions such as skull fractures and metastatic tumors [65].

Villaret syndrome

Maurice Villaret (1877–1946) was a French physician who made significant contributions to neurology. He received his doctorate from the University of Paris in 1906 and trained under renowned physicians, including Charles Joseph Bouchard and Joseph Jules Babinski [66]. Villaret served as associate professor and chief physician at Necker Hospital in Paris. In 1916, he described two patients with bullet wounds to the posterior retroparotid space during World War I. These patients exhibited symptoms from nerve lesions affecting the hypoglossal, sympathetic, vagus, and glossopharyngeal nerves, including lingual paralysis, miosis, and hoarseness [30]. Villaret syndrome refers to these cranial nerve lesions.

Frey syndrome

Łucja Frey Gottsman (1889–1942) was a Polish Ukrainian neurologist born in Lwów (now Lviv, in Ukraine). She began her medical studies in 1917, completed her degree in 1923, and later worked under Kazimierz Orzechowski in Warsaw [67]. During World War II, Frey was forced into the Lemberg ghetto, where she worked in a polyclinic, but her ultimate fate remains uncertain [67]. Frey’s publication Le Syndrome du Nerf Auriculo-Temporal (The Auriculotemporal Nerve Syndrome) described a vasomotor disorder linked to gustatory sweating following a gunshot injury. She identified autonomic symptoms involving the auriculotemporal nerve and glossopharyngeal reflex pathways, with potential mixed symptoms when parasympathetic conduction is disrupted [31].

Lhermitte sign

Jacques Jean Lhermitte (1877–1959) was a French neurologist who made significant contributions to the study of multiple sclerosis and neurological disorders. He served as the chief of the Department of Neurological Diseases at Salpêtrière Hospital and later became an associate professor at the University of Paris [68]. Lhermitte identified a distinct phenomenon, later called the Lhermitte sign, which is characterized by electric shock-like sensations radiating from the head to the upper limbs and legs upon head flexion. This sign is commonly used and associated with multiple sclerosis [32]. Lhermitte’s work significantly advanced the understanding of neurological pain syndromes [69].

Meleney ulcer

Frank Lamont Meleney (1889–1963) was an American surgeon who earned his medical degree in 1916. He served in the US Army during World War I and later held faculty positions in China and at the University of Miami [70,71]. Meleney described infections caused by hemolytic Streptococcus leading to gangrene, often originating from injuries such as hypodermic injections or boils, though some patients reported no prior injury [33]. The condition progresses rapidly, with symptoms including swelling, redness, and tenderness, followed by fever, numbness, and the formation of blisters filled with yellow fluid. The disease, now known as necrotizing fasciitis, is characterized by its swift progression and severe tissue destruction [33].

Raeder (paratrigeminal) syndrome

Johan Georg Raeder (1889–1959) was a Norwegian physician known for his contributions to ophthalmology and neurology. After earning his medical degree in 1915, Raeder worked in Norway and abroad, including Portuguese West Africa. He later obtained his doctorate with a thesis on the lens in the human eye [72]. In 1924, Raeder described a syndrome involving oculopupillary sympathetic paresis (incomplete Horner syndrome) and trigeminal nerve involvement, which can arise from tumors or traumatic skull fractures. This condition, termed paratrigeminal syndrome, also includes facial pain, epiphora, and pterygoid muscle paresis [34]. The syndrome is caused by lesions near the Gasserian ganglion and the internal carotid artery, affecting both sympathetic and trigeminal nerves.

Frenkel syndrome

Henri Frenkel (1864–1934), a Polish-born French ophthalmologist, made noteworthy contributions to our understanding ocular trauma. He earned his medical degree in 1892 from the University of Lyon and later became chair of the Ophthalmology Clinic at the University Hospital in Toulouse [73]. In 1931, Frenkel described “anterior traumatic syndrome,” a condition resulting from traumatic contusions affecting the anterior segment of the eye. Symptoms range from temporary paralytic mydriasis to more severe cases, including iridoplegia and iris lesions. Frenkel attributed these changes to partial rupture of the lens zonule, leading to pupil and iris alterations [35]. The condition is also known as ocular contusion syndrome.

Coleman syndrome

Claude C. Coleman (1879–1953), an American neurosurgeon, earned his medical degree from the Medical College of Virginia in 1903. He completed surgical training in New York and Richmond, Virginia, and served as a major in the US Army during World War I, where he played a key role in brain surgery [74]. In 1918, Coleman and Meredith identified the relationship between cervical spine injuries and head and shoulder injuries in unconscious patients, emphasizing the need to examine the cervical spine in those with shoulder girdle injuries [36]. This condition is now referred to as the “posttraumatic occipital cervical shoulder girdle syndrome” or “occipital cervical shoulder girdle syndrome.”

Mondor disease

Henri Mondor (1885–1962), a French surgeon, made significant contributions to surgical pathology. He earned his medical degree in 1909 and held prominent roles, including the chair of surgical pathology at the Hôtel-Dieu [75]. Mondor described a condition characterized by phlebitis of the superior epigastric veins, presenting as a firm, tender cord beneath the skin following trauma or inflammation [37]. The disease, known as Mondor disease, is a form of sclerosing superficial thrombophlebitis, often affecting the anterior chest wall and causing symptoms such as erythema, nodules, and tenderness along the cord [76]. It is also referred to as Mondor phlebitis or Mondor syndrome.

Bywaters syndrome

Eric George Lapthorne Bywaters (1910–2003), a British physician, made significant contributions to the understanding of crush injury syndrome. Bywaters held various positions, including professor of rheumatology at the Royal Postgraduate Medical School, University of London [77]. During World War II, he and Desmond Beall documented symptoms and renal failure in crush injury patients, leading to the recognition of crush syndrome [38]. They identified muscle necrosis as a key factor and described acute tubular necrosis, which is now associated with rhabdomyolysis and compartment syndrome [78].

Fegeler syndrome

Ferdinand Fegeler (1920–2007) was a German physician known for his work in dermatology and mycology [79]. In 1949, he described a syndrome following a traumatic head injury in a 43-year-old man, characterized by left-sided facial nevus flammeus, hyperesthesia, Horner syndrome, and weakness in the left arm and leg [39]. Fegeler hypothesized that the nevus developed due to sympathetic nerve disruption following trauma, affecting vasoconstriction in areas supplied by the trigeminal nerve. This syndrome is also referred to as posttraumatic nevus flammeus [39].

DISCUSSION

Trauma-related eponyms encompass a wide range of conditions affecting various organ systems, including the gastrointestinal, neurological, musculoskeletal, and ophthalmological systems. These terms not only commemorate pioneering physicians but also represent milestones in the historical development of trauma medicine, particularly during wartime and periods of scientific advancement. While some eponyms, such as Laugier sign and Secrétan syndrome, have fallen out of use due to the adoption of more descriptive terminology, others remain widespread in contemporary clinical practice.

Among these, Morel-Lavallée syndrome, Kümmell disease, Hoffa disease, Purtscher syndrome, and Bywaters syndrome continue to be relevant due to their well-defined pathophysiology and association with distinct trauma mechanisms. These conditions are still encountered in orthopedic, emergency, and critical care settings.

Morel-Lavallée syndrome (1863), initially observed in industrial accidents, is now more often associated with high-energy trauma such as motor vehicle collisions. Advances in plastic and reconstructive surgery have improved its management. As a closed soft tissue degloving injury caused by shearing forces, it presents a diagnostic challenge in polytrauma cases, where subtle early findings may delay recognition and increase the risk of infection or necrosis if not promptly addressed [80].

Kümmell disease (1895), characterized by delayed vertebral collapse, gained recognition after the introduction of x-rays and is now more accurately diagnosed via magnetic resonance imaging (MRI), making it a relevant concept in posttraumatic orthopedic care. Often resulting from minor spinal trauma, it reflects a delayed complication involving avascular necrosis at the fracture site, which can lead to vertebral instability or kyphosis if left untreated [81].

Hoffa disease (1904), involving impingement of the infrapatellar fat pad, remains clinically relevant due to continued advancements in sports medicine and physical therapy. Frequently triggered by repetitive microtrauma in active individuals, it demonstrates how friction syndromes within the knee’s biomechanical structure can manifest as anterior knee pain [82].

Purtscher syndrome (1912), associated with traumatic retinal hemorrhages, remains significant in ophthalmology and critical care, particularly in cases of severe blunt trauma. Thought to result from embolic occlusion of precapillary arterioles, it exemplifies the complex vascular responses to systemic trauma that can cause acute visual loss [83].

Bywaters syndrome (1941), which is related to crush injuries and acute kidney failure, is an important condition in disaster medicine that clinicians should be aware of for managing trauma-induced rhabdomyolysis. The recognition of this condition highlights how pathological insights can directly inform effective treatment strategies, especially in recognizing renal failure resulting from skeletal muscle breakdown after prolonged compression [84].

The geographical origins of trauma-related eponyms reflect the dominance of European medical research in the 19th and early 20th centuries. France and Germany produced the most entries, followed by the United Kingdom and the United States. The concentration of musculoskeletal and nervous system-related eponyms corresponds with the high incidence of fractures, nerve injuries, and vascular trauma, which were accessible to clinical observation in a pre–imaging era.

The continued use of these eponyms is closely linked to major medical advancements. The introduction of x-rays in 1895, followed by MRI and computed tomography, transformed the diagnosis of trauma-related conditions. Advances in surgical disciplines, particularly in plastic and reconstructive surgery, have reinforced the clinical relevance of injuries first described in industrial and wartime settings. The emergence of specialized fields such as sports medicine, nephrology, and critical care has further expanded the diagnostic and therapeutic applications of these eponyms.

Ultimately, the persistence of trauma-related eponyms underscores both their diagnostic clarity and historical significance. Originating from wartime experiences, industrial injuries, and early radiological exploration, these terms continue to inform clinical reasoning and therapeutic strategies. Their survival attests to the enduring impact of past medical discoveries on modern trauma care.