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Tabes dorsalis
Other namesSyphilitic myelopathy
Axial section of the spinal cord showing syphilitic destruction (whitened area, upper center) of the posterior columns which carry sensory information from the body to the brain
SpecialtyNeurology

Tabes dorsalis is a late consequence of neurosyphilis, characterized by the slow degeneration (specifically, demyelination) of the neural tracts primarily in the dorsal root ganglia of the spinal cord (nerve root). These patients have lancinating nerve root pain which is aggravated by coughing, and features of sensory ataxia with ocular involvement.

Signs and symptoms

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Signs and symptoms may not appear for decades after the initial infection and include weakness, diminished reflexes, paresthesias (shooting and burning pains, pricking sensations, and formication), hypoesthesias (abnormally diminished sense of touch), tabetic gait (locomotor ataxia), progressive degeneration of the joints, loss of coordination, episodes of intense pain and disturbed sensation (including glossodynia), personality changes, urinary incontinence, dementia, deafness, visual impairment, positive Romberg's test, and impaired response to light (Argyll Robertson pupil). The skeletal musculature is hypotonic due to destruction of the sensory limb of the spindle reflex. The deep tendon reflexes are also diminished or absent; for example, the "knee jerk" or patellar reflex may be lacking (Westphal's sign). A complication of tabes dorsalis can be transient neuralgic paroxysmal pain affecting the eyes and the ophthalmic areas, previously called "Pel's crises" after Dutch physician P.K. Pel. Now more commonly called "tabetic ocular crises", an attack is characterized by sudden, intense eye pain, tearing of the eyes and sensitivity to light.[1][2]

"Tabes dorsalgia" is a related lancinating back pain.[citation needed]

"Tabetic gait" is a characteristic ataxic gait of untreated syphilis where the person's feet slap the ground as they strike the floor due to loss of proprioception. In daylight the person can avoid some unsteadiness by watching their own feet.[citation needed]

Cause

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Tabes dorsalis is caused by demyelination by advanced syphilis infection (tertiary syphilis) when the primary infection by the causative spirochete bacterium, Treponema pallidum, is left untreated for an extended period of time (past the point of blood infection by the organism).[3] The spirochete invades large myelinated fibers, leading to the involvement of the dorsal column medial leminiscus pathway rather than the spinothalamic tract.[citation needed]

Diagnosis

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Routine screening for syphilis. Treponemal antibody usually positive both in blood and in CSF also. In CSF lymphocytosis and elevated protein found. Serological tests are usually positive.[citation needed]

Treatment

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Intravenously administered penicillin is the treatment of choice. Associated pain can be treated with opiates, valproate, or carbamazepine. Those with tabes dorsalis may also require physical therapy and occupational therapy to deal with muscle wasting and weakness. Preventive treatment for those who come into sexual contact with an individual with syphilis is important.[citation needed]

Prognosis

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Left untreated, tabes dorsalis can lead to paralysis, dementia, and blindness. Existing nerve damage cannot be reversed.[citation needed]

Epidemiology

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The disease is more frequent in males than in females. Onset is commonly during mid-life. The incidence of tabes dorsalis is rising, in part due to co-associated HIV infection.[citation needed]

History

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Although there were earlier clinical accounts of this disease, and descriptions and illustrations of the posterior columns of the spinal cord, it was the Berlin neurologist Romberg whose account became the classical textbook description, first published in German[4] and later translated into English.[5]

Sir Arthur Conan Doyle, author of the Sherlock Holmes stories, completed his doctorate on tabes dorsalis in 1885.[6]

Society and culture

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Notable patients

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  • German storywriter E.T.A. Hoffmann appears to have had and died in 1822 from tabes dorsalis.
  • Mary Todd Lincoln [Dec 12, 1818 - Jul 16, 1882], wife of U.S. President Abraham Lincoln and America's First Lady from 1861 to 1865 most probably suffered from tabes dorsalis as early as 1869, at age 51. [1] She died of a stroke at age 63 in Springfield, IL.
  • The French novelist Alphonse Daudet kept a journal of the pain he experienced from this condition which was posthumously published as La Doulou (1930) and translated into English as In the Land of Pain (2002) by Julian Barnes.
  • Poet Charles Baudelaire contracted syphilis in 1839 and resorted to opium to help alleviate the pain of tabes dorsalis ascending his spine.
  • Painter Édouard Manet died of syphilis complications, including tabes dorsalis, in 1883, aged 51.
  • Boxer Charley Mitchell
  • Meyer Nudelman, the father of author and doctor Sherwin Nuland, who described his father's condition extensively in his book Lost in America; A Journey with my Father (2003).

See also

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References

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[edit]
Revisions and contributorsEdit on WikipediaRead on Wikipedia

Tabes dorsalis

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from Grokipedia
Tabes dorsalis, also known as , is a rare neurodegenerative disorder and a manifestation of tertiary caused by the bacterium subspecies pallidum. It primarily affects the dorsal columns and dorsal roots of the , leading to progressive , demyelination, and sensory loss due to chronic inflammation and direct treponemal invasion. This late-stage complication typically emerges 20 to 30 years after initial infection, following untreated , and is characterized by , abnormal sensations, and impaired coordination. The condition arises from the progression of , a , where the spirochete T. pallidum invades the , triggering an immune-mediated inflammatory response that damages sensory neurons. Pathophysiologically, it involves selective degeneration of the posterior columns, resulting in loss of and vibratory sense, while motor functions remain relatively spared until advanced stages. Historically prevalent before the widespread use of antibiotics in the early , tabes dorsalis now occurs in approximately 1.5% to 9% of syphilis cases, primarily in untreated or inadequately managed infections, and is exceedingly rare in regions with effective screening and treatment protocols. As of 2025, rising syphilis rates worldwide have led to increased cases of , heightening concerns for late-stage manifestations like tabes dorsalis in untreated individuals, though it remains exceedingly rare overall due to screening and treatment. Clinically, patients often present with lancinating pains (sharp, lightning-like episodes in the limbs or trunk), sensory ataxia exacerbated by visual deprivation (positive Romberg sign), and visceral crises such as gastric or bladder dysfunction. Other hallmark features include Argyll Robertson pupils (accommodate but do not react to light), absent deep tendon reflexes, paresthesias, and potential complications like Charcot joints (neuropathic arthropathy) or optic atrophy leading to vision impairment. Diagnosis relies on clinical suspicion, serological tests (e.g., nontreponemal RPR or treponemal FTA-ABS), and cerebrospinal fluid analysis confirming reactive VDRL, distinguishing it from other ataxic or neuropathic disorders. Treatment centers on eradicating the infection with high-dose intravenous penicillin G (18-24 million units daily for 10-14 days), which halts progression but cannot reverse existing neural damage; alternatives like are used for penicillin-allergic individuals. Supportive care includes analgesics for pain, physical therapy for , and management of complications such as or joint deformities. Prognosis is favorable with early intervention, preventing further deterioration, though untreated cases can lead to severe disability, including , , or blindness.

Introduction and Background

Definition and Classification

Tabes dorsalis, also known as , derives its name from the Latin term "tabes," meaning wasting or consumption, and "dorsalis," referring to the dorsal aspect of the , highlighting the condition's characteristic degenerative involvement of posterior spinal structures. It is defined as a slowly progressive, rare of the dorsal columns and dorsal roots of the , resulting from chronic by Treponema pallidum subspecies pallidum. This late manifestation primarily affects the sensory pathways, leading to progressive neurodegeneration. As a subtype of neurosyphilis—the infection of the central nervous system by the syphilis spirochete—tabes dorsalis is classified within the parenchymatous form of tertiary or late neurosyphilis, alongside general paresis of the insane. This classification distinguishes it from the meningovascular subtype, which involves vascular inflammation and earlier onset, and the meningeal form, characterized by acute inflammatory responses in the meninges. Parenchymatous neurosyphilis specifically targets neural parenchyma, resulting in degenerative changes rather than prominent acute inflammation. Core pathological features include demyelination and subsequent axonal degeneration of the dorsal root ganglia, posterior roots, and dorsal columns of the , with histologic findings showing pale, atrophic dorsal columns due to loss of sheaths and axons. Although an initial inflammatory response with perivascular lymphocytic infiltrates contributes to early pathogenesis, the late-stage process is predominantly degenerative with minimal ongoing . Onset typically occurs 10 to 30 years after the initial syphilitic infection, often averaging around 20 years, marking it as having the longest latent period among manifestations. A hallmark clinical correlate is , reflecting the sensory pathway disruption.

Historical Development

The term "tabes dorsalis," meaning "wasting of the back," originated from ancient descriptions of spinal cord afflictions, but its modern clinical recognition began in the early 19th century. In 1846, German physician Moritz Heinrich Romberg provided a seminal description, coining the synonymous term "locomotor ataxia" to characterize the progressive sensory ataxia and gait disturbances observed in affected patients. Romberg also developed the Romberg test, a simple clinical maneuver where a patient stands with eyes closed to assess proprioceptive loss, which became a cornerstone for diagnosing sensory deficits in the condition. Prior to Romberg, early 19th-century accounts, such as those by Ernst Horn in 1813, described similar spinal symptoms but lacked a unified clinicopathological framework. The mid-19th century marked a "golden age" of observations on tabes dorsalis, driven by detailed clinical studies and postmortem examinations that revealed characteristic dorsal column atrophy and demyelination as the pathological hallmark. Researchers like Romberg, collaborating with pathologist Robert Froriep, conducted autopsies demonstrating degeneration in the posterior columns and dorsal roots of the , distinguishing the disease from other myelopathies. These findings, corroborated by contemporaries such as , who detailed limb incoordination in the 1850s, shifted understanding toward a degenerative spinal process. Before 1875, outdated theories attributed tabes dorsalis to non-syphilitic causes, including , trauma, damp living conditions, or social impoverishment, often conflating it with or . A pivotal advancement came in 1875 when French physician Jean Alfred Fournier explicitly linked tabes dorsalis to , proposing it as a late manifestation based on epidemiological patterns in syphilitic patients; this "parasyphilitic" hypothesis was later solidified by statistical and pathological evidence. In the , Paul Ehrlich's 1910 introduction of salvarsan (), the first effective chemotherapeutic agent against , dramatically reduced the incidence of late-stage complications like tabes dorsalis by targeting the causative spirochete early in infection. The post-World War II era saw further decline with the advent of penicillin in the 1940s, which became the standard treatment and rendered tabes dorsalis a rare entity in developed regions due to its efficacy in eradicating .

Etiology and Pathogenesis

Causative Agent

Tabes dorsalis is primarily caused by a chronic infection with subspecies pallidum, a motile, gram-negative spirochete bacterium that is the etiologic agent of . This pathogen is transmitted primarily through sexual contact with an infected individual or congenitally from mother to during . The infection progresses through stages, with tabes dorsalis emerging as a late manifestation of untreated in the tertiary phase. The latency period from initial primary to the onset of tabes dorsalis typically spans 15 to 30 years, reflecting a prolonged phase where the bacterium persists at low levels without eliciting strong immune clearance. This extended allows T. pallidum to evade host defenses, maintaining viability in tissues despite the absence of overt symptoms. Key risk factors for progression to tabes dorsalis include untreated early-stage , which permits unchecked dissemination of the pathogen, and male gender, associated with higher historical and epidemiological rates of . Co-infections such as further accelerate the development of manifestations like tabes dorsalis by impairing immune control over the spirochete. The bacterium invades the via hematogenous spread shortly after initial , establishing a persistent presence that culminates in tertiary without necessarily requiring active bacterial replication in the later stages. This invasion leads to downstream effects such as demyelination in the dorsal columns of the .

Disease Mechanisms

Tabes dorsalis arises as a late manifestation of infection by , the spirochete responsible for , leading to specific neurodegenerative changes in the central and peripheral nervous systems. The primary pathology involves demyelination and of the posterior columns of the , specifically the fasciculus gracilis and cuneatus, along with degeneration of the dorsal roots. This selective damage impairs the transmission of proprioceptive and vibratory sensory information to the brain, as these pathways rely on large myelinated fibers that are particularly vulnerable to the inflammatory process. Immune-mediated damage plays a central , characterized by chronic inflammation triggered by treponemal antigens, which provokes perivascular infiltrates of lymphocytes, plasma cells, and macrophages without evidence of active bacterial replication. This persistent induces and in the affected neural tissues, culminating in progressive neuronal loss and scarring, distinct from the acute meningovascular phase of . Ocular involvement manifests as Argyll Robertson pupils, resulting from lesions in the midbrain's and Edinger-Westphal nucleus, which disrupt the pathway while sparing the near reflex for accommodation. This leads to miotic, irregular pupils that fail to constrict to light but respond to convergence. Systemic effects include known as Charcot joints, particularly in weight-bearing areas like the knees and spine, resulting from the loss of deep pain and proprioceptive sensation that leads to repeated unnoticed trauma and joint destruction. The disease progresses through a model of slow axonal degeneration, initiating in the sensory neurons of the dorsal root ganglia and extending to the posterior columns over a latency period of approximately 15 to 30 years post-, eventually resulting in irreversible fibrotic scarring and permanent sensory deficits.

Clinical Presentation

Primary Signs and Symptoms

Tabes dorsalis manifests primarily through a constellation of sensory, motor, ocular, and visceral symptoms resulting from demyelination in the dorsal columns and roots of the . The condition typically emerges insidiously in mid-to-late adulthood, approximately 20 years after initial syphilitic , with symptoms progressing gradually and featuring intermittent exacerbations often triggered by stress, , or spontaneously. Sensory symptoms are hallmark features, including lancinating "lightning" pains—sharp, intense, stabbing sensations in the legs, back, or that can last from seconds to days—and paresthesias such as numbness or tingling in the extremities. Patients commonly experience profound loss of and vibration sense due to dorsal column involvement, leading to where coordination is impaired without visual cues. Motor signs arise secondary to sensory deficits and include an ataxic, wide-based known as tabetic gait, characterized by foot slapping or stomping due to absent ankle jerks and other deep tendon reflexes. The Romberg test is positive in about 60% of cases, with patients demonstrating instability when standing with eyes closed, underscoring the reliance on vision to compensate for proprioceptive loss. Ocular manifestations feature bilateral Argyll Robertson pupils in roughly 50% of patients; these are miotic, irregular pupils that fail to react to light but constrict during accommodation to near objects. Visceral crises involve episodic, severe gastric crises mimicking acute abdominal conditions, with intense epigastric pain, , and , alongside genitourinary disturbances such as , , and impotence.

Associated Complications

Untreated tabes dorsalis, a late manifestation of , leads to several secondary complications arising from progressive , proprioceptive deficits, and ongoing syphilitic inflammation in the . , commonly known as Charcot joints, develops in approximately 6-10% of cases due to repeated painless trauma to weight-bearing joints from impaired deep sensation and . This destructive process most frequently affects the knees, hips, and spine, resulting in joint instability, effusion, and eventual deformity without significant pain, as the loss of protective reflexes allows unchecked microtrauma. In the spine, this manifests as Charcot spine, characterized by vertebral collapse, , and potential nerve root compression, further exacerbating mobility issues. Ocular complications include optic atrophy, which occurs in up to 20% of patients and progresses to irreversible blindness through demyelination and vascular damage to the . Additionally, (cranial nerve IV) palsy can arise from meningeal involvement, leading to vertical diplopia and head tilt as compensatory mechanisms fail. In advanced stages, neurological progression may overlap with general , a form of syphilitic , presenting as tabo-paresis with combined features of spinal degeneration and cerebral involvement; this includes marked by memory impairment and cognitive decline, alongside featuring hallucinations and delusions. Other sequelae encompass trophic ulcers, which form on the feet or pressure points due to insensate skin and poor , often becoming chronic and infected from unnoticed injuries. Spinal deformities, such as those from tabetic collapse (sometimes termed tabes equina), contribute to and disability, while heightens fall risk through instability and positive Romberg sign. In rare modern contexts, co-infection accelerates the disease course, with more frequent abnormalities, earlier onset of neurosyphilitic symptoms, and increased incidence of meningovascular events like ischemic strokes due to enhanced treponemal invasion of the blood-brain barrier.

Diagnosis

Clinical Assessment

The clinical assessment of suspected tabes dorsalis begins with a detailed taking, focusing on remote exposure, including sexual history and any prior untreated infections, as the condition typically manifests 20 to 30 years after initial infection. Patients should be queried about the timeline of neurological symptoms, such as progressive sensory ataxia, lancinating pains, paresthesias, and visceral disturbances like gastric or bladder crises, to establish the insidious onset characteristic of this late neurosyphilis form. Physical examination emphasizes neurological testing to identify dorsal column and root involvement. is evaluated using a for vibration sense and joint position sense, often revealing profound deficits in the lower extremities. includes the Romberg test, which is positive in approximately 60% of cases, demonstrating with a wide-based, stamping due to proprioceptive impairment. Reflex assessment typically shows absent or diminished deep tendon reflexes in the lower limbs, while pupillary examination may reveal Robertson pupils—small, irregular pupils that accommodate but do not react to light—in about 50% of patients. Differential diagnosis requires careful consideration of symptom patterns to rule out mimics like causing subacute combined degeneration, with distal sensory loss, or featuring progressive areflexia and ataxia. Tabes dorsalis is distinguished by its , lancinating pains, and selective dorsal column involvement without systemic or . Red flags such as acute crises, including severe lightning pains—sudden, stabbing sensations in the limbs or trunk—or visceral crises with intense and autonomic symptoms, warrant urgent evaluation to prevent complications like joint destruction. Multidisciplinary input, particularly from a neurologist, is essential for comprehensive assessment and coordination of care, often involving infectious disease specialists for historical correlation.

Laboratory Confirmation

Laboratory confirmation of tabes dorsalis, a late manifestation of neurosyphilis, relies on serological testing, cerebrospinal fluid (CSF) analysis, and supportive imaging or electrophysiological studies to demonstrate Treponema pallidum infection and central nervous system involvement. Blood tests begin with non-treponemal assays such as the Venereal Disease Research Laboratory (VDRL) or rapid plasma reagin (RPR) for initial screening, which detect nonspecific antibodies and are quantitative to assess disease activity; elevated titers suggest active infection, though they may decline or become nonreactive in late-stage disease. Confirmation requires treponemal-specific tests like the fluorescent treponemal antibody absorption (FTA-ABS) or Treponema pallidum particle agglutination (TP-PA), which remain positive for life in most cases and indicate prior or current syphilis exposure. CSF examination via is essential for diagnosing , including tabes dorsalis, as it provides direct evidence of infection. Typical findings include with more than 5 per microliter (or greater than 20 per microliter in patients with ), elevated protein levels exceeding 45 mg/dL, and a reactive CSF-VDRL test, which is highly specific (though less sensitive) for and unaffected by blood-brain barrier integrity. The CSF-VDRL is considered diagnostic when positive in the context of neurological symptoms, while treponemal CSF tests like FTA-ABS or TP-PA offer higher sensitivity but lower specificity due to potential passive antibody diffusion from serum. Imaging and electrophysiological tests support the diagnosis by revealing dorsal column pathology. Magnetic resonance imaging (MRI) often shows T2-weighted hyperintensities in the dorsal columns of the , reflecting demyelination and characteristic of tabes dorsalis. Somatosensory evoked potentials (SSEPs), particularly tibial nerve SSEPs, can detect subclinical involvement by demonstrating delayed or absent responses due to posterior column dysfunction, aiding in early or cases. According to Centers for Disease Control and Prevention (CDC) guidelines, definitive diagnosis of such as tabes dorsalis requires compatible clinical signs (e.g., ataxic ) plus either a reactive CSF-VDRL or a reactive treponemal test (e.g., CSF-FTA-ABS) accompanied by CSF abnormalities like pleocytosis or elevated protein. No single test is fully diagnostic, emphasizing the need for integrated serological, CSF, and clinical data. Diagnostic challenges in late-stage tabes dorsalis include false-negative results from non-treponemal tests due to waning levels, occurring in up to 30% of tertiary cases, and occasional negative CSF-VDRL despite active . co-infection increases the risk of and atypical presentations, necessitating routine testing in all suspected cases to guide interpretation and management.

Management

Pharmacological Treatment

The primary pharmacological treatment for tabes dorsalis, a manifestation of , involves high-dose intravenous penicillin G to eradicate the underlying infection. The recommended regimen is aqueous crystalline penicillin G at 18–24 million units per day, administered as 3–4 million units intravenously every 4 hours or via continuous infusion, for 10–14 days. This bactericidal approach aims to achieve treponemicidal levels in the (CSF), halting disease progression, though it cannot reverse preexisting neural damage. For patients with penicillin allergy, desensitization protocols are preferred to enable treatment with penicillin, as no alternative has proven equivalent efficacy for . In penicillin-allergic patients unable to undergo desensitization, alternative regimens include 1–2 grams daily (intramuscularly or intravenously) for 10–14 days; however, this option has limited supporting data and is less effective for , necessitating close clinical and CSF monitoring. To prevent progression to tabes dorsalis, early-stage should be treated promptly with intramuscular benzathine penicillin G 2.4 million units in a single dose, which effectively interrupts the infection cascade. Symptomatic management targets the characteristic , including lightning-like pains and tabetic crises. Analgesics such as opiates and may be helpful for severe pain crises. Opiates, such as or , should be used cautiously and short-term for acute crises due to risks of dependence and respiratory depression. Post-treatment monitoring is essential to assess response and manage complications. The Jarisch-Herxheimer reaction, characterized by fever, chills, and worsening symptoms due to bacterial antigen release, occurs in approximately 10% of cases within 24 hours of initiating penicillin and requires supportive care without altering the regimen. Follow-up involves clinical and serologic testing every 3–6 months until stable; repeat CSF examination is unnecessary if serum RPR normalizes and clinical response is observed.

Supportive Therapies

Supportive therapies for tabes dorsalis focus on mitigating the functional impairments caused by dorsal column degeneration, such as , , and , thereby enhancing patient mobility, independence, and . These interventions complement antimicrobial treatment, such as penicillin, by addressing residual neurological deficits that persist despite infection control. Physical therapy plays a central role in managing ataxia and weakness, incorporating targeted exercises to improve coordination and proprioception. Frenkel's exercises, originally developed for tabetic ataxia, involve systematic, graded movements performed with visual guidance to retrain balance and reduce reliance on impaired sensory feedback; these include heel-toe walking, rhythmic heel tapping, and coordinated arm-leg patterns to enhance postural stability. Balance retraining and strengthening exercises further prevent muscle wasting, while gait aids like canes or walkers provide external support to compensate for proprioceptive loss and minimize fall risk during ambulation. Patients are educated on sensory precautions to avoid injuries from unnoticed trauma due to diminished sensation. Occupational therapy supports daily functioning by introducing adaptive devices and strategies tailored to sensory and motor deficits. Therapists recommend tools such as reachers, button hooks, or modified utensils to facilitate activities like dressing and eating, particularly for those with involvement or general weakness. is emphasized through environmental modifications, including grab bars and non-slip mats, alongside training in techniques to sustain and reduce fatigue. These interventions help maintain overall functional capacity despite progressive neuropathy. Pain management in tabes dorsalis employs non-pharmacological adjuncts to alleviate lancinating neuralgias and joint discomfort. Modalities like (TENS) units deliver low-level electrical currents to disrupt pain signals, offering relief for neuropathic symptoms when used regularly over affected areas. Heat or cold applications provide symptomatic easing for acute episodes, while may serve as an alternative for by modulating neural pathways, though evidence is drawn from broader neuropathic contexts. For Charcot joints, a common complication involving painless , orthopedic interventions include bracing to immobilize and protect the joint, preventing further ; in advanced cases, surgical options like fusion or resection address instability and ulceration. Multidisciplinary care coordinates specialists to address associated impairments holistically. Urologists manage and incontinence through behavioral training or catheterization protocols, while ophthalmologists evaluate and treat visual disturbances, such as Argyll Robertson pupils, to preserve remaining sight. Neurologists oversee overall progression, and psychologists provide support for coping with chronic pain and disability, using cognitive-behavioral techniques to mitigate emotional distress. This team approach ensures comprehensive symptom control and prevents secondary complications. Lifestyle measures emphasize compensatory strategies for proprioceptive deficits and avoidance. Visual cues, such as high-contrast flooring or illuminated pathways, aid by enhancing reliance on sight to offset , as demonstrated in gait assessments like the Romberg test. Patients are advised to abstain from alcohol, which can exacerbate and worsen through additive neurotoxic effects. Regular monitoring and adherence to these adaptations promote long-term safety and functionality.

Outcomes and Public Health

Prognosis

Tabes dorsalis, if left untreated, follows a progressive course leading to severe , including , loss of , and potential complications such as , blindness, and . Historical data from untreated tertiary cases indicate a of approximately 20%, often due to secondary infections, falls, or cardiovascular issues. The disease typically manifests 15 to 30 years after initial infection, with gradual deterioration in mobility and sensory function over 5 to 10 years without intervention. With appropriate treatment using intravenous penicillin, the progression of tabes dorsalis can be halted, though existing neurological is irreversible and symptoms like often persist. Early and intervention significantly improve functional outcomes, allowing many patients to maintain , whereas delayed treatment correlates with poorer mobility and higher dependency rates. Co-infection with accelerates disease onset and worsens prognosis, increasing the risk of and complicating response to due to immune dysregulation. Onset after age 50 is associated with more rapid functional decline and reduced recovery potential compared to younger patients. Quality of life in tabes dorsalis is markedly impacted by , instability, and sensory deficits, often resulting in high dependency on assistive devices or caregivers for daily activities. Studies highlight elevated risks of falls and joint deformities, such as Charcot joints, further limiting mobility and self-sufficiency. In the modern era, tabes dorsalis has become exceedingly rare in developed regions due to widespread penicillin use for early , but resurgence risks persist in untreated populations amid rising incidence, particularly among those with .

Epidemiology

Tabes dorsalis, a late manifestation of , is a rare condition globally, affecting an estimated 1.5% to 9% of individuals with infections. In untreated cases, 25% to 35% progress to late , of which tabes dorsalis represents a subset, though exact proportions vary by population and access to care. Due to widespread penicillin use since the and routine screening, incidence rates in developed countries remain extremely low, typically below 0.01 per 100,000 population annually. Demographically, tabes dorsalis disproportionately affects males in a 3:1 ratio compared to females, with onset typically occurring between ages 40 and 60 years, reflecting the 15- to 30-year latency from initial infection. It is more prevalent among men who have sex with men (MSM), where rates are elevated, and rates of coinfection can reach 45%, increasing the risk of progression to up to 10%. In the United States, higher incidence is observed among Black individuals relative to White individuals, aligning with broader disparities. Geographically, tabes dorsalis has declined sharply in high-income regions following antibiotic introduction, but recent syphilis resurgences—driven by untreated cases—have led to upticks in neurosyphilis, including tabes, in and . In lower-income areas of Africa and , syphilis prevalence remains highest, with age-standardized incidence rates exceeding 1,200 per 100,000 in Central Sub-Saharan Africa as of 2021, heightening risks for late complications like tabes dorsalis. Congenital tabes dorsalis is exceedingly rare but possible in untreated maternal syphilis cases. Key risk factors include untreated latent , inadequate prenatal screening, and substance use—particularly among MSM—which facilitates transmission and delays . Public health surveillance indicates that comprises 4% to 10% of cases overall, with U.S. Centers for Disease Control and Prevention (CDC) data showing 1% to 2% of reported progressing to amid a 28.6% rise in primary/secondary cases from 2020 to 2021. This resurgence, with over 8 million global adult acquisitions as of 2022, underscores ongoing prevention needs, though provisional U.S. data as of 2024 show a 22% decline in primary and secondary cases from 2023 levels.

Societal Impact

Notable Individuals

Ernst Theodor Amadeus Hoffmann (1776–1822), the German writer known for his fantastical tales such as The Nutcracker and the Mouse King, suffered from in his later years, manifesting in symptoms including , severe pains, and progressive neurological decline that influenced the nightmarish and uncanny elements in his literature. His condition, likely as a late complication of , contributed to his physical deterioration and early death at age 46, amid a backdrop of exacerbating the symptoms. Mary Todd Lincoln (1818–1882), the of the as wife of President , exhibited gait disturbances, lightning-like pains, and visceral crises consistent with tabes dorsalis, a syphilitic complication that complicated her history and led to her institutionalization in 1875. A 1999 analysis of her physicians' records confirmed these as hallmarks of tertiary , distinguishing her neurological symptoms from purely psychiatric ones and highlighting the disease's role in her pallor, weakness, and unsteady walk over decades. Her case underscores how tabes dorsalis intertwined with personal tragedy, including the loss of her children and the assassination of her husband, amplifying public perceptions of her instability. Alphonse Daudet (1840–1897), the French novelist famous for works like Tartarin of Tarascon, endured tabes dorsalis for over two decades following syphilis infection in his youth, experiencing intense "lightning pains," ataxia, and gastric crises that he meticulously documented in his posthumously published notebook La Doulou (The Pain). This intimate chronicle not only captured the relentless, stabbing neuralgias and loss of coordination but also raised early public awareness of the disease's torment, portraying it as a "one-man band of pain" that isolated him socially and artistically in his final years. Édouard Manet (1832–1883), the pioneering French painter and father of , developed tabes dorsalis around 1875, suffering from progressive leg pains, sensory ataxia, and Argyll Robertson pupils that severely impaired his mobility and forced him to adapt his studio work. The condition culminated in of his left foot, leading to just days before his death at age 51, and likely contributed to sensations posthumously inferred from his symptoms; his late paintings, such as A Bunch of Asparagus, reflect a shift toward still lifes amid his physical decline. Other notable cases include the French poet (1821–1867), who contracted in 1839 and later experienced the ascending spinal pains of tabes dorsalis, which he managed with opium and which infused the decadent themes of . Oscar Wilde's (1854–1900) potential tabes dorsalis remains debated, with some contemporaries attributing his final to tertiary , though modern analyses favor an ear infection as the primary cause. English boxer Charley Mitchell (1861–1918), a champion who fought , succumbed to tabes dorsalis at age 57, the disease causing fatal loss of coordination after a marked by bare-knuckle bouts.

Cultural Representations

Tabes dorsalis, as a manifestation of late-stage , has appeared in 19th-century literature reflecting the era's medical and social concerns. , who completed his medical thesis on the changes in tabes dorsalis in 1885, incorporated allusions to —a common term for the condition—in his short story "The Doctors of Hoyland" (1894), where a character references reading Doyle's paper on the topic during a consultation. This depiction highlights the dramatic symptom of , portraying it as a professional interest for physicians while underscoring the disease's neurological impact. Similarly, French writer chronicled his own experience with tabes dorsalis in his posthumously published memoir In the Land of Pain (1930, based on 1880s notes), detailing excruciating neuropathic pains and criticizing the medical inadequacies of the time in treating syphilis-related suffering. In art, the condition influenced the work of Impressionist painter , who suffered from tabes dorsalis in his later years, experiencing severe lightning-like pains, proprioceptive , and gait instability that culminated in leg in 1883. These symptoms, including post-amputation sensations, may have intensified Manet's focus on themes of physical discomfort and transience in his paintings, contributing to the expressive qualities of by channeling personal pain into innovative visual representations of the human form and movement. During the , tabes dorsalis carried significant stigma due to its established link to , often interpreted as a consequence of moral failings like , which permeated literary and cultural narratives and reinforced societal judgments against affected individuals. In modern media, representations of tabes dorsalis are rare, largely diminished by the advent of antibiotics like penicillin in the mid-20th century, but it occasionally appears in historical dramas to illustrate the perils of untreated venereal diseases; for instance, the 2017 episode of the series Victoria references manifestations including tabes to dramatize Victorian-era crises. The societal legacy of tabes dorsalis extended to early 20th-century efforts against , where its visible neurological horrors—such as —motivated campaigns for premarital screening and serological testing, exemplified by the widespread adoption of the after to detect latent infections and prevent late complications.

References

  1. https://www.ncbi.nlm.nih.gov/books/NBK557891/
  2. https://medlineplus.gov/ency/article/000729.htm
  3. https://journalfeed.org/article-a-day/2025/is-neurosyphilis-increasing-yes-but-whos-at-risk/
  4. https://emedicine.medscape.com/article/1169231-overview
  5. https://www.sciencehistory.org/education/scientific-biographies/paul-ehrlich/
  6. https://www.cdc.gov/std/treatment-guidelines/syphilis.htm
  7. https://pmc.ncbi.nlm.nih.gov/articles/PMC6493817/
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