General Paresis Research Articles

Neurosyphilis Presenting as Primary Progressive Aphasia

Back to table of contents Previous article Next article LettersFull AccessNeurosyphilis Presenting as Primary Progressive AphasiaPanagiotis Ioannidis, M.D., Ph.D., Athanasios Lourbopoulos, M.D., Ph.D., Dimitra Mamouli, M.D., Eleni Polichroniadou, M.D., George Papadopoulos, M.D., and Dimitris Karacostas, M.D., Ph.D.Panagiotis IoannidisSearch for more papers by this author, M.D., Ph.D., Athanasios LourbopoulosSearch for more papers by this author, M.D., Ph.D., Dimitra MamouliSearch for more papers by this author, M.D., Eleni PolichroniadouSearch for more papers by this author, M.D., George PapadopoulosSearch for more papers by this author, M.D., and Dimitris KaracostasSearch for more papers by this author, M.D., Ph.D.Published Online:1 Jan 2014https://doi.org/10.1176/appi.neuropsych.13010018AboutSectionsPDF/EPUB ToolsAdd to favoritesDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InEmail To the Editor: Primary progressive nonfluent aphasia (PPnfA) is an aphasic disorder that is classified in the spectrum of frontotemporal dementia diseases.1 It is characterized by disturbed grammatical comprehension and expression, as well as reduction of speech sound production. We present a adult man whose initial symptoms and signs were compatible with PPnfA in whom later work-up surprisingly unmasked neurosyphilis.Case ReportA 52-year-old normotensive native man was admitted from the outpatient memory clinic of our department for evaluation of speech difficulties that started 6 months earlier. His past medical history was otherwise unremarkable. Neurological examination revealed mild cogwheel rigidity, positive grasp reflexes, and bilateral Babinski signs. MMSE score was 28, and the Addenbrooke Cognitive Examination–Revised (ACE–R) test score was 74/100. He presented reduced verbal fluency, with word-finding difficulties. Brain MRI showed bilateral perisylvian cortical atrophy, more prominent in the left hemisphere (Figure 1), and routine EEG revealed theta-wave activity in the left frontotemporal area. Extensive serology and hematological tests were normal except for positive Venereal Disease Research Laboratory (VDRL) test (titer: 1/128). Subsequently, serum tests for rapid plasma regain (RPR) and fluorescent treponemal antibody absorption (FTA-Abs) were both positive, with RPR titer: 1/128. Spinal tap demonstrated clear CSF with 160 cells/mm3 (50% neutrophils), along with protein: 135 mg/dl, glucose: 28 mg/dl, and positive VDRL (1:16), RPR (1:32), and positive FTA-Abs.FIGURE 1. Neurosyphilis Patient’s MRI[A]: T1-weighted image with contrast medium; [B]: T2-weighted image shows ventricular enlargement due to parenchymal atrophy, incompatible with his age.The patient was treated with IV 4×106 units of penicillin administrated 6 times daily for 15 days and followed by 2.4 million units of benzathine penicillin 5 IM once a week for 3 weeks. A second spinal tap showed clear, acellular CSF, with protein 95 mg/dl, glucose 37 mg/dl, positive VDRL (1:8), and RPR (1:16).On follow-up 6 months later, a significant improvement of language production was observed; his ACE–R score was 92/100; MMSE score was 30; and the rest of the neurological signs remained unchanged.DiscussionNeurosyphilis can present with progressive cognitive deterioration accompanied by psychiatric manifestations,2 and it is considered one of the treatable and reversible causes of dementia.3 With the present progress of socioeconomic globalization, the spread of migration from developing countries, and the recently-published increasing spread of syphilis,4 we have to reconsider neurosyphilis even in immunocompetent adults. The correct diagnosis could be crucial because early therapy could dramatically affect prognosis.5 Also, our case was atypical because it presented with progressive aphasic disturbances resembling PPnfA. Had we omitted the special serological tests for syphilis, our case could had probably remained undiagnosed.In conclusion, syphilis should be included in the differential diagnosis of early-onset dementias, even if the initial symptoms and neuroimaging findings point toward a degenerative dementing process.Dept. of Neurology, AHEPA University Hospital, Aristotle University School of Medicine, Thessaloniki, Macedonia, GreeceCorrespondence: Dr. Ioannidis; e-mail: [email protected]grThe authors report no conflict of interest related to the present study.References1 Gorno-Tempini ML, Hillis AE, Weintraub S, et al.: Classification of primary progressive aphasia and its variants. Neurology 2011; 76:1006–1014Crossref, Medline, Google Scholar2 Nagappa M, Sinha S, Taly AB, et al.: Neurosyphilis: MRI features and their phenotypic correlation in a cohort of 35 patients from a tertiary care university hospital. Neuroradiology 2013; 55:379–388; available at doi: 10.1007/s00234-012-1017-9Crossref, Medline, Google Scholar3 Yu Y, Wei M, Huang Y, et al.: Clinical presentation and imaging of general paresis due to neurosyphilis in patients negative for human immunodeficiency virus. J Clin Neurosci 2010; 17:308–310Crossref, Medline, Google Scholar4 Mayer KH, Mimiaga MJ: Resurgent syphilis in the United States: urgent need to address an evolving epidemic. Ann Intern Med 2011; 155:192–193Crossref, Medline, Google Scholar5 Ghanem KG: Review: Neurosyphilis: a historical perspective and review. CNS Neurosci Ther 2010; 16:e157–e168Crossref, Medline, Google Scholar FiguresReferencesCited byDetailsCited ByLanguage impairments and CNS infections: a review29 July 2021 | Aphasiology, Vol. 36, No. 10Neurosyphilis Mimicking Behavioral Variant of Frontotemporal Dementia in a 59-Year-Old Man1 June 2022 | Cognitive and Behavioral Neurology, Vol. 35, No. 2Current Infectious Disease Reports, Vol. 17, No. 5 Volume 26Issue 1 Winter 2014Pages E27-E28 Metrics PDF download History Published online 1 January 2014 Published in print 1 January 2014

MRI findings and early diagnosis of general paresis of the insane

The objective of this study was to improve the knowledge of the clinical and MRI presentation of general paresis of the insane (GPI) and achieve its early diagnosis. Fifteen patients with GPI were gathered. Their clinical data and brain MRI information were analyzed. The age range was 33–62 years (mean: 48·8 years). The disease lasted 34 days–28 months (mean: 10·87 months). Treponema pallidum hemagglutination assays (TPHAs) on the cerebrospinal fluid (CSF) and sera were positive. All patients were human immunodeficiency virus (HIV) negative and primarily showed progressive cognitive impairment, mostly accompanied with emotional disturbance and psychosis. The accompanying symptoms included epilepsy (n = 7), ataxia (n = 5), cerebral vascular disease (n = 3), and limbs tremor (n = 2). Typical Argyll Robertson's pupil was observed in two cases. A CSF examination showed elevated white blood cell (WBC) and protein level. Purely cerebral atrophy was found in three cases. Abnormal high signals were found in nine cases in different brain area, mainly in bilateral temporal, insular, and frontal lobes and hippocampus in T2-weighted and fluid-attenuated inversion recovery (FLAIR), which was accompanied by cerebral and/or hippocampus atrophy. Purely atrophy of bilateral or unilateral hippocampus was found in two cases. Cerebral infarction lesions were found in three cases. Contrary to the previous reports, the hippocampal atrophy and bilateral abnormal signals of hippocampus and temporal lobe in brain MRI were more common in cases with GPI. Abnormal signals were probably related to proliferation of glial cells rather than cytotoxic edema. The pathogenesis of the abnormal signals needs to be further explored. General paresis of the insane has a wide variety of central nervous system manifestations, either clinically or neuroradiologically. Identification of these presentations could be important for early diagnosis.

Dying to Get Out of the Asylum: Mortality and Madness in Four Mental Hospitals in Victorian Canada, c. 1841–1891

This article examines the status of lunatic cadavers during the second half of the nineteenth century. The first section summarizes cause of death data of over three thousand patients who were admitted to the four principal lunatic asylums in the province of Ontario (Canada). The results illuminate the alleged causes of death, revealing, among other factors, the impact of tuberculosis and general paralysis of the insane. The data also suggest that there was a steady increase in life chances of those entering the mental hospital over the five decades under study. The second section of the article investigates the tension between medical schools and asylum superintendents as educational requirements for nineteenth-century medical education necessitated more and more material for dissection, elevating the status of alienists as gatekeepers to cadavers. The article then concludes by reflecting on what implications these findings have for our understanding of the Victorian lunatic asylum.

Syphilitic polyradiculoneuropathy in an immunocompetent patient

Background: Although the incidence of neurosyphilis has decreased, it is still prevalent. Its most common clinical presentation includes tabes dorsalis and general paresis. In contrast, polyradiculoneuritis has rarely been reported during syphilis. The authors report /INS;a case of acute polyradiculoneuritis caused by Treponema pallidum in an immunocompetent patient.

Neurosyphilis manifesting with rapidly progressive dementia: report of three cases

Neurosyphilis is rather an unusual cause of dementia characterized by a rapidly progressive course and psychiatric symptoms. Diagnosis of neurosyphilis should be suspected in the presence of a global cognitive impairment consisting in disorientation, amnesia and severe impairment of speech and judgement and psychiatric symptoms such as depression, mania and psychosis, with a subacute onset. More commonly, clinical manifestations of neurosyphilis include general PARESIS (involvement of Personality, Affect, Reflexes, Eye, Sensorium, Intellect and Speech). Upon clinical suspicion, diagnosis of neurosyphilis is confirmed by a reactive cerebrospinal fluid (CSF)-Venereal Disease Research Laboratory. Here we report three Human Immunodeficiency Virus (HIV)-negative male patients presenting with psychiatric symptoms and a rapidly evolving dementia. Although magnetic resonance imaging did not address to diagnosis, CSF examination was mandatory in neurosyphilis diagnosis. Other diagnostic tools such as neuropsychology and single-photon emission computed tomography resulted supportive in the diagnosis. We showed that a prompt antibiotic treatment might stop disease progression. Therefore, neurosyphilis should be always considered even in HIV-negative patients in the presence of unexpected psychiatric symptoms accompanied by a rapidly evolving cognitive decline.

Elevated CSF Cytokines in the Jarisch-Herxheimer Reaction of General Paresis

The Jarisch-Herxheimer reaction (JHR) is a well-recognized transient worsening of signs and symptoms occurring soon after the first dose of an appropriate antibiotic for several spirochetal infections. The pathogenesis of this reaction is poorly understood. In this case study of cerebrospinal fluid (CSF) cytokines, we aimed to improve understanding of the pathogenesis of JHR in patients with neurosyphilis who develop transient neurologic signs. Four hours after receiving penicillin for general paresis, a 55-year-old man developed a severe JHR characterized by fever, tachycardia, hypertension, obtundation, seizures, and a neutrophilia lasting 18 hours. Cerebrospinal fluid obtained at the peak of the JHR demonstrated a switch from a mild lymphophilia to a moderate neutrophilia. He had markedly elevated CSF interleukin (IL) 8 and likely elevated IL-1β, IL-10, and IL-15 levels, which returned to normal in follow-up CSF examination results. To our knowledge, this is the first report of elevated CSF cytokines in a patient with a JHR, which possibly contributed to the neurologic signs of JHR. Further studies on the innate inflammatory response during episodes of acute infection and inflammation are needed to develop targeted therapies to modulate this system, which could, in turn, improve future outcomes and modify the JHR.

The bones of the insane.

This article examines alienist explanations for fracture among British asylum patients in the late nineteenth to early twentieth centuries. A series of deaths in asylums came to light in the 1870s which, in placing the blame for such incidents on asylum staff, called for a response from the psychiatric profession. This response drew upon other medical fields and employed novel pathological techniques to explain why fractures occurred among the insane, in many cases aligning bone fragility with particular forms of insanity (namely, General Paralysis of the Insane). Although such research aimed to provide a medical explanation for the ‘fracture death’, it also called into question the value of pathological research and the utility of quantitative measurement in understanding mental disease.

Clinical Spectrum of Neurosyphilis among HIV-Negative Patients in the Modern Era

Background: The clinical spectrum of neurosyphilis (NS) has changed over time. Objective: To describe the clinical spectrum and characteristics of NS in HIV-negative patients. Methods: A retrospective chart review was performed for 149 in patients with NS. Result: All patients were >25 years old, including 16.8% asymptomatic for NS, 15.4% with syphilitic meningitis, 24.2% with meningovascular NS, 38.9% with general paresis, 4.0% with tabes dorsalis and 0.7% with gummatous NS. The original misdiagnosis rate was 84.6%. All 149 patients had positive serum Treponema pallidum particle agglutination (TPPA) and rapid plasma reagin (RPR). The overall positive rates of cerebrospinal fluid RPR (CSF-RPR) and CSF-TPPA were 57.0 and 89.9%, respectively. CSF pleocytosis and elevated CSF protein were found in 40.3% of patients. Nonspecific abnormal brain magnetic resonance imaging and electroencephalography findings were present in 60.4 and 54.8% of NS patients, respectively. Conclusions: NS has various clinical manifestations, laboratory findings and magnetic resonance imaging and electroencephalography findings, but all studies lack specificity. Every patient with neurological or psychiatric symptoms that are without unambiguous causes should have blood tests for syphilis. When serology proves positive, patients should undergo CSF examination.

Laboratory findings in neurosyphilis patients with epileptic seizures alone as the initial presenting symptom

A retrospective chart review was performed to characterize the clinical presentation, the characteristic combination of serologic and cerebrospinal fluid (CSF) abnormalities, and the neuroimaging findings of neurosyphilis (NS) patients who had epileptic seizures alone as an initial presenting symptom. In a 6.75-year period, 169 inpatients with NS were identified at Zhongshan Hospital (from June 2005 to February 2012). We demonstrated that 13 (7.7%) of the 169 NS patients had epileptic seizures alone as an initial presenting feature. Epileptic seizures occurred in NS patients with syphilitic meningitis (2 cases), meningovascular NS (5 cases), and general paresis (6 cases). The types of epileptic seizures included simple partial, complex partial with secondary generalization (including status epilepticus), and generalized seizures (no focal onset reported). Nine of NS patients with only epileptic seizures as primary symptom were misdiagnosed, and the original misdiagnosis was 69.23% (9/13). Ten (10/13, 76.9%) patients had an abnormal magnetic resonance imaging, and 7 (7/13 53.8%) patients had abnormal electroencephalogram recordings. In addition, the sera rapid plasma reagin (RPR) and Treponema pallidum particle agglutination (TPPA) from all 13 patients were positive. The overall positive rates of the CSF-RPR and CSF-TPPA were 61.5% and 69.2%, respectively. Three patients demonstrated CSF pleocytosis, and 9 patients exhibited elevated CSF protein levels. Therefore, NS with only epileptic seizures at the initial presentation exhibits a lack of specificity. It is recommended that every patient with clinically evident symptoms of epileptic seizures should have a blood test performed for syphilis. When the serology results are positive, all of the patients should undergo a CSF examination to diagnose NS.

Spectrum and characterization of movement disorders secondary to neurosyphilis

There have been frequent reports of Neurosyphilis with atypical features. Syphilitic infection of the central nervous system can result in various movement disorders (MD). The few reports of MD patients with neurosyphilis have been mainly of single patient. Between June 2005 and February 2012 we identified, 169 in-patients with neurosyphilis at Zhongshan Hospital. We performed a retrospective chart review to characterize MD findings, clinical signs and symptoms, misdiagnosis rate, laboratory findings, and brain magnetic resonance imaging results. We found that seven of the 169 neurosyphilis patients presenting with MD, had originally been misdiagnosed with Parkinsonism (4), laryngeal dystonia (1), corticobasal syndrome (1), and sensory ataxia (1). None of these patients were initially suspected of having neurosyphilis. The correct diagnosis was syphilitic meningitis (1), meningovascular neurosyphilis (2), general paresis (3), and tabes dorsalis (1). Among them, six patients had abnormal imaging studies, and sera rapid plasma reagin (RPR) and Treponema pallidum particle agglutination (TPPA) from all seven patients were positive. The cerebrospinal fluid (CSF) examinations showed that four patients were CSF-RPR positive (titers ≤1:16) by CSF syphilitic serologic testing, but all seven patients were CSF-TPPA reactive. Moreover, two patients had CSF pleocytosis and four patients had elevated CSF protein expression. Our findings reinforced the importance of routine serologic testing for syphilis should be a part of the evaluation of patients with atypical MD presentations or in whom alternative diagnoses are not forthcoming. When serology is positive, all patients should be examined more thoroughly for neurosyphilis by lumbar puncture.

Mental disorders as “brain diseases” and Jaspers’ legacy

Mental disorders as “brain diseases” and Jaspers’ legacy

Alterations of CSF Cystatin C Levels and Their Correlations with CSF Αβ40 and Αβ42 Levels in Patients with Alzheimer's Disease, Dementia with Lewy Bodies and the Atrophic Form of General Paresis

Immunohistochemical studies have revealed that cystatin C (CysC) co-localizes with amyloid-β (Αβ) in amyloid-laden vascular walls and in the senile plaque cores of amyloid. In vitro and in vivo animal studies suggest that CysC protects against neurodegeneration by inhibition of cysteine proteases, inhibition of Αβ aggregation, induction of autophagy and induction of cell division. CysC levels may be altered and may have a potential link with cerebrospinal fluid (CSF) Aβ levels in various types of dementia with characteristic amyloid deposits, such as Alzheimer's disease (AD), dementia with Lewy bodies (DLB) and the atrophic form of general paresis (AF-GP). We assessed the serum and CSF levels of CysC and the CSF levels of Aβ40 and Aβ42 in patients with AD (n = 51), DLB (n = 26) and AF-GP (n = 43) and normal controls (n = 30). Using these samples, we explored the correlation between CSF CysC and CSF Aβ levels. We found that in comparison to the normal control group, both CSF CysC and CSF Aβ42 levels were significantly lower in all three dementia groups (all p<0.001); serum CysC levels were the same in the AD and DLB groups, and were lower in the AF-GP group (p = 0.008). The CSF CysC levels were positively correlated with both the CSF Aβ40 and Aβ42 levels in the AD, AF-GP and normal control groups (r = 0.306∼0.657, all p<0.05). Lower CSF CysC levels might be a common feature in dementia with characteristic amyloid deposits. Our results provide evidence for the potential role of CysC involvement in Aβ metabolism and suggest that modulation of the CysC level in the brain might produce a disease-modifying effect in dementia with characteristic amyloid deposits.

Diagnostic and statistical manual of mental disorders 5: A quick glance

Byline: Vihang. Vahia Dr. Dilip Jeste, the then President of the American Psychiatric Association, released the Fifth Edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM 5) [sup][1] on May 18, 2013 at the 166 [sup]th Annual Meeting of the APA at San Francisco. This was a landmark achievement for the APA. Indian psychiatrists should take additional pride in the fact that Dr. Dilip V. Jeste is actually one of us. He used to be an Overseas Member of the Indian Psychiatric Society (IPS). History of the DSM Earliest documented efforts to gather epidemiological data on mental illness commenced in the USA in the year 1840. Mental illnesses were then classified under a single category of idiocy/insanity. Inaccurately defined categories of mental illness like mania, melancholia, monomania, general paralysis of the insane, dementia, and dipsomania were included in the US Census of 1880. In 1918, the American Medico-Psychological Association published a manual of classification of mental illnesses that listed 22 categories. The manual was designed for the use of Institutions for the Insane. The American Medico-Psychological Association was later renamed APA in 1921. During World War II, the US army prepared a manual of medical illnesses called the ' Medical 203 '. The US Navy revised the Medical 203 to formulate the Classified Nomenclature of Disease or the Standard. Office of the US Surgeon General adopted the Standard to classify illnesses on the battle grounds and among veterans returning from the war. The Veterans Administration adopted the Standard with few modifications. After the war, psychiatrist with experience of using the Standard during the Second World War continued to use it in civilian practice. The World Health Organization (WHO) included a chapter on Mental Disorders in its International classification of Diseases (ICD) 6 (1949). It resembled the Standard . In the year 1950, the APA set up a committee on nomenclature and statistics. This committee published the first DSM in the year 1952. [sup][2],[3],[4],[5],[6] The first edition of DSM (1952) was titled 'Diagnostic and Statistical Manual of Mental Disorders'. It did not carry any number attached to its title. Authors of the manual had perhaps not envisaged that the manual would be revised periodically. The second edition (1968) was titled Diagnostic and Statistical Manual of Mental Disorders, Second Edition. The trend of fixing a roman suffix to the newer editions of the DSM commenced with the third edition which was titled DSM III (1980). DSM III also pioneered the multiaxial system of evaluation and classification of mental disorders. A revised version was christened DSM III R (1987). The trend continued while publishing the DSM IV (1994) and its text revised edition the DSM IV TR (2000). [sup][2],[3],[4],[5],[6] The most recent edition of the DSM was initially labeled DSM V. As the process of developing the manual progressed, the Roman numerical 'V' was replaced by the alpha numerical '5'. This would facilitate subsequent revisions being numbered as 5.1, 5.2 and so forth. While facilitating the numbering, it is also a tacit acceptance that the DSM 5 is not the ultimate manual of classification of mental disorders. It is a document that reflects current consensus of the leading academicians, clinicians, and researchers in the field of mental health. [sup][5],[6],[7] Methodology By the year 1999, even as the DSM IV TR was being published, clinicians and researchers had noticed several flaws in the DSM IV. The DSM IV TR (2000) did not propose any substantial modifications to the doctrine of DSM IV (1994). The diagnostic criteria continued to result in rather frequent diagnosis of comorbidity. Heterogeneity within the diagnostic groups was unacceptable to the researchers and it contaminated treatment outcome. The erratic thresholds for inclusion and exclusion could not differentiate the normal from abnormal or syndromal from subsyndromal disorders. …

535 – The clinical spectrum of neurosyphilis today

Introduction Neurosyphilis is a complication of syphilis, due to invasion into the central nervous system of Treponema pallidum, subspecies pallidus. Although neurosyphilis may remain asymptomatic, symptoms can develop at any time after initial infection. Early forms include syphilitic meningitis, meningovasculitis and ocular disease. Dementia paralytica, or “general paralysis of the insane”, and tabes dorsalis used to be the most frequent forms of late neurosyphilis. Several reports, however, suggest a changing clinical presentation of neurosyphilis. Atypical neuropsychiatric syndromes seem to be more prevalent than in the past. Inadvertent treatment with antibiotics prescribed for unrelated diseases and improved serological methods are probably the most important contributing factors. Accelerated progression from syphilis to neurosyphilis in HIV seropositive patients has also been reported. Objectives This prospective study aims to investigate the clinical spectrum of neurosyphilis in patients whose cerebrospinal fluid was tested positive for neurosyphilis by the Laboratory for Infectious Diseases, a large reference laboratory in the North-East part of the Netherlands. Methods From 2004 to 2013 all patients with a new diagnosis of neurosyphilis, proven by cerebrospinal fluid serology, were included. Each patient’s clinical record was reviewed for demographic, clinical and laboratory data. Results Our inclusion criteria were met by 24 patients, all male. The clinical spectrum ranged from asymptomatic to dementia paralytica. Age varied from 31 to 71. At the time of neurosyfilis diagnosis, 7 patients were HIV seropositive. Conclusions Further analysis is currently being done and definite results and conclusions will be presented at the meeting.

Chronic or late lyme neuroborreliosis: analysis of evidence compared to chronic or late neurosyphilis.

Whether spirochetes persist in affected host tissues and cause the late/chronic manifestations of neurosyphilis was the subject of long-lasting debate. Detection of Treponema pallidum in the brains of patients with general paresis established a direct link between persisting infection and tertiary manifestations of neurosyphilis. Today, the same question is in the center of debate with respect to Lyme disease. The goal of this review was to compare the established pathological features of neurosyphilis with those available for Lyme neuroborreliosis. If the main tertiary forms of neurosyphilis also occur in Lyme neuroborreliosis and Borrelia burgdorferi can be detected in brain lesions would indicate that the spirochete is responsible for the neuropsychiatric manifestations of late/chronic Lyme neuroborreliosis. The substantial amounts of data available in the literature show that the major forms of late/chronic Lyme neuroborreliosis (meningovascular and meningoencephalitis) are clinically and pathologically confirmed. Borrelia burgdorferi was detected in association with tertiary brain lesions and cultivated from the affected brain or cerebrospinal fluid. The accumulated data also indicate that Borrelia burgdorferi is able to evade from destruction by the host immune reactions, persist in host tissues and sustain chronic infection and inflammation. These observations represent evidences that Borrelia burgdorferi in an analogous way to Treponema pallidum is responsible for the chronic/late manifestations of Lyme neuroborreliosis.Late Lyme neuroborreliosis is accepted by all existing guidelines in Europe, US and Canada. The terms chronic and late are synonymous and both define tertiary neurosyphilis or tertiary Lyme neuroborreliosis. The use of chronic and late Lyme neuroborreliosis as different entities is inaccurate and can be confusing. Further pathological investigations and the detection of spirochetes in infected tissues and body fluids are strongly needed.

The great pox

How many physicians have seen a patient with tabes dorsalis or an Argyll Robertson pupil? In the 1960s, they turned up in the MRCP examinations but it was always a surprise to see a new patient with neurosyphilis in the clinic. I remember the last one in whom I, working as a registrar in that era, made the diagnosis. He had worked for decades in West Africa and his ataxia and high-stepping gait, which he had attributed to old age, was quite distinctive. Some time before I saw him, I met a man with general paralysis of the insane (GPI). Indeed, I met several. My father used to take me, a schoolboy, to see his patients on the tropical diseases ward on Saturday mornings, presumably to give my mother respite. It was the early 1950s and penicillin was not widely available in the new NHS. This man was friendly and very talkative; he believed that he was a wireless and invited me to tune him in by turning knobs that he said were on his arm. He then produced an imitation of the home, light or third programmes. The story has a happy ending. He responded well and went home to his sweetie …

Making Sense of Pain: Delusions, Syphilis, and Somatic Pain in London County Council Asylums, c. 1900

During the late nineteenth century, a high percentage of male deaths in asylums was attributed to various forms of tertiary syphilis, most notably General Paralysis of the Insane (GPI) and tabes dorsalis. It was not unusual for patients to present symptoms of both conditions, the latter of which could be agonizingly painful. Some patients also suffered from persecutory delusions, believing that electricity was running through them or that their limbs were gnawed by lions and wolves at night. Drawing on a theory advanced by a number of key alienists and pathologists of the period, I suggest that these delusions were misinterpretations of felt sensations and, as such, illusions rather than delusions. Despite the well-known problems around using these historical sources, I contend that recorded delusions in asylum case notes can be treated as narratives of pain that provide invaluable insights into patients' subjective experiences.

Cadaver Brains and Excesses in Baccho and Venere: Dementia Paralytica in Dutch Psychiatry (1870-1920)

This article explores the approach of dementia paralytica by psychiatrists in the Netherlands between 1870 and 1920 against the background of international developments. The psychiatric interpretation of this mental and neurological disorder varied depending on the institutional and social context in which it was examined, treated, and discussed by physicians. Psychiatric diagnoses and understandings of this disease had in part a social-cultural basis and can be best explained against the backdrop of the establishment of psychiatry as a medical specialty and the specific efforts of Dutch psychiatrists to expand their professional domain. After addressing dementia paralytica as a disease and why it drew so much attention in the late nineteenth and early twentieth century, this essay discusses how psychiatrists understood dementia paralytica in asylum practice in terms of diagnosis, care, and treatment. Next we consider their pathological-anatomical study of the physical causes of the disease and the public debate on its prevalence and causes.

Vivid Visual Hallucinations Manifested as the Initial Symptom in a Patient with Neurosyphilis

Late neurosyphilis tends to affect the brain and spinal cord parenchyma, typically presenting as dementia, tabes dorsalis, general paresis, sensory ataxia, or bowel/ bladder dysfunction. We present a case of neurosyphilis with manifestations of vivid visual hallucinations as the initial symptom. Only later did the patient develop agitation, auditory hallucinations, and monopolizing conversation. In patients with neurosyphilis, auditory hallucinations are common, but visual hallucinations have rarely been reported.

The most deadly disease of asylumdom: general paralysis of the insane and Scottish psychiatry, c.1840–1940

General paralysis of the insane (GPI) was one of the most devastating diseases observed in British psychiatry during the century after 1840, in terms of the high number and type of patients diagnosed, the severity of its symptoms and, above all, its utterly hopeless prognosis. With particular reference to the physicians and patients of the Royal Edinburgh Asylum, this article explores the diagnostic process and the social and medical significance of the 'death sentence' that accompanied the GPI diagnosis.