“<i>Hirnsymptome bei Carcinomatose</i>” — Hermann Oppenheim and an Early Description of a Paraneoplastic Neurological Syndrome

Schulz, Paulina; Prüß, Harald

doi:10.1080/0964704x.2015.1021120

Cited by 14 publications

(5 citation statements)

References 5 publications

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“…The concept that patients with cancer could develop syndromes of neurological injury in the absence of tumor metastasis or direct spread—conditions that are now termed “paraneoplastic neurological syndromes”—was introduced by Oppenheim in 1888, who reported the occurrence of central nervous system symptoms in a patient with uterine cancer in whom no evidence of tumor metastasis in the brain could be found at autopsy ( 6 , 7 ). Around the same time, in 1890, M. Auché described peripheral nervous system symptoms in cancer patients ( 8 ).…”

Section: Paraneoplastic Neurological Disease and The Discovery Of Antineuronal Antibodiesmentioning

confidence: 99%

Paraneoplastic and Other Autoimmune Encephalitides: Antineuronal Antibodies, T Lymphocytes, and Questions of Pathogenesis

et al. 2022

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Autoimmune and paraneoplastic encephalitides represent an increasingly recognized cause of devastating human illness as well as an emerging area of neurological injury associated with immune checkpoint inhibitors. Two groups of antibodies have been detected in affected patients. Antibodies in the first group are directed against neuronal cell surface membrane proteins and are exemplified by antibodies directed against the N-methyl-D-aspartate receptor (anti-NMDAR), found in patients with autoimmune encephalitis, and antibodies directed against the leucine-rich glioma-inactivated 1 protein (anti-LGI1), associated with faciobrachial dystonic seizures and limbic encephalitis. Antibodies in this group produce non-lethal neuronal dysfunction, and their associated conditions often respond to treatment. Antibodies in the second group, as exemplified by anti-Yo antibody, found in patients with rapidly progressive cerebellar syndrome, and anti-Hu antibody, associated with encephalomyelitis, react with intracellular neuronal antigens. These antibodies are characteristically found in patients with underlying malignancy, and neurological impairment is the result of neuronal death. Within the last few years, major advances have been made in understanding the pathogenesis of neurological disorders associated with antibodies against neuronal cell surface antigens. In contrast, the events that lead to neuronal death in conditions associated with antibodies directed against intracellular antigens, such as anti-Yo and anti-Hu, remain poorly understood, and the respective roles of antibodies and T lymphocytes in causing neuronal injury have not been defined in an animal model. In this review, we discuss current knowledge of these two groups of antibodies in terms of their discovery, how they arise, the interaction of both types of antibodies with their molecular targets, and the attempts that have been made to reproduce human neuronal injury in tissue culture models and experimental animals. We then discuss the emerging area of autoimmune neuronal injury associated with immune checkpoint inhibitors and the implications of current research for the treatment of affected patients.

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Section: Paraneoplastic Neurological Disease and The Discovery Of Antineuronal Antibodiesmentioning

confidence: 99%

Paraneoplastic and Other Autoimmune Encephalitides: Antineuronal Antibodies, T Lymphocytes, and Questions of Pathogenesis

et al. 2022

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“…Neuroimmunological researchers suggest (Schulz and Prüss 2015 ) that paraneoplastic autoimmune encephalitis was first described over 130 years ago by the neurologist Oppenheim 1888 (Fig. 1 ).…”

Section: Resultsmentioning

confidence: 99%

Autoimmune encephalitis with psychiatric features in adults: historical evolution and prospective challenge

Hansen

Timäus

2020

J Neural Transm

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Our review aims to delineate the psychiatric spectrum of autoantibody-associated autoimmune encephalitis over time through its discoveries of antibodies. We searched in PubMed for appropriate articles depicting the first appearance and spectrum of psychiatric symptomatology in autoantibody-positive encephalitis for this narrative review. Memory impairment was first associated with autoantibodies against intracellular antigens such as anti-HuD antibodies in 1993. 8 years later, autoantibodies against cell membrane surface antigens such as voltage-gated potassium channels were described in conjunction with memory dysfunction. The spectrum of psychiatric syndromes was amplified between 1990 and 2020 to include disorientation, behavior, cognitive dysfunction, obsessive compulsive behavior and suicidality in encephalitis patients occurring together mainly with antibodies against surface antigens, less so against intracellular antigens. In general, we found no specific psychiatric symptoms underlying specific autoantibody-associated encephalitis. As fundamental data on this issue have not been systemically assessed to date, we cannot know whether our specific findings would remain from systematic studies, i.e., on the association between cerebrospinal fluid N-methyl-D-aspartate receptor antibodies in catatonia. The psychiatric symptomatology overlaps between psychiatric domains and occurs frequently in antibody-positive encephalitis. No specific psychiatric symptoms imply an underlying, specifically autoantibody-associated encephalitis. The psychiatric phenotypology associated with antibody-positive encephalitis has evolved tremendously recently, and this new evidence reveals its relevance for future diagnostic and treatment aspects of autoimmune encephalitis patients.

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“…According to the National Cancer Institute (NCI, Dictionary of Cancer Terms, https://www.cancer.gov/publications/dictionaries/cancer-terms) a paraneoplastic syndrome is defined as follows: "A group of symptoms that may develop when substances released by some cancer cells disrupt the normal function of surrounding cells and tissue". This definition implies that a cancer patient may develop symptoms that are not directly attributable to tumor invasion or compression [23]. Paraneoplastic syndromes may have impact on different organs, such as endocrine, neurologic, hematologic, rheumatologic and dermatologic systems.…”

Section: Potassium In Paraneoplastic Syndromesmentioning

confidence: 99%

Potassium in Solid Cancers

Iorio¹,

Lastraioli²,

Lastraioli³

2022

Physiology

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Electrolyte disorders are a frequent finding in cancer patients. In the majority of cases the etiologies of such disorders are common to all cancer types (i.e. diuretic-induced hyponatremia or hypokalemia). Sometimes, electrolyte disorders are caused by paraneoplastic syndromes or are due to cancer therapy. Potassium is one of the most important electrolytes of the human body since it is involved in the regulation of muscle contraction, maintenance of the integrity of the skeleton, blood pressure and nerve transmission as well as in the normal function of cells. Potassium homeostasis is strictly regulated since the gap between the recommended daily dietary intake (120 mEq/day) and the levels stored in the extracellular fluid (around 70 mEq) is huge. Alterations of potassium homeostasis are frequent in cancer patients as well alterations in potassium channels, the transmembrane proteins that mediate potassium fluxes within the cells. The present chapter is focused on the clinical significance of potassium homeostasis and potassium channels in patients with solid tumors.

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“Hirnsymptome bei Carcinomatose” — Hermann Oppenheim and an Early Description of a Paraneoplastic Neurological Syndrome

Cited by 14 publications

References 5 publications

Paraneoplastic and Other Autoimmune Encephalitides: Antineuronal Antibodies, T Lymphocytes, and Questions of Pathogenesis

Paraneoplastic and Other Autoimmune Encephalitides: Antineuronal Antibodies, T Lymphocytes, and Questions of Pathogenesis

Autoimmune encephalitis with psychiatric features in adults: historical evolution and prospective challenge

Potassium in Solid Cancers

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