Abstract: paraneoplastic limbic encephalitis (PLE) is clinical form of paraneoplastic neurological syndrome, an autoimmune disorder of the central nevrous system. The incidence of PLE is about 3 cases per 1,000 patients with cancer. PLE is characterized by acute or subacute development of memory disorders, symptomatic epilepsy, psychiatric disorders. The authors present the current data on the pathogenesis, clinical presentation, diagnosis, and treatment of PLE, a clinical case of symptomatic epilepsy in the 38-year-old man with PLE associated with testicular cancer.

Paraneoplastic cerebellar degeneration (PCD) is a rare form of the paraneoplastic neurological syndrome (PNS). PCD is an autoimmune disease of the central nervous system (CNS) affecting the Purkinje cells and possibly other cells of the cerebellum. PCD is characterized by a rapid onset resulting in disability for a few days or weeks; a slow progredient increase in cerebellar symptomatology is observed less often. PCD develops in 1–3% of cancer patients; its fraction accounts for 25% of all forms of PNS. The mean incidence rate of PCD is about 2 cases per 1,000 cancer patients. PCD develops in patients with cancer of the ovary, uterus and fallopian tubes, with small cell lung cancer and Hodgkin's lymphoma. The incidence rate among females is 3 times higher than that among males. Females aged 50–65 years are most likely to suffer from PCD. PCDs are divided into four main subgroups that differ in terms of prognosis and range of associated antineuronal antibodies. In the last decade, different classes of anti-onconeuronal antibodies associated with PCD have been described; 9 of them have been best studied. Anti-Yo and anti-Hu antibodies are most frequently detected upon PCD. PCD can be also diagnosed without anti-onconeuronal antibodies associated with it or their titer in the blood can be low. Differential diagnosis of PCD is complex and is conducted for a wide range of CNS diseases. No single approach to treating PCD currently exists. Surgical removal of the tumor, the source of production of anti-onconeuronal antigens, followed by radiotherapy and/or chemotherapy, does not solve the problem completely, but may reduce severity of the clinical manifestations of PCD or stabilize the pathological process. This explains the need for rapid and profound search for a tumor in patients suspected with PCD. The authors described a clinical case of an acute debut of PCD in 47-year-old female, 6 months after which, the patient was diagnosed with breast cancer. The problems of PCD diagnosis by neurologists are discussed. The importance of the interdisciplinary approach to diagnosis and follow-up monitoring of patients with this nosology is noted.

Paraneoplastic cerebellar degeneration (PCD) is a rare form of the paraneoplastic neurological syndrome (PNS). PCD is an autoimmune disease of the central nervous system (CNS) affecting the Purkinje cells and possibly other cells of the cerebellum. PCD is characterized by a rapid onset resulting in disability for a few days or weeks; a slow progredient increase in cerebellar symptomatology is observed less often. PCD develops in 1–3% of cancer patients; its fraction accounts for 25% of all forms of PNS. The mean incidence rate of PCD is about 2 cases per 1,000 cancer patients. PCD develops in patients with cancer of the ovary, uterus and fallopian tubes, with small cell lung cancer and Hodgkin's lymphoma. The incidence rate among females is 3 times higher than that among males. Females aged 50–65 years are most likely to suffer from PCD. PCDs are divided into four main subgroups that differ in terms of prognosis and range of associated antineuronal antibodies. In the last decade, different classes of anti-onconeuronal antibodies associated with PCD have been described; 9 of them have been best studied. Anti-Yo and anti-Hu antibodies are most frequently detected upon PCD. PCD can be also diagnosed without anti-onconeuronal antibodies associated with it or their titer in the blood can be low. Differential diagnosis of PCD is complex and is conducted for a wide range of CNS diseases. No single approach to treating PCD currently exists. Surgical removal of the tumor, the source of production of anti-onconeuronal antigens, followed by radiotherapy and/or chemotherapy, does not solve the problem completely, but may reduce severity of the clinical manifestations of PCD or stabilize the pathological process. This explains the need for rapid and profound search for a tumor in patients suspected with PCD. The authors described a clinical case of an acute debut of PCD in 47-year-old female, 6 months after which, the patient was diagnosed with breast cancer. The problems of PCD diagnosis by neurologists are discussed. The importance of the interdisciplinary approach to diagnosis and follow-up monitoring of patients with this nosology is noted.

Paraneoplastic limbic encephalitis is a rare disorder characterized by personality changes, irritability, depression, seizures, memory loss and sometimes dementia. The diagnosis is difficult. Clinical symptoms are often lacking, and symptoms usually mimic other brain pathology. Early recognition of paraneoplastic limbic encephalitis and prompt intervention with immune therapies will probably translate into more favorable neurological outcomes.

Paraneoplastic limbic encephalitis (PLE) is clinical form of paraneoplastic neurological syndrome, an autoimmune disorder of the central nevrous system. The incidence of PLE is about 3 cases per 1,000 patients with cancer. PLE is characterized by acute or subacute development of memory disorders, symptomatic epilepsy, psychiatric disorders. The authors present the current data on the pathogenesis, clinical presentation, diagnosis, and treatment of PLE, a clinical case of symptomatic epilepsy in the 38-year-old man with PLE associated with testicular cancer.

The literature review is devoted to the problems of the incidence of thoracic cancer and paraneoplastic syndrome (PNS) associated with thoracic cancer. The most common PNS manifestations in thoracic cancer are: Lambert-Eaton myastenic syndrome, paraneoplastic cerebellar degeneration, paraneoplastic encephalomyelitis, opsoclonus-myoclonus syndrome, paraneoplastic retinopathy, syndrome of rigid man syndrome, paraneoplastic subacute sensory neuropathy, dermatomyositis, neuromyotonia and chronic gastrointestinal pseudoobstruction.

The review presents data on the role of tumor antigens and antionconeural antibodies in the development of paraneoplastic neurological syndrome.

The review presents data on the role of tumor antigens and antionconeural antibodies in the development of paraneoplastic neurological syndrome.