Cerebellar degeneration associated with a remote neoplasm. Clinical manifestations include progressive limb and GAIT ATAXIA; DYSARTHRIA; and NYSTAGMUS, PATHOLOGIC. The histologic type of the associated neoplasm is usually carcinoma or lymphoma. Pathologically the cerebellar cortex and subcortical nuclei demonstrate diffuse degenerative changes. Anti-Purkinje cell antibodies (anti-Yo) are found in the serum of approximately 50% of affected individuals. (Adams et al., Principles of Neurology, 6th ed, p686)
In patients with neoplastic diseases a wide variety of clinical pictures which are indirect and usually remote effects produced by tumor cell metabolites or other products.
Diseases that affect the structure or function of the cerebellum. Cardinal manifestations of cerebellar dysfunction include dysmetria, GAIT ATAXIA, and MUSCLE HYPOTONIA.
Degenerative or inflammatory conditions affecting the central or peripheral nervous system that develop in association with a systemic neoplasm without direct invasion by tumor. They may be associated with circulating antibodies that react with the affected neural tissue. (Intern Med 1996 Dec;35(12):925-9)
An autoimmune disease characterized by weakness and fatigability of proximal muscles, particularly of the pelvic girdle, lower extremities, trunk, and shoulder girdle. There is relative sparing of extraocular and bulbar muscles. CARCINOMA, SMALL CELL of the lung is a frequently associated condition, although other malignancies and autoimmune diseases may be associated. Muscular weakness results from impaired impulse transmission at the NEUROMUSCULAR JUNCTION. Presynaptic calcium channel dysfunction leads to a reduced amount of acetylcholine being released in response to stimulation of the nerve. (From Adams et al., Principles of Neurology, 6th ed, pp 1471)
Incoordination of voluntary movements that occur as a manifestation of CEREBELLAR DISEASES. Characteristic features include a tendency for limb movements to overshoot or undershoot a target (dysmetria), a tremor that occurs during attempted movements (intention TREMOR), impaired force and rhythm of diadochokinesis (rapidly alternating movements), and GAIT ATAXIA. (From Adams et al., Principles of Neurology, 6th ed, p90)
A heterogenous group of degenerative syndromes marked by progressive cerebellar dysfunction either in isolation or combined with other neurologic manifestations. Sporadic and inherited subtypes occur. Inheritance patterns include autosomal dominant, autosomal recessive, and X-linked.
Endoscopes used for examining the interior of the stomach.
The output neurons of the cerebellar cortex.
The part of brain that lies behind the BRAIN STEM in the posterior base of skull (CRANIAL FOSSA, POSTERIOR). It is also known as the "little brain" with convolutions similar to those of CEREBRAL CORTEX, inner white matter, and deep cerebellar nuclei. Its function is to coordinate voluntary movements, maintain balance, and learn motor skills.
A diffuse or multifocal peripheral neuropathy related to the remote effects of a neoplasm, most often carcinoma or lymphoma. Pathologically, there are inflammatory changes in peripheral nerves. The most common clinical presentation is a symmetric distal mixed sensorimotor polyneuropathy. (Adams et al., Principles of Neurology, 6th ed, p1334)
Loss of functional activity and trophic degeneration of nerve axons and their terminal arborizations following the destruction of their cells of origin or interruption of their continuity with these cells. The pathology is characteristic of neurodegenerative diseases. Often the process of nerve degeneration is studied in research on neuroanatomical localization and correlation of the neurophysiology of neural pathways.
Antibodies that react with self-antigens (AUTOANTIGENS) of the organism that produced them.
'Nerve tissue proteins' are specialized proteins found within the nervous system's biological tissue, including neurofilaments, neuronal cytoskeletal proteins, and neural cell adhesion molecules, which facilitate structural support, intracellular communication, and synaptic connectivity essential for proper neurological function.
Endogenous tissue constituents that have the ability to interact with AUTOANTIBODIES and cause an immune response.
An anaplastic, highly malignant, and usually bronchogenic carcinoma composed of small ovoid cells with scanty neoplasm. It is characterized by a dominant, deeply basophilic nucleus, and absent or indistinct nucleoli. (From Stedman, 25th ed; Holland et al., Cancer Medicine, 3d ed, p1286-7)
A paraneoplastic syndrome marked by degeneration of neurons in the LIMBIC SYSTEM. Clinical features include HALLUCINATIONS, loss of EPISODIC MEMORY; ANOSMIA; AGEUSIA; TEMPORAL LOBE EPILEPSY; DEMENTIA; and affective disturbance (depression). Circulating anti-neuronal antibodies (e.g., anti-Hu; anti-Yo; anti-Ri; and anti-Ma2) and small cell lung carcinomas or testicular carcinoma are frequently associated with this syndrome.
Tumors or cancer of the LUNG.
A condition marked by progressive CEREBELLAR ATAXIA combined with MYOCLONUS usually presenting in the third decade of life or later. Additional clinical features may include generalized and focal SEIZURES, spasticity, and DYSKINESIAS. Autosomal recessive and autosomal dominant patterns of inheritance have been reported. Pathologically, the dentate nucleus and brachium conjunctivum of the CEREBELLUM are atrophic, with variable involvement of the spinal cord, cerebellar cortex, and basal ganglia. (From Joynt, Clinical Neurology, 1991, Ch37, pp60-1)
Ocular manifestations secondary to various NEOPLASMS in which antibodies to antigens of the primary tumor cross-react with ocular antigens. This autoimmune response often leads to visual loss and other ocular dysfunctions.
Impairment of the ability to perform smoothly coordinated voluntary movements. This condition may affect the limbs, trunk, eyes, pharynx, larynx, and other structures. Ataxia may result from impaired sensory or motor function. Sensory ataxia may result from posterior column injury or PERIPHERAL NERVE DISEASES. Motor ataxia may be associated with CEREBELLAR DISEASES; CEREBRAL CORTEX diseases; THALAMIC DISEASES; BASAL GANGLIA DISEASES; injury to the RED NUCLEUS; and other conditions.
An autosomal recessive inherited disorder characterized by choreoathetosis beginning in childhood, progressive CEREBELLAR ATAXIA; TELANGIECTASIS of CONJUNCTIVA and SKIN; DYSARTHRIA; B- and T-cell immunodeficiency, and RADIOSENSITIVITY to IONIZING RADIATION. Affected individuals are prone to recurrent sinobronchopulmonary infections, lymphoreticular neoplasms, and other malignancies. Serum ALPHA-FETOPROTEINS are usually elevated. (Menkes, Textbook of Child Neurology, 5th ed, p688) The gene for this disorder (ATM) encodes a cell cycle checkpoint protein kinase and has been mapped to chromosome 11 (11q22-q23).
A retrogressive pathological change in the retina, focal or generalized, caused by genetic defects, inflammation, trauma, vascular disease, or aging. Degeneration affecting predominantly the macula lutea of the retina is MACULAR DEGENERATION. (Newell, Ophthalmology: Principles and Concepts, 7th ed, p304)
Degenerative changes in the RETINA usually of older adults which results in a loss of vision in the center of the visual field (the MACULA LUTEA) because of damage to the retina. It occurs in dry and wet forms.

Cdr2, a target antigen of naturally occuring human tumor immunity, is widely expressed in gynecological tumors. (1/27)

The paraneoplastic neurological disorders provide perhaps the best known example of naturally occurring tumor immunity in humans. For example, patients with paraneoplastic cerebellar degeneration (PCD) appear to suppress the growth of occult breast or ovarian tumors that express a neuronal antigen termed cdr2. PCD patients harbor cdr2-specific CTLs in their peripheral blood, and these cells are likely mediators of the tumor suppression. Whereas cdr2 therefore appears to be the target of an effective immune response in patients with PCD, the general relevance to cancer patients has been unclear, due in part to reports indicating that cdr2 is not expressed in tumors obtained from neurologically normal patients. We have reexamined this question, and we find that cdr2 is widely expressed in such tumors, indicating that cdr2 is in fact an important tumor antigen in the general population of breast and ovarian cancer patients.  (+info)

A case of paraneoplastic syndrome accompanied by two types of cancer. (2/27)

A case of paraneoplastic syndrome accompanied by two types of cancer is reported. The patient was a 62 year old man who progressively developed cerebellar ataxia, especially an abnormal gait. The anti-Hu antibody titre was high. A small tumour was detected in the middle lobe of the right lung and was surgically treated. The histology was adenocarcinoma. After lobectomy, however, the ataxia deteriorated, and plasma exchange, 250 ml/kg/day, was conducted for 6 days. After plasma exchange, the anti-Hu antibody titre decreased and the ataxia temporarily ceased to progress. A week after the last plasma exchange, a mass appeared in the anterior cervical region and rapidly increased in size. The biopsy of the neck tumour disclosed a small cell carcinoma. Five months later small cell carcinoma appeared in the left lung. This case shows the importance of searching for small cell carcinoma when anti-Hu antibodies are detected. It is assumed that plasma exchange removed not only a pathogenic factor of ataxia but also a factor which inhibited the growth of the small cell carcinoma. It is recommended that plasmapheresis should be performed with caution in paraneoplastic syndrome when the origin of a tumour is obscure.  (+info)

The immunopathogenesis of paraneoplastic neurological syndromes. (3/27)

Paraneoplastic neurological syndromes are rare non-metastatic complications of cancer that have an immune-mediated aetiology. The central and peripheral nervous systems are considered to be immune-privileged sites, since the presence of the 'blood-brain/nerve barrier' means that antigens sequestered within the nervous system do not normally induce an immune response. Aberrant expression of a neuronal antigen by a tumour arising outside this barrier can lead to the breakdown of immune tolerance to the nervous system. However, in many cases the immune mechanisms that result in neurological dysfunction remain poorly defined. Furthermore, aberrant expression of neuronal antigens can be detected in many tumours that are not complicated by non-metastatic neurological syndromes. This review article examines current concepts in the immunopathogenesis of paraneoplastic neurological syndromes.  (+info)

Paraneoplastic cerebellar degeneration associated with antineuronal antibodies: analysis of 50 patients. (4/27)

Paraneoplastic cerebellar degeneration (PCD) is a heterogeneous group of disorders characterized by subacute cerebellar ataxia, specific tumour types and (often) associated antineuronal antibodies. Nine specific antineuronal antibodies are associated with PCD. We examined the relative frequency of the antineuronal antibodies associated with PCD and compared the neurological symptoms and signs, associated tumours, disability and survival between groups of PCD with different antibodies. Also, we attempted to identify patient-, tumour- and treatment-related characteristics associated with functional outcome and survival. In a 12-year period, we examined >5000 samples for the presence of antineuronal antibodies. A total of 137 patients were identified with a paraneoplastic neurological syndrome and high titre (> or =400) antineuronal antibodies. Fifty (36%) of these patients had antibody-associated PCD, including 19 anti-Yo, 16 anti-Hu, seven anti-Tr, six anti-Ri and two anti-mGluR1. Because of the low number, the anti-mGluR1 patients were excluded from the statistical analysis. While 100% of patients with anti-Yo, anti-Tr and anti-mGluR1 antibodies suffered PCD, 86% of anti-Ri and only 18% of anti-Hu patients had PCD. All patients presented with subacute cerebellar ataxia progressive over weeks to months and stabilized within 6 months. The majority of patients in all antibody groups had both truncal and appendicular ataxia. The frequency of nystagmus and dysarthria was lower in anti-Ri patients (33 and 0%). Later in the course of the disease, involvement of non-cerebellar structures occurred most frequently in anti-Hu patients (94%). In 42 patients (84%), a tumour was detected. The most commonly associated tumours were gynaecological and breast cancer (anti-Yo and anti-Ri), lung cancer (anti-Hu) and Hodgkin's lymphoma (anti-Tr and anti-mGluR1). In one anti-Hu patient, a suspect lung lesion on CT scan disappeared while the PCD evolved. Seven patients improved by at least 1 point on the Rankin scale, while 16 remained stable and 27 deteriorated. All seven patients that improved received antitumour treatment for their underlying cancer, resulting in complete remission. The functional outcome was best in the anti-Ri patients, with three out of six improving neurologically and five were able to walk at the time of last follow-up or death. Only four out of 19 anti-Yo and four out of 16 anti-Hu patients remained ambulatory. Also, survival from time of diagnosis was significantly worse in the anti-Yo (median 13 months) and anti-Hu (median 7 months) patients compared with anti-Tr (median >113 months) and anti-Ri (median >69 months). Patients receiving antitumour treatment (with or without immunosuppressive therapy) lived significantly longer [hazard ratio (HR) 0.3; 95% confidence interval (CI) 0.1-0.6; P = 0.004]. Patients > or =60 years old lived somewhat shorter from time of diagnosis, although statistically not significant (HR 2.9; CI 1.0-8.5; P = 0.06).  (+info)

Acute onset paraneoplastic cerebellar degeneration in a patient with small cell lung cancer. (5/27)

A patient with small cell lung cancer presented with a rare presentation of an acute onset pancerebellar dysfunction. His clinical condition markedly improved following the surgical removal of the tumor and chemo- and radiotherapy.  (+info)

Anti-Yo antibody-mediated paraneoplastic cerebellar degeneration in a man with esophageal adenocarcinoma. (6/27)

We report a case of paraneoplastic cerebellar degeneration (PCD) associated with adenocarcinoma of the esophagus and anti-Yo antibodies in a male patient. The patient presented with progressive ataxia, dysarthria, and significant weight loss. Extensive work-up suggested paraneoplastic neurologic syndrome. A wide search for a cancer was undertaken and a small mass was identified in the distal esophagus on upper endoscopy. Biopsies of this lesion revealed well-differentiated invasive adenocarcinoma of the esophagus. The endoscopic ultrasound staged the tumor as T3N1M0. Despite trials of multiple therapeutic modalities, the patient's cerebellar dysfunction progressed. This is only the second report of PCD caused by esophageal adenocarcinoma and the fourth report of anti-Yo antibodies occurring in a male patient.  (+info)

Paraneoplastic cerebellar degeneration (PCD) associated with squamous cell carcinoma of the lung. (7/27)

We report a case of a 71-year-old man who presented with cerebellar dysfunction. He was diagnosed as having squamous cell carcinoma of the lung (T2N3M0, Stage IIIB). No anti-onconeural antibodies were found in his serum. Cerebral spinal fluid (CSF) examination showed mild mononuclear pleocytosis alone. Magnetic resonance imaging (MRI) of the brain and spinal cord revealed no abnormalities. At autopsy, there was complete disappearance of Purkinje cells with reactive astrocytosis. These findings are compatible with paraneoplastic cerebellar degeneration (PCD). To our knowledge, no case of PCD has been reported previously in patients with squamous cell carcinoma of the lung.  (+info)

A pre-senile case of limbic encephalitis and cerebellar degeneration, with subacute onset of progressive dementia. (8/27)

In case a pre-senile patient presented subacutely progressive dementia, secondary dementia, such as paraneoplastic neurological syndrome (PNS), hypothyroidism, confusion, early phase of primary degenerative dementia and prion diseases are to be considered. It is a case of pathologically confirmed, and clinico-pathologically assessed limbic encephalitis with cerebellar degeneration. The patient was a 63-year old male, with a well followed up medical history of gastric cancer 8 years earlier. Four weeks after he presented himself at our hospital his memory and disorientation progressively declined. A neurological examination revealed gaze nystagmus, with potential secondary dementia. However, no abnormal findings were detected from systemic radiological examination, or from chemical analyses. Two months later, after the onset of the disease, he presented additional symptoms, including seizure, gait disturbance, and insomnia. On admission, neurological examinations revealed gaze nystagmus and progression of dementia; however, his thought process was relatively preserved. No paroxysmal synchronized discharge was seen on electroencephalogram. Chest X-rays showed an inflammatory infiltration. In spite of anti-biotic medication, he died due to respiratory failure. The autopsy was limited to the brain. Histologically, limited lymphocytic infiltration into the hippocampus through the entorhinal cortex, with marked neuronal loss and gliosis was observed. Neuronophagia, microglial nodules, and perivascular lymphocytic infiltration were also seen. Additionally, most of the Purkinje cells in the cerebellum were lost, with Bergmann's gliosis and sparse lymphocytic infiltration. No tumor was observed in the brain. Pathological findings of the brain were compatible with paraneoplastic limbic encephalitis and cerebellar degeneration, though no neoplasm, clinically or pathologically, was detected in this patient. Consequently, it is suggested that when a senile patient presents sub-acute onset of progressive dementia, with a variety of neurological symptoms, paraneoplastic syndrome is to be taken into consideration, even if a tumor or an auto-antibody is not detected since the resection of the tumor is still the best therapeutic means. Otherwise immuno-suppressive and steroid therapies should be used.  (+info)

Paraneoplastic cerebellar degeneration (PCD) is a rare disorder characterized by progressive damage to the cerebellum, the part of the brain responsible for coordinating muscle movements. It is considered a paraneoplastic syndrome, which means it is caused by an abnormal immune system response to a cancerous tumor (neoplasm) located elsewhere in the body.

In PCD, antibodies produced by the immune system to fight the tumor mistakenly attack proteins in the cerebellum that are similar to those found in the tumor. This leads to inflammation and degeneration of the Purkinje cells, a type of neuron critical for maintaining balance and coordinating movements.

PCD can present with symptoms such as unsteady gait, loss of coordination, slurred speech, nystagmus (involuntary eye movement), and tremors. These symptoms often develop rapidly, over the course of days to weeks, and may progress even after the tumor has been removed or treated.

PCD is associated with several types of cancers, including small cell lung cancer, breast cancer, ovarian cancer, Hodgkin's lymphoma, and others. Early diagnosis and treatment of the underlying cancer are essential to slowing down the progression of PCD and improving outcomes.

Paraneoplastic syndromes refer to a group of rare disorders that are caused by an abnormal immune system response to a cancerous (malignant) tumor. These syndromes are characterized by symptoms or signs that do not result directly from the growth of the tumor itself, but rather from substances produced by the tumor or the body's immune system in response to the tumor.

Paraneoplastic syndromes can affect various organs and systems in the body, including the nervous system, endocrine system, skin, and joints. Examples of paraneoplastic syndromes include Lambert-Eaton myasthenic syndrome (LEMS), which affects nerve function and causes muscle weakness; cerebellar degeneration, which can cause difficulty with coordination and balance; and dermatomyositis, which is an inflammatory condition that affects the skin and muscles.

Paraneoplastic syndromes can occur in association with a variety of different types of cancer, including lung cancer, breast cancer, ovarian cancer, and lymphoma. Treatment typically involves addressing the underlying cancer, as well as managing the symptoms of the paraneoplastic syndrome.

Cerebellar diseases refer to a group of medical conditions that affect the cerebellum, which is the part of the brain located at the back of the head, below the occipital lobe and above the brainstem. The cerebellum plays a crucial role in motor control, coordination, balance, and some cognitive functions.

Cerebellar diseases can be caused by various factors, including genetics, infections, tumors, stroke, trauma, or degenerative processes. These conditions can result in a wide range of symptoms, such as:

1. Ataxia: Loss of coordination and unsteady gait
2. Dysmetria: Inability to judge distance and force while performing movements
3. Intention tremors: Shaking or trembling that worsens during purposeful movements
4. Nystagmus: Rapid, involuntary eye movement
5. Dysarthria: Speech difficulty due to muscle weakness or incoordination
6. Hypotonia: Decreased muscle tone
7. Titubation: Rhythmic, involuntary oscillations of the head and neck
8. Cognitive impairment: Problems with memory, attention, and executive functions

Some examples of cerebellar diseases include:

1. Ataxia-telangiectasia
2. Friedrich's ataxia
3. Multiple system atrophy (MSA)
4. Spinocerebellar ataxias (SCAs)
5. Cerebellar tumors, such as medulloblastomas or astrocytomas
6. Infarctions or hemorrhages in the cerebellum due to stroke or trauma
7. Infections, such as viral encephalitis or bacterial meningitis
8. Autoimmune disorders, like multiple sclerosis (MS) or paraneoplastic syndromes
9. Metabolic disorders, such as Wilson's disease or phenylketonuria (PKU)
10. Chronic alcoholism and withdrawal

Treatment for cerebellar diseases depends on the underlying cause and may involve medications, physical therapy, surgery, or supportive care to manage symptoms and improve quality of life.

Paraneoplastic syndromes of the nervous system are a group of rare disorders that occur in some individuals with cancer. These syndromes are caused by an immune system response to the cancer tumor, which can lead to the damage or destruction of nerve cells. The immune system produces antibodies and/or activated immune cells that attack the neural tissue, leading to neurological symptoms.

Paraneoplastic syndromes can affect any part of the nervous system, including the brain, spinal cord, peripheral nerves, and muscles. Symptoms vary depending on the specific syndrome and the location of the affected nerve tissue. Some common neurological symptoms include muscle weakness, numbness or tingling, seizures, memory loss, confusion, difficulty speaking or swallowing, visual disturbances, and coordination problems.

Paraneoplastic syndromes are often associated with specific types of cancer, such as small cell lung cancer, breast cancer, ovarian cancer, and lymphoma. Diagnosis can be challenging because the symptoms may precede the discovery of the underlying cancer. A combination of clinical evaluation, imaging studies, laboratory tests, and sometimes a brain biopsy may be necessary to confirm the diagnosis.

Treatment typically involves addressing the underlying cancer with surgery, chemotherapy, or radiation therapy. Immunosuppressive therapies may also be used to manage the immune response that is causing the neurological symptoms. While treatment can help alleviate symptoms and improve quality of life, paraneoplastic syndromes are often difficult to cure completely.

Lambert-Eaton Myasthenic Syndrome (LEMS) is a rare autoimmune disorder characterized by muscle weakness and fatigability. It is caused by the presence of antibodies against voltage-gated calcium channels (VGCC) in the neuromuscular junction, which disrupts the normal transmission of signals between nerves and muscles.

The symptoms of LEMS include proximal muscle weakness, which may affect the legs more than the arms, and autonomic dysfunction such as dry mouth and constipation. The weakness tends to improve with exercise but worsens after periods of rest. In some cases, LEMS can be associated with cancer, particularly small cell lung cancer.

Diagnosis of LEMS typically involves a combination of clinical evaluation, electromyography (EMG) studies, and blood tests to detect VGCC antibodies. Treatment may include medications such as pyridostigmine, which improves neuromuscular transmission, or intravenous immunoglobulin and plasma exchange, which help to reduce the immune response. In cases where LEMS is associated with cancer, treatment of the underlying malignancy can also improve muscle strength and function.

Cerebellar ataxia is a type of ataxia, which refers to a group of disorders that cause difficulties with coordination and movement. Cerebellar ataxia specifically involves the cerebellum, which is the part of the brain responsible for maintaining balance, coordinating muscle movements, and regulating speech and eye movements.

The symptoms of cerebellar ataxia may include:

* Unsteady gait or difficulty walking
* Poor coordination of limb movements
* Tremors or shakiness, especially in the hands
* Slurred or irregular speech
* Abnormal eye movements, such as nystagmus (rapid, involuntary movement of the eyes)
* Difficulty with fine motor tasks, such as writing or buttoning a shirt

Cerebellar ataxia can be caused by a variety of underlying conditions, including:

* Genetic disorders, such as spinocerebellar ataxia or Friedreich's ataxia
* Brain injury or trauma
* Stroke or brain hemorrhage
* Infections, such as meningitis or encephalitis
* Exposure to toxins, such as alcohol or certain medications
* Tumors or other growths in the brain

Treatment for cerebellar ataxia depends on the underlying cause. In some cases, there may be no cure, and treatment is focused on managing symptoms and improving quality of life. Physical therapy, occupational therapy, and speech therapy can help improve coordination, balance, and communication skills. Medications may also be used to treat specific symptoms, such as tremors or muscle spasticity. In some cases, surgery may be recommended to remove tumors or repair damage to the brain.

Spinocerebellar degenerations (SCDs) are a group of genetic disorders that primarily affect the cerebellum, the part of the brain responsible for coordinating muscle movements, and the spinal cord. These conditions are characterized by progressive degeneration or loss of nerve cells in the cerebellum and/or spinal cord, leading to various neurological symptoms.

SCDs are often inherited in an autosomal dominant manner, meaning that only one copy of the altered gene from either parent is enough to cause the disorder. The most common type of SCD is spinocerebellar ataxia (SCA), which includes several subtypes (SCA1, SCA2, SCA3, etc.) differentiated by their genetic causes and specific clinical features.

Symptoms of spinocerebellar degenerations may include:

1. Progressive ataxia (loss of coordination and balance)
2. Dysarthria (speech difficulty)
3. Nystagmus (involuntary eye movements)
4. Oculomotor abnormalities (problems with eye movement control)
5. Tremors or other involuntary muscle movements
6. Muscle weakness and spasticity
7. Sensory disturbances, such as numbness or tingling sensations
8. Dysphagia (difficulty swallowing)
9. Cognitive impairment in some cases

The age of onset, severity, and progression of symptoms can vary significantly among different SCD subtypes and individuals. Currently, there is no cure for spinocerebellar degenerations, but various supportive treatments and therapies can help manage symptoms and improve quality of life.

A gastroscope is a type of endoscope that is used to examine the inside of the stomach. It is a long, thin, flexible tube with a light and camera at the end, which allows doctors to view the lining of the stomach in detail on a screen. Gastroscopes are commonly used to diagnose and monitor conditions such as gastritis, ulcers, and stomach cancer. They can also be used to take tissue samples for biopsy or to perform certain treatments, such as removing polyps or cauterizing bleeding vessels.

Purkinje cells are a type of neuron located in the cerebellar cortex, which is the outer layer of the cerebellum, a part of the brain that plays a crucial role in motor control and coordination. These cells have large branching dendrites and receive input from many other neurons, particularly granule cells. The axons of Purkinje cells form the principal output pathway of the cerebellar cortex, synapsing with deep cerebellar nuclei. They are named after Johannes Evangelista Purkinje, a Czech physiologist who first described them in 1837.

The cerebellum is a part of the brain that lies behind the brainstem and is involved in the regulation of motor movements, balance, and coordination. It contains two hemispheres and a central portion called the vermis. The cerebellum receives input from sensory systems and other areas of the brain and spinal cord and sends output to motor areas of the brain. Damage to the cerebellum can result in problems with movement, balance, and coordination.

Paraneoplastic polyneuropathy is a rare neurological disorder that can occur in some individuals with cancer. It's caused by the immune system producing antibodies or cells that attack the nervous system (neurons, nerve axons, or myelin sheath) as a response to the presence of a tumor or cancer in the body.

The term "polyneuropathy" refers to damage or dysfunction affecting multiple peripheral nerves simultaneously. This can lead to various symptoms such as numbness, tingling, muscle weakness, and pain, typically starting in the hands and feet and progressing upwards.

In paraneoplastic polyneuropathy, these symptoms are related to the immune system's response to the cancer rather than direct invasion of the nerves by the tumor itself. The specific type of polyneuropathy can vary between individuals, and it may present as sensorimotor polyneuropathy, autonomic neuropathy, or a combination of both.

Early diagnosis and treatment of the underlying cancer are crucial for managing paraneoplastic polyneuropathy. Immunotherapy, plasma exchange, and intravenous immunoglobulin may be used to help control the immune response and alleviate symptoms.

Nerve degeneration, also known as neurodegeneration, is the progressive loss of structure and function of neurons, which can lead to cognitive decline, motor impairment, and various other symptoms. This process occurs due to a variety of factors, including genetics, environmental influences, and aging. It is a key feature in several neurological disorders such as Alzheimer's disease, Parkinson's disease, Huntington's disease, and multiple sclerosis. The degeneration can affect any part of the nervous system, leading to different symptoms depending on the location and extent of the damage.

Autoantibodies are defined as antibodies that are produced by the immune system and target the body's own cells, tissues, or organs. These antibodies mistakenly identify certain proteins or molecules in the body as foreign invaders and attack them, leading to an autoimmune response. Autoantibodies can be found in various autoimmune diseases such as rheumatoid arthritis, lupus, and thyroiditis. The presence of autoantibodies can also be used as a diagnostic marker for certain conditions.

Nerve tissue proteins are specialized proteins found in the nervous system that provide structural and functional support to nerve cells, also known as neurons. These proteins include:

1. Neurofilaments: These are type IV intermediate filaments that provide structural support to neurons and help maintain their shape and size. They are composed of three subunits - NFL (light), NFM (medium), and NFH (heavy).

2. Neuronal Cytoskeletal Proteins: These include tubulins, actins, and spectrins that provide structural support to the neuronal cytoskeleton and help maintain its integrity.

3. Neurotransmitter Receptors: These are specialized proteins located on the postsynaptic membrane of neurons that bind neurotransmitters released by presynaptic neurons, triggering a response in the target cell.

4. Ion Channels: These are transmembrane proteins that regulate the flow of ions across the neuronal membrane and play a crucial role in generating and transmitting electrical signals in neurons.

5. Signaling Proteins: These include enzymes, receptors, and adaptor proteins that mediate intracellular signaling pathways involved in neuronal development, differentiation, survival, and death.

6. Adhesion Proteins: These are cell surface proteins that mediate cell-cell and cell-matrix interactions, playing a crucial role in the formation and maintenance of neural circuits.

7. Extracellular Matrix Proteins: These include proteoglycans, laminins, and collagens that provide structural support to nerve tissue and regulate neuronal migration, differentiation, and survival.

Autoantigens are substances that are typically found in an individual's own body, but can stimulate an immune response because they are recognized as foreign by the body's own immune system. In autoimmune diseases, the immune system mistakenly attacks and damages healthy tissues and organs because it recognizes some of their components as autoantigens. These autoantigens can be proteins, DNA, or other molecules that are normally present in the body but have become altered or exposed due to various factors such as infection, genetics, or environmental triggers. The immune system then produces antibodies and activates immune cells to attack these autoantigens, leading to tissue damage and inflammation.

Carcinoma, small cell is a type of lung cancer that typically starts in the bronchi (the airways that lead to the lungs). It is called "small cell" because the cancer cells are small and appear round or oval in shape. This type of lung cancer is also sometimes referred to as "oat cell carcinoma" due to the distinctive appearance of the cells, which can resemble oats when viewed under a microscope.

Small cell carcinoma is a particularly aggressive form of lung cancer that tends to spread quickly to other parts of the body. It is strongly associated with smoking and is less common than non-small cell lung cancer (NSCLC), which accounts for about 85% of all lung cancers.

Like other types of lung cancer, small cell carcinoma may not cause any symptoms in its early stages. However, as the tumor grows and spreads, it can cause a variety of symptoms, including coughing, chest pain, shortness of breath, hoarseness, and weight loss. Treatment for small cell carcinoma typically involves a combination of chemotherapy, radiation therapy, and sometimes surgery.

Limbic encephalitis is a rare type of inflammatory autoimmune disorder that affects the limbic system, which is a part of the brain involved in emotions, behavior, memory, and sense of smell. It is characterized by inflammation of the limbic system, leading to symptoms such as memory loss, confusion, seizures, changes in behavior and mood, and problems with autonomic functions.

Limbic encephalitis can be caused by a variety of factors, including viral infections, cancer, or autoimmune disorders. In some cases, the cause may remain unknown. Diagnosis typically involves a combination of clinical evaluation, imaging studies (such as MRI), and analysis of cerebrospinal fluid. Treatment usually involves immunosuppressive therapy to reduce inflammation, as well as addressing any underlying causes if they can be identified.

It is important to note that limbic encephalitis is a serious condition that requires prompt medical attention and treatment. If you or someone else experiences symptoms such as sudden confusion, memory loss, or seizures, it is essential to seek medical care immediately.

Lung neoplasms refer to abnormal growths or tumors in the lung tissue. These tumors can be benign (non-cancerous) or malignant (cancerous). Malignant lung neoplasms are further classified into two main types: small cell lung carcinoma and non-small cell lung carcinoma. Lung neoplasms can cause symptoms such as cough, chest pain, shortness of breath, and weight loss. They are often caused by smoking or exposure to secondhand smoke, but can also occur due to genetic factors, radiation exposure, and other environmental carcinogens. Early detection and treatment of lung neoplasms is crucial for improving outcomes and survival rates.

Myoclonic cerebellar dyssynergia is not a widely recognized or formally defined medical term. However, based on its individual components, it can be inferred to refer to a neurological condition characterized by:

1. Myoclonus: These are sudden, involuntary jerking movements of a muscle or group of muscles. They typically occur as a result of hyperexcitability of the neurons in the brain that control movement (motor neurons).
2. Cerebellar: The cerebellum is a part of the brain responsible for coordinating muscle movements, maintaining posture and balance, and fine-tuning motor skills. When a condition is described as "cerebellar," it implies that there is some dysfunction or abnormality in this region of the brain.
3. Dyssynergia: This term refers to a lack of coordination between muscles and muscle groups during voluntary movements. It can result from damage to the cerebellum or other parts of the nervous system involved in motor control.

Therefore, myoclonic cerebellar dyssynergia could be interpreted as a condition characterized by involuntary muscle jerks (myoclonus) and impaired coordination of voluntary movements (dyssynergia), likely due to cerebellar dysfunction. However, it is essential to consult with a medical professional for an accurate diagnosis and treatment plan if you or someone else experiences symptoms that may align with this description.

Paraneoplastic syndromes are a group of rare disorders that occur in some individuals with cancer. These syndromes are caused by substances produced by the tumor or the body's immune response to the tumor, which can affect distant organs and cause various symptoms.

Ocular paraneoplastic syndromes refer to a subset of these disorders that specifically affect the eyes. They are caused by an abnormal immune response directed against antigens shared by both the tumor and the nervous tissue of the eye. This results in damage to the nerve cells and can lead to various visual symptoms, such as:

1. Visual loss or blurring
2. Double vision (diplopia)
3. Light sensitivity (photophobia)
4. Abnormalities in pupil size or reactivity
5. Jerky eye movements (nystagmus)
6. Loss of peripheral vision (visual field defects)
7. Impaired color vision
8. Deterioration of the optic nerve (optic neuropathy)

Some examples of ocular paraneoplastic syndromes include:

1. Paraneoplastic retinopathy: A condition characterized by damage to the light-sensitive cells in the retina, leading to visual loss and other visual disturbances.
2. Paraneoplastic optic neuropathy: Damage to the optic nerve that can result in visual loss and visual field defects.
3. Cancer-associated retinopathy (CAR): A condition characterized by progressive vision loss, night blindness, and abnormalities in the electroretinogram (ERG), a test used to assess retinal function.
4. Melanoma-associated retinopathy (MAR): Similar to CAR but specifically associated with melanoma, this condition can cause visual loss, night blindness, and abnormal ERG results.
5. Opsoclonus-myoclonus syndrome: A rare disorder characterized by rapid, involuntary eye movements (opsoclonus) and muscle jerks (myoclonus), which can be associated with various types of cancer, including breast, lung, and ovarian cancer.

It is important to note that these conditions are relatively rare but can significantly impact a patient's quality of life. Early diagnosis and treatment of the underlying cancer can help improve outcomes for patients with ocular paraneoplastic syndromes.

Ataxia is a medical term that refers to a group of disorders affecting coordination, balance, and speech. It is characterized by a lack of muscle control during voluntary movements, causing unsteady or awkward movements, and often accompanied by tremors. Ataxia can affect various parts of the body, such as the limbs, trunk, eyes, and speech muscles. The condition can be congenital or acquired, and it can result from damage to the cerebellum, spinal cord, or sensory nerves. There are several types of ataxia, including hereditary ataxias, degenerative ataxias, cerebellar ataxias, and acquired ataxias, each with its own specific causes, symptoms, and prognosis. Treatment for ataxia typically focuses on managing symptoms and improving quality of life, as there is no cure for most forms of the disorder.

Ataxia telangiectasia is a rare, inherited genetic disorder that affects the nervous system, immune system, and overall development. The condition is characterized by progressive difficulty with coordination and balance (ataxia), as well as the development of small, dilated blood vessels (telangiectasias) on the skin and eyes.

The underlying cause of ataxia telangiectasia is a mutation in the ATM gene, which provides instructions for making a protein that plays a critical role in DNA repair and maintaining genetic stability. When this gene is mutated, cells are unable to properly repair damaged DNA, leading to an increased risk of cancer and other health problems.

Individuals with ataxia telangiectasia typically begin to show symptoms during early childhood, with progressive difficulties in coordination and balance, slurred speech, and recurrent respiratory infections due to weakened immune function. Over time, these symptoms can worsen, leading to significant disability and reduced life expectancy.

There is currently no cure for ataxia telangiectasia, and treatment is focused on managing the symptoms and complications of the condition. This may include physical therapy, speech therapy, and medications to help control infections and other health problems.

Retinal degeneration is a broad term that refers to the progressive loss of photoreceptor cells (rods and cones) in the retina, which are responsible for converting light into electrical signals that are sent to the brain. This process can lead to vision loss or blindness. There are many different types of retinal degeneration, including age-related macular degeneration, retinitis pigmentosa, and Stargardt's disease, among others. These conditions can have varying causes, such as genetic mutations, environmental factors, or a combination of both. Treatment options vary depending on the specific type and progression of the condition.

Macular degeneration, also known as age-related macular degeneration (AMD), is a medical condition that affects the central part of the retina, called the macula. The macula is responsible for sharp, detailed vision, which is necessary for activities such as reading, driving, and recognizing faces.

In AMD, there is a breakdown or deterioration of the macula, leading to gradual loss of central vision. There are two main types of AMD: dry (atrophic) and wet (exudative). Dry AMD is more common and progresses more slowly, while wet AMD is less common but can cause rapid and severe vision loss if left untreated.

The exact causes of AMD are not fully understood, but risk factors include age, smoking, family history, high blood pressure, obesity, and exposure to sunlight. While there is no cure for AMD, treatments such as vitamin supplements, laser therapy, and medication injections can help slow its progression and reduce the risk of vision loss.

No FAQ available that match "paraneoplastic cerebellar degeneration"

No images available that match "paraneoplastic cerebellar degeneration"