Optic Neuritis
Neuritis
Neuritis, Autoimmune, Experimental
Vestibular Neuronitis
Brachial Plexus Neuritis
Neuromyelitis Optica
Multiple Sclerosis
Optic Nerve
Evoked Potentials, Visual
Visual Acuity
Caloric Tests
Scotoma
Aquaporin 4
Retinal Ganglion Cells
Demyelinating Diseases
Vision Disorders
Facial Nerve Diseases
Color Vision Defects
Myelitis, Transverse
Vestibular Diseases
Rats, Inbred Lew
Papilledema
Visual Fields
Tomography, Optical Coherence
Encephalomyelitis, Autoimmune, Experimental
Reflex, Pupillary
Vestibular Nerve
Magnetic Resonance Imaging
Myelin Proteins
Myelin Sheath
Nystagmus, Pathologic
Sciatic Nerve
Nerve Fibers
Optic Atrophy
Myelitis
Myelin-Oligodendrocyte Glycoprotein
Ophthalmology
Neurology
Color Perception
Myelin P2 Protein
Visual Field Tests
Salsola
Vestibular Function Tests
Optic Neuropathy, Ischemic
Color Vision
Polyradiculopathy
Retinal Neurons
Optic Nerve Diseases
Heterogeneity of T-cell receptor usage in experimental autoimmune neuritis in the Lewis rat. (1/58)
In experimental autoimmune neuritis (EAN), T-cell receptor (TCR) variable (V)-region gene usage by neuritogenic T cells has been reported to be clonally restricted at the RNA level. This study was designed to verify TCR usage by neuritogenic T cells at the protein level. We generated two monoclonal antibodies (mAbs) 7H4 and 8G8 specific for a Vbeta4/Valpha11 associated idiotype expressed by the majority of neuritogenic cells of P2-specific T-cell lines. The remaining neuritogenic P2-specific T cells either exhibited a dominant usage of the TCR Vbeta13 chain recognized by the recently generated mAbs 17D5 and 18B1 or showed diverse Vbeta usage. Treatment of adoptive-transfer (AT)-EAN or of EAN actively induced with the neuritogenic P2 peptide by mAbs 7H4 and 8G8 led to a partial, but significant, reduction of clinical disease. Treatment with Vbeta13-specific mAb 17D5 had no clear effect on active EAN. Our data show that at least three different TCR are used by P2-specific pathogenic T cells in EAN, an animal model for human inflammatory neuropathies. (+info)A complementary peptide vaccine that induces T cell anergy and prevents experimental allergic neuritis in Lewis rats. (2/58)
We have developed and described a new method of altering T cell-mediated autoimmune diseases by immunization with the complementary peptide against T cell epitopes. The complementary peptide (denoted NAE 07-06) to the bovine P2 protein, residues 60-70 (denoted EAN 60-70), was tested in the Lewis rat model of experimental allergic neuritis (EAN). Immunization with NAE 07-06 induced polyclonal and monoclonal Abs that inhibited the proliferation of the P2-specific T cell line, stimulated with EAN 60-70, and recognized Vbeta, but not Valpha, of TCRs. Proliferation of T cells treated with anti-NAE 07-06 Abs could be partially restored by treatment with rIL-2, in accordance with an anergy model. A homologous sequence was found between NAE 07-06 and the VDJ junction of the TCR beta-chain from an EAN 60-70-specific T cell line. Rats preimmunized with NAE 07-06 in vivo before EAN induction showed less disease severity clinically and histologically. These data suggest a new therapeutic approach for T cell-mediated autoimmune disorders through the induction of anti-TCR Abs with complementary peptide Ags. (+info)Suppression of chronic experimental autoimmune neuritis by nasally administered recombinant rat interleukin-6. (3/58)
Experimental autoimmune neuritis (EAN) is a CD4+ T-cell-mediated demyelinating disease of the peripheral nervous system (PNS) and serves as experimental model for human immune-demyelinating neurophathies, especially the Guillain-Barre syndrome. In this study, we examined the effect of recombinant rat interleukin-6 (rrIL-6) on chronic EAN in Lewis rats induced by immunization with P2 peptide 57-81 and Freund's complete adjuvant (FCA). Nasal administration of rat rIL-6 (1 microg/rat/day) beginning in the initial phase of EAN as a therapeutic agent, decreased the severity and the duration of clinical EAN. Low-grade inflammation and suppression of regional demyelination within the sciatic nerves were seen in rrIL-6-treated rats. Hyporesponsiveness of lymph node T cells, down-regulation of serum tumour necrosis factor-alpha (TNF-alpha) and increased levels of P2-specific immunoglobulin G1 (IgG1) antibodies document that nasal administration of rrIL-6 was effective systemically. However, because of the non-specific nature of the treatment and multiple effects of IL-6, more experience and great caution are needed, before nasal administration of IL-6 can be considered as a treatment of human autoimmune demyelinating neurophathies. (+info)Transfer of myelin-specific cells deviated in vitro towards IL-4 production ameliorates ongoing experimental allergic neuritis. (4/58)
A causal role of IL-4 (Th2) production for recovery in experimental allergic neuritis (EAN) was indicated by experiments where Th1-like autoreactive cell populations, taken from the induction phase of the disease, were deviated to extensive secretion of IL-4 in a selective fashion, by ex vivo stimulation with autoantigen in the presence of IL-4. The deviated cells were adoptively transferred to EAN rats at a time just prior to the onset of clinical signs. This treatment ameliorated EAN compared with sham treatment. This therapeutic approach, with generation of autoreactive IL-4-secreting cells ex vivo followed by subsequent adoptive transfer, may become a new selective treatment of organ-specific autoimmune diseases since, in contrast to previous attempts, it is done in a physiological and technically easy way. (+info)Suppression of experimental autoimmune neuritis by leflunomide. (5/58)
Leflunomide is a new immunosuppressive drug whose active metabolite, A77 1726, impairs cellular nucleotide metabolism by inhibiting the dihydroorotate dehydrogenase (DHODH), a rate-limiting enzyme of de novo pyrimidine synthesis. Furthermore, A77 1726 suppresses tyrosine kinases involved in signal transduction pathways. We investigated the immunosuppressive effects of leflunomide in experimental autoimmune neuritis (EAN) in rats, which is a model of immune-mediated neuropathies. In EAN that was actively induced by subcutaneous injection of peripheral nerve myelin, leflunomide completely prevented paraparesis if applied orally from the day of immunization. Leflunomide was much more effective than azathioprine, which did not mitigate EAN at all. Even when leflunomide was administered therapeutically after the appearance of the first neuropathical signs, it halted the progression and markedly reduced the severity and duration of EAN. Inflammatory infiltrates, demyelination and axonal degeneration in sciatic nerve sections of leflunomide-treated EAN rats were strongly reduced. Leflunomide-treated rats did not mount autoantibodies as specified by ELISA (enzyme-linked immunosorbent assay) with a mixture of peripheral myelin proteins, including P2 and myelin basic protein. In EAN that was adoptively transferred by injection of neuritogenic cells of a P2-specific T-helper line, application of leflunomide also clearly reduced signs of disease. Additional injection of uridine did not neutralize the effect of leflunomide. Similarly, transfer of neuritogenic P2-specific T cells, which were activated in the presence of A77 1726 plus uridine in vitro, still resulted in reduced severity of adoptive transfer EAN in vivo, although proliferation of these cells in vitro was identical to that of control cells. The T-cell receptor-mediated in vitro activatability of a P2-specific T-cell hybridoma was diminished by high concentrations of A77 1726, as evidenced by reduced Ca(2+) flux into the cytosol. Together with the findings in adoptive transfer EAN, this indicates that the antiproliferative effect is probably not the only mechanism of immunosuppressive action by leflunomide. In summary, leflunomide suppresses EAN efficiently and may constitute a promising therapy for immune-mediated neuropathies. (+info)Vaccination, prevention, and treatment of experimental autoimmune neuritis (EAN) by an oligomerized T cell epitope. (6/58)
Using a polypeptide oligomer harboring 16 repeats of the neuritogenic epitope (aa 58-73) of myelin P2 protein separated by spacers, enhancement of the immune response to the P2 protein, an important neuritogenic autoantigen in experimental autoimmune neuritis (EAN), was attempted. In contrast to a previous study with PLP-16-mer antigen-specific response of T cells was attenuated at all doses examined to a variable degree. Treatment of Lewis rats with the P2-16-mer up to 2 months before immunization with P2(53-78) (vaccination) or after immunization but before appearance of disease (prevention) had a strong tolerizing effect against the induction of EAN on immunization with P2(53-78). Moreover, rats injected with 200 microg of the P2-16-mer i.v. on day 11 after disease induction, at which time the initial signs of disease had appeared, were almost completely protected against progression of clinical disease, whereas animals treated with the same amount of monomeric control peptide developed severe disease (treatment). Similar results were obtained by i.v. treatment of adoptive-transfer EAN with the P2-16-mer. The lack of clinical signs of disease after 16-mer therapy could be correlated with a reduced proliferative response of P2(53-78)-specific lymph node cells. The frequency of apoptotic T cells in sciatic nerve or in lymph node cells, however, was not increased by the 16-mer treatment, suggesting that induction of anergy or other forms of peripheral tolerance may be responsible for the effect. Thus, the oligomerized P2 peptide antigen was highly effective in all three treatment modalities examined in this specific autoreactive T cell-mediated immune response. (+info)Treatment of rats with experimental allergic neuritis using high dose immunoglobulin. (7/58)
OBJECTIVE: To investigate the therapeutic potential of high-dose immunoglobulin (HIG) in experimental allergic neuritis (EAN) to provide a theoretical basis of its clinical use in the treatment of human inflammatory demyelinating neuropathies. METHODS: Female Lewis rats were induced to EAN, and divided into experimental and control groups. The rats were treated with either 0.3 g/kg.day-1 of IgG or an equivalent volume of 0.15 mol/L glycine. Clinical, electrophysiologic, and histologic evaluations were carried out in a blind fashion. RESULTS: Clinically, rats treated with IgG had significantly less severe symptoms (P < 0.001) and slower progression (P < 0.001) than controls. Electrophysiologically, the mean conduction latency of the experimental group was significantly shorter than controls (P < 0.05). Histologically, rats treated with IgG prepared from normal Lewis rats had a significantly lower percentage of demyelinated fibers (P = 0.01) and total abnormal fibers (P < 0.001) than controls. Statistically, clinical, electrophysiologic and morphologic data were all significantly correlated. CONCLUSIONS: The EAN animal model is reliable for observation of HIG effects, and useful to provide data for clinical work. HIG has a significant therapeutic effect in EAN when given soon after disease onset. It can reduce clinical disease severity and decrease the number of demyelinated fibers as well as the number of total abnormal fibers. For the current controversy over whether HIG is effective, the results of this research support the clinical use of HIG in human demyelinating neuropathy. (+info)Experimental autoimmune autonomic neuropathy. (8/58)
Antibodies specific for the neuronal ganglionic nicotinic acetylcholine receptor (nAChR) are found in high titer in serum of patients with subacute autonomic failure. This clinical disorder is known as autoimmune autonomic neuropathy (AAN). Rabbits immunized with a neuronal nAChR alpha3 subunit fusion protein produce ganglionic nAChR antibodies and develop autonomic failure (experimental AAN, or EAAN). We used quantitative measures of autonomic function to demonstrate that this animal model of neuronal nAChR autoimmunity recapitulates the cardinal autonomic features of AAN in humans. The severity of dysautonomia in the rabbit ranges from isolated cardiovagal impairment to severe panautonomic failure with fixed mydriasis, gastroparesis, dry eyes, impaired heart rate variability, hypotension, and low plasma catecholamines. The severity of autonomic failure correlates with serum antibody levels. Immunohistochemical staining of superior cervical ganglia and myenteric plexus neurons demonstrates intact presynaptic nerve terminals and intact postsynaptic neurons containing cytoplasmic nAChR, but lacking surface nAChR. These findings define the autonomic physiology and histopathology of this novel animal model and support the concept that AAN in humans is a disorder of ganglionic cholinergic synaptic transmission caused by ganglionic nAChR antibodies. (+info)Optic neuritis is a medical condition characterized by inflammation and damage to the optic nerve, which transmits visual information from the eye to the brain. This condition can result in various symptoms such as vision loss, pain with eye movement, color vision disturbances, and pupillary abnormalities. Optic neuritis may occur in isolation or be associated with other underlying medical conditions, including multiple sclerosis, neuromyelitis optica, and autoimmune disorders. The diagnosis typically involves a comprehensive eye examination, including visual acuity testing, dilated funduscopic examination, and possibly imaging studies like MRI to evaluate the optic nerve and brain. Treatment options may include corticosteroids or other immunomodulatory therapies to reduce inflammation and prevent further damage to the optic nerve.
Neuritis is a general term that refers to inflammation of a nerve or nerves, often causing pain, loss of function, and/or sensory changes. It can affect any part of the nervous system, including the peripheral nerves (those outside the brain and spinal cord) or the cranial nerves (those that serve the head and neck). Neuritis may result from various causes, such as infections, autoimmune disorders, trauma, toxins, or metabolic conditions. The specific symptoms and treatment depend on the underlying cause and the affected nerve(s).
I'm sorry for any confusion, but "Autoimmune Experimental Neuritis" is not a widely recognized medical term or diagnosis. It seems that this term might be referring to a specific experimental model used in research to study autoimmune neuritis.
Neuritis generally refers to inflammation of a nerve or nerves, which can cause symptoms such as pain, tingling, numbness, or weakness. Autoimmune neuritis is a condition where the immune system mistakenly attacks the peripheral nerves, leading to these symptoms.
In research settings, an "experimental" model refers to a controlled study in a laboratory setting, often using animals, to investigate a particular medical condition or test new treatments. Therefore, "Autoimmune Experimental Neuritis" might refer to a specific animal model used to study the mechanisms and potential treatments of autoimmune neuritis.
However, without more context, it's difficult to provide a precise definition. If you have more information about where you encountered this term or its intended meaning, I would be happy to help further!
Vestibular neuronitis, also known as vestibular neuritis, is a medical condition that affects the inner ear's vestibular system. It is characterized by sudden and severe vertigo (a spinning sensation), nausea, vomiting, and unsteadiness, typically lasting for several days to weeks.
The condition results from an inflammation of the vestibular nerve, which carries information about balance and motion from the inner ear to the brain. The exact cause of the inflammation is not always clear, but it is thought to be due to a viral infection or an autoimmune response.
Vestibular neuronitis is differentiated from labyrinthitis, another inner ear disorder, by the absence of hearing loss in vestibular neuronitis. In labyrinthitis, there may be hearing loss as well as vertigo and balance problems. Treatment for vestibular neuronitis typically involves medication to manage symptoms such as nausea and vertigo, along with physical therapy exercises to help retrain the brain to maintain balance.
Brachial plexus neuritis, also known as Parsonage-Turner syndrome or neuralgic amyotrophy, is a medical condition characterized by inflammation and damage to the brachial plexus. The brachial plexus is a network of nerves that originates from the spinal cord in the neck and travels down the arm, controlling movement and sensation in the shoulder, arm, and hand.
In Brachial plexus neuritis, the insulating covering of the nerves (myelin sheath) is damaged or destroyed, leading to impaired nerve function. The exact cause of this condition is not fully understood, but it can be associated with viral infections, trauma, surgery, or immunological disorders.
Symptoms of Brachial plexus neuritis may include sudden onset of severe pain in the shoulder and arm, followed by weakness or paralysis of the affected muscles. There may also be numbness, tingling, or loss of sensation in the affected areas. In some cases, recovery can occur spontaneously within a few months, while others may experience persistent weakness or disability. Treatment typically involves pain management, physical therapy, and in some cases, corticosteroids or other medications to reduce inflammation.
Neuromyelitis optica (NMO), also known as Devic's disease, is an autoimmune disorder that affects the central nervous system (CNS). It primarily causes inflammation and damage to the optic nerves (which transmit visual signals from the eye to the brain) and the spinal cord. This results in optic neuritis (inflammation of the optic nerve, causing vision loss) and myelitis (inflammation of the spinal cord, leading to motor, sensory, and autonomic dysfunction).
A key feature of NMO is the presence of autoantibodies against aquaporin-4 (AQP4-IgG), a water channel protein found in astrocytes (a type of glial cell) in the CNS. These antibodies play a crucial role in the development of the disease, as they target and damage the AQP4 proteins, leading to inflammation, demyelination (loss of the protective myelin sheath around nerve fibers), and subsequent neurological dysfunction.
NMO is distinct from multiple sclerosis (MS), another autoimmune disorder affecting the CNS, as it has different clinical features, radiological findings, and treatment responses. However, NMO can sometimes be misdiagnosed as MS due to overlapping symptoms in some cases. Accurate diagnosis of NMO is essential for appropriate management and treatment, which often includes immunosuppressive therapies to control the autoimmune response and prevent further damage to the nervous system.
Multiple Sclerosis (MS) is a chronic autoimmune disease that affects the central nervous system (CNS), which includes the brain, spinal cord, and optic nerves. In MS, the immune system mistakenly attacks the protective covering of nerve fibers, called myelin, leading to damage and scarring (sclerosis). This results in disrupted communication between the brain and the rest of the body, causing a variety of neurological symptoms that can vary widely from person to person.
The term "multiple" refers to the numerous areas of scarring that occur throughout the CNS in this condition. The progression, severity, and specific symptoms of MS are unpredictable and may include vision problems, muscle weakness, numbness or tingling, difficulty with balance and coordination, cognitive impairment, and mood changes. There is currently no cure for MS, but various treatments can help manage symptoms, modify the course of the disease, and improve quality of life for those affected.
The optic nerve, also known as the second cranial nerve, is the nerve that transmits visual information from the retina to the brain. It is composed of approximately one million nerve fibers that carry signals related to vision, such as light intensity and color, from the eye's photoreceptor cells (rods and cones) to the visual cortex in the brain. The optic nerve is responsible for carrying this visual information so that it can be processed and interpreted by the brain, allowing us to see and perceive our surroundings. Damage to the optic nerve can result in vision loss or impairment.
Evoked potentials, visual, also known as visually evoked potentials (VEPs), are electrical responses recorded from the brain following the presentation of a visual stimulus. These responses are typically measured using electroencephalography (EEG) and can provide information about the functioning of the visual pathways in the brain.
There are several types of VEPs, including pattern-reversal VEPs and flash VEPs. Pattern-reversal VEPs are elicited by presenting alternating checkerboard patterns, while flash VEPs are elicited by flashing a light. The responses are typically analyzed in terms of their latency (the time it takes for the response to occur) and amplitude (the size of the response).
VEPs are often used in clinical settings to help diagnose and monitor conditions that affect the visual system, such as multiple sclerosis, optic neuritis, and brainstem tumors. They can also be used in research to study the neural mechanisms underlying visual perception.
Visual acuity is a measure of the sharpness or clarity of vision. It is usually tested by reading an eye chart from a specific distance, such as 20 feet (6 meters). The standard eye chart used for this purpose is called the Snellen chart, which contains rows of letters that decrease in size as you read down the chart.
Visual acuity is typically expressed as a fraction, with the numerator representing the testing distance and the denominator indicating the smallest line of type that can be read clearly. For example, if a person can read the line on the eye chart that corresponds to a visual acuity of 20/20, it means they have normal vision at 20 feet. If their visual acuity is 20/40, it means they must be as close as 20 feet to see what someone with normal vision can see at 40 feet.
It's important to note that visual acuity is just one aspect of overall vision and does not necessarily reflect other important factors such as peripheral vision, depth perception, color vision, or contrast sensitivity.
Caloric tests are a type of diagnostic test used in otology and neurotology to evaluate the function of the vestibular system, which is responsible for maintaining balance and eye movements. The tests involve stimulating the vestibular system with warm or cool air or water, and then observing and measuring the resulting eye movements.
During the test, the patient sits in a chair with their head tilted back at a 30-degree angle. A special goggles device is placed over their eyes to measure and record eye movements. Then, warm or cool air or water is introduced into each ear canal, alternately, for about 20-30 seconds.
The stimulation of the inner ear with warm or cold temperatures creates a difference in temperature between the inner ear and the brain, which activates the vestibular system and causes eye movements called nystagmus. The direction and intensity of the nystagmus are then analyzed to determine if there is any damage or dysfunction in the vestibular system.
Caloric tests can help identify lesions in the vestibular system, such as vestibular neuritis or labyrinthitis, and can also help differentiate between peripheral and central vestibular disorders.
A scotoma is a blind spot or area of reduced vision within the visual field. It's often surrounded by an area of less distinct vision and can be caused by various conditions such as eye diseases, neurological disorders, or brain injuries. A scotoma may be temporary or permanent, depending on its underlying cause.
There are different types of scotomas, including:
1. Central scotoma - a blind spot in the center of the visual field, often associated with conditions like age-related macular degeneration and diabetic retinopathy.
2. Paracentral scotoma - a blind spot located slightly away from the center of the visual field, which can be caused by optic neuritis or other optic nerve disorders.
3. Peripheral scotoma - a blind spot in the peripheral vision, often associated with retinal diseases like retinitis pigmentosa.
4. Absolute scotoma - a complete loss of vision in a specific area of the visual field.
5. Relative scotoma - a partial loss of vision in which some details can still be perceived, but not as clearly or vividly as in normal vision.
It is essential to consult an eye care professional if you experience any changes in your vision or notice a scotoma, as early detection and treatment can help prevent further vision loss.
Methylprednisolone is a synthetic glucocorticoid drug, which is a class of hormones that naturally occur in the body and are produced by the adrenal gland. It is often used to treat various medical conditions such as inflammation, allergies, and autoimmune disorders. Methylprednisolone works by reducing the activity of the immune system, which helps to reduce symptoms such as swelling, pain, and redness.
Methylprednisolone is available in several forms, including tablets, oral suspension, and injectable solutions. It may be used for short-term or long-term treatment, depending on the condition being treated. Common side effects of methylprednisolone include increased appetite, weight gain, insomnia, mood changes, and increased susceptibility to infections. Long-term use of methylprednisolone can lead to more serious side effects such as osteoporosis, cataracts, and adrenal suppression.
It is important to note that methylprednisolone should be used under the close supervision of a healthcare provider, as it can cause serious side effects if not used properly. The dosage and duration of treatment will depend on various factors such as the patient's age, weight, medical history, and the condition being treated.
Aquaporin 4 (AQP4) is a water channel protein that is primarily found in the membranes of astrocytes, which are a type of glial cell in the central nervous system. AQP4 plays a crucial role in the regulation of water homeostasis and the clearance of excess fluid from the brain and spinal cord. It also facilitates the rapid movement of water across the blood-brain barrier and between astrocytes, which is important for maintaining proper neuronal function and protecting the brain from edema or swelling.
Mutations in the AQP4 gene can lead to various neurological disorders, such as neurodegenerative diseases and neuromyelitis optica spectrum disorder (NMOSD), a severe autoimmune condition that affects the optic nerves and spinal cord. In NMOSD, the immune system mistakenly attacks AQP4 proteins, causing inflammation, demyelination, and damage to the nervous tissue.
Retinal Ganglion Cells (RGCs) are a type of neuron located in the innermost layer of the retina, the light-sensitive tissue at the back of the eye. These cells receive visual information from photoreceptors (rods and cones) via intermediate cells called bipolar cells. RGCs then send this visual information through their long axons to form the optic nerve, which transmits the signals to the brain for processing and interpretation as vision.
There are several types of RGCs, each with distinct morphological and functional characteristics. Some RGCs are specialized in detecting specific features of the visual scene, such as motion, contrast, color, or brightness. The diversity of RGCs allows for a rich and complex representation of the visual world in the brain.
Damage to RGCs can lead to various visual impairments, including loss of vision, reduced visual acuity, and altered visual fields. Conditions associated with RGC damage or degeneration include glaucoma, optic neuritis, ischemic optic neuropathy, and some inherited retinal diseases.
Color perception tests are a type of examination used to evaluate an individual's ability to perceive and distinguish different colors. These tests typically consist of a series of plates or images that contain various patterns or shapes displayed in different colors. The person being tested is then asked to identify or match the colors based on specific instructions.
There are several types of color perception tests, including:
1. Ishihara Test: This is a commonly used test for red-green color deficiency. It consists of a series of plates with circles made up of dots in different sizes and colors. Within these circles, there may be a number or symbol visible only to those with normal color vision or to those with specific types of color blindness.
2. Farnsworth D-15 Test: This test measures an individual's ability to arrange colored caps in a specific order based on their hue. It is often used to diagnose and monitor the progression of color vision deficiencies.
3. Hardy-Rand-Rittler (HRR) Test: This is another type of color arrangement test that measures an individual's ability to distinguish between different colors based on their hue, saturation, and brightness.
4. Color Discrimination Tests: These tests measure an individual's ability to distinguish between two similar colors that are presented side by side or in close proximity.
5. Anomaloscope Test: This is a more sophisticated test that measures the degree of color vision deficiency by asking the person to match the brightness and hue of two lights.
Color perception tests are often used in occupational settings, such as aviation, military, and manufacturing, where color discrimination is critical for safety and performance. They may also be used in educational and clinical settings to diagnose and monitor color vision deficiencies.
Demyelinating diseases are a group of disorders that are characterized by damage to the myelin sheath, which is the protective covering surrounding nerve fibers in the brain, optic nerves, and spinal cord. Myelin is essential for the rapid transmission of nerve impulses, and its damage results in disrupted communication between the brain and other parts of the body.
The most common demyelinating disease is multiple sclerosis (MS), where the immune system mistakenly attacks the myelin sheath. Other demyelinating diseases include:
1. Acute Disseminated Encephalomyelitis (ADEM): An autoimmune disorder that typically follows a viral infection or vaccination, causing widespread inflammation and demyelination in the brain and spinal cord.
2. Neuromyelitis Optica (NMO) or Devic's Disease: A rare autoimmune disorder that primarily affects the optic nerves and spinal cord, leading to severe vision loss and motor disability.
3. Transverse Myelitis: Inflammation of the spinal cord causing damage to both sides of one level (segment) of the spinal cord, resulting in various neurological symptoms such as muscle weakness, numbness, or pain, depending on which part of the spinal cord is affected.
4. Guillain-Barré Syndrome: An autoimmune disorder that causes rapid-onset muscle weakness, often beginning in the legs and spreading to the upper body, including the face and breathing muscles. It occurs when the immune system attacks the peripheral nerves' myelin sheath.
5. Central Pontine Myelinolysis (CPM): A rare neurological disorder caused by rapid shifts in sodium levels in the blood, leading to damage to the myelin sheath in a specific area of the brainstem called the pons.
These diseases can result in various symptoms, such as muscle weakness, numbness, vision loss, difficulty with balance and coordination, and cognitive impairment, depending on the location and extent of the demyelination. Treatment typically focuses on managing symptoms, modifying the immune system's response, and promoting nerve regeneration and remyelination when possible.
Vision disorders refer to a wide range of conditions that affect the visual system and result in various symptoms, such as blurry vision, double vision, distorted vision, impaired depth perception, and difficulty with visual tracking or focusing. These disorders can be categorized into several types, including:
1. Refractive errors: These occur when the shape of the eye prevents light from focusing directly on the retina, resulting in blurry vision. Examples include myopia (nearsightedness), hyperopia (farsightedness), astigmatism, and presbyopia (age-related loss of near vision).
2. Strabismus: Also known as crossed eyes or walleye, strabismus is a misalignment of the eyes where they point in different directions, which can lead to double vision or loss of depth perception.
3. Amblyopia: Often called lazy eye, amblyopia is a condition where one eye has reduced vision due to lack of proper visual development during childhood. It may be caused by strabismus, refractive errors, or other factors that interfere with normal visual development.
4. Accommodative disorders: These involve problems with the focusing ability of the eyes, such as convergence insufficiency (difficulty focusing on close objects) and accommodative dysfunction (inability to maintain clear vision at different distances).
5. Binocular vision disorders: These affect how the eyes work together as a team, leading to issues like poor depth perception, eye strain, and headaches. Examples include convergence insufficiency, divergence excess, and suppression.
6. Ocular motility disorders: These involve problems with eye movement, such as nystagmus (involuntary eye movements), strabismus, or restricted extraocular muscle function.
7. Visual processing disorders: These affect the brain's ability to interpret and make sense of visual information, even when the eyes themselves are healthy. Symptoms may include difficulty with reading, recognizing shapes and objects, and understanding spatial relationships.
8. Low vision: This term refers to significant visual impairment that cannot be fully corrected with glasses, contact lenses, medication, or surgery. It includes conditions like macular degeneration, diabetic retinopathy, glaucoma, and cataracts.
9. Blindness: Complete loss of sight in both eyes, which can be caused by various factors such as injury, disease, or genetic conditions.
Facial nerve diseases refer to a group of medical conditions that affect the function of the facial nerve, also known as the seventh cranial nerve. This nerve is responsible for controlling the muscles of facial expression, and it also carries sensory information from the taste buds in the front two-thirds of the tongue, and regulates saliva flow and tear production.
Facial nerve diseases can cause a variety of symptoms, depending on the specific location and extent of the nerve damage. Common symptoms include:
* Facial weakness or paralysis on one or both sides of the face
* Drooping of the eyelid and corner of the mouth
* Difficulty closing the eye or keeping it closed
* Changes in taste sensation or dryness of the mouth and eyes
* Abnormal sensitivity to sound (hyperacusis)
* Twitching or spasms of the facial muscles
Facial nerve diseases can be caused by a variety of factors, including:
* Infections such as Bell's palsy, Ramsay Hunt syndrome, and Lyme disease
* Trauma or injury to the face or skull
* Tumors that compress or invade the facial nerve
* Neurological conditions such as multiple sclerosis or Guillain-Barre syndrome
* Genetic disorders such as Moebius syndrome or hemifacial microsomia
Treatment for facial nerve diseases depends on the underlying cause and severity of the symptoms. In some cases, medication, physical therapy, or surgery may be necessary to restore function and relieve symptoms.
Color vision defects, also known as color blindness, are conditions in which a person has difficulty distinguishing between certain colors. The most common types of color vision defects involve the inability to distinguish between red and green or blue and yellow. These deficiencies result from an alteration or absence of one or more of the three types of cone cells in the retina that are responsible for normal color vision.
In red-green color vision defects, there is a problem with either the red or green cones, or both. This results in difficulty distinguishing between these two colors and their shades. Protanopia is a type of red-green color vision defect where there is an absence of red cone cells, making it difficult to distinguish between red and green as well as between red and black or green and black. Deuteranopia is another type of red-green color vision defect where there is an absence of green cone cells, resulting in similar difficulties distinguishing between red and green, as well as between blue and yellow.
Blue-yellow color vision defects are less common than red-green color vision defects. Tritanopia is a type of blue-yellow color vision defect where there is an absence of blue cone cells, making it difficult to distinguish between blue and yellow, as well as between blue and purple or yellow and pink.
Color vision defects are usually inherited and present from birth, but they can also result from eye diseases, chemical exposure, aging, or medication side effects. They affect both men and women, although red-green color vision defects are more common in men than in women. People with color vision defects may have difficulty with tasks that require color discrimination, such as matching clothes, selecting ripe fruit, reading colored maps, or identifying warning signals. However, most people with mild to moderate color vision defects can adapt and function well in daily life.
Transverse Myelitis is a neurological disorder that involves inflammation of the spinal cord, leading to damage in both sides of the cord. This results in varying degrees of motor, sensory, and autonomic dysfunction, typically defined by the level of the spine that's affected. Symptoms may include a sudden onset of lower back pain, muscle weakness, paraesthesia or loss of sensation, and bowel/bladder dysfunction. The exact cause is often unknown but can be associated with infections, autoimmune disorders, or other underlying conditions.
Vestibular diseases are a group of disorders that affect the vestibular system, which is responsible for maintaining balance and spatial orientation. The vestibular system includes the inner ear and parts of the brain that process sensory information related to movement and position.
These diseases can cause symptoms such as vertigo (a spinning sensation), dizziness, imbalance, nausea, and visual disturbances. Examples of vestibular diseases include:
1. Benign paroxysmal positional vertigo (BPPV): a condition in which small crystals in the inner ear become dislodged and cause brief episodes of vertigo triggered by changes in head position.
2. Labyrinthitis: an inner ear infection that can cause sudden onset of vertigo, hearing loss, and tinnitus (ringing in the ears).
3. Vestibular neuronitis: inflammation of the vestibular nerve that causes severe vertigo, nausea, and imbalance but typically spares hearing.
4. Meniere's disease: a disorder characterized by recurrent episodes of vertigo, tinnitus, hearing loss, and a feeling of fullness in the affected ear.
5. Vestibular migraine: a type of migraine that includes vestibular symptoms such as dizziness, imbalance, and disorientation.
6. Superior canal dehiscence syndrome: a condition in which there is a thinning or absence of bone over the superior semicircular canal in the inner ear, leading to vertigo, sound- or pressure-induced dizziness, and hearing loss.
7. Bilateral vestibular hypofunction: reduced function of both vestibular systems, causing chronic imbalance, unsteadiness, and visual disturbances.
Treatment for vestibular diseases varies depending on the specific diagnosis but may include medication, physical therapy, surgery, or a combination of these approaches.
I'm happy to help! "Rats, Inbred Lew" is a specific strain of laboratory rats that have been inbred for research purposes. The "Lew" part of the name refers to the location where they were first developed, the Lewis Institute in Lake Bluff, Illinois, USA.
Inbreeding is a process of mating closely related individuals over many generations to create a genetically homogeneous population. This results in a high degree of genetic similarity among members of the strain, making them ideal for use as experimental models because any differences observed between individuals are more likely to be due to the experimental manipulation rather than genetic variation.
Inbred Lew rats have been widely used in biomedical research, particularly in studies related to hypertension and cardiovascular disease. They exhibit a number of unique characteristics that make them useful for these types of studies, including their susceptibility to developing high blood pressure when fed a high-salt diet or given certain drugs.
It's important to note that while inbred strains like Lew rats can be very useful tools for researchers, they are not perfect models for human disease. Because they have been bred in a controlled environment and selected for specific traits, they may not respond to experimental manipulations in the same way that humans or other animals would. Therefore, it's important to interpret findings from these studies with caution and consider multiple lines of evidence before drawing any firm conclusions.
Papilledema is a medical term that refers to swelling of the optic nerve head, also known as the disc, which is the point where the optic nerve enters the back of the eye (the retina). This swelling can be caused by increased pressure within the skull, such as from brain tumors, meningitis, or idiopathic intracranial hypertension. Papilledema is usually detected through a routine eye examination and may be accompanied by symptoms such as headaches, visual disturbances, and nausea. If left untreated, papilledema can lead to permanent vision loss.
Visual fields refer to the total area in which objects can be seen while keeping the eyes focused on a central point. It is the entire area that can be observed using peripheral (side) vision while the eye gazes at a fixed point. A visual field test is used to detect blind spots or gaps (scotomas) in a person's vision, which could indicate various medical conditions such as glaucoma, retinal damage, optic nerve disease, brain tumors, or strokes. The test measures both the central and peripheral vision and maps the entire area that can be seen when focusing on a single point.
Optical coherence tomography (OCT) is a non-invasive imaging technique that uses low-coherence light to capture high-resolution cross-sectional images of biological tissues, particularly the retina and other ocular structures. OCT works by measuring the echo time delay of light scattered back from different depths within the tissue, creating a detailed map of the tissue's structure. This technique is widely used in ophthalmology to diagnose and monitor various eye conditions such as macular degeneration, diabetic retinopathy, and glaucoma.
Autoimmune encephalomyelitis (EAE) is a model of inflammatory demyelinating disease used in medical research to study the mechanisms of multiple sclerosis (MS) and develop new therapies. It is experimentally induced in laboratory animals, typically mice or rats, through immunization with myelin antigens or T-cell transfer. The resulting immune response leads to inflammation, demyelination, and neurological dysfunction in the central nervous system (CNS), mimicking certain aspects of MS.
EAE is a valuable tool for understanding the pathogenesis of MS and testing potential treatments. However, it is essential to recognize that EAE is an experimental model and may not fully recapitulate all features of human autoimmune encephalomyelitis.
A pupillary reflex is a type of reflex that involves the constriction or dilation of the pupils in response to changes in light or near vision. It is mediated by the optic and oculomotor nerves. The pupillary reflex helps regulate the amount of light that enters the eye, improving visual acuity and protecting the retina from excessive light exposure.
In a clinical setting, the pupillary reflex is often assessed as part of a neurological examination. A normal pupillary reflex consists of both direct and consensual responses. The direct response occurs when light is shone into one eye and the pupil of that same eye constricts. The consensual response occurs when light is shone into one eye, causing the pupil of the other eye to also constrict.
Abnormalities in the pupillary reflex can indicate various neurological conditions, such as brainstem injuries or diseases affecting the optic or oculomotor nerves.
The vestibular nerve, also known as the vestibulocochlear nerve or cranial nerve VIII, is a pair of nerves that transmit sensory information from the balance-sensing structures in the inner ear (the utricle, saccule, and semicircular canals) to the brain. This information helps the brain maintain balance and orientation of the head in space. The vestibular nerve also plays a role in hearing by transmitting sound signals from the cochlea to the brain.
Medical Definition:
Magnetic Resonance Imaging (MRI) is a non-invasive diagnostic imaging technique that uses a strong magnetic field and radio waves to create detailed cross-sectional or three-dimensional images of the internal structures of the body. The patient lies within a large, cylindrical magnet, and the scanner detects changes in the direction of the magnetic field caused by protons in the body. These changes are then converted into detailed images that help medical professionals to diagnose and monitor various medical conditions, such as tumors, injuries, or diseases affecting the brain, spinal cord, heart, blood vessels, joints, and other internal organs. MRI does not use radiation like computed tomography (CT) scans.
Myelin proteins are proteins that are found in the myelin sheath, which is a fatty (lipid-rich) substance that surrounds and insulates nerve fibers (axons) in the nervous system. The myelin sheath enables the rapid transmission of electrical signals (nerve impulses) along the axons, allowing for efficient communication between different parts of the nervous system.
There are several types of myelin proteins, including:
1. Proteolipid protein (PLP): This is the most abundant protein in the myelin sheath and plays a crucial role in maintaining the structure and function of the myelin sheath.
2. Myelin basic protein (MBP): This protein is also found in the myelin sheath and helps to stabilize the compact structure of the myelin sheath.
3. Myelin-associated glycoprotein (MAG): This protein is involved in the adhesion of the myelin sheath to the axon and helps to maintain the integrity of the myelin sheath.
4. 2'3'-cyclic nucleotide 3' phosphodiesterase (CNP): This protein is found in oligodendrocytes, which are the cells that produce the myelin sheath in the central nervous system. CNP plays a role in maintaining the structure and function of the oligodendrocytes.
Damage to myelin proteins can lead to demyelination, which is a characteristic feature of several neurological disorders, including multiple sclerosis (MS), Guillain-Barré syndrome, and Charcot-Marie-Tooth disease.
The myelin sheath is a multilayered, fatty substance that surrounds and insulates many nerve fibers in the nervous system. It is essential for the rapid transmission of electrical signals, or nerve impulses, along these nerve fibers, allowing for efficient communication between different parts of the body. The myelin sheath is produced by specialized cells called oligodendrocytes in the central nervous system (CNS) and Schwann cells in the peripheral nervous system (PNS). Damage to the myelin sheath, as seen in conditions like multiple sclerosis, can significantly impair nerve function and result in various neurological symptoms.
Pathological nystagmus is an abnormal, involuntary movement of the eyes that can occur in various directions (horizontal, vertical, or rotatory) and can be rhythmical or arrhythmic. It is typically a result of a disturbance in the vestibular system, central nervous system, or ocular motor pathways. Pathological nystagmus can cause visual symptoms such as blurred vision, difficulty with fixation, and oscillopsia (the sensation that one's surroundings are moving). The type, direction, and intensity of the nystagmus may vary depending on the underlying cause, which can include conditions such as brainstem or cerebellar lesions, multiple sclerosis, drug toxicity, inner ear disorders, and congenital abnormalities.
The sciatic nerve is the largest and longest nerve in the human body, running from the lower back through the buttocks and down the legs to the feet. It is formed by the union of the ventral rami (branches) of the L4 to S3 spinal nerves. The sciatic nerve provides motor and sensory innervation to various muscles and skin areas in the lower limbs, including the hamstrings, calf muscles, and the sole of the foot. Sciatic nerve disorders or injuries can result in symptoms such as pain, numbness, tingling, or weakness in the lower back, hips, legs, and feet, known as sciatica.
An acute disease is a medical condition that has a rapid onset, develops quickly, and tends to be short in duration. Acute diseases can range from minor illnesses such as a common cold or flu, to more severe conditions such as pneumonia, meningitis, or a heart attack. These types of diseases often have clear symptoms that are easy to identify, and they may require immediate medical attention or treatment.
Acute diseases are typically caused by an external agent or factor, such as a bacterial or viral infection, a toxin, or an injury. They can also be the result of a sudden worsening of an existing chronic condition. In general, acute diseases are distinct from chronic diseases, which are long-term medical conditions that develop slowly over time and may require ongoing management and treatment.
Examples of acute diseases include:
* Acute bronchitis: a sudden inflammation of the airways in the lungs, often caused by a viral infection.
* Appendicitis: an inflammation of the appendix that can cause severe pain and requires surgical removal.
* Gastroenteritis: an inflammation of the stomach and intestines, often caused by a viral or bacterial infection.
* Migraine headaches: intense headaches that can last for hours or days, and are often accompanied by nausea, vomiting, and sensitivity to light and sound.
* Myocardial infarction (heart attack): a sudden blockage of blood flow to the heart muscle, often caused by a buildup of plaque in the coronary arteries.
* Pneumonia: an infection of the lungs that can cause coughing, chest pain, and difficulty breathing.
* Sinusitis: an inflammation of the sinuses, often caused by a viral or bacterial infection.
It's important to note that while some acute diseases may resolve on their own with rest and supportive care, others may require medical intervention or treatment to prevent complications and promote recovery. If you are experiencing symptoms of an acute disease, it is always best to seek medical attention to ensure proper diagnosis and treatment.
Nerve fibers are specialized structures that constitute the long, slender processes (axons) of neurons (nerve cells). They are responsible for conducting electrical impulses, known as action potentials, away from the cell body and transmitting them to other neurons or effector organs such as muscles and glands. Nerve fibers are often surrounded by supportive cells called glial cells and are grouped together to form nerve bundles or nerves. These fibers can be myelinated (covered with a fatty insulating sheath called myelin) or unmyelinated, which influences the speed of impulse transmission.
Optic atrophy is a medical term that refers to the degeneration and shrinkage (atrophy) of the optic nerve, which transmits visual information from the eye to the brain. This condition can result in various vision abnormalities, including loss of visual acuity, color vision deficiencies, and peripheral vision loss.
Optic atrophy can occur due to a variety of causes, such as:
* Traumatic injuries to the eye or optic nerve
* Glaucoma
* Optic neuritis (inflammation of the optic nerve)
* Ischemic optic neuropathy (reduced blood flow to the optic nerve)
* Compression or swelling of the optic nerve
* Hereditary or congenital conditions affecting the optic nerve
* Toxins and certain medications that can damage the optic nerve.
The diagnosis of optic atrophy typically involves a comprehensive eye examination, including visual acuity testing, refraction assessment, slit-lamp examination, and dilated funduscopic examination to evaluate the health of the optic nerve. In some cases, additional diagnostic tests such as visual field testing, optical coherence tomography (OCT), or magnetic resonance imaging (MRI) may be necessary to confirm the diagnosis and determine the underlying cause.
There is no specific treatment for optic atrophy, but addressing the underlying cause can help prevent further damage to the optic nerve. In some cases, vision rehabilitation may be recommended to help patients adapt to their visual impairment.
Myelitis is a medical term that refers to inflammation of the spinal cord. This inflammation can cause damage to the myelin sheath, which is the protective covering of nerve fibers in the spinal cord. As a result, the transmission of nerve impulses along the spinal cord may be disrupted, leading to various neurological symptoms.
Myelitis can affect any part of the spinal cord and can have many different causes, including infections (such as viral or bacterial infections), autoimmune disorders (such as multiple sclerosis), and other conditions (such as spinal cord injuries or tumors). The specific symptoms of myelitis depend on the location and severity of the inflammation. They may include muscle weakness, numbness or tingling sensations, pain, bladder or bowel dysfunction, and difficulty with coordination and balance.
Myelitis can be a serious condition that requires prompt medical attention and treatment. Treatment typically focuses on addressing the underlying cause of the inflammation, as well as managing symptoms and supporting recovery.
Myelin-Oligodendrocyte Glycoprotein (MOG) is a protein found exclusively on the outermost layer of myelin sheath in the central nervous system (CNS). The myelin sheath is a fatty substance that surrounds and insulates nerve fibers, allowing for efficient and rapid transmission of electrical signals. MOG plays a crucial role in maintaining the integrity and structure of the myelin sheath. It is involved in the adhesion of oligodendrocytes to the surface of neuronal axons and contributes to the stability of the compact myelin structure. Autoimmune reactions against MOG have been implicated in certain inflammatory demyelinating diseases, such as optic neuritis, transverse myelitis, and acute disseminated encephalomyelitis (ADEM).
Ophthalmology is a branch of medicine that deals with the diagnosis, treatment, and prevention of diseases and disorders of the eye and visual system. It is a surgical specialty, and ophthalmologists are medical doctors who complete additional years of training to become experts in eye care. They are qualified to perform eye exams, diagnose and treat eye diseases, prescribe glasses and contact lenses, and perform eye surgery. Some subspecialties within ophthalmology include cornea and external disease, glaucoma, neuro-ophthalmology, pediatric ophthalmology, retina and vitreous, and oculoplastics.
Neurology is a branch of medicine that deals with the study and treatment of diseases and disorders of the nervous system, which includes the brain, spinal cord, peripheral nerves, muscles, and autonomic nervous system. Neurologists are medical doctors who specialize in this field, diagnosing and treating conditions such as stroke, Alzheimer's disease, epilepsy, Parkinson's disease, multiple sclerosis, and various types of headaches and pain disorders. They use a variety of diagnostic tests, including imaging studies like MRI and CT scans, electrophysiological tests like EEG and EMG, and laboratory tests to evaluate nerve function and identify any underlying conditions or abnormalities. Treatment options may include medication, surgery, rehabilitation, or lifestyle modifications.
Color perception refers to the ability to detect, recognize, and differentiate various colors and color patterns in the visual field. This complex process involves the functioning of both the eyes and the brain.
The eye's retina contains two types of photoreceptor cells called rods and cones. Rods are more sensitive to light and dark changes and help us see in low-light conditions, but they do not contribute much to color vision. Cones, on the other hand, are responsible for color perception and function best in well-lit conditions.
There are three types of cone cells, each sensitive to a particular range of wavelengths corresponding to blue, green, and red colors. The combination of signals from these three types of cones allows us to perceive a wide spectrum of colors.
The brain then interprets these signals and translates them into the perception of different colors and hues. It is important to note that color perception can be influenced by various factors, including cultural background, personal experiences, and even language. Some individuals may also have deficiencies in color perception due to genetic or acquired conditions, such as color blindness or cataracts.
Myelin P2 protein, also known as proteolipid protein 1 (PLP1), is a major structural component of the myelin sheath in the central nervous system. The myelin sheath is a protective and insulating layer that surrounds nerve cell fibers (axons), allowing for efficient and rapid transmission of electrical signals.
The P2 protein is a transmembrane protein, with four transmembrane domains, and it plays a crucial role in maintaining the stability and integrity of the myelin sheath. Mutations in the gene that encodes for this protein (PLP1) have been associated with several demyelinating diseases, including Pelizaeus-Merzbacher disease (PMD), a rare X-linked recessive disorder characterized by abnormalities in the development and maintenance of the myelin sheath.
The P2 protein is also involved in various cellular processes, such as signal transduction, ion transport, and immune response regulation. However, the precise mechanisms through which these functions are carried out remain to be fully elucidated.
Stilbamidines are a class of chemical compounds that are primarily used as veterinary medicines, specifically as parasiticides for the treatment and prevention of ectoparasites such as ticks and lice in livestock animals. Stilbamidines belong to the family of chemicals known as formamidines, which are known to have insecticidal and acaricidal properties.
The most common stilbamidine compound is chlorphentermine, which has been used as an appetite suppressant in human medicine. However, its use as a weight loss drug was discontinued due to its addictive properties and potential for serious side effects.
It's important to note that Stilbamidines are not approved for use in humans and should only be used under the supervision of a veterinarian for the intended purpose of treating and preventing ectoparasites in animals.
A visual field test is a method used to measure an individual's entire scope of vision, which includes what can be seen straight ahead and in peripheral (or side) vision. During the test, the person being tested is asked to focus on a central point while gradually identifying the appearance of objects moving into their peripheral vision. The visual field test helps detect blind spots (scotomas) or gaps in the visual field, which can be caused by various conditions such as glaucoma, brain injury, optic nerve damage, or retinal disorders. It's an essential tool for diagnosing and monitoring eye-related diseases and conditions.
"Salsola" is a term that refers to a genus of plants, rather than a medical concept. The plants in this genus are commonly known as Russell or Prickly Pear cactuses, and they are native to Asia, Africa, and Europe. They are not typically associated with medical definitions or conditions. If you have any questions about a specific medical term or condition, I would be happy to help you with that instead!
Vestibular function tests are a series of diagnostic assessments used to determine the functionality and health of the vestibular system, which is responsible for maintaining balance and spatial orientation. These tests typically include:
1. **Caloric Testing:** This test evaluates the response of each ear to stimulation with warm and cold water or air. The resulting responses are recorded and analyzed to assess the function of the horizontal semicircular canals and the vestibular-ocular reflex (VOR).
2. **Rotary Chair Testing:** This test measures how well the vestibular system adapts to different speeds of rotation. The patient sits in a chair that moves in a controlled, consistent manner while their eye movements are recorded.
3. **Videonystagmography (VNG):** This test uses video goggles to record eye movements in response to various stimuli, such as changes in head position, temperature, and visual environment.
4. **Electronystagmography (ENG):** Similar to VNG, this test records eye movements but uses electrodes placed near the eyes instead of video goggles.
5. **Dix-Hallpike Test:** This is a clinical maneuver used to diagnose benign paroxysmal positional vertigo (BPPV). It involves rapidly moving the patient's head from an upright position to a position where their head is hanging off the end of the examination table.
6. **Head Shaking Test:** This test involves shaking the head back and forth for 15-20 seconds and then observing the patient's eye movements for nystagmus (involuntary eye movement).
These tests help diagnose various vestibular disorders, including benign paroxysmal positional vertigo, labyrinthitis, vestibular neuritis, Meniere's disease, and other balance disorders.
Ischemic optic neuropathy (ION) is a medical condition that refers to the damage or death of the optic nerve due to insufficient blood supply. The optic nerve is responsible for transmitting visual information from the eye to the brain.
In ION, the blood vessels that supply the optic nerve become blocked or narrowed, leading to decreased blood flow and oxygen delivery to the nerve fibers. This results in inflammation, swelling, and ultimately, damage to the optic nerve. The damage can cause sudden, painless vision loss, often noticed upon waking up in the morning.
There are two types of ION: anterior ischemic optic neuropathy (AION) and posterior ischemic optic neuropathy (PION). AION affects the front part of the optic nerve, while PION affects the back part of the nerve. AION is further classified into arteritic and non-arteritic types, depending on whether it is caused by giant cell arteritis or not.
Risk factors for ION include age (most commonly occurring in people over 50), hypertension, diabetes, smoking, sleep apnea, and other cardiovascular diseases. Treatment options depend on the type and cause of ION and may include controlling underlying medical conditions, administering corticosteroids, or undergoing surgical procedures to improve blood flow.
Color vision is the ability to perceive and differentiate colors, which is a result of the way that our eyes and brain process different wavelengths of light. In the eye, there are two types of photoreceptor cells called rods and cones. While rods are more sensitive to low levels of light and help us see in dim conditions, cones are responsible for color vision.
There are three types of cone cells in the human eye, each containing a different type of pigment that is sensitive to specific wavelengths of light. One type of cone cell is most sensitive to short wavelengths (blue light), another is most sensitive to medium wavelengths (green light), and the third is most sensitive to long wavelengths (red light). When light enters the eye, it is absorbed by these pigments in the cones, which then send signals to the brain. The brain interprets these signals and translates them into the perception of color.
People with normal color vision can distinguish between millions of different colors based on the specific combinations of wavelengths that are present in a given scene. However, some people have deficiencies or abnormalities in their color vision, which can make it difficult or impossible to distinguish between certain colors. These conditions are known as color vision deficiencies or color blindness.
Polyradiculopathy is a medical term that refers to a condition affecting multiple nerve roots. It's a type of neurological disorder where there is damage or injury to the nerve roots, which are the beginning portions of nerves as they exit the spinal cord. This damage can result in various symptoms such as weakness, numbness, tingling, and pain in the affected areas of the body, depending on the specific nerves involved.
Polyradiculopathy can be caused by a variety of factors, including trauma, infection, inflammation, compression, or degenerative changes in the spine. Some common causes include spinal cord tumors, herniated discs, spinal stenosis, and autoimmune disorders such as Guillain-Barre syndrome.
Diagnosing polyradiculopathy typically involves a thorough neurological examination, imaging studies such as MRI or CT scans, and sometimes nerve conduction studies or electromyography (EMG) to assess the function of the affected nerves. Treatment for polyradiculopathy depends on the underlying cause but may include medications, physical therapy, surgery, or a combination of these approaches.
Retinal neurons are the specialized nerve cells located in the retina, which is the light-sensitive tissue that lines the inner surface of the eye. The retina converts incoming light into electrical signals, which are then transmitted to the brain and interpreted as visual images. There are several types of retinal neurons, including:
1. Photoreceptors (rods and cones): These are the primary sensory cells that convert light into electrical signals. Rods are responsible for low-light vision, while cones are responsible for color vision and fine detail.
2. Bipolar cells: These neurons receive input from photoreceptors and transmit signals to ganglion cells. They can be either ON or OFF bipolar cells, depending on whether they respond to an increase or decrease in light intensity.
3. Ganglion cells: These are the output neurons of the retina that send visual information to the brain via the optic nerve. There are several types of ganglion cells, including parasol, midget, and small bistratified cells, which have different functions in processing visual information.
4. Horizontal cells: These interneurons connect photoreceptors to each other and help regulate the sensitivity of the retina to light.
5. Amacrine cells: These interneurons connect bipolar cells to ganglion cells and play a role in modulating the signals that are transmitted to the brain.
Overall, retinal neurons work together to process visual information and transmit it to the brain for further analysis and interpretation.
Vision tests are a series of procedures used to assess various aspects of the visual system, including visual acuity, accommodation, convergence, divergence, stereopsis, color vision, and peripheral vision. These tests help healthcare professionals diagnose and manage vision disorders, such as nearsightedness, farsightedness, astigmatism, amblyopia, strabismus, and eye diseases like glaucoma, cataracts, and macular degeneration. Common vision tests include:
1. Visual acuity test (Snellen chart or letter chart): Measures the sharpness of a person's vision at different distances.
2. Refraction test: Determines the correct lens prescription for glasses or contact lenses by assessing how light is bent as it passes through the eye.
3. Color vision test: Evaluates the ability to distinguish between different colors and color combinations, often using pseudoisochromatic plates or Ishihara tests.
4. Stereopsis test: Assesses depth perception and binocular vision by presenting separate images to each eye that, when combined, create a three-dimensional effect.
5. Cover test: Examines eye alignment and the presence of strabismus (crossed eyes or turned eyes) by covering and uncovering each eye while observing eye movements.
6. Ocular motility test: Assesses the ability to move the eyes in various directions and coordinate both eyes during tracking and convergence/divergence movements.
7. Accommodation test: Evaluates the ability to focus on objects at different distances by using lenses, prisms, or dynamic retinoscopy.
8. Pupillary response test: Examines the size and reaction of the pupils to light and near objects.
9. Visual field test: Measures the peripheral (side) vision using automated perimetry or manual confrontation techniques.
10. Slit-lamp examination: Inspects the structures of the front part of the eye, such as the cornea, iris, lens, and anterior chamber, using a specialized microscope.
These tests are typically performed by optometrists, ophthalmologists, or other vision care professionals during routine eye examinations or when visual symptoms are present.
Optic nerve diseases refer to a group of conditions that affect the optic nerve, which transmits visual information from the eye to the brain. These diseases can cause various symptoms such as vision loss, decreased visual acuity, changes in color vision, and visual field defects. Examples of optic nerve diseases include optic neuritis (inflammation of the optic nerve), glaucoma (damage to the optic nerve due to high eye pressure), optic nerve damage from trauma or injury, ischemic optic neuropathy (lack of blood flow to the optic nerve), and optic nerve tumors. Treatment for optic nerve diseases varies depending on the specific condition and may include medications, surgery, or lifestyle changes.
Apolipoprotein E
Abaucin
Acute disseminated encephalomyelitis
Stephen Waxman
Myelin oligodendrocyte glycoprotein
List of MeSH codes (C20)
List of MeSH codes (C10)
Experimental autoimmune encephalomyelitis
Psychoneuroimmunology
Guillain-Barré syndrome
List of MeSH codes (E05)
Corticosteroid
Sudden acquired retinal degeneration syndrome
Vestibular nerve
Anne Haney Cross
MOG antibody disease
Neuromyelitis optica spectrum disorder
Inflammatory demyelinating diseases of the central nervous system
Side effects of cyproterone acetate
Polyneuropathy
Graves' disease
Multiple sclerosis
Neuritis
Anti-AQP4 disease
Collapsin response mediator protein family
Demyelinating disease
Aquaporin-4
Human herpesvirus 6
Pathology of multiple sclerosis
Lyme disease
Enhanced glycolysis contributes to the pathogenesis of experimental autoimmune neuritis | Journal of Neuroinflammation | Full...
Apolipoprotein E - Wikipedia
Innate IFN-γ ameliorates experimental autoimmune encephalomyelitis and promotes myeloid expansion and PDL-1 expression |...
Il5 (interleukin 5) - Rat Genome Database
Research | Department of Ophthalmology / Hu Lab | Stanford Medicine
Guillain‑Barré syndrome associated with Covid‑19: A close relationship or just a coincidence? (Review)
PE Mouse Anti-Rat αβ T-Cell Receptor
Low Endotoxin/Azide Free Anti-Mouse CD19, 6D5 | SouthernBiotech
Frontiers | Emerging Therapeutics for Immune Tolerance: Tolerogenic Vaccines, T cell Therapy, and IL-2 Therapy
Upregulated Retinal Neurofilament Expression in Experimental Optic Neuritis | Lund University Publications
AP Donkey Anti-Goat IgG(H+L), Cross Adsorbed | SouthernBiotech
IL-17A Monoclonal Antibody (eBio17B7), APC (17-7177-81) ...
Factor VII, EPCR, aPC Modulators: novel treatment for neuroinflammation | Journal of Neuroinflammation | Full Text
Mitochondrial damage and "plugging" of transport selectively in myelinated, small-diameter axons are major early events in...
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"Forced-Exercise Dependent Changes in Cellular Immunity: Effects on Exp" by Michael W. Calik
Biomolecules
Anti Rat CD43 Antibody, clone W3/13 | Bio-Rad
Glial pathology and retinal neurotoxicity in the anterior visual pathway in experimental autoimmune encephalomyelitis - List...
Encephalomyelitis17
- The myelin-oligodendrocyte-glycoprotein (MOG) induced experimental autoimmune encephalomyelitis (EAE) model was used to investigate the retinas of Brown Norway rats with (i) visual evoked potentials (VEP) confirmed ON, (ii) VEP confirmed absence of ON and (iii) control animals. (lu.se)
- The animal model experimental autoimmune encephalomyelitis (EAE) has been used extensively in the past to test mechanisms that target peripheral immune cells for treatment of multiple sclerosis (MS). While there have been some notable successes in relapsing MS, the development of therapies for progressive multiple sclerosis (MS) has been hampered by lack of an appropriate animal model. (listlabs.com)
- Here we characterized the transcriptome of the choroid plexus (CP), which is part of the blood-brain barriers (BBBs) and the major site of cerebrospinal fluid production, in the experimental autoimmune encephalomyelitis (EAE) mouse model of MS. In addition, cerebrospinal fluid samples from two cohorts of patients with MS and with optic neuritis (ON) were analyzed to confirm the clinical relevance of the findings. (escholarship.org)
- Inhibition of experimental autoimmune encephalomyelitis by an antibody to the intercellular adhesion molecule ICAM-1. (2medicalcare.com)
- In recent years, oral tolerance induction has been used successfully to prevent a number of experimental autoimmune diseases, including T cell-mediated experimental autoimmune encephalomyelitis, experimental autoimmune neuritis, experimental autoimmune uveitis, arthritis, and diabetes in the nonobese diabetic mouse ( 1 , 2 , 3 ) as well as Ab-mediated experimental autoimmune myasthenia gravis (EAMG) 4 ( 4 , 5 ). (aai.org)
- Mesenchymal stem cells have been demonstrated to ameliorate experimental autoimmune encephalomyelitis (EAE), a model of MS, prompting clinical trials in MS which are currently ongoing. (ms-selfie.blog)
- and non-T cell mediated settings using the MOG35-55 experimental autoimmune encephalomyelitis (EAE) and cuprizone-mediated demyelination models respectively. (bio-cavagnou.info)
- However, when there are multiple attacks of acute disseminated encephalomyelitis followed by optic neuritis, it is defined as acute disseminated encephalomyelitis-optic neuritis. (biomedcentral.com)
- To the best of our knowledge, there are no previous reports of acute disseminated encephalomyelitis and optic neuritis preceded by autoinflammation, triggered by periodic fever syndrome. (biomedcentral.com)
- We report on a case of acute disseminated encephalomyelitis with optic neuritis and periodic fever syndrome in a 12-year-old Ecuadorian Hispanic boy with several relapses over the past 10 years, always preceded by autoinflammatory manifestations and without evidence of infectious processes. (biomedcentral.com)
- Macrophage inflammatory products including tumor necrosis factor (TNF) and interleukin-12/p40 are implicated in demyelinating diseases such as multiple sclerosis (MS), Guillain-Barré syndrome, and animal models experimental autoimmune encephalomyelitis and neuritis. (unicamp.br)
- MOGAD is typically associated with acute disseminated encephalomyelitis (ADEM), optic neuritis (ON), and transverse myelitis (TM) and is less commonly associated with cerebral cortical encephalitis, brainstem or cerebellar symptoms, and clinical presentations including the combination of several phenotypes and sometimes accompanies other autoantibodies such as anti- N -methy-D aspartate receptor (NMDAR) autoantibodies with symptoms of autoimmune encephalitis. (encyclopedia.pub)
- In fact, MOG was initially identified as an immunodominant target for demyelinating autoantibodies in a guinea pig model of experimental autoimmune encephalomyelitis (EAE) [ 2 ] [ 3 ] . (encyclopedia.pub)
- ER Chaperone BiP/GRP78 Is Required for Myelinating Cell Survival and Provides Protection during Experimental Autoimmune Encephalomyelitis. (uchicago.edu)
- Inhibition of midkine alleviates experimental autoimmune encephalomyelitis through the expansion of regulatory T cell population. (uchicago.edu)
- Chronological changes of CD4(+) and CD8(+) T cell subsets in the experimental autoimmune encephalomyelitis, a mouse model of multiple sclerosis. (uchicago.edu)
- Multiple sclerosis (MS) and acute disseminated encephalomyelitis (ADEM) bear a close pathological resemblance, each resembling the pathology of experimental allergic encephalomyelitis (EAE). (medscape.com)
Optic5
- In optic neuritis (ON), transient thickening of the macular retinal nerve fibre layer (RNFL) can be observed. (lu.se)
- In the present study, we describe the time course of glial activation and retinal neurodegeneration in the EAE model, and highlight the utility of studying the anterior visual pathway for modeling mechanisms of neuronal injury that may recapitulate critical aspects of the pathology described in people with MS following optic neuritis and subclinical optic neuropathy. (listlabs.com)
- Emerging concepts in the treatment of optic neuritis: mesenchymal stem cell-derived extracellular vesicles. (uchicago.edu)
- Risk Factors for Multiple Sclerosis Development After Optic Neuritis Diagnosis Using a Nationwide Health Records Database. (cdc.gov)
- Moreover, other conditions along the suggested continuum include optic neuritis, transverse myelitis, and neuromyelitis optica - clinical entities that may occur as manifestations of either MS or ADEM. (medscape.com)
Myasthenia Gravis1
- Autoantigen administration via nasal mucosal tissue can induce systemic tolerance more effectively than oral administration in a number of experimental autoimmune diseases, including Ab-mediated experimental autoimmune myasthenia gravis, a murine model of myasthenia gravis. (aai.org)
Diseases20
- GBS is a group of autoimmune diseases with acute/subacute evolution characterized by progressive and ascending motor deficit in the limbs, often with sensory, cranial nerve involvement ( 4 , 6 ). (spandidos-publications.com)
- Autoimmune diseases affect roughly 5-10% of the total population, with women affected more than men. (frontiersin.org)
- The standard treatment for autoimmune or autoinflammatory diseases had long been immunosuppressive agents until the advent of immunomodulatory biologic drugs, which aimed at blocking inflammatory mediators, including proinflammatory cytokines. (frontiersin.org)
- These therapies inhibit the proinflammatory action of TNF-α in common autoimmune diseases such as rheumatoid arthritis, psoriasis, ulcerative colitis, and Crohn's disease. (frontiersin.org)
- TNF-α blockade quickly became the "standard of care" for these autoimmune diseases due to their effectiveness in controlling disease and decreasing patient's adverse risk profiles compared to broad-spectrum immunosuppressive agents. (frontiersin.org)
- However, anti-TNF-α therapies have limitations, including known adverse safety risk, loss of therapeutic efficacy due to drug resistance, and lack of efficacy in numerous autoimmune diseases, including multiple sclerosis. (frontiersin.org)
- Loss of immune tolerance to autoantigens associated with a specific organ results in the activation of organ-specific T and B cells that in turn cause organ-specific inflammation and the development of autoimmune diseases such as multiple sclerosis (MS) ( 5 ), rheumatoid arthritis (RA) ( 6 ), psoriasis ( 7 ), and type 1 diabetes (T1D) ( 8 ). (frontiersin.org)
- Thus, therapeutics that induce, restore, and maintain immune tolerance toward these autoantigens represent the "Holy Grail" of treatments for autoimmune diseases. (frontiersin.org)
- Exercise attenuates the onset and progression of autoimmune diseases. (luc.edu)
- The K+ efflux was found to be reduced in experimental models of these diseases, resulting in abnormally prolonged depolarization and incomplete repolarization, thereby interfering with repetitive discharges in the cells. (bvsalud.org)
- An important question is whether this therapeutic effect generalises to other autoimmune neurological diseases. (ms-selfie.blog)
- MSCs have been shown to improve experimental models of several autoimmune diseases including Type 1 Diabetes systemic lupus erythematosus rheumatoid arthritis and multiple sclerosis (MS) [1-5]. (bio-cavagnou.info)
- The global burden has risen with the near tripling in the last half-century of multiple sclerosis (MS) ( 2 , 3 ), type 1 diabetes (T1D) ( 4 ), and other autoimmune diseases. (frontiersin.org)
- This review highlights recent advances in vitamin D and T-lymphocyte biology in an effort to harness vitamin D's potential to reduce the impact of autoimmune diseases. (frontiersin.org)
- Autoimmune diseases represent a failure of self-identification leading to an immune-mediated assault on host tissues. (frontiersin.org)
- We drew mainly on MS and T1D research because intensive investigation has generated detailed insights into vitamin D mechanisms in these diseases and provided valuable guidance for research on other autoimmune diseases. (frontiersin.org)
- Other autoimmune diseases are included where robust mechanistic data exist. (frontiersin.org)
- A recent chapter ( 6 ) and a review ( 7 ) have summarized vitamin D mechanisms in autoimmune diseases more generally. (frontiersin.org)
- OBJECTIVE: In this review the authors discuss evidence from the literature concerning vitamin D and temporal bone diseases (benign paroxysmal positional vertigo [BPPV], Menière's disease [MD], vestibular neuritis, idiopathic facial paralysis, idiopathic acute hearing loss). (kl.ac.at)
- abstract = "OBJECTIVE: In this review the authors discuss evidence from the literature concerning vitamin D and temporal bone diseases (benign paroxysmal positional vertigo [BPPV], Meni{\`e}re's disease [MD], vestibular neuritis, idiopathic facial paralysis, idiopathic acute hearing loss). (kl.ac.at)
Encephalitis1
- The association of vitamin D deficiency with demyelination has already been established in other entities such as multiple sclerosis and experimental autoimmune encephalitis. (kl.ac.at)
Vestibular neuritis2
- In a randomized, controlled trial by Strupp et al, steroids (methylprednisolone) were found to be more effective than antiviral agents (valacyclovir) for recovery of peripheral vestibular function in patients with vestibular neuritis. (medscape.com)
- CONCLUSIONS: MD, BPPV, vestibular neuritis, idiopathic facial paralysis, idiopathic acute hearing loss may all have several etiological factors, but a common feature of the current theories is that an initial viral infection and a subsequent autoimmune/autoinflammatory reaction might be involved. (kl.ac.at)
Inflammatory7
- Multiple sclerosis (MS) is a neuroinflammatory disease with an autoimmune component that is characterised by activation of self-reactive lymphocytes, which enter the central nervous system (CNS) and cause destruction of myelin producing cells and neurons leading to the formation of inflammatory lesions. (nature.com)
- Selective expression and cellular localization of pro-inflammatory chemokine ligand/receptor pairs in the sciatic nerves of a severe murine experimental autoimmune neuritis model of Guillain-Barré syndrome. (southernbiotech.com)
- Guillain-Barré Syndrome (GBS) is a debilitating inflammatory autoimmune disease of the peripheral nervous system that is characterized by rapid-onset paraparesis with areflexia progressing to neuromuscular paralysis. (luc.edu)
- We performed two trials of efficacy of MSCs in experimental autoimmune neuritis (EAN, an autoimmune demyelinating disease of the peripheral nervous system) in Lewis rats, a model of human autoimmune inflammatory neuropathies. (ms-selfie.blog)
- Given the proposed wider application of these medicines and their potentially important advantages in treatment of inflammatory and autoimmune disorders, more studies are needed with special focus on the molecular targets of statins included in regulating the immune response. (archivesofmedicalscience.com)
- Acute inflammatory demyelinating polyneuropathy (AIDP) is an autoimmune process that is characterized by progressive areflexic weakness and mild sensory changes. (medscape.com)
- Experimental evidence suggests that inflammatory proteins play a critical role in the pathogenesis of cytomegalovirus-induced hearing loss. (medscape.com)
Inhibition2
- Inhibition of experimental autoimmune neuritis by an antibody to the lymphocyte function-associated antigen-1. (2medicalcare.com)
- Mesenchymal Stem Cells Lack Efficacy in the Treatment of Experimental Autoimmune Neuritis despite In Vitro Inhibition of T-Cell Proliferation. (ms-selfie.blog)
Pathogenesis1
- Evidence for CD4 + T-cell involvement in autoimmune disease pathogenesis and for paracrine calcitriol signaling to CD4 + T lymphocytes is summarized to support the thesis that calcitriol is sunlight's main protective signal transducer in autoimmune disease risk. (frontiersin.org)
Inflammation2
- METHODS: We used in vivo confocal microscopy to compare the effects of inflammation in experimental autoimmune neuritis (EAN), a model of Guillain-Barré syndrome (GBS), on mitochondrial function and transport in large- and small-diameter axons. (ucl.ac.uk)
- MS is usually a debilitating central nervous system (CNS) autoimmune disease that consists of CNS-directed inflammation demyelination and axonal degeneration. (bio-cavagnou.info)
Peripheral3
- Neurologic manifestations may be the result of virus neurotropism which can reach the central nervous system (CNS) through cranial nerves and olfactory pathways or via circulation, while damage to the peripheral nervous system (PNS) is likely the result of a parainfective autoimmune reaction ( 3 , 5 ). (spandidos-publications.com)
- In vivo treatment with mAb R73 can suppress immune function of peripheral αβ TCR-expressing T cells, and reduce the severity of experimental autoimmune, transplant rejection, and graft-versus-host responses. (bdbiosciences.com)
- [ 2 ] An autoimmune process was supported by Waksman and Adams when they created the experimental allergic neuritis model by injecting peripheral nerve tissue into rodents. (medscape.com)
Demyelination models1
- Therefore the efficacy of MSCs observed in autoimmune CNS demyelination models do not necessarily generalise to the treatment of other forms of neurological autoimmunity. (ms-selfie.blog)
MSCs2
- These results highlight the potential variability of MSCs as a Desacetylnimbin biologic therapeutic tool in the treatment of autoimmune disease and the need for further investigation into the multifaceted functions of MSCs in diverse microenvironments and the mechanisms behind the diversity. (bio-cavagnou.info)
- presentations of suppression also have not really been recapitulated in a few configurations as MSCs lacked significant influence on experimental autoimmune neuritis [17]. (bio-cavagnou.info)
AIDP1
- In this study, we determined the effects of forced-exercise on development and progression of experimental autoimmune neuritis (EAN), an animal model of AIDP. (luc.edu)
Suppression2
- Suppression of experimental allergic neuritis by an antibody to the intracellular adhesion molecule ICAM-1. (2medicalcare.com)
- Suppression of experimental autoimmune neuritis by the oxygen radical scavengers superoxide dismutase and catalase. (foryou01.com)
Model2
- Clinical, electrophysiological and pathologic correlations in a severe murine experimental autoimmune neuritis model of Guillain-Barré syndrome. (southernbiotech.com)
- An experimental animal model for central nervous system demyelinating disease. (nih.gov)
Clinical1
- Clinical and experimental dermatology 2023 0 0. (cdc.gov)
Type 1 Diabet1
- Evidence linking sunlight, vitamin D, and the risk of multiple sclerosis and type 1 diabetes is summarized to develop the thesis that vitamin D is the environmental factor that most strongly influences autoimmune disease development. (frontiersin.org)
Extracellular1
- Detection and quantification of antibodies to the extracellular domain of P0 during experimental allergic neuritis. (2medicalcare.com)
Arthritis1
- The suppressive effect of MoAb against either L3T4 or Lyt-2 on diabetes development suggests that the pathomechanism involved is different from that in experimental autoimmune neuritis and adjuvant arthritis where Lyt-2 cells are not involved. (ox.ac.uk)
Hepatic1
- 2009) Experimental models of hepatic encephalopathy: ISHEN guidelines. (aimspress.com)
Reaction1
- Given the immunomodulatory effect of vitamin D, we postulate that it may play a role in suppressing an eventual postviral autoimmune reaction. (kl.ac.at)
Lewis1
- Attenuation of experimental autoimmune neuritis in the Lewis rat by treatment with an antibody to L-selectin. (2medicalcare.com)
Treatment1
- A deep understanding of molecular mechanisms relevant to gene-environment interactions is needed to deliver etiology-based autoimmune disease prevention and treatment strategies. (frontiersin.org)
Oxygen1
- The experimental group needed less oxygen (p (bvsalud.org)
Multiple1
- Multiple sclerosis (MS) is considered to be an autoimmune disease that is caused by the immune system attacking the central nervous system (CNS) leading to myelin loss and axonal damage, resulting in long-term disability. (touchneurology.com)
Mechanisms2
- Gene-environment interactions, sunlight and vitamin D, and T lymphocytes as autoimmune disease initiators and vitamin D targets are discussed to explain the rationale for reviewing vitamin D mechanisms in T cells. (frontiersin.org)
- Finally, unanswered questions relating to vitamin D mechanisms in CD4 + T cells are highlighted to promote further research that may lead to a deeper understanding of autoimmune disease molecular etiology. (frontiersin.org)
Vitamin1
- This review summarizes and integrates research on vitamin D and CD4 + T-lymphocyte biology to develop new mechanistic insights into the molecular etiology of autoimmune disease. (frontiersin.org)
Profiles1
- Below are the most recent publications written about "Nervous System Autoimmune Disease, Experimental" by people in Profiles. (rush.edu)
Cell1
- B cell responses to the PNS protein P0 in experimental autoimmune neuritis. (2medicalcare.com)
Cells1
- both CD4 and CD8 T cells have been implicated in a secondary autoimmune response ( 6 ). (cdc.gov)
Research1
- Finally, unanswered questions and potentially informative future research directions are highlighted to speed delivery of etiology-based strategies to reduce autoimmune disease. (frontiersin.org)
Patients1
- Methods: A retrospective quasi-experimental study design compared patients admitted pre- and post-intervention. (bvsalud.org)
People1
- This graph shows the total number of publications written about "Nervous System Autoimmune Disease, Experimental" by people in this website by year, and whether "Nervous System Autoimmune Disease, Experimental" was a major or minor topic of these publications. (rush.edu)