Early symptoms of multiple sclerosis and how they are 10 years later – optic neuritis
Early symptoms of multiple sclerosis and how they are 10 years later – optic neuritis
optic neuritis
Anti-cell death agent a potential treatment for vision loss associated with Multiple Sclerosis
This image shows myelin (blue) in the optic nerve of a normal mouse (top), a mouse with optic neuritis (middle), and an optic neuritis mouse treated with ST266 (bottom) .Ken Shindler, MD, PhD, Perelman School of Medicine, University of Pennsylvania
A new therapeutic agent tested in a mouse model of multiple sclerosis (MS) produced anti-inflammatory activity and prevented loss of cells in the optic nerve, according to a new study by researchers in the Perelman School of Medicine at the University of Pennsylvania, with Pittsburgh-based Noveome Biotherapeutics. The research was conducted in the laboratory of Kenneth Shindler, MD, PhD, an associate professor of Ophthalmology and Neurology, and published in Scientific Reports.
The team demonstrated the therapeutic potential of the agent, called ST266, for treating optic neuritis, inflammation that damages the optic nerve and is a common presenting feature of MS. About half of patients diagnosed with MS experience optic neuritis, which can cause mild to moderate permanent loss of vision, but rarely complete blindness. ST266 is a solution of molecules that stimulate paracrine signaling. This is one way in which cells “talk” to each other: One cell produces a chemical signal that induces changes in nearby cells.
“In this case, the idea is that the many factors in ST266 not only bind to cell receptors and cause changes within the cells they bind to, but those cells then alter their own secretions and provide additional signals to other neighboring cells, thus propagating an effect from a relatively small amount of protein present in the therapy itself,” Shindler said. “To the best of our knowledge, this study demonstrates, for the first time, the ability to treat the optic nerve via the intranasal route of administration.”
When ST266 was given to the MS mice via their nose, it reached the central nervous system within 30 minutes and was detected at higher concentrations in parts of the eye and optic nerve compared to other areas of the brain. These findings demonstrated that this type of delivery can target tissues of the eye, which is easier, less painful, and less invasive than injecting medication directly into the eye.
In mice with optic neuritis, the team showed that early treatment with ST266 prevented damage and dysfunction, marked by significantly reduced loss of optic nerve cells, and suppression of inflammatory cell infiltration into the optic nerve. This in turn was associated with limitation of the degree of demyelination caused by MS- related optic neuritis. However, “it’s not known if these effects are independent effects of the therapy or interdependent effects,” Shindler said.
Treatment of later-stage optic neuritis in the MS mice showed similar results, resulting in improved visual function compared to untreated groups. The data suggest that ST266 helps promote optic neuron survival by potentially activating multiple pathways, including those that prevent cell death.
“These results are particularly important as the preservation of retinal cells is a significant factor when treating optic neuritis,” Shindler said. “There is an increased need for combination treatment options that are able to prevent nerve-cell axon loss for patients with optic neuritis.”
Currently, the only acute treatment for MS-related optic neuritis is IV steroids, which only hasten whatever amount of visual recovery will occur even without treatment. Steroids do not prevent nerve damage or permanent vision loss. “ST266’s ability to preserve vision in the preclinical model and reduce neuronal loss would be a huge advance if it translates to human patients,” Shindler said.
The study also has implications beyond MS-related optic problems. “We also showed an effect on cultured neurons, suggesting that effects may translate to other optic nerve diseases, as well as other brain neurodegenerative diseases,” Shindler said.
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Devic’s disease – what are the signs of Devic’s disease? Is this a type of MS?
Devic’s disease
Neuromyelitis optica (NMO), also known as Devic’s disease, is a rare neurological condition.
Neurological conditions are caused by disease or damage to the brain, spinal cord or nerves.
NMO most commonly affects the optic nerves and spinal cord, which can lead to optic neuritis and transverse myelitis (see below).
Some people may only experience optic neuritis or myelitis but may have the aquaporin-4 antibody (also see below). In such cases, a person is said to have an NMO spectrum disorder (NMOSD).
Each person with NMO will experience different symptoms and require individually tailored care and support.
Some of the main symptoms of NMO include:
muscle weakness – reduced strength in one or more muscles that can affect mobility
impaired eyesight
nerve pain – which can be a sharp, burning, shooting or numbing pain
spasms and increased muscle tone – from nerve damage that affects muscle control
bladder, bowel and sexual problems
NMO UK has more information about the symptoms of NMO.
Optic neuritis
Optic neuritis is inflammation of the nerve that leads from the eye to the brain. It causes a reduction or loss of vision, and can affect both eyes at the same time.
Other symptoms of optic neuritis include eye pain, which is usually made worse by movement, and reduced colour vision where colours may appear ‘washed out’ or less vivid than usual.
Transverse myelitis
Transverse myelitis is inflammation of the spinal cord. It causes weakness in the arms and legs which can range from a mild ‘heavy’ feeling in one limb, to complete paralysis in all four limbs.
It may cause numbness, tingling or burning below the affected area of the spinal cord and increased sensitivity to touch, cold and heat. There may also be tight and painful muscle contractions (known as tonic muscle spasms).
Relapses in NMO
An attack or relapse of NMO results in the nervous system becoming inflamed. The inflammation usually occurs in the optic nerve and spinal cord, and causes new symptoms or the recurrence of previous symptoms.
Less common symptoms of NMO can include unexplained nausea and vomiting, unexplained itching and tonic spasms (painful muscle contractions). In someone with known NMO, these symptoms may signify a new relapse.
NMO symptoms can range from mild to severe. In some cases, there may only be one attack of optic neuritis or transverse myelitis, with good recovery and no further relapses for a long time.
However, in severe cases, there can be a number of attacks which lead to disability. Disability occurs because the body can’t always fully recover from damage caused by the attacks on the spinal cord and optic nerve.
NMO UK has more information about NMO relapses.
What causes NMO?
NMO is an autoimmune condition, which means a person’s immune system (the body’s natural defence against illness and infection) reacts abnormally and attacks the body’s tissues and organs.
An antibody against a protein called aquaporin-4 is present in the blood of up to 80% of people with NMO.
Antibodies are proteins produced by the body to destroy disease-carrying organisms and toxins.
In NMO, the immune system attacks aquaporin-4 which damages the myelin sheath (the protective layer that surrounds nerve cells in the brain and spinal cord and helps transmit nerve signals).
Who’s affected by NMO?
NMO is a rare condition. In Europe, it’s estimated that there’s one case of NMO for every 100,000 people. In the UK, it’s thought that NMO affects less than 1,000 people.
NMO can affect anyone but it’s more common in women than men, with about four females being affected for every male.
Although the condition is thought to be more common in people of Asian and African descent, an increasing number of white (Caucasian) people are also being diagnosed.
Diagnosing NMO
It’s important that NMO is correctly diagnosed. It can sometimes be confused with multiple sclerosis, which also affects the brain and spinal cord and has similar symptoms. However, the treatment is different.
A neurology specialist will discuss your symptoms and medical history with you.
You’ll have a magnetic resonance imaging (MRI) scan of your brain and spinal cord. Some people with NMO (up to 60%) have lesions on their brain and spine, which are different to the lesions of someone with MS.
A blood sample will be taken and tested for aquaporin-4 antibodies.
A lumbar puncture is another test you may have. A sample of cerebrospinal fluid (CSF) is taken from the spine using a hollow needle that’s inserted into the lower part of the spine.
The fluid sample will be sent to a laboratory to be tested and to look for evidence of conditions affecting the brain, spinal cord or other parts of the nervous system.
In some cases of transverse myelitis, there’s an increase in the level of proteins or white cells.
NMO UK has more information about how NMO is diagnosed.
Treating NMO
There’s no cure for NMO, so treatment aims to manage attacks and symptoms, and prevent relapses.
Every person with NMO is affected differently and some may have much milder symptoms than others. However, early treatment is usually needed to prevent further episodes and permanent disability.
Medication is used to reduce nerve inflammation, suppress the immune system and treat any pain. Rehabilitation techniques, such as physiotherapy, can also help with any reduced mobility that the relapses cause.
At these centres, research is ongoing to find possible future treatments for NMO.
To be referred to one of these centres, a GP referral letter is all that’s needed. These specialist services are nationally funded, so GP practices won’t have any additional costs for referring.
NMO UK has more information about treatments for NMO.
Driving
Optic neuritis (inflammation of the optic nerve) could affect your ability to drive.