BeCare Link, New York, NY (2026)

11/02/2026

𝗩𝗲𝘀𝘁𝗶𝗯𝘂𝗹𝗮𝗿 𝗠𝗶𝗴𝗿𝗮𝗶𝗻𝗲: 𝗪𝗵𝗲𝗻 𝗗𝗶𝘇𝘇𝗶𝗻𝗲𝘀𝘀 𝗦𝘁𝗿𝗶𝗸𝗲𝘀 𝗪𝗶𝘁𝗵𝗼𝘂𝘁 𝗮 𝗛𝗲𝗮𝗱𝗮𝗰𝗵𝗲
Can you have a migraine without a headache? Absolutely. For some people, migraines cause dizziness, vertigo, and balance problems rather than the throbbing head pain most people associate with migraine. This condition, called vestibular migraine, is one of the most common causes of recurrent vertigo.
Vestibular migraine is a neurological condition that affects the brain’s processing of balance and motion. The vestibular system helps us maintain balance and understand where our body is in space. During a vestibular migraine, changes in brain activity can disrupt these processes, creating sensations of spinning, rocking, or unsteadiness.
A headache does not have to occur during an episode. Some people have a history of traditional migraines but later develop episodes of vertigo without any head pain.

Symptoms vary considerably from person to person and may include:
· Vertigo: A spinning sensation, even when sitting or lying still.
· Dizziness:
· Motion sensitivity
· Nausea.
· Light sensitivity
· Sound sensitivity

Episodes typically last anywhere from five minutes to 72 hours, although some lingering imbalance may persist longer.
Many triggers are similar to those associated with traditional migraines. Common examples include stress, inadequate sleep, dehydration, skipped meals, hormonal fluctuations, and certain foods or alcohol. Weather changes, bright lights, and prolonged screen exposure may also provoke symptoms in susceptible individuals. Not everyone has identifiable triggers.

No single blood test or brain scan confirms vestibular migraine. Diagnosis is based on symptoms, migraine history, and examination. A neurologist may recommend testing appropriate to exclude other causes.

Conditions such as benign paroxysmal positional vertigo (BPPV), Ménière’s disease, and inner ear disorders can produce similar symptoms. Sudden dizziness accompanied by double vision, difficulty speaking, weakness, or inability to walk requires emergency evaluation because these can be signs of a stroke.

Treatment of a vestibular migraine is similar to that of classic migraines with or without aura. Vestibular rehabilitation therapy can improve balance and motion tolerance, particularly when dizziness persists between episodes.

The BeCare Headache app can help you to track your headaches and your vestibular migraines with our headache tracker. Our headache classification used by all headache specialists, enhanced by BeCare’s AI can help direct you correct diagnosis and treatment. Join our headache communityand pose your questions to our AI assistant. Be aware with BeCare. Be a driver in your own headache journey.

10/29/2026

𝗕𝗹𝘂𝗿𝗿𝘆 𝗩𝗶𝘀𝗶𝗼𝗻: 𝗜𝘀 𝗜𝘁 𝗠𝗦, 𝗮 𝗡𝗲𝗲𝗱 𝗳𝗼𝗿 𝗚𝗹𝗮𝘀𝘀𝗲𝘀, 𝗼𝗿 𝗮 𝗦𝘁𝗿𝗼𝗸𝗲?
Blurry vision is a common complaint, but not all vision problems have the same cause. For people living with multiple sclerosis (MS), changes in vision can be particularly concerning. Is it an MS relapse, a simple need for glasses, or something more serious, such as a stroke? Understanding the differences can help you recognize when to seek medical attention.

Optic neuritis occurs when inflammation damages the optic nerve, which carries visual information from the eye to the brain. It is a common visual manifestation of MS and can sometimes be the first symptom of the disease.
Typical symptoms include:
• Blurred or dimmed vision, usually in one eye
• Pain behind the eye, especially when moving it
• Colors appearing faded or washed out, particularly red
• A dark or blurry spot in the center of vision
• Vision worsening over hours to several days
Unlike ordinary blurry vision, optic neuritis generally cannot be corrected with glasses. Vision often begins improving within several weeks, although recovery may take months.

Nearsightedness (myopia) and farsightedness (hyperopia) are refractive errors. They occur when the eye does not focus light properly onto the retina. Nearsightedness makes distant objects blurry while nearby objects remain relatively clear. Farsightedness may cause difficulty focusing on nearby objects, particularly when reading.
These conditions generally develop gradually, do not cause pain with eye movement or faded colors, and improve with properly prescribed glasses or contact lenses. Age-related difficulty focusing up close, called presbyopia, is another common cause of blurry reading vision, particularly after age 40.

A stroke can affect the parts of the brain responsible for processing vision. Unlike optic neuritis, which usually develops over hours or days, stroke-related visual changes typically occur suddenly, within seconds or minutes.
Warning signs include:
• Sudden loss of vision in one or both eyes
• Missing the same side of the visual field in both eyes
• Sudden double vision
• Vision changes accompanied by dizziness, imbalance, weakness, numbness, or difficulty speaking
Importantly, a stroke affecting vision may occur without weakness or speech problems. Sudden painless vision loss can also result from a retinal vascular blockage, another medical emergency.
Call 911 immediately for sudden vision loss or a new visual field defect, even if symptoms improve.
Not every visual change in someone with MS is caused by MS. Gradually worsening distance or reading vision may simply require glasses. Painful vision loss developing over days raises concern for optic neuritis and warrants prompt medical evaluation.
Sudden vision loss should always be treated as an emergency until a stroke or another vascular cause has been ruled out.
Recognizing these differences can help protect your vision and ensure you receive the right treatment at the right time. The BeCare MS App can help not only by monitoring your overall neurologic function, but also by offering two activities that can assess your visual acuity and suggest if optic neuritis is occurring. Be aware with BeCare. Become a driver in your own MS journey.

10/20/2026

𝗗𝗲𝗽𝗿𝗲𝘀𝘀𝗶𝗼𝗻 𝗮𝗻𝗱 𝗠𝘂𝗹𝘁𝗶𝗽𝗹𝗲 𝗦𝗰𝗹𝗲𝗿𝗼𝘀𝗶𝘀: 𝗜𝘀 𝗜𝘁 𝗖𝗮𝘂𝘀𝗲𝗱 𝗯𝘆 𝗠𝗦 𝗼𝗿 𝗯𝘆 𝗟𝗶𝘃𝗶𝗻𝗴 𝗪𝗶𝘁𝗵 𝗠𝗦?
Depression is one of the most commonly overlooked symptoms experienced by people with multiple sclerosis (MS). Up to half of individuals with MS will experience depression during their lifetime. The question is: is depression an emotional reaction to living with MS, or is it directly caused by the disease itself? Both mechanisms can contribute, sometimes simultaneously.

MS patients face uncertainty about the future, unpredictable symptoms, physical limitations, and concerns about employment, relationships, and independence. Depression related to these challenges may develop following a diagnosis, relapse, or major lifestyle change, including grief over lost abilities or independence mood following a relapse or functional decline. Emotional improvement when circumstances become more manageable may suggest this depression is a reaction to having MS.

However, the disease itself can cause depression. Inflammatory damage to brain regions involved in emotional regulation, including connections between the frontal lobes and limbic system, as well as changes in neurotransmitter signaling may also influence mood. Unlike depression primarily associated with difficult life circumstances, biologically mediated depression may appear even when someone feels they are coping well with their diagnosis.

MRI findings alone cannot distinguish the two causes. Further, depression
in MS patients could be related to something else entirely, such as fatigue, difficulty concentrating, sleep disturbances, and reduced motivation. Medication side effects, chronic pain, thyroid disease, and sleep disorders may also contribute.

Fortunately, both forms of MS-related depression are treatable, and treatment often overlaps. Antidepressant medications, cognitive behavioral therapy, exercise adapted to physical abilities, and improved sleep can all help. Addressing pain, fatigue, and social isolation is equally important.

For many people with MS, depression reflects a combination of biological changes and the emotional challenges of chronic illness. Rather than focusing exclusively on identifying one cause, patients should recognize that depression is neither a personal weakness nor an inevitable consequence of MS.
Discussing mood changes openly with a neurologist or mental health professional is the first step toward effective treatment and a better quality of life.

The BeCare MS App can help both with standardized evaluation for mental health disorders, including depression, and by monitoring your neurological status to determine if your MS is progressing. Be aware with BeCare. Become a driver in your own healthcare journey.

09/28/2026

𝗦𝗺𝗼𝗹𝗱𝗲𝗿𝗶𝗻𝗴 𝗠𝗦: 𝗪𝗵𝘆 𝗠𝘂𝗹𝘁𝗶𝗽𝗹𝗲 𝗦𝗰𝗹𝗲𝗿𝗼𝘀𝗶𝘀 𝗖𝗮𝗻 𝗣𝗿𝗼𝗴𝗿𝗲𝘀𝘀 𝗘𝘃𝗲𝗻 𝗪𝗶𝘁𝗵𝗼𝘂𝘁 𝗥𝗲𝗹𝗮𝗽𝘀𝗲𝘀

For many years, multiple sclerosis (MS) was viewed largely as a disease of relapses. A person would develop new neurological symptoms, an MRI might show a new area of inflammation, and treatment would focus on preventing the next attack.

We now know that this is only part of the story.

Some people with MS experience gradual neurological changes even when they haven't had a relapse and their routine MRI scans appear relatively stable. Researchers sometimes describe the ongoing disease activity behind this progression as “smoldering MS.”

In relapsing MS, immune cells enter the brain and spinal cord and cause episodes of inflammation that can produce new MRI lesions and clinical relapses. Today's disease-modifying therapies can be extremely effective at reducing this type of inflammation.

But inflammation may also persist more quietly within the central nervous system. Older MS lesions can remain biologically active around their edges, with immune cells continuing to contribute to tissue injury. These areas are sometimes called chronic active lesions or slowly expanding lesions.

At the same time, damage to nerve fibers and other processes within the brain may gradually accumulate.

Another important concept is PIRA, which stands for progression independent of relapse activity.

PIRA describes a gradual increase in disability that cannot be explained by a recent MS relapse. Someone might notice that walking is becoming a little more difficult, balance isn't quite as good, or hand coordination has slowly declined—even though there hasn't been a dramatic MS attack.

This has changed how neurologists think about relapsing MS. Progression isn't necessarily something that begins only after a person develops secondary progressive MS. It can occur much earlier in the disease.

Routine MRI remains one of our most important tools for monitoring MS, but it doesn't capture everything happening in the brain.A scan may show no obvious new lesions while microscopic inflammation, nerve-fiber injury, brain-volume loss, or activity around older lesions continues.

Preventing relapses and MRI changes remains important, but neurologists are increasingly looking beyond these traditional measures. Subtle changes in walking, balance, cognition, hand function, fatigue, and other neurological abilities reflect the behavior of the inividual's disease.

The next generation of MS treatments will go further by no longer simply preventing the next relapse but also by preventing the quiet progression that can occur between relapses as well.

The BeCare MS app can pick up subtle changes before clinicians and patients. Catching subtle changes from smoldering disease prompts a proactive rather than reactive treatment approach. Be Aware with BeCare. Become a driver in your own MS journey.

09/23/2026

𝗧𝗵𝗲 𝗚𝗲𝗻𝗲𝘁𝗶𝗰𝘀 𝗕𝗲𝗵𝗶𝗻𝗱 𝗣𝗮𝗿𝗸𝗶𝗻𝘀𝗼𝗻’𝘀 𝗗𝗶𝘀𝗲𝗮𝘀𝗲: 𝗪𝗵𝗮𝘁 𝗪𝗲 𝗞𝗻𝗼𝘄
Parkinson’s disease (PD) is usually described as a disorder caused by the loss of dopamine-producing brain cells. But why those cells become vulnerable is more complicated. Research increasingly shows that genetics can play an important role—although PD is not simply an inherited disease.

About 10–15% of people with PD have an identifiable genetic link. In most people, however, the disease probably develops through a combination of aging, genetic susceptibility and environmental factors. Having a PD-related gene variant therefore does not necessarily mean that someone will develop PD.

Several genes have become especially important in PD research. GBA1 is the most common genetic risk factor identified in people with PD. The gene helps cells make an enzyme involved in the lysosome—the cell’s “recycling” system. Certain GBA1 variants may interfere with the removal of abnormal proteins, including alpha-synuclein, the protein that accumulates in Lewy bodies.
LRRK2 is another major PD gene. Some LRRK2 variants are inherited in an autosomal dominant pattern, meaning one altered copy can increase the chance of developing the disease. Importantly, not everyone who inherits a disease-associated LRRK2 variant develops PD, a concept known as reduced penetrance.

Other genes are less common but have provided important clues about PD biology. Variants in SNCA, the gene that produces alpha-synuclein, can cause rare inherited forms of PD. PRKN (parkin), PINK1 and PARK7 are associated particularly with younger-onset forms and are often inherited in an autosomal recessive pattern. VPS35 is another rare cause of dominantly inherited PD.
Why does this matter? Genetics is helping researchers divide PD into biological subtypes rather than treating it as one single disease. Clinical trials are already investigating therapies aimed at pathways involving genes such as GBA1 and LRRK2. In the future, a person’s genetic profile may help guide treatment choices.

Genetic testing is becoming more accessible, but results can be complicated. A positive result may indicate increased risk rather than certainty, while a negative result does not rule out PD. Testing may be particularly worth discussing in people with young-onset disease, a strong family history or ancestry associated with certain variants. Genetic counseling can help patients and families understand what a result does—and does not—mean.

The larger lesson from PD genetics is that genes are not destiny. Instead, they are providing a window into the cellular mechanisms that cause PD—and potentially pointing the way toward treatments designed to slow or prevent the disease.

The BeCare Parkinson’s App can help you track your symptoms to help you decide when to get evaluation for PD, and, if you are diagnosed, help guide treatment decisions. Be Aware with BeCare. Become a driver in your own neurologic journey.

09/14/2026

𝗖𝗮𝗻 𝗖𝗶𝗴𝗮𝗿𝗲𝘁𝘁𝗲 𝗦𝗺𝗼𝗸𝗲 𝗧𝗿𝗶𝗴𝗴𝗲𝗿 𝗠𝗶𝗴𝗿𝗮𝗶𝗻𝗲𝘀?
For people who live with migraine, triggers can sometimes seem to be everywhere—stress, lack of sleep, bright lights, weather changes, certain smells, and even changes in eating habits. Cigarette smoke is another potential trigger that deserves attention.

Importantly, you don't have to be a smoker yourself. Exposure to someone else's cigarette smoke may be enough to provoke or worsen a migraine in some people.

Ni****ne has complex effects on blood vessels and brain signaling. It also influences neurotransmitters involved in pain processing. These effects may contribute to headache susceptibility in some individuals.

The trigeminal nerve is one of the major nerve pathways involved in migraine. Irritating chemicals in to***co smoke can stimulate sensory nerve endings in the nose, sinuses, and airways. In someone with a migraine-prone nervous system, that irritation may help initiate an attack.

People with migraine frequently have heightened sensitivity to smells, known as osmophobia. Cigarette smoke is a particularly strong and persistent odor, and some patients report developing headache, nausea, or other migraine symptoms shortly after exposure.

Cigarette smoke contains carbon monoxide, which reduces the blood's ability to carry oxygen. Although typical secondhand-smoke exposure generally produces much lower carbon-monoxide levels than active smoking, it may be one of several factors contributing to headache during substantial smoke exposure.
Secondhand smoke is the combination of smoke released from a burning cigarette and smoke exhaled by the person smoking.

For someone susceptible to migraine, sitting near a smoker, spending time in a smoke-filled room, or riding in a car where someone has been smoking may potentially trigger symptoms. The amount of exposure necessary to provoke a migraine varies considerably from person to person.

There is no single exposure level at which everyone with migraine will develop a headache. Some people are extremely sensitive to cigarette smoke, while others notice little or no relationship.
Thirdhand smoke refers to to***co-related chemicals that remain on clothing, furniture, carpets, walls, and other surfaces after a cigarette has been extinguished.

The relationship between thirdhand smoke and migraine is much less established than that of direct smoke exposure. However, the lingering odor can be significant for people who are particularly sensitive to smells.

Research has found associations between cigarette smoking and headache disorders, including migraine, but that does not necessarily prove that smoking directly causes migraine. Smoking, stress, sleep problems, anxiety, caffeine use, alcohol use, and other factors can overlap, making the relationship difficult to untangle.

What is clearer is that cigarette smoke can act as an individual trigger for some people who already have migraine.

One important point is that sensitivity to smells can sometimes be an early symptom of migraine rather than the actual cause of the attack. In other words, a migraine may already be developing when cigarette smoke suddenly becomes particularly unpleasant. This can make identifying true triggers challenging.

Look for a reproducible pattern.If migraine attacks repeatedly occur after exposure to cigarette smoke but are less likely to occur when that exposure is absent, smoke becomes a more convincing trigger.

A headache diary can be helpful. Record when the migraine began, how much smoke exposure occurred, sleep the night before, meals, caffeine and alcohol intake, stress, menstrual-cycle timing when applicable, and other potential triggers.Over several weeks, patterns often become easier to recognize.

The BeCare Headache App can help by tracking your migraine frequency, associated symptoms, and triggers. Be Aware with BeCare. Become a driver in your own headache journey.

08/31/2026

𝗦𝗽𝗵𝗲𝗻𝗼𝗽𝗮𝗹𝗮𝘁𝗶𝗻𝗲 𝗚𝗮𝗻𝗴𝗹𝗶𝗼𝗻 𝗕𝗹𝗼𝗰𝗸 𝗳𝗼𝗿 𝗠𝗶𝗴𝗿𝗮𝗶𝗻𝗲
Migraine can be difficult to treat, particularly when headaches are frequent, severe, or do not respond well to standard medications. One treatment that may be considered for certain patients is a sphenopalatine ganglion (SPG) block. This minimally invasive procedure targets a cluster of nerve cells located deep behind the nose that plays an important role in headache and facial pain.

The sphenopalatine ganglion is a collection of nerve cells located behind the nasal passages. It is connected to the trigeminal nerve, one of the major nerves involved in migraine. It also contains autonomic nerve fibers that can contribute to symptoms such as tearing, nasal congestion, and facial pressure that sometimes accompany severe headaches.Because of these connections, temporarily reducing activity in the SPG may interrupt some of the pain signals involved in a migraine attack.

Despite the name “nerve block,” an SPG block usually does not require an injection through the face or skull. For migraine treatment, a physician typically administers a local anesthetic, such as lidocaine, through the nostril. Depending on the technique, the medication may be delivered using a small catheter or applicator designed to reach the back of the nasal cavity, close to the SPG.

The procedure generally takes only a few minutes and is usually performed in the office. Patients remain awake, and sedation is typically unnecessary.

An SPG block may provide relatively rapid relief for some patients with an acute migraine. Studies have reported reductions in headache pain shortly after treatment, although results vary considerably from person to person.Some physicians also use a series of SPG blocks in patients with frequent or chronic migraine. However, the evidence for long-term migraine prevention is less established than it is for standard preventive treatments such as CGRP-targeting medications, certain oral medications, or Botox for chronic migraine.

For this reason, SPG blocks are generally considered one potential tool in a broader migraine treatment plan rather than a cure for migraine.

Patients may notice temporary numbness in the nose, throat, or roof of the mouth. A bitter taste, watery eyes, or mild nasal irritation can also occur. Occasionally, a small nosebleed develops. Because the treatment uses a local anesthetic and does not involve surgery, serious complications are uncommon.

An SPG block may be worth discussing if migraines are severe, prolonged, or difficult to control with usual rescue medications. It may also be considered when medication side effects or other medical circumstances limit treatment choices.

The most important point is that migraine treatment should be individualized. An SPG block will not work for everyone, but for selected patients it may offer a relatively quick, minimally invasive option for reducing migraine pain—without adding another daily medication.

The BeCare Headache App can help by tracking your headaches and associated symptoms, response to medications, a supportive online community and interactive AI assistant to answer your questions. Be Aware with BeCare. Become a driver in your own headache journey.

08/17/2026

𝗡𝗲𝘄 𝗣𝗮𝗿𝗸𝗶𝗻𝘀𝗼𝗻’𝘀 𝗠𝗲𝗱𝗶𝗰𝗮𝘁𝗶𝗼𝗻𝘀 𝗶𝗻 𝗖𝗹𝗶𝗻𝗶𝗰𝗮𝗹 𝗧𝗿𝗶𝗮𝗹𝘀: 𝗥𝗲𝗮𝘀𝗼𝗻𝘀 𝗳𝗼𝗿 𝗛𝗼𝗽𝗲

For decades, medications for Parkinson’s disease (PD) have focused primarily on replacing dopamine or helping the brain use dopamine more effectively. Levodopa remains the most effective treatment for many PD symptoms. But an important shift is occurring in Parkinson’s research: scientists are increasingly testing treatments designed not simply to improve symptoms, but potentially to slow the underlying disease itself.

GLP-1 receptor agonists are best known as medications used for diabetes and weight management. Researchers became interested in them after laboratory studies suggested they might also reduce inflammation and protect nerve cells in the brain.

One drug, lixisenatide, was studied in 156 people with early PD. After 12 months, participants receiving lixisenatide had less worsening of motor symptoms than those receiving placebo. However, nausea and vomiting were common, and researchers emphasized that larger and longer studies are necessary to determine whether the drug truly slows Parkinson’s progression.
The findings are encouraging, but they do not yet establish GLP-1 medications as Parkinson’s treatments.

Another major strategy focuses on alpha-synuclein, a protein that accumulates abnormally in the brains of many people with Parkinson’s disease.

One experimental treatment, prasinezumab, is an antibody designed to target alpha-synuclein. Its initial Phase 2 trial did not meet its primary endpoint, meaning it did not clearly slow overall Parkinson’s progression. However, subsequent analyses suggested that some patients—particularly those whose disease was progressing more rapidly—might experience slower worsening of motor symptoms.

These intriguing findings have kept alpha-synuclein therapies an active area of investigation.

Researchers are also developing treatments directed at specific genetic pathways.One important target is LRRK2, a gene associated with some inherited and sporadic cases of Parkinson’s. Researchers have been studying experimental treatments designed to reduce activity of the LRRK2 pathway, including antisense oligonucleotide approaches.

Early-stage trials are primarily designed to evaluate safety and whether these treatments have the intended biological effects. Much more research is needed before we know whether targeting LRRK2 can slow Parkinson’s disease.

Researchers are also investigating drugs already used for other conditions. Ambroxol, for example, is a respiratory medication used in some countries that affects an enzyme called glucocerebrosidase, or GCase. Clinical trials are evaluating whether ambroxol could have a role in slowing Parkinson’s progression.

None of these experimental approaches has yet replaced standard Parkinson’s therapy, and there is currently no medication proven to stop Parkinson’s disease. But the direction of research is changing. Instead of treating Parkinson’s as one identical disease in everyone, researchers are increasingly using genetics and biological markers to identify different types of Parkinson’s and match treatments to the biology driving an individual patient’s disease.

For patients, this represents an important reason for optimism. The next generation of Parkinson’s medications may not simply provide more dopamine. The ultimate goal is much bigger: to protect brain cells, slow progression, and eventually change the course of Parkinson’s disease itself.

The BeCare Parkinson’s App can help you track your disease for worsening symptoms and cognitive decline. Become aware with BeCare. Be a driver in your own neurologic health journey.

08/10/2026

𝐏𝐚𝐫𝐤𝐢𝐧𝐬𝐨𝐧’𝐬 𝐓𝐫𝐞𝐚𝐭𝐦𝐞𝐧𝐭 𝐇𝐚𝐬 𝐂𝐡𝐚𝐧𝐠𝐞𝐝: 𝐖𝐡𝐲 𝐃𝐨𝐜𝐭𝐨𝐫𝐬 𝐀𝐫𝐞 𝐔𝐬𝐢𝐧𝐠 𝐋𝐞𝐯𝐨𝐝𝐨𝐩𝐚 𝐄𝐚𝐫𝐥𝐢𝐞𝐫

For many years, people newly diagnosed with Parkinson’s disease were often started on a dopamine agonist rather than levodopa. Today, that approach has changed. For many patients—particularly adults over age 60—carbidopa/levodopa (Sinemet) is now the preferred first treatment when Parkinson’s symptoms begin to interfere with daily life.

The Old Concern: “Save Levodopa for Later”

Parkinson’s disease causes symptoms such as slowness, stiffness and tremor because the brain gradually loses cells that produce dopamine. Levodopa is converted into dopamine in the brain and is generally the most effective medication for improving these movement symptoms.

In the past, doctors sometimes delayed levodopa because of concerns that long-term treatment would lead to dyskinesias, or involuntary extra movements, and fluctuations in how well the medication worked. There was also a belief that starting levodopa early might cause it to “stop working” sooner.

Because of these concerns, younger patients in particular were often started on dopamine agonists such as pramipexole (Mirapex), ropinirole (Requip), or rotigotine (Neupro). These medications stimulate dopamine receptors directly and can improve Parkinson’s symptoms without using levodopa.

What Have We Learned?

Over time, research has changed how neurologists think about levodopa.

We now know that levodopa does not simply “wear out” because someone starts taking it early. Motor fluctuations and dyskinesias appear to be strongly related to the progression of Parkinson’s itself, as well as the dose and duration of levodopa exposure.
Importantly, levodopa generally provides better improvement in movement symptoms than dopamine agonists.

This has shifted the balance toward treating symptoms effectively now rather than withholding the most effective medication because it might be needed later.

Dopamine Agonists Have Their Own Risks

Another important change has been greater recognition of dopamine agonist side effects.

These drugs can cause sleepiness, dizziness, swelling of the legs, hallucinations and confusion. Of particular concern are impulse-control disorders. Some people develop new or unusually strong urges involving gambling, shopping, eating or sexual behavior. These changes can sometimes be difficult for the person taking the medication to recognize.

The risk of hallucinations and confusion can also make dopamine agonists less attractive for older adults or people who already have cognitive difficulties.

Are Dopamine Agonists Still Used?

Absolutely. Dopamine agonists remain useful medications for selected patients. They may be used alone in some younger people with relatively mild symptoms or added to levodopa when symptoms are no longer controlled throughout the day.
The difference is that doctors are generally less focused on avoiding levodopa at all costs.

The Bottom Line

For many people with Parkinson’s disease today, carbidopa/levodopa is the preferred initial medication when movement symptoms require treatment. Dopamine agonists still have an important role, but their potential behavioral, cognitive and sleep-related side effects are considered more carefully than they were in the past.

The goal of Parkinson’s treatment has evolved: rather than “saving” levodopa for the future, treatment is increasingly individualized to provide the best symptom control and quality of life right now.

The BeCare Neuro and Parkinson's apps can help by tracking neurological function and mental health issues that can be due to Parkinson's meds or to the disease itself. Be Aware with BeCare. Become a driver in your own neurologic care.

08/02/2026

𝗧𝗵𝗲 𝗙𝘂𝘁𝘂𝗿𝗲 𝗼𝗳 𝗕𝗹𝗼𝗼𝗱 𝗧𝗲𝘀𝘁𝘀 𝘁𝗼 𝗗𝗶𝗮𝗴𝗻𝗼𝘀𝗲 𝗮𝗻𝗱 𝗠𝗼𝗻𝗶𝘁𝗼𝗿 𝗠𝘂𝗹𝘁𝗶𝗽𝗹𝗲 𝗦𝗰𝗹𝗲𝗿𝗼𝘀𝗶𝘀
If you have multiple sclerosis (MS), you are probably familiar with MRI scans and neurological examinations. These tools remain the foundation for diagnosing MS and monitoring disease activity. But researchers are now studying blood tests that may one day give doctors additional information about what is happening inside the brain and spinal cord. Although these tests are promising, it is important to understand that they are still emerging tools. They do not replace MRI scans, neurological exams, or conversations with your MS specialist.

A biomarker is something that can be measured in the body to provide information about a disease. For MS, scientists are searching for biomarkers that can help estimate disease activity, monitor treatment response, or identify nerve damage earlier than current methods.

Neurofilament light chain, often called NfL, is a protein found inside nerve cells. When nerves are damaged, small amounts of NfL are released into the cerebrospinal fluid and eventually into the bloodstream.
Research has shown that people with active MS often have higher NfL levels than healthy individuals. NfL levels may also rise during a relapse or when new inflammatory lesions develop on MRI. In some studies, NfL levels decrease after effective treatment with disease-modifying therapies, suggesting that the test may reflect reduced disease activity.
However, NfL is not specific to MS. Levels can also increase with normal aging and in other neurological conditions, such as stroke, traumatic brain injury, Alzheimer's disease, or other disorders that injure nerve cells. Because of this, doctors cannot diagnose MS using NfL alone.
Another biomarker being studied is glial fibrillary acidic protein (GFAP). Unlike NfL, which reflects damage to nerve fibers, GFAP is released by astrocytes, a type of support cell in the brain and spinal cord.
Early research suggests that GFAP may provide information about disease progression, particularly in progressive forms of MS. Scientists are still learning exactly how this marker can be used in clinical practice.
Will these blood tests replace MRI?

The short answer is no—at least not with today's evidence.
MRI remains the best tool for detecting new MS lesions and monitoring changes over time. Blood biomarkers are more likely to become an additional piece of the puzzle rather than a replacement for imaging. They may help neurologists identify subtle disease activity, guide discussions about treatment effectiveness, or determine when closer monitoring is needed.
While these tests are becoming increasingly available in research settings and some specialty centers, they are not yet considered standard care for every person with MS. As more studies are completed, doctors will better understand when and how to use them to improve patient care.
BeCare MS App can be an additional tool to diagnose and monitor MS. With a quantified neurologic examination, tracking of individual performance over time and compared with the general population, and calculation of gold standard disability scores, the BeCare App can empower patients to become a partner in their own MS journey. Be Aware with BeCare.