DISABLED ITEM

Multiple System Atrophy (MSA) is a rare and rapidly progressing neurodegenerative disorder that affects various systems within the nervous system. It impacts the autonomic nervous system, leading to problems with bladder and bowel control, as well as blood pressure and heat regulation. MSA also affects motor systems, resulting in coordination issues and slow motor function. It can manifest with a wide range of symptoms, including balance problems, movement difficulties, and sleep disturbances. MSA is not strongly associated with specific genetic or environmental factors and is primarily considered sporadic, although a few rare cases have been observed in families.

Distinguishing between multiple system atrophy (MSA) and Parkinson’s disease can be a challenge, even for experienced clinicians. However, several clues can help in the differentiation.

1. Clinical Presentation: In the cerebellar variant of MSA, individuals typically experience balance problems, whereas those with Parkinson’s appear slowed down and hunched over.
2. Early Symptoms: MSA patients may experience early and pronounced issues with balance, unlike Parkinson’s patients who typically develop these problems much later in the disease.
3. Response to Medication: While the classic Parkinson’s drug, LDOPA, may provide temporary relief in MSA, it stops working quickly. In contrast, it can continue to be effective for 10-15 years in Parkinson’s.
4. Dementia: Significant dementia is not a common feature of MSA but is present in Parkinson’s disease.
5. Autonomic Nervous System: Early and severe involvement of the autonomic nervous system, such as low blood pressure and bladder issues, is more indicative of MSA.
6. Vocal Cord Involvement: Vocal cord issues, like Laryngeal Stridor, speech difficulties, and sleep disturbances, are distinct to MSA and unusual in Parkinson’s.
   
   

MSA typically has an earlier onset, often in the early 50s, and patients may initially be misdiagnosed with Parkinson’s. Symptoms like sleep disturbances and vocal cord problems can be critical indicators for MSA, and the diagnosis is primarily clinical, although neuroimaging can sometimes assist in confirming the suspicion.

Multiple System Atrophy (MSA) commonly presents in the fifth decade of life, with the typical age range for onset being between the late thirties and forties, around age 40. The peak incidence of MSA occurs in the age group of 50 to 60 years. However, it’s important to note that there are cases where individuals may experience onset as early as their late thirties or in their forties, and others who may develop symptoms as late as their seventies or eighties. MSA can, therefore, exhibit a broad age range at onset.

Understanding the normal progression of multiple system atrophy (MSA) is essential. MSA, like other neurodegenerative disorders such as ALS and Parkinson’s disease, typically follows a gradual and linear deterioration pattern. This means that if you weren’t using a wheelchair last month, you’re unlikely to suddenly need one this month. The progression is gradual and can span several months, or even up to a year.

If there’s a sudden change in your condition, it’s essential to investigate what might have been added to the situation. For instance, it could be due to a urinary tract infection, pneumonia, or even depression. Some patients may become despondent and give up, leading to a rapid decline. So, if you were walking without difficulty just a month ago and are now reliant on a wheelchair, it’s crucial to consider that something may have transpired in the interim.

MSA typically advances through various stages, and it’s advisable to consult with a doctor to evaluate your condition carefully and identify any factors that may have influenced the change. In most cases, there’s a specific reason for sudden alterations in symptoms that need to be addressed and managed.

To address the question of a treatment versus a cure for multiple system atrophy (MSA), it’s important to distinguish between the two. In terms of treatment, there is a more optimistic outlook in the short term. Various avenues are being explored to modify the disease’s progression and slow it down. These include potential treatments involving metalloproteinases, myeloperoxidase, anti-inflammatory agents, and gaining a deeper understanding of the genetics or epigenetics underlying the condition.

However, when it comes to finding a cure, the timeline appears significantly longer. The reason for this cautious outlook is that, as of now, there is no convincing evidence that any of the exciting findings in MSA research are the root cause of the disease. Discovering an actual cause is a complex process, and it might take a while to identify it. One key challenge is the fact that there is often a gap of many years between the onset of initial symptoms and the formal diagnosis of MSA. This means that the triggering event or events that occurred years before the motor symptoms began remain unclear.

Additionally, MSA is a complex condition, and akin to cancer, it might require a multi-pronged approach to halt degeneration. While treatments are on the horizon and may become available within the next five years, finding a cure for MSA remains a long-term and challenging goal.

Orthostatic hypotension (OH) is a condition where your blood pressure drops when you stand up. This might not be something people commonly think about, but maintaining stable blood pressure while walking around is a complex process. It’s akin to pushing a boat upstream at Niagara Falls – a challenging task that our bodies effortlessly manage. This feat relies on the autonomic coordinating centers in the brain. These centers detect when you’re transitioning from sitting or lying down to standing, and they send signals to your blood vessels to constrict, which helps push blood back up to your brain, thus maintaining your blood pressure.

In multiple system atrophy (MSA), a debilitating neurodegenerative disorder, these coordinating centers cease to function properly. They no longer sense the drop in blood pressure when you stand up, and they fail to send the necessary signals. As a result, your blood pressure can plummet, for instance, from 160/90 when lying flat to 90/50 when standing. This condition significantly impacts MSA patients and is one of the most debilitating symptoms of the disease.

What’s also noteworthy is that these malfunctioning centers not only fail to keep blood pressure up when standing but also send signals to raise it when you’re lying flat, essentially reversing the normal regulatory processes.

Elevating the head of the bed is a valuable non-pharmacological approach to manage orthostatic hypotension (OH). In fact, about 70% of the efficacy in addressing OH comes from non-pharmacological strategies like salt intake regulation and tilt training, with medications providing the remaining 30%. Elevating the head of the bed helps tackle a particular issue known as “nocturnal microgravity.”

Nocturnal microgravity refers to the state of having little or no gravity, much like astronauts experience in space. Astronauts returning from space wear special suits because their bodies adapt to the microgravity environment, affecting their ability to maintain blood pressure. Similarly, when we sleep flat in bed for eight hours, we undergo a period of microgravity, similar to what astronauts encounter. As a result, when we first wake up, whether or not we have MSA, we may experience some lightheadedness as we begin to move around.

In cases where the autonomic system is already impaired, as in multiple system atrophy, the added challenge of microgravity can be particularly troublesome. Elevating the head of the bed, ideally as high as possible without sliding to the foot of the bed, helps mitigate this issue. This elevation should be achieved by placing supports under the bed’s head legs, such as a couple of bricks or a large cinder block.

It’s crucial not to mistake this with using pillows, as raising your upper body with pillows won’t be effective. The key is to position your legs below your waist and your waist below your heart, maintaining a specific angle. Elevating the entire bed helps reduce the effects of microgravity, making you feel less lightheaded when you wake up and potentially decreasing nighttime trips to the bathroom due to reduced fluid elimination. This approach offers numerous benefits in managing orthostatic hypotension.

Water plays a crucial role in the treatment of orthostatic hypotension, and it offers two distinct benefits.

Firstly, water is essential for the effective utilization of salt. When you consume approximately four grams of salt throughout the day, it’s recommended to also drink around 96 ounces of water. This combination of salt and water is essential for regulating blood pressure.

The second property of water is particularly intriguing. Drinking about 16 ounces of water relatively quickly, within five minutes, triggers a reflex from the stomach. This reflex causes an almost immediate increase in blood pressure, usually within ten minutes, with a rise of about 30 to 40 millimeters of mercury, and this effect can last for about an hour. This rapid increase in blood pressure is notably quicker than the time it takes for medications to take effect, which is typically around an hour to an hour and a half.

This makes water an ideal tool for managing orthostatic hypotension. For example, if you’re lying in bed at night, you can keep a 16-ounce glass of water by your bedside. When you wake up, you can quickly consume the water within 5 to 10 minutes. This will help raise your blood pressure significantly, providing you with the necessary blood pressure to get up, take your medications, use the bathroom, and carry out your morning activities. So, water has two essential properties that are vital for addressing orthostatic hypotension effectively.

Dietary salt plays a vital but often underappreciated role in the treatment of orthostatic hypotension, and its importance cannot be overstated. The reason for this lies in the fundamental issue at the heart of orthostatic hypotension: the constriction of blood vessels. While many available drugs assist in this vessel constriction process, they are most effective when you combine them with an increased blood volume.

To visualize this, consider a well that has stopped providing fluid. You can attempt to pump it harder, which is analogous to what drugs do – helping the vessels constrict better. However, this pumping won’t be very effective if the well isn’t adequately filled first. This filling of the well represents the role of dietary salt. You need to increase your blood volume before relying on medications to enhance vessel constriction.

Typically, you might require an additional two to four grams of salt, taken once or twice a day in addition to your dietary salt intake. Attempting to achieve this solely through salting your food isn’t practical, so acquiring over-the-counter salt pills from a pharmacy is often necessary. In fact, some patients have reported a reduction in the need for certain medications once they increased their salt intake.

It’s important to note that some individuals with multiple system atrophy may experience gut-related issues that hinder salt absorption. If salt appears ineffective in such cases, a simple 24-hour urine test can be conducted to determine if salt is being absorbed adequately. The key is to measure how much salt is being retained and utilized within the body.

Regarding the type of salt, any kind of salt will suffice, but it’s advisable to avoid those high in iodine content, as the added iodine can be excessive when you’re increasing your salt intake. Opting for a product like Thermotabs, which provides pure salt, is a prudent choice.

Salt has two distinct properties worth noting. The first is related to volume expansion: increasing salt and water intake leads to greater blood volume, facilitating better blood pressure maintenance. This property explains why individuals with hypertension are often advised to limit salt intake.

However, the second, less-known property of salt comes into play over a more extended period. After about two weeks of increased salt consumption, the body reduces its nitric oxide levels, a vasodilator. In cases of high blood pressure, vasodilation can be beneficial. However, when dealing with low blood pressure, as in orthostatic hypotension, the aim is to constrict vessels rather than dilate them, which helps in maintaining blood pressure, particularly when transitioning from sitting or lying to standing. This chronic effect of salt, taking around two weeks to manifest, further contributes to reducing the tendency of blood vessels to dilate when they should remain constricted, especially upon standing.