#myoclonic spasms

[storybookprincess]

having another flare up of whatever weird undiagnosed potentially autoimmune bullshit i have going on so i might be online less than usual. good vibes appreciated 💖💖💖

[neuroticboyfriend]

i see the neurologist today, would anyone be able to give me advice on how to get my concerns addressed properly? for context, i'm going for:

spinal nerve (mayhaps cord?) compression, causing pain, spasms, and weakness. i need medication for the pain & spasms, and nerve tests done on my limbs (mainly legs).

..myoclonic jerks and attacks? triggered by loud noise and fatigue, but sometimes the trigger is unclear. i have it on video, thankfully.

i'm nervous they won't give me medication and won't test properly, causing me to be misdiagnosed with FND, if I don't have it. like.. what tests should they be doing before they even think about diagnosing me with FND?

(im ok with this being reblogged for reach btw)

[pearlypairings]

I love the clarkelley snippet 😍 but I NEED to hear more about Chrissy’s Retribution!

I've talked about a subverted 80s horror AU on here before where Chrissy, after being killed by a Jason/Krueger-type supernatural killer, would be resurrected with the same strength and mystique of the villain....ready to seek vengeance on her killer and those who wronged before she died 🤬

Today I reformatted and reimagined the resurrection part:

Her finger twitched first. A small myoclonic spasm crunched her knuckles down toward her palm. The rest of her hand followed suit in a rippling of uncomfortable pops. And suddenly she was aware; aware that it should be impossible for her to be awake, that her body should not be moving, and that her deep inhale shouldn't reach her lungs.

Is that spooky enough? I don't know I'll save it for later 😁

[thethermocline]

A fun true fact about me is I have a tremor in both hands and myoclonic jerks (muscle spasms), and every time I paint something beautiful I feel I've pulled off a heist >:)

[qvackjack]

google reallt does just hit you with the "remember the scariest moment of your life?? that was actually a myoclonic seizure!! teehee!! 🤗" and now i have to do research to make sure thats not what happened and that it was in fact just some bad muscle spasms.

[elderflowerprince]

this isn't me trying to comment on anyone else's story or perspective or circumstances, it's just my own venting

my medication is killing me. it's ruining me.

i used to have no trouble walking up a hill after flights and flights of stairs, with a backpack of ten kilograms on my back and an extra couple kilos in a separate bag, every day. i also used to have seizures every morning. so much spilt tea. so many broken plates. so many bruises.

after a while, my doctor finally told me she would put me on new medication. that'll make three kinds at once, but the other two alone aren't working. the new one, it's only just out of the trial stage, they know it works for a lot of people but they're not sure of all the side effects yet. it seems safe, though. that's fine. that's fine. いいですよ、なんでも。i can't keep doing this anyway. i hate sitting around for hours every morning, waiting for the twitching and jerking to stop, unable to even have a conversation because my thoughts are lost to the void of a seizure every few seconds.

now i can sleep a full eight hours at night. now i don't have to wake up a few hours early every morning just to make sure i don't have any accidents trying to get myself ready for the day. now i'm blurry and dizzy and stumbly all the time. now i can barely walk straight. now i can't climb a single flight of stairs without getting so out of breath it hurts. i'm no longer exhausted for a lack of sleep, but i am just as impaired anyway, in a permanent haze of inability to focus. worse, you used to be able to tell with the twitching of my arms when i'd lost my train of thought. these days, i look like an idiot for forgetting what i was doing, or rude for not paying attention to you. i feel hot and cold and like i'm going to throw up half the time. i feel distant. i feel like it's all falling apart and i could not tell you why.

i can't go back. epilepsy was killing me too. you can't really take days off in this country, and tonic-clonic seizures are incapacitating in that sense--i can't move right for about a day or two for the muscle pain, every time. and i can't convey how awkward it is to constantly look like you're throwing things and poking or punching people, unable to explain that it's an uncontrollable arm spasm, when you're around anyone who doesn't know what "juvenile myoclonic epilepsy" is... and why would they know? that's such a specific condition, it just got highlighted by my spellchecker as a misspelling of "cyclonic".

i can't go back off medication, because it would kill me from stress or suffocation or maybe i'd hit my head or drown. but this is killing me in a different way too. just, probably, slower.

“do you really wanna be on medication for the rest of your life” if you knew me unmedicated you’d want me to be on medication for the rest of my life too

[evieville]

Every time our leg involuntarily kicks I just start thinking about that season one episode of House where he figures out a kid has an Issue because of a myoclonic jerk and then I get very distracted thinking about the difference between the early seasons of House and the later ones. This would not matter if we didn't have muscle spasms and thus fairly frequent involuntary kicking but alas

[cinivia]

The only way they can test you for MS and see it on your brain, is with an MRI WITH CONTRAST. Which my doctors failed to order for me. My MRI was without contrast.

There’s honestly a high probability that I have MS. I have every symptom.

It’s been one year already and I still have no answers for why I’m experiencing the symptoms that I’m having. Seizures, Dystonia, involuntary limb movements, spasms, limb jerks all over my body, vibrating sensations all over my body, brain fog, constant migraines, constant fatigue. Focal seizures, myoclonic seizures, I stop breathing when I sleep sometimes.

this is all autoimmune triggered.

Now I have to ask my neurologist for a referral to see a rheumatologist. and if you’re a new patient you have to wait months to see a new specialist.

I don’t have the patience for this. It’s insane how long you have to wait. They order one test and you have to wait a month for it to be performed because your insurance has to approve it. It’s just absolutely diabolical.

Me once again complaining about the healthcare industry. And I work in it. 💀

[xtruss]

'Exploding Head Syndrome'? Inside A Mysterious, Disturbing Sleep Condition

This Little Understood Disorder Leads Some to Hear Loud Crashes or Booms as They're Drifting Off to Sleep.

— By Karen Peterson | March 12, 2024

Brain and brain waves during deep sleep, as depicted by a computer illustration. Exploding head syndrome is characterized by a loud boom heard just as one drifts off to sleep (A Brain, Outlined in Yellow with a Kaleidoscope of Colors with Purple, Electric, Squiggly Lines). Illustration By Kateryne Kon, Science Photo Library, Getty Images

A musician and guitar luthier who's no stranger to loud noises, Dave Lovos admits to being a bit undone by the boom he heard in his head one night earlier this year. It hit just as Lovos was drifting off to sleep, the force of it snapping him to attention.

"It was a very sharp sound inside my head at the top of my skull," says Lovos, and along with the deafening internal explosion he saw the flash of a car crash. "The two seemed to happen at once."

What Lovos experienced is known by the unscientific but evocative moniker "exploding head syndrome" (EHS), a mysterious example of a parasomnia, or sleep disorder. Parasomnias include sleepwalking, sleep talking, sleep paralysis, and pesky muscle spasms known as "myoclonic jerks." In most cases, these parasomnias are normal and harmless, except when physical danger or pain is involved.

"My office would be a lot messier if heads were actually exploding," says Brian Sharpless, a licensed clinical psychologist who specializes in sleep. Sharpless is among the handful of psychologists and others researching EHS. He says the condition is harmless.

"As long as you're not having pain during [an episode], it's not anything really to worry about," he says.

What Causes the Condition

Very few people who experience EHS seek medical advice, or even bring it up to their doctors or loved ones, says Sharpless.

In one study, only 11 percent had reported EHS to a professional, and only eight percent of patients with recurring episodes sought prevention. Some are embarrassed about admitting to "hearing noises"; most go on with life when there's no sign of continued distress or pain.

Jennifer McDonald Slowik, sleep medicine physician with Frederick Health Medical Group in Frederick, Maryland, and board member of the Maryland Sleep Society, also says it is uncommon for someone to seek EHS treatment.

EHS usually comes up as part of a sleep clinic's extended evaluation, she says. "We usually ask questions about narcolepsy," symptoms of which can include hallucinogenic sounds.

"If there is any concern about something more serious, we do an [additional test] as part of a sleep study to make sure nothing else is there," she adds.

Like Slowik, Sharpless warns that diligence is always the best policy when it comes to the head. In the worst-case scenario, EHS with pain could be a sign of the more dangerous and deadly subarachnoid brain hemorrhage.

Usually lasting less than a second, the first misconception about EHS is its timing: Rather than waking a person up, EHS is experienced in the ephemeral moment of the "sleep-wake" transition before slumber, known as the "hypnagogic state."

According to Sharpless, studies, including those with EEG brain monitoring, have yet to identify EHS activity during sleep. Rather, it is thought to be a type of neuronal misfiring as the brain begins to shut down areas associated with awake-time auditory, visual, and motor activity.

"You could even say they were just in a state of being really, super relaxed," he adds. "That's when it seems people have these events."

By loose definition, EHS is an "auditory hallucination," and in clinical terms expresses itself as a "paroxysmal sensory parasomnia," or sleep disorder presenting as a "sudden outburst" of sound. EHS is not tinnitus, a common misconception.

Crashes, Gunshots, and Slamming Doors

Lovos heard something akin to a car crash, which is among the many descriptions given by EHS study participants. The range of examples is broad, but the end results are the same: disturbing noises.

Among the many common descriptions, as told to researchers including Sharpless, people hear an explosion or bomb; a door slamming; something hitting the wall; a gunshot or fireworks; metal pans banging together; a scream; waves crashing; lightning; "an enormous roar"; cars driving by.

"You're not hearing symphonies, you're not hearing articulate speech, you're hearing big, massively loud noises," said Sharpless. He says the best description he’s heard is a patient who described it as "Wily Coyote trying to drop a piano on the Road Runner."

EHS was first named and discovered in 1876 by Philadelphia neurologist Silas Weir Mitchell, who wrote of patients who had heard "gunshots" and "pistols." He called the phenomenon "sensory shock." In the 1980s, neurologist J.M.S. Pearce changed it to EHS. Sharpless and colleague Peter Goadsby, a neuroscientist at King’s College London, are pushing for a name change to "episodic cranial sensory shock."

Pearce, who gave EHS its name in 1989, reported "little evidence of relevant past illness and no other CNS [central nervous system] disease in evidence, adding, "It is entirely benign, and I suspect quite common, but underreported."

"What causes the bomb-like noise remains a mystery," wrote Peace, an observation that Sharpless and other researchers also conclude three decades later.

Classified as a sleep disorder in 2005 by the American Academy of Sleep Medicine, the small number of studies to date have dismissed earlier clinical claims that women over 50 were more prone to EHS. Data today show that the incidents are almost equally divided among men and women. In a study out of Washington State University, authored by Sharpless, upwards of 13 percent of college students reported at least one episode.

While EHS has been "named" since the mid-1800s, records of earlier occurrences are missing, with one exception. One 2018 paper suggested that 17th century philosopher Rene Descartes had a head explosion between two dreams that he said helped answer the question, "What path in life should I pursue?”

"Despite being harmless, those affected are understandably concerned that it may be a sign of a serious brain condition," the paper noted, "and they usually feel too embarrassed to talk about their experience in case they are judged or disbelieved."

[treatmentguidelines]

Merrf syndrome

Merrf Syndrome, also known as Myoclonic Epilepsy with Ragged Red Fibers, is a rare genetic disorder that affects the functioning of the mitochondria, the powerhouse of the cells. In this blog post, we will explore what Merrf Syndrome is, its causes, and the various symptoms and signs associated with it. Furthermore, we will delve into the genetic mutations linked to this syndrome and how it is diagnosed. Additionally, we will discuss the available treatment options, including managing the symptoms and providing supportive care for individuals living with Merrf Syndrome. Moreover, we will highlight the ongoing research and advancements in the field, as well as provide insights into the prognosis and life expectancy of those affected. Lastly, we will shed light on the challenges faced by individuals living with Merrf Syndrome and the available resources and support available to them.

What Is Merrf Syndrome

MERRF syndrome, which stands for Myoclonic Epilepsy with Ragged Red Fibers, is a rare and progressive neurological disorder that affects both children and adults. It is a mitochondrial disease characterized by a variety of symptoms including epilepsy, muscle weakness, and developmental delays. The name "ragged red fibers" refers to the appearance of muscle fibers under a microscope, which show red staining and abnormal shapes. This condition is caused by mutations in the mitochondrial DNA, specifically in the MT-TK gene. MERRF syndrome is a genetic disorder that is inherited in a mitochondrial pattern, meaning it is passed down from the mother to her children. Mitochondria are responsible for producing energy in our cells, and when there is a mutation in the mitochondrial DNA, it can disrupt the normal functioning of the cells. This can lead to the symptoms associated with MERRF syndrome, such as seizures and muscle weakness. There are several symptoms and signs that are commonly associated with MERRF syndrome. One of the most prominent features is myoclonic epilepsy, which is characterized by sudden, involuntary muscle jerks or twitches. These can occur at any time and can be triggered by various factors such as stress or physical activity. Other symptoms may include muscle weakness, hearing loss, problems with balance and coordination, and developmental delays in children. Additionally, individuals with MERRF syndrome may experience progressive deterioration of their cognitive abilities. - Genetic mutations play a crucial role in the development of MERRF syndrome. Specifically, mutations in the MT-TK gene are responsible for disrupting the normal functioning of mitochondria, leading to the characteristic features of the condition. These mutations can vary among individuals, resulting in a wide range of symptoms and severity. - Diagnosing MERRF syndrome can be challenging, as its symptoms overlap with other neurological disorders. However, genetic testing can help identify mutations in the mitochondrial DNA and confirm the diagnosis. Additionally, doctors may perform other tests such as electroencephalogram (EEG) to evaluate brain activity and muscle biopsy to examine the ragged red fibers in the muscle tissue. - Treatment for MERRF syndrome focuses on managing the symptoms and improving the individual's quality of life. This may involve a combination of medications to control seizures and muscle spasms, physical therapy to maintain muscle strength and mobility, and occupational therapy to address any developmental delays or difficulties with daily activities. Research and Advancements Ongoing research in MERRF syndrome is exploring potential treatments and interventions to target the underlying genetic mutations and improve outcomes. Scientists are also investigating potential gene therapy approaches to correct the mitochondrial defects in the affected individuals. Living with MERRF syndrome can be challenging, both for the individuals diagnosed and their families. It is important to seek supportive care from healthcare professionals who specialize in mitochondrial disorders. These experts can provide guidance and resources to help manage the symptoms, monitor the disease progression, and address any emotional or psychological impacts. While MERRF syndrome is a progressive disorder, it is important to remember that every individual's experience with the condition is unique. The prognosis and life expectancy of MERRF syndrome can vary depending on the severity of symptoms and overall health of the individual. However, with appropriate management and support, individuals with MERRF syndrome can lead fulfilling lives and participate in activities they enjoy. It is essential for individuals with MERRF syndrome and their families to have access to resources and support networks. Organizations such as the United Mitochondrial Disease Foundation and the Myoclonic Epilepsy with Ragged Red Fibers Community can provide valuable information, advocacy, and connections to other individuals who are going through similar experiences. These resources not only offer support but also contribute to raising awareness and promoting further research into MERRF syndrome.

Causes Of Merrf Syndrome

MERRF syndrome, which stands for Myoclonic Epilepsy with Ragged Red Fibers, is a rare genetic disorder that affects the mitochondria, the energy-producing centers in cells. This condition is characterized by a variety of symptoms, including muscle weakness, myoclonic seizures, ataxia, and hearing loss. The exact cause of MERRF syndrome is due to mutations in the mitochondrial DNA. Mutations in the MT-TK gene are the most common cause of this syndrome, although other genes can also be involved. One of the main causes of MERRF syndrome is the presence of genetic mutations in the mitochondrial DNA. These mutations often occur spontaneously and are not inherited from either parent. However, in some cases, MERRF syndrome can be inherited from a person's mother, who may have the same genetic mutation. This is because mitochondria are passed down from the mother to the child. Therefore, if the mother carries the mutated mitochondrial DNA, there is a risk of passing on the syndrome to her offspring. In addition to genetic mutations, other factors can also contribute to the development of MERRF syndrome. Environmental factors, such as exposure to toxins or certain medications, may increase the risk of developing this condition. However, these factors are believed to play a smaller role compared to the genetic component. Researchers have made significant advancements in understanding the causes of MERRF syndrome. Through genetic testing, they have identified specific mutations in the mitochondrial DNA that are associated with the syndrome. This has allowed for more accurate diagnosis and has provided insights into the underlying biology of the disorder. Ongoing research continues to explore other potential causes and contributing factors, as well as potential treatment options for individuals living with MERRF syndrome. Common Causes of MERRF Syndrome: 1. Genetic mutations in the mitochondrial DNA, particularly the MT-TK gene. 2. Inheritance of the mutated mitochondrial DNA from the mother. 3. Environmental factors, although their role is not well-understood. It is important to note that while the exact causes of MERRF syndrome have been identified, there is currently no cure for this condition. Treatment options focus on managing the symptoms and providing supportive care to improve the quality of life for affected individuals. Genetic counseling is also recommended for individuals who may be at risk of passing on the syndrome to their children. In conclusion, MERRF syndrome is primarily caused by genetic mutations in the mitochondrial DNA, particularly the MT-TK gene. The inheritance of these mutations from the mother can also contribute to the development of the syndrome. Ongoing research and advancements continue to shed light on the underlying causes and potential treatment options for this rare genetic disorder.

Symptoms And Signs Of Merrf Syndrome

MERRF syndrome, which stands for Myoclonic Epilepsy with Ragged Red Fibers, is a rare genetic disorder that affects the mitochondria, the energy-producing structures within cells. This syndrome is typically characterized by a combination of neurological symptoms and multi-systemic involvement. The symptoms and signs of MERRF syndrome can vary greatly between individuals, but there are several common features that may help in its identification. Muscle problems: One of the key symptoms of MERRF syndrome is muscle weakness and wasting (atrophy). Affected individuals may experience difficulty with fine motor skills, such as writing or buttoning a shirt. They may also have muscle stiffness, spasms, or involuntary jerking movements known as myoclonus. These symptoms can greatly impact a person's mobility and coordination. Epilepsy: Another prominent feature of MERRF syndrome is the presence of seizures, particularly myoclonic epilepsy. These seizures are characterized by sudden, brief muscle jerks or twitches. They may occur spontaneously or be triggered by various factors such as stress, sleep deprivation, or certain medications. Seizures can vary in intensity and frequency, and their management is an essential aspect of MERRF syndrome treatment. Neurological and sensory involvement: MERRF syndrome can also affect the central nervous system and peripheral nerves. Individuals may experience cognitive impairment, such as difficulties with learning, attention, and memory. Sensory abnormalities may include deafness, hearing loss, or vision problems, including retinal changes that can be detected through an eye exam. These neurological and sensory symptoms further contribute to the complexity of the condition.

Genetic Mutations And Merrf Syndrome

Genetic Mutations And MERRF Syndrome MERRF Syndrome, which stands for Myoclonic Epilepsy with Ragged Red Fibers, is a rare genetic disorder that affects the mitochondria, the powerhouse of our cells. This syndrome is caused by mutations in the genetic material of the mitochondria rather than the nuclear DNA. Mitochondrial DNA mutations can be inherited from one or both parents, or they can occur spontaneously during the formation of reproductive cells. The genetic mutations associated with MERRF Syndrome can lead to a range of symptoms and complications, making it essential to understand the underlying genetic factors. One of the key genetic mutations linked to MERRF Syndrome is the mitochondrial DNA A8344G mutation. This specific mutation affects the transfer RNA*Lys gene and is most commonly associated with MERRF Syndrome. This mutation disrupts the production of proteins within the mitochondria, leading to the impaired function of these vital organelles. As a result, affected individuals may experience a wide array of symptoms, including muscle weakness, seizures, ataxia, and cognitive impairment. Another genetic mutation related to MERRF Syndrome is the mitochondrial DNA T8356C mutation. This mutation affects the transfer RNA*Ser gene and has been found in individuals diagnosed with MERRF Syndrome. Similar to the A8344G mutation, the T8356C mutation impairs mitochondrial protein synthesis, leading to the characteristic features of the syndrome. It is worth noting that these genetic mutations are not the only ones associated with MERRF Syndrome. Researchers continue to explore different mutations and their specific implications to gain a better understanding of this complex disorder. Common Genetic Mutations in MERRF Syndrome Associated Features A8344G Impacts transfer RNA*Lys gene T8356C Affects transfer RNA*Ser gene The identification of these genetic mutations plays a crucial role in diagnosing MERRF Syndrome. Genetic testing, including mitochondrial DNA sequencing, can help confirm the presence of these mutations in affected individuals. It is important to note that not all individuals with MERRF Syndrome will have these specific mutations, highlighting the genetic heterogeneity of the disorder.

Diagnosing Merrf Syndrome

MERRF syndrome, also known as Myoclonic Epilepsy with Ragged Red Fibers, is a rare genetic disorder that affects the mitochondria, which are the energy-producing structures within cells. People with MERRF syndrome have various symptoms, including muscle weakness, seizures, and developmental delays. In order to diagnose MERRF syndrome, healthcare professionals utilize a combination of genetic testing, medical history review, physical examination, and laboratory tests. Genetic testing plays a crucial role in diagnosing MERRF syndrome. By analyzing a person's DNA, doctors can identify mutations in the mitochondrial DNA or nuclear DNA, which are responsible for causing the condition. This testing is usually done using a blood sample or a saliva sample. If a known mutation is found, it can confirm the diagnosis. However, in some cases, the genetic testing may not identify any known mutations, making the diagnosis more challenging. Medical history review and physical examination are also important steps in the diagnostic process. Doctors will ask about the individual's symptoms, family history, and any other relevant information. During the physical examination, they may look for specific signs, such as muscle weakness, myoclonus (involuntary muscle jerks), and the presence of ragged red fibers in muscle biopsies. Laboratory tests can provide additional information to support the diagnosis of MERRF syndrome. These tests may include blood tests, urine tests, and muscle biopsies. Blood tests can measure the levels of lactate, pyruvate, and creatine kinase, which can be elevated in individuals with MERRF syndrome. Urine tests may reveal high levels of certain metabolites, further indicating the presence of the disorder. Muscle biopsies, where a small sample of muscle tissue is removed and examined under a microscope, can show characteristic ragged red fibers, which are abnormally structured muscle fibers. In conclusion, diagnosing MERRF syndrome involves a comprehensive approach that combines genetic testing, medical history review, physical examination, and laboratory tests. It is essential for healthcare professionals to diligently investigate the presence of this rare condition to ensure accurate diagnosis and appropriate management strategies. Early diagnosis is crucial in providing individuals with MERRF syndrome the necessary care and support to improve their quality of life.

Treatment Options For Merrf Syndrome

MERRF syndrome, or Myoclonic Epilepsy with Ragged Red Fibers, is a rare genetic disorder that affects the mitochondria in the body's cells. This syndrome is characterized by a variety of symptoms, including myoclonic seizures, muscle weakness, and progressive neurological deterioration. Although there is currently no cure for MERRF syndrome, there are treatment options available to help manage the symptoms and improve quality of life for individuals affected by this condition. One of the primary treatment options for MERRF syndrome is medication. Anticonvulsant drugs can be prescribed to help control seizures and reduce the frequency and intensity of myoclonic jerks. These medications work by stabilizing the electrical activity in the brain and preventing abnormal firing of neurons. It is important for individuals with MERRF syndrome to work closely with a healthcare provider to find the most effective medication and dosage for their specific symptoms. In addition to medication, individuals with MERRF syndrome may benefit from other forms of therapy. Physical therapy can help improve muscle strength and coordination, while occupational therapy can assist with maintaining independence in daily activities. Speech therapy may also be useful in managing any speech or swallowing difficulties that may arise due to muscle weakness. These therapies can be tailored to the individual's needs and can be instrumental in maximizing their functional abilities. - Home modifications can also be an important part of treatment for individuals with MERRF syndrome. Simple adaptations to the home environment, such as grab bars in the bathroom or ramps for wheelchair accessibility, can enhance safety and independence. It is important to consult with a healthcare professional or occupational therapist for guidance on specific home modifications that may be beneficial. Moreover, patients with MERRF syndrome may also benefit from palliative care interventions. The goal of palliative care is to improve the quality of life for individuals with serious illnesses, such as MERRF syndrome. This type of care focuses on providing relief from symptoms, managing pain, and addressing emotional and psychosocial needs. Palliative care can be provided alongside other treatments and is aimed at supporting the overall well-being of the individual. Advancements in research While there is currently no cure for MERRF syndrome, ongoing research is aimed at better understanding the condition and developing potential treatments. Scientists are studying the underlying genetic mutations responsible for MERRF syndrome, which may open up opportunities for targeted therapies in the future. Advances in mitochondrial replacement therapies and gene editing techniques may hold promise for individuals affected by MERRF syndrome, offering hope for improved treatment options in the years to come. In conclusion, although there is no cure for MERRF syndrome at present, there are treatment options available to help manage the symptoms and improve the quality of life for individuals with this condition. Medications can help control seizures, while therapies such as physical and occupational therapy can enhance functional abilities. Home modifications and palliative care interventions can also play a significant role in providing support and improving overall well-being. Ongoing research holds promise for future advancements in treatment options for MERRF syndrome, potentially offering hope for individuals and their families.

Managing The Symptoms Of Merrf Syndrome

Managing the Symptoms of MERRF Syndrome MERRF syndrome, which stands for Myoclonic Epilepsy with Ragged Red Fibers, is a rare genetic disorder that affects the mitochondria, the powerhouses of the cells. Individuals with MERRF syndrome often experience a variety of symptoms that can significantly impact their daily lives. While there is currently no cure for MERRF syndrome, there are various strategies and treatments available to help manage the symptoms and improve quality of life. One of the primary goals in managing MERRF syndrome is to control the seizures and reduce their frequency. Antiepileptic medications, such as valproic acid or carbamazepine, are commonly prescribed to help decrease seizure activity. Read the full article

[coloradopharmacyonline]

WHAT IS CLONAZEPAM AND HOW DOES IT WORK?

Clonazepam is a medication that belongs to the benzodiazepine class, which is commonly prescribed for its effects on the central nervous system. It is used primarily for its anxiolytic (anti-anxiety), anticonvulsant (anti-seizure), and muscle relaxant properties.

Mechanism of Action:

Clonazepam works by enhancing the effects of a neurotransmitter called gamma-aminobutyric acid (GABA) in the brain. GABA is an inhibitory neurotransmitter, meaning it reduces the activity of nerve cells (neurons) in the brain. It helps to regulate neuronal excitability and has a calming effect on the nervous system.

When Clonazepam is ingested, it binds to specific receptors in the brain known as GABA-A receptors. This binding increases the effectiveness of GABA, leading to an overall increase in inhibitory signaling. As a result, Clonazepam helps to reduce the excessive neuronal activity that can contribute to anxiety, seizures, and other conditions.

Effects and Uses:

Anxiolytic Effects: Clonazepam's enhancement of GABA activity results in a calming effect on the brain. This makes it effective for reducing symptoms of anxiety disorders by reducing feelings of worry, nervousness, and restlessness.

Anticonvulsant Effects: By increasing GABA-mediated inhibition, Clonazepam helps to prevent or reduce abnormal electrical activity in the brain, which can lead to seizures. It is used to treat various seizure disorders, including absence seizures and myoclonic seizures.

Muscle Relaxant Effects: Clonazepam's ability to suppress neuronal activity also extends to muscle cells. This makes it useful for managing conditions characterized by muscle spasms, such as myoclonus and certain forms of spasticity.

Sleep Improvement: The calming effects of Clonazepam can help improve sleep quality in conditions like restless legs syndrome (RLS) or insomnia associated with anxiety.

Adjunctive Treatment: In some cases, Clonazepam is used alongside other medications to manage certain aspects of bipolar disorder or alcohol withdrawal.

It's important to note that while Clonazepam has therapeutic benefits, it also carries potential risks, especially with long-term use. It can lead to tolerance (requiring higher doses for the same effect), dependence (resulting in withdrawal symptoms upon discontinuation), and cognitive impairments. Clonazepam should be taken under the supervision of a healthcare professional and used at the lowest effective dose for the shortest duration necessary. It's essential to follow medical guidance to minimize potential side effects and risks.

WHAT ARE DOSES OF CLONAZEPAM?

The appropriate dosage of Clonazepam (brand name: Klonopin) can vary widely depending on the specific condition being treated, an individual's medical history, their response to the medication, and other factors. It's crucial to follow your healthcare provider's instructions and recommendations regarding dosing. Clonazepam is available in various forms, including tablets and orally disintegrating tablets. The dosages listed here are general guidelines and may not apply to every individual:

For Anxiety Disorders:

Starting dose: 0.25 to 0.5 mg taken orally 2 to 3 times per day.

Maintenance dose: The dose can be increased gradually based on response, typically not exceeding 4 mg per day.

The maximum recommended daily dose is usually around 4 mg.

For Panic Disorder:

Starting dose: 0.25 mg taken orally twice per day.

Maintenance dose: The dose can be adjusted based on the individual's response, but it usually ranges from 1 to 4 mg per day.

The maximum recommended daily dose is generally around 4 mg.

For Seizure Disorders:

Dosage can vary widely based on the specific type of seizure disorder and the individual's needs.

Starting doses are generally lower and then gradually increased to find the optimal dosage that effectively controls seizures while minimizing side effects.

Maintenance doses can range from 1 to 20 mg per day or even higher in some cases.

For Restless Legs Syndrome (RLS):

The dose for RLS is generally lower compared to anxiety or seizure disorders.

Starting dose: 0.25 mg taken orally before bedtime.

Maintenance dose: The dose can be increased based on response, but it typically doesn't exceed 3 mg per day.

It's important to note:

Clonazepam should be taken as prescribed by a healthcare professional.

Dosages may be adjusted gradually to achieve the desired effect while minimizing side effects.

The duration of treatment can vary based on the condition being treated, but long-term use should be carefully evaluated due to the potential for dependence and other risks.

Dosages may need to be lowered for individuals with liver or kidney impairment.

Never adjust your Clonazepam dosage or stop taking it without consulting your healthcare provider. Suddenly stopping Clonazepam can lead to withdrawal symptoms and other complications. Always communicate openly with your doctor about your symptoms, concerns, and any changes you experience while taking this medication.

ARE THERE ANY SIDE EFFECTS TO USING CLONAZEPAM (KLONOPIN)?

Clonazepam (brand name: Klonopin) is associated with various side effects, ranging from mild to potentially serious. Not everyone will experience these side effects, and their severity can vary. It's important to be aware of the possible side effects and to communicate with your healthcare provider if you experience any concerning symptoms. Here are some common side effects associated with Clonazepam:

Common Side Effects:

Drowsiness

Dizziness

Fatigue

Impaired coordination or balance

Difficulty concentrating

Memory problems

Increased salivation

Slurred speech

Less Common Side Effects:

Confusion

Changes in appetite

Muscle weakness

Blurred vision

Gastrointestinal disturbances (nausea, diarrhea)

Skin rash

Rare or Serious Side Effects:

Allergic reactions (rash, itching, swelling, severe dizziness, difficulty breathing)

Mood changes (agitation, aggression, mood swings)

Hallucinations or delusions

Suicidal thoughts or behavior

Severe drowsiness or sleepiness

Memory loss or amnesia

Changes in sexual desire

Dependence and Withdrawal:

Long-term use of Clonazepam can lead to physical and psychological dependence, which means that abruptly stopping the medication can result in withdrawal symptoms. These withdrawal symptoms can include anxiety, insomnia, tremors, muscle cramps, and seizures in severe cases. It's important to work with your healthcare provider to gradually reduce the dosage if you're planning to discontinue Clonazepam.

Tolerance and Rebound Symptoms:

With prolonged use, some individuals might develop tolerance to Clonazepam's effects, which means the medication becomes less effective over time. Additionally, there could be a rebound worsening of symptoms, especially anxiety, when the medication's effects wear off.

Interactions and Overdose:

Clonazepam can interact with other medications, especially central nervous system depressants like alcohol, opioids, and certain sleep medications. Combining these substances can lead to increased sedation and respiratory depression. An overdose of Clonazepam can result in serious complications and should be treated as a medical emergency.

It's essential to discuss any concerns or unusual symptoms with your healthcare provider. If you experience severe or concerning side effects, seek medical attention immediately. Your healthcare provider can help you weigh the benefits of Clonazepam against potential side effects and work with you to adjust your treatment plan if necessary.

[relahospital-16]

The different types of epilepsy are idiopathic epilepsy, symptomatic epilepsy, cryptogenic epilepsy, juvenile myoclonic epilepsy and absence epilepsy. Some types specific to childhood are infantile spasms and Lennox-Gastaut syndrome.

[nursingscience]

SLEEP MYOCLONUS

You have been experiencing some strange things in your body during sleep.

It sounds like you might have sleep myoclonus,, which is a form of involuntary muscle twitching that occurs either as you fall asleep or during sleep. It is also known as a hypnic jerk or hypnagogic jerk.

Sleep myoclonus is not a disease but a symptom of several different conditions.

▪️Some possible causes of sleep myoclonus are:

1. Sleep disorders, such as periodic limb movement disorder or rhythmic movement disorder.

2. Epilepsy, especially juvenile myoclonic epilepsy

3. Anxiety and stress

4. Physical stress from exercise before bedtime

5. Caffeine intake

6. Alcohol consumption

7. Medications or drugs

Sleep myoclonus can affect your sleep quality and cause daytime fatigue. If you are concerned about your condition, you should consult a doctor for a proper diagnosis and treatment. They may prescribe medications to reduce the muscle spasms or suggest lifestyle changes to improve your sleep hygiene.

▪️Some medications that can help treat sleep myoclonus are:

1. Antiseizure and anticonvulsant medications, such as clonazepam (Klonopin), phenytoin (Dilantin), and levetiracetam (Keppra)

2. Sedatives, such as barbiturates

5-hydroxytryptophan, an amino acid in serotonin1

3. Botulinum toxin (Botox)

These medications may reduce the frequency and severity of the muscle spasms, but they may also cause side effects, such as drowsiness, dizziness, or nausea.

You should consult your doctor before taking any medication for sleep myoclonus. They can prescribe the appropriate dosage and monitor your condition. Do not stop taking your medication without your doctor’s advice.

[brooklynislandgirl]

@kylo-wrecked   {{And angels weep}}

A single word ought not bite and make the wound bleed, but it does. She feels it slink its way into her at too-damn-late in the early morning, reeking of stale beer and blue jazz flavoured smoke. Helps itself to left over cold sobe noodles right out of the carton in the fridge. She doesn't remember giving it a key or extending him that kind of invitation but there they have it. She still manages to roll over ~all of her body turned toward him~ and let it stay. Regardless of his intentions perhaps she's fallen pray to the depth of potency that he holds, the faint strains of a sonata she cannot remember the name of, if he's an original composition created in the moment or something classic from a time long before they were even born. He slices through everything else with a clean edge. Scores her in a way she can't put a finger on. He leaves behind the kind of desecration with that duality of expression, which itself hinges the world on her own empathy. She cannot make herself look away.

At least not until the waitress edges her way into the middle of this stunted conversation, a wall built with speed as if by Hadrian. It's enough to shunt her nearly back into her liminal space. Not the first time she's been culled from a conversation, not the first time she's experienced the sudden and bitter realisation that she's competing outside of her weight class. As such the surprise when she notices him still casting his Stygian gaze her way is genuine and not one she can easily hide behind a mask of feigned apathy. He draws over himself, night over a starless sea. No. That isn't right, implies a seamless fluidity. Neither is it chorea or myoclonic muscle disorder. It's the spasm of a jellyfish on the body of a robust and beautiful orchid mantis. Does he eat lotuses? She's a hundred percent sure that if he did, they would melt on his tongue, just to be that much closer to him. But she isn't blind, she can see a glimpse of something darkly fragile beneath his gilded facade. She gets completely blind-sided. "How...." did you know what I was going to ask you? "How you know dat word?" It's a co-opted word from when missionaries came, the advanced scouts of what would become a occupying force, one that would illegally overthrow the monarchy and drag her kingdom into pampered slavery. A much larger scale than what was done to her very own mother. It can mean half, or it can mean part, and is used, sometimes welcome and sometimes scornfully for those with island blood. Later it was borrowed by others and Beth can't really blame them for stealing a stolen word.  For him to know it? A new flare of intrigue lights her gaze as she gazes more boldly. Just in time to see the mouthed words. What Beth lacks in aural capacity she more than makes up for with sight and smell and taste. Her tongue flirts with the edge of her lower lip and she swallows. She nods even as her face screams in red. They really are beautiful. He rises like a wave and the feel of his crashes over her. As her head tilts up to meet his face she finds her hand of its own accord reaching out. She'd intended to catch him by the wrist, halt his inevitable flight. Instead, she brushes his hip. She nods and in turn climbs off the couch. She’s all sand coloured skin and the skeleton of some kind of perfume that’s subtle but sweet. The whisper of a dress she wears hugs her in shadow as she asks "Go wheah? Some place mo' quiet?"

[blue-opossum]

50+ Years of Knowledge of Dream Content Causality, 1

        3 minutes to read.

        Tuesday afternoon, 20 December 2022.

          50+ Years of Knowledge of Dream Content Causality, 1

        Upon entering sleep at the beginning of every sleep cycle, dream content naturally confirms the absence of real-world physicality and mobility and presents two narratives in a sequence that has remained virtually the same for over 50 years.

        My inability to keep walking in each first post-hypnagogic dream (loss of real-world leg mobility) results in the intense but imaginary sensation of my right foot slipping forward as I fall backward, rapidly waking with leg myoclonus. Sometimes, it seems to be both of my feet and legs responding - more intense if I had walked more the previous day. Typically, the effect is like spontaneously attempting to kick a ball with my right foot and missing it while falling backward (even though my dream only implies I am merely walking). The sensation is blissful and amusing, not alarming.

        My second dream typically involves someone dropping something (corresponding with an absence of arm mobility and dexterity). Curiously, my second dream often involves another character dropping something.

        Myoclonus in my shoulders or back sometimes correlates with my degree of liminality, the state between dreaming and viable consciousness. My anticipation of it (whether or not it seems imminent) affects its intensity. As such, it sometimes has the curious essence of trying to control an impending sneeze (even when there is only a vague perception of its possibility), which is self-evident, as sneezing occurs with myoclonic dynamics.

        People might think that experiencing the same liminal perceptions and dream themes at the start of every sleep cycle for over 50 years would encourage intentional directing of the transition. My response is spontaneous and occurs too quickly to gain control (unlike hypnagogic dreams that I explore and influence). The event typically happens because I suddenly (rather than gradually) recognize that I am fully within an illusion with imaginary physical modeling (in contrast to when I "walk with intent" in stabler dreams later in my sleep cycle). (Most people spontaneously wake up once they know they are dreaming, even so-called lucid dreamers, though "walking with intent" is one method I use to stabilize and vivify the dream state later in my sleep cycle.) It is as reliable as compartmentalized virtual amnesia when only one strand of real-world recall is active. It does not matter because deliberate summoning and direction of dream content occur in the first stage of every sleep cycle regardless (which I have never written much about online).

        With REM atonia becoming more established and myoclonus more unlikely, the illusory sensations of distorted proprioception and vestibular-motor nuances inspire me to pretend I am riding in a car, bus, boat (typically a skiff or canoe), or on a train. (Illusory physical responses develop before imagined visual content and usually remain a short time after the rest of a dream has faded.) This imaginary movement is smoother and does not result in myoclonus or expectation of wakefulness. It brings me into a peaceful, comfortable state. Later, I experience at least one flying dream, as I have every sleep cycle since my earliest memories.

        As a child and young adult, my back myoclonus was always in the small of my back. As an adult, it is now solely one or both shoulders or in the middle of my upper back. The intensity varies from a light shoulder twitch to an intense spasm in my upper back.

        Illusory perceptions in liminal states include the "three knocks." For over 50 years, it has always been three knocks, no more, no less, with the same rhythm and essence (though in the dream state proper, various narratives continue from here). My reticular activating system (RAS) responds to my state of liminality (when there is no imagery) to focus my attention to wake me. A door (even unseen) signifies the threshold of wakefulness between dreaming and viable consciousness.

        Sometimes these physiological responses occur in a sequence. While myoclonus results from my vestibular-motor response to entering or leaving deeper sleep with incomplete or decreasing REM atonia, the knocking exemplifies a hallucinatory auditory response when perceptual attention to real-world surroundings is minimal. With this mode, a dream narrative (with imagery) only occurs after the three knocks when I allow my sleep to continue.

        A typical combination is hearing the three knocks and, rather than waking up, I open a door in a post-hypnagogic dream, not necessarily corresponding to where I am living at the time and seeing someone who has dropped packages or bags outside "my" door.

[nuditorium]

having ptsd can be one of the most lonesome things to deal with. i have been experiencing myoclonic jerks (sudden and involuntary muscle/body spasms) since the summer time. this is a new symptoms for me. i am embarrassed of it. i feel alone. i feel ashamed. i feel wrong. i feel broken. i see the way people react whenever these spasms occur and I just want to run and hide forever. anytime someone touches me, hugs me, or even during medical checkups- i experience it. any physical touch or any reminders/triggers creates this reaction and i don't know what to do about it but feel intense shame. i feel extremely alone and i have nobody to talk to about this other than posting it into the tumble void. i want to cry. i hate this. and i moreso hate the individual who did this to me. i just wish i could remember how it felt like to feel safe. to feel normal. to not feel broken and wrong. i am sad. i am having a very difficult night tonight.