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#ropinirole
bpod-bpod · 10 months
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Delaying Tactics
A fatal neurodegenerative disease, amyotrophic lateral sclerosis (ALS) causes the progressive loss of motor neurons, cells that send signals from the brain to muscles. Patients gradually lose the ability to move, and ultimately even breathe on their own, often succumbing to respiratory failure. There is no cure, and existing therapies to mitigate symptoms have only limited effects, but new methods of drug discovery offer some hope. Researchers recently reprogrammed induced pluripotent stem cells derived from ALS patients (pictured) to make motor neurons, then used these to identify a potential drug candidate, known as ropinirole hydrochloride. Early clinical trials with small numbers of patients suggest the drug is safe, and that its protective effect on cultured cells translates to real benefits: taking the drug for 48 weeks led to slower declines in motor function, delaying disease progression. More extensive trials will help determine if this promising drug can yield new treatments.
Written by Emmanuelle Briolat
Image from work by Satoru Morimoto and Shinichi Takahashi, and colleagues
Department of Physiology, Keio University School of Medicine, Tokyo, Japan
Image copyright held by the original authors
Research published in Cell Stem Cell, June 2023
You can also follow BPoD on Instagram, Twitter and Facebook
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kingdrawcse · 6 months
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Ropinirole: Balancing Benefits and Risks🎲🍔
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Ropinirole is a dopamine agonist used for Parkinson's and restless leg syndrome. Like other dopamine boosters, it triggers our brain's 'reward system.' Some experience impulsive behaviors with potentially risky side effects, like gambling, overeating, shopping, or internet addiction. The severity of symptoms is linked to the dosage, and they gradually fade after discontinuation. However, quitting Ropinirole can lead to severe withdrawal reactions, making it challenging for long-term users to break free from the medication.
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kunalp1234 · 2 years
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agentnatesewell · 5 months
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It’s embarrassing that, due to my line of work, when the detective asks Verda if Garrett could have been given any drugs that would have increased his dopamine levels and I immediately thought of carbidopa-levodopa or ropinirole 🤦‍♀️
(anyway i love n going rogue in this scene and asking the question about saliva in front of a)
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Yet case reports are not hard to find. According to a 2010 article in the journal Sleep, a grandfather who was prescribed the dopamine agonist ropinirole for restless legs syndrome gained 200 pounds from binge eating and had his home raided by the police for illegal sexual activity on the Internet. In 2011, neurologists in Buenos Aires reported a Parkinson’s patient taking pramipexole who “was found by one of his sons attempting to have sexual intercourse with a female family dog.” In 2016, a 54-year-old Oregon man taking a dopamine agonist for Parkinson’s was sentenced to prison for exposing himself to 15 women in three different cities while wearing a wig. Once off the drug, many patients are so ashamed of their behavior that they are desperate to keep it secret. As Hannah put it, “You’re a professor, and you’re middle-aged, and you have esteem, and you’re walking around in a prostitute’s outfit with the word bitch across your chest. You might as well put me on a leash and walk me like a dog. It’s total degradation.”
“The Degradation Drug” from The American Scholar
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its-ticsticstics · 1 year
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Medications for Tourettes Syndrome
*This is not intended to be taken as medical advice. This is purely for educational purposes*
Goal of pharmaceutical treatment of TS
The goal of using medications in the treatment of Tourettes syndrome is not to completely remove tics but to help them become more managable along with any comorbid disorders.
Currently approved drugs for the treatment of TS
Neuroleptics: Haloperidol (Haldol), Pimozide (Orap), Aripiprazole (Abilify). Neuroleptics act to antagonize dopamine, through the blockade of type 2 dopamine receptors. In general, the higher the potency of dopamine blockade, the more effective a drug is in ameliorating tics.
Drugs used off-label for the treatment of TS
Atypical Antipsychotics: Risperidone (Risperdal), Clozapine, Olanzapine (Zyprexa), Quetiapine (Seroquel). Atypical antipsychotics are more selective dopamine receptor D2 blockers, although they can also affect serotonin. These drugs include risperidone, clozapine, olanzapine, quetiapine and the partial agonist aripiprazole. Atypical antipsychotics may be considered a safer treatment for tics due to the reduced risk of developing acute or subacute side effects. Risperidone may also treat comorbid aggression and obsessive-compulsive symptoms, and Olanzapine may help with morbid ADHD and aggression.
Experimental pharmalogical agents in the treatment of TS
Benzamides: Sulpiride, Tiapride; may also help treat echophenomena, aggression, tension, and obsessive-compulsive comorbidities.
Tetrabenazine: acts as dopamine antagonist, by reducing the presynaptic storage of monoamines and blocking postsynaptic DA receptors.
Alpha adrenergic agonists: Clonidine (Catapres), Guanfacine. These drugs may also help with comorbid oppositional defience, aggression, and obessive-compulsive symptoms.
Benzodiazepines: Clonazepam (Klonopin); addictive and generally best for transient use.
Anticonvulsants: Topiramate (Topamax), Levetiracetam (Keppra); better tolerated than neurleptics but conflicting evidence efficacy.
Dopamine Agonists: Pergolide (Permax), Apomorphine, Buspirone (Buspar), Ropinirole (Requip); typically medications that are used in the treatment of Parkinsonism, low doses may also treat tics.
Cannabinoids: THC in particular may also help with comorbid self-injurious behaviours, obsessive-compulsive symptoms, and ADHD.
*This is not an exhaustive list*
Sources: (x) (x)
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mcatmemoranda · 2 years
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My attending in clinic told me yesterday that the bone marrow makes blood at night, which is why restless leg syndrome occurs at night. Requip (ropinirole) has been used to treat RLS, but it actually makes it worse! You should check transferrin in pts with RLS. Low iron is common in people with RLS and treating low iron treats RLS.
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melissacastro · 2 years
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Time for bed as it has been a really long day. The pain has been really bad and I had a bout of chest pain. So here's hoping tomorrow is better than today!
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Tonight's Medication:
Lyrica 200mg
Pantoprazole 40mg
Atorvastatin 40mg
Cetirizine 10mg
Tizanidine HCL 2mg×2
Lithium Carbonate ER 300mg×3
Ropinirole 1mg
Sildenafil 10mg
Rizatriptan 10mg
Zofran 4mg×2
Percocet 10-325mg
Lorazepam 1m×2
Vitamins:
Biotin
Fish Oil
B 100 Complex
Women's Multi Vitamin
Probiotic
Co q 10
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writer59january13 · 8 months
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Self destructive wickedness arrested, convicted, and gaoled...
with kidnapping little boy
ordered to suffer
life sentence without parole. The deadly scourge of one obsessive/compulsive disorder
nearly left me starving to death.
Anorexia nervosa absent bulimia nadir of onset diagnoses schizoid personality disorder severe social anxiety still legion I aire behavior which agonizingly elicited slow suicide
courtesy self starvation
maelstrom within psyche of self as prepubescent lad
(particularly devastated immediate family members)
as emaciation pitted existential revulsion from unseen
wuthering heights betook courtesy yours truly
teased, hectored, and called “professor,”
when riding the school bus
nearly wrung death knell
annihilating fragile entity christened Matthew Scott Harris
with peremptory imprimatur yielding covalent bond to life
readily obvious to kith and kin
via zorro like signature per profound perilous depressive psychological state.
Now - at about
three decades plus six years from attaining rank of centenarian
perfect 20/20 hindsight
offers supreme advantage from swift current near drowning alluded earlier when das scribe juiced thwarted leapfrogging from pollywog tad metamorphosed
to witness puberty, whence devastating emotional crisis tripped, trilled,
and tricked aborted
natural healthy development
chronological denouement demise
jump/kick started
theorizing numerous educated guesses
within mind of
middle progeny and sole sol
(of the both late father and mother
Boyce and Harriet Harris) respectively
why he willfully hurtled his flesh at light speed
down the abyss toward death.
Literal and physical lightness of being
manifested within nooks and crannies
prior to full blown symptoms
to eliminate sustenance
drawing the curtain on brief residence
way before high noon of life.
Metamorphosis from boyhood
kindled burning man
found solace in attempting
to keep at bay of pigs hijacked
natural cycle, which seminal
transformation grieved me
to pine for nostalgic childhood’s end (albeit one fraught with romanticism)
vengefully interpreted attempt
to halt dead in the tracks intervention of mother,
whose nursing experience helped fend off passive attempt
to promulgate passive
silent plan to fruition.
She whipped various nutritious concoctions in the blender
to ensure minimal essentials to this, I readily admit) famished body
in conjunction with applying vital supplements into
one or the other skeletal
gluteus maximus
thru fuel injection,
which submissiveness to acquiesce, and bare bony buttocks
to receive iron injections
did absolutely nothing to squelch death wish.
I inexorably did buzzfeed
hashtagged eating disorder to go on a deadly hunger strike,
which essentially constituted declaration of independent control
despite horrendous craving for food jabbed innards like a pike
bifurcated psychic division
to live ousted coeval death wish goal
to seize yore reminiscent blissful, (albeit fictional) childhood over flooded self made damned dike
engaging, engendering, engineering
propensity to catapult yours truly into abysmal emotional hole
and way before the invention of Facebook, I mentally clicked like
to surrender mailer daemons all of me healthy development stole.
Imprimatur indelibly etched decades after bout with passive exit from life
crimp on psycho/social skills plus stunted physical growth cuts like a knife
affecting mental health with panic attacks and anxiety although existence
considerably less riddled qua debilitating symptoms
(such as vertigo, racing heart, profuse sweating, nausea, irritable bowels)
relying on the following prescription medications: BUSPIRONE HCL 15 MG TABLET
CLOMIPRAMINE 50 MG CAPSULE CLONAZEPAM 0.5 MG TABLET
FLUOXETINE HCL 40 MG CAPSULE
GLYCOPYRROLATE 2 MG TABLET
PRAZOSIN 1 MG CAPSULE PRAZOSIN 5 MG CAPSULE
RISPIRIDONE 1 MG TABLET
ROPINIROLE HCL 1 MG TABLET.
To add insult to injury yours truly also gifted
courtesy split uvula
but did little to ameliorate
the writer of these words
suffering brickbats as scape goat, whereby severe adenoidal vocalizations
allowed, enabled, and provided an easy target viz black barbs poised to strike, hurled,
and bullied me by peers.
Up until I entered six grade
(at Henry Kline elementary -
a one classroom per grade school)
classmates bullied, derided,
and feigned to hammer -
jabbing leering, nasty pimping ragout as a rule
which boyhood self of mine availed
a perfect bullseye target
with combination of diminutiveness,
being painfully quiet,
essentially remaining mum the entire day except when called upon
to answer question thence utterance emanating between lips
produced and emitted
a strong nasal sound to boot
grist for the mill
sans malice meted, mimicked, and mocked mashup
of mine warped congestion
ah, twas only by a fluke conversation,
whence speech pathologist
informed my parents about
The Lancaster cleft palate clinic,
where oral an examination
revealed minor birth defect
identified as a submucous cleft palate,
which explained the severe pinched twang
somewhat mitigated by wearing
a removable prosthetic
fastened with clasps to upper teeth
whereby a makeshift miniature
plastic protuberance closed the gap (at the expense of practically gagging me)
so air would be prevented
passing thru my button nose,
and thus gentle and soft as a shutterfly
shunted air out oral opening
though congenital defect disallowed
returning merchandise back to sender nor could blame be affixed
at either father nor mother
who both harbored the genetic mutation
now such admissions
re: aforementioned impediment allows,
enables and provides boasting rights if in a mood temper
any curiosity or satisfying a rumor whispered down the alley whence I said “ah”
left nagging nincompoops
as if pie hole filled with a gobstopper.
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statesandcounties · 10 months
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Understanding the Optimal Medication for Parkinson's Disease Tremors 1. Levodopa 2. Carbidopa-levodopa 3. Pramipexole 4. Ropinirole 5. Rotigotine Medication For Tremors From Parkinson's Parkinson's disease is a progressive neurological disorder that affects movement and coordination. One of the most common symptoms of Parkinson's disease is tremors, which can affect various parts of the body, including the hands, arms, legs, and head. Tremors can be distressing and can interfere with daily activities, such as writing, eating, and dressing. Fortunately, there are medications available that ... Read More. https://statesandcounties.com/2023/06/22/medication-for-tremors-from-parkinsons-best-medication-for-hand-tremors-from-parkinsons-disease/?feed_id=5315&_unique_id=649b23b7a79ad
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cavenewstimes · 11 months
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Parkinson's disease drug ropinirole safely slowed the progression of ALS for over 6 months in a clinical trial
2023-06-02 15:51:00Parkinson’s illness drug ropinirole securely slowed the development of ALS for over 6 months in a medical trialAmyotrophic lateral sclerosis (ALS), likewise referred to as Lou Gehrig’s illness, is a deadly motor nerve cell illness that triggers individuals to slowly lose control of their muscles. There is no remedy, Amyotrophic lateral sclerosis (ALS), likewise referred to as…
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psikologline · 1 year
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Huzursuz Bacak Sendromu Nedenleri ve Tedavisi
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Huzursuz Bacak Sendromu (HBS), sinir sistemiyle ilgili nörolojik bir rahatsızlık olan ve bacaklarda rahatsız edici hislerle karakterize bir durumdur. HBS genellikle istirahat halindeyken, özellikle akşam ve gece saatlerinde ortaya çıkar ve bacaklarda karıncalanma, yanma, sızlama ve ağrı gibi hislere neden olur. HBS'li kişiler bu rahatsız hislerin hafiflemesi için bacaklarını hareket ettirmeye, sallamaya veya ovuşturmaya ihtiyaç duyarlar. Bu durum, uyku problemlerine yol açarak yaşam kalitesini önemli ölçüde düşürebilir. Huzursuz Bacak Sendromu'nun kesin nedeni tam olarak bilinmemekle birlikte, genetik faktörler, demir eksikliği, böbrek yetmezliği, gebelik ve bazı ilaçlar gibi faktörlerin HBS'nin gelişiminde rol oynadığı düşünülmektedir. Tedavi, altta yatan nedenlere yönelik olabilir veya belirtileri hafifletmeye odaklanabilir. İlaç tedavisi, demir takviyeleri, dopamin agonistleri ve antikonvülsanlar gibi ilaçlar içerebilir. Ayrıca, yaşam tarzı değişiklikleri ve bacak kaslarını gevşetmeye yönelik fiziksel terapi de HBS belirtilerini hafifletmeye yardımcı olabilir. İşte huzursuz bacak sendromu nedenleri:
Huzursuz Bacak Sendromu ve Genetik Faktörler
Huzursuz Bacak Sendromu (HBS), genetik faktörlerle ilişkilendirilebilir. Ailede HBS öyküsü olan bireylerin, sendroma sahip olma olasılığı daha yüksektir. Genetik çalışmalar, HBS'nin kalıtımının çoğunlukla otosomal dominant olduğunu göstermektedir.
Demir Eksikliği ve Anemi
Demir eksikliği ve anemi, HBS'nin gelişiminde önemli faktörlerdendir. Beyindeki demir eksikliği, dopamin üretimindeki düşüşle ilişkilendirilmiştir ve dopamin eksikliği HBS'nin ortaya çıkmasına neden olabilir.
Böbrek Yetmezliği
Böbrek yetmezliği olan hastalar, HBS riski taşır. Böbrek yetmezliği, demir ve dopamin metabolizmasındaki değişikliklerle ilişkili olarak HBS belirtilerinin ortaya çıkmasına neden olabilir.
Gebelik
Gebelik sırasında HBS gelişme riski artar. Özellikle üçüncü trimesterde ortaya çıkan HBS, doğumdan sonra genellikle düzelir. Gebelikte HBS'nin nedeni tam olarak bilinmese de, hormonal değişiklikler ve demir eksikliği gibi faktörler rol oynayabilir.
İlaçlar ve İlaç Etkileşimleri
Bazı ilaçlar HBS belirtilerini tetikleyebilir veya kötüleştirebilir. Antidepresanlar, antipsikotikler, antihistaminikler ve bazı antiemetikler bu ilaçlar arasındadır. Wikipedia'da antiemetik
Nöropati (Sinir Hasarı)
Sinir hasarı ve nöropati, HBS belirtileriyle ilişkilendirilmiştir. Diyabet ve alkol kullanımı gibi nedenlerle oluşan nöropati, HBS riskini artırabilir.
Uyku Bozuklukları
HBS, uyku bozukluklarıyla sıkça ilişkilidir. HBS'li kişilerde uyku süresi ve kalitesi azalır ve bu durum, günlük yaşamda işlevselliği etkileyebilir.
Huzursuz Bacak Sendromu ve Diyabet
Diyabetik nöropati, HBS belirtilerinin ortaya çıkmasına neden olabilir. Diyabetli hastaların HBS riski, sinir hasarı ve dopamin düzeyindeki değişiklikler nedeniyle artabilir. Huzursuz bacak sendromu tedavi yöntemleri:
Huzursuz Bacak Sendromu İlaç Tedavisi
a. Dopamin Agonistleri: HBS belirtilerini hafifletmeye yardımcı olan dopamin agonistleri, dopamin düzeylerini artırarak sinir iletimini düzenler. Ropinirol, pramipeksol ve rotigotin örnek olarak verilebilir. b. Antikonvülsanlar (Nöbet Önleyici İlaçlar): Gabapentin ve pregabalin gibi antikonvülsanlar, sinir sistemi üzerinde sakinleştirici etkileri nedeniyle HBS belirtilerini hafifletir. c. Benzodiazepinler: Clonazepam gibi benzodiazepinler, uyku kalitesini artırarak ve kas gevşemesine yardımcı olarak HBS semptomlarını azaltır. d. Opioidler: Şiddetli HBS belirtileri için kullanılan düşük doz opioidler, ağrıyı azaltarak ve uyku kalitesini artırarak etki eder. Örnek olarak kodein ve tramadol verilebilir. e. Demir Takviyeleri: Demir eksikliği olan HBS hastaları için demir takviyeleri, dopamin düzeylerini düzenleyerek belirtileri hafifletebilir. Huzursuz bacak sendromu hakkında ilaç tedavisine başlamak için Psikiyatristler sayfamızdan önerilen bir doktor seçimi yapabilirsiniz.
Huzursuz Bacak Sendromu: Yaşam Tarzı Değişiklikleri
a. Düzenli Egzersiz: Egzersiz, HBS belirtilerini hafifletir ve uyku kalitesini artırır. Ancak, egzersizin şiddetine ve zamanlamasına dikkat etmek önemlidir. b. Uyku Hijyenine Özen Gösterme: Düzenli uyku saatleri ve iyi uyku ortamı, HBS belirtileri ve uyku kalitesi üzerinde olumlu etkiler yapar. c. Sigara ve Alkol Kullanımını Azaltma: Sigara ve alkol tüketimi HBS belirtilerini kötüleştirebilir. Bu nedenle, tüketimi azaltmak veya bırakmak önemlidir. d. Kafein Alımını Kısıtlama: Kafein, sinir sistemi üzerinde uyarıcı etkiye sahiptir ve HBS belirtilerini kötüleştirebilir. Kafein alımını azaltmak faydalı olabilir. e. Stres Yönetimi ve Meditasyon: Stres yönetimi ve meditasyon, rahatlama sağlayarak HBS belirtilerini hafifletebilir.
Huzursuz Bacak Sendromu: Fiziksel Terapi ve Masaj
Fiziksel terapi ve masaj, kas gerginliğini azaltarak ve sirkülasyonu artırarak HBS belirtilerini hafifletmeye yardımcı olabilir. Ayrıca, esneklik ve hareket kabiliyetini artırarak, genel yaşam kalitesini iyileştirir.
Huzursuz Bacak Sendromu: Sıcak ve Soğuk Uygulamalar
Sıcak ve soğuk uygulamalar, HBS belirtilerini hafifletmeye yardımcı olabilir. Sıcak uygulamalar kasları gevşetirken, soğuk uygulamalar şişliği ve ağrıyı azaltır. Bu yöntemlerin etkinliği, kişiden kişiye değişebilir ve her iki uygulamayı deneyerek en iyi sonucu elde etmek mümkündür.
Huzursuz Bacak Sendromu ve Bilişsel Davranışçı Terapi
Bilişsel Davranışçı Terapi (BDT), HBS belirtileriyle başa çıkmayı öğretir ve uyku kalitesini artırmaya yardımcı olur. BDT, düşünce ve davranış kalıplarını değiştirerek stres, endişe ve HBS belirtileriyle başa çıkmada etkilidir. BDT, diğer tedavi yöntemleriyle birlikte kullanılabilir ve yaşam kalitesinde önemli iyileşmelere yol açar.
Huzursuz Bacak Sendromu - Sıkça Sorulan Sorular
Huzursuz bacak sendromunun belirtileri nelerdir?Genellikle bacaklarda istemsiz hareket etme isteği ve rahatsızlık hissi olarak ortaya çıkar. Bu durum, özellikle dinlenme anlarında ve geceleri daha belirginleşir, hareket ettikçe hafifler.Huzursuz bacak sendromu için ne iyi gelir?Düzenli egzersiz ve stres yönetimi gibi yaşam tarzı değişiklikleri faydalı olabilir. Ayrıca, uygun ilaç tedavisi ve doktor önerisiyle demir takviyeleri de belirtileri hafifletmeye yardımcı olabilir.Huzursuz bacak sendromu psikolojik midir?Temelde nörolojik bir bozukluktur ve dopamin dengesizliği gibi fizyolojik faktörlerle ilişkilidir. Bununla birlikte, psikolojik faktörler, özellikle stres, huzursuz bacak sendromu belirtilerini kötüleştirebilir. İlginizi çekebilecek diğer yazılar; - Mutsuzluk Hissi Nedenleri ve Nasıl Geçer? - Psikolojik Rahatlama Yöntemleri - Belirsizlik ve Psikolojideki Etkileri Read the full article
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kunalp1234 · 2 years
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lasclreality · 2 years
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Cheesy pakoda from rasoi show colors gujarati june 2015
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welevelup1 · 2 years
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Opiate withdrawal restlessness
Opiate Withdrawal Restlessness (RLS)
Restless Leg Syndrome (RLS) is a neurological condition that causes overwhelming urges to move the legs. It is a serious cause of chronic insomnia, and it affects more than 7 million Americans – and it’s also frequently a symptom of opiate withdrawal. While not life-threatening, restless leg syndrome is uncomfortable and irritating, as are the other symptoms of opiate withdrawal. Restless leg syndrome during opiate withdrawal may be particularly unpleasant due to the existence of other withdrawal symptoms. An individual may be experiencing anxiety, nausea, intense sweating and runny nose, and a number of other symptoms along with RLS.
There are two kinds of RLS:
Idiopathic – primary condition without a known cause.
Secondary – caused by another medication or condition (such as when caused by opiate discontinuation.
Symptoms and Features of RLS include:
Irresistible urges to move the legs. Legs feel creepy-crawly.
Symptoms typically get worse as you lay at rest and worsen as your rest deepens and lengthens.
Symptoms go away when you move your legs – but only for so long as you continue to move.
Symptoms cause significant sleep disruption and affect energy levels and mood.
Fentanyl Withdrawal Restless Legs
Fentanyl is an opioid analgesic. Specifically, transdermal fentanyl is a well-used and highly effective form of opioid analgesia for individuals suffering from severe chronic pain. It is also an opioid that is widely abused and results in significant withdrawal symptoms. Fentanyl withdrawal can lead to restlessness, nausea, vomiting, sweating, diarrhea, and myoclonus, all in addition to RLS.
There has been a report of a 58-year-old male with fentanyl patch withdrawal-induced RLS. He utilized the patch for two months after having surgery on his right shoulder. After the discontinuation of the patch, he complained of severe insomnia. He experienced an unpleasant sensation in both legs that was aggravated in the nighttime, and which could only be improved only by moving his legs. The patient thus met all the diagnostic criteria for RLS.
<a href="https://welevelup.com/addiction/opiate-withdrawal-restlessness/">opiate withdrawal restlessness</a>
He readministered the patch because of his insomnia, after which his RLS symptoms disappeared. His RLS symptoms recurred repeatedly whenever he stopped using the patch. His orthopedic surgeon then referred him for psychiatric consultation. The patient had no disease related to secondary RLS. He was also taking no medication except for the patch. Finally, his RLS symptoms disappeared following the commencement of ropinirole/clonazepam therapy.
Oxycodone Withdrawal Restless Legs Syndrome
Oxycodone is an alternative treatment option for RLS as a semisynthetic opioid. The κ-opioid and the μ-opioid receptor mediate its analgesic effect, but this has not been clearly confirmed. Oxycodone withdrawal-induced RLS has also been reported as follows. A 42-year-old male patient was medicated with an analgesic (oxycodone 60 mg bid) for 10 weeks with embolization because of a hepatocellular carcinoma rupture and hematoperitoneum with pain. Thereafter, his pain was relieved, and he arbitrarily stopped taking the oxycodone.
Seven days later, he complained of a tickling sensation in both his legs. This sensation began in the evening and become increasingly aggravated until midnight. These symptoms worsened at rest and were mitigated only when he moved his legs. His symptoms satisfied all the diagnostic criteria for RLS. The severe abdominal pain recurred, and he restarted taking the oxycodone at his own discretion. The irresistible and tickling sensations in both his legs then dramatically disappeared.
Heroin Addict Restless Legs Syndrome
Heroin is an addictive drug made from morphine. It has been used as a recreational drug and is often abused. Heroin withdrawal-induced RLS has also been reported as follows. A 34-year-old male patient with a five-year history of heroin addiction. Two days after he discontinued his use of heroin, he complained of all four of RLS’s diagnostic symptoms. L-dopa and subsequent naltrexone treatment were then utilized and relieved both his RLS symptoms and heroin addiction.
In another study, 19 patients with opioid dependence, who were admitted to a hospital for detoxification, were enrolled. After abstaining from opioids, 10 of the 19 patients developed RLS symptoms. Six of these 10 patients had taken heroin, with the rest of them having taken dextropropoxyphene (n=2), tramadol (n=1), pentazocine (n=1), and crude opium (n=1). Their RLS symptoms appeared after a mean of 1.7 days following their ceasing their use of opioids. Pregabalin leads to significant improvement in their RLS symptoms and overall sleep quality.
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dongysaigon · 2 years
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Bệnh Parkinson Là Gì? (Parkinson’s Disease and Caregiving)
Bệnh Parkinson (Parkinson’s Disease, PD) là một bệnh thần kinh tăng tiến, tác động chủ yếu đến khả năng vận động, nhưng cũng có thể tác động đến khả năng nhận thức. Nguyên nhân gây ra bệnh Parkinson là do sự phá hủy các tế bào thần kinh ở một vùng trong não bộ có tên là hạch cơ bản.
Các vùng khác nhau của não bộ phối hợp làm việc bằng cách truyền tín hiệu cho nhau để phối hợp mọi suy nghĩ, vận động, cảm xúc và giác quan. Khi chúng ta muốn di chuyển, một tín hiệu được phát đi từ hạch cơ bản tới đồi não, sau đó tới vỏ não và tất cả các vùng khác trên não bộ. Tế bào thần kinh trong não bộ liên lạc bằng các chất.
Một chất (chất dẫn truyền thần kinh) có tên là dopamine được tạo ra trong một nhóm tế bào có tên là chất đen, và rất cần thiết cho sự vận động bình thường. Khi những tế bào này chết đi, chúng không còn khả năng tạo và tiết ra dopamine, vì vậy tín hiệu vận động không thể truyền đi được.
Vào thời điểm một người bắt đầu gặp các triệu chứng về vận động của bệnh Parkinson thì người đó đã mất đi khoảng 50% tế bào tạo dopamine.
Con người có thể gặp các triệu chứng không liên quan đến vận động do mất đi các chất dẫn truyền thần kinh khác trong thời gian tối đa mười năm, trước khi nhận ra các triệu chứng về vận động.
Điều trị bệnh Parkinson
Mục đích điều trị
Làm giảm các triệu chứng của bệnh như run, cứng đờ, giảm động tác.`
Nâng thể trạng.
Phương pháp điều trị
Bệnh cần được điều trị kéo dài suốt đời, gồm liệu pháp dùng thuốc và tập phục hồi chức năng. Tùy từng trường hợp, có thể phối hợp với phẫu thuật hoặc ghép tế bào gốc...
Liệu pháp dùng thuốc
Hiện nay có rất nhiều loại thuốc điều trị bệnh Parkinson nhưng tùy theo triệu chứng lâm sàng, tùy theo tuổi và giai đoạn bệnh mà có sự phối hợp thuốc khác nhau.
Các thuốc điều trị Parkinson:
Thuốc L-dopa (Modopar, Madopar):
Đây là loại thuốc tác dụng tốt nhất với những triệu chứng của bệnh Parkinson, đặc biệt với các triệu chứng tăng trương lực và giảm động tác nhưng ít tác dụng với triệu chứng run.
Tác dụng của thuốc được ghi nhận tốt nhất trong những năm đầu điều trị “giai đoạn tuần trăng mật”, giai đoạn này kéo dài 3 – 4 năm. Sau đó thuốc sẽ chậm tác dụng và hiệu quả tác dụng ngắn (hiện tượng ON/OFF)
Tác dụng không mong muốn (tác dụng phụ): buồn nôn, nôn, đau dạ dày, hạ huyết áp tư thế đứng, loạn nhịp tim, lú lẫn, ảo giác (nhìn hoặc nghe, ngửi thấy bất thường...), loạn động (những động tác bất thường nhưng xuất hiện muộn).
Tránh dùng L- dopar với Vitamin B6 liều cao vì gây giảm tác dụng của thuốc.
Thuốc giảm run (Anticholinergiques): Trihexyphenidil (Artan).
Thuốc có tác dụng với triệu chứng run và tăng trương lực, không có tác dụng đối với giảm động tác.
Tác dụng không mong muốn: lú lẫn, ảo giác (nhất là ở người lớn tuổi), khô miệng, táo bón, bí đái.
Tránh sử dụng đối với người trên 70 tuổi, u xơ tuyến tiền liệt, Glocom.
Thuốc chủ vận Dopamin: Pramipexole và Ropinirole, thuốc có thể dùng đơn trị liệu hoặc phối hợp với thuốc L-dopar để tránh tăng liều thuốc L-dopar (vì L-dopar ở liều cao có thể gây loạn động)
Thuốc ức chế COMT (Tolcapone, Entacapone): kéo dài thời gian sử dụng L-Dopar bằng cách ngăn chặn quá trình chuyển hóa của dopamine. Chỉ được sử dụng ở những người đã điều trị bằng L-dopar nhưng kém hiệu quả (hiện tượng ON/OFF) hoặc khi đáp ứng với điều trị không đầy đủ.
Chất ức chế MAO (Rasagiline, Selegiline) là một tác nhân đơn lẻ hoặc một thuốc bổ sung cho L-dopar, ngăn chặn sự thoái giáng của Dopamine để kéo dài tác dụng của thuốc L-dopar.
Amantadine: Thuốc điều trị cúm A, tuy nhiên được chỉ định trong bệnh Parkinson phối hợp với Levodopar khi xuất hiện tác dụng phụ (loạn động) hoặc kém tác dụng. Thuốc được dùng với liều tăng dần và không được dừng thuốc đột ngột. Một số tác giả Khuyên nên sử dụng khoảng vài tháng sau đó tạm nghỉ.
Liệu pháp không dùng thuốc
Bên cạnh việc dùng thuốc, hồi phục chức năng có một vai trò quan trọng giúp cho người bệnh nâng cao chất lượng cuộc sống, gồm tập phục hồi chức năng vận động, ngôn ngữ, tập thể dục, đi bộ...
 Điều trị phẫu thuật
Ngày nay với sự phát triển của Y học, ở Việt nam và các nước tiên tiến trên thế giới, đã áp dụng phương pháp điều trị phẫu thuật (đặt điện cực kích thích não sâu) ở những trường hợp không đáp ứng với thuốc điều trị giúp cho bệnh nhân Parkinson cải thiện chất lượng cuộc sống.
Ghép tế bào gốc
Với sự tiến bộ của khoa học kỹ thuật, trong tương lai các nhà khoa học trên thế giới có thể tiến hành ghép tế bào gốc cho bệnh nhân Parkinson.
Phòng khám ứng dụng những phương pháp Y học cổ truyền như châm cứu, bấm huyệt…. kết hợp với các bài thuốc Đông y 100% thiên nhiên để hồi phục sức khỏe cho bệnh nhân - SĐT: 0931 225 777 - Website: dongy.org
[CHIA SẺ] 6 ĐỊA CHỈ CHỮA BỆNH PARKINSON TỐT Ở TPHCM-HÀ NỘI
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