Guillain-Barré syndrome 2

Freddie Freeman's 3-year-old son, Maximus, who is battling Guillain-Barré syndrome, has returned home from the hospital and is on the road to recovery, the Los Angeles Dodgers star and his wife, Chelsea, announced.

"Last Friday, Max rapidly declined and went into full body paralysis," Freeman and his wife wrote in a shared statement on social media. "We are very fortunate to have gotten him to the hospital in time so they could reinforce his lungs. Freddie was in Houston at the time and rushed to the first flight back home. After many tests, Max is battling a severe case of Guillain-Barré syndrome. A rare neurological condition that is especially rare in children.

"These have been the hardest and scariest days of our lives. Maximus is such a special boy and he has been fighting SO hard."

Guillain-Barré syndrome is a disease where the body's immune system attacks the nerves, causing weakness, numbness and paralysis, according to the Mayo Clinic. The rare disease can be spotted by tingling in the limbs before turning into paralysis. The cause of the disease isn't known and there isn't a known cure. However, there are numerous treatment options for the disease and most people who've been diagnosed with the disease completely recover, though more serious versions of the illness can be fatal.

Maximus had been dealing with transient synovitis, temporary inflation of the hip joint, and a viral infection when the family attended the MLB All-Star Game in July, Chelsea Freeman shared on social media last week.

After several stressful days in the hospital, the Freemans announced that Max was able to return home and is making progress in his recovery.

Chelsea Freeman wrote in an Instagram post, "After 8 long days in the Pediatric ICU we are officially HOME! Max still has a long road ahead of him to regain his strength and relearn how to walk. But we are so thankful to have our family back together. Thank you God for this miracle. Also, thank you to our incredible team of doctors and angel nurses for taking such good care of our boy. And to our village for helping so much with Charlie and Brandon."

Freeman was placed on the family emergency list Saturday and has been out of the Dodgers' lineup since then. It isn't clear when he'll make his return.

Freeman is in the midst of another standout season, earning his eighth All-Star nod. He's hitting .288 with a .888 OPS to go with 16 homers and 67 RBIs. Los Angeles has lost four of its last five games, causing its lead in the NL West to shrink to 4.5 games, as Cavan Biggio and Kiké Hernández have filled in at first base for Freeman.

https://www.foxnews.com/sports/freddie-freeman-3-year-old-son-battling-guillain-barre-syndrome

An Australian father of three has been left fighting for his life after contracting Guillain-Barré syndrome while visiting Bali, Indonesia, and is now unable to move or breathe on his own.

Craig Hardy, who at first thought he was suffering from “Bali belly,” a condition commonly associated with travel-related digestive issues, has been hospitalized since June, news.com.au reported.

The 52-year-old, whose family nickname is “Rock,” drove himself to Royal Perth Hospital when he realized his symptoms were intensifying. His sister-in-law told the news outlet that during the 15-minute drive Hardy became paralyzed.

“They took him straight into emergency and by that night he was paralyzed from head to toe and in an induced coma,” Deborah Hardy told news.co.au.

Ten weeks after the family was told Hardy has Guillain-Barré, they said he can slightly move his head but there’s no expression on his face and he can’t speak. He uses a letter board and blinking to spell out sentences.



“He’s completely cognizant and awake lying there but he’s not able to move,” Deborah told news.com.au. “His mind is 100 percent perfect but he’s trapped; it’s like being buried alive. Every now and again he gets the feeling he is drowning because of the fluid on his lungs, which they have to pump out, but he can’t say anything.”

According to the Mayo Clinic, Guillain-Barré syndrome is a rare disorder that causes the body’s immune system to attack a patient’s nerves. Symptoms typically begin with tingling and weakness in the feet and legs before spreading upward. It can progress to unsteady gait, severe pain, difficulty with bowel function or bladder control and difficulty breathing among other issues. While it is not known what causes Guillain-Barré, it is often preceded by an infectious illness.

According to Mayo Clinic, muscle weakness can progress into paralysis, and while there is no cure, several treatments can help reduce symptoms and duration of the illness. Most people recover, while other patients may experience lingering effects.

A post on the family’s GoFundMe page said doctors predict that it may take Hardy up to two years to recover from his illness.

“He’s a hard-working dedicated family man,” Deborah told news.com.au of her brother-in-law. “He’d do anything for anyone, he’s very funny, a strong man, hence his nickname Rock, but a heart of gold.”

https://www.foxnews.com/health/dad-struck-by-guillain-barre-syndrome-unable-to-speak-move-3-months-later

East Metropolitan Health Service is at Royal Perth Hospital.
A Perth father paralysed by the rare Guillain-Barré Syndrome received a well-earned boost to his spirits with a visit from the West Coast Eagles.
Doctors from Royal Perth Hospital's Intensive Care Unit noticed small improvements in Craig Hardy's condition whenever an Eagles game was on the TV in ICU.
Our wonderful staff were able to arrange a special visit from former club champions Daniel Kerr and Andrew Embley, in addition to some pre-recorded words of encouragement from Captain Shannon Hurn.
Guillain-Barré Syndrome is a debilitating form of nerve inflammation and sufferers can take between six months to two years to recover.

https://www.facebook.com/EastMetropolitanHealthService/posts/a-perth-father-paralysed-by-the-rare-guillain-barr%C3%A9-syndrome-received-a-well-ear/1114523535365831/

ALS

Chicago Bears legend Steve McMichael was inducted into the Pro Football Hall of Fame on Saturday, and he made an appearance on the video board during the ceremony in Canton, Ohio.

McMichael, dressed in his bronze Hall of Fame jacket, was in a hospital bed surrounded by loved ones. He couldn’t make it to the festivities as the battle with ALS had left him bedridden.

"You are on a team that you can never be cut from and never be released from. When you die, you’ll always be on this team. Welcome home, Steve. You’re in football heaven forever," former Bears star Richard Dent said.

Misty McMichael was in tears as she turned her husband toward the bronze bust.

"That’s you, baby, forever," she said.

McMichael, lovingly known as "Mongo," was a standout defensive tackle with the Bears from 1981 to 1993. He played for the New England Patriots and Green Bay Packers as well – bookends to his 15-year NFL career.

He had 847 total stacks and was a staple on the fearsome 1985 Bears defense. He played a Bears franchise record 191 consecutive games and was second in sacks with 92.5 while with Chicago.

"I want to thank the Chicago Bears and the fans, the best city to play football in," Kathy McMichael said in a speech she worked on with her brother before he lost the ability to move and speak. "I played 15 years in the NFL and loved every minute of every down. I played with the greatest players and the greatest defense to this day."

McMichael also performed in World Championship Wrestling and was a United States champion.

He announced he was diagnosed with AL in 2021.

https://www.foxnews.com/sports/nfl-legend-steve-mcmichael-hospital-bed-hes-inducted-hall-fame-heartbreaking-ceremony

DDX23 mutations

Inspired by a patient

Burns W, Bird LM, Heron D, Keren B, Ramachandra D, Thiffault I, Del Viso F, Amudhavalli S, Engleman K, Parenti I, Kaiser FJ, Wierzba J, Riedhammer KM, Liptay S, Zadeh N, Porrmann J, Fischer A, Gößwein S, McLaughlin HM, Telegrafi A, Langley KG, Steet R, Louie RJ, Lyons MJ. Syndromic neurodevelopmental disorder associated with de novo variants in DDX23. Am J Med Genet A. 2021 Oct;185(10):2863-2872. doi: 10.1002/ajmg.a.62359. Epub 2021 May 29. PMID: 34050707.

Abstract

The DEAD/DEAH box RNA helicases are a superfamily of proteins involved in the processing and transportation of RNA within the cell. A growing literature supports this family of proteins as contributing to various types of human disorders from neurodevelopmental disorders to syndromes with multiple congenital anomalies. This article presents a cohort of nine unrelated individuals with de novo missense alterations in DDX23 (Dead-Box Helicase 23). The gene is ubiquitously expressed and functions in RNA splicing, maintenance of genome stability, and the sensing of double-stranded RNA. Our cohort of patients, gathered through GeneMatcher, exhibited features including tone abnormalities, global developmental delay, facial dysmorphism, autism spectrum disorder, and seizures. Additionally, there were a variety of other findings in the skeletal, renal, ocular, and cardiac systems. The missense alterations all occurred within a highly conserved RecA-like domain of the protein, and are located within or proximal to the DEAD box sequence. The individuals presented in this article provide evidence of a syndrome related to alterations in DDX23 characterized predominantly by atypical neurodevelopment.

Thys L, Beysen D, Jansen A, Janssens K, Meuwissen M. Confirmation of gray matter heterotopia as part of the DDX23 phenotypic spectrum. Am J Med Genet A. 2023 Sep;191(9):2451-2453. doi: 10.1002/ajmg.a.63347. Epub 2023 Jul 10. PMID: 37596899.

No abstract

John Stephenson, MD 1935-2024

Missing a most engaging colleague, always a world of fun. Stephenson J, Breningstall G, Steer C, Kirkpatrick M, Horrocks I, Nechay A, Zuberi S. Anoxic-epileptic seizures: home video recordings of epileptic seizures induced by syncopes. Epileptic Disord. 2004 Mar;6(1):15-9. PMID: 15075063.



Trudie Lobban’s young daughter, Francesca, was fainting up to eight times a day. Unconvinced that she would “grow out of it” after hospital tests reported nothing wrong, Lobban wrote letters to paediatric neurologists all over the world.

Professor John Stephenson, of what was then the Royal Hospital for Sick Children, Glasgow, responded. Extremely concerned about children like Francesca, he had coined a name for their condition: reflex anoxic seizures (RAS). Occurring mainly in young children, RAS can stop the heart, make arms and legs jerk, and stiffen the body. The attacks often left Lobban fearing that Francesca had died, but the condition was not life-threatening.

However, RAS was often misdiagnosed as temper tantrums, breath-holding, and, most critical of all, epilepsy. Nearly a third of children with supposed epilepsy were reported to have been misdiagnosed and prescribed unnecessary drugs that induced debilitating side-effects such as abdominal pain, nausea, dizziness and mood changes.

Renowned for getting people to do things and generating enthusiasm where none may have existed before, the deep-voiced Stephenson persuaded Lobban to set up a parental support group. He reassured her that this would involve only “about ten families a year”. Lobban launched Stars (Syncope Trust & Reflex Anoxic Seizures) in 1993.

Thirty years later, in 2023, Stephenson apologised to Lobban for misleading her because, she explained, “Stars had taken over my life and tens of thousands of people have made contact over the years.” But she added: “I would not change anything.” The group became international and led to Lobban also founding the Arrhythmia Alliance.

Recognising that medical progress is often more drip-drip than bang-bang, Stephenson spent years trying to educate fellow doctors about RAS in reports showcasing his erudition and witty way with words.

Writing in the British Medical Journal in 1977 he raged: “Although once upon a time epilepsy encompassed any kind of seizure, syncope [temporary loss of consciousness] cut loose several centuries ago. Please let us keep it that way and not blur the fundamental distinction between epileptic and anoxic [oxygen-deficient] fits.”

His monograph, Fits and Faints (1990), quietly but firmly chastised medical colleagues for overly casual use of common words such as convulsion, faint, fit and syncope. Words, he stressed, had specific meanings with diagnostic significance.

Fits and Faints built on his pioneering use of video in the 1970s for teaching, diagnosing and monitoring disease. He used the revolutionary Kodak Super 8 camera, the catalyst of the first home movies for millions of families, to distinguish between different involuntary movements such as spasms and seizures. Stephenson lent patients VHS video cameras to record night-time seizures.

He was an idiosyncratic teacher. His last senior registrar, now Professor Sameer Zuberi of the Royal Hospital for Children, Glasgow, said: “John encouraged a learning environment where scientific discourse accompanied discussion of literature and music. Clinical points were illustrated by references to the work of Sir Arthur Conan Doyle and examination taught by comparing the use of a tendon hammer to a cellist playing Dvorak’s Concerto in B Minor.”

Sharing a birthday with Scotland’s national bard Robert Burns, Stephenson invited students to an annual Burns supper to deliver a poem or speech. Burns would have toasted Stephenson’s delight in identifying several malt whiskies while blindfolded and his love of the island of Islay, where the family had a holiday home.

His birthday Burns parties were hosted by his wife Phillippa. She and their five children survive him: David, a retired finance director; Philip, a university lecturer; Michael, a health and safety adviser; Wendy, a retired paediatric nurse; and Ian, a software engineer.

Although he was highly sociable, Stephenson never backed away from controversy. Zuberi remembers how the words “Stephenson, Glasgow” struck fear in many neurologists at medical meetings, provoking a penetrating and sometimes witty question.

John Burdett Primmer Stephenson was born in 1935. Brought up initially in Fife, he was the son of Keith Stephenson OBE, a Second World War naval commander who later worked in military intelligence. His wife Jane (neé) Robertson was a teacher with degrees in English, French and drama.

Young John won scholarships to the private St Edward’s School, Oxford, and Balliol College, Oxford, before completing medical training at St Thomas’ medical school, London. Deciding to specialise in neurology in Glasgow after initial jobs in paediatrics, he won a fellowship at the internationally renowned Toronto Hospital for Sick Children. He described his time in Canada as “one year, a lifetime of education”.

Medical careers, like many others, need a bit of luck or serendipity if they are to take off. Toronto was Stephenson’s luck — as was his timing. Paediatric neurology in the early 1970s was still in its infancy and he became one of its pioneers. Only ten years after graduating he returned to Glasgow, in 1973, as the city’s first consultant paediatric neurologist.

In his first year in Glasgow he founded the Fraser of Allander Unit, one of the UK’s first multidisciplinary child neurology and development centres. Four years later the Department of Health and Social Security recognised paediatric neurology as a speciality in its own right.

Zuberi recalled how Stephenson would focus at times “almost obsessively” on certain fields such as Aicardi-Goutières syndrome (AGS), a rare inherited disease affecting mainly the brain, immune system and the skin. But as his hunches often paid big dividends, he persuaded a young genetics trainee to investigate the disorder.

Yanick Crow identified many of AGS’s genetic causes, leading to an explanation for several other genetic disorders and the development of a new branch of medicine, “the interferonopathies” (interferon plays a role in the body’s immune system and was implicated in AGS).

Stephenson was both an outstanding researcher and physician. He was renowned for putting stressed children at ease through his humour and for having what his former colleague Rod Duncan called “a modest frame and the constitution of an ox”.

Duncan added: “Despite being 20 years his junior (and no shrinking violet myself), I could only marvel at it: his need for sleep seemed negligible and his resistance to the adverse effects of large amounts of whisky was nothing short of prodigious. I have the feeling that modern algorithms for the selection of medical students would instantly identify and exclude him and his like. Fortunately for us he lived in more enlightened times.”

Professor John Stephenson, doctor, was born on January 25, 1935. He died of progressive frailty and cerebral small vessel disease on April 16, 2024, aged 89

https://www.thetimes.com/uk/obituaries/article/professor-john-stephenson-2g0m0bxzx

Trudie Lobban, Founder and CEO of STARS remembers Professor John Stephenson:

STARS Founding Patron Professor John Stephenson died peacefully in his sleep on Wednesday 17 April 2024. Some of you will not be familiar with the name, but there are many families who remain forever grateful to this wonderful doctor.

It was 1978 when Prof Stephenson gave a name to the unexplained loss of consciousness young children were experiencing. Reflex Anoxic Seizures (RAS). Until then, many children were being misdiagnosed with epilepsy and prescribed what would have been unnecessary anti-epileptic medication. My daughter, Francesca, could have been one of those children, but after writing to numerous paediatric neurologists, I was contacted by Prof John Stephenson himself, who diagnosed RAS. It was Prof Stephenson who then asked whether I would like to start a small ‘support group to help about ten families a year’. This was March 1993 when STARS was conceived.

I last spoke to my friend and mentor at Christmas 2023, and he again apologised for ‘misleading’ me all those years ago because STARS has taken over my life and tens of thousands (maybe over 100,000) of people have made contact over the years – but I would not change anything.

He had a vision no child would be misdiagnosed with epilepsy as long as RAS was recognised and understood by the medical profession. STARS will continue to support his work and ensure it has not been in vain.

Dr Ailsa McLellan, BPNA President and Professor Sameer Zuberi Consultant Paediatric Neurologist Royal Hospital for Children, pay tribute to Professor John Stephenson

John was one of the Founders of Paediatric Neurology and set up the Fraser of Allander Unit at the Royal Hospital for Sick Children in Glasgow, one of the first comprehensive multidisciplinary child neurology and development centres in the United Kingdom. He remained a full-time NHS Consultant until he retired in 2000 and was an Honorary Professor in the University of Glasgow. He attended the first British Paediatric Neurology Association meeting in 1975 and was elected to the inaugural committee of the BPNA.

Defining the physiology and differential diagnosis of epilepsy and other paroxysmal disorders was one of John’s principal research and clinical interests. His classic monograph “Fits and Faints” was published in 1990 and contains over 140 case histories. He taught generations of trainee doctors that history is key to making a diagnosis and wrote ‘complete acquisition may not be possible, but no effort is too great in attempting to reach this goal’.

John pioneered the use of home and clinic video recordings for teaching and to aid differentiation of paroxysmal events and follow the course of chronic neurological disease. This, of course, is a routine part of clinical assessment now with the use of smart phones, but he did this from the 1970s using Super 8 cameras and lent out VHS cameras and tripods to families in the 1990s to record nocturnal seizures at home.

John collaborated widely with research groups around the world to further the understanding of the pathophysiology of paediatric neurology conditions. He did this with great enthusiasm but always with the premise of trying to give an explanation of the clinical condition of a patient to their families and offer targeted treatments. Like all paediatric neurologists he had many unsolved cases in his working career, but as newer diagnostics evolved, he reviewed his cases and made many new diagnoses which he relished in sharing with colleagues as ‘updates’ at the Scottish Paediatric Neurology Group.

John revelled in the environment of clinical meetings and spent as much time as possible in the hospital and University library. The words “Stephenson, Glasgow” (and more recently ‘’Stephenson, Islay’) as he asked a penetrating and often witty question was heard at academic meetings for over 40 years.

He will be missed.

https://heartrhythmalliance.org/stars/pl/trudie-lobban-remembers-prof-john-stephenson

Blood test offers hope for early detection of Alzheimer's

Blood test offers hope for early detection of Alzheimer's

A simple blood test has been shown to detect Alzheimer’s disease in routine health care settings with up to 90% accuracy, according to Swedish researchers.

The findings were presented at the Alzheimer’s Association International Conference in Philadelphia on Sunday.

The test works by measuring the levels of Plasma Phospho-Tau217, a biomarker that is linked to the presence of Alzheimer’s pathology in the brain.

It has been shown to detect the disease even before the person begins experiencing symptoms, researchers say.

"The tested blood test can detect Alzheimer’s disease with high accuracy even in real-life settings in primary care," said study author Oskar Hansson, M.D., head of the Clinical Memory Research Unit at Lund University, Sweden, in an email to Fox News Digital.

It is currently difficult for primary care physicians to diagnose Alzheimer’s disease due to a lack of adequate tools, he said. 

In the most recent study — also published in the journal JAMA — 1,213 people who were experiencing mild memory loss were evaluated by either primary care doctors or memory specialists. 

The patients then underwent both the blood test and cerebrospinal fluid tests, and researchers compared the results.

"Primary care doctors’ accuracy in identifying Alzheimer’s disease was 61%, while specialist physicians were correct 73% of the time," study author Sebastian Palmqvist, associate professor of neurology at Lund University, stated in a press release.

By comparison, the blood test had an accuracy of 90%.

"I was surprised by how well the blood test worked in real-life settings in primary care, where the patients are older and have more comorbidities like kidney disease, which can affect the blood test results," Hansson told Fox News Digital.

The main limitation of the research was that it was only conducted in Sweden. 

"We need studies in the U.S. and other countries to better understand the generalizability of the findings," Hansson said.

"I think it will take one or two years before there are clinical guidelines in place for use of blood tests in primary care."

Looking ahead, there is a need for clear guidelines on how doctors should use these tests in clinical practice, according to the researchers. 

"My prediction is that highly accurate blood tests will very soon be recommended for use in patients with cognitive impairment who are assessed at clinics specialized in memory disorders," Hansson said. 

This could help to reduce the need for more advanced and expensive methods, like PET scans and cerebrospinal tests.

"I think it will take one or two years before there are clinical guidelines in place for use of blood tests in primary care," Hansson also noted. 

The researchers do not currently recommend screenings for "cognitively normal people" — as there are not any approved treatments for people with Alzheimer’s disease pathology who do not have cognitive impairment, the researcher said.

Added Hansson, "Further, we propose that the blood test should be used as an adjunct to, and not replacement for, the clinical assessments used today."

Approximately one in five women and one in 10 men develop dementia due to Alzheimer’s disease, according to the Alzheimer’s Association.

The condition is misdiagnosed in 25% to 35% of patients who are treated at specialized clinics, previous studies have shown — and researchers believe that number is even higher for patients assessed by their primary care physicians.

https://www.foxnews.com/health/alzheimers-blood-test-detects-disease-accuracy-routine-doctors-appointments-study

Janelidze S, Barthélemy NR, Salvadó G, Schindler SE, Palmqvist S, Mattsson-Carlgren N, Braunstein JB, Ovod V, Bollinger JG, He Y, Li Y, Raji CA, Morris JC, Holtzman DM, Ashton NJ, Blennow K, Stomrud E, Bateman RJ, Hansson O. Plasma Phosphorylated Tau 217 and Aβ42/40 to Predict Early Brain Aβ Accumulation in People Without Cognitive Impairment. JAMA Neurol. 2024 Jul 28. doi: 10.1001/jamaneurol.2024.2619. Epub ahead of print. PMID: 39068669.

Abstract

Importance: Phase 3 trials of successful antiamyloid therapies in Alzheimer disease (AD) have demonstrated improved clinical efficacy in people with less severe disease. Plasma biomarkers will be essential for efficient screening of participants in future primary prevention clinical trials testing antiamyloid therapies in cognitively unimpaired (CU) individuals with initially low brain β-amyloid (Aβ) levels who are at high risk of accumulating Aβ.

Objective: To investigate if combining plasma biomarkers could be useful in predicting subsequent development of Aβ pathology in CU individuals with subthreshold brain Aβ levels (defined as Aβ levels <40 Centiloids) at baseline.

Design, setting, and participants: This was a longitudinal study including Swedish BioFINDER-2 (enrollment 2017-2022) and replication in 2 independent cohorts, the Knight Alzheimer Disease Research Center (Knight ADRC; enrollment 1988 and 2019) and Swedish BioFINDER-1 (enrollment 2009-2015). Included for analysis was a convenience sample of CU individuals with baseline plasma phosphorylated tau 217 (p-tau217) and Aβ42/40 assessments and Aβ assessments with positron emission tomography (Aβ-PET) or cerebrospinal fluid (CSF) Aβ42/40. Data were analyzed between April 2023 and May 2024.

Exposures: Baseline plasma levels of Aβ42/40, p-tau217, the ratio of p-tau217 to nonphosphorylated tau (%p-tau217), p-tau231, and glial fibrillary acidic protein (GFAP).

Main outcomes and measures: Cross-sectional and longitudinal PET and CSF measures of brain Aβ pathology.

Results: This study included 495 (BioFINDER-2), 283 (Knight ADRC), and 205 (BioFINDER-1) CU participants. In BioFINDER-2, the mean (SD) age was 65.7 (14.4) with 261 females (52.7%). When detecting abnormal CSF Aβ-status, a combination of plasma %p-tau217 and Aβ42/40 showed better performance (area under the curve = 0.949; 95% CI, 0.929-0.970; P <.02) than individual biomarkers. In CU participants with subthreshold baseline Aβ-PET, baseline plasma %p-tau217 and Aβ42/40 levels were significantly associated with baseline Aβ-PET (n = 384) and increases in Aβ-PET over time (n = 224). Associations of plasma %p-tau217 and Aβ42/40 and their interaction with baseline Aβ-PET (%p-tau217: β = 2.77; 95% CI, 1.84-3.70; Aβ42/40: β = -1.64; 95% CI, -2.53 to -0.75; %p-tau217 × Aβ42/40: β = -2.14; 95% CI, -2.79 to -1.49; P < .001) and longitudinal Aβ-PET (%p-tau217: β = 0.67; 95% CI, 0.48-0.87; Aβ42/40: β = -0.33; 95% CI, -0.51 to -0.15; %p-tau217 × Aβ42/40: β = -0.31; 95% CI, -0.44 to -0.18; P < .001) were also significant in the models combining the 2 baseline biomarkers as predictors. Similarly, baseline plasma p-tau217 and Aβ42/40 were independently associated with longitudinal Aβ-PET in Knight ADRC (%p-tau217: β = 0.71; 95% CI, 0.26-1.16; P = .002; Aβ42/40: β = -0.74; 95% CI, -1.26 to -0.22; P = .006) and longitudinal CSF Aβ42/40 in BioFINDER-1 (p-tau217: β = -0.0003; 95% CI, -0.0004 to -0.0001; P = .01; Aβ42/40: β = 0.0004; 95% CI, 0.0002-0.0006; P < .001) in CU participants with subthreshold Aβ levels at baseline. Plasma p-tau231 and GFAP did not provide any clear independent value.

Conclusions and relevance: Results of this cohort study suggest that combining plasma p-tau217and Aβ42/40 levels could be useful for predicting development of Aβ pathology in people with early stages of subthreshold Aβ accumulation. These biomarkers might thus facilitate screening of participants for future primary prevention trials.

Giant intracranial hydatid cysts

Inspired by: https://www.youtube.com/watch?v=vrwX-jx2maU (10:21-11:28)

Gautam S, Sharma A. Intracranial Hydatid Cyst: A Report of Three Cases in North-West India. J Pediatr Neurosci. 2018 Jan-Mar;13(1):91-95. doi: 10.4103/JPN.JPN_141_17. PMID: 29899780; PMCID: PMC5982502.

Abstract

Human echinococcus is caused by tapeworm, Echinococcus granulosus, which forms larval cysts in the human tissue. Incidence in the cerebral form is only 1–2%. This localization can be associated with the involvement of other organs such as liver or lung or may be an isolated infestation of the brain or spinal column. Surgical removal of the intact and unruptured cyst is advised to prevent local recurrence that may require further surgery and long-term treatment with parasiticidal agents. We report three cases who presented with headache, vomiting, hemiparesis with decreased visual acuity, and convulsions. MRI showed a giant hydatid cyst in all three cases which was removed surgically and the patient was successfully discharged. Successful treatment of hydatid cyst requires preoperative diagnosis and meticulous surgical technique for complete excision of cyst without rupture under perioperative coverage of albendazole to avoid recurrence and anaphylaxis.

Alomari MS, Almutairi MK, Alali HM, Elwir JS, Alola SA, Alfattoh NI, Alharthy NA, Azzubi MA. Primary Giant Cerebral Hydatid Cyst in an 8-year-old Girl. Asian J Neurosurg. 2018 Jul-Sep;13(3):800-802. doi: 10.4103/ajns.AJNS_240_16. PMID: 30283551; PMCID: PMC6159100.

Abstract

Echinococcosis, also called hydatid disease, is a parasitic disease that passes from animals to humans. Literature reports suggest very rare cases of cerebral hydatid cysts. Brain involvement with hydatid disease occurs in 1%–2% of all Echinococcus infections. In this report, we aim to emphasize the presentation of such an isolated primary cerebral hydatid cyst, discuss its radiological features, Emergency department management, inpatient medical management, referral to neurosurgery, consequent operative procedures, postoperative care, and outcome.

Ashraf M, Ahmed S, Ahmad S, Ahmad A. A Large Hydatid Cyst in the Brain of a 10-year Child. J Coll Physicians Surg Pak. 2022 Apr;32(4):538-540. doi: 10.29271/jcpsp.2022.04.538. PMID: 35330534.

Abstract

Hydatid cyst is the larval form of the parasite, echinococcus granulosus. We operated upon a case of a giant hydatid cyst in the left cerebral hemisphere of a 10-year male child. The patient presented to us with a history of headache, vomiting, vertigo and difficulty in walking. On the examination, there was hemiparesis on the right side and left-sided papilledema. The CT scan showed a large extra-axial cystic lesion in the left frontotemporoparietal area. Craniotomy and excision of the cyst by hydro-dissection was performed. The patient recovered uneventfully and was discharged. Albendazole was given postoperatively for a period of one month. The follow-up CT scan, performed after three months, showed complete resolution of the disease.

Gök H, Başkurt O. Giant Primary Intracranial Hydatid Cyst in Child with Hemiparesis. World Neurosurg. 2019 Sep;129:404-406. doi: 10.1016/j.wneu.2019.06.129. Epub 2019 Jun 26. PMID: 31254691.

Abstract

Hydatid cyst is the larval form of the parasite Echinococcus. Echinococcus granulosus and less commonly Echinococcus multilocularis species cause the disease. Intracranial hydatid disease is relatively rare; the incidence is approximately 1%-2%. Intracranial hydatid cyst can be classified as primary and secondary. A primary cyst, the most common type, is always solitary. The treatment of hydatid cyst is surgical, and the aim of surgery is to remove the cyst without rupture to prevent recurrence or anaphylactic reaction. The Dowling technique (improved by Arana-Iniguez and San Julian) has been widely used for the excision. Albendazole and praziquantel are the medical treatment of choice. In recurrent cases or cases with rupture during surgery, medical therapy has been reported to be effective. Preoperative and postoperative albendazole may be considered to sterilize the cyst, decrease the chance of anaphylaxis, lower the tension in the cyst wall, and reduce the recurrence.

Ganjeifar B, Ghafouri M, Shokri A, Rahbarian Yazdi F, Hashemi SA. Giant Cerebral Hydatid Cyst: A Rare Case Report. Clin Case Rep. 2021 Feb 10;9(3):1774-1778. doi: 10.1002/ccr3.3908. PMID: 33768934; PMCID: PMC7981697.

Abstract

The diagnosis of hydatid cyst should be considered in children with seizure in endemic regions.

MIT-educated neurosurgeon

MIT educated neurosurgeon reveals shocking reason why he QUIT his lucrative medical career after 20 years

Dr. Goobie went through years of rigorous training to be a neurosurgeon

But, after 20 years, he made the decision to leave the medical field behind

The expert has now candidly opened up about the real reason why he quit

An MIT-educated neurosurgeon has candidly revealed the shocking reason he quit his job and left the medical field behind after 20 years.

Dr. Goobie went through years of rigorous training, completed medical school and finished a six-year neurosurgery residency before getting to the peak of his career - which saw him performing multiple successful surgeries each day.

But, after spending 10 years practicing and working to relieve patients of their suffering, the neurosurgeon said he had gained 40 pounds from stress and a lack of sleep.

And while the feelings of burn out were plaguing the MIT alum, the 38-year-old also couldn't shake a nagging thought about greed.

In a 50-minute clip shared to his YouTube account, Dr. Goobie confessed that he had realized the medical system in the US was not built to 'help heal' but was instead created so that 'hospitals could make money.'

MIT-educated neurosurgeon Dr. Goobie has candidly revealed the shocking reason he quit his job and left the medical field behind after 20 years

In the intimate video, the health expert spoke directly to viewers while in the mountains as he shared the real reasons behind his decision to ditch the medical field.

He explained: 'So I used to be a neurosurgeon. I went to college at MIT and did four years of medical school and six years of neurosurgery training. I was a neurosurgeon for almost 10 years after all of that, so that's 20 years of my life.

'I quit last year and nobody understood why I quit. People would ask but a decision like that involves 20 years of your life, you can't really answer that in a couple minutes...

'I'm making this video to help sort my own thoughts out about the whole thing because there's a lot of factors but also to help somebody else who's in a tough spot.

'If they're in a tough spot like I was, maybe hearing my story will help them get out of that tough spot.'

Despite being well paid and having a well-respected role, he admitted: 'Something was not right, I was very unhappy. I was the most unhappy I have ever been and I couldn't really figure it out for a long time.'

He explained that while he was a surgeon, he undertook several surgeries using advanced technologies, but was never able to address the root cause of the illness.

'I was trying to help people but these surgeries weren't fixing the problem. It would help some people feel better, some people would feel the same, some people would be worse,' Dr. Goobie dished.

In a 50-minute clip shared to his YouTube account, Dr. Goobie confessed that he had realized the medical system in the US was not built to 'help heal' but was instead created so that 'hospitals could make money'

'I thought if I did a perfect surgery people would get better but that wasn't always the case... It really bothered me,' he dished.

And he soon began asking his patients more questions about their lives - which proved to be the key to his understanding.

He claimed that people who ate a low-sodium and mostly-plant based diet, exercised daily, had good group of social support, didn't smoke, didn't drink often, slept well and found ways to manage their stress would often heal from pain the quickest - sometimes even before they underwent surgery.

But the medical expert said that despite this being his 'aha moment' it actually caused him a bigger problem due to systemic greed.

Dr. Goobie said: 'The problem is that our medical system is not set up this way... The way that things are set up is that the hospital needs to make money. They need to grow economically.

'The problem there is that if you figure out a way to help patients heal in a way that doesn't include a pill or a surgery then the hospital and the doctor are in big trouble.

'If you figure out a way to help patients heal and you can't charge them for it, well then you just worked yourself out of a job.'

He continued: 'I really felt like the focus of medicine wasn't in the right place - it wasn't in healing, it was in making money from surgeries and pills and images and whatever you can make money from...

'The incentives were not right. Once I figured out what was going on it was a huge problem for me ethically.

'I was doing a job I didn't believe in anymore.'

But Dr Goobie admitted that he had to keep doing surgeries to ensure he and his wife still had a paycheck coming in.

'That tore me apart. I gained 40lbs. I was really sad. I was really angry, frustrated, didn't have hope. I thought I was stuck...

'I knew that I was dying inside and my body was dying,' he shared.

However, after discussing his problems with his wife, she supported him to leave the medical field behind entirely and go on without a clear plan.

Dr. Goobie admitted that he was 'embarrassed' and 'uncomfortable' at first but admitted it was ultimately 'freeing' getting to decide what he wanted to do with his life.

At the end of the clip, he added: 'When you let go of something that you're holding too tightly, even though it's hurting you, and you let go of it, then you're able to pick up something else that hopefully is better for you...

'Trust your heart, lean on people that love you and do what you need to do - whatever that is.'

https://www.dailymail.co.uk/femail/article-13637435/mit-neurosurgeon-reason-quit-medical-career.html

See: https://www.youtube.com/watch?v=25LUF8GmbFU&t=3s

https://www.youtube.com/watch?v=riB2xAWcxoQ