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American Academy of Neurology

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The official account of the American Academy of Neurology. Discover what’s next in brain health… and see why 44,000+ members call us home!

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न्यूरोफिजिशियन डॉ नरेश शर्मा डी० एम० (न्यूरोलॉजी)
क्लीनिक पता- कपीश्वर न्यूरो हेल्थ केयर प्रा० लि० - 77, गाँधी नगर पेट्रोल पम्प बाई पास रोड, साकेत मॉल के पास, सुल्तानगंज की पुलिया, आगरा।
Mobile No- 8239544307, 6398733626

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🗞️ EXTRA! EXTRA! 🗞️
Hot off the press... Dr. Lamees Alhallaq has been accepted into the American Academy of Neurology’s 2027 Enhanced Resident Leadership Program! 🎉🧠

Only 15 residents nationwide were selected — and she’s one of them!
We’re so proud of @lamees_alhallaq leadership, dedication, and drive. 💪✨

#Neurology #NeurologyResident #Nmatch2027 #insidethematch #Geisingergme #GeisingerNeurology #Geisingerneurds #LeadershipInNeurology #AAN2027 #ResidentSpotlight #FutureLeader #NeurologyStrong #aanbrain
@geisingergme @nmatch2027

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Folks w/ GBA1 Parkinson's should NOT automatically be excluded from DBS! GBA1 is a gene associated w/ an increased risk of Parkinson's disease and a greater likelihood of cognitive decline. Deep brain stimulation is a surgical treatment that uses electrical stimulation to improve movement symptoms. Evridiki Asimakidou and colleagues describe in a new paper in Movement Disorders how the timing of DBS may influence cognitive trajectories in folks w/ GBA1-associated Parkinson's disease.
Key points:
- This multicenter study included 343 folks w/ Parkinson's disease who underwent subthalamic nucleus (STN) DBS, including 91 GBA1 carriers and 252 non-carriers.
- Folks w/ GBA1 Parkinson's who underwent DBS later in their disease course experienced significantly faster cognitive decline than those receiving DBS earlier. The strongest differences emerged around the 7- to 8-year disease duration thresholds.
- Cognitive decline was greater overall in GBA1 carriers compared to nocarriers, however the severity of the GBA1 genetic variant did not clearly predict the cognitive trajectory.
My take: This study addresses an important clinical dilemma. Should we deny a potentially life-changing therapy to someone simply because they carry a GBA1 variant and may be at greater risk for cognitive decline? I would argue absolutely not. We must have thoughtful and transparent discussions about cognitive trajectories, including the possibility of worsening memory and thinking over time. However, an increased risk of cognitive decline does not automatically mean someone should be excluded from DBS. We should be discussing motor benefits, current cognitive function, quality of life, disease duration, individual goals and the potential window of opportunity for treatment. Importantly, this observational study does not prove that earlier DBS prevents cognitive decline or that DBS itself causes the decline.

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What sticks with me about this fascinating case of adult-onset bobble-head doll syndrome is how a rare and potentially reversible neurological condition can masquerade as a more familiar movement disorder. Shibayama and colleagues describe a 24 year old man who had been working and living independently but developed progressive memory loss, urinary incontinence, severe gait instability, and unusual side-to-side no-no head movements. The paper appears in the journal Tremor and Other Hyperkinetic Disorders. His cognitive testing was striking, with a Montreal Cognitive Assessment score of only 12 out of 30. Even more fascinating was that touching his face temporarily stopped the head movements, a sensory trick we commonly associate with cervical dystonia. Brain MRI revealed massive enlargement of the ventricles caused by a thin membrane, or aqueductal web, blocking the normal flow of cerebrospinal fluid. Following ventriculoperitoneal shunt surgery, his head movements completely disappeared within one week, and his walking, cognition, and bladder control gradually improved. At 18 months, he was independent in daily activities, although mild memory difficulties persisted and he had not returned to work. The differential diagnosis of unusual head movements should include cervical dystonia and dystonic tremor, essential tremor, cerebellar tremor, functional movement disorders, and less commonly tics or other structural brain disorders. When head bobbing is accompanied by cognitive decline, gait dysfunction, or urinary symptoms, we should particularly consider hydrocephalus, including obstruction from aqueductal stenosis or webs, third ventricular cysts, and tumors. Treatment depends on the cause: botulinum toxin injections for cervical dystonia, selected medications for essential tremor, and neurosurgical treatment for obstructive hydrocephalus, including endoscopic third ventriculostomy or shunting. In this case, the anatomy made shunting the safer choice, although a postoperative subdural hematoma required valve adjustment and monitoring.

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Grocery Shopping with Parkinson's: What Should You Buy? | The Parkinson's Plate. What should you put in your grocery cart if you have Parkinson's disease? Join me and registered dietitian Emily Truscott, MS, RD, LD, as we take The Parkinson's Plate to the grocery store. Eating well with Parkinson's does not have to be complicated, and there is no single diet that works for everyone. Our goal is to help folks living with Parkinson's and their families think about everyday food choices, build healthy shopping habits, and make nutrition a practical part of their Parkinson's plan. Good nutrition starts with choices we can make every day, and sometimes the best place to begin is in the grocery aisle.
https://youtube.com/shorts/D0ZzFXByuCQ

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Could obesity be quietly aging our brains and increasing our risk of dementia? Obesity refers to excess body fat that can negatively affect health, including brain health. Cali McEntee, Eva Feldman and colleagues describe in a new review in Nature Reviews Neurology how obesity may affect memory, thinking and the biological pathways involved in dementia.
Key points:
- Midlife obesity is associated w/ cognitive decline and an increased risk of dementia, even when weight decreases later in life.
- Obesity may affect the hippocampus and prefrontal cortex, brain regions essential for memory, attention and decision-making, through inflammation, insulin resistance and vascular dysfunction.
- Exercise, healthier nutrition, weight-loss surgery and newer weight-management medications offer potential opportunities to improve metabolic health and possibly protect cognition, although more definitive trials are needed.
My take: What resonates w/ me is that obesity is not simply a number on a scale. It is a biological condition that can influence how our brains function and age. The brain and body are not separate universes. Inflammation, blood vessel health, insulin signaling and metabolism all matter. Perhaps most importantly, the timing of obesity matters. Carrying excess weight in midlife may have consequences that are not completely reversed by losing weight decades later.
Here are 5 points that resonated w/ me:
1- Midlife may represent an important window of opportunity for protecting long-term brain health.
2- Where fat accumulates may matter as much as how much we weigh, particularly when it collects around the abdomen.
3- Obesity can create a vicious cycle in which inflammation disrupts the brain circuits controlling appetite, potentially promoting further weight gain.
4- Exercise, nutrition and appropriate medical treatment should be viewed as investments in brain health, not simply strategies for changing appearance or body weight.
5- We still need randomized trials to establish whether treating obesity actually prevents dementia, but the opportunity to improve metabolic and vascular health is already in front of us.
https://www.nature.com/articles/s41582-026-01251

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The Sheila Essey Award for ALS Research honors outstanding contributions to ALS research and highlights the importance of continued discovery, innovation, and collaboration in the search for better treatments and, ultimately, a cure.⁣
⁣
Become a candidate! Applications are open until October 20, 2026, 10:59 p.m. PT.⁣
⁣
Learn more about the award and the researchers making a difference: LINK IN BIO⁣
⁣
#ALSresearch #ALS

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The Braak Paradox: When Parkinson’s pathology and clinical progression disconnect. For more than two decades, the Braak hypothesis has shaped how we think about Parkinson’s disease, suggesting that abnormal alpha-synuclein pathology spreads through the brain in a predictable sequence as the disease advances. What resonates with me about this new study by di Biase and colleagues, and the accompanying thoughtful editorial by Rodríguez-Violante in Neurology, is that the biology may be far more complicated than the model. In 61 people with autopsy-confirmed Parkinson’s disease, Braak stage did not correlate with motor disability, disease duration, age at death, or brain weight. In other words, having more widespread alpha-synuclein pathology did not necessarily mean having more advanced clinical disease. The editorial importantly reminds us that this finding does not invalidate Braak staging or the importance of alpha-synuclein, but rather exposes the limitations of using pathology as a clock for clinical progression. Parkinson’s is not one disease following one predictable path, and the frequent presence of other pathologies, including tau, amyloid, and vascular disease, further complicates the picture. For me, the lesson is that we must be careful not to confuse what we see under the microscope with what patients actually experience. As we develop biological staging systems, biomarkers, and disease-modifying therapies, we need to measure not only abnormal proteins but also neuronal loss, clinical disability, and the individual trajectories of people living with Parkinson’s. The patient, not the pathology, must remain at the center of our science.
https://www.neurology.org/doi/10.1212/WNL.0000000000218469

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Could ADHD be a risk factor for dementia later in life? An important new study raises questions. What really resonates with me about this new study published in JAMA Psychiatry is the possibility that attention-deficit/hyperactivity disorder (ADHD), a condition we often associate with childhood, may also be an important risk factor for cognitive decline later in life. Researchers followed data from more than 187,000 adults and found that people diagnosed with ADHD had a substantially higher risk of developing mild cognitive impairment or dementia. In fact, 6.7% of those with ADHD developed cognitive impairment compared with 3.4% of those without ADHD, and the association remained significant even after accounting for several other health conditions and risk factors. Interestingly, genetic markers associated with ADHD also predicted a modest increase in risk. We must be careful here: this study does not prove that ADHD causes dementia, and having ADHD certainly does not mean you are destined to develop cognitive problems. What strikes me is that we may need to rethink ADHD as more than a disorder of attention and behavior and consider its potential implications across the lifespan. The message is not to create fear, but to recognize risk, pay attention to changes in memory and thinking, and invest in research to understand whether earlier recognition and better management of ADHD can improve long-term brain health.
https://cutt.ly/UyWH9uHB

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Registros do XXXII Congresso Brasileiro de Neurologia 2026, no Rio de Janeiro. 🧠

São dias de atualização científica, discussões interessantes, tecnologia, inovação, e troca de experiências e reencontros com amigos e colegas de diferentes partes do Brasil.

Tive a oportunidade de apresentar resultados em construção do projeto DigiTAU, pesquisa que investiga a relação entre habilidades digitais e desempenho cognitivo. Foi muito bom compartilhar parte desse trabalho e acompanhar as discussões sobre os avanços da Neurologia.

Tivemos também a escolha de Salvador como sede do Congresso Brasileiro de Neurologia de 2030. Uma excelente notícia para a Neurologia baiana e uma oportunidade de receber colegas de todo o país em nossa cidade.

Além da programação científica, ficam também as boas conversas, os reencontros e as novas conexões, que fazem parte desses eventos.

Volto com boas lembranças, novos aprendizados e a expectativa de nos encontrarmos novamente em Salvador, em 2030!

#neuro2026 #congressobrasileirodeneurologia #neurologia #pesquisacientífica #inovação

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Whirlwind trip to Vegas to speak for the American Academy of Neurology.Grateful for the opportunity to be part of this organization and continue advocating for APPs in neurology. 🧠

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🧠⚡ Proud and honored to announce a new publication in Anesthesia & Analgesia @iars_journals .💡Is there a connection between Post-surgical pain and dystonia❓

Current dystonia classifications don’t explain how peripheral nerve injury after surgery can produce a dystonic phenotype tied to chronic pain. These presentations are frequently mistaken for spasticity, contributing to misdiagnosis, yet they are two distinct pathophysiologic entities.

In this first report, we propose the peripheral nerve generator as a therapeutic target. In susceptible individuals, peripheral injury may drive maladaptive sensorimotor plasticity and central sensitization, leading to the dystonic phenotype. Diagnostic nerve block–guided cryoneurolysis improved pain, dystonic posture, and quality of life in all three patients.

This is what collaboration across anesthesiology, pain medicine, and neurology can uncover together. The future of pain medicine, movement disorders, and neuromuscular physiology is bright.

📄 Full article link 🔗 available in the my bio

With gratitude. Special thanks to @drkalava , EDRA for your mentorship, guidance, and the invaluable opportunity to make this project happen.

I’m also grateful to Dr. Paul Winston, MD who connected me with Dr. Kalava and brought the intellectual spark that drew me into the fascinating world of cryoneurolysis.

Sincere thanks to the Neurology (@larkinneurons) and Movement Disorders departments at @larkinhospitalsm, for their collaboration on this project, with special thanks to Dr. Simon Starosta-Rubinstein, MD .

Thanks to Dr. @wilsoncuevamusic, my Neurology Program Director, and Dr. Hector Lalama, MD , Attending Neurologist, for their unwavering mentorship; and to Dr. @jmichelmd MD and the GME committee @larkingme . #neurology #movementdisorder #medicine #dystonia @aanbrain @nowyouknowneuro @florida_sipp #pain

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