Liam Ramsey

Interested in brains, people and culture

[Jordi Serra-Mestres @JordiSM_]

Comparative effectiveness of lorazepam versus diazepam for acute catatonia: A retrospective analysis https://t.co/HOelrtPssT

[JAMA Psychiatry @JAMAPsych]

💬 Editor's Note by Dost Öngür, MD, PhD: In a RCT, semaglutide reduced hemoglobin A1c and body weight and improved physical quality of life in patients with #schizophrenia, #prediabetes, and #obesity, without negative effects on mental health status.

https://t.co/J2xmDSBujn

[Oliverio @LuisOliverio]

Hace poco salió una revisión de Alzheimer en The Lancet (2026). Aquí van las notas (muy) sintetizadas:

🟡60% de los casos de demencia
🟡 Si <65 años: pensar en monogénica dominante (por mutación en APP, PSEN1, PSEN2) (1%)
🟡 Late-onset Alzheimer, es 80% de los casos, por APOE epsilon4; aunque hay 100 loci, el estilo de vida saludable sí reduce el riesgo
🟡80% de los casos son con amnesia hipocampal (olvidas rápido, no aprendes); 20% son en la corteza, disfunción visuoespacial, síndrome de Gerstmann, agnosia visual, dificultad para encontrar una palabra (afasia primaria progresiva lopogénica), cambios en comportamiento, estereotipia, crisis, mioclonía
🟡No poder recordar palabras con pistas, es sugestivo de inicio de Alzheimer (si la pista ayuda a recuperar, sugiere fronto-subcortical, vascular o depresión)
🟡No poder funcionar fuera de casa define la demencia como “moderada”; ser dependiente lo cataloga como grave
🟡Patogenia: agregados de beta-amiloide que forman placas y acumulación de tau fosforilada
🟡Es frecuente que coexista con angiopatía amiloide (80%, leve), enfermedad argirofílica (otra tauopatía) o astrogliopatía de la edad, microinfartos - demencia vascular
🟡Aunque la genética importa mucho, 45% del riesgo es modificable con: educación, buena audición, salud cardiovascular, peso, ejercicio
🟡La RM es importante para los diferenciales, clásicamente en Alzheimer hay atrofia en el lóbulo temporal medial - pero no es suficiente
🟡El PET con 18-FDG es más sensible; y aun mejor PET con beta-amiloide (Aβ PET - bueno para descartar, puedes usar escala de Centiloid) o Tau-PET. Otros biomarcadores para PET en investigación: Synaptic Vesicle Glucoprotein (SVA2), Translocator protein 18 kda (TSPO), MAO-B PET
🟡Biomarcadores en LCR: radio beta-amiloide 42/ beta-amiloide 40, tau total, tau-fosforilada 181 alto. Otros: cadena ligera de neurofilamento (NfL), proteínas sinápticas (beta-sinucleina, GAP-43, NPTX2, SNAP-25, SV2A, sTREM2, YKL-40, GFAP
🟡Biomarcadores sanguíneos p-tau181, p-tau217, p-tau231, GFAP, NfL, Beta-sinucleina
🟡Para el diagnóstico una sociedad dice que debes tener datos clínicos y otra no (como diabetes, no requiere síntomas solo HbA1c - un debate interesante)
🟡Mejorar la salud cardiovascular y ejercicio es parte del tratamiento
🟡 Tratamiento: inhibidores de acetilcolina y memantina, y sintomáticos
🟡Modificadores: Lecanemab y Donanemab están aprobados. En prueba: Trontinemab
🟡Otras en estudio: esitmulación gamma, estimulación magnética transcraneal, estimulación profunda cererbral, agonistas muscarínicos parciales, agonistas de receptor de cannabinoies, inhibidores de la MAO-B, litio.

El tema es gigante y muy interesante. Está completo con mucho más en Accio - incluye algoritmo de los nuevos criterios diagnósticos (https://t.co/FQyQuLPcWG).

[JAMA Psychiatry @JAMAPsych]

Individualized, connectivity-based targeting of accelerated transcranial magnetic stimulation produced significantly greater antidepressant effects than scalp-based targeting in adults with treatment-resistant #Depression.

https://t.co/mHdQIS4NVG

[Brain @Brain1878]

Xin et al. found that tau PET is as effective as amyloid PET for diagnosing Alzheimer’s disease. It also provides valuable information for identifying non-AD tauopathies and refining diagnoses, thereby increasing diagnostic confidence. https://t.co/nxq8thk9fs

[Jesus Ramirez-Bermudez @JRBneuropsiq]

Dear fellows: We published this systematic review to figure out the Neuropsychiatric Phenotyope of Klüver-Bucy syndrome.
🧵🧠💭
This condition involves a deep transformation of behavior, characterized by hypersexuality, hyperorality, hyperphagia, visual agnosia, (1/5)

[Shan Siddiqi @shansiddiqi.bsky.social @shansiddiqi]

We all thought this study would fail, for different reasons.

Joe Taylor (1st author) thought it'd be a takedown of fMRI-guided TMS.

@foxmdphd and I (co-senior authors) thought the effect would be too small to detect in just 40 patients.

We were wrong.

https://t.co/MlFghE9hBX

[Nature Mental Health @NatMentHealth]

🚨@SaraStampacchiaet al. investigated minor hallucinations in patients with Parkinson’s Disease using a connectome-based brain fingerprinting approach and examined their association with cognitive decline. @BernasconiFosco,@OlafBlankeLab,@Neuro_X_EPFL
https://t.co/GrLGY4wqVZ

[JAMA Psychiatry @JAMAPsych]

💬 Editorial: Connectivity-based targeting for transcranial magnetic stimulation demonstrated greater antidepressant effects and precision than scalp-based approaches in adults with treatment-resistant #Depression. https://t.co/U0tyKb6lO3

[JAMA Psychiatry @JAMAPsych]

This narrative review suggests mental disorders are statistical clusters of biopsychosocial properties, not sharply defined categories, mirroring concepts in species classification and supporting dimensional #MentalHealth frameworks. https://t.co/SfES3sUTlh

[Jonathan Shedler @JonathanShedler]

🎙️

Watch or listen👇

[Sara Stampacchia @SaraStampacchia]

🧠 New paper in @NatMentHealth !

In Parkinson's Disease, we show that patients at risk of cognitive decline have a distinct brain fingerprint, and that patient-specific networks associate with clinical outcomes and neurochemical substrate.

Paper 👇

[JAMA Psychiatry @JAMAPsych]

In individuals at clinical high risk for #psychosis, reduced temporal stability of EEG microstates was associated with earlier conversion and increased positive symptom severity. https://t.co/zFnnkHeCQT

[JAMA Psychiatry @JAMAPsych]

💬 Editorial: Reduced temporal stability of #EEG microstates shows promise as a scalable biomarker for predicting clinical outcomes in individuals at high risk for psychosis.

https://t.co/aicAIEKYJs

[Kemtrup @KemtrupTweets]

I have a lot to say about POSSIBLE psychosomatic symptoms but here is the most important thing:

Individual clinicians MUST take the patient and the symptoms seriously. BOTH must FEEL and explore the possibility that the symptoms aren’t or aren’t entirely psychosomatic AND the 1/

[Sultan @Sultan__Shehri]

Video Atlas of the Detailed Neurologic Examination by Dr. Martin Samuels

A classic neurologic examination series that was included as part of Harrison’s. Highly recommended for anyone learning or refining their neurological exam

https://t.co/2SukhwUvIB

[Michael Okun @MichaelOkun]

Big challenge in Parkinson’s is that synuclein seeding assays can be positive across many diseases. Nice plenary this morning showing how this group uses synuclein seeding + 4 R TAU + NFL to sort this out using a multi-modal biomarkers approach. This is one such approach used at the University of Toronto and presented today at the World Parkinson Congress.

[Mayo Florida AutoImmune Neurology Group @Mayo_AING]

Pragmatic. Full of information. Cutting edge. Cool figs!

Honored to lead The Lancet review on Encephalitis. With amazing Sophie B, Ava E, Kiran T &amp; @DeannaSaylor1

We hope you enjoy reading it:
https://t.co/0baEHVhjeH

@mayoneurores @mayocliniclabs @MayoClinic @NDCNOxford

[John D. Arena, MD @JohnDArenaMD]

CTE cannot be diagnosed during life. Our work published today in @NatureMedicine demonstrates that most individuals meeting proposed clinical criteria do not have evidence of #CTE neuropathology at autopsy (1/5)

https://t.co/5euKrqf8vq

@PennNSG @PennMedCSO @WillStewNeuro

[Awais Aftab @awaisaftab]

@DrAnnieHickox Pair with:

https://t.co/WBHm9jgPM5