Lawrence Robbins, M.D. Riverwoods, Ill Neurology
2.4K posts

Lawrence Robbins, M.D. Riverwoods, Ill Neurology
@lrobb98
New book: Neurology and Psychiatry: Lectures and Clinical Pearls (great reviews)...Neurology educator, headache specialist, psychopharmacologist, professor;


I have never talked to the press about being a creationist missionary, how I left etc - and I do feel really conflicted about sharing this profile. I’ll be clarifying and giving context to lots of things in it over time. 1/ @ObserverUK observer.co.uk/news/science-t…

9. Ten Years After performing "I’m Going Home"

@BenPopeCST Some franchises play the long game when rebuilding… the Hawks are playing the long, long looooonnnng game

Dear Neurology Residents Starting in the ED Next Month, You will frequently encounter “?GBS” or “GBS rule out” consults. Please remember to carry your reflex hammer, save this post for future reference, and read the open-access review that I share ⬇️. 🤓 Since you won’t have much time for history taking, make sure to ask about important details such as falls, the use of gait aids, the ability to climb stairs, difficulty walking, using zippers, and washing their hair. These activities can help you gather an accurate timeline. I also suggest asking when they last felt like their usual selves, as this can help pinpoint when the symptoms began, along with their prior level of disability, which is crucial. Don't forget to ask about potential triggers, including recent vaccinations, infections, surgery, and trauma. The following physical examination features make GBS very unlikely and may assist you in “ruling it out”: - A sensory level - Unilateral weakness - Markedly asymmetric weakness (excluding cranial nerves) - Weakness confined to either the upper or lower limbs - Normal (or preserved) ankle reflexes - Fever or skin rash - Normal gait GBS is the most common cause of ascending weakness and paresthesias. So, if history suggests it, the patient is unable to walk, the weakness is symmetric, and the reflexes are reduced/absent, please admit the patient and start IVIg overnight. Time is nerve! 😅

@AnswerTheColl False. Dan Marino


📚🧠5 Essential Neurology Books (Residency basics) 1. Clinical Neurology & Neuroanatomy @AaronLBerkowitz 2. How to think like a neurologist @emeltzermd 3. The Acute Neurology Survival Guide @caseyalbin 4. The Code Stroke Handbook @MicieliA_MD 5. Brainspotting @ajlees #NeuroTwitter #stroke #Neurology #brain #MedStudentTwitter #match2025 @NMatch2026 #meded


A missing puzzle piece in Alzheimer’s and other dementias may be 'modifiable' and right in front of us. This study in Journal of Neurology by Montero‑Odasso and colleagues brings into focus vascular risk factors like high blood pressure, diabetes, obesity, cholesterol, and smoking. Spoiler alert: These risk factors are common across neurodegenerative diseases and modifiable. Key Points: - These risks are linked to increased white matter damage in the brain, especially in cerebrovascular disease (CVD), frontotemporal dementia (FTD), and Alzheimer’s/MCI. - White matter damage shows up both as visible lesions (white matter hyperintensities) and as subtle microstructural changes detectable on advanced MRI. - The APOE ε4 genetic risk for Alzheimer’s only slightly modified these vascular effects, meaning vascular risks acted independently. - The vascular risk index (VRI) was a strong predictor of neurodegenerative disease presence and severity. My take: Here are 5 Takeaways from this article: 1- Vascular risk is not just noise, it's a signal. Alzheimer's and related diseases aren’t just about amyloid and tau. Small vessel disease and vascular burden are co-conspirators in brain decline. 2- Brains don't forget blood pressure. Hypertension and cholesterol were more common in people with Alzheimer's, FTD, and CVD. These are treatable targets. 3- The MRI never lies (at least most of the time). Higher vascular risk scores were tied to worse white matter integrity, both the kind you can see (lesions) and the kind you can’t (microstructure changes). 4- Genetics isn’t destiny. APOE ε4 status didn’t erase the impact of vascular risks. That means even genetically at-risk individuals can benefit from better vascular control. 5- It's time to treat what we can fix. We may not yet have a cure for Alzheimer’s, but we can reduce stroke risk, treat blood pressure, and manage cholesterol. This study adds urgency to acting now. When it comes to health be sure you nosce te ipsum – know thyself and think about what may be modifiable. link.springer.com/article/10.100… @ParkinsonDotOrg @FixelInstitute @HeartAssocMN #Alzheimers #Dementia #BrainHealth #StrokePrevention #Hypertension #Cholesterol

Up to 80% of individuals with Autism Spectrum Disorder (ASD) show ADHD symptoms, and up to 50% of those with ADHD meet ASD criteria (Lau-Zhu et al., 2019). DSM-5 formally recognised co-diagnosis, reshaping how we assess, manage, and support neurodevelopmental overlap. Let’s examine the neurobiological overlap, diagnostic complexities, and treatment considerations driving clinical care. 🧵👇

I really don’t understand how dudes traveled the seas 500 years ago

Rickey Henderson is on first, and he’s looking to run. You can have any Catcher from any era try and gun him down. Who gets the nod?

We have just updated our Parkinson's disease pain checklist with this paper ow.ly/oFaP50Qyr8Z

A common misconception regarding the treatment of Guillain-Barré syndrome (GBS) is the idea that it can be categorized as either "IVIg responsive" or "resistant." The only two therapies that are effective for GBS—plasma exchange and intravenous immunoglobulin (IVIg)—do not change mortality rates or long-term disability outcomes. Yes, you read that correctly. Both treatments are quite expensive, and clinical trials have shown that, compared to placebo, they only lead to accelerated recovery, with no significant difference in disability at one year or mortality rates. Some of you may think I’m crazy for repeatedly stating that "Time is Nerve," but I strongly believe this to be true. The variation in response to immunotherapy in GBS is most likely related to the timing of starting treatment for an individual patient's disease course. This is why it is crucial to initiate therapy as soon as possible. I believe that starting treatment early may change the trajectory for many patients on an individual level. Research indicates that the neuropathic process in GBS begins several days before patients exhibit any symptoms. After antibodies have been deposited in the nerves and complement activation occurs, plasma exchange or IVIg cannot effectively treat the damage that has already taken place in the nerves. While these treatments may help prevent further injury caused by antibodies or complement/cytokines, they cannot reverse the damage that has already been activated. As a result, patients with severe GBS who present to the hospital within less than three days or who become unable to walk in that same timeframe are likely to require mechanical ventilation and face a poor prognosis. 1/x



Psych Scene Snapshots 🧠📷⚡ Q: How do you differentiate the mood dysregulation of BPD from Bipolar Disorder? A: Mood shifts in BPD are rapid (minutes to hours), often reactive to interpersonal stress, and closely tied to identity disturbance and fear of abandonment. In contrast, bipolar episodes are sustained (≥4–7 days), often arise without external triggers, and involve clear changes in energy, sleep, and cognition. BPD is characterised by heightened affective reactivity to interpersonal stressors, particularly intense anger, shame, and fear of abandonment. In contrast, bipolar disorder features sustained mood episodes (mania, hypomania, or depression) lasting days to weeks, interspersed with periods of relative euthymia and functional recovery. Psych Scene Tip💡: Ask about duration, trigger, and trajectory. If mood swings are moment-to-moment and relational, think BPD. If mood states dominate for days to weeks, think bipolar. *About 20% of bipolar II patients and 10% of bipolar I patients have comorbid BPD, and there is a robust relationship between BPD and bipolar disorder II (Zimmerman and Morgan, 2013)

The nucleus accumbens, the brain's reward center, can fuel impulsive behaviors like overeating and addiction. Fascinating @NatureMedicine study found that stimulating this region in a temporally precise fashion can reduce overeating and promote weight loss.

📢 NEW Course | NEUROLOGY MADE EASY • 26 July 2025 🗓️ • 7:30am - 4:10pm ⏱️ Target Audience : • 1- Internal Medicine Residents • 2- Family Medicine residents • 3- Junior Neurology residents • 4-Hospitalist / Family medicine practitioners • 5- Interns
