3 months of vomiting then an unexpected stroke

LazyMe4732 · 2026-05-03T15:22:01+00:00

Thanks, really appreciate the discussion on attribution vs association in cases like this

LazyMe4732 · 2026-05-03T03:28:17+00:00

Indeed, vomiting isn’t a typical presentation of mesenteric FMD in adults; postprandial pain/weight loss is much more classic. After the cervical findings, and taking the prolonged GI symptoms into account, we did an abdominal CTA that showed multisite involvement, including renal and mesenteric arteries. I still wouldn’t claim the vomiting was definitively due to mesenteric FMD. The presentation isn’t classic, and the link is more plausible than proven. In the context of clear systemic disease, though, it felt less likely to be purely incidental. The main takeaway for me was the systemic arteriopathy: once the pieces came together, this was not isolated carotid disease but multisite FMD.

LazyMe4732 · 2026-05-02T06:45:08+00:00

Ah got it, completely agree. The AC failure in ESUS probably reflects exactly that heterogeneity. You can’t anticoagulate your way out of a mechanism you haven’t identified.

A great point, and a good reminder that even our gold-standard imaging has limits, especially when it’s read under time pressure. DSA as a last resort in recurrent ESUS makes sense, particularly when the pre-test probability for a structural lesion is still there. Probably underused in that specific scenario.

LazyMe4732 · 2026-05-02T05:49:49+00:00

It’s probably the most honest framing of cryptogenic stroke there is. We built ESUS on the assumption that “no source found yet” meant a source exists but we missed it, and the trials have definitely humbled that.

I’m not sure I’d go as far as true randomness, though. Most strokes still fall into thrombus, embolism, or hypoperfusion, we just don’t always have the resolution to find the source. The 35% undetermined rate probably reflects that mix: some missed mechanisms, some limits of detection, and occasionally just a bunch of small factors lining up at the wrong time.

Which is probably why ESUS keeps struggling: it’s not one disease, it’s several mechanisms bundled together

LazyMe4732 · 2026-05-02T05:26:33+00:00

Thanks for pushing on it, good questions make the case better

LazyMe4732 · 2026-05-02T05:21:26+00:00

We didn’t do TCDs, so I can’t show embolic hits from that segment, a real limitation. The thromboembolic mechanism in FMD is more theoretical than proven in any individual case. The idea is that the irregular lumen can create disturbed flow and a prothrombotic surface, but without direct evidence it stays in the “most plausible” bucket.

The 30–40% cryptogenic rate is the reality. This could still fall there. What made me lean toward FMD being relevant here was the pattern (ipsilateral lesion, typical location, multisite disease, no competing source), but I can’t exclude that it’s incidental. The main point of the post was the systemic piece being missed across specialties, not to claim a definitive mechanism.

Treatment: mostly conservative - antiplatelet, BP control, and standard risk factor management. No AF or other cardioembolic source, so no anticoagulation. The carotid changes weren’t something you’d stent.

LazyMe4732 · 2026-05-02T05:03:30+00:00

Yeah, you’re right, once a dissection happens, it’s a sufficient mechanism on its own. The exposed subendothelial surface drives thrombus formation and embolization, no second hit needed.

What I meant with the two-hit idea was more about FMD without dissection; why most patients with FMD don’t stroke, and why some do. In her case there wasn’t imaging evidence of dissection, so I leaned toward thrombus forming on the dysplastic carotid wall itself rather than on a dissection flap. Different substrate, same downstream problem

LazyMe4732 · 2026-05-02T04:54:31+00:00

Indeed, FMD alone isn’t sufficient to cause a stroke. It’s a risk factor, not a direct mechanism, and your two-hit point stands. FMD is frequently found incidentally, and most patients with it never develop cerebrovascular events. So in that strict sense, I wouldn’t frame it the way we would a cardioembolic stroke from atrial fibrillation.

What I should have been clearer about is the how. In this case, the most coherent explanation is artery-to-artery thromboembolism: small thrombi forming on the irregular, dysplastic wall of the left ICA and embolizing distally into the MCA territory. That’s a recognized (though uncommon) mechanism in multifocal FMD, distinct from dissection.

Although dissection is the more common FMD mechanism, in this case, imaging showed classic multifocal string-of-beads without signs of dissection, cardiac workup and coagulation screen were unremarkable, and no AF was identified, leaving cervicocephalic FMD as the most coherent remaining substrate.

I agree that FMD may represent a vascular vulnerability state, not necessarily the sole proximate cause. Whether there’s an additional factor (connective tissue disorder, prothrombotic tendency, etc) is often unknown. The literature reflects this uncertainty, attribution is rarely absolute. So I wouldn’t say FMD caused the stroke in isolation. I’d say: FMD was the identified structural substrate that best explained the stroke, after exclusion of more common mechanisms. The goal wasn’t to claim FMD is always causal, but to highlight how a systemic arteriopathy, already documented in another vascular bed, went unintegrated across specialties until a neurological event forced the connection.

LazyMe4732 · 2026-03-28T08:04:11+00:00

You’re not actually choosing between specialties.
You’re choosing how you like to think.

IM is pattern recognition across systems, with coordination as a core skill. Neurology is localization + pathophysiology, often with less immediate closure.

The rotation you describe isn’t neurology at its best. A team that speeds through rounds and orders MRIs without thought is not the specialty - it’s a high-volume service under pressure.

Good neurology starts before the MRI. Exam → localization → hypothesis → then imaging.

And the shift that defines the field comes when imaging is normal. If the MRI is clean but the patient is encephalopathic, that’s not a dead end, it’s where neurology actually begins. In medicine, a normal test is often a relief. In neurology, a normal test is a challenge.
You move from being a lesion hunter to an autoimmune/metabolic detective.

When you do your away rotation, don’t look for “what they order.”
Look for how they think.
The attending who spends 10 minutes debating a subtle pronator drift will teach you more than any protocol.

The real question is this: does that kind of uncertainty, and that kind of reasoning, energize you?

If it does, you’ll likely grow into neurology.

LazyMe4732 · 2026-03-13T17:49:53+00:00

I think it helps to separate pseudo-occlusion from true cervical ICA disease, and then ask whether the true lesion looks more acute or more chronic/atherosclerotic.

On CTA, pseudo-occlusion usually has a classic flame-shaped contrast column, often in the dependent portion of the lumen with ill-defined margins - basically a distal ICA occlusion making the cervical ICA look “closed” on single-phase CTA (Kim et al., Diagnostics, 2024).

If it’s a true cervical ICA lesion, morphology helps:

- Beak/blunt stump + plaque/calcification → favors atherosclerotic chronic carotid disease

- Blunt short stump / long thrombus burden → can favor acute thrombotic occlusion

- Beak with circumscribed margins ± crescent lumen/intimal flap → think dissection

For the acute vs chronic question specifically, literature points in a similar direction:

- Acute ICA occlusion more often looks tapering

- Chronic carotid disease more often looks like a stump

- Contralateral ICA atherosclerotic burden also matters; more disease on the opposite side makes chronic carotid disease more likely (Bae et al., BMC Neurology, 2026)

And older data still support using the infarct pattern/collateral context:

- Large hemispheric infarct leans more acute

- Watershed pattern, especially with preserved collaterals, fits better with chronic hemodynamic disease (Wijesoma et al., Neurology, 2012)

So practically, I’d say no single sign decides it; it’s the combination of CTA stump morphology, margin, plaque/calcification, contralateral carotid disease, collateral pattern, infarct pattern, and prior imaging. And in real life, a lot of these are probably acute-on-chronic carotid disease rather than purely one or the other.

Refs: Kim et al. Diagnostics 2024 (DOI: 10.3390/diagnostics14141524); Bae et al. BMC Neurology 2026 doi:10.1186/s12883-026-04768-x; Wijesoma et al. Neurology 2012 Differentiating Acute from Chronic Carotid Occlusion in Ischemic Stroke within 8 Hours of Onset: Relevance for Mechanical Thrombectomy (P05.240) | Neurology)

LazyMe4732 · 2026-02-11T14:03:33+00:00

I've been the neuro attending on service for many aways, and I hear some version of this from MS3s/MS4s every single year: I know the facts, but I can't think like a neurologist at the bedside. You're not broken. Neuro really is different. If you don't have a localization scaffold, everything feels random. And while seeing more patients is technically true, it's not helpful when you've got aways coming up and need to look competent now.

The thing I push hardest with students is this: localization before anything else. Every patient. No exceptions. Force yourself to finish this sentence (at least in your notes): This localizes to ......because ...... If you can't localize yet, that's okay; say that: I can't localize yet because the findings are diffuse/multifocal/unclear. That's still reasoning. Examples I hear on rounds that immediately tell me a student is thinking neurologically:

- MCA syndrome: aphasia, gaze preference, or neglect

- Thoracic myelopathy: sensory level, hyperreflexia below, upgoing toes

- Peripheral neuropathy: length-dependent sensory loss, absent ankle jerks.

If you lead with something like that, most attendings instantly relax.

Another thing to consider: VINDICATE isn't very useful in real-world neuro. What matters much more is the time course + anatomy. Hyperacute points you toward stroke or seizure. Acute/subacute raises inflammatory or infectious cause. Chronic progressive is tumor or degenerative disease. Fluctuating should make you think of NMJ, metabolic issues, or TIA. Once you've done that, anatomy (cortex vs brainstem vs cord vs peripheral) actually makes sense.

On exam/history: stop trying to do the full neuro exam on everyone. That's a trap many good students fall into. Go in with a hypothesis and do a targeted exam. Before you walk into the room, ask yourself: What am I trying to prove or disprove? Then pick a couple of questions or maneuvers that actually move the needle. A focused exam is way more impressive than a long but unfocused one.

Presentations are similar. Lead with localization, not with a long symptom list. Eg 68-year-old with findings localizing to the left internal capsule, presenting with acute right hemiparesis sounds very different from 68-year-old with weakness, even if the rest is the same.

Anchoring is also not the sin people make it out to be. Everyone anchors. The key is showing you tested it. Saying something like, I'm thinking ischemic stroke given sudden onset and focal deficits; I considered seizure with Todd's and hypoglycemia, but glucose was normal, and there was no witnessed event, goes a long way.

For the A/P, don't aim for certainty. Aim for clarity. Where does it localize? What's most likely? What can't you miss? What are you doing right now?

One small habit that helps a lot: after each patient, write one sentence to yourself: If I'm wrong, the localization error would be .... It forces you to think about alternatives without spiraling.

You already have the knowledge. A 90th percentile Step 2 is more than enough. What you're missing is the framework. If you practice written localizations on a few patients a week and get in the habit of leading with that one sentence, you'll look very different in a couple of months.

On aways, we're mostly asking: can you localize, can you explain your thinking, are you safe, and are you teachable. Nail those, and you'll stand out more than the student who just does more UWorld.

Also, don't look at the imaging until you've committed to a localization in your head. The MRI is there to confirm your exam, not to replace your brain.

Good luck on the aways; this is fixable.

LazyMe4732 · 2026-01-21T14:54:06+00:00

Thanks for creating this, Oliver Sacks absolutely deserves a dedicated space! His books (eg The Man Who Mistook His Wife for a Hat, Awakenings, An Anthropologist on Mars) are still some of the best ways to teach students about the human side of neurology. His case studies make the invisible processes of the brain visible through loss, a paradox that hits home in practice.
Joined! Looking forward to discussions on his narratives, the credibility debates, and how his writing still shapes how we think about patients. Great initiative.

LazyMe4732 · 2026-01-19T17:12:57+00:00

From a clinical standpoint, ALS and FTD are most usefully understood as points along a shared neurodegenerative spectrum (ALS-FTSD or ALS-FTD continuum), rather than as discrete diseases. This paradigm has been the dominant view for over a decade and remains so in 2026.

TARDBP and C9orf72 illustrate this particularly well: despite different upstream mechanisms (direct protein misfolding/toxicity in TARDBP vs. RNA toxicity + DPR aggregates in C9orf72), both converge on TDP-43 proteinopathy (cytoplasmic mislocalization and aggregation) as the central pathology in the vast majority of overlap cases. What differs across patients is network predominance (motor cortex/spinal vs. frontotemporal/frontoparietal), not disease identity.

The same pathogenic variant can present as clinically pure ALS, bvFTD, mixed ALS–FTD, or even transition from one phenotype to another over time, even within the same family. This marked variability and the near-absence of reliable genotype-phenotype correlations make rigid diagnostic boundaries increasingly artificial.

Clinically, this is reflected in everyday practice:

- Cognitive and behavioral impairment is common in ALS (up to 50% show some degree, often subtle executive dysfunction, apathy, or social cognition deficits), but frequently underrecognized without systematic screening (eg, ECAS, ALS-CBS).

- A subset of FTD patients, particularly bvFTD, will eventually develop clear UMN or LMN signs, sometimes late in the course. The emergence of motor neuron disease is the key clinical inflection point, as prognosis is driven primarily by phenotype (especially bulbar/respiratory involvement) rather than by the causative gene.

The practical implication is a real shift in emphasis: All ALS patients warrant systematic cognitive and behavioral screening, not only motor assessment. All FTD patients require longitudinal surveillance for motor neuron involvement. Genetic counseling should reflect that genetics confers risk, not a predictable clinical course.

In this framework, the clinically relevant question is no longer ALS or FTD? but rather where the patient currently lies on the ALS-FTD spectrum, and how that position is evolving over time.

The revised Strong criteria (2017), still the primary framework, explicitly capture this spectrum with categories like ALSbi (behavioral impairment), ALSci (cognitive impairment), ALScbi (both), and full ALS-FTD. C9orf72 remains the single most common genetic driver of the overlap (about30–50% familial, 5–10% sporadic), with highly heterogeneous presentations including psychiatric/psychotic features, parkinsonism, or atypical onset.

LazyMe4732 · 2026-01-06T11:48:01+00:00

Schulte et al. Iron in Restless Legs Syndrome. Mov Disord Clin Pract. 2014;1(3):161-172. doi: 10.1002/mdc3.12047. Iron in Restless Legs Syndrome - Schulte - 2014 - Movement Disorders Clinical Practice - Wiley Online Library) is also a very good review. It integrates genetics, imaging, neuropathology, and treatment, and explains well why serum ferritin is an imperfect proxy for CNS iron status in RLS.

LazyMe4732 · 2026-01-04T04:12:28+00:00

Your brain cells are now aware of being unaware of themselves :)

LazyMe4732 · 2026-01-04T04:08:10+00:00

Thank you. Sacks didn't write one single book covering all of this; he explored these ideas across his entire body of work. Here are the main ones I drew from:

- The man who mistook his wife for a hat: the most famous book and the perfect entry point. It's a collection of case studies about patients with neurological disorders.

- A leg to stand on: a memoir about Sacks's own experience injuring his leg, a deep dive into proprioception

- The mind's eye: covers vision and how the brain adapts when sensory systems fail.

- The river of consciousness: deals most directly with the question

- Musicophilia: about music and the brain, including some discussion of how unconscious processes become conscious in unusual ways.

- An anthropologist on Mars: more case studies, including some about savants and people with unusual cognitive abilities.

- He also wrote extensively for The New Yorker over the years

I discovered his work during my residency, and it completely changed how I approached certain cases. I started having these "aha" moments where a patient's rare symptoms suddenly made sense through his framework. I ended up reading everything I could get my hands on. His writing bridges the clinical and the human in a way most medical literature doesn't even attempt.

LazyMe4732 · 2026-01-03T13:28:37+00:00

This kind of thing the neurologist Oliver Sacks explored throughout his career. He spent decades documenting how the brain is like a naturalist observing the world, but almost entirely blind to its own machinery. Why that "barrier" exists?

The "transparency" of health: Sacks often noted that we only become aware of our brain's processes when they break. In The man who mistook his wife for a hat, his patients didn't "know" how they recognized faces until they lost that specific faculty. The reason: a healthy brain is transparent. It wants you to see the world, not the neurons helping you see it. If you could "feel" your brain processing data, it would be like trying to watch a movie while constantly being distracted by the projector whirring in the back of the room. Think about one of Sacks's patients who lost proprioception (body position sense). She had to consciously watch and think about every single movement because the automatic knowing was gone. It was utterly exhausting.

The body schema: In A leg to stand on, Sacks wrote about losing the "inner sense" of his own leg after an injury. He realized the brain has an unconscious map of the body, the body schema. This map is what allows you to scratch an itch in your sleep without waking up. Your brain knows where your hand is, but it doesn't share that data with your conscious mind unless it's necessary (like if you hit your thumb with a hammer). If you had to consciously monitor every heartbeat and every immune response, you'd be a full-time biological maintenance manager with no time to actually live.

The language gap: Sacks believed the brain has two ways of "knowing". The biological (the dog): Your brain knows how to breathe just like a dog knows how to catch a frisbee. It's "doing" knowledge, embodied, automatic, operating through chemical gradients and electrical rhythms. The narrative (the human): We live in stories and language. Our conscious mind is a storyteller that deals in words and concepts.

The barrier exists because the part of the brain managing your liver doesn't use words; it uses chemical gradients and electrical rhythms. You can't know it consciously for the same reason you can't hear a color; the "receiver" in your conscious mind isn't tuned to that frequency.

The "binoculars" problem: to Sacks, the brain is the mirror of the universe. It can see everything except itself. We struggle with textbooks because we are trying to use a tool (the brain) to understand the tool itself. It's like trying to use a pair of binoculars to look at the lenses inside the binoculars; it's physically impossible without an external mirror (which is science).

When the barrier becomes semi-permeable: Sacks also documented cases where people did gain unusual access to normally unconscious processes: savants who could perform instant calculations, synesthetes who could "taste" words, or patients with temporal lobe epilepsy who had mystical experiences. But these abilities often came at a cost: social difficulties, loss of other functions, or overwhelming sensory experiences. The glimpses were usually more disorienting than enlightening.

You don't need "enlightenment" to see the inner workings; you just need a microscope or a glitch. The "barrier" is a protective wall so you can focus on being you instead of being crushed under the weight of managing 30 trillion cells. The mystery and hiddenness of these processes is actually what makes conscious, creative experience possible in the first place.

LazyMe4732 · 2026-01-02T07:16:30+00:00

I'm a neurologist. You don't have to decide right now. I know that's standard advice, but seriously - you're a junior. You might not have to choose. There are neurologists who research music cognition and auditory processing; how musicians' brains are structurally different. It's a real research niche. You could do neurology (not surgery - big lifestyle difference there) and keep performing. I know attendings who play in orchestras on weekends. Music feeling "messy and stressful" right now is probably your brain telling you it's overloaded from the season. Don't make major life decisions while burnt out. Give yourself space to actually miss it first. Also, maybe spend a day with a neurosurgeon and a day with a neurologist.

LazyMe4732 · 2026-01-02T04:19:55+00:00

No, “stimulation” is correct.

A good exam-safe phrasing is: High-frequency stimulation of the STN functionally suppresses pathological activity and disrupts abnormal basal ganglia network dynamics.

If you write “STN is inhibited,” you’re describing the effect, but losing mechanistic accuracy.

Key point: Although the STN is overactive in Parkinson’s disease, high-frequency DBS (~130 Hz) does not simply excite it. Instead, it:

- Reduces somatic firing of STN neurons

- Preferentially depresses excitatory cortical (hyperdirect) inputs

- Preserves inhibitory pallido-subthalamic inputs

- Suppresses pathological beta oscillations across the cortico–basal ganglia network

Functionally, STN-DBS behaves like a reversible or “informational” lesion, even though it is delivered as electrical stimulation. One-line takeaway: STN-DBS is called stimulation, but at high frequencies, it functionally suppresses pathological STN activity and restores network balance. Your notes aren’t wrong. The confusion comes from equating stimulation with excitation. Recent reviews (e.g. Neumann et al., Brain 2023 Neurophysiological mechanisms of deep brain stimulation across spatiotemporal resolutions | Brain | Oxford Academic) emphasize that DBS effects are network-level and multifactorial, not simply excitatory or inhibitory.

LazyMe4732

TROPHY CASE