Avraham Z. Cooper, MD Profile picture
Oct 3, 2020 19 tweets 9 min read Read on X
1/
What is the mechanism of brain freeze?

Why do some people (myself included) get piercing headaches when eating cold food or drinks while others are totally unaffected?

#medtwitter #tweetorial
2/
Brain freeze, formally known as cold stimulus headache, actually has a diagnostic classification:

Transient frontal, temporal, or occipital headaches caused by passage of cold liquids or food over the palate and posterior oropharynx.

pubmed.ncbi.nlm.nih.gov/29368949/
3/
The first question that I had was how common is susceptibility to brain freeze?

I asked #medtwitter what percentage experience it and 82% said they do.

4/
A cross-sectional, population-based German study found a prevalence of 51% among adults.

💡 Brain freeze is clearly not universal and only happens to some of us.

pubmed.ncbi.nlm.nih.gov/31645112/
5/
So what causes brain freeze?

One clue is a symptom that can accompany it: lacrimation (aka tearing).

Lacrimation occurred in up to 49% of those who experienced brain freeze, in a study where subjects were exposed to ice water/cubes.

pubmed.ncbi.nlm.nih.gov/27206961/
6/
Why is lacrimation significant?

It turns out that the lacrimal glands of the eye are innervated by the lacrimal nerve, a branch of the trigeminal nerve (CN V).

🔑 This effectively localizes brain freeze to stimulation of the trigeminal nerve.

link.springer.com/chapter/10.100…
7/
We now know that the trigeminal nerve is involved, but how does ingesting cold substances cause headache?

Let's walk through the series of events that culminates with brain freeze.
8/
Upon ingesting cold food or drinks, the temperature of the palate and posterior oropharynx decreases.

This stimulates branches of the trigeminal nerve entering the sphenopalatine ganglion (SPG), a parasympathetic ganglion near the zygomatic arch.

ncbi.nlm.nih.gov/pmc/articles/P…
9/
Parasympathetic stimulation causes the lacrimation we already discussed, but also may impact cerebral vasculature.

This study looked at the effects of drinking ice water (compared w/ lukewarm) on cerebrovascular tone and headache symptoms.

pubmed.ncbi.nlm.nih.gov/31316454/
10/
Amazingly, drinking ice water was associated w/ cerebral vasodilation, whether or not the participant experienced brain freeze.

⚡️And those who experienced brain freeze had more vasodilation than those who didn't.

pubmed.ncbi.nlm.nih.gov/31316454/
11/
Those w/ both brain freeze + lacrimation had the most vasodilation.

🔑 This suggests the following mechanistic chain:

Decreased posterior pharyngeal temperature ➡️ trigeminal signaling through SPG ➡️ vasodilation ➡️ brain freeze

pubmed.ncbi.nlm.nih.gov/31316454/
12/
Let’s return to one of the questions from the lead tweet.

Why do some people get brain freeze but not everyone?

While the answer isn’t entirely clear, it may have to do w/ predisposition to headaches in general, particularly migraines.
13/
In an observational study in adolescents, 55% of those with a history of migraines experienced brain freeze, versus only 39% of those without migraines.

pubmed.ncbi.nlm.nih.gov/14984231/
14/
In the same study, those w/ the most migraine aura/symptoms actually had the highest prevalence of brain freeze.

💥 Incredibly, more than half reported that cold-induced headaches occurred in the exact same location as their migraines.

pubmed.ncbi.nlm.nih.gov/14984231/
15/
This apparent link b/w migraines and brain freeze actually makes physiologic sense.

Although migraines likely result from cortical spreading depressions and brain freeze from cerebral vasodilation, both involve trigeminal nerve system activation.

ncbi.nlm.nih.gov/pmc/articles/P…
16/
Let's close w/ some strategies to prevent and "treat" brain freeze.

A cheeky BMJ study showed that slowly eating ice cream reduced brain freeze risk.

💡Eating slowly allows cold substances to warm up in the mouth and reduces trigeminal activation.

ncbi.nlm.nih.gov/pmc/articles/P…
17/
Another preventative strategy:

Keep cold food and drinks in the front of the mouth, prior to swallowing.

💡This decreases SPG and trigeminal nerve stimulation, as they are more sensitive to posterior temperature changes (b/c of anatomic location).

bit.ly/3cJZAc5
18/
Thankfully, brain freeze is transient and typically resolves within seconds to minutes.

Pressing your tongue to the roof of the mouth - which warms the mucosa and decreases stimulation of the trigeminal nerve/SPG - can help it resolve a bit faster.

bit.ly/2SfJQUU
19/
🔑 Brain freeze results from cold-induced trigeminal and sphenopalatine ganglion stimulation
🔑 This induces cerebral vasodilation, which seems to be the source of headache
🔑 Predisposition to headaches (eg migraines) may account for why only some people get brain freeze

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More from @AvrahamCooperMD

Mar 3
1/THREAD

How could eating black licorice cause life-threatening hypokalemia?

Why in the world could specifically eating this food cause serum potassium levels to dangerously drop?

#medtwitter #tweetorial Image
2/
Let's first review what black licorice is actually made from.

Black licorice is a sweetener found in candy, tea, sweet drinks, and even beer.

It's extracted from the root of the legume Glycyrrhiza glabra plant.

licorice.com/blogs/news/wha…
Image
3/
Thousands of years ago, ancient Egyptians drank licorice as a sweet drink, and archaeologists found licorice in King Tut's tomb.

Alexander the Great and Napoleon both chewed on black licorice root during battle for its soothing properties.

klepperandklepper.com/knowledge-base…
Image
Read 16 tweets
Sep 24, 2023
1/
Why can multiple sclerosis symptoms worsen with heat exposure, something known as the Uhthoff phenomenon?

This question is especially relevant in the era of record-breaking heat waves and climate change.

#tweetorial #medtwitter Image
2/
In 1890, Wilhelm Uhthoff noted multiple sclerosis (MS) patients having a “marked deterioration of visual acuity during exercise" or after a hot bath, which ⬆️ body temperature.

1 patient lost vision just by walking vigorously in Uhthoff's clinic.

pubmed.ncbi.nlm.nih.gov/20375511/

Image
Image
3/
The Uhthoff phenomenon is now recognized as exceedingly common in MS.

Up to 80% of patients experience ⬆️ neurological symptoms w/ even small body temp increases. These can include diminished physical (eg gait) and cognitive (eg mental fog) function.

journals.sagepub.com/doi/abs/10.117…
Image
Read 15 tweets
Jun 25, 2023
1/THREAD
Has it ever occurred to you that Graves' disease presents a conundrum?

Graves' involves an autoimmune antibody that ACTIVATES a receptor, which is relatively unique in the landscape of human disease.

Let's unpack this fascinating mechanism.
#medtwitter #tweetorial
2/
Graves’ disease was first described by English physician Caleb Parry in 1786, when he noted an association between thyroid enlargement, tachyarrythmias, and exopthalmos in 8 patients.

Parry’s son posthumously published his description in 1825.

https://t.co/sklIBMwyzDlitfl.com/graves-disease/


3/
In 1835, 10 years after publication of Parry's description, Irish surgeon Robert Graves described a patient w/ thyromegaly + exophthalmos.

Although clearly not the first description, Trousseau proposed the name Graves' disease in 1862 and it stuck.

https://t.co/D3DY4WwF7dlitfl.com/graves-disease/


Read 18 tweets
Apr 23, 2023
1/THREAD
Ever wonder why amphotericin B can cause severe infusion reactions, including chills/rigors + hypotension?

These infusion reactions are so awful that it carries the nickname "amphoterrible".

Why does this happen? The answer is mind-blowing.

#medtwitter #tweetorial Image
2/
First let's review amphotericin B's history.

In 1953, analysis of a fermentation broth from Venezuelan soil found 2 antifungal compounds: amphotericin A and B.

B had a broader antifungal activity spectrum and so underwent further drug development.

pubmed.ncbi.nlm.nih.gov/33261213/ Image
3/
Amphotericin B (AmB) contains a hydrophobic polyene "tail" and a hydrophilic amine "head".

This amphipathic profile allows AmB to bind ergosterol in fungal membranes, which is thought to cause ion-leaking pores to form, killing the fungus.

pubmed.ncbi.nlm.nih.gov/33261213/ Image
Read 19 tweets
Mar 5, 2023
1/THREAD
Ever wonder why fluoroquinolones increase the risk of tendon rupture?

It seems so random that a whole class of antibiotics could cause tendon injuries, but the risk is real.

#medtwitter #tweetorial
2/
Fluoroquinolones inhibit bacterial function by blocking topoisomerase activity.

They first emerged as an antibiotic class in the 1960s, as byproducts of antimalarial quinine development.

Nalidixic acid = the first quinolone discovered.

pubmed.ncbi.nlm.nih.gov/14056431/
3/
The first report of fluoroquinolone-associated tendinopathy occurred in 1983.

2 renal transplant patients received norfloxacin and subsequently developed achilles tenosynovisitis.

Their symptoms spontaneously resolved w/ cessation of the norfloxacin.

pubmed.ncbi.nlm.nih.gov/6223241/
Read 16 tweets
Jan 22, 2023
A short 🧵 on my 3️⃣-prong approach to rounding with resident teams in the MICU…

I emphasize 3️⃣ themes to the residents and fellows:

1️⃣ Clinical care
2️⃣ Education
3️⃣ Development

#MedTwitter #MedEd
1️⃣ Clinical care

I ask teams to focus on efficiency, ⬆️ time for teaching/ discussion

⏳⬇️ transitions b/w patients by alerting next RN
⏳Enter orders on rounds, w/ clearly defined roles as to who will do that
⏳Present from memory (if possible), focusing on critical issues
2️⃣ Education

🧠I ❤️ to teach but avoid overwhelming residents by teaching high yield points on 2-3 patients max. I supplement w/ PM chalk talks after lunch and notes are done

🧠 I also ask each learner to share one learning point from rounds, and do so myself as well
Read 5 tweets

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