medicowesome

Evaluating axis from ECG (Mnemonic)

Hi everyone! We are going to learn how to determine the axis from an electrocardiogram =D

First of all, do you know which two leads should be looked at to determine whether axis is in the normal quadrant or if it is Left Axis Deviation (LAD) or Right Axis Deviation (RAD)?

Look at lead I and lead II. Sounds simple! ^__^

An upright (positive) QRS in leads I and II is normal (–30 degrees to +105 degrees).
In left-axis deviation, there is an upright QRS in lead I and a downward (negative) QRS in lead II ( +105 degrees).

How do I remember this? @_@

Thumbs up method: Lead I = Left thumb, Lead II = Right thumb.

Wait, why lead I is left thumb and lead II is the right thumb?
Because left is a smaller word and it gets the smaller number, that is, one!
Right has more alphabets and it gets the bigger number, that is, two.

Left thumb up (I) + Right thumb up (II) = Normal.
Left thumb up (I) + Right thumb down (II) = LAD.
Left thumb down (I) + Right thumb up (II) = RAD.

Mnemonic method:
Left leaves, right returns.

That’s all!
Have a splendid week everyone

HLA associations mnemonic

Hi everyone!
Here’s a complete guide on how to remember the HLA associations. Let’s catch em all!

Doctors (DR) will turn into MD’s someday.. The thought makes you go, “Aah”
Starting with 2 and ending with 5, your mnemonic for DR associations is "MD.. AAH!"
HLA DR2 - Multiple sclerosis
HLA DR3  - Diabetes mellitus type 1
HLA DR4  - Arthritis (Rheumatoid, also the one associated with Lyme’s disease)
HLA DR5  - Anemia (Pernicious, causing B12 deficiency)
HLA DR5  - Hashimoto’s thyroiditis

If it’s not too much, you can remember “Hey! This Doctor is going to be good MS someday” to remember Hay fever, Goodpasture’s syndrome and Multiple Sclerosis for HLA DR 2.

Hi5 is another way you can remember about Hashimoto’s relation to DR5.
HiPA5 will help you remember Pernicious Anemia with it too (If the A’s of Arthritis and Anemia confuse you!)

I use rhymes for all the other associations, make sure you sing em with a funny tone!

"Two, three S-L-EE.
Three, four, not so sour.”

HLA DR2 and HLA DR3 is associated with SLE
HLA DR3 and HLA DR4 is associated with Diabetes mellitus type 1
(not sour - sweet - sugar - diabetes lol)

You can also remember with the pokemon, "Two, three, butterfree" for the butterfly rash in SLE.. Whatever suits you.

A threeFrEaking three.
HLA A3 is associated with Hemochromatosis.
(fe3+ - iron - hemochromatosis)

Be there at eight, don’t be late.
HLA B8 is associated with Grave’s disease.
(late - dead - grave)

Seven, heavenly pee.
 HLA DR7 is associated with steroid-responsive nephrotic syndrome.
(pee - kidney - nephrotic syndrome)
Seven rhymes with heaven, lee rhymes with pee, I don’t know what I was even thinking when I made this!

For HLA B27, the PAIR mnemonic is famous.
Psoriasis, Ankylosing spondylitis, Inflammatory bowel disease, Reiter’s syndrome.

The above mnemonics will suffice for the exam.

The below facts are not very high yield, but for the sake of completion here you go -
SCAM 3 - Sjogrens syndrome, Chronic active hepatitis, diabetes mellitus type 1 for HLA DR3.

If you extend the line in 4, it looks like an A.
A for Arthritis. Flip the A and it looks like V.
V for vulgaris, pemphigus vulgaris.
So HLA DR 4 is associated with Arthritis as well as Pemphigus vulgaris,

That’s all!
Hope it helps you all < 3

Credits here.

This post is awesome!

How to differentiate between Lateral Pontine Syndrome vs Lateral Medullary Syndrome.

What is lateral medullary syndrome?

Neurological symptoms due to injury to lateral part of the medulla. Also called Wallenberg’s syndrome.

 When does it happen?

When the posterior inferior cerebellar artery (PICA) is occluded.

What is lateral pontine syndrome?

Neurological symptoms due to injury to lateral part of the pons.

When does it happen?

When the anterior inferior cerebellar (AICA)  artery is occluded.

What do both the lesions have in common?

  •  Ipsilateral horner’s syndrome.

Why? Descending hypothalamic tracts affected.

  • Contralateral loss of pain and temperature.

Why? Lateral spinothalamic tract affected.

  • Ipsilateral cerebellar ataxia.

Why? Cerebellar peduncles affected. (Inferior cerebellar peduncle in medullary and middle cerebellar peduncle in pons.

  • Nausea, nystagmus, vertigo, vomiting.

Why? Vestibular nuclei involved.

  • Ipsilateral loss of pain and temperature sensation from the face (facial hemianesthesia).

Why? Spinal trigeminal nucleus and tract involved.

  • Ipsilateral hearing loss.

Why? Cochlear nuclei and intraxial nerve fibers involved.

So how do I tell the difference between the two?

 Lateral medullary syndrome:

 Dysphagia, dysarthria, dysphonia

Why? Nucleus ambiguous involved.

Lateral pontine syndrome:

  •  Ipsilateral paralysis of the upper and lower face (lower motor neuron lesion).
  • Ipsilateral loss of lacrimation and reduced salivation.
  • Ipsilateral loss of taste from the anterior two-thirds of the tongue.
  • Hyperacusis.

Why? Facial nucleus and facial nerve involved.

 All the credits go to the brilliant medicowesome !!

For more posts like these follow medicowesome on tumblr or http://medicowesome.blogspot.in/p/blog-page_1239.html

Awesome blog: MEDICOWESOME

Hey guys! there’s this blog that i’ve recently started following and reblogging a lot! 

If you haven’t started follow her/him, start now!!! She/he explains everything perfectly and in a very easy to learn way :) 

This is the blog: medicowesome

Enjoy ;)

R.

youtube

How to draw the tympanic membrane

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Aortic arch derivatives mnemonic images  -HD images here

I made these diagrams guessing these will be helpful ^__^

The greater part of the first and second artery disappear. In adult life first arch artery is represented by the maxillary artery and the second arch persists for some part of fetal life as the stapedial artery.
The mnemonic people use for that is, “First is max" & "Second is Stapedial" =)

Mnemonic for third arch artery:
C for Carotid, C the third letter of the alphabet.”

The third arch artery gives off a bud that grows cranially to form the external carotid artery.

The internal carotid artery is derived from the distal part of the third arch artery and cranial most part of the dorsal aorta.

The brachiocephalic trunk is formed by the right horn of the aortic sac.

Mnemonic for fourth arch artery:
"fOUR rhymes with AOR for Aorta.
fouRS for Right Subclavian.”

The ascending aorta is formed from the truncus arteriosus.

The arch of aorta is derived from the vental part of the aortic sac, it’s left horn and the left fourth arch artery.

Mnemonic for sixth arch artery:
Well, this is lame but the letter 6 looks like lungs to me =D

Pulmonary trunk is derived from truncus arteriosus.

Mnemonic for subclavian artery:
"7 is S."
Seventh InterSegmental Subclavian!

The right subclavian artery is derived from the right fourth arch artery and right seventh cervical intersegmental artery.

On the left side, the subclavian is derived entirely from the seventh cervical intersegmental artery.

That’s all!

Hope you had fun learning ^__^

-IkaN

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How to remember lipoprotein disorders

Hello everyone!

Click here to read about Lipoproteins and apoproteins if you need a quick revision before we get started :)

In this blog post, I’ll be talking about lipoprotein disorders, how to remember them and some facts that you need to know about the disorders. Type I hyperlipoproteinemia
Chylomicrons increased in childhood.
VLDL increased later in life.

Lab findings: Increase in serum triglycerides.

Why?
CPL (Capillary lipprotein lipase) hydrolyzes triglycerides in lipoproteins.
It requires apo-CII as a co-factor.

Clinical findings: Acute pancreatitis (Pancreatic vessels filled with chylomicrons rupture), eruptive xanthomas. Type II hyperlipoproteinemia
Serum LDL is increased.

Lab findings:
In IIa, only cholesterol is increased.

Why?
Liver cholesterol synthesis is deprived of negative feedback.

In IIb, cholesterol and triglycerides are increased.

Why?
Liver overproduces VLDL in IIb

Acquired causes: Primary hypothyroidism, nephrotic syndrome, extrahepatic cholestasis.

Clinical findings: Tendon xanthomas, Xanthelasma, premature coronary artery disease and stroke. Type III hyperlipoproteinemia
This dysbetalipoproteinemia is also known as “remnant disease”.

Lab findings: Elevation in cholesterol and triglyceride levels.

Why?
Apo E is required to remove chylomicron remnants and IDL (remnant of VLDL).

Clinical findings: Palmar xanthomas, increased risk for coronary artery and peripheral vascular disease. Type IV hyperlipoproteinemia
Increase in VLDL.

Lab findings: TG accumulates
in preference to cholesterol, like IIb.

Acquired causes: Excess alcohol, OCPs, Diabetes mellitus, chronic renal failure, thiazides, beta blockers.

Clinical findings: Eruptive xanthomas, increased risk for coronary artery and peripheral vascular disease.
Type V hyperlipoproteinemia Increase in chVlomicrons and VLDL. It is a mixture of types I and IV familial dyslipidemias. Lab findings: TG levels are high, whereas cholesterol concentration increases only moderately. Clinical findings: Like type I, but unlike type IV, there is no major risk of atherosclerosis, so that pancreatitis and eruptive xanthomas remain the main complications. For the sake of completion, I’d like to add another disease -
Tangier disease is due to lack of ABC1 cholesterol transporter gene.
Cholesterol accumulates inside cells. Blood HDL and cholesterol are low.
The disease is characterized by atherosclerosis, hepatosplenomegaly, polyneuropathy and orange tonsils.

*phew* That’s all!

Like I always say, if you stare at a word long enough, you find the mnemonic in the word itself :P
I made these myself, hope you find them helpful ^__^

Happy Indian Independence Day :)

-IkaN

Hey! Everybody has their moments of low self esteem. We have different reasons for why we doubt our abilities.

I’ll tell you about mine, for example. After I cleared my exam and got into med school, I thought, "What if I really got through the entrance based on pure luck? What if I just marked the right answers, got a good score and I don’t really deserve to be here?" After being transferred to an academically better med school, "These kids are really smart. I just got here because of the transfer. I don’t belong here."


Honestly, no one knows for sure whether they deserve it, whether anyone deserves anything. So that’s not even a valid question to ask ourselves, but we are so programmed to be negative that we still do. We drown ourselves with doubt and fear. We need to tell that negative inner voice to shut up!

You are not average. You have infinite potential within you. Your premed score doesn’t determine who you can or can not be. At this present moment of time, I think it doesn’t matter who you are or where you came from or how you got here - Here you are. So let’s do this!

Your dreams will drive you to work when you have low self, hold on to it. Write it down, why you really wanted to be here. Write about how your passion will separate you from others. Anything positive about you, write it down and read it thrice a day. It’ll really help you get out of the negativity you’ve created for yourself.

Once you get rid of your low self esteem and self doubt, you’ll start to work towards your dream. And it’s an uphill from there. The work reinforces you to learn more. You discipline yourself to achieve what you desire. Your work starts to speak for you. It glows out of your personality from within. Who you were separates out from what you do.

Also, in the movie Kung Fu Panda, Po thinks he fell out of the sky and didn’t deserve to be the Dragon warrior. But look what happens once he starts to believe in himself! So don’t doubt yourself. Believe and just start working. And watch the movie if you haven’t :)

Oh and here’s something by Les Brown that you should read:

"Be careful of your self-talk. Without monitoring your mind and your mouth, the majority of what you say to yourself can poison your attitude, weaken your spirit, drain your energy. Be aware that, left unchecked, the negative storyteller in your brain can shut down your faith, amplify your fears and activate a spirit of hopelessness and self-sabotage. Turn off and banish the automatic negative thoughts that will ruin your life if you let them.


Learn to keep your heart open and love yourself unconditionally. The universe is on your side waiting for your next move. Celebrate what’s working in your life. Focus on the positive and on what you can do right now. Give thanks for what you have and that you’re still here. That alone says that your life still matters. You have something special. You have GREATNESS within you!”

Competitive and non competitive inhibitors simplified

Let me present to you the most understandable, simplified, awesome analogy for explaining competitive and non competitive inhibitors =D

When you are hungry, you have affinity for food.
Hunger has affinity for food like enzymes have affinity for substrates.

Rice is the substrate for your hunger.
You happily eat it at some random rate.

But *plot twist* if you’re given a hamburger at the same time..
OBVIOUSLY, your affinity for the burger is more so you eat the burger instead.
The burger acts as a competitive inhibitor.
Lesson learnt: Competitive inhibitors reduces enzyme-substrate affinity.

Say you’re still hungry and your burger is surrounded by rice.. *Another twisted plot*
The only way to reach the burger is to eat the rice..
So you eat the rice (since you are hungry anyway, duh!)
Lesson learnt: Competitive inhibitor concentration can be overcome by increasing the substrate concentration.

What ultimately made you eat the rice?
The increased concentration of the substrate!
Km, the substrate concentration to produce half of Vmax, had increased.
Lesson learnt: Km increases in presence of a competitive inhibitor.

Say, you were hungry.. Until you saw something gross and it ruined your appetite.
The “gross thing” is a non competitive inhibitor.

Even if there is food on the table, you won’t wanna eat it or uhh, say if you were gonna eat it really fast, now you roll your eyes and yeah, eat slowly.
Vmax, the maximum rate of a chemical reaction, decreases.
Lesson learnt: Vmax decreases in presence of a non competitive inhibitor.

And since you have a decreased appetite, no matter how much rice is given to ya, you’ll eat it at the same slow rate.
Lesson learnt: Increasing substrate concentration will not affect the action of a non-competitive inhibitor.

When it comes to drugs, there are terms such as efficacy, potency and complex things such as graphs you need to remember - Here are some mnemonics that may help you out.

That’s all! <3

-IkaN

2

Hey everyone!

We recently got 500 followers on tumblr & I couldn’t think of a more fun way to celebrate it!! =D

I missed the 500th follower though ^__^”

I’d love to thank all of my followers for reblogging & liking my posts :)

Especially, My Notes for USMLEDr. Cranquis’ Mumbled Gripes

Thank you so much everyone for your love and support <3

As for the emoticon game, I won’t be posting the answers online but you can email me on medicowesome@gmail.com for the answers and I’ll get back to you as soon as I can!

That’s all!

-IkaN

Southern, Northern, and Western blot mnemonic

Hello everyone!

The mnemonic to remember blotting techniques is “SNoW DRoP

S -    Southern - DNA     - D
N -   Northern - RNA     - R
O -   Oooooo - Ooooo    - O
W -  Western - Protein   - P

That’s all!

Hope you won’t go, “Which direction was that again?” in the exam =P

-IkaN

Medicowesome study group on Whatsapp

Some of my friends discuss questions and concepts on Whatsapp. So for a long time, I’ve been wanting to do this. Make a huge all time accessible study group where we can learn!

This is the first trial attempt, of course. It may not work. It might work brilliantly.

If it doesn’t work out, we dissolve the group and pretend it never happened T_T

If it does, we’ll be learning something new on a daily basis *_*

So who’s in?

All you’ve got to do is message me your number. You can email me at medicowesome@gmail.com with “Whatsapp study group” in the subject.

DO NOT ignorantly leave your contact details publicly in the comments for everyone to see! *whispers* Keep it secret, keep it safe.

I’ll message you in a week max.

I have a lot in mind but it varies with the response. Let’s try this out first and see how it goes!

PS: I’ll also try posting what we discuss on the group out here as well for those who don’t have access / are uncomfortable with Whatsapp.

*hoping for the best*
-IkaN

Preparing for the USMLE Step 1 exam

"How do I prepare for the USMLE Step 1 exam?" -The most requested post ever!

The essentials - Kaplan videos & notes (for basics) + Goljan book & audio + uWorld + First Aid is the general way to go for most IMG students.

Kaplan videos and notes: They are a good start. If you are time restricted, you may want to skip stuff, fast forward through it.

Pathology: Do Goljan and Pathoma. Know them cold. I had studied Goljan really well. I wish I had the time to complete Pathoma as well. The videos and concepts are awesome.

uWorld: Do it really well the first time. You are gonna get bored doing it the second time so get the concepts in the first go. Take your time if you have to.

While doing it the first time, the 2 blocks per day and 20 days scheme didn’t work for me. I got frustrated with the time constraints I had put on myself. The best I could do was 1 block per day. So give yourself 45 days, just in case you are slow with uWorld like me.

I did it in random just because I assumed studying subject-wise would get too monotonous. Subject-wise goes faster. I did it timed. You may do it untimed, tutorial, subject-wise. It doesn’t matter. Do what you are comfortable with.

First Aid: It’s your quick review book. Write uWorld notes all over it. Make it messy, draw diagrams on it. It’s the only book that’s gonna stick with you till the end of time.

NBMEs: Give as many as you can. But do them only for feedback, not for learning.

Other stuff you can do -

BRS behavioural science: I highly recommend it. You can easily do important chapters like stuff on defense mechanisms even 20 days before the exam. There are good quality, minimal in number, doable questions at the end of every chapter.

Be flexible: If you find yourself weak in any random subject, quickly Google for good sources and review the doable ones. People advice not to look into new resources a few days prior to the exam but that’s bull. Your old sources are obviously did not help you and that’s the reason you are weak in the subject… Look for new ones! I did BRS behavioural science 20 days before my step and it is one of the best decisions that I made. I tried ANKI flashcards for brain stem sections a week before. As long as you keep a balance, new resources won’t hurt you.

Flashcards: Download or make your own flashcards. It helps you revise frequently.

Other Qbanks: Yes, I had done bits of Kaplan Qbank and USMLE Rx. I had time when I started them, they helped me get what the questions are like and I did make a few notes. They did freak me out (since I got most of the questions wrong) and hence, helped me study more early in my preps. But they are not essential if you are out of time.

Doctors In Training: It’s very boring. But the worksheets do help you memorize and revise. I don’t recommend it, but I did review some of it once upon a time.

Random advice -

Be attentive during rounds: Because the USMLE will have questions on clinical stuff. If you have done your core rotations, it’s not an issue. But if you are in your basic sciences years, the only way you can get these right is by being attentive in rounds. There are very simple common clinical questions like urge incontinence on Step 1 which are not covered in First Aid. You can easily get them right. Read x-rays, especially the fracture ones.

Don’t forget to revise Kaplan and Goljan: Read a little bit of Kaplan and lots of Goljan even in your busy 2 block per day + First Aid schedule. The bain of knowledge is to forget.

Revise as much as you can before the exam: I remember antidepressants and antipsychotics being a bit foggy in my head during the step. I should have revised properly and in a more organized way before the exam.

Solving questions: The questions are scary. I made a lot of silly mistakes during the preps. I agree that the margin for error is small. You miss one word and the question goes wrong. The exam seems hard before you take it and easy after you’re done with it. Keep going. All you can do is give your best :)

Don’t delay dates too much: I delayed my exam for a month. I gave an NBME on the previous exam date. The NBME score and the test score came out to be the same. Life! xD

Social isolation: It’s normal. Friends will demand to see you, even after you’ve explained how important and hard this exam is. You will feel bad for not meeting them and have mood swings, it is okay. Don’t let it consume you. Focus. You may completely ignore the existence of any other species on the planet, it’s allowed. The good ones will stick with you anyway.

That’s all! 

Feel free to ask any questions.

-IkaN

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I feel reviewing from Blogger is easier in such long posts.. Click here to view the post on the website.

Darrow-Yannet Diagrams simplified

What are Darrow Yannet diagrams?

They are graphs that tell you the osmolarity and volume changes of body fluids.

X axis represents volume.
Y axis represents solute concentration.

Total body water = 2/3 ICF (Intracellular fluid) + 1/3 ECF  (Extracellular fluid)

Remember:
All volume disturbances originate in the ECF compartment.
Changs in ICF are in response to changes in ECF.

How to make the graph in your head -
Step 1. Figure out what happens to the osmolarity and volume in theECF compartment (ECF is the smaller compartment)
Step 2. Think how is ICF affected?

Let’s review some examples to make sure we understand the concept! Loss of whole blood, adult diarrhea.

What will happen to volume in ECF compartment?
Will decrease.

What will happen to osmolarity in ECF compartment?
Will not change. (Why? Isotonic fluid is lost.)

What will happen to ICF volume and osmolarity?
No osmotic gradient, therefore, will not change :)

That was easy!
Let’s look at a similar example. Infusion of excessive isotonic saline.

What will happen to volume in ECF compartment?
Will increase.

What will happen to osmolarity in ECF compartment?
Will not change. (Why? Isotonic fluid is lost.)

What will happen to ICF volume and osmolarity?
No osmotic gradient, therefore, will not change.

See? It’s very simple! Loop diuretics, Addison’s disease.

(Loops make you lose sodium and water, but more of sodium than water.
Addison’s disease is adrenal insufficiency. Aldosterone makes you retain sodium so in the absence of aldosterone, you will lose sodium.)

What will happen to osmolarity in ECF compartment?
Will decrease. (Why? You are losing sodium.)

What will happen to volume in ECF compartment?
Will decrease. (Why? Fluid moves from ECF to ICF)

What will happen to ICF volume?
Will increase. (Decrease in osmolarity shifts the fluid into ICF) SIADH, compulsive water drinker.

(SIADH: You are conserving too much water due to ADH.
Water drinker: You are having too much water =P )

What will happen to osmolarity in ECF compartment?
Will decrease. (Why? You are diluting by adding water.)

What will happen to volume in ECF compartment?
Will  increase. (Why? You are adding fluid.)

What will happen to ICF volume?
Will increase. (Decrease in osmolarity shifts the fluid into ICF) Right heart failure, Cirrhosis, Nephrotic syndrome.

What will happen to osmolarity in ECF compartment?
Will decrease.

What will happen to volume in ECF compartment?
Will  increase.

What will happen to ICF volume?
Will increase.

Can’t figure why? Well.. Here’s why!

In all three conditions, there is a decreased effective circulatory volume (Effective arterial blood volume)
[See diagram]

This leads to decreased renal blood flow and pressure and increased ADH secretion and activates the renin angiotensin aldosterone system, increasing sodium and water reabsorption.

Note: Total body sodium is increased, however, serum sodium is decreased.
Why?
The alteration in Starling forces redirects the sodium containing fluid in the interstitial space (leading to edema)

*phew* That was work! Let’s see what happens during sweating ;) Sweating.
What will happen to volume in ECF compartment?
Will decrease.

What will happen to osmolarity in ECF compartment?
Will increase. (Why? Hypotonic fluid is lost.)

What will happen to ICF volume?
Will decrease.

Your sweat doesn’t taste salty.. That’s how I remember it’s hypotonic, not hypertonic like tears T_T Insensible water loss in fever, diabetes insipidus, alcohol.

What will happen to volume in ECF compartment?
Will decrease. (Water is lost. Why? ADH action is lost in Diabetes insipidus, alcohol inhibits pitutary secretion of ADH, water evaporates from the warm skin surface in fever)

What will happen to osmolarity in ECF compartment?
Will increase.

What will happen to ICF volume?
Will decrease.

Note: The ECF contraction is mild because there has been no loss of sodium.

Next one is easy too.. Keep going! <3
Infusion of sodium bicarbonate, sodium containing antibiotics.

What will happen to osmolarity in ECF compartment?
Will increase.

What will happen to volume in ECF compartment?
Will increase. (Why? Fluid moves from the ICF to ECF)

What will happen to ICF volume?
Will decrease.

..And the last one!!! :D Hyperosmolar nonketotic coma, diabetic ketoacidosis.


What will happen to osmolarity in ECF compartment?
Will increase. (Why? Glucose is an osmotically active particle)

What will happen to ICF volume?
Will decrease. (Why? Fluid moves from the ICF to ECF)

This gets a little tricky.. ^__^” What will happen to volume in ECF compartment?
Will decrease.
Why?
Glucose in urine acts as an osmotic diuretic and the water from ECF is lost.


That’s all!

This blog post took me forever to write.. I feel the color coding makes it easier to see the changes in the diagrams :)
Hope you had fun learning and revising with me and see you in the next post <3

-IkaN

I was super super excited to share this mnemonic with you ^__^

What is lateral medullary syndrome?
Neurological symptoms due to injury to lateral part of the medulla
(also called Wallenberg syndrome)

When does it happen?
When the posterior inferior cerebellar artery is occluded

What is lateral pontine syndrome?
Neurological symptoms due to injury to lateral part of the pons

When does it happen?
When the anterior inferior cerebellar artery is occluded


What do both the lesions have in common?
 

Ipsilateral horner’s syndrome
Why? Descending hypothalamic tracts affected

Contralateral loss of pain and temperature
Why? Lateral spinothalamic tract affected

Ipsilateral cerebellar ataxia
Why? Cerebellar peduncles affected
(Inferior - medulla, middle - pons)

Nausea, nystagmus, vertigo, vomiting
Why? Vestibular nuclei involvement

Ipsilateral loss of pain and temperature sensation from the face (facial hemianesthesia)
Why? Spinal trigeminal nucleus and tract involved

Ipsilateral hearing loss
Why? Cochlear nuclei and intraxial nerve fibers involved


So how do I tell the difference between the two? @__@


Lateral medullary syndrome:
Dysphagia, dysarthria, dysphonia
Why? Nucleus ambiguus involved

Lateral pontine syndrome:
Ipsilateral paralysis of the upper and lower face (lower motor neuron lesion)
Ipsilateral loss of lacrimation and reduced salivation
Ipsilateral loss of taste from the anterior two-thirds of the tongue

Hyperacusis
 Why? Facial nucleus & facial nerve involved


Cool fact:

There is a loss of pain and temperature sensation on the contralateral (opposite) side of the body and ipsilateral (same) side of the face This finding is diagnostic

That’s all!

I created the mnemonic all by myself =D
Hope that was fun and helpful :)

-IkaN