Hemiplegia History-taking : Case-related Clinical Pearls

Hi everyone !
Just a short summary of what not to miss in your case taking of a Hemiplegia case - on the Boards or the Wards ! Here goes.

In the History of Present Illness
- Ask Onset - Time of onset very imp. And sudden or gradual. (To decide Ischemic or Hemorrhagic)

- Progress - If maximal at onset -- likely embolic. If progressive gradually -- Thrombotic stroke. If rapidly progressive -- Hemorrhagic stroke. 

- Hemiplegia / Paresis - what position was pt in ;
Upper Limb (UL) more than Lower Limb (LL) or equal. 
(ASK FOR PROXIMAL AND DISTAL MUSCLE INVOLVEMENT IN EACH LIMB)
( Proximal UL = Raise hands above head to take an object/Comb hair ;
Distal UL = Button Tee shirt or Eat food.
Proximal LL = Get up from Squatting position
Distal LL = Walking).

- Ask for facial deviation ; Drooling of food after feeding ? -- Facial palsy 
- Hemianaesthesia - ask for sensory loss or paraesthesias. 

- The Episode -->

• Seizures ? Urinary / faecal incontinence?  - suggests increased severity / Cortical involvement

•Speech disturbances ?
- Likely cortical lesion if Aphasia ; or dysarthria due to UMN lesions

•Symptoms of cranial nerves --> Vision changes, Diplopia , Facial sensations , repeated aspiration of food , tongue problems. ( Localise the lesion to Brainstem)

• Gets better for a while and then Symptoms re appear - Lucid interval of extradural Hemorrhage

• Preceded by headache, vomiting , photophobia ?
( Meningitis/ SAH or PCA stroke) (Thunderclap headache in SAH) 

• Any h/o Alcoholism / Trauma - Could be Subdural Hemorrhage

Always rule out a simple Syncopal episode and a plain Seizure.

In the Past History :
- H/O similar episodes - how were they treated and what were the residual deficits.
- H/O similar episodes that spontaneously resolved - TIA's
- H/O Other occlusive events - Myocardial Infarction, Peripheral Vascular Disease , Pulmonary embolism
- Ask h/o heart disease - Skipped beats for Atrial Fibrillation and other Valvular problems.
_________________________________________

What is expected out of the history-taking for Stroke :

1. What is the topographic distribution of weakness -
Hemiplegia / Monoplegia / Quadriplegia / Diplegia

2. Is the likely Etiology a vascular event in the Cerebral Circulation?
(From : typical elderly to middle aged presentation in a Hypertensive , Diabetic patient with sudden onset Focal Neurological deficit).

3. If fairly certain that this is Vascular : is it Thrombotic , Embolic or Hemorrhagic ?

4. What is the possible site of lesion in terms of :
A. Structure(s) involved
B. Vessel involved

Quick Rules of Thumb for diagnosis of CVA on history

<> Thrombotic Strokes have an insiduous onset , are progressive in their deficit but gradually , and may occur during earlier hours of the day.

<> Embolic Strokes have a sudden onset and are non progressive - Maximal deficit at onset ; May have History of Atrial Fibrillation or Valvular Heart disease and may have H/O recurrent emboli.

<> Hemorrhagic strokes are sudden in onset , very rapidly progressive and may be Preceded by Thunderclap headache in Subarachnoid Hemorrhage. Almost invariably the patient is hypertensive.

<> RISS = Rapidly Improving Stroke Symptoms are a feature of TIA (Transient Ischemic Attack) - generally resolving within about an hour , but the technical definition is the Deficit relieving in 24 hours or lesser.

<> Diabetic patients on Insulin must be watched out for Hypoglycemia which is highly common.

<> If no focal deficits and just a 'Confused' state of the patient or Diffuse CNS features must prompt a search for Electrolyte imbalance especially in the elderly for a Metabolic Encephalopathy.

<> Hypertensive Encephalopathy must be suspected if the patient is an Uncontrolled Hypertensive and has headaches and evidence of End organ damage.

<> Todd's palsy must be suspected in a young man who has recurrent attacks of 'Apparent Paresis' that occurs after some form of a seizure - it's a post ictal confused state.

<> Acephalgic Migraine is a rare form of Migraine where the headache is absent. So the patient would experience an Aura , go through non ache features of migraine and then followed by post migraine weakness.
The weakness can be perceived as a stroke.

Hope this was helpful !
Will be doing another one on stuff not to miss on examination and the questions asked generally!
Happy studying !
Stay Awesome !

~ A.P.Burkholderia

Neurology Nuggets : Trigeminal neuralgia in Multiple Sclerosis.

Hello everybody!

A short nugget to start your Day with.

Let's see the reason behind the occurrence of Trigeminal Neuralgia in Multiple Sclerosis.

Multiple Sclerosis is basically a disorder of oligodendrocytes - derived Myelin which leads to blocks of varied degrees in Nerve impulse conduction.

The Trigeminal nerve is myelinated by Schwann cells, like rest of the Peripheral nervous System.
But still we see a high frequency of Trigeminal Neuralgia in Multiple Sclerosis.

The reason for this is-

*The trigeminal nerve is ensheathed by oligodendrocytes - derived myelin, rather than Schwan cells - derived myelin for upto 7mm after it leaves the Brainstem.*

This explains the high frequency of Trigeminal Neuralgia in Multiple Sclerosis which is a disorder of oligodendrocyte myelin.

Let's Learn Together!
-Medha Vyas.

My NEET experience

I could start off by mentioning how daunting it is to study for this particular exam, but I don’t think I need to. Nearly everyone, from their own experience or that of others has known and feared the NEET preparation. 19 subjects, 10 months, and in my case, the year of internship. Weekdays were spent running around the wards, weekends, trying to stay awake in 10-12 hour long classes. This was essentially 2017 for me.

It took me a while to get used to the amount of work and studying, both of which were never ending. The first week was like being thrown headfirst into a deep pool without knowing how to swim! Several coin sized haematomas later, I finally learnt the basics of what an intern was supposed to do.

Then came the first class of the year. If having 500 students in the batch wasn’t intimidating enough, the teacher more than made up for it. And so began my journey of fear, hurtling towards the NEET with no idea how to brake. Things became clearer in retrospect, as they should, for that is what retrospection is for. I wonder if I have had a calmer, even happier year if not for the constant weekly badgering. That being said, I knew I would have never stood a chance if not for the highly concise and valuable course material given to us by our classes.

In the weeks that followed, I managed to juggle both my duties with difficulty, not quite succeeding at doing justice to either. Nevertheless, I was happy, probably because the gravity of the situation hadn’t quite caught up with me.

‘There’s always a next year’, I thought to myself every time the dark thoughts about the exam loomed nearby.

Now, this blissful ignorance was beneficial in some ways, because it allowed me to adapt to and deal with the various perks of my job. The daunting working hours of the heavier departments, being constantly exposed to blood and bodily fluids and being in a frightful sense of awareness about the the hazards they carried, being addressed as ‘sister’ while my male colleagues had the privilege of being ‘doctor saab’ and the eventual satisfaction that came with staring a patient down till they squirmed and called me ‘doctor’, to name a few.

Reality caught up with me sometime around July, and brought with it a portion of self esteem issues and demotivation, much to my dismay. Try as I might, I just couldn’t rid myself of the notion that I would falter and fail. The previous mantra of ‘there’s always a next year’ didn’t seem comforting anymore, not when I saw my batchmates grinding it out everyday in the library. I tried to buck up my pace but kept zoning out, distracted by the very thing I was supposed to focus on. This mental inertia lasted for almost 2 months, relapsing and remitting, for lack of better words.

It spilled over to aspects of my life other than studying. I began to lose interest in work. It didn’t help that I was posted in Surgery, which is one of the more trying postings with shifts running upto 30 hours on emergency days. Imagine being an intern in surgery and not wanting to learn suturing. That is how demotivated I had become and that is how worthless I felt.

In the midst of this, there was a marathon 3 day session from our classes. Maybe it was the 42 hours worth of lectures that finally pushed me off the edge, but I ended up having one of the worst breakdowns of my life on the last day of the marathon session.

Thankfully, crying it out is something that has always made me feel better and this time was no exception. “Where there’s tears, there’s hope.” the Twelfth Doctor had said, and I truly realised the significance of that simple but powerful statement that day.

After that, I made a vow to pull up my socks and put in every effort towards my goal. Regret is a terrible thing, and nothing hurts more than knowing one could have done better. I made a list of the subjects I was not good at, and allotted more hours to them. I signed up for a series of mock tests which helped me keep track of my progress. I split the remainder of my time into revision sessions of 15-20 days, as per the advice of my extremely helpful seniors. When I was actively doing all the things, it was easier to put the crippling self doubt to the back of my mind, and assure myself that I was doing everything I possibly could.

Did I falter every now and then? Of course I did. My mock test scores had reached a plateau I couldn’t seem to overcome. There were times when I couldn’t remember the simplest of things that would lead to gross errors, at times simply because I did not read the question properly. This was more distressing than it should have been, mainly because I was functioning on such low levels of self esteem, and tended to be very harsh with myself for making errors.

With time, I realised this attitude was getting me nowhere. However, changing something that is so deeply ingrained in yourself is easier said than done. Nevertheless, I tried my best to build up my confidence by working on my weaker subjects, cutting myself some slack, and when things got difficult, confiding in my parents and friends and basking in their endless love and support. I also pampered myself with my favourite Murakami novels and endless mugs of tea. It didn’t make the stress go away, but it certainly made it more bearable.

Before I knew it, my time was up and it was time for the exam. I went in, promising myself that no matter what happened, I would not be drawn into the pit of self loathing I had escaped from. Surprisingly, I didn’t need to be. The weeks after the exam passed in a blur and then the results arrived, when I was on a train to Gwalior. My mother’s excited phone call rang through the sleeping compartment at 5am and I could barely stop smiling when I heard that I’d sailed through, and with a good score to boot!

I could hear the relief and pure joy in my mother’s voice, and then the tears fell, for what it had cost to get here. Back then it was almost impossible to believe, but in the end, it was worth it. Every extra hour, every missed question, every mediocre mock test, every stepping stone that had eventually paved the way for this.

If I had a few words of advice for the next batch of students preparing for the NEET, it’d be this. Surround yourself with people who love and support. Keep encouraging yourself and don’t be too hard on yourself when you make mistakes. Don’t ever withhold the things you love as a twisted form of positive reinforcement. It never works and ends up being a punishment for something you haven’t even done wrong. Be nice to yourself. You’re doing your best. Have faith and never stop believing in what you can achieve!

- Written by Aditi

Aditi decided to write the emotional aspect of NEET which very few students address. Hope it is helpful and relatable to those beginning the journey :)

Opportunistic infections in AIDS

AIDS is a retroviral disease caused by HIV. It is characterized by the triad of immunosuppression associated with:
1) Opportunistic infections.
2) ‎Secondary neoplasms.
3) ‎Neurological manifestation.

Opportunistic infections seen are:

1) Bacterial infections:

MANS.

M-M.tuberculosis
A-Atypical mycobacterial infections
N-Nocardiosis
S-Salmonella

M.tuberculosis is the most common infection with HIV in India.

2) Viral infection:

H.C. verma of John Cunningham.

H-Herpes simplex virus
C-Cytomegalovirus
V-Varicella zoster virus
John Cunningham -JC virus causing     progressive multifocal leukoencephalopahty.

3) Fungal infections:

H P computers creates crossword

H-Histoplasmosis
P-Pneumocystis jiroveci
computers-Cryptococcosis
creates-Coccidiomycosis
crosswords-Candidiasis

Candidiasis is the most common fungal infection of AIDS in India

Pneumocystis jiroveci is the most common fungal infection of AIDS in world.

4) Protozoal infection:
CITy

C-Cryptosporidium
I-Isosporidium
T-Toxoplasmosis

-Demotional bloke.

Metabolism of HDL notes

Hello, 

Here is a short post on the metabolism of HDL.

USMLE Step 3 - My two cents by Dr. B

USMLE step 3 - My two cents!

My name is Dr. B and I have recently finished my Step 3 - results aren’t out yet, but I hope I can stay as just the author of this article and not have to read it once more. Fingers crossed!!

Pearls on polyps

Hey everyone, this is my first blog! So I realised recently that Ear, Nose, Throat (or ENT for short) has a lot of theory so here's a short post on nasal polyps, for remembering this short, important but a little tedious topic. 

Antrochoanal and ethmoidal polyps are the commonly found types of polypoid growths found in the nasal cavity. They can be fleshy growth of tissue due to various causes, and usually leads to complaints of nasal obstruction and breathing difficulties. Here's a guide to remember the points of difference between the antrochoanal and ethmoidal polyps. For the following:

A - age 

A - aetiology

N - number

L - laterality

O - origin

G - growth

S - size and shape

R - recurrence

T - treatment 

The mnemonic is: "An Apple Never Lives On Green Shrubs (and) Red Trees" 

Interesting imagery, ain't it? 

So what are the differences between the two types of polyps based on these points? 

Age - antrochoanal polyps are found in children, whereas ethmoidal are found in adults. 

Aetiology - usually antrochoanal are having an infectious aetiology, whereas ethmoidal have allergic or other factors as cause for their origin. 

Number- only one antrochoanal polyp usually is present, whereas ethmoidal is usually multiple in number. 

Laterality - antrochoanal are unilateral, the other kind is bilateral mostly. 

Origin - Antrochoanal begins from the ostium of maxillary sinus but ethmoidal, as the name suggests, originates from the ethmoidal sinuses, uncinate process, middle turbinate and middle meatus. 

Growth - As the name suggests, this polyp grows behind towards the choana and hangs down behind the soft palate. The ethmoidal polyp, grows forward and may present at the nares. 

Size and shape - interestingly, antrochoanal polyps are trilobed with the three parts being antral, choanal and nasal. Ethmoidal are grape- like round masses. 

Recurrence - antrochoanal has lesser chance of recurrence as compared to ethmoidal polyps. 

Treatment - antrochoanal polyps are removed by polypectomy, endoscopic removal or Caldwell-Luc operation. Ethmoidal polyps are treated by ethmoidectomy, polypectomy or endoscopic surgery. 

I hope this has been helpful to you! Best of luck for your studies! 

Also, Fact Fatigue: Polyps growing in the ear, middle ear cavity ones, are never avulsed, because it's dangerous and could lead to damage to the branches of facial nerve passing through the walls of the middle ear.

This mnemonic was written by our Medical Student Guest Author, Devanshi Shah

Read more about MSGAI: http://www.medicowesome.com/2018/01/medical-student-guest-author-internship.html

Headaches : Fun Facts

Here's just a list of fun facts about headaches :p
You might find some of them lame but hey, I can write whatever interests me - this is My-Graine you see ! (Sorry about that, had to crack that graine up since it's mine ;;) )

1. Coffee is actually an Anti Migraine substance ! It helps in vasodilation of cerebral vessels since it contains Caffeine and  Theobromine (Compare : Theophylline) which are PDE Inhibitors.
There are drugs that combine Caffeine with Aspirin for this purpose ! Who would've thought ! Surprisingly, through mysterious mechanisms , Caffeine may Trigger migraine in few people.
(Go figure.)

2. Telcagepant is a novel drug being tried for treatment of Migraines. It's a CGRP Antagonist - Calcitonin Gene Related Peptide - Which is said to be a molecular mediator for Migraine headaches.

3. Constipation was said to cause headache. There's no evidence to prove this but old timers might still prescribe laxatives to treat headache.

4. Oxygen therapy helps treat Cluster headache !

5. Migraines may sometimes occur without headache ! Yeah , who would've thought.
So the patient would experience all other symptoms : Aura , Photo-phonophobia with vomiting and nausea , a mild headache And the post headache weakness !
It may actually become a stroke mimic at times as the weakness is pretty severe.
It's called "Acephalgic migraine"

6. Bickerstaff Migraine is a type of migraine where brainstem features are prominent. Also called Basilar migraine.

7. Tension type headache is the most common type of Primary headache ! But it may not have anything to do with being stressed at all.

8. People with cluster headaches may get so worked up and agitated they may actually want to bang their head and beg you to kill them , it's so severe ! (Talk about banging your head against a wall?)

9. There is a type of headache called 'Analgesic Overuse Headache'. The person with a known headache disorder begins to abuse NSAIDs to such an extent that taking the NSAID causes the headache ! So the solution is simple right ? STOP the NSAID?! BUT NO. IT'S NOT AS SIMPLE.
There is a sort of Physical dependence on it. And the withdrawal period is also characterized by headaches for a couple of of days/ weeks till the headaches finally stop. (What a pain!)

10. A subarachnoid Hemorrhage may be preceded by a series of minor headaches called 'Sentinel Headaches'. They can be warning signs in a known hypertensive and must be taken seriously.

That's all!
Hope this helps.
Happy Studying!
Stay awesome!
~ A.P.Burkholderia

Headache : Clinical Overview of Primary Headache Disorders

Primary headache disorders are poorly understood and the treatment isn't satisfactory. Hence it's super important to rule out Secondary causes before labelling a patient to have primary headache.

Here's a summary of clinical profiles of patients with Primary Headache disease.

Patient profiles for primary headache disorders

1. Migraine headache

Age : 30-40 years

Sex : Females >>> Males

Frequency : May be random, usually following a trigger.

Trigger : Subjective ; Lack / excess sleep , Menses , Starving , Chocolate for some people , Excess sunlight , oily food , etc.

Character : Throbbing / Pulsatile headache

Distribution : generally hemicranial to begin with but may Generalise over 1-2 hours.

Associated features : 
Preceded by an Aura - in the form of halos / fortification Spectra / floaters etc.

The attack is associated with Nausea, vomiting , photophobia and phonophobia.

Post Headache state : weakness after the headache subsides. Generally 4-48 h is the duration.

> 72 h = Status Migranosus.

_______________________________________
2 . Tension type headache

Age : 30-40 years

Sex : Females = Males

Frequency : May be random. Can occur daily.

Trigger :  unclear ; Stress or Tension may or may not be an established risk factor.

Character : constriction/ band like sensation around the head - Like a helmet.

Distribution : band like around the head. Fronto occipital region affected more than others.

Associated features : 
NO nausea vomiting ; may have photo and phonophobia. Not as rapidly progressive as migraine headaches.

Post Headache state : weakness not as severe as in migraine headache.

_______________________________________

3. Cluster headache

Age : 20-30 years

Sex : Females <<< Males

Frequency : Can occur daily - classically at the same time every day or at similar intervals during the day.

Trigger :  unclear ; alcohol , smoking , hot weather may precipitate

Character : Throbbing / can be sharp pain. May be sudden in onset. Very severe.

Distribution : always unilateral and involves Peri and retrorbital area.

Associated features : 
Ipsilateral miosis , conjunctival injection , chemosis , rhinorrhea , sweating over forehead.
Patient may become agitated and restless.

Post Headache state : weakness not as severe as in migraine headache.
_______________________________________

Hope this post actually helped and wasn't merely a headache ;)
Happy Treating !
Stay awesome !

~ A.P. Burkholderia

Headache : An Overview of Secondary Headaches

Headache

Headaches are possibly the most common symptoms patients might present with to Neurologists , and even to a General Practitioner!

Here's a more practical and clinical approach to identifying the cause of a headache.

Headache disorders can be secondary to a systemic or neurological condition such as Meningitis or Dengue ; or can be due to a primary headache disorder such as Migraine or Tension headache.

In this post I'd like to summarize causes of secondary headaches.

Important  Causes of Secondary Headache

- Refractive Errors : if an Adolescent or person in his 20's comes with headache , it's important to look into the possibility of a Myopia causing headache.

- Hypertension : especially occipital headache in a 40-50 year old obese male.

- Sinusitis : Maxillary and Frontal sinusitis can commonly cause headache and may confuse for a primary headache disorder.
Associated with Post nasal drip , upper respiratory tract infection , sinus pain on bending over and tender sinuses.

- Systemic Infections :
Dengue - Especially a bifrontal headache
Malaria
Typhoid fever

- Meningitis , Encephalitis, Brain Abscess
Meningitis is typically fever , headache and altered sensorium with neck stiffness.
If these features are present with Diffuse Neurological depression it can be Encephalitis and if Focal features it could be an Abscess.
Tuberculous Meningitis is an important entity to be considered for Chronic headache in India.

- Venous Sinus thrombosis : Suspect in Females on OC Pills / Hormone Replacement or Men on chemotherapy.
Presents with chronic headache and may be accompanied by focal features occassionally.

- Trauma

- Sub Arachnoid Hemorrhage : the typical Thunder clap headache followed by complete collapse of the person is typically for SAH.
Typically in 30-40 year old men , with history of senitnel headaches and generally hypertensive.

- Brain Tumors

- Temporal Arteritis : 60 years and above - Large vessel Vasculitis causing sharp superficial headache especially in temporal region , raised ESR and responsive to steroids to a good extent.

_____________________________

The next post will be a summary of clinical profiles of primary headache disorders.

Hope this helped !
Happy Studying!
Stay awesome !
~ A.P. Burkholderia.

Crepts : An Overview

Hi everyone ! Just a short summary post on Crepts. Would like to thank Upasana for suggesting this topic ! 

Crepts

1 . Synonyms = Rales , Crepitations , Crackles

2 . Character = Rustling/  Bubbling type of sounds
Short , sharp, interrupted sounds.
(Wet Sounds)

3 . Types =

Fine and Coarse crepts -
Differentiation is clinical - fine crepts have a shorter amplitude while Coarse crepts have a higher amplitude and are usually louder with a lower frequency.

So ,  if you hear crepts of mellow tone (lighter quality) , with a very small gap between two crepts they are fine.
If they are very harsh and widely spaced they're likely to be Coarse crepts. 

As a thumb rule , fine crepts are generally Cardiac and Coarse are of Respiratory origin (with exceptions).

4 . Special types of Crepts :

Velcro crepts = Fine crepts of Interstitial Lung Disease

Coarse leathery crepts = Harsh Coarse crepts of Bronchiectasis

5 . Mechanism of Crepts :
- unclear but certain reasons are hypothesized.
- When an Alveolus is in a  collapsed state and then bursts open it produces a crept.
So for example -  in a pneumonia due to the exudates accumulated in the alveolus there is very little air in it and the alveolus is in a collapsed state at the end of expiration. Due to this, when a person inspires the collapsed alveolus and airway suddenly open with a snap and produce a sharp sound due to sudden pressure equalisation.
When many such alveoli open in a serial fashion from top to bottom we hear the typical bubbling sound of 'Crepts'.

- Older reasons - Air bubbling through exudative alveolus. But rejected as other forms of airway Obstruction like Bronchiectasis and Fibrosis causing collapsed airways also causes crepts.

6 . Causes of Crepts :

- Pneumonia / Consolidation
- Interstitial Lung Disease and Pulmonary Fibrosis
- Bronchiectasis
- Bronchitis
- Lung Abscess
- At times in COPD patients - Expiratory crepts may be heard.

Cardiac causes :
- Pulmonary edema due to Left Ventricular Failure.

7 . Cardiac vs Respiratory crepts :

Cardiac crepts are typically Basal and Bilateral , are fine crepts , associated with features of Heart Failure and may disappear on adminstering diuretics.
The opposite is true for Respiratory crepts.

Hope this was concise enough and helped !
Happy Studying!
Stay Awesome!

~ A.P.Burkholderia

Transamination

Have you ever wondered about the difference between non-essential and essential amino acids? 

I’m pretty sure you know the difference :))

If non-essential amino acids are not delivered to the body through diet then how are they made in the body? 

Answer is simple it is by the process of transamination

I hope my notes will help you! If you have any doubts, don’t hesitate to comment or send a message on WhatsApp group :)

Maxillary Artery notes

Hello Friends! This is Anisha :))

Maxillary artery is divided into three branches. Again, each branch is subdivided. 

We also have to learn their course which is very confusing and we forget it during our exam :( 

So, I came up with an easy way to learn it. I decided that I will show the course of the artery in form of a diagram ( you will get more marks! ) and write down what it supplies. 

I hope my notes will help you :)) All the best