Can watching Pokémon cause seizures?

Hello everybody,

So this is an interesting post about Stimulus Sensitive seizures also known as Reflex Seizures.

The major stimuli precipitating these seizures are Sensory in nature but as there is no known "Reflex" to cause such seizures they are better termed as Stimulus Sensitive Seizures!

So in order to study these seizures Japanese children were exposed to   Pokémon  cartoon that induced seizures, surprisingly​ out of all the children who had an episode of seizure only 24% had a  history of spontaneous seizures. These children had the Photosensitive type of Stimulus Sensitive seizures.

Photosensitive or pattern-induced  seizures as experimented in the Japanese kids are, well-recognized and stimulated by bright or flashing lights  (TV,  video  games,  discotheques,  concert  light  shows)  or  by patterns  (lines on the road  while traveling).  These may occur 1 in 4,000 people in age group of 5-25yr but are outgrown in their 30s.

For patients with isolated  photosensitive  or pattern-induced seizures, avoidance  or  modification of stimuli is the initial  approach in the form of wearing blue or  polarized  sunglasses, avoiding  highcontrast flashing-light video games, 
avoiding discotheques, watching TV in a  well-lit room at a distance of  >8  feet,  and covering 1 eye when in a provocative  situation.

Well generally it is observed that many patients with epilepsy can identify precipitating or provoking events that  predispose them to having a seizure. 

Common events include :
stress
lack of sleep
fever
fatigue.

In another group, patients have seizures in response to a very specific, identifiable sensory stimulus or activity.
These stimuli may be :
External :(light, patterns,  music,  brushing  teeth)
Internal :(math, reading, thinking, self-induced). 

The manifestation of these seizures can be either:
Generalized
Partial
Nonconvulsive
Absence
Myoclonic. 

One common pattern is photomyoclonic seizures characterized by forehead  muscle twitching or repetitive eye opening or closing.

So till the next time you play Pokèmon Go or you see Pikachu in action do remember about Stimulus Sensitive Seizures!  ;)

Hope this was informative!

-Medha!

Sudden Unexpected Death in Epilepsy - SUDEP.

Hello everybody,

Let's today learn about Sudden  Unexpected  Death  in  Epilepsy.

It is the most common epilepsy related  mortality in patients with chronic  epilepsy.

Incidence: ranges  from  1-5 per 1000 patients.

Etiology:  unknown, but some of the risk factors include :

1)Polypharmacology, 
2) Poorly controlled generalized  tonic clonic seizures
3) Male gender, 
4) Age  younger than 16 yr, 
5) Long duration of epilepsy, and  frequent seizures. 

Potential mechanisms include :
1) Respiratory  arrest  or  dysfunction, 
2) Drug-induced  cardiac  toxicity, 
3) CNS dysfunction  (hypoventilation,  arrhythmia,  suppression  of  brain  electrical  activity)
4) Pulmonary  edema.

Patients are usually found dead in their  bed in prone  position  with  evidence  suggestive of a recent seizure.   

Some of the Preventive measures include:

1)Reduction of tonic–clonic seizures:  optimum  treatment,  good drug  compliance,  lifestyle  advice  (e.g. avoiding sleep deprivation)

2)Treatment changes: change drugs in a  gradual staged manner; when switching, introduce the new drug before  withdrawing the old one.

3)Supervision at night for patients at high risk.

4) Choice of drugs:  caution  with  antiepileptic drugs with potential cardiorespiratory adverse  effects.
 
5) Action on ictal warning signs: 
tonic–clonic  seizures  that  are prolonged, associated  with  marked  cyanosis, severe bradycardia or apnea,    complex  partial seizures with marked  atonia  (drop  attacks); 

Lastly counseling on the risks, lifestyle modifications. The treatment  decisions are the patient’s  prerogative, the physician’s role is to provide a risk-vs-benefit analysis.

Hope it was informative.

Let's learn together!
-Medha!

Micro-organism series -Salmonella

Introduction: Salmonella belongs to the type of parasites which infects the intestine of vertebrates and causes infection.It causes following infections  (Mnemonic - "GAS".)
G - Gastro-enteritis
A - Abdominal fever or enteric fever
S - Septicemia

The species Salmonella-typhi was first observed by Eberth in mesenteric lymph nodes and  spleen and was first isolated by Gaffky and hence is also known as Eberth -Gaffky or Eberthella -typhi .
S.cholerae - suis the first organism to be isolated from animals and human beings.

Salmonella is divided into two groups :-
1)Typhoidal Salmonella :Causes typhoid fever eg S.typhi and  S.paratyphi A,B,C
Man is the only reservoir
2)Non-typhoidal : They have many animal reservoir .To remember species name, here is a mnemonic
"Hodor held typhimurium  to enter into port "

Hodor -S.hadar

Held- S.heidelbrurg

typhimurium-S.typhimurium (to)

Enter-S.enteridies

Port-S.new port

Morphology:
Aerobes and facultative anaerobes
Gram negative bacilli
It is motile with peri-trichate flagella except S.Gallinarum and S.Pullorum .
Non-capsulated and non-sporing .

Cultural characteristics:
Can grow on simple media over pH-6-8
Temperature:15-41℃
Colonies are circular ,low-convex and smooth .
1)Mac-Conkey's agar(Differential media) :Non-lactose fermenting colonies

2)Deoxycholate citrate and XLD(Selective media): Black head due to hydrogen sulphide production
(Deoxycholate citrate agar and Mac-Conkey's agar are selective as well as differential media)

3)Wilson & Blair bismuth sulphite medium(Indicator medium):Black colony with metallic sheen due to production of hydrogen sulphide.Only S.typhi produces black colony .Paratyphi A produces green colony as it does not form hydrogen sulphide.

4)Selenite F broth and tetrathionate broth  is the enrichment media used for both shigella and salmonella

Biochemical tests:-
1)It ferments Glucose ,mannitol and maltose producing acid and gas
2)IMViC : - + - +
3)Most salmonella produces hydrogen sulphide in Triple sugar iron(TSI) test except S.parathyphi A and S.Cholerae suis .
4)S.Gallinarum and Pullorum cannot be differentiated but can be identified by biochemical reactions .S Gallinarum ferments dulcitol unlike Pullorum .

Resistance:
Killed in 1 hour at 55℃ or in 15 mins at 60℃
Boiling ,chlorination and pasteurisation destroys bacteria .
Killed in 5 minutes by using mercuric cholride / 5% Phenol .
Survives for weeks in polluted air & water
Survives for months in ice
Survives for years  if prevented from drying .

Antigenic structure:
There are 3 antigens present in salmonella
1)Flagellar antigen H:
- Heat labile
- Present on flagella
- Highly immunogenic and hence form high titre of antibodies
- Destroyed by alcohol or boiling
- When mixed with antisera  , agglutination is rapid producing large ,loose and fluffy clumps.
- H persists longer than O agglutinins

2)Somatic antigen "O"
- Integral part of cell wall
- Identical to endotoxin
- Less immunogenic

3)Vi antigen :
- Heat labile polysaccharide and it prevents the agglutination of O antigen
- Act as virulence factor by preventing phagocytosis.
- Persistance of Vi antigen indicates carrier state

Pathogenesis:
Transmission:Normally food contaminated by the faeces of the animal or humans who carries salmonella

Mode of transmission:Ingestion

Incubation period :7-14 days for enteric fever

Pathogenicity :
Salmonella infection usually causes
Gastroenteritis
Enteric fever
Septicemia

Clinical symptoms:
Clinical course  may vary from mild to undifferentiated pyrexia (Also called as ambulant typhoid)
- Onset :Gradual with headache ,malaise ,anorexia ,a coated tongue and constipation or diarrhea.
- Step ladder pyrexia.
- Palpable spleen
- Rose spot appearence on chest during 3rd or 4th week .
- Complications occurs in 3rd and 4th week causing intestinal perforation and GI hemorrhage (most common )
- Pea soup stools in 3rd week of typhoid fever
- Some degree of bronchitis or bronchopulmonary spasm is always seen
- Osteomyelitis is rarely seen mainly in patients affected with  sickle cell anemia  .

Laboratory diagnosis :
Specimen :
Blood is collected for culture ,as in urine or stool .
Serum for Widal test .
(A very famous mnemonic for collection of sample depending upon time duration is
"BASU")
B - Blood culture in 1st week of infection
A - Antibody (Widal in 2nd week of infection)
S - Stool culture in 3rd week of infection
U - Urine  culture for 4th week of infection.
Best diagnosis is  made by blood culture at any stage .
Detection of Vi antigen indicates carrier state.
If antibiotics is started we must use faeces or bone marrow for laboratory diagnosis .Since antibiotics kills bacteria from the circulation  and if not started then we can use blood culture .

Treatment:
Ceftriaxone is the DOC
Ciprofloxacin is the DOC for susceptible organism .
Other drugs used are azithromycin ,amoxicillin,chloramphenicol
Carrier :Ampicillin or amoxicillin given for six weeks

Salmonellosis:
Non Thyphoidal salmonellosis(NTS) is -commonest type of salmonellosis

Factor causing NTS
Immunosuppressive agents like increase in age ,Disease such as HIV etc.

Clinical manifestation:
Gastroenteritis most common .Diagnosis is done by gastroenteritis .
Localized infection like abscess ,meningitis , Osteomyelitis.

Treatment:
DOC either ceftriaxone or Ciprofloxacin .

That's it :P
Stay awesome and cool:)

~Khushboo and Ojas

Testosterone and Dihydrotestosterone

Hello awesomites today I am going to share my notes on functions of Testosterone and Dihydrotestosterone .

Testosterone is regarded as the circulating prohormone.In most of the target cells , testosterone is reduced to Dihydrotestosterone (DHT) which is more potent than the testosterone.

Testosterone function:

Remember: LISE
-LH inhibition .
-Internal genitals development .
-Spermatogenesis
-Erythropoiesis.

Dihydrotestosterone function

Remember :"PG says hair growth,behaviour changes and development of external genitals is due to DHT "

(Half of the things you all  must have got through it!)
PG-Prostrate growth .
Behaviour changes ,Sexual growth .
Hair growth .
External genital development.

Function which is done by both hormones?

-Increase in muscle  mass and strength of bones

Stay cool and awesome:)
~Ojas

Watermelon stomach- GAVE!

Helloooo everybody....

So today's post is summer special ... A condition called as Watermelon stomach...

I am sharing here the most important points related to it... 

Do lemme know your thoughts on the same....And any important points that I may have missed...

Let's learn together!!

-Medha!

Ion-exchange resins and Laxatives

In my last post on Hyperkalemia, I asked this question that why do we give laxatives with ion-exchange resins, eg. Sodium polystyrene sulfonate.

The reason is that if there is constipation due to Hyperkalemia or any other condition we are treating, besides these ion-exchange resins can themselves cause constipation; these resins will be stuck in the colon and the ion to which it is bound to will be reabsorbed into the circulation hence foiling the whole agenda.

-VM

Difference between polysaccharide vaccines and conjugated vaccines

Polysaccharides are strings of sugars. Some bacteria, such as Streptococcus pneumoniae and Neisseria meningitidis, have large amounts of polysaccharide on their surface, which encapsulate the bacteria. The polysaccharide capsules protect the bacteria from the host’s immune system and can make the bacteria more virulent. 

Polysaccharide vaccines are poorly immunogenic. They produce low affinity antibodies (which do not bind well to the antigen) and, because they do not elicit T-cell responses, immune memory does not develop. 

The new generation conjugate vaccines contain carrier proteins that are chemically attached to the polysaccharide antigens. Attaching relatively non-immunogenic polysaccharides to the highly immunogenic carrier proteins means that by activating a T-cell response, conjugate vaccines induce both high-affinity antibodies against the polysaccharide, and immune memory.

So in conclusion:

Polysaccharide vaccine - T cell independent B cell response

Conjugate vaccine -  Carrier proteins - T cell dependent B cell response

Mnemonic:
CT (Like a CT scan?)
ConjugaTe has a T cell response

That's all! 

-IkaN 

Trastuzumab notes + mnemonic

Trastuzumab (Herceptin) is a humanized monoclonal antibody directed against the extracellular domain of the tyrosine kinase receptor HER2.

ARDS pathophysiology Q&A

In Acute Respiratory Distress Syndrome (ARDS), what happens to the following parameters? (Increase / decrease / normal) 

Compliance
Pulmonary artery pressure
Pulmonary capillary wedge pressure
A-a gradient (Alveolar-arterial gradient)
PaO2 / FiO2

Answers given below!

Medicowesome secret project: Cyclothymia

What is the secret project? How can I participate?

Fact of the day : Neuroticism and creative thinking

Hey Awesomites

While the medial prefrontal cortex is a part of the brain that shows high levels of activity in the neurotics, innovation of new ideas is also something the frontal areas of our ( mainly right ) brain function for.

There is often a preponderance to generation of self - generated thoughts and a perception of threat appraisal when there is no such actual external stimulus. The neurotics tend to 'create' situations of threat in their mind and respond accordingly, but they also come up with creative ideas to find solutions to such 'internal' problems by overthinking and overactivating their thought - provoking areas of brain. They also have oversensitive amygdalae, that is concerned with panic attacks, excess fear and anxiety.


Thats all
- Jaskunwar Singh

Did you know? Sir Isaac Newton suffered from bouts of depression and once had a mental breakdown. Inspite of that he made use of his creative mind and formulated laws of gravity, and fathomed several mathematical theories.

Pregnancy risks related to hypertension

Important for multiple choice questions (=

Pre-eclampsia
Post partum hemorrhage
Placental abruption
Gestational diabetes

Preterm delivery
Oligohydramnios
Growth restriction (Asymmetric IUGR, Head spared, Head abdominal ratio increased)
Still birth

-IkaN

Calcium Gluconate in Hyperkalemia

Hey guys!!

In this post I will try to explain why Calcium gluconate is the first line drug in managing hyperkalemia.

First of all, please form a mental image of normal cardiac action potential with the-
1- Very steep phase 0 caused by Na+ influx,
[Note: Vmax is the rate of build-up of membrane potential in phase 0]

2- A short, sharp phase 1 caused by K+ efflux via Transient outward K+ channel
( and some books say Cl- influx)

3- Phase 2 plateau phase caused by Ca2+ influx and K+ efflux via slow delayed rectifier channels.

4- And finally, the downsloping, not so steep repolarization phase caused by K+ efflux via Ikr (Rapid delayed rectifier channels) and also a few other channels which you can afford to forget.

Now what changes Hyperkalemia bring in this sequence of normal action potential?

1. Initially it increases myocardial excitability by raising the RMP from -90mv to approx -75mv; hence bringing it closer to the threshold potential. This is coz of the K+ concentration gradient alteration.

2. But as Hyperkalemia progresses, it causes myocardial depression by decreasing Vmax, essentially slowing down phase 0, hence causing increase in QRS complex duration. This is because the no of Na+ channels activated decreases if RMP becomes less negative.

3. Conversely, it increases the rate of Repolarization, hence causing shortening of QT interval. This is because of a strange reason. The Ikr which I have mentioned above becomes more active if the extracellular K+ levels are high.

Now that we know what happens in Hyperkalemia, let us learn how calcium gluconate amends these changes.

1. It makes the threshold potential become less negative, thereby restoring the normal difference between it and RMP. Myocardial excitability amended!

2. It increases Vmax. Myocardial depression amended!

3. It acts on the SA node and AV node and increases their automaticity further rectifying myocardial depression.

A word of caution! In patients having Hyperkalemia due to digitalis toxicity, hypercalcemia can potentially kill the patient. So in such conditions we use calcium gluconate cautiously only if-
1. There is loss of P waves
2. Widened QRS complex.

Other treatment modalities:

1. Insulin with Dextrose
2. Beta-2 Agonists​ like Albuterol

Both 1 and 2 work by increasing the activity of Na+-K+ ATPase.

3. Bicarbonate. It will cause increased pH which will increase the activity of H+-K+ exchangers.

4. Haemodialysis if it's readily available

5. Ion exchange resins like Sodium Polystyrene Sulfonate along with a laxative like Sorbitol.

A question for you guys, Why is it recommended to give a laxative with an ion exchange resin? ;)

-VM

Education - a vaccine for violence

Hello

We are often so engulfed with racks of books to study and revise for exams that some might even go unrevised or untouched !! Many a times we notice poor children roaming on the streets and asking for coins and notes that are not of much value in their life. These children need education and proper guidance to re - track their life routes and help them fulfil their dreams. Poverty and lack of education in life makes such people feel helpless and force them to use illegal ways to fill their pockets.

" Brian was a poor boy. Born to a poor family, he worked all day to help his parents earn some money. Wearing a half - torn  white - turned - black tee and a faded brownish - black shorts, the eight -year old roamed here and there on the roads while holding some beautiful soft toys for being sold to the so-called 'high class' passers - by. Little did he know why was he doing all that. He was just told that he has to give the toys to some people and in return, he would get something called 'money'.

Then one day, he saw other boys of his age, carrying bags full of books and going to school. Fully energized, cheerful and in high spirits, they went on to their place. And Brian just saw them going. At that moment, he decided to change his life for the better. :)

Brian squandered his bag of toys on the roadside and started searching for a book store. A few hours passed but he couldn't find one. He knew nothing about shops, places, or any people around. He felt lone. It was a new place for him. He felt suffocated in the rising shades of darkness. The sun was getting closer to the horizon. The street lights scattered blue on the dusty road. He felt helpless and tired. Unable to get back to his home, he just slept on the footpath. Not even one eye focused on him inspite of busy streets and the flux of vehicles on the roads.

It was 8 in the morning. Seeing him still there and crying, an old man came up to him. Brian couldn't respond to any of his questions. The old man gave him some food to eat, and then took him to his house. There the little boy saw a library of books - just what he was finding since so long. He got overjoyed and went on to reach the shelves. The old man felt his curiosity to study. He asked the boy if he goes to school.

Brian told him his story after which the old man decided to help the little boy. He got him admitted to a reputed school. He gave him all he could. Books, clothes, food, shelter and work so that the little boy could help his family. And so now the boy was not poor any more. He got the treasure of his life - the books. :) "

In view of the Dhule incident a few days back, it is unethical and unacceptable for parents and relatives to demonstrate any act of physical and mental abuse towards a doctor if a patient with head injury cannot be saved due to the unfortunate circumstances such as the patient being brought late to the hospital and shortage of staff and equipment. These factors attract the need to shift the patient to a higher centre for provision of better treatment facilities and medical care.

The poor prefer to visit government hospitals and clinics because it suits their pockets. Referring the patient to a higher centre means more expensive and more delay in treatment. But that absolutely does not mean you argue with and abuse the doctor to force the treatment which cannot be done !!

Education is a key component to ensure that the person who has met with an accident and severely injured is immediately brought under medical care and treated successfully with suitable measures to save the life.

We, as responsible and educated citizens of the country must take steps to help the poor children and give them their weapons to fulfil dreams which seemed impossible to them. :)


That's all
- Jaskunwar Singh

Fact of the day: Histoplasmosis can present like sarcoidosis

Patients with histoplasmosis who have hilar lymphadenopathy, arthralgias, and erythema nodosum can be mistakenly given the diagnosis of sarcoidosis (“pseudosarcoidosis.”)

Steroids mistakenly given for sarcoidosis can cause acute exacerbation of histoplasmosis.

Fact of the day: Ferritin is an inflammatory disease marker

Ferritin is an acute phase reactant.

Serum ferritin arises from damaged cells, and is thus a marker of cellular damage.

Medicowesome secret project: Hemispheres of the brain

What is the secret project? How can I participate?

An overview of the NEET PG entrance exam

AN OVERVIEW OF THE NEET PG ENTRANCE EXAM
by Dr. Prateek Charuchandra Joshi (DNB AIR 291, MH state rank 51)

Brainstem Syndromes-Pons!

Hellooo people!

After travelling from the Midbrain  I we have reached  the Pons.. which literally means a Bridge... So .... Let's study the important eponymous Pontine syndromes today...

1) Millard-Gubler Syndrome:
Lesion location:Pons
Structures affected: CN VII ,Corticospinal tracts!!
Clinical features: Ipsilateral peripheral facial palsy; contralateral hemiparesis ,CN VI not involved

Foville's Syndrome(Raymond-Foville) :
Lesion location:Pons
Structures affected:CN VII; lateral gaze center; Corticospinal tracts.
Clinical features • Ipsilateral facial palsy and horizontal gaze palsy; contralateral hemiparesis

Raymond's (Yelloly, Landry) Syndrome: Lesion Location: Pons
Structures affected: CN VI; Corticospinal tracts
Clinical Features: Ipsilateral abducens palsy; contralateral hemiparesis ,it is  often lumped with Foville's syndrome.

There are other Pontine syndromes ...And an Anatomical classification of them makes them easy to understand !

I shall in the next post put up the respective syndromes along with associated diagrams..

Till then... Study Well Guys!
Also I would like to say... Medicine is not just science and theory but also an art to be understood.... So we all need to have the artists eyes and spot out the subtle presentations of the  diseases in our patients and treat them with all our hearts!

-Medha!

Fact of the day: High maternal cortisol good for foetal brain

Hey Awesomites

Neurodevelopment attained in the foetal period is greater than in any other period of an individual's life. Foetal exposure to "optimal levels" of maternal cortisol in third trimester has been linked to better cognitive and functional performance in the child.

Maternal cortisol acts on its receptors present in amygdala, hippocampus and the pre - frontal cortex ( PFC ) in high amounts. This hormone influences various stages of neurodevelopment including neurogenesis, axonal development, and myelination of nerve fibres and thus it leads to increased cortical thickness in frontal part of the brain and increased brain maturity.
( Source )

Thats all
- Jaskunwar Singh

Brutons disease (X linked agammaglobulinemia) mnemonic

Hello! 

Guess who made a new video?