CMS neurology form 2: Question on numbness, tingling and decreased grip strength

Disclaimer: This is an CMS neurology form 2 question for step 2 CK. If you are planning to take USMLE step 2 CK in the future, I would recommend that you DO NOT read this post because it will bias your assessments.

Differentiating C8 radiculopathy from ulnar neuropathy

Hello. This is a very short post (because I am super busy studying)

It's on differentiating C8 radiculopathy from Ulnar neuropathy based on a question I solved the other day. How would you differentiate the two in clinical practice?

C8 radiculopathy:
- Thumb abduction weakness: abductor pollicis brevis (C8, T1)

- Triceps affected (C6, C7, C8)

- Radiculopathies are often painful.

Ulnar neuropathy:
- Hand intrinsics (C8, T1) affected:
Palmar and dorsal interossei
Lumbricals III & IV
Abductor/opponens/flexor digiti minimi

- Basically, all hand intrinsics except for the median-supplied "LOAF" muscles (lumbricals I & II, opponens/ abductor/flexor pollicis brevis)

- Triceps not affected.

- Focal neuropathies aren't painful.

Conclusion: The ulnar nerve innervates all intrinsic hand muscles, except the abductor and flexor pollicis brevis, opponens pollicis, and lateral two lumbricals, which are innervated by C8 and T1 via the median nerve which helps differentiating the ulnar neuropathy from C8 radiculopathy.

That's all!
-IkaN

Pills of knowledge in Ophthalm- Anterior ciliary artery

The point where the anterior ciliary artery pierces the sclera is often marked by a pigment. This is of particular importance while cauterization as in a bid to make everything look neat and shiny, the pigmented part shouldn't be cauterized as it will cause necrosis of the structures supplied by the artery. 

Effects of Angiotensin-II on GFR

So this is a highly confusing topic. No matter how many times you read it, some amount of doubt is always there in your mind. So an advice to the readers, bookmark this post because you will be needing to read it more than once to get the drift.

First of all, let us review the effects of Angiotensin II on Glomerulus.

It constricts both the afferent and efferent arterioles but preferentially increases efferent resistance. Why? 3 reasons:

1. Efferent arterioles have a smaller diameter in their basal state.

2. Ang II stimulates the release of vasodilator NO from the afferent arteriole.

3. Ang II minimizes vasoconstriction at the afferent arteriole via the stimulation of Ang II type 2 (AT-2) receptors, which result in vasodilatation through a CYP450 dependent pathway.

The net effect of preferential rise in efferent arteriolar resistance is that the glomerular pressure is increased or stabilized(in hypoperfusion states), which helps to maintain or increase GFR. But in the long run, lots of fluid have been filtered out leaving behind the proteins which raise the colloid osmotic pressure, eventually enough to overrule the hydrostatic pressure and hence it leads to decrease in GFR.

Ang II also reduces GFR by causing constriction of the mesangial cells which reduces the effective surface area for filtration. 


-VM

Pills of knowledge in Ophthalmology- Squint and refractive errors

1.A refractive error should be thoroughly assessed prior to surgical squint correction or the squint may recur.

2. Divergent squint occurs in myopes as the divergent system of muscles is more active during far vision. So, the far vision in myopes being hampered, the eyes try to diverge more.

3. Same goes for hypermetropes. They end up with a convergent squint if left uncorrected.

-That's all!

Sushrut Dongargaonkar

Differentiating peroneal neuropathy, sciatic nerve injury and L5 radiculopathy

This post is on differentiating weak dorsiflexion of foot - I made a little algorithm on it. (I'll add images later)

If there's weakness in foot dorsiflexion, check plantar flexion and inversion.

If plantar flexion and inversion is normal: Peroneal neuropathy.

If plantar flexion and inversion is weak: Check hip movements.

If weakness at hip joint: S5 radiculopathy.

If no weakness at hip joint: Sciatic nerve compression.

You can differentiate based on sensory levels and reflexes too but this is easier.

Conclusion:
Peroneal nerve supplies the dorsiflexors and evertors of the foot. There will be no weakness in plantar flexion and inversion in peroneal nerve injury.

Hip abduction is an action of Gluteus medius and minimus muscles. These are Superior gluteal nerve innervated muscles. This nerve arises from L4, L5 and S1 roots . If there is hip abduction deficit with foot drop, it means pathology at the radicular ( root) level. 

Here's the reading material.

Common peroneal neuropathy presentation:
- Acute foot drop (difficulty dorsiflexing the foot against resistance or gravity).
- Patients describe the foot as limp; there is a tendency to trip over it unless they compensate by flexing the hip higher when walking, producing what is called a "steppage" gait.
- Patients may also complain of paresthesias and/or sensory loss over the dorsum of the foot and lateral shin.
- Examination typically reveals weakness in foot dorsiflexion and foot eversion (deep and superficial peroneal nerve-innervated, respectively), with normal inversion and plantar flexion (posterior tibial nerve).
- Sensory disturbance is confined to the dorsum of the foot, including the web space between digits 1 and 2 and the lateral shin.
- Reflexes are normal.

Sciatic nerve injury presentation:
- Weakness affecting most of the lower leg musculature, including the hamstrings.
- Hip flexion, extension, abduction and adduction, and knee extension are normal.
- Sensory loss involves the entire peroneal, tibial, and sural territories.
- In the lower leg, however, the medial calf and arch of the foot may be spared secondary to innervation by the preserved saphenous nerve (a branch of the femoral nerve). Sensation is also spared above the knee both anteriorly and posteriorly.
- The knee jerk is normal, but the ankle jerk is unobtainable.

L5 radiculopathy presentation:
- Back pain that radiates down the lateral aspect of the leg into the foot.
- On examination, strength can be reduced in foot dorsiflexion, toe extension, foot inversion, and foot eversion.
- Mild weakness in leg abduction may also be evident in severe cases due to involvement of gluteus minimus and medius. Atrophy may be subtle; it is most readily observed in extensor digitorum brevis.
- Sensory loss is confined to the lateral shin and dorsum of the foot.
- Reflexes are generally normal.

That's all!
-IkaN

Alvarado Score Parameters Mnemonic ; For Appendicitis

Alvarado score is one of the most famous scores to clinically diagnose Appendicitis. Without further adieu let us delve into it.

            Anorexia or ketones in urine           - 1 
            Leukocytosis >10,000                      -2  
            Vomiting/Nausea                             -1
     migrAtory pain to right iliac fossa            -1
           Rebound tenderness                         -1
 temperAture above 37.3 celsius                 -1
      tenDerness in right iliac fossa              -2
   neutrOphilia >70%                                 -1

Of these the second parameter from above and second parameter from below have 2 points credited for each. Every other parameter is credited with 1 point each.

The overall aggregate comes out of 10, which the highest possible score for Alvarado score.

If, the aggregate is,

<3 - Low risk for appendicitis
4-6 - Mid risk for appedicitis
>=7 - High risk for appendicitis

In some hospitals where a differential count is difficult to find, use a modified score with 9.

That's all guys, if you find any mistake let me know.

With love,
Jay~

P.S. - yayyy.....missed me much awesomites? I was away from the blog for the last 6 months from posting, because I had very disastrous scores for surgery in my university and I didn't feel worthy enough to write for you guys. (So my activity was largely concentrated in the Whatsapp Medicowesome groups, and the Author's page.) Anyways, I had to take a remedial exam for Surgery 2 weeks ago. And BAAM!!!!.....the results were released today, and yayyyyy.....I passed surgery! :)

I must thank all my Medicowesome admin/author collegues for tolerating my rants and, help me to push through the hellish scary time together. Thanks everyone. Finally I'm through it, and I'm back to writing for you all guys. So thought to start the first post after returning, with a General Surgery Diagnosing score with the help of Schwartz Textbook of Surgery.

See ya soon peepz! :)

Pills of knowledge in Ophthalm- Posterior staphyloma

A posterior staphyloma is common because the durability of the layers of the eye where the optic nerve enters the eye is lesser in comparison.

-That's all!

Sushrut Dongargaonkar

Pills of knowledge in Ophthalm- Moxifloxacin

Moxifloxacin is the preferred antibiotic in Ophthalmic surgeries and pathologies because it gets concentrated into the anterior chamber and the aqueous.

That's all!


-Sushrut Dongargaonkar

EMG and NCS - Review

Hello there!

Today we'll see some important points on Electromyography (EMG) and Nerve conduction studies (NCS).

EMG evaluates abnormal electrical activity in muscles, and NCS investigates how electricity flows through a nerve.

They help to locate and determine the causes of diseases that affect muscles and peripheral nerves.

Procedure:
In EMG, a small needle is inserted into a muscle, to measure its electrical activity. In NCS, electrodes are placed on the skin overlying a nerve, and other recording electrodes are attached at a different point over the same nerve and a small shock is applied, and the electrical impulse is recorded​.

Understanding the terminologies and results of these tests-

 Amplitude: The electrical signal is represented as a wave, and the amplitude is its height.

ConductionVelocity (CV): The conduction velocity describes the speed at which the electrical impulse travels along the nerve.D

Duration This describes the width of an electrical wave.

ConductionBlock: The diminution of signal across an anatomical region such as the wrist. This suggests nerve entrapment.

So when a nerve stimulates a muscle to contract, there is a brief burst of electrical activity called a motor unit action potential (MUP).

Some of the abnormal responses seen are:

1)Fibrillations & positive sharp waves on the monitor seen in diseases of peripheral nerves.

Muscles sometimes start having spontaneous activity on their own.

2)Fasciculations: Sometimes the abnormality causes visible muscle twitches.

3)Abnormally large MUPS : These are seen If a nerve has been injured and then regrows.

 On regeneration the nerve tends to branch out to include a wider area of the muscle and hence we get large motor unit potentials on the screen.

4) Abnormally small MUPS: When they're  abnormally small or brief it suggests the presence of a disease of a muscle (a myopathy) where the muscle is unable to contract to and fails to provide the normal amplitude of the wave.

5)"Recruitment pattern":  As a muscle is contracted, nerve fibers signal more and more bits of muscle (called motor units) to join in and help. 

In a neuropathic disorder, the amplitude of different motor units is strong, but there are fewer of them because the nerve is unable to connect to as many units.

 In myopathies, the number of motor units is normal, but the amplitude is smaller

You may never come across an actual EMG for an interpretation,but it is always good to know the investigation.

The interpretation of EMG and NCSs is not always straightforward and may not always lead to just one possible diagnosis — but the tests can reduce the number of diagnostic possibilities.

Hope this was helpful!

Let's Learn Together!

-Medha.

New TB Risk Factor

People with low levels of vitamin A who live with individuals who were sick with tuberculosis were 10 times more likely to develop the disease than people with high levels of the nutrient, according to research led by investigators at Harvard Medical School.

Vit A rich foods: Liver, fish, hard-boiled egg(not omelette), cheese, butter, cheddar etc

And now some vegetables: Sweet potato, Carrot, Squash, Spinach, Lettuce

Some fruits: Mango, Papaya, Guava, Watermelon, Apricot, Passion fruit

Another reason to love Mango!

-VM

Research update: Statins may increase risk of Parkinsons' disease

Hey Awesomites

A new research by neuroscientists has updated our knowledge about the association between high cholesterol levels in people and prevalence of neurodegenerative diseases such as the Parkinson's.

Mind - wandering : How your body reacts to it?

Hey Awesomites

First lets have a word about mind - wandering.. "Mind- wandering (or task-unrelated thoughts) is an experience of thoughts which are totally unrelated to the task you are doing right now, especially when it demands attention. It involves activities such as reading, driving, attending lectures, etc."

Dibucaine Number.

Hello !
Let's see what this Dibucaine number is.

So Dibucaine is a local anesthetic.

Dibucaine inhibits 80% of the normal Pseudocholinesterase enzyme and 20% of the Atypical enzyme.

The number is determined by measuring the percentage of Pseudocholinesterase enzyme that remains unchanged in the blood of individuals administered a standard dose of Dibucaine intravenously.

Normal Dibucaine number is 70-80% i.e 70-80%of normal enzyme is inhibited by Dibucaine.
If there is a point mutation in the enzyme making it a Atypical Pseudocholinesterase then Dibucaine will not be able to inhibit it and the number will decrease.

This number is used to measure the activity of Atypical Pseudocholinesterase,and to assess the likely hood of prolonged apnea after succinylcholine administration.

Sodium Fluoride can also be used in place of Dibucaine.

If you know more on it Add to this information.

Let's learn Together!
-Medha.

Contraindications for Noninvasive Ventilation Mnemonic

Hey guys

This is one of my rare mnemonic posts. I don't post much on this coz most of my mnemonics are kinda personal if not socially inappropriate :p

So Noninvasive ventilation, imagine having a mask on ur face, all air tight, almost strangulating and as if this isn't enough, with multiple tiny outlets giving jets of air which are titillating your highly itchable nasal area.

Unpleasant, right?

Talking of unpleasant, you do remember Hitler, right?
He GAAASED the Jews, since that's not a possibility for us since we all love Zuckerberg let's think about something on a similar note.

"GAAAS the HOEs"

G- GI bleeding
A- Aspiration
A- Angina( including MI)
A- Arrest( Cardiac and Respiratory)
S- Surgery on ur face

H- Haemodynamic instability
O- Obstruction ( in upper airway)
E- Encephalopathy ( Severe)
S- _____

I've left the last one blank for the reader to fill up. Hint: It has something to do with​ obstruction of the lower airways.

Hope this is helpful!

-VM

Study Group Discussion: Salisbury Phenomenon

Whats Salisbury effect?

It's a very interesting phenomenon.

It states that when coronary collaterals develop in the face of myocardial ischemia, they improve the blood supply. However they physically restrict left ventricular dilation and thereby raise LVEDP(LV end diastolic pressure) and reduce LV compliance.
This is because they act like tendrils/scaffold which prevent ventricular dilation.

Nice one!

-VM

Ductus Arteriosus : Review of Key Points

Hi everyone ! Just a short review on Ductus Arteriosus.

- Ductus Arteriosus is basically a communication between the Pulmonary trunk and the Systemic Aorta.
- This communication is between pulmonary trunk and the end of Arch of aorta. Just after the Brachiocephalic trunk , and Left Common carotid and Subclavian have branched off.
- In embryonic life this communication helps transport blood from RV- Pulmonary artery to the Systemic circulation.

So ,
Remember :
Prostaglandins Persist

-Prostaglandins, especially PGE1 , act on the Ductal muscle tissue and keep it Open.
-So the Ductus arteriosus stays open.

-This is important in certain Duct dependent lesions
- Duct dependent heart lesions are those which need the presence of an Open ductus to receive blood in systemic / Pulmonary circulation.

- For example -->
✓ Duct dependent lesions for Systemic Circulation are those that cause obstruction to the Left side heart to pump blood into the aorta. These include :

- Coarctation of Aorta ( especially pre Ductal ) : Here there is a constriction of the aorta just before the ductus Arteriosus. So , a persistent Ductus would transport blood from pulmonary circulation into the systemic. 
If ductus gets closed , there would be minimal blood flow to the Lower limbs and abdomen.

- Critical Aortic stenosis.
- Left side Hypoplastic heart.

~~~~~~~~~~~~~~~~~~~~~~~~~

✓ Duct dependent lesions for pulmonary circulation
-These are lesions where pulmonary blood flow would be severely reduced due to some RV- Outflow tract Abnormality and the only source to the lungs would be through the ductus shunting some blood from aorta into the pulmonary vein.

- These include : 

- Critical Pulmonary Stenosis
- Hypoplastic Right heart syndrome
- Tetrology of Fallot
- Tricuspid Atresia
- Ebstein Anomaly

Another important disease is Transposition of the great vessels where this sort of corrects the defect.
~~~~~~~~~~~~~~~~~~~~~~~~~

So. We've seen in what conditions we'd like to keep the Ductus Arteriosus open / persistent.
Normally this Ductus closes functionally within 24 hours of birth. And anatomically between 10 and 14 days post natally.

If this persists on its own for a long time it causes a Congenital Heart Disease called Patent Ductus Arteriosus.
This defect is characterised by shunting of blood into the pulmonary trunk constantly during systole and diastole causing a Continuous murmur.

To close this ductus , we could try using Indomethacin / Ibuprofen especially in preterm children.
These drugs inhibit Prostaglandin synthesis , thus causing Ductus Smooth muscle to constrict and eventually close.

So that's all about the ductus !

Happy studying !
And Stay Awesome !

~ A.P.Burkholderia

Jaundice Syndromes : Mnemonic

Hey everyone. Just a short post on how to remember the Jaundice Syndromes.

So.

Remember :
CGI
(As in the CGI special effects in movies.)

C - Criggler Najjar Syndrome
G - Gilbert Syndrome
I  - Indirect Jaundice ( Unconjugated Bilirubin).

So this would make Dublin Johnson and Rotor Syndromes Direct Jaundice.

Another useful fact :
All are inherited as Autosomal recessive trait except Gilbert and Criggler Najjar 1.

Hope this helped !
Happy studying.
~ A.P.Burkholderia

Lowe syndrome mnemonic

Lowe Syndrome (Oculocerebrorenal dystrophy) mnemonic

Think of Lowe = Love and it'll make sense.

Lowe makes you blind (cataracts, glaucoma)

Lowe makes you HAPpy (High Alkaline Phosphatase along with normal calcium, low phosphate)

Lowe messes with your head (intellectual disability)

LoveR - Renal defects (proximal tubular acidosis, aminoaciduria, and low-molecular-weight proteinuria)

Lowes syndrome is a cause of Fanconi syndrome.

That's all!

-IkaN

Renal Cell Carcinoma Etiology : Summary

Hi everyone. Here's a short summary of the causes for Renal cell carcinoma !

Renal Cell Carcinoma ( or RCC) is a common tumor of the kidneys and is essentially an Adenocarcinoma.
It's quite often called as the 'great mimic' as it is relatively hard to diagnose.

Here's the list of causes of this tumor.

Remember :
CCCC or C4

C = Cigarette smoking and Tobacco usage.
C = Chronic Kidney Disease / Cystic (Acquired) Disease of kidneys.
C = Cadmium, Asbestos and other occupational Exposures.
C = Cancer Syndromes.
Important Cancer Syndromes =

- Von Hippel Lindau Syndrome :
3p mutation in VHL Gene which is a tumor suppressor --> Tumors seen include Cerebellar and Retinal Hemangioblastomas , Pheochromocytoma, RCC (Clear type) and various other Cystic tumors.

- Tuberous Sclerosis

- Birt Hogg Dube Syndrome : Associated with various weird skin changes and chromophobe type RCC.
Skin changes include --> Tumors of Hair disc (Tricho-discoma) , Tumors of Hair follicle - Fibrofolliculoma and Acrochordons ( skin tags).

- Hereditary Papillary Cancer : Associated with MET Gene mutations

- Hereditary Leiomyomatosis with RCC : Associated with multiple Fibroids in the uterus.

That's​ all for today!
Hope this helped.
Happy Studying !
And, as always , Stay awesome !

~ A.P.Burkholderia

Step 2 CK: Differentiating ileus from SBO

Hello! Short post.

SBO: Small bowel obstruction.

Both: Nausea, vomiting, abdominal distension

Ileus: Hypoactive bowel sounds
Dull and constant pain
Dilated bowel but no air fluid levels

SBO: Initially hyperactive, later hypoactive
Colicky abdominal pain
Air fluid levels seen

That's all!
Back to studying.
-IkaN

Neuroblastoma mnemonic

Hello!

The term neuroblastoma is commonly used to refer to a spectrum of neuroblastic tumors (including neuroblastomas, ganglioneuroblastomas, and ganglioneuromas) that arise from primitive sympathetic ganglion cells and, like paragangliomas and pheochromocytomas, have the capacity to synthesize and secrete catecholamines.

Remember the N myc mnemonic for neuroblastoma :

N - Neuroblastoma, N myc gene
M - Crosses midline (differentiates from Wilms)
MY - MYoclonus (Opoclonus myoclonus)
C - Calcifications in tumor present
C - Catecholamine secretion

You can also remember "High BP" for additional findings seen in neuroblastoma:

Horner syndrome
Heterochromia iridis (different colors of the iris or portions of the iris)
Hypertension
Homovanillic acid and vanillylmandelic acid elevated in urine
Bombesin positive
Back pain
Bone pain
Beckwith-wiedemann syndrome association
Posterior mediastinum or retroPeritoneal mass
Pseudorosette
Purple skin lesions
Proptosis
Periorbital ecchymoses

That's all!
-IkaN

Doyne's macular degeneration

So, the other day the head of my department asked us about Doyne's maculopathy. Couldn't find rest until I searched it up on Google. Here what it is in short-

1. Accumulation of material between
the Bruch's membrane and the retinal pigment epithelium.

2. This results into the formation of a drusen, which is a radially localised
white, large one which spreads over
time.

3. The cause is a mutation in the
EFEMP1 gene,on chromosome
2p16, inherited as an autosomal
dominant trait which results in the
formation of a misfolded protein
which is poorly secreted as well.

4. All this results into a gradual loss of
vision.

5. Photodynamic therapy forms the
mode of treatment for subfoveal nets which may also occur in the disease.

It is also known as 'Honeycomb retinopathy'

That's all!

-Sushrut Dongargaonkar

The Romberg's Test.

Hello,
Today's review is on Rombergs test.

Romberg/Brauch-Romberg sign:
In cases where the proprioception is disturbed, patient may be able to stand with eyes open but sways or falls with eyes closed.

Romberg described this test, in patients with tabes dorsalis where the Dorsal Columns are damaged.
Well he did not state that the feet should be placed together; it was added later.. Nor did he comment on where the arms were to be positioned.

It is just a common practice to have the patient hold the arms outstretched in front, in order to check simultaneously for pronator drift or to perform finger-to-nose testing; it is not what the original test was.

The Romberg sign is often misunderstood and misinterpreted. 

The essential finding is a difference between standing balance with eyes open and closed. To test this function, the patient must have a stable stance, eyes open and then demonstrate a decrease in balance with eyes closed, when visual input is eliminated.
This is the time patient must rely on proprioception to maintain balance.

The Romberg sign is used primarily as a test of proprioceptive, not cerebellar, function, patients with cerebellar disease, particularly disorders of the vestibulocerebellum or spinocerebellum, may have some increase in instability with eyes closed, but not usually to the degree seen with impaired proprioception.

A patient with an acute unilateral vestibulopathy may fall toward the side of the lesion when standing with eyes closed.

Additional Manuevers for this Sign.

1) Ropper's Refined Rombergs Test :
Turning the head side to side eliminates vestibular clues and increases the reliance on proprioception.

2) The Sharpened Romberg Test :
It is done by having the patient stand in tandem position with eyes open and closed; the limits of normality for this variation are conjectural.

Hope this was helpful!

Let's Learn Together!
-Medha.

MCQ Pointers - Pityriasis Versicolor.

Hello!

If you see some of the below "pointer" words in MCQs the ans would most likely be pointing towards Pityriasis Versicolor.

-Acquired lesions.
-Hypopigmented small macules coalescing to form Patches classically on the chest (m/c),back,face.
-Perifollicular (around hair follicles) distribution.
-Fine scaling on lesions which becomes prominent on scratching - Scratch sign+.
-Pale yellow fluorescence of the lesions on Wood's lamp examination.

Finally the classic - Indicating the causative organism : Malasessia.
Spaghetti and meat balls appearance or Banana and Grapes appearance on KOH mount.

Lemme know more of pointers you know about.
Let's Learn Together!
-Medha.

Step 2 CK: Psychiatry tip for possible depression questions

Hello! 

Whenever I come across a possible major depression question, I write SIGECAPS (full form at the end of the post) down and strike out the alphabets as and when I come across the symptoms.

For example, weight loss - strike out A for appetite change, fatigue because staying up at night - strike out S for sleep change, E for loss of energy.

Then re-read the stem and see for symptoms I missed out due to twisted wording (she stopped singing a month ago - strike out I for loss of interest)

It REALLY helps in figuring out 5/9 SIGECAPS for diagnosis of MDD because if you are not actively looking for the symptoms in the question stem, you'll miss them out. Also, if you are not counting, you might wrongly over diagnose MDD.

Writing it down also saves time because you don't have to keep re-reading the stem over and over.

It also helps getting the count right because if you have already striked out an alphabet, you can't strike it out again. So you won't get the count wrong for possible rephrasing of the same symptom in the question stem. (patient says she has lost appetite, there is weight loss - it is one alphabet in SIGECAPS, so you can't strike A out again - you will get the symptom count right!)

That's all!

I've read so many comments by students in forums where people get MDD wrong just because they didn't see the obvious 5/9 SIGECAPS. Don't miss it out guys, it's very easy to diagnose with this trick! :)
Hope that helps!

-IkaN

For those who don't know what SIGECAPS stands for :

S: Sleep changes: Increase during day or decreased sleep at night

I: Interest (loss): of interest in activities that used to interest them

G: Guilt (worthless): Devalue themselves, feel guilty

E: Energy (lack): common presenting symptom (fatigue) 

C: Cognition / Concentration: Reduced cognition &/or difficulty concentrating

A: Appetite (weight loss): Usually declined, occasionally increased

P: Psychomotor: Agitation (anxiety) or retardations (lethargic)

S: Suicide / preoccupation with death

Originally when a physician would write a prescription, the abbreviation “SIG” would be written which was to mean directions. The "E" CAPS was to remind the prescriber to write “Energy” capsules for depression (antidepressants).

Hence:  SIG:  E. CAPS

Therapist near me, BetterHelp

GLP-1 analogues mnemonics

Hello!

Mechanism of action of GLP 1 analogues
- Increase glucose dependent insulin release
- Decrease glucagon release

Motor Neurone Disease : Why and How to rule it out.

Hi everyone ! Here's a short post on How and why to rule out Motor Neuron diseases.

Motor Neurone Disease includes a group of conditions where the Motor Neurons of your body begin to degenerate.
If these neurons are located above the level of the Alpha motor neuron of spinal cord , the result is UMN lesions , like Primary Lateral Sclerosis.
If the degeneration occurs in the Alpha motor neurons themselves , the result is LMN type paralysis, like Spinal Muscular Atrophy..
A combination of the two - UMN + LMN features as seen in - Amyotrophic Lateral Sclerosis.

Now a few set of conditions are used as a way to exclude to MND.
MND itself isn't very common , and carries an extremely poor prognosis. Treatment options are extremely limited. So it's important to rule it out whenever you come across a Paraplegia , Quadriplegia, Bulbar or Pseudobulbar palsy patient .

An MND has No COBS.
C - No Cognitive changes
O - No Ocular motility involvement till late.
B - No Bladder bowel involvement till late.
S - No Sensory involvement.

There are a few exceptions to this -
Cognitive changes can be present if it's associated with Fronto temporal dementia. A lot of the familial cases are associated with this.

Behavorial changes can also be seen in a Pseudobulbar palsy patient. (More on that some other day !)

Sensory involvement may be seen in Hereditary spastic paraplegia - a variant of MND.

So that's all !
Happy studying !
Stay awesome !

~ A.P.Burkholderia.

Clonus - A review.

Hello everybody!
Let's review Clonus breifly today.

So what is it?
It is a series of rhythmic involuntary muscular contractions induced by the sudden passive stretching of a muscle or tendon.

Clonus occurs most frequently at the ankle, knee, and wrist, occasionally elsewhere.

The important Clonus that we all frequently examine is the Ankle Clonus so let's see that in detail here.

Ankle clonus is a series of rhythmic alternating flexions and extensions of the ankle.

How to do it?
The leg and foot should be well relaxed, the knee and ankle in moderate flexion, and the foot slightly everted.
The examiner supports the leg, with one hand under the knee or the calf, grasps the foot from below with the other hand, and quickly dorsiflexes the foot while maintaining slight pressure on the sole at the end of the movement.
A single tap on the tendon to elicit the ankle jerk may occasionally provoke clonus.

Unsustained clonus fades away after a few beats; sustained clonus persists as long as the examiner continues to hold slight dorsiflexion pressure on the foot.

Unsustained (transient) symmetric ankle clonus may occur in normal individuals with physiologically fast Deep Tendon Reflexes. Nonorganic clonus occurs rarely. False clonus (pseudoclonus) in psychogenic disorders is poorly sustained and irregular in rate, rhythm, and excursion.

Sustained clonus is never normal. In severe spasticity, clonus may occur spontaneously or with the slightest stimulus. At the ankle, true clonus can usually be stopped by sharp passive plantar flexion  of the foot or the great toe; false clonus is not altered by such a maneuver

Mechanism:
Part one - For ankle clonus, the sudden stretch of the gastrosoleus muscle elicits a contraction essentially analogous to a stretch reflex that causes a contraction with resultant plantar flexion of the foot. The foot goes down. 
Part two - This contraction increases tension in the Golgi tendon organs in the gastrosoleus tendon, sending a volley of impulses via the Ib fibers that then inhibit the contraction of the gastrosoleus and facilitate contraction of its antagonist, the tibialis anterior muscle.  The foot goes up. 
This in turn passively stretches the gastrosoleus, and the cycle is repeated.

A simpler explanation is alternating stretch reflexes.

A few other Clonus' seen are :

1) Patellar clonus :
It consists of a series of rhythmic up-and-down movements of the patella. It may be elicited if the examiner grasps the patella between index finger and thumb and executes a sudden, sharp, downward thrust, holding downward pressure at the end of the movement. 

The leg should be extended and relaxed. Patellar clonus may appear when eliciting the patellar or suprapatellar reflex.

2) Wrist Clonus :
It is produced by a sudden passive extension of the wrist or fingers.

3) Jaw Clonus occurs occasionally.

So that's all about clonus.
Hope it was helpful!

Let's learn Together!
-Medha!

Alternate methods of Eliciting Toe Dorsiflexion in Corticospinal tract lesions.

Hello!

Let's review few minor signs of eliciting toe dorsiflexion when we are suspecting  a Corticospinal tract lesion.

Gordon’s sign :
Squeezing of calf muscles.

Schaefer’s sign :
Deep pressure on Achilles tendon.

Bing’s sign :
Pricking dorsum of foot with a pin.

Moniz’ sign :
Forceful passive plantar flexion at ankle.

Throckmorton’s sign :
Percussing over dorsal aspect of metatarsophalangeal joint of great toe just medial to Extensor Hallucis Longus tendon.

Marie Foix sign :
Squeezing the toes or strongly plantar   flexing toes or foot.

Gonda (Allen) :
Forceful downward stretching or snapping of second, third, or fourth toe; if response is difficult to obtain, flex toe slowly, press on nail, twist the toe, and hold it for a few seconds.

Stransky :
Small toe forcibly abducted, then released.

Allen and Cleckley :
Sharp upward flick of second toe or pressure applied to ball of toe.

Strümpell’s  phenomenon :
Forceful pressure over anterior tibial region.

Cornell response :
Scratching dorsum of foot along inner side of Extensor Hallucis Longus tendon.

All the above signs may not be always seen and sometimes these may be the Only signs present and hence it is necessary for us as students to screen as many patients as we can and increase our understanding and clinical acumen, cause the eyes can't see what the brain doesn't know.

Let's learn Together!
-Medha.

Tetralogy of fallot mnemonic

Hello!

Here is a short note on tetralogy of fallot. Tetralogy of fallot is a congenital disorder of heart. It shows four signs, as indicated in it's name (tetra).

Mnemonic for it is - PRVO virus ( parvo virus )

1. Pulmonary stenosis
2. Right ventricular hypertrophy
3. Ventricular septal defect
4. Overriding of aorta.

That's all :)

H@Mid.

Ano-Rectal anatomy: Above and below pectinate line

Here's an illustration I made :)

It shows the embryology, pathology, innervation, blood supply, venous drainage and lymphatic drainage on the rectum above and below pectinate line.

Examination of Subtle Hemiparesis - Barré's Sign.

Hello everybody!

So today let's learn about examination of subtle hemiparesis, a very important inspectory finding.

Sometimes patients with mild CST (Corticospinal Tract) lesions may have normal strength to routine testing, but the deficit may be brought out using ancillary maneuvers like the examination for pronator drift (Barré’s sign).

With the patient’s upper extremities outstretched to front, palms up and with the eyes closed, we have to observe the position of hands.
Normally patient should hold this position for at least 20 to 30 seconds and the palms will remain straight with the elbows straight, and the limbs horizontal.

Any deviation from this position should be similar on the two sides.

(One exception to the usual symmetry is that the dominant hand occasionally may pronate slightly more than the nondominant, perhaps because the nondominant extremities tend to be more flexible than the dominant extremities, making it more difficult to stretch the dominant hand to a horizontal position.)

However, greater pronation of the nondominant arm is sometimes an indication of subtle hemiparesis.

Three types of drifts may occur when the patient attempts to hold the arms outstretched with eyes closed: pyramidal drift, parietal drift, and cerebellar drift. In pronator drift (Barré’s sign) due to a pyramidal lesion, the arm sinks downward and there is accompanying pronation of the forearm.

In parietal drift, the arm usually rises and strays outward (updrift).  

With cerebellar drift, the arm drifts mainly outward, either at the same level, rising, or less often sinking.

The patient with a mild CST deficit may demonstrate “pronator drift” to varying degrees.

Mild drift : there is slight pronation of the hand and slight flexion of the elbow on the abnormal side. 

Severe drift : there is more prominent pronation and obvious flexion of the elbow, and there may be downward drift of the entire arm.

Mechanism: Because of the innervation pattern of the CST, the minimally weak CST innervated muscles are overcome by the non-CST muscles.

With a mild CST lesion, the minimally weak muscles in the upper extremity are the extensors, supinators, and abductors.  These are overcome by the uninvolved and therefore stronger muscles: the pronators, biceps, and internal rotators of the shoulder. As these overcome the slightly weakened CST innervated muscles, the hand pronates, the elbow  flexes, and the arm drifts downward.

The tendency to pronation and flexion in mild hemiparesis has also been attributed to subtle hypertonicity in the pronator and flexor muscle groups.

Imagine what would occur if this motion continued to the extreme: the hand would become hyperpronated, the elbow fully exed, and the shoulder internally rotated, that is, the position of spastic hemiparesis.

The abnormal upper limb positions in minimal pronator drift and in severe spastic hemiparesis are due to the same underlying phenomenon: strong non-CST muscles overcome variably weak CST muscles involved by the disease process.

The examination for pronator drift is a very important part of the neurologic examination. If only one motor test could be done on a patient, the best single test to use would probably be examining for drift.

Hope this was informative!
Let's learn Together!
-Medha.

Glargine insulin mnemonic

Mini post!

Pathophysiology of anorexia in chronic kidney disease

Normal appetite regulation: Appetite regulation involves the gastrointestinal tract (ghrelin as an appetite stimulant, and cholecystokinin, glucagon-like peptide-1, and neuropeptide YY as appetite inhibitors); the adipose tissue with leptin, a potent appetite inhibitor; the vagal system; and the brain, which integrates the stimuli in the hypothalamus area. Satiety relies on the melanocortin receptors with serotonin as the main neurotransmitter and is challenged with hunger peptides, namely, neuropeptide Y and agouti-related peptide.

What happens in CKD?

Pharmacotherapy for PTSD in pregnancy mnemonic

The two FDA approved drugs for PTSD are: Paroxetine and Sertaline.

Fact of the day: Valbenazine for treatment of tardive dyskinesia

Here's a cool fact: Valbenazine is a highly selective vesicular monoamine transporter 2 (VMAT2) inhibitor. It modulates dopamine release during nerve communication.

CMS psychiatry form 4 question on tardive dyskinesia

Disclaimer: This is an CMS neurology form 2 question for step 2 CK. If you are planning to take USMLE step 2 CK in the future, I would recommend that you DO NOT read this post because it will bias your assessments.

Tetrology of Fallot Causes : Mnemonic and discussion

Hello everyone !

Tetrology of Fallot refers to the tetrad of features occuring in the heart -

1. Ventricular septal defect
2. Pulmonary stenosis
3. Right Ventricular Hypertrophy
4. Overriding aorta.

Now. The factors associated with this disease include a decent bit of things.  And while I was revising I remembered I didn't remember them at all. :) :) :) :) :)

-_-

So here's a mnemonic.
CATCH NATE

CATCH = CATCH 22 Syndrome
(DiGeorge Syndrome is represented by CATCH 22 popularly).

N - NOTCH 1 Gene mutations.
A - Alagille syndrome - Associated with a very peculiar set of features - Bile duct hypoplasia. So random .
T - Trisomies 13,18,21
E - Et cetera = Maternal Diabetes , Maternal progesterone , Drugs like Retinoic acid.

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

Step 2 CK: Manometric findings of achalasia and scleroderma

In achalasia:
Basal LES pressure - Increases / decreases?
Peristalsis - Increases / decreases?

In scleroderma:
Basal LES pressure - Increases / decreases?
Peristalsis - Increases / decreases?

This is high yield for CK!

Cauda equina syndrome

Hello!

What is cauda equina syndrome (CES)?
The cauda equina syndrome is caused by an intraspinal lesion caudal to the conus that injures two or more of the 18 nerve roots constituting the cauda equina within the lumbar spinal canal.

Cauda equina syndrome causes

Non lactose fermenters mnemonic

Shigella, Salmonella, Proteus, Yersinia - Motile or non motile? produces H2S or not?

Step 2 CK: Oral contraceptive pills and cancer

Hello!
Back with a mini post!

Wifi-allergy !

Now,being teenager we all know how much we are addicted to word "Wi-fi" or let's say  "Free Wi-fi".But today I came to know about a weird disorder "Wifi-allergy" .

Electromagnetic hypersensitivity is popularly known as "Wifi-allergy".
Adverse reaction to electromagnetic field is seen even if a victim is exposed to EM field below threshold level .
There are no scientific basis for Wi-fi allergy .

No scientific signs and symptoms are specified,but non-specific symptoms such as headache,fatigue,stress,sleep distractions,skin prickling,burning sensation,rashes pain,and acne in muscles,ringing in the ear,tinnitus,unexpected earache,memory loss,inability to concentrate,nausea,insomnia,fluctuation in heart rate,deteriorating vision,weakness and spasm of muscles,
bladder problems can develop.

Many of these symptoms overlaps with other syndromes such as Idiopathic Environmental Intolerance(IEI)

Cause:

No relation is found between exposure of electromagnetic field and symptoms.Studies shows it is a psychological disorder rather than a physiological .Many scientists claims that it is actually a nacebo effect.

Diagnosis:

Electromagnetic hypersensitivity is not an accepted diagnosis.No case definition /clinical practice guidelines are performed.No specific tests are performed.A French scientist Dr Belpomme has developed a technique using a computer and a Pulsed Eco-doppler which envelops diagnosis of electrical sensitivity.

Treatment:

There are no specific protocols for treatment of this psychological disorder.The basic treatment involes less use of devices which emits electromagnetic fields.

Stay awesome and cool:)
 
~Ojas

Lesions of the Central Nervous System.

Hello everybody!

So today we'll review a series of lesions and their presentation starting from the cortex till the spinal cord.

Will try and include as many lesions as I can without making it redundant or boring.

To start with.

1)Disorders of the Meninges and Ventricular System.

Many conditions can affect the meninges, like infections, neoplasia, sarcoidosis.The most common being infections.

Some meningeal infections may be extremely indolent and lack the classical signs associated with infection.
Chronic meningitis can also present as dementia or AMS.
Abnormalities of the ventricular system can occur due to congenital anomalies, such as aqueductal stenosis leading to dilatation of the ventricular system and may cause increased head circumference in children.
In adults, acquired conditions, such as normal pressure hydrocephalus usually present with evidence of increased intracranial pressure or with dementia, AMS, gait problems,difficulty with bladder control. The classic triad of Normal pressure hydrocephalus is - WET WHACKY WOBBLY.

2)Cerebral Hemisphere Disorders. Characteristic of unilateral hemispheric pathology is a “hemi” deficit.
Hemisensory loss,
Hemiparesis,
Hemianopsia,
Hemiseizures.

Other manifestations are hyperreflexia and pathologic reflexes.

Disease affecting the cerebral cortex behave differently from disease of subcortical structures.

Cortical involvement:
Aphasia,
Apraxia,
Astereognosis,
Impaired two-point discrimination, Memory loss,
Cognitive defects,
Focal seizures, or other abnormalities that reflect integrative role of the cortex.

Dominant hemisphere involvement:
Language dysfunction in the form of aphasia, alexia, or agraphia. 

Non dominant hemisphere involvement:
Higher cortical function disturbances involving functions other than language, such as apraxia.

Subcortical structures :
The clinical picture includes the hemidistribution of dysfunction but lacks those elements that are typically cortical (e.g., language disturbance, apraxia, seizures, dementia).

Certain processes involve wide areas of the cerebrum, causing diffuse dysfunction.

3) Basal Ganglia Disorders:
Diseases of the basal ganglia cause movement disorders such as Parkinson’s disease (PD) or Huntington's Disease. Movement disorders may be hypokinetic or hyperkinetic, referring to whether movement is in general decreased or increased.
PD causes bradykinesia and rigidity. Huntington’s disease, in contrast, causes increased movements, which are involuntary and beyond the patient’s control (chorea).  Tremor is a frequent accompaniment of basal ganglia disease.

4)Brainstem Disease: (So I have a  separate blog on these do check them out,where I have enlisted individual syndromes.)

The classic distinguishing feature of brainstem pathology is that deficits are “crossed,” with cranial nerve dysfunction on one side and a motor or sensory deficit on the opposite side.

There are often symptoms reflecting  dysfunction of other posterior fossa structures, such as vertigo, ataxia, dysphagia, nausea - vomiting, and abnormal eye movements.

Unless the process has impaired the reticular activating system, patients are normal, mentally awake, alert, able to converse (though perhaps dysarthric), not confused, and not aphasic. 

DeepTendon Reflexes are usually hyperactive with accompanying pathologic reflexes in the involved extremities; pain is rare untill Thalamus is involved and sphincter dysfunction occurs only if there is bilateral involvement.

5) Cranial Neuropathy Disease :
Selectively involve one, or more than one, cranial nerve.
The long tract abnormalities, vertigo, ataxia, and similar symptoms and findings that are otherwise characteristic of intrinsic brainstem disease are lacking.

Common cranial neuropathies include Optic neuropathy due to MS,
Third nerve palsy due to aneurysm
Bell’s palsy.
Involvement of more than one nerve occurs in conditions such as Lyme disease, sarcoidosis, and lesions involving the cavernous sinus

6)Cerebellar Disease:
Leads to combinations of tremor, incoordination, difficulty walking, dysarthria, and nystagmus, depending on the parts of the cerebellum involved. 

There is no weakness, sensory loss, pain, hyperreflexia, pathologic reflexes, sphincter dyscontrol, or abnormalities of higher cortical function.

Cerebellar abnormalities resulting​ from dysfunction of the cerebellar connections in the brainstem, usually are accompanied by other brainstem signs.

7)Spinal cord disorders:
Produce characteristic patterns of clinical abnormalities, with motor and sensory deficits in a certain distribution.

In addition to weakness below the level of the lesion, patients with spinal cord lesions also have paresthesias, numbness, tingling, and sensory loss with a discrete sensory level, usually on the trunk.

The pattern of weakness is typically more localizing than sensory abnormalities in lesions of the cervical spinal cord, while demonstration of a sensory level on the trunk is more helpful in localizing lesions of the thoracic cord.

Some important findings depicting the syndromes are :

Dorsal cord syndrome : Loss of position and vibratory sensation in the feet with preserved ankle jerks.

Central cord Syndrome (syringomyelia) :
Bilateral segmental sensory loss (i.e., sensory loss in the hands and forearms), not in a peripheral nerve distribution, with normal sensation in the legs and trunk and in the upper arms and neck.

Thoracic Cord Syndrome : Bilateral loss of position and vibratory sensation in the feet with a definite level of pinprick loss on the abdomen or chest.

Brown-Séquard syndrome : Loss of pinprick sensation on one side of the body with loss of position and vibration sensation on the other.

Intramedullary lesion or anterior extramedullary compression :
Loss of pinprick sensation over the legs and trunk with normal sensation in the perianal area.

Conus medullaris or L5–S1 cauda  equina lesion:
Loss of pinprick sensation in the perianal area and in the upper part of both posterior thighs.

Anterior Cord Syndrome :
Loss of pinprick sensation on the legs and trunk with normal position and vibration sense in the toes and fingers.

Phew😅 that was alot.
I hope this was helpful.
If you have any doubts or you need a detailed explanation of some part, do let me know.

Let's learn Together!
-Medha.

Authors diary: Have fun while studying

If you are not having fun while studying, you are doing it wrong.

I crack really lame jokes. It keeps me sane :P

Low Weight in Cerebral Palsy : Possibilities

Hi everyone ! Here's a short post on Causes of Weight loss or Poor gain of weight in Cerebral palsy (CP) patients.

1. Feeding problems due to motor deficit -
- Patients with CP have poor feeding due to problems with sucking and swallowing. - They may have  palato-pharyngeal incoordination due to the UMN lesions - especially if there's an accompanying Bulbar or Pseudobulbar palsy.
-So there's impaired oral motor control.
- Repeated aspirations may be present.

2. GERD -
- Gastro esophageal reflux is a common co-morbidity with CP.
- This can be very bothersome for the baby and reduces appetite and may even cause repeated vomiting.

3. Reliance on Care taker -
- The child cannot use his own hands to feed a lot of times.
- This causes excess reliance on the caretaker.
- The caretaker may underfeed the baby weary of the aspirations and Dysphagia of the baby.

4. Poor hygiene -
- Poor hygiene practices are more likely to cause infections (Feco-oral ).
- This is more likely to cause undernutrition due to the infective agents.

Hope this felt clinically relevant and helpful to you !
Stay awesome !

~A.P.Burkholderia

Syndromes associated with Ventricular Septal Defect : Mnemonic

Here's a short post.
So a fair bit of genetic mutations are associated with VSD's.

Remember :
ACED 2
(As in You ACED your exam ! )

A- Apert Syndrome
Features are mainly Cranio-digital. Causes Craniosynostosis, Syndactyly and mandibulo-facial deformities.

C- Cri du chat Syndrome
Notorious for the kitten like cry.
Other features are hyperagrresivenes, skin tags in front of eyes , microcephaly and wide eyes.

E - Edwards Syndrome
Trisomy 18. Other features - Omphalocele , esophageal atresia, low set ears, Microcephaly, Ptosis and Rocker bottom feet , Hypertelorism. Also associated with ASDs.

D - DiGeorge Syndrome
CATCH 22
C - CHD
A - Abnormal facies
T - thymic aplasia
C - Cleft palate
H - Hypocalcemia
22 - Chr 22 abnormality.

D - Down Syndrome
(You all know about that one !)

That's all!
Hope this helped.
Happy Studying and like always , Stay awesome !

~ A.P.Burkholderia

Medicowesome secret project : Lets talk about 'adjustments'

“Hello, I'm sure you would relate to me,
You will understand how I feel,
Because you might have felt it for a few moments like I feel most of the time.”

I was diagnosed with clinical depression a year back. Although the labeling never led to any improvement but it made me understand that I have a medical problem and I need help. Being from a smaller city, where everyone knew each other, where life moved at its own pace and where things were easier to understand, moving to Delhi away from my family proved stressful for me. The constant pressure to fit in, to dress, talk, sit in a particular manner and being ridiculed for being little different only made things worse. There would be days in row when I wouldn't feel like getting up, the day would stretch far too long and I wouldn't understand what exactly was I going through. I would stay awake till 4am crying with feeling of helplessness. From being the topper of my school I became one of the lowest scorers of my class.  Nothing would seem to motivate me to keep going because I had already given up. Fortunately, two failed suicide attempts made me feel like seeking for help. My treatment is ongoing. People close to me understand that it's something which I wasn't in control of. Depression is something which can break you into innumerable pieces, loosen your ability to look at positivity and get up to fight back with zeal. I hope you understand. - maybe this is what someone with depression goes through (I guess). So will you help them stay strong? :)

You, out of all these people have the capacity to love yourself the most, trust yourself the most and build yourself stronger with each passing day. Then why be worried if someone doesn't love you back or breaks your trust? It's you who is important. It's your life, you make your own decisions. Let no one ever tell you your worth or take away your happiness. You deserve all of the good things like everyone else.  You is important. Yes, you are :)

Thanks Purnima Bhatia for sharing this story ( a part of it is hers, rest is fiction ) with us and spread awareness on the matter. :)

Ewing's Sarcoma- A review.

Hello everybody!

Let's review a few important points on Ewing's sarcoma.

Ewing sarcoma is one of the small, round cell lesions of bone

Second most common malignant bone tumor in children (after osteosarcoma)
Common in males than females.

Occurs between the ages of 5-30 years.

 Location:

Arise in medullary cavity, usually of long bones in the lower extremities. Commonly involves metadiaphysis of long bones.

Most commonly occurs in long bones and pelvis but they can occur in virtually any bone.

Clinical Findings:

Most common symptoms are localized pain and swelling.

Additional symptoms:

Fever

Weight loss

Anemia

Leukocytosis

Elevated erythrocyte sedimentation rate 

Imaging Findings:

Most lesions are visible on conventional radiographs

However, their degree of spread is better evaluated with MRI

Common manifestations on conventional radiography include

1)Poorly marginated, lytic, destructive lesion

2)Permeative (small holes) or moth-eaten (mottled) appearance

3)Rarely, they can be sclerotic,Soft tissue mass or infiltration is common

4)Soft tissue mass may occur without destruction of cortex.Soft tissue mass may produce saucerization (scalloped depression in cortex)

5)Periosteal reaction is common

6)Lamellated - onion-skinning due to successive layers of periosteal development

7)Sunburst or spiculated - hair-on-end appearance when new bone is laid down perpendicular to cortex along Sharpey’s fibers.

8)Codman’s triangle - formed between elevated periosteum with central destruction of cortex

9)Osteosclerosis may be present secondary to reactive bone formation

Prognosis:60-75% five-year survival.

Treatment:Systemic chemotherapy is the mainstay of treatment with surgery and/or radiotherapy playing a role depending of the location and size of the tumour.

Hope this was useful.

Let's Learn Together!

-Medha.