Pathophysiology: Multiple Sclerosis

Hey guys, let’s look at the fundamentals of multiple sclerosis.

Multiple sclerosis is an autoimmune disease of the CNS characterised by

- chronic inflammation

- demyelination

- reactive gliosis/ scarring

- neuronal loss

with a course that is relapsing-remitting or progressive

and lesions that are disseminated in time and space.

Here’s how it happens:

[Please click on the image to enhance it]

- Ashish Singh

Step 2 CS: Neurology Case mnemonic

The following mnemonic (HDFC ST) helps me cover all bases in a Neurology case.

Types of Sphenoid Sinues.

Hello Guy's!

Here's a sneak peek into the world of Neurosurgery!

In cases of Pituitary Adenomas, the general surgical approach is a TransNasal TransSphenoidal Approach for the excision of the lesion.

To know the type of sphenoid sinus is an important step in the pre-operative planning for the surgery. It also helps in estimating the site where we are most likely to encounter the tumor and the pituitary gland.

Hamburger classified 3 types of pneumatization based on its relationship to the sella turcica.

1)Conchal (rudimentary or absent sphenoid sinus)

2)Presellar (a posterior sphenoid sinus wall that is separated from sella by thick bone).

3)Sellar (a posterior sphenoid sinus wall that is adjacent to sella).

That's all for now... Time to Scrub.

Let's learn Together!

~Medha Vyas.

POTS Syndrome

●The postural tachycardia syndrome (POTS) is defined as a form of orthostatic intolerance characterized by an excessive increase in heart rate that occurs on standing without arterial hypotension.

●The etiology of POTS is not clear, but the disorder may be heterogeneous. Abnormalities in autonomic regulation that may either be genetic or acquired are described. Proposed mechanisms include partial sympathetic denervation leading to discordant cardiac and vascular sympathetic control, hypovolemia and impairment of the renin-angiotensin-aldosterone system, venous abnormalities and baroreflex dysfunction.

●The clinical symptoms of POTS are varied and nonspecific, and include dizziness, lightheadedness, weakness, blurred vision, and fatigue upon standing. The orthostatic nature of the symptoms is the primary clue to the diagnosis.

●The diagnosis of POTS is established from the history and head-up tilt testing which demonstrates a heart rate increase of >30 bpm over baseline or to >120 bpm. Dehydration, prolonged bedrest, medications, and other dysautonomias should be excluded as etiologies.

●The optimal therapy of POTS is not established. Patients should avoid precipitating factors, and physical activity should be encouraged. We suggest volume repletion and fludrocortisone (0.05 to 0.2 mg per day) as the first line of therapy . Some patients may benefit from midodrine or beta blocking agents. Other therapies remain under investigation, and further confirmation of benefit is needed before they can be recommended.

Bhopalwala. H

Simpson's Grading for Brain Tumors.

Hello Everyone!

So my Neurosurgery residency diaries continue and I continue sharing as I learn.

Learnt about the Grades of Tumor resection while operating on a Glioma.

These are Simpsons Grades of Tumor resection and are correlated as the degree of surgical resection completeness with with symptomatic recurrence. 

Grade I-complete removal including resection of underlying bone and associated dura.

9% symptomatic recurrence at 10 years

Grade II-complete removal and coagulation of dural attachment.

19% symptomatic recurrence at 10 years

Grade III-complete removal without resection of dura or coagulation.

29% symptomatic recurrence at 10 years

Grade IV-subtotal resection of the tumor.

44% symptomatic recurrence at 10 years

Grade V-simple decompression with or without biopsy

100% symptomatic recurrence at 10 years.

That was it!

Let's Learn Together!

-Medha Vyas 

Horner Syndrome

Horner syndrome is a classic neurologic syndrome whose signs include miosis, ptosis, and anhidrosis.

NEUROANATOMY - Horner syndrome can result from a lesion anywhere along a three-neuron sympathetic pathway that originates in the hypothalamus:
●The first-order neuron descends caudally from the hypothalamus to the first synapse, which is located in the cervical spinal cord (levels C8-T2, also called ciliospinal center of Budge).

●The second-order neuron travels from the sympathetic trunk over the lung apex. It then ascends to the superior cervical ganglion, located near the bifurcation of the common carotid artery.

●The third-order neuron from superior cervical ganglia then ascends within the adventitia of the internal carotid artery, through the cavernous sinus. In the orbit and the eye, the oculosympathetic fibers innervate the iris dilator muscle as well as Müller's muscle, a small smooth muscle in the eyelids responsible for a minor portion of the upper lid elevation and lower lid retraction.

First-order syndrome - Lesions of the sympathetic tracts in the brainstem or cervicothoracic spinal cord can produce a first-order Horner syndrome.
The most common causes are:
(a)occlusion of PICA, which produces Horner syndrome as part of the Wallenberg syndrome.
(b)Brown-Séquard syndrome above T1, patient may present with ipsilateral Horner syndrome due to damage of oculosympathetic pathway.

Second-order syndrome — Second-order or preganglionic Horner syndromes can occur with trauma or surgery involving the spinal cord, thoracic outlet, or lung apex.Other causes include pancoast tumor involving the lung apex.

Third-order syndrome — Third-order Horner syndromes often indicate lesions of the internal carotid artery such as an arterial dissection, thrombosis, or cavernous sinus aneurysm

CLINICAL FEATURES -The classic signs of a Horner syndrome are ptosis, miosis, and anhidrosis.
1)The ptosis occurs as a result of paralysis of the Müller's muscle.
2)The degree of anisocoria is more marked in the dark than in light.
3)Anhidrosis is present in central or preganglionic (first- or second-order) lesions because the sympathetic fibers responsible for facial sweating branch off at the superior cervical ganglion along the external carotid artery and its branches.
4)Horner syndrome is also a common feature of cluster headache.

SOURCE-UpToDate, Kaplan.

-Srikar Sama.

True or False #6

1. Nightmare is a REM sleep behavior disorder. T or F

2. Night Terror is a REM sleep behavior disorder. T or F

ANSWERS

1. True

Things you should REMember for Nightmare disorder are :

REM

Second half of the night

Responsive to comfort

REMembers the dream

2. False

Night terrors:  Abrupt arousals from sleep (panicked scream, terror, autonomic arousal, unresponsive to comfort)

- Little or no dream recall

- Amnesia for episodes

Sleep is a gift, always be grateful for it.

True or False #5

1. Narcolepsy exhibits a reduced REM latency. T or F

ANSWER

1. True

Narcolepsy: depletion of hypocretin secreting neurons in lateral hypothalamus that are involved in maintaining wakefulness

Diagnostic: recurrent lapses into sleep or napping several times in the same day, >3 times a week for >3mo. and at least 1 of the following
-Cataplexy: Conscious of bilateral loss of muscle tone precipitated by emotions or abnormal facial movement (without emotional triggers)

-Hypocretin - 1 (orexin A) deficiency in CSF

- REM sleep latency <15 minutes

Tetrad:
-Sleep attacks

-Cataplexy

-Hypnagogic or hypnopompic hallucinations

-Sleep paralysis

Dx: Shortened REM sleep latency on polysomnografy
Low levels of hypocretin 1 in CSF

You may feel weak, you may fall down, say no to Cataplexy, say yes to CATA GETUP!!

True or False #1

1. Vareniciline increases the risk of suicide and depression. T or F

2. Vareniciline increases the risk of CVS events. T or F

ACHOO SYNDROME.

HELLO PEOPLEEEE!

Well this is not a medical joke or something that I made up. This syndrome is legit and very irritatting for the people who suffer from it. As said by Pryse Phillips the acronym is slightly forced but remains the best of the decade.

The acronym ACHOO is for Autosomal Dominant Compelling Helio-Opthalmic Outburst reflex which is basically sneezing in response to looking at a bright light, there can be a burst of 2-10 sneezes at a time.

Photic sneeze reflexes don't seem to make any sense at first. The purpose of sneezing is to clear unwanted irritants or germs from the nose. Bright light produces neither.

The phenomenon was first described in the 1950s, after a French doctor discovered several patients sneezing in response to the light of his ophthalmoscope, (the device doctors use to examine the retina). Further investigation revealed that it wasn't just any light that brought on the sneezing, but sudden flashes. These patients would reliably sneeze when quickly exposed sunlight, flash photography, and, in a few cases, even ultraviolet light.

There is no clear understanding on how photic sneez reflex works and hence a variety of theories have been proposed. 

For us its important to understand the basics of a normal sneez reflex arc.

The opthalmic division of the trigeminal nerve innervates the the nasal mucosa over the nasal septum and the anterior nasal passages. The afferent limb of the reflex arc is carried over the opthalmic nerve and the efferent limb is by the cranial nerves 5 and 7,9,10 and the motor nerves of the cervical and thoracic spinal cord.

The reflex centre is situated in the brainstem and upper spinal cord.

Any stimulation of the afferent limb of this reflex arc by dust or any foreign material sets the reflex arc in action which ultimately makes us sneez!

The primary clinical use of this sneez (sternutatory) reflex is a cross check on the corneal reflex.

Are there any other weird stimuli that cause people to involuntarily sneeze?

• Sneezing induced by feeling full. (One case study of a relatively normal 32-year-old man found that "fullness of the stomach immediately after meals invariably results in three or four uncontrollable sneezes."

• And the weirdest: For some, eating chocolate can induce some unwanted sneezes how barbaric.

Well I hope this information was helpful. So the next time you hear some sneezing (ACHOO!) do remember this phenomenon.

Let's Learn Together.
-Medha Vyas.
x

Significance of ictal head turning in frontal and temporal lobe seizure

Hello Awesomites!

Let us begin.

My patient had an episode of seizure. As she was not aware during the episode I asked the one who saw her during the episode. She had head turning to one side.

The patient had other complain also but for time being I am focusing on this sign.

When you begin from symptoms to localization and then lateralization, you will get following answers.

Non versive head turning - Ipsilateral temporal lobe.

Forced (versive) head turning - Contralateral Frontal lobe.

I want to thank my professor.

I hope it will help you to be more observant during history taking.

-Upasana Y. :)

Cincinnati pre-hospital stroke scale

Hey Awesomites

Cincinnati Pre - Hospital Stroke scale is one of the most common scale to detect stroke early on. Remember the mnemonic - FAST

Adverse reactions of Digitalis mnemonic

Hey guys
I am back :D

My first blog post of the year - Adverse effects of Digitalis ( Digitalis toxicity ) mnemonics

Though the ADRs are divided into extra-cardiac and cardiac symptoms, I will present a more systematic mnemonification ;p

Management of Stroke

Hello, seeker of knowledge! Let’s see how we manage one the most common emergencies in medicine, stroke or cerebrovascular accident.


PRE-HOSPITAL CARE:

Cincinnati Pre-Hospital Stroke Scale (CPSS) helps make a prompt diagnosis and includes FAST -

Face drooping

Arm weakness

Speech difficulty

Time to call Emergency Medical Services

HOSPITAL CARE:

TIA = Transient Ischemic Attack
ABC = Airway, Breathing and Circulation
BGL = Blood Glucose Level; Both HYPO- and HYPER- glycemia are to be corrected
Hhg = Hemorrhage
Lytes=Electrolytes; ABG =Arterial Blood Gas; RFT=Renal Function Test; LFT=Liver Function Test
rTPA = recombinant tissue plasminogen activator
ASA = Acetyl Salicylic Acid = Aspirin
UFH = Unfractionated Heparin;  LMWH = Low Molecular Weight Heparin

ADDITIONAL INVESTIGATIONS MAY BE DONE - PROVIDED THROMBOLYSIS, IF INDICATED PER CT - IS NOT DELAYED


TREATMENT PRINCIPLES:

To minimize:
Ischemic penumbra (area around umbra/ ischemia)
Secondary brain injury
Risk of recurrence


THROMBOLYSIS:

INDICATIONS -

Mnemonic: ADD 1/3rd to CT after consent

Age 18 years or more
Diagnosis of Acute Ischemic Stroke(AIS)
Duration of symptoms 4.5 hours or less
AIS involves more than 1/3rd MCA territory
CT reveals no hemorrhage or edema
Consent of the patient or surrogate decision maker

CONTRAINDICATIONS -

Mnemonic: SHIP BLAST

Stroke in the last 3 months
Head injury in last 3 months
Intracranial hemorrhage
Prothrombin Time > 15 sec
BP > 185/110
Lumbar puncture in last 7 days
Anticoagulants use / Arterial puncture in last 7 days
Surgery within last 14 days
Thrombocytopenia < 100,000

PRECAUTIONS:
No anti-thrombotics for 24 hours
No Foley’s catheter for 2 hours

ADVERSE DRUG REACTIONS:
Intra-cranial hemorrhage
Allergy


ANTI-COAGULANTS:

INDICATIONS:

Mnemonic: My L.A.P.D. job

Recent MI
Left ventricle aneurysm or dyskinesia
Atrial fibrillation
Prosthetic heart valve
Deep vein thrombosis prophylaxis


MEDICINE PEARL: MI and stroke have essentially the same pathophysiology. Clots blocking arteries! However, we give DUAL anti-platelet therapy [DAPT], i.e. Aspirin and Clopidogrel for MI while there’s only Aspirin administered to a patient with stroke.


NURSING CARE:
Bowel and bladder care
Prevention and treatment of bed sores

REHABILITATION:
Use of walkers and crutches
Full range of active and passive joint movements


FURTHER READING:
Other rehabilitative therapies offered
Risk factors and preventive strategies
Alternative drugs and procedures


Hope this helps. Happy studying!
-- Ashish Singh.

Introduction to neuroanatomy

This video was made by our Medicowesome Student Guest Author, Salman!!!!

Stroke Series: Cortical lobar functions

This is a basic post on our stroke series -
CORTICAL LOBAR FUNCTIONS.

1. Frontal lobe:
Okay guys, for frontal lobe, I think of an average guy (not the musician, not the good looking) trying to get a relationship - well, that's were you need your frontal lobe for.

• Personality - definitely, it's one of the prime qualities an average guy should have.

• Flirting skills - Social behaviour and language.

• Emotional control - you have to have good emotional control even if you fail at it multiple times.

• Other functions are Motor and Micturition.

2. Parietal lobe:
It has dominant as well as a non dominant side. For the dominant side, think of a calculator and for the non dominant side think of playing Tetris video game.

• Dominant side - Calculation and language.

• Non dominant side - Spatial orientation and constructional skills  (Tetris game).

3. Temporal lobe:
For the temporal lobe, it has both dominant as well as non dominant side. For this, you have to think of the position of temporal lobe near your temples, near which you have your ears, mouth and nose and for the non dominant side it's the musicians area.

• Dominant side - Auditory perception and balance, Smell, Verbal memory, Language.

• Non dominant side - Melody, Pitch, Non verbal memory (musicians remember music, not words, it's a weird way to remember!)

4. Occipital lobe:
O looks like an Eye to me O_o for vision.

    • Visual processing

That's all!

This is a basic post. I'll come up with a detailed one soon. Enjoy studying!

The Stroke Series is written by our Medicowesome Student Guest Author, Nikhil. More to come soon!

Urinary Bladder and Clinical Correlates

Hello everyone! This write-up attempts to organize the seemingly confusing nerve supply of the bladder and associated pathology aka the neurogenic bladder.

NERVE SUPPLY :

(beta 2 and alpha 1 are adrenergic receptors of SANS ; muscarinic type 3 is a cholinergic receptor of PANS)

• SANS inhibits micturition while PANS facilitates micturition. You don’t want to pee when you’re running a 100m sprint, an SANS-dominant activity but you can comfortably pee at rest, a PANS-dominant activity.

• Sensory fibres of pudendal nerve tell your CNS when the bladder is full. The motor fibres of pudendal nerve maintain EUS tonic contraction by default so that you’re not always peeing.

• The reflex arc, after higher centre commands, causes voluntary micturition by inhibiting the “contraction-effect” of motor fibres of pudendal nerve.

•  To oversimplify matter (so that it’s easy to understand and remember): Level 2 control inhibits reflex arc. Level 3 control facilitates reflex arc, causing micturition at will, once the bladder is full.

CLINICAL CORRELATES:

• CORTICAL BLADDER

-- Aka Incomplete Spastic OR Uninhibited bladder.

LESION	CLINICAL  FEATURE
Postcentral cortex	--  Loss of awareness of bladder fullness          --  Incontinence
Precentral cortex	--  Hesitancy = Difficulty in initiating micturition
Frontal cortex	--  Precipitancy = micturition with ‘easy’ stimulus, eg: sound of running water          -- Inappropriate micturition/ loss of social inhibition (infant-like)

Associated with:

Multiple Sclerosis

Parkinson’s disease

Stroke, among others.

• HYPERTONIC/ AUTOMATIC  BLADDER

-- UMNL/ Complete spastic type of bladder.

LESION	CLINICAL  FEATURE
Spinal cord ABOVE S2, S3 and S4.	--  Urge incontinence = patient passes low-volume urine frequently         --  Less post-voidal urine volume, so less risk of UTIs         --   More intra-vesical pressure, more risk reflux nephropathy

• HYPOTONIC/ AUTONOMOUS BLADDER

-- LMNL/ Flaccid type of bladder.

LESION	CLINICAL FEATURE
--  Spinal cord AT S2, S3, S4         --  Cauda equina/ Conus medullaris         --   Peripheral nerves	--  Overflow incontinence =  urine retention, overtime, forces IUS to mechanically open causing dribbling micturition         --  More post-voidal urine volume, more risk UTIs

2 subtypes are:

• Motor Paralytic bladder – Motor (efferent) pathway is damaged. However, patient can sense bladder fullness, resulting in prompt diagnosis. Associated with:

--  Complication of abdominal/ pelvic surgery

--  Lumbar canal stenosis

--  Lumbo-sacral meningo-myelocele

• Sensory Paralytic bladder – Sensory (afferent) pathway is damaged and hence, patient canNOT sense bladder fullness, resulting in delayed diagnosis. Associated with:

--  Diabetes mellitus

--  Syringomyelia

--  Tabes dorsalis

Medicine pearl: When we talk about bladder pathology, we only refer to PANS (lesions above/ at/ below it) as SANS lesions doNOT cause bladder pathology per se. However, bilateral lesion to L1 causes retrograde ejaculation and hence, infertility.

Topics for further reading:

--  Age-related urine continence

--  Nocturnal enuresis

--  Barrington reflexes

Hope this helps! Let me know if anything needs clarification. Happy studying!

-- Ashish Singh.

Hemiplegia Evaluation : Case-related Clinical Pearls

Here's a couple of special pointers for a CNS Case with the Viva Questions asked commonly !

General Examination (In addition to what you would routinely mention)

- GCS / MMSE depending on status of the patient

- Regular Temperature, Pulse , Respiratory Rate and Blood Pressure.

(Pulse could have irregularly irregular rhythm which indicates Atrial Fibrillation. Very strong Etiological clue)

(Blood pressure is super important : to be brought down rapidly if Hemorrhagic suspected and to be brought down below 185/110 of planning to Thrombolyse.
Do not reduce to very low levels too rapidly to prevent damage to the Ischemic penumbra)

- Carotid Bruit : indicates Carotid artery stenosis due to Atherosclerosis. Before palpating for the carotid pulse always auscultate to rule out a Thrombus as you may dislodge it when you press it.

- Signs of Hyperlipidemia :
Xanthoma , Xanthelesma , Arcus Senilis , Locomotor Brachii

- Check for Bed Sores - will find in long term Hemiplegics

- Check for an Indwelling Catheter.

- Neurocutaneous markers :
(Cafe au lait for Neurofibromatosis , Shahgreen patches , Ash leaf macules for Tuberous Sclerosis, Port wine stain for Sturge Weber Syndrome)

After this perform the routine neurological examination.

_______________________________________
Specific Questions that can be asked on Hemiplegia , and we must be aware of for exams (and for life) :

1. Elicit :
Tone
Power
Any deep tendon reflex (Commonly Biceps , Triceps , Knee , Ankle)
Clonus
Plantar Reflex (Babinski)

Glabellar tap
Jaw jerk
Facial Movements (7th nerve )
Gag reflex (Never forget to check for gag - it decides whether Ryles tube is needed or not and is super important to prevent Aspirations).
Extra Ocular movements
Tongue examination

2. Viva Questions :

A. Plegia vs Paresis?
Total paralysis = Plegia
Incomplete paralysis / Weakness = Paresis

B. What is Hemiplegia, Quadriplegia, Diplegia , Monoplegia , Cruciate Hemiplegia?
Diplegia = All 4 limbs involved but Lower Limb involved more than the upper.

Cruciate Hemiplegia= Upper limb of one side and lower limb of the other.
(I'm sure you know the others )

Complete Hemiplegia is when Facial involvement is present as well.

C. Hemiplegia vs Paraplegia site of lesions?
Hemiplegia is brainstem and above upto the cortex.
Paraplegia is spinal cord and below - upto the nerve.
(Paraplegia = Both lower limbs )

D. Rigidity vs Spasticity
- Lead pipe and Cogwheel Rigidity in Extra Pyramidal lesions like Parkinson's
- Clasp Knife Spasticity in UMN pyramidal tract lesion

E. UMN vs LMN lesions
(What is UMN ? What is LMN?)

F. Root values for all reflexes ?
(Deep + Superficial)

G. Plantar reflex components? What is a positive Babinski Sign? (5 components)

H. Causes of Babinksi positive other than Pyramidal tract lesions ?
(Deep sleep , Infancy , Coma.)

I. Alternatives to Elicit Babinski :
Gordon = Squeeze the Calves
Shaefer = Squeeze Tendoachilles
Oppenheim = Slide the knuckles down the tibial shaft
Chaddock = Strike along the medial aspect of the malleolus.

Hoffman Sign in Upperlimb

J. What is Jendrassik's maneuver ? What's its use?

K. Grades of Power ? (Should be pit pat)

L. Grades of Reflexes ? (In terms of + ++ +++ and ++++)

M. Causes of Hypo and Hypertonia?
Remember : Cerebellar disease causes Hypotonia

N. Clonus definition ?

O. What is Spinal Shock ?

P. Importance of aphasia ?
Wernicke vs Broca with area numbers ?
Conduction aphasia ?
How are these different from dysarthria?

Q. Know your blood supply : Anterior vs Posterior Circulation
- Middle Cerebral Artery - Superior vs Inferior Branch how to distinguish?
- Features of MCA territory stroke ?

R. Know Brainstem Syndromes names - the Crossed Hemiplegias.

Weber , Claude , Benedikt in Midbrain
Milliard Gubler and Foville in Pons
Medial and Lateral medullary Syndrome in Medulla.

S. Frontal lobe lesion features ! Especially Frontal release signs can be asked - Palmar grasp , Palmomental reflex , glabellar tap.
What is Gegenhalten phenomenon?

T. Then if you answer some of these they'll ask Management!
In that Basic Routine Ix. Don't forget Bloor Sugars and ECG.
NCCT best initial (Non contrast CT Scan)
Diffusion weighted MRI is very accurate for localisation!

U. Thrombolysis can ask everything about !
rTPA 0.9 mg/kg 
CONTRA INDICATIONS and Indications.

V. BP control in stroke - Which agents ? Target BP ? How to Reduce?

W. Raised ICT management?

X. What drugs would the patient be on life long ?
Aspirin and Statins

Y. Neuroprotective agents , name a few?
Citicholine , Piracetam , Adavarone

Hope this was a good list !
Do message on the Medicowesome Group or comment down below if any answers are needed or you have doubts !
Happy studying!
Stay awesome.

~ A.P. Burkholderia.

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.