Conus medullaris syndrome vs. Cauda equina syndrome

Both of these are orthopedic/neurosurgical emergencies! But in general, CM syndrome is more severe than CE syndrome.

Here's a comparison between the two...

Neurology examination template

Hi everyone!

Here is my template for documenting the basic bare minimum neurology examination.

CNS practical higher examination function.

This is the first video of the series - Neurology practical examination.

GCS Glasgow Coma scale video

In this video, I'll be talking about GCS. Please do give your comments regarding the video.

GCS explained

By Ojas Gite

Gerstmann's syndrome physical examination

 Gerstmann's syndrome is caused by lesions in the dominant parietal lobe (usually left).

Hoffman sign in neurology

Hello! Let's learn about the Hoffman sign.

The Hoffman sign: Involuntary flexion of the thumb and/or index finger when the fingernail of the middle finger is flicked down. 

Fact- Reversible ADP-r inhibitors cause breathlessness

Hi

 Reversible inhibitors of ADP-r (P2Y12) such as ticagrelor, cangrelor, and elinogrel used as anti-platelet drugs have a unique side effect of dyspnea, unlike the irreversible ones. This is hypothesized to occur because of reversible inhibition of ADP-r on sensory neurons. Since half-life of the reversible inhibitors is shorter than that of irreversibles, repeated doses lead to permanent inhibition of the P2Y12 receptors on sensory neurons.

 Moreover, oral administration is found to cause more severe effects on the breathing difficulties than the parenteral route.

 Source- Research gate 

 

That's  all

- Jaskunwar Singh

Tympanogram.

Hello Everybody!

Let us quickly review the different curves of a tympanogram. 

The following are the yypes of curves in you'll see on a tympanogram:

Type A – Normal pressure and normal compliance in normal ear.

Type A_s – Reduced compliance (‘s’ means stiffness leading to reduced compliance) and normal pressure.

• Seen in
  • Otosclerosis or other ossicular fixation
  • Tympanosclerosis

Type A_d – Increased compliance (‘d’ means discontinuity leading to increased mobility) and normal pressure.

• Seen in
  • Ossicular discontinuity
  • Thin and lax TM

 

Type B – Flat or dome shaped graph i.e. reduced compliance.

Seen in case of:Serous otitis media.

Thick tympanic membrane.

Type C – Normal compliance but negative pressure due to eustachian tube obstruction.

• Seen in case of:
• Retracted tympanic membrane,
• Early stages before collection of fluid in middle ear.

Hope this was helpful. 

Let's Learn Together! 

Dr. Medha Vyas 

Apraxia vs autotopagnosia

Hello Awesomites !

Here we will discuss two from many parietal lobe lesion.

1.APRAXIA

Inability to carry out well organized voluntary movement correctly.
Despite motor, sensory & coordinated functions are not significantly impaired.

Ideomotor : It is a type of apraxia.
Patient performs the task but makes errors; there is a common tendency to substitute a body part for an object.

2.AGNOSIA

Abnormalities of perception of sensation despite normal sensory pathways.

Visual & body perception are impaired in parietal lobe lesions 

Agnosia of body scheme or autotopagnosia

Inability to locate, identify & orient one’s body parts.

Suppose while on rounds in neurology ward:- You see a patient brushing his knee early morning.(according to above discussion)

Apraxia -Patient has forgotten how to use toothbrush.Brushing knee as a toothbrush rather than pretending to hold one.

Autotopagnosia- the patient has forgotten the body part itself.

In either case localisation of lesion is PARIETAL LOBE.

Isn't the interpretation of one neurological sign seems interesting?

"Eyes see what mind knows"

Below is the link which is very descriptive and I came across it while reading more on this topic.

Parietal lobe

Happy studying !

-Upasana Y.

Friedreich's Ataxia Mnemonic

Check out this mnemonic if you have difficulty memorizing it :)

Clinical vignette: Meningitis due to Listeria monocytogenes

Hello

Listeria monocytogenes is the 3rd most common organism that causes bacterial meningitis.
Cephalosporins do not cover this gram - positive bacteria under its spectrum. More aptly saying, the cephs do not kill this bacteria. So, especially in high-risk patients such as neonates, elderly, and the immunocompromised, cephalosporins are given in combination with ampicillin, and never alone.

Ceftriaxone is avoided for use in neonates due to its decreased biliary metabolism and sludging.
The choice of ceph in neonates and other high-risk groups in the case of meningitis is cefotaxime.

That's all
- Jaskunwar Singh

COVID-19: Neurological manifestations

Since the Chinese health authorities confirmed the first case of novel coronavirus infection, almost all of the clinical focus has been on the viral's prodromal symptoms and severe life-threatening adverse effects such as ARDS. However, neurologists all over the world have been reporting the neurological manifestations of COVID-19 such as, ataxia, encephalopathy, myelitis among others. One neurological symptom in particular received inordinate attention, anosmia, even though it barely has any diagnostic relevance. It is safe to say that the neurological deficits are ongoing in this pandemic without getting noticed appropriately. However, since we are in the early phases of understanding the clinical conundrum of the COVID-19, such relative blindness is expected.

How does SARS-CoV-2 enter the CNS?

Two pathways have been postulated:
1. Through the cribriform plate
2. Systemic circulatory dissemination after infecting the lungs.

Reported neurological manifestations:

1. Anosmia - Can be explained by the proximity of the olfactory bulb to the cribriform plate
2. Hypoguesia, dysguesia
3. Headache, malaise
4. Unstable walking or ataxia, dizziness
These four can occur in the early phase of the disease.

5. Cerebral hemorrhage - This has been hypothesized to be due to decrease in expression and function of ACE2 proteins, especially in hypertensive patients in whom the expression of ACE2 is already low. Given that ACE2 signaling lowers BP, lack of ACE2 function would lead to higher BP which might precipitate cerebral hemorrhage.
6. Cerebral infarction (acute cerebrovascular disease causing stroke)
7. Ondine's curse - The central respiratory centres lose their function, which consequently impairs involuntary respiration severely.
8. Acute encephalopathy - headache, altered mental status, convulsions.
9. Myopathy

Interestingly, the CSF in the patients were normal, which implies that COVID-19 does not cross the blood brain barrier and hence cannot cause meningitis or encephalitis. We should keep in mind that the neurological manifestations could be secondary to hypoxia, respiratory or metabolic acidosis and other complications of the COVID-19 infection.

Thank you!

-Vinayak

References:

1. Necrotizing Encephalopathy: CT and MRI Features

https://pubs.rsna.org/doi/10.1148/radiol.2020201187

2. Neurological Complications of Coronavirus Disease (COVID-19): Encephalopathy

https://www.cureus.com/articles/29414-neurological-complications-of-coronavirus-disease-covid-19-encephalopathy

3. Neurological Manifestations of Hospitalized Patients with COVID-19 in Wuhan, China: a retrospective case series study

https://www.medrxiv.org/content/10.1101/2020.02.22.20026500v1

AVPU Scale

Hello Awesomites !

LONG TIME .

AVPU scale is like glasgow coma scale to determine the level of responsiveness.

A=ALERT AND AWARE

• Eyes open 
• Knows name,date,time,place

V=RESPONDS TO VERBAL STIMULUS 

• Not oriented to time and place
• Responds in a meaningful way
  

P=RESPONDS TO PAINFUL STIMULUS 

• Eyes do not open

• Responds when trapezium muscle is pinched

U=UNRESPONSIVE

• Eyes do not open
• Does not respond to pinching of muscles 

Best (A) to Worst (U)

Happy Studying :)
 -Upasana Y.  

Fact of the day: AHN in old age

Hi!

Fact: New neurons proliferate as we age, in both physiologically and pathologically aging brains, even in the ninth decade of life.

How to read CSF analysis report?

Video by Jay!

Mnemonic: Cerebellar Signs

Hey guys,

Here's a short and sharp mnemonic post.

Hope it helps.

Post-LP Headache

Hey guys! 

Here's all you need to you know about that nasty headache some patients get, after a lumbar puncture (LP).

How common?
Up to one-thirds of all cases.

What are the risk factors?
None. Despite years of anecdotal advice to the contrary, none of the following has ever been scientifically shown to be a risk factor: position during or after the procedure; hydration status before, during or after; amount of CSF removed; immediate activity or rest post-LP.

When does it happen?
Within 24 hours of LP.

How does it present?
Let's SOCRATES the pain here.

Site: Frontal > Occipital
Onset: Acute
Character: Dull aching
Radiation: None
Association: Mild neck stiffness, nausea
Time Course: Lasts for 2 days to 2 weeks
Exacerbating factor: Sitting upright or standing, and so the relieving factor is lying down
Severity: Varies 

What is the pathology?
Thought to be continued leakage of CSF from the puncture site and intracranial hypotension. Other neuro-vascular mechanisms may be involved.

How do I prevent it?
Using the smallest practical needle and keeping the bevel facing up. Before withdrawing the needle, reinserting the stilette.

How do I treat it?
It's self limiting. Can use analgesia, as per WHO Pain Ladder. In extreme cases, can also involve an anaesthetist for an epidural 'blood patch'.



Know something you'd like to add? Let me know.

Thank you for reading. Have a nice rest of the day, you.



- Ashish Singh

Lamotrigine: A depression mood stabilizer

Lamotrigine is used primarily as an anticonvulsant for the treatment of generalized and partial seizures and is effective for treating focal epilepsies in the presence or absence of secondary generalization.

Definition of generalized convulsive status epilepticus

Hi everyone,

Historically, the International League Against Epilepsy (ILAE) and others defined status epilepticus as a single epileptic seizure of >30 minutes duration or a series of epileptic seizures during which function is not regained between ictal events in a 30-minute period.

However, a 30-minute definition is neither practical nor appropriate in clinical practice.

What Is Going On In Migraine?

Despite the high prevalence of migraines, the underlying pathophysiology is poorly understood.

What was thought?
Cerebral and meningeal arteries dilatation. Now largely disproven.

What do we think?
- MRI says episodic cerebral edema with dilatation of intracereberal vessels and less water diffusion that doesn’t respect vascular territories.

- PET says it’s a subcortical disorder affecting modulation of sensory processing.

- Magneto-EncepaloGraphic (MEG) scan suggests failure of inhibitory circuitry in the visual cortex.

- Hormones play a role. Migraines occur just as commonly in males as in pre-pubertal and post-menopausal females but the ratio tilts towards women of reproductive age group by 3:1. About half of the women complain of migraine synchrony with menses.

- 5-HT overload as suggested by its metabolites in the urine. While the exact significance is controversial, the efficacy of Triptans (5-HT 1b/1d agonists) supports its role.

- Trigeminal nerve dysfunction suggested by blockade of trigeminal nerve impulses by Triptans. They also inhibit release of substance P and pro-inflammatory neuropeptides.

This is what we know so far. To thread this string is your responsibility, future Dr. Neurologist. Good luck!



- Ashish Singh