Lhermitte's sign Variants!

Helloooo....

Well we all know about the Lhermitte’s sign... The famous Barber's Chair sign!

For the people who are reading for the first time... Lhermitte's sign  is a sensation of tingling or electric shocks running down the back and legs on flexion of the neck.

Some other actions giving rise to similar sensations are:  Neck rotation, arm abduction, coughing ,Yawning 

It is common in multiple sclerosis, and other demyelinating diseases  but can occur with other conditions involving the cervical spinal cord.

But...Some variants to Lhermitte’s sign have also been described.

1) Delayed typical Lhermitte phenomenon can follow contusion of the spinal cord from neck trauma.

2) Reverse Lhermitte phenomenon
Paresthesias induced by neck extension have been described in extrinsic compression of the cervical spinal cord.

3) Inverse Lhermitte's sign:
Upward moving paresthesias with neck   flexion have been described in myelopathy from nitrous oxide inhalation.

I hope this was informative!

-Medha!😊

Brainstem syndromes-Midbrain!

Here we shall review three syndromes in the Midbrain occuring majorly due to a vascular event.

Weber's Syndrome:
Lesion Location: Midbrain base

Structures involved :CN III fibers; cerebral peduncle

Features: Ipsilateral CN III palsy; contralateral hemiparesis

(The image showing the involved 3 nerve and the crus! The lesion is anterior—in the cerebral peduncle—in  Weber’s syndrome, causing hemiparesis.)

Claude's Syndrome:
Lesion location :Midbrain tegmentum

Structures involved: CN III fibers; red nucleus; SCP

Clinical features: Ipsilateral CN III palsy; contralateral ataxia and tremor (“rubral tremor”)

(The sky blue line depicts the sup. Cerebellar peduncle! Lesion is more posterior—in the tegmentum—in Claude’s syndrome, causing hemiataxia.)

Benedikt's Syndrome:
Lesion location: Midbrain tegmentum

Structures involved: CN III fibers; red nucleus; CST (corticospinal tract)SCP(superior cerebellar peduncle)

Clinical features:
•Ipsilateral CN III palsy; contralateral hemiparesis with ataxia, hyperkinesia and tremor “rubral tremor

(The blue fibers being the sup. Cerebellar peduncle. In Benedikt’s syndrome, the lesion is more extensive, involving both the tegmentum and the peduncle, causing hemiparesis with tremor and ataxia of the involved limbs)

These three midbrain syndromes are variations on a theme.

Benedikt’s is essentially  Weber’s + Claude’s.

Because the fascicles of cranial nerve (CN) III are scattered in their course through the midbrain, the third nerve palsy in any of these syndromes may be partial.

Last on the list....
 Nothnagel's Syndrome mainly due to neoplasms ...affecting the Midbrain tectum involving Ipsilateral or bilateral CN 3 causes Oculomotor palsies; ataxia.

We finish Alll the midbrain syndromes !!!!!😎

Hope it helps!

-Medha😊

Facts and Fallacies: Vitamin D link to cancer

Hey Awesomites

Vitamin D has been shown beneficial for a variety of disorders and diseases. Recent studies now suggest that those deficient in vitamin D are at a  higher risk of developing cancer compared to those with adequate levels.

Brainstem Syndromes!

So let's get done with all the important brainstem syndromes once and for all !

I would be writing on all of them one by one...

Also ...I will try and incorporate many of my diagrams to help you guys make it seem less daunting...

Starting from the Midbrain the first syndrome is..

(The image shows the level of the lesion)

1):Parinaud's Syndrome

Lesion location:Midbrain dorsum ,superior  collicculi.

Structures involved: Quadrigeminal plate region; pretectum; periaqueductal gray matter

Etiology: •Due to mass lesion in the region of the posterior third ventricle, most often pinealoma, or due to midbrain infarction.

Clinical features:
•Impaired upgaze as centre for upward gaze is affected
convergence retraction nystagmus;
Argyll Robertson pupil :dilated pupils with light near dissociation.

A closer look at the structures involved .

I hope it helped !Also do share your Neuroanatomy diagrams and and more information on Parinaud Syndrome.

Have a nice day!

-Medha!

How I remember the duration of symptoms for Generalized anxiety disorder (GAD) required for diagnosis

The symptoms of generalized anxiety disorder should be present for at least 6 months. For me, it's hard to remember the duration of the symptoms in psychiatry. So I mnemonic-ify them :D

I remember G6PD, and say G6AD instead!

For those who don't know what GAD is here is the DSM V criteria for diagnosis of Generalized Anxiety Disorder...

Transposition of Great Arteries!

Hello!

So I have divided the post into two parts - A short summary for those who don't have the time to read everything (#TLDR) and a nice long explanation for those who want to read everything :)

Let's start with TLDR.

Buzz words for congenital syphilis!

Following are some important signs and buzzwords that are testable ...And high yeild for entrances.

Olympian Brow: Bony prominence of the forehead caused by persistent or recurrent periostitis

Clavicular or Higoumenakia sign:Unilateral or bilateral thickening of the sternoclavicular third of the clavicle

Saber shins :Anterior bowing of the midportion of the tibia

Scaphoid scapula :Convexity along the medial border of the scapula

Hutchinson teeth:Peg-shaped upper central incisors; they erupt during 6th yr of life with abnormal enamel, resulting in a notch along the biting surface

Mulberry molars :Abnormal 1st lower (6 yr) molars characterized by small biting surface and excessive number of cusps

Saddle nose :Depression of the nasal root, a result of syphilitic rhinitis destroying adjacent bone and cartilage

Rhagades:Linear scars that extend in a spoke-like pattern from previous mucocutaneous fissures of the mouth, anus, and genitalia

Juvenile paresis :Latent meningovascular infection; it is rare and typically occurs during adolescence with behavioral changes, focal seizures, or loss of intellectual function

Juvenile tabes : Rare spinal cord involvement and cardiovascular involvement with aortitis

Hutchinson triad :Hutchinson teeth, interstitial keratitis, and 8th nerve deafness

Clutton joint :Unilateral or bilateral painless joint swelling (usually involving knees) from synovitis with sterile synovial fluid; spontaneous remission usually occurs after several weeks

Interstitial keratitis: Manifests with intense photophobia and lacrimation, followed within weeks or months by corneal opacification and complete blindness

8th nerve deafness: May be unilateral or bilateral, appears at any age, manifests initially as vertigo and high-tone hearing loss, and progresses to permanent deafness.

Well all these are late manifestations of congenital syphilis occuring after 2 years of life.
It is important to recognise these signs clinically and also on the exams...

-Medha.

Pathophysiology of myopathy caused during hypothyroidism and hyperthyroidism

Hello awesomites! Today's topic of discussion is - Myopathy in thyroid disease.

Interestingly, it is caused by both, hypothyroidism as well as hyperthyroidism.

What is myopathy?

It is a disease of muscle tissue where, ultimately, muscles get weak and are unable to perform work due to deficiency of ATP.

Why is there myopathy in hyperthyroidism?

The thyroid hormone is a catabolic hormone. Hyperthyroidism increases energy expenditure, glucose turnover, lipolysis, and protein breakdown (proteolysis). But here is the catch - Hyperthyroidism increases whole-body protein turnover and breakdown before any measurable changes in energy expenditure or glucose and fat metabolism, suggesting that amino acid and protein metabolism is an early and primary target for thyroid hormone action in humans. It was therefore concluded that the thyroid-hormone concentration may be an important factor in regulating muscle proteolysis. The altered protein metabolism causes myopathy.

Then, one may ask, why myopathy in hypothyroidism? Less thyroid hormone should lead to less protein breakdown, shouldn't it?

Well, this is a good question! Slightly complex and tricky to answer though. 

In hypothyroidism, there is abnormal glycogenolysis, defective mitochondrial oxidative metabolism and triglyceride storage.

Abnormal glycogenolysis and triglyceride storage: Less glucose is released and utilised because of this. The body starts using more proteins usually derived from muscles leading to myopathy.

Mitochondrial oxidative metabolism defect: Thyroid hormone is responsible for activation of bc1 complex also known as complex 3 & succinate dehydrogenase. Less activation of bc1 leads to less formation of ATP from glucose.... So again, the body switches to proteins from muscles as a source of energy!

That's all!
Stay cool :)

~Ojas

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Fact of the day: Regulate brain activity with your type of music

Hey Awesomites

Which genre or type of music do you like the most? Well, it surely has to do a lot with the functioning of our brain. Some of you may like slow music while others like to rock n roll on the floor while listening to their favourite beats. I am more of the latter type too, depending on the mood. ;p