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.

Types of barium-contrast imaging.

Hello everybody!

Let's quickly revise the types of Barium investigations.

So to enlist the investigations are: Barium swallow, barium meal, barium follow-through, and barium enema.

The barium swallow, barium meal, and barium follow-through are together also called an upper gastrointestinal series (study), whereas the barium enema is called a lower gastrointestinal series (study).

Procedure:

In upper gastrointestinal series examinations, the barium sulfate is mixed with water and swallowed orally, whereas in the lower gastrointestinal series (barium enema), the barium contrast agent is administered as an enema through a small tube inserted into the rectum.

Let's review individual examinations breifly:

Barium swallow X-ray examinations are used to study the pharynx and esophagus.

Barium meal examinations are used to study the lower esophagus, stomach and duodenum.

Barium follow through examinations are used to study the small intestine.

Enteroclysis also called small bowel enema is a Barium X-ray examination used to display individual loops of the small intestine by intubating the jejunum with a small tube and administering Barium sulfate followed by methylcellulose or air.

Barium enema examinations are used to study the large intestine and rectum.

Hope this was useful!

Let's learn Together!

-Medha.

Authors' diary: How to study during Ramzaan

This video has been requested since last year! Finally made it! :)

Autism and ADHD : The clinical intersection

Hello

Autism and Attention - Deficit Hyperactivity Disorder (ADHD) may co - occur in upto 80% of children and they share about 50 - 75% of their genetic factors and pathologic features, thus resulting in some clinical intersection.

NBME 7 question on muscle weakness

Disclaimer: This is an NBME form 7 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.

CMS neurology form 2 question on fibromuscular dysplasia with paresis, occulomotor palsy

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.

CMS neurology form 2 question on headache, seizures, urinary incontinence, broad based gait

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.

NBME 7 question on intoxication

Disclaimer: This is an NBME form 7 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.

Fact of the day : Pinenes for refreshing your Airways

Hello

Did you know? One of the reasons your lungs feel refreshed ( increased mental focus and energy ) when you walk through the shades of beautiful pine forest is because of an anti - inflammatory compound called alpha -Pinene, that is found in conifers. It is used as a bronchodilator in the treatment of asthma and is abundantly present in marijuana.

- Jaskunwar Singh

Pill induced esophagitis mnemonic

Pill induced esophagitis is caused by a pill! :D

Causes of pill induced esophagitis mnemonic: A PILL.

Aspirin
Alendronate
Antibiotics like tetracycline, clindamycin

Potassium chloride
Iron
Less water
Lying down immediately

Interesting anatomy correlation:
The most common sites of injury are the proximal esophagus near the compression from the aortic arch and the distal esophagus in patients with left atrial enlargement.

The typical endoscopic appearance of pill-induced esophageal injury is a discrete ulcer with relatively normal surrounding mucosa.

That's all!
-IkaN

Motor nuclei in the brainstem : An overview

Hi everyone. Just thought of doing an overview of the various motor nuclei of cranial nerves in the brain stem.

So we can classify the motor nuclei into 3 groups -

1. Somatic motor efferent - 4
2. Branchial motor efferent - 4
3. Visceral motor efferent - 4

Now how are these classified ?

1. Somatic Motor Efferent

- In the embryological stage , there are certain precursors to muscle and skin segment groups called 'Somites'. These are processes of the paraxial mesoderm.
- Sach somite gives rise to a particular set of muscles called its myotome. 

- There 4 such important somite groups -->

A. Pre otic somites = 3.
So this is simple.
There are 3 pre otic somites giving rise to distinct groups of extraocular muscles supplied by their own cranial nerve.

Somite 1  =
Muscles -
All Extra ocular muscles except Lateral Rectus and Superior oblique.
Nerve -
Oculomotor nerve (III)
Nucleus -
Oculomotor nucleus in the Upper Midbrain.

Somite 2  =
Muscles -
Superior oblique.
Nerve -
Trochlear nerve (IV)
Nucleus -
Trochlear motor nucleus in the Lower Midbrain.

Somite 3  =
Muscles -
Lateral Rectus.
Nerve -
Abducent nerve (VI)
Nucleus -
Abducent motor nucleus in the Pons.

(I'm sure you remember the popular mnemonic - LR6 SO4)

B. Occipital somites

Muscles -
All muscles of the tongue except Palatoglossus
Nerve -
Hypoglossal I'm nerve (XII)
Nucleus -
Hypoglossal nucleus in the Medulla.

Since these nuclei represent the motor innervation to the derivatives of Somites , they're called Somatic Motor or General Somatic Efferent (GSE) Fibres. 

2. Branchial Motor Efferent - 

- In the embryological stage , there are various branchial or Pharyngeal arches that give rise to muscles , bones and cartilage supplied by a particular nerve of that arch.

- Each nucleus that supplies the muscles from such a Branchial arch is called Branchiomotor Efferent or Special Visceral Efferent. (SVE) 

- There are 4 such important arches - 

A. 1st Pharyngeal arch (mandibular arch)

Muscles -
All muscles of mastication + TT (Tensor tympani + Tensor veli Palatini) + Digastric anterior belly. ( And Meckel cartilage)
Nerve -
Mandibular branch of Trigeminal
Nucleus - 

Trigeminal motor nucleus in Pons 

B. 2nd Pharyngeal arch (hyoid arch) 

Muscles -
All muscles of facial expressions + Stapedius + Digastric posterior belly.  ( And Reichter cartilage)
Nerve -
Facial nerve (VII)
Nucleus - 

Facial motor nucleus in Pons 

C. 3rd Pharyngeal arch

Muscles -
Stylopharyngeus

(And the hyoid bone funnily.)
Nerve -
Glossopharyngeal nerve (IX)
Nucleus - 

Nucleus Ambiguus in Medulla

D. 4th and 6th Pharyngeal arches

Muscles -
- All muscles of  Soft palate ( except Tensor veli which is up in the 1st arch) by the 4th. + cricothyroid muscle of Larynx. 

- All muscles of Larynx by the 6th except cricothyroid which is by the 4th. 

(All laryngeal cartilage as well)
Nerve -
4th arch - Superior laryngeal nerve of the Vagus.(X)

6th arch - Recurrent laryngeal nerve of the Vagus (X)
Nucleus - 

Nucleus Ambiguus of Medulla 

Now there's another Motor nucleus - The Accessory nerve. It supplies Trapezius and Sternomastoid muscles but it's doubtful if it's Branchial or Somatic. 

3. Visceral Motor Efferent - General. 

- These nuclei are parasympathetic and stimulate a particular gland to secrete or a ganglion to function. 

- These are called Secretomotor or General Visceral Efferent Fibres 

Again , there are 4 of these. 

A. Ciliary ganglion 

Function mediated by - 
Sphincter pupillae - Constricts pupil 

(Mnemonic = Remember C and C - Cholinergic Constricts )
Nerve -
Oculomotor nerve
Nucleus - 

Edinger Westphal in Midbrain 

B. Pterygopalatine ganglion 

Function mediated by - 
Lacrimal glands, nasal mucosal, sinuses mucosal glands and pharynx mucosal - Secretomotor. 

Nerve -
Facial nerve  (Greater Petrosal)
Nucleus - 

Superior salivatory nucleus - Pons. 

C. Submandibular ganglion 

Function mediated by - 
Submandibular glands , sublingual glands - Secretomotor.

Nerve -
Facial nerve  (Chorda tympani)
Nucleus - 

Superior salivatory nucleus - Pons. 

D. Otic ganglion 

Function mediated by - 
Parotid gland

Nerve -
Glosspharyngeal nerve  (Lesser Petrosal)
Nucleus - 

Inferior salivatory nucleus - Pons. 

The Vagus nerve has the largest parasympathetic discharge and supplies a lot of visceral with this input in the guy as well.

Hope this helps you to re-orient yourself to neuroanatomy and grasp the roles of various brainstem structures ! 

Happy studying ! 

~ A.P.Burkholderia

Lacunar strokes : An Overview

      Hi everyone ! Here's a short post on Lacunar infarcts. Credits to IkaN without whom IKant have done this post. Haha ;;) here goes.

- A Lacunar infarct is an infarction occurring    in the deep penetrating branches supplying the deep subcortical structures - Mainly the Internal capsule and parts of thalamus. 

- These are some of the most common infarctions seen. 

- Causes of lacunar infarction include Hypertensive bleeds and Microthrombi. 

- So these infarcts can present as one of the following​ Syndromes --> 

1. Pure Motor 

2. Pure Sensory 

3. Combined Sensorimotor 

4. Ataxic 

5. Dysarthria- Clumsy hand syndrome. 

- The illustrations I've drawn below clearly depict the syndromes , their anatomical localization and the arteries commonly involved. 

- The commonest of the lot is the Pure Motor type of stroke that affects mainly the Internal capsule containing the motor corticospinal fibres. Since a multitude of Fibres is concentrated very judciously in the Internal capsule , the hemiplegia resulting from this type is a 'Dense' or total hemiplegia affecting both upper and lower limbs in equal measure. 

(click on the image to see them in better resolution ) 

- The management is much like the other strokes - 

1. Airway Breathing Circulation to be established. 

2. Check Blood sugar and BP.

3. Send for an emergency Non contrast CT scan to rule out hemorrhage. 

4. If within 3-4.5 hours and absence of hemorrhage = Thrombolyse. 

5. If hemorrhage - BP control and ICT management.

6. If beyond 4.5 hours = Symptomatic and Palliative care and treat risk factors.

- I hope all of these Syndromes are clear to you now !

 Let me know if you'll have any doubts. 

Happy Studying ! 

Stay awesome.

~ A.P.Burkholderia

Fact of the day: Marchiafava-Bignami disease

Marchiafava-Bignami disease is a rare disorder of demyelination or necrosis of the corpus callosum and adjacent subcortical white matter that occurs predominantly in malnourished alcoholics. Dementia, spasticity, dysarthria, and inability to walk may present as an acute, subacute or chronic condition.

Lesions appear as hypodense areas in portions of the corpus callosum on CT and as discrete or confluent areas of decreased T1 signal and increased T2 signal on MRI. Alcohol abusers without liver disease, amnesia, or cognitive dysfunction show thinning of the corpus callosum at autopsy and on MRI, suggesting that alcohol or malnutrition damages the corpus callosum commonly in the absence of the necrotic lesions of Marchiafava-Bignami disease.

Interesting, isn't it?
-IkaN

High ankle and low ankle sprain mnemonic

Hello!

High ankle and low ankle sprain

Atrial fibrillation begets Atrial fibrillation: Explanation

Hi ! Short post on pathophysiology of Atrial Fibrillation!

- Atrial Fibrillation is a fairly common disorder of rhythm, where the atria begin to beat at random , irregular and very high rates. Like 300-600 beats / min !
- Some of these MANY contractions get transmitted to the ventricles causing an Irregular , yet High , Ventricular rate - around 100-160 per minute or even higher.

Now how this occurs is a very interesting yet much-ignored mechanism.

- Due to some pre existing factors like Rheumatic heart disease , Myocardial ischemia or Thyroid abnormalities among many others, the atria get electrically irritated and begin to fire on their own.

- These ectopic foci are common along the opening of the pulmonary veins = called the pulmonary sleeve.
This area of hyperactivity and automaticity begins to fire from the left Atrium creating a wavefront of abnormal impulses.

- Say one of these myocytes becomes ectopic one day and produces an abnormal wavefront. This wavefront progresses across the atrium and in turn stimulates the other Atrial myocytes to inturn fire ectopically -- causing formation of multiple Daughter ectopic foci.

- These daughter ectopic foci produce daughter wavelets that then propagate through the atria , in turn producing more duaghter wavefronts.

- Eventually there are A LOT of Atrial foci causing multiple wavelets to produce multiple electrical wavefronts.

- Thus A-Fib causes multiple wavefronts which in turn cause more wavefronts eventually propogating A fib as a positive feedback mechanism​.

- In the long term, due to this constant irregular beating there is fibrosis and electrophysiological remodelling making the atrium more irritable and automatic.

Thus A-Fib begets A-Fib!

Hope you liked this !
Happy Studying !
Stay awesome.
~A.P.Burkholderia

Mitral Regurgitation Begets Mitral Regurgitation : Explanation

Hi everyone  ,just a short explanation of the famous phrase 'MR begets MR'.
Here goes.

- Mitral Regurgitation is a disease where the mitral valve is incompetent or insufficient and leaks or pukes when it should be shut. (Rather like a blithering idiot who keeps talking at the wrong time. =}. )

- So it allows the blood to puke back into the Left Atrium from the Ventricle during systole.

- So assume - 100 ml of blood would flow into LV from the LA normally which the LV would pump into the Aorta.

- Now because of the weird and incompetent valve , the LV can pump only like 70 ml into the Aorta and the rest of the 30 ml goes back into the LA.

- So now the LA volume is 30 ml + 100 ml
And it'll pour in 130 ml into the LV.

- So effectively, the LV has an overload of volume in it and over a period of time it would undergo Dilatational changes and increase in size.

- As the Ventricle increases in size , the mitral valve apparatus is stretched all the more.

-This is because the mitral valve is attached to the Ventricular myocardial tissue directly at the annulus as well as via the papillary muscles. Both of these are stretched. 

- The stretching causes further increase in MR. This causes further volume overload. Which causes further MR.

- Thus it is like a positive feedback response and a vicious cycle is formed.

This phenomenon is referred to as ' MR begets MR' which means MR basically causes Ventricular changes which stretch the heart and cause more MR which continues the cycle further.

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

Microbiology of Actinomyces vs Nocardia mnemonic

Hello! Let's go back to Microbiology today.

Nocardia typically appear as delicate filamentous gram-positive branching rods that appear similar to Actinomyces species.

Nocardia can usually be differentiated from Actinomyces by acid-fast staining, as Nocardia typically exhibit varying degrees of acid fastness due to the mycolic acid content of the cell wall.

Another useful clue is that Nocardia grow under aerobic conditions, whereas Actinomyces grow under anaerobic conditions.

How to remember this? Remember one mnemonic, the other one is the other one. Okay?

So let's start with nocardia.
nocarDIA. nocarDICA. ACID fast!
noCARDIA. Heart needs oxygen. Aerobic organism.

Therefore, the other one, Actinomyces is anaerobic, non acid fast.

Treatment mnemonic: PANT
Penicillin Actinomyces
Nocardia TMP-SMX

That's all!
-IkaN

Tay-Sachs disease notes and mnemonic

Hello!

Tay-Sachs disease is an autosomal recessive, neurodegenerative disease.

Plasma Proteins Mnemonic

Hello Everyone,
 Lets discuss plasma proteins.

1.How do we classify them?

• They are classified into Albumin, Globulin and Fibrinogen.
• Globulins are further classified into Alpha , Beta Globulins and Gamma Globulin.
• Alpha Globulin is further divided into Alpha 1 and Alpha 2 Globulins.

Memorising the examples of them is simple. 

Examples of Beta Globulins can be remembered as follows:

         B PTH

B-Beta Lipoproteins(LDL)

P-Plasminogen

T-Transferrin

H-Hemopexin

Interesting Fact:

Acute-phase proteins are a class of proteins whose plasma concentrations increase (positive acute-phase proteins) or decrease (negative acute-phase proteins) in response to inflammation. This response is called the acute-phase reaction.

• Positive acute-phase proteins increase in inflammation e.g., C-reactive protein, mannose-binding protein, complement factors, ferritin, ceruloplasmin, serum amyloid A and haptoglobin.
• Negative acute-phase proteins decrease in inflammation. Examples include albumin, transferrin, transthyretin, retinol-binding protein, antithrombin, transcortin. 

Thats all,

Thank you,

Chaitanya Inge

No cyanosis in cyanide poisoning. Why?

I was reading about cyanide poisoning today and saw "Cherry red skin" in the clinical manifestations. I know that carbon monoxide poisoning causes a cherry red color to blood. But why cyanide?

The curiosity lead to this post.

In normal cellular metabolism, most adenosine triphosphate (ATP) is generated from oxidative phosphorylation. .

Cyanide avidly binds to the ferric ion (Fe3+) of cytochrome oxidase a3, inhibiting this final enzyme in the mitochondrial cytochrome complex. When this enzyme's activity is blocked, oxidative phosphorylation ceases. The cell must then switch to anaerobic metabolism of glucose to generate ATP.

Anaerobic metabolism leads to the formation of lactic acid and the development of metabolic acidosis. Hydrogen ions produced by ATP hydrolysis are no longer consumed in aerobic ATP production, exacerbating this acidosis. Serum bicarbonate decreases as it buffers excess acid, leading to an increased anion gap.

Despite an ample oxygen supply, cells cannot utilize oxygen because of their poisoned electron transport chain. This functional (or "histotoxic”) hypoxia is particularly deleterious to the cardiovascular and central nervous systems (especially the basal ganglia).

Because of the decreased utilization of oxygen by tissues, the venous oxyhemoglobin concentration will be high, making venous blood appear bright red.

Therefore, despite hypotension, apnea, and/or bradycardia, the patient does not usually appear cyanotic in the setting of cyanide poisoning.

Clinical features:
Central nervous system toxicity is the most prominent in cyanide toxicity – Headache, anxiety, confusion, vertigo, coma, seizures.

Which should you suspect cyanide poisoning?
Victims of fires
Reported ingestions
Treatment with sodium nitroprusside

Antidote:
Hydroxocobalamin
Sodium thiosulfate
Nitrites (to induce methemoglobinemia)

That's all!
-IkaN

CT scans and role of Contrast enhancement

Contrast enhancement and it's role in CT scan
The concept of Contrast enhancement in radiology is not new and it has been in practice even before the Advent of CT scans.
CT scan as a modality of imaging was invented by a British engineer Godfrey Hounsfield in the year 1972.

Purpose of Contrast enhancement

Contrast enhancement is a method of exaggerating  the visible difference between adjacent structures on scan by administrating contrast agents.The term Contrast enhancement in CT scan includes usage of radio opaque substances for better visualization of the anatomic structures as well as better localization and characterization of the pathologies, better differentiation of the pathology from the normal surrounding structures.

Principle of Contrast enhancement

The diffusion of contrast agents from the blood stream to the body tissue is physiologically limited. In pathologies such as cancer, blood vessels grow (angioneogenesis) with increased leaking of contrast agents resulting in lesions much more visible on Contrast enhanced scans.
In CNS, contrast diffusion is limited by Blood brain barrier. Disruption of BBB lead to enhancement after administration of contrast agents.

Indications of Non Contrast CT (NCCT )
For detection of
1.Stones in kidney,ureter, cbd
2.Calcification
3. Fat in various tumors
4. Head injury
5. Acute hemorrhage
6. Stroke
7. SAH


CECT

The pathologic lesions show enhancement or attenuation depending upon the phase of contrast enhancement. So if you are looking for a particular pathology,it is important to know in which phase of CECT to look for.
For that purpose,I've enumerated the phase in which CT scan is done and can be recorded.

1. Non enhanced phase (NECT)
Uses are same as those of Ncct. Many a times this scan is done before administration of the dye to compare pre and post contrast enhancement study.
Calcification, fat in tumors, inflammation and infarction can be seen in this phase well.

2. Early arterial phase (15-20 secs post injection)
When contrast is still in the arteries, it has not enhanced the organs.
This phase is useful to look for vascular abnormalities such as aneurysms, vascular stenosis, etc

3. Late arterial phase (35-40 secs post injection)
Sometimes known as arterial phase.
All the structures that get their blood supply from arteries will show optimal enhancement in this phase.

4. Hepatic or late portal phase (70-80 secs post injection)
Liver parenchyma enhance trough blood supply by portal vein and some enhancement of hepatic veins.

5. Nephrogenic phase (100 secs post injection)
This is when all of the renal parenchyma including medulla enhances. Particularly helpful for small renal cell carcinoma which are otherwise missed.

6. Delayed phase (6-10 mins post injection) called as wash out phase or equilibrium phase
Washout of contrast in all abdominal structures except for fibrotic tissues which become relatively more dense in this phase.

Factors affecting CECT
The timings depend on
1. Organs to be scanned and focussed
2. Type of CT machine available, number of slice
3. Amount of contrast given depending upon the body weight of the patient
4. Injection rate of the contrast
5. Route by which contrast given. (Mainly IV but can be oral,rectal too)

Lesions / pathologies visualized on CECT
1. Liver tumors
Due to it's dual blood supply, 80% by portal vein and 20% by hepatic artery normal parenchymal enhancement maximally in hepatic phase . On the contrary, all all liver tumors are supplied 100% by hepatic artery. So hyper vascular tumors are best seen in late arterial phase. Hypovascular tumors on the other hand are better seen in hepatic phase.
2. Fibrotic lesions
Fibrotic lesions like cholangiocarcinoma and fibrotic mets hold contrast much longer than normal parenchyma hence best seen in delayed phase.
3. Pancreatic tumors most of them being hypovascular are seen best in late arterial phase. In cases of acute pancreatitis, late arterial phase best detects necrosis. Remember chronic pancreatitis can be very well appreciated on NCCT due to calcification.
4. Anastomosis leakage 
CECT done in post op patients to check anastomosis leakage. Oral contrast play a role here for check scans done in post op bowel anastomosis.

5. Pulmonary embolism - 
Good quality scans are required to delineate the emboli in the pulmonary vasculature.
6.CT angiography 
For vascular studies.

Dr. Shil Pill

Coccidioidomycosis mnemonic

Coccidioidomycosis is caused by Coccidioides immitis!