How are Ketone Bodies formed?

In the liver, ketone bodies are synthesized in the mitochondrial matrix from acetyl-CoA generated from fatty oxidation and this process is known as ketogenesis. Acetyl-CoA results from the breakdown of carbohydrates, lipids and certain amino acids. Normally, the acetyl group of acetyl-CoA enters the citric acid cycle to generate energy in the form of ATP, but it can also form ketone bodies; this happens if acetyl-CoA levels are high and the TCA cycle capacity is exceeded (the limiting factor is the availability of oxaloacetate).

Steps in ketogenesis:

1. Catalyzed by enzyme thiolase, 2 molecules of acetyl-CoA condense to form acatoacetyl-CoA.
2. Catalyzed by enzyme HMG-CoA synthase, acetoacetyl-CoA combines with another molecule of acetyl-CoA to produce HMG-CoA (β-hydroxy β-methyl glutaryl-CoA).
3. HMG-CoA lyase cleaves HMG-CoA to produce acetoacetate and acetyl-CoA.
4. Acetoacetate can undergo spontaneous decarboxylation to form acetone.
5. Acetoacetate can be reduced by a dehydrogenase to β-hydroxybutyrate.

The dehydrogenase reaction is readily reversible and interconverts the 2 ketone bodies, which exist in an equilibrium ratio determined by NADH/NAD+ ratio of the mitochondrial matrix. Under normal conditions, the ratio of the 2 ketone bodies in the blood is approxiamtely 1:1.

Regulation:

When fat enters liver it has 2 fates: either

1. Beta oxidation (Occurs during glucose deficiency)
2. Storage as triacylglycerol (Occurs when liver has sufficient supplies of glycerol 3 phosphate from glycolysis)

Hormones:

1. Hunger stimulates Glucagon hormone responsible for stimulating Fatty acid oxidation and Ketogenesis
2. Fed state stimulates Insulin hormone responsible for inhibiting ketogenesis

How are Ketone Bodies utilized?

The ketone bodies being water soluble, are easily transported from the liver to various tissues. Acetoacetate and β-hydroxybutyrate can be oxidized as fuels in most tissues includin skeletal muscle, brain, certain cells of kidney and cells of the intestinal mucosa. The tissues which lack mitochondria (eg. erythrocytes) cannot utilize ketone bodies. During prolonged starvation, ketone bodies are the major sources of fuel for the brain and other parts of central nervous system (CNS).

Steps in oxidation of ketone bodies (ketogenolysis):

1. β-hydroxybutyrate is converted back to acetoacetate.
2. Acetoacetate is activated to Acetoacetyl-CoA by a mitochondrial enzyme thiophorase (succinyl-CoA : acetoacetate-CoA transferase). Thiophorase is absent in liver, hence ketone bodies are not utilized in the liver.
3. Thiolase cleaves acetoacetyl-CoA to 2 moles of acetyl-CoA
4. The principal fate of the acetyl-CoA synthesized is the oxidation in TCA cycle.

Ketosis:

The concentration of ketone bodies in blood is maintained around 1 mg/dl. The excretion in urine is very low and undtectable by routine tests (Rothera’s test).

When the rate of synthesis of ketone bodies exceeds the rate of utilization, their concentration in blood increases, this is known as ketonemia. This is followed by ketonuria – excretion of ketone bodies in urine. The overall picture of ketonemia and ketonuria is commonly referred to as ketosis. Smell of acetone in breathe is a common feature of ketosis. It is most commonly associated with following conditions:

Starvation: Starvation is accompanied by increased degradation of fatty acids to meet energy needs of the body. This causes an overproduction of acetyl-CoA which cannot be entirely handled by TCA or citric acid cycle. Furthermore, TCA cycle is impaired due to deficiency of oxaloacetate, since most of it is diverted for glucose synthesis (gluconeogenesis) to meet the essential requirements (often unsuccessful) for tissues like brain. The result is an accumulation of acetyl-CoA and overproduction of ketone bodies leading to ketosis.

Diabetes Mellitus type I (Insulin Dependent):

1. Hyperglycaemia occurs due to decreased glucose uptake in fat and muscle cells due to insulin deficiency
2. Lipolysis in fat cells now occurs promoted by the insulin deficiency releasing Free fatty acids (FFA) into the blood which provide substrate to the liver
3. A switch in hepatic lipid metabolism occurs due to the insulin deficiency and the glucagon excess, so the excess FFA is metabolised resulting in excess production of acetyl CoA
4. The excess hepatic acetyl CoA (remaining after saturation of TCA cycle) is converted to ketone bodies which are released into the blood
5. Ketoacidosis and hyperglycaemia both occur due to the lack of insulin and the increase in glucagon and most of the clinical effects follow from these two factors

Countercurrents exist when fluids flow in opposite directions in parallel and adjacent tubes. There are 2 countercurrent systems and an osmotic equilibrating device:

1. Countercurrent multiplier (Loop of Henle): Establishes gradient of osmolarity from cortex (300mOsm/L) to the papilla (1200mOsm/L) aided by Urea recycling
2. Countercurrent exchanger (Vasa recta): Maintains the corticopapillary osmotic gradient established by Countercurrent multiplier
3. Osmotic equilibrating device (Collecting duct): Depending on the plasma level of ADH, collecting duct urine is allowed to equilibrate with the hyperosmotic medullary gradient resulting from countercurrent system

Countercurrent Multiplication:

Remember 2 exceptions on which the countercurrent multiplier is based:

1. Descending limb of loop of Henle doesn’t reabsorb solute but does reabsorb water (Concentrates Urine)
2. Ascending limb of loop of Henle doesn’t reabsorb water but does reabsorb solute actively (Dilutes Urine and the urine leaving ascending limb of loop of henle is hypo-osmotic ~100 mOsm/L)

Steps:

1. As NaCl is reabsorbed from the thick ascending limb by the Na+ K+ 2Cl- cotransport it creates a gradient in the interstitium (maximum 200 mOsm/L at a time because paracellular diffusion of ions back into eventually counterbalances transport of ions out of lumen when 200mOsm/L concentration gradient is achieved)
2. Urine in the descending limb now equilibrate osmotically with the interstitium and water leaves
3. Flow of urine now moves hyperosmotic urine into the ascending limb and the NaCl transport creates another gradient
4. The loop configuration creates a counter-current multiplier for the effect of the Na+ pump to create the cortico-medullary gradient (300-1200 mOsm/Kg)

Countercurrent Exchange:

Remember 3 things:

1. Vasa recta is freely permeable to both solute and water throughout the length. Water diffuses along the osmotic gradient and NaCl diffuses along its concentration gradient.
2. Blood entering the descending limb of vasa recta is ~ 300mOsm/L and Blood leaving the ascending limb of vasa recta is ~ 325mOsm/L. Only slight increase in the solute content of the blood going out of the medulla shows that the medullary concentration gradient is maintained as most of the solute is left in the interstitium.
3. Urine osmolarity is inversely related to medullary (vasa recta) blood flow. Faster the blood flows, there is less time for equilibration and increased solute leave blood leading to decreased medullary concentration gradient.

Steps:

1. As the blood descends through the descending limb of vasa recta, water diffuses out and NaCl diffuses in to equilibrate with the increasing osmolarity of medullary interstitial fluid (ISF) from top to bottom established by countercurrent multiplier.
2. As the blood ascends through the ascending limb of vasa recta, water diffuses in and NaCl diffuses out to equilibrate with the decreasing osmolarity of medullary interstitial fluid (ISF) from bottom to top.
3. The process continues and the equilibrium is never reached.

Role of Urea recycling in Medullary Concentration Gradient

Absorption of urea in the collecting tubules, under the influence of ADH, and secreation in the loop of henle contributes ~ 50% of the medullary concentration gradient.

Osmotic Equilibrating Device:

1. When ADH plasma levels are increased during negative water balance:

The collecting ducts become highly permeable to water and water moves out of the collecting duct into the hyperosmotic medullary interstitium down its chemical gradient until the collecting duct lumen and corresponding medullary interstitium have equal water concentrations. So much water leaves by the end of the collecting duct that urine volume is low (perhaps 500 ml/day) and the urine osmolality is high (~ 1200 mOsm/L). The kidneys have saved volume.

2. When ADH plasma levels are decreased during positive water balance:

Water is trapped in the collecting ducts and some solute removal still occurs in the collecting ducts; therefore a very large volume of dilute urine (upto 100 mOsm/L) is formed.

Obligatory urine volume:

If maximal urine concentrating ability is 1200 mOsm/L, the minimal volume of urine that must be excreted is: Concentration of solute to be excreted per day / Maximal urine concentration ability.

To excrete 600 mOsm of solute each day, the obligatory urine volume is 0.5 L/day (600/1200).

Why drinking sea water leads to dehydration?

Ans: This is due to limited ability of human kidney to concentrate the urine to maximal concentration of 1200 mOsm/L. Osmolarity of sea water is ~ 1200 mOsm/L. Hencer for each litre of sea water drunk, 1L of water is required to excrete 1200 mOsm of sodium. But still dehydration occurs. This is because of requirement to excrete other substances as well. At maximal concentration ability, urea contributes 600 mOsm/L. Hence meximum concentration of NaCl that can be excreted by kidney is 600 mOsm/L. Hence, for every 1L of sea water drunk, 2L of fluid loss occurs.

Function:
The brachial plexus is responsible for cutaneous and muscular innervation of the entire upper limb, with two exceptions:

1. the trapezius muscle innervated by the spinal accessory nerve (CN XI)
2. an area of skin near the axilla innervated by the intercostobrachial nerve

Anatomy:
The plexus consists of roots, trunks, divisions, cords and branches.

Mnemonic: Real (Root) Teen (Trunk) Drinks (Division) Cold (Cord) Beer (Branch)

• The roots lie between the anterior and middle scalene muscles.
• The trunks traverse the posterior triangle of the neck.
• The divisions lie behind the clavicle.
• The cords lie in the axilla.

a. Roots: The five roots are derived from the anterior primary rami of C5, 6, 7, 8 and T1. It also recieves contribution from anterior primary rami of C4 and T2. Depending on this there are 2 types of plexus:

1. Prefixed: Contribution by C4 is large and that from T2 is often absent
2. Postfixed: Contribution by T1 is large, T2 is always present, C4 is absent and C5 is reduced in size.

b. Trunks: These roots link up to form 3 trunks:

1. Superior or upper (C5 and C6)
2. Middle (C7)
3. Inferior or lower (C8 and T1)

c. Divisions: Each trunk then splits in 2 (ventral and dorsal divisions), to form 6 divisions:

1. Anterior divisions of the upper, middle, and lower trunks
2. Posterior divisions of the upper, middle, and lower trunks

d. Cords: These 6 divisions will regroup to become the 3 cords. The cords are named by their position with respect to the axillary artery.

1. Posterior cord: from the union of all 3 posterior divisions
2. Lateral cord: from the fused anterior divisions of the upper and middle trunks
3. Medial cord: from the anterior division of the lower trunk

e. Branches:

The cords continue distally to form the main nerve trunks of the upper limb, thus:

1. Lateral cord continues as the musculocutaneous nerve
2. Medial cord, as the ulnar nerve
3. Posterior cord, as the radial nerve and the axillary nerve
4. Cross-communication between the lateral and medial cords forms the median nerve

Median nerve supplies LOAF muscles in hand

1. Lumbricals ( 1st and 2nd)
2. Opponens pollicis
3. Abductor pollicis brevis
4. Flexor pollics brevis

Median nerve gives following cutaneous supply in hands:

1. Lateral 3 and 1/2 on palamar side
2. Middle 3 fingers on dorsal side

The derivatives of brachial plexus are:

From the roots

1. Nerve to rhomboids (Dorsal scapular nerve) – C5
2. Nerve to serratus anterior (Long thoracic nerve) – C5,C6 and C7

From the trunk

1. Nerve to subclavius from the upper trunk – C5 and C6
2. Suprascapular nerve from the upper trunk (supplies supraspinatusand infraspinatus) – C5 and C6.

From the lateral cord

Mnemonic: LML

Root of origin: C5, C6, C7

1. Musculocutaneous nerve (coracobrachialis, brachialis and biceps brachi, lateral cutaneous nerve of forearm)
2. Lateral pectoral nerve (pectoralis major)
3. Lateral root of median nerve

From the medial cord

Mnemonic: MMMMU

Root of origin: C8, T1

1. Medial pectoral nerve (pecotralis major and minor)
2. Medial cutaneous nerves of arm and forearm
3. Ulnar nerve (flexor carpi ulnaris, the medial 2 bellies of flexor digitorum profundus, most of the small muscles of the hand including 3rd and 4th lumbricals, the skin of the medial side of the hand and medial 1 and 1/2 fingers on the palmar side and medial 2 and 1/2 fingers on the dorsal side)
4. Medial root of median nerve

From the posterior cord

Mnemonic: ULTRA

1. Subscapular nerves (subscapularis and teres major) – C5, C6
2. Nerve to latissimus dorsi (thoracodorsal nerve) – C6, C7, C8
3. Axillary nerve (deltoid muscle, teres major, upper lateral cutaneous nerve of arm) – C5, C6
4. Radial nerve (brachialis, brachioradialis, extensor muscle of forearm, anconeus, supinator, triceps, posterior cutaneous nerve of the arm) – C5, C6, C7, C8 and T1

Mnemonic: Radial Nerve Supplies BEAST muscles (brachialis, brachioradialis, extensor muscle of forearm, anconeus, supinator, triceps)

Note that the posterior cord supplies the skin and muscles of the posterior aspect of the limb whereas the anteriorly placed lateral and medial cords supply the anterior compartment structures.

Clinical Anatomy:

It may be damaged in open, closed or obstetrical injuries, be pressed uponby a cervical rib or be involved in tumour. It is encountered, and hence putin danger, in operations upon the root of the neck.

There are 4 types of brachial plexus injuries:

1. Avulsion: most severe type, in which the nerve is torn from the spine
2. Rupture: the nerve is torn but not at the spinal attachment
3. Neuroma: the nerve has tried to heal itself but scar tissue has grown around the injury, putting pressure on the injured nerve and preventing the nerve from conducting signals to the muscles
4. Neurapraxia or stretch: the nerve has been damaged but not torn. Neurapraxia is the most common type of brachial plexus injury.

Lesions of Brachail Plexus: Bird’s Eye View

Correlate the numbers below with the numbers in the picture to find the part involved:

1. Waiter’s tip (Erb’s palsy)
2. Total claw hand (Klumpke’s palsy)
3. Wrist drop
4. Winged scapula
5. Deltoid paralysis
6. Saturday night palsy (wrist drop)
7. Difficulty flexing elbow,variable sensory loss
8. ↓ thumb function (“ape hand”)
9. Intrinsic muscles of hand,claw hand (“Pope’s blessing”)

Erb’s Palsy:

A child with Erb's Palsy

Site of injury: Erb’s point (meeting point of 6 nerves in upper trunk)

Causes: Undue separation of the head from the shoulder commonly encountered in: birth injury, fall of the shoulder or during anaesthesia

Nerve roots involved: C5, C6

Muscles paralysed: Mainly biceps, deltoid, brachialis and brachioradials. Partly supraspinatus, infraspinatus and supinator.

Deformity (Position of the limb): The deformity is known as ‘policeman’s tip hand’ or ‘porter’s tip hand’.
a. Arm: hangs by the side; it is adducted and medially rotated
b. Forearm: extended and pronated

Disability:
a. Abduction and lateral rotation of the arm
b. Flexion and supination of the forearm
c. Biceps and supinator jerks are lost
d. Sensations are lost over a small area over the lower part of deltoid.

Klumpke’s Paralysis:

Klumpke's Paralysis

Site of injury: Lower trunk of the brachial plexus

Cause of injury: Undue abduction of the arm, as in clutching something with hands after a fall from a height, or sometimes in birth injury.

Nerve roots involved: C8, T1

Muscles Paralysed:
a. Intrinsic muscle of the hand (T1).
b. Ulnar flexors of the wrist and fingers (C8).

Deformity (position of the hand):
a. Claw hand due to the unopposed action of the long flexors and extensors of the fingers.
b. In a claw hand there is hyperextension and the metacarpopharyngeal joints and flexion at the interphalangeal joints.

Disability:

• Claw hand.
• Cutaneous anaesthesia and analgesia in a narrow zone along the ulnar border of the forearm and hand.
• Horner’s syndrome: ptosis, mitosis, anhydrosis, enopthalmos, and loss of ciliospinal reflex- may be associated. This is because of injury to sympathetic fibers to the head and neck that leave the spinal cord through nerve T1.
• Vasomotor changes: The skin areas with sensory loss is warmer due to arteriolar dilation. It is also due to the absence of sweating as there is loss of symphatetic activity.
• Trophic changes: Long-standing case of paralysis leads to dry and scaly skin. The nails crack asily with atrophy of the pulp of fingers.

Injury to the Nerve to Serratus Anterior (Nerve of Bell):

Causes:
a. Sudden pressure on the shoulder from above.
b. Carrying heavy loads on the shoulder.

Deformity:
a. Winging of the scapula i.e. excessive prominence of the medial border of the scapula.
b. The pull of the muscle keeps the medial border agains thoracic wall.

Disability:
a. Loss of pushing and punching actions. During attempts and pushing, there occurs winging of the scapula.
b. Arm cannot be raised beyond 90° i.e. overhead abduction which is performed by the serratus anterior is not possible).

Injury to Lateral Cord:

Cause: Dislocation of humerus.

Nerves involved:
a. Musculocutaneous
b. Lateral part of median nerve

Muscles paralysed:
a. Bicpes and coracobrachialis.
b. All muscles supplied by the median nerve, except those of the hand.

Deformity and disability:
a. Midprone forearm.
b. Loss of flexion of forearm.
c. Loss of flexion of the wrist.
d. Sensory loss on the radial sode of the forearm.
e. Vasomotor and trophic changes as above.

Carpal Tunnel Syndrome:

It is a syndrome characterized by the compression of the median nerve as it passes beneath the flexor retinaculum in carpal tunnel.

Read more Carpal Tunnel Syndrome: Features and Treatment | Medchrome

Drawing Brachial Plexus:

Learn to draw well labelled diagram of brachail plexus in 5 minutes

1. Length of Vas deferens or ductus deferens
2. Length of thoracic duct
3. Length of Spinal cord
4. Femur (for 6 feet person)
5. Length of transverse colon
6. Distance from the incisor teeth to the cardiac end of the stomach
7. Umbilical cord at birth
8. Length of sartorius muscle

All are about 25 cms or 10 inches:

1. Length of Esophagus
2. Length of Ureter
3. Length of Duodenum
4. Length of Descending colon

All are about 10 cms or 4 inches:

1. Length of Trachea
2. Length of Fallopian or Uterine tube
3. Length of Common bile duct
4. Length of 3rd part of Duodenum (Transverse Duodenum)
5. Length of Posterior wall of Vagina
6. Anteroposterior measurement of Inlet of Pelvis
7. Transverse measurement of Outlet of Pelvis

All are about 4 cms or 1.5 inches:

1. Length of Auditory tube
2. Length of Anal canal
3. Length of Female urethra
4. Length of Cystic duct
5. Length of Common hepatic duct
6. Length of External acoustic/auditory meatus when measured from tragus
7. Length of Optic nerve
8. Length of Ovary
9. Length of Inguinal canal
10. Length of Femoral sheath
11. Thickness of Kidney
12. Width of Pons

All are about 1 inch or 2.5 cm

1. Length of Medulla
2. Length of Midbrain
3. Length of Pons
4. Length of 4th part of Duodenum (Ascending Duodenum)
5. Length of Ducts of Bartholin’s gland (Greater vestibular glands)
6. Diameter of Trachea
7. Diameter of Right main bronchus
8. Distance between Ureteric orifice in Empty bladder

Structures whose width is greater than length:

1. Pons varioli
2. Cecum
3. Prostate

Descent of Testis:

1. 3rd month: Reaches Iliac fossa
2. 6th month: Rests at Deep Inguinal ring
3. 7th month: Traverses Inguinal canal
4. 8th month: Reaches Superficial Inguinal ring
5. 9th month: Descneds into Scrotum

Rule of 2s for Meckel’s Diverticulum:

Meckel’s Diverticulum is a congenital outpouching of the ileum that is a normal variant and is the remnant of omphalomesenteric (vitellointestinal) duct. It is a true diverticulum, that consists of all the layers of the intestinal wall (mucosa, submucosa and muscularis).

1. Occurs in 2% population
2. 2 times more common in male
3. 2 feet proximal to ileocecal valve
4. 2 inches in length
5. 2 years of age is typical for onset of symptoms
6. 2 % are symptomatic
7. 2 types of mucosa possible (Small intestine and Gastric)

Rule of 2s: 2nd week of Development (Embryology)

1. Trophoblast differentiates into 2 layers: Cytotrophoblast and Sycytiotrophoblast
2. Embryoblast forms 2 layers: Epiblast and Hypoblast
3. Extraembryonic mesoderm splits in 2 layers: Somatopleure and Splanchnopleure
4. 2 cavities are formed: Amniotic cavity and Yolk sac cavity

Rule of 3s: Thoracic spine levelling

1. T1-3 (and T12) transverse processes are at the level of the corresponding thoracic spine.
2. T4-6 (and T11) transverse processes lie superiorly between its level’s spine and the spine of the thoracic segment above it.
3. T7-9 (and T10) transverse processes lie superiorly at the level of the superior segment’s spine.

Rule of 3s: 3rd week of Development

1. Bilaminar germ disc changes into trilaminar germ disc with 3 layers ectoderm, mesoderm and endoderm
2. Formation of 3 important structures: Notochord, Neural plate and Primitive streak
3. 3 layered chorionic villi
4. 3 carnegie stages

Dalley/Voss Rule of 3s of 2s: Sacral Plexus

For 3 sets of 3 nerves:

• 1st set of 3 nerves will all have 3 spinal contributions (3,3,3)
• 2nd set of will have 2 nerves with 3 spinal contributions and 1 nerve with 2 spinal contributions (3,3,2)
• 3rd set will have 1 nerve with 3 spinal contributions and 2 nerves with 1 spinal contribution (3,2,2)

1st set of nerves (3,3,3):

1. Superior gluteal nerve: 3 spinal contributions beginning from L4 (L4,L5,S1)
2. Inferior gluteal nerve: 3 spinal contributions beginning from L5 (L5,S1,S2)
3. Posterior femoral cutaneous nerve: 3 spinal contributions beginning from S1 (S1,S2,S3)

2nd set of nerves (3,3,2):

1. Nerve to Quadratus femoris: 3 spinal contributions beginning from L4 (L4,L5,S1)
2. Nerve to Obturator internus: 3 spinal contributions beginning from L5 (L5,S1,S2)
3. Nerve to Piriformis: 2 spinal contributions beginning from S1 (S1,S2)

3rd set of nerves (3,2,2):

1. Pudendal nerve: 3 spinal contributions beginning from S2 i.e. where you left off with pyriformis (S2,S3,S4)
2. Nerve to levator ani: 2 spinal contributions beginning from S3 (S3,S4)
3. Nerve to coccygeus:2 spinal contributions beginning from S4 (S4,S5)

Gate’s Rule of 4s: For Detecting Brainstem Lesion

There are 4 rules in Rules of 4s:

1. 4 structures in the “M“idline begins with “M“: Motor pathway (Corticospinal Tract), Medial Lemniscus, Medial longitudinal fasciculus, Motor nucleus and nerves (CN 3,4,6,12)
2. 4 structures to the “S“ide begins with “S“: Spinothalamic, Spinocerebellar tract, Sensory nucleus of CN V, Sympathetic pathway
3. 4 Cranial nerves in Each of:
• Medulla: 9,10,11,12
• Pons: 5,6,7,8
• Above Pons: 1,2,3,4
4. The 4 midline motor nuclei can exactly divide 12 (excluding 1 and 2 which are purely sensory) – 3, 4, 6 and12 (Remaining 4 motor nuclei are on sides/laterally i.e 5, 7, 9 and 11).

Associated deficits of 4 Midline “M” structures:

1. Motor pathway (or corticospinal tract): contralateral weakness of the arm and leg.
2. Medial Lemniscus: contralateral loss of vibration and proprioception in the arm and leg.
3. Medial longitudinal fasciculus: ipsilateral internuclear ophthalmoplegia (failure of adduction of the ipsilateral eye towards the nose and nystagmus in the opposite eye as it looks laterally).
4. Motor nucleus and nerve: Ipsilateral loss of affected cranial nerve function (3, 4, 6 or 12).

Associated deficits of 4 Side “S” structures:

1. Spinocerebellar pathways: ipsilateral ataxia of the arm and leg.
2. Spinothalamic pathway: contralateral alteration of pain and temperature affecting the arm, leg and rarely the trunk.
3. Sensory nucleus of 5th Cranial nerve: ipsilateral alteration of pain and temperature on the face in the distribution of the 5th cranial nerve (this nucleus is a long vertical structure that extends in the lateral aspect of the pons down into the medulla).
4. Sympathetic pathway: Ipsilateral Horner’s syndrome i.e ptosis, miosis, anhydrosis.

Associated deficits of 4 Cranial nerves in Medulla:

1. 9th or Glossopharyngeal: ipsilateral loss of pharyngeal sensation
2. 10th or Vagus: ipsilateral palatal weakness
3. 11th or Spinal accessory: ipsilateral weakness of the trapezius and sternocleidomastoid muscles
4. 12th or Hypoglossal: ipsilateral weakness of the tongue

Associated deficits of 4 cranial nerves in Pons:

1. 5th or Trigeminal: ipsilateral alteration of pain, temperature and light touch on the face back as far as the anterior two-thirds of the scalp and sparing the angle of the jaw
2. 6th or Abducens: ipsilateral eye abduction weakness
3. 7th or Facial: ipsilateral facial weakness
4. 8th or Auditory: ipsilateral deafness

Associated deficits of 4 cranial nerves above Pons:

1. 1st or Olfactory: not in midbrain.
2. 2nd or Optic: not in midbrain.
3. 3rd or Occulomotor: impaired adduction, supraduction and infraduction of the ipsilateral eye (eye is turned out and slightly down)
4. 4th or Trochlear: eye unable to look down when the eye is looking in towards the nose

Applying the knowledge:

Pathways and tracts pass through the entire length of brainstem and can be likened  to “meridians of longitude” whereas the cranial nerves can be likened to “parallels of latitude”. To establish the site of brainstem lesion, you need to detect the point of intersection of the meridians of longitude and parallels of latitude. Thus a medial brainstem syndrome will consist of the deficits of 4 “M”s and the relevant motor cranial nerve, and a lateral brainstem syndrome will consist of the deficits of 4 “S”s and either the 9–11th cranial nerve if in the medulla, or the 5th, 7th and 8th cranial nerve if in the pons.

Example:

58 years old lady with left hemiparesis, Left side loss of proprioception and right sided tongue deviation.

1. Left hemiparesis is associated with deficit of Motor or corticospinal pathway of Right side which lies medially
2. Left sided loss of proprioception is associated with deficit of medial lemniscus of Right side which lies medially
3. Right sided tongue deviation is associated with deficit of Cranial nerve 12 on Right side which lies medially in medulla

Diagnosis: Medial medullary syndrome due to lesion in right vertebral artery

Rule of 7s: For Orbit

There are 7 bones, 7 intraorbital muscles and 7 nerves in orbit

• 7 Bones: Frontal, Ethmoid, Lacrimal, Sphenoid, Zygomatic, Palatine, Maxilla
• 7 intraorbital muscles: Levator palpebrae, 4 recti (Superior, Inferior, Medial and Lateral), 2 oblique (Superior and Inferior)
• 7 orbital nerves: Optic (CN II), Occulomotor (CN III), 3 branches of Opthalmic nerve (CN V1) – Frontal, Nasociliary, Lacrimal, Abducens nerve (CN VI)