CMF tutorial

Question 1

Where can lesions occur?

Answer 1

1) Brain/Brainstem 2) Spinal Cord 3) Anterior white commisure 4) Dorsal spinocerebellar tract 5) Primary somatosensory cortex 6) Internal cortex

Question 2

What would you observe when the Anterior White commisure is damaged

Answer 2

Pain and Temperature - loss on both sides

Question 3

What would you observe when the dorsal spinocerebellar tract is damaged?

Answer 3

Impaired joint position (propriocception) on the SAME side

Question 4

What would you observe when the Primary somatosensory cortex is damaged?

Answer 4

Loss of touch and pressure on the opposite side NO loss of pain and temp unless it’s a deep lesion

Question 5

What would you observe when the Internal capsule is damaged?

Answer 5

Loss of pain, temp, touch and pressure The only place where all four come together. If you lose all four, chances are you’ll find the lesion here.

Question 6

Describe the 5 parts of the Internal Capsule

Answer 6

1) Anterior limb (inter-brain connections) 2) Genu (cortico-bulbar tract, face and head) 3) Posterior limb (corticospinal) 4) Retrolenticular (visual radiation from/to LGB) 5) Sub-lenticular (auditory radiation from/to MGB)

Question 7

Where is the lesion for this case? (to a minimal to maximal extent) 1) The patient has loss of discriminative touch and pressure sensation on the left side below the nipple line. 2) Pain and temp sensation is normal on the left but impaired on the right side below the nipple line 3) Joint sensation is impaired in all joints on the left leg 3) Patient has an upper motor neuron weakness in the left leg with increased reflexes 4) Extensor plantar response

Answer 7

MINIMAL -all the following is starting 1) Dorsal column (discrim/touch/pressure) 2) Dorsal spinocerebllar tract 3) Lateral spinothalamic tract (pain/temp of contralateral side) 4) Corticospinal tract (UMN) MAXIMAL 1) Ruberospinal pathway 2) Reticulospinal pathway 3) Parts of dorsal gray horn over a few spinal segments 4) LMN over a few spinal segments (faccid paralysis may not be detectable) 5) Anterior spinothalamic tract (crude/non-discriminative tough and pressure sensation)

Question 8

Where is the lesion for this case? (to a minimal to maximal extent) 1) The patient has difficulty in understanding what is said to her 2) Difficulty reading and understanding the written word 3) She has hesitancy, fragmentation and slurring of speech and has difficulty producing the words she wants to use 4) UMN weakness of the muscles of the lower part of the face on the right side and in the right arm and hand 5) Two point discrim is impaired in the right hand and on the right side of the face 6) Diminished hearing in the right ear 7) Okay pain and temp 8) Okay visual field

Answer 8

Minimal 1) Wernike’s area 2) Supramarginal and angular gyri 3) Broca’s area 4) Postcentral gyrus (from face to hand area) 5) Precentral gyrus (from face to hand) 6) Primary auditory cortex Maximal 1) Arcuate fasiculus 2) Cerebellum (slurring of speech) 3) Could extend anteriorly into the inferior frontal gyrus, inferiorly into middle temporal gyrus, superiorly into superior parietal lobule (because no detectable clinical effects).

Question 9

Describe Parkinson’s Disease -Anatomy -Symptoms

Answer 9

1) Loss of dopimergic cells in the substantia nigra 2) Loss of inhibition of D2-positive GABA-ergic cells of the striatum 3) Loss of motor initiation 4) Symptoms -bradykinesia -tremor at rest -rigidity -flattened mood

Question 10

How does an ear detect different frequencies of sound?

Answer 10

1) Place principle: -Different areas of the cochlear responds to different frequencies (are tonotopically organised) due to different stiffness of the basilar membrane. -At the base the basilar membrane is hard. Therefore responds to high frequencies -At the tip, the basilar membrane is floppy and therefore responds to low frequencies. 2) Volley principle -Low (low only) frequencies are detected by temporal frequency of the stimulus -e.g. if the sterocilia move 500times/sec, they’ll stimulate the nerve 500times/sec. A nerve cannot follow a stimulus beyond 2000hz, so we need the place principle for higher frequencies.

Question 11

What is the function of the middle ear?

Answer 11

-Air conduction of sound by displacement of airdrum and ossicular chain -Transformer to overcome resistance of inner ear fluids, matching the low impedence (density) of air to high impedence of inner ear fluid. 1) Greater area of eardrum transfers more pressure on smaller stapes footplate 2) Malleus arm is longer than the incus, which generates a larger force on the stapes

Question 12

What kind of hearing loss is there?

Answer 12

1) Conductive (outer/middle ear)- problem with air conduction. 2) Sensorineural (cochlear, cochlear nerve) 3) Mixed 4) Central

Question 13

How do you decide what sort of learing loss has occured?

Answer 13

History Examination (otoscopy, whisper test, Rinne and Weber test, audiogram, cranial nerve exam)

Question 14

What are some causes of conductive hearing loss?

Answer 14

1) Foreign substance 2) Tympanic membrane perforation 3) Fluid in middle ear due to colds 4) Wax build up

Question 15

How can you tell if someone has conductive or sensorineural hearing loss by looking at the audiogram?

Answer 15

Air-bone gap in the conduction auditory loss No air-bone gap in the sensorineural auditory loss

Question 16

What does the tympanometry measure?

Answer 16

Assess ear drum motility (transfer of sound across the middle ear) e.g. glue ear Assesses middle ear pressure (is pressure on inside and outside of ear drum the same?) Assesses integrity of middle ear muscles and related neural pathways Low compliance - if conductive deafness Normal- can be sensorineural deafness

Question 17

What does the vestibule sense?

Answer 17

1) Linear acceleration (utricle, sacule) 2) Angular acceleration (semi-circular canal ampulla) It mainly provides info about the position of the head. The brain integrates this information with all the other information it receives

Question 18

Describe the detection of linear acceleration

Answer 18

-Sensory hair cells cover the interior of the vestibule -Hairs stick inwards. -Covered by gelatinous mass -Otoconia (little stones) sit on the gel. Otoconia increase membrane mass and give it greater inertia. So when you move horizontally, the sterocilia (hairs) displace towards the kinocilium (longest hair) and your brain decides you’re moving. When you tilt your head, one macula will depolarise and the other hyperpolarise, since the saccule and utricle have their hairs oriented in the opposite direction.

Question 19

Utricle is ______ Saccule is ______

Answer 19

Utricle is horizontal Saccule is vertical

Question 20

Describe why you get nystagmus when you have vestibular disease

Answer 20

A loss of function on one side will cause the brain to think the other side has increased its output. Good side becomes dominant. Your brain will think that you are rotating towards the good/dominant side Therefore your eyes try to “compensate” by looking towards the bad/non-dominant side. When they turn as far as they can go, they rapidly flick back towards the good side. Called nystagmus.

Question 21

Describe the cause of BPPV and BPPV diagnosis and treatment

Answer 21

BPPV is caused by an otoconium escaping from the vestibule and entering a canal, touching off a cupula. This causes vertigo (surroundings moving/spinning) & nystagmus. Short duration of attacks. Attacks caused when the head is in specific postiions. Get a proper history Diagnose by: Dix-Hallpike Treat by: Epley’s maneuver

Question 22

What are the 4 basic processes of pain?

Answer 22

1) Transduction 2) Transmission 3) Perception 4) Modulation

Question 23

If you rub an area that is in pain, why does the perceived pain reduce?

Answer 23

-Activation of the A(B) fibres. -According to the gate control theory, this will activation will synapse onto specialised interneurons -These specialised interneurons releases enkephalin into the dorsal horn. -This blocks the neurotransmitter release from A-delta and C fibres, which ‘keeps the gate closed’ i.e. prevents 2nd order neurons from the dorsal horn sending pain signals to the brain.

Question 24

Why can your back pain become worse over the months?

Answer 24

Windup Windup is the process where there’s increased AP output from DH cells in response to sustained low frequency input from nociceptive afferents via C fibres to the DH neurons. Therefore of pain is heightened. Repetitive release of Glutamate from the C and A(delta) fibres will result in repetitive/excessive stimulation of the NMDA/AMPA receptors of the DH neurons and therefore influx of Calcium Consequently, the excessive activation of NMDA receptors and increased Ca2+ influx can lead to neurological and pathological changes in the DH neurons, by upregulating of receptors and lowering of the receptor’s threshold. As a result, they become more responsive to all of its inputs- resulting in central sensitization (secondary hyperalgesia and allodynia).

Question 25

Describe the mechanism around chronic pain

Answer 25

Windup occurs. If the pain is not treated for a long time, the neurotransmitter released from the 1st order neuron affects the glial cells in the dorsal root. This results in physiological changes and the glial cells start producing cytokines The cytokines act on the terminal end of the 1st order neurons to produce MORE neurotransmitters Therefore automatic viscious cycle of neurotransmitter release occurs, independent of the stimulus = chronic pain.

Question 26

What are some advantages of Pethidine over Morphine

Answer 26

Pethidine causes less miosis and biliary spasm They have higher oral availability than morphine so a lower dose is needed Some disadvantages: -Tachycardia -Accumulates in renal failure

Question 27

How do local anaesthetics provide pain relief?

Answer 27

Local anaesthetics cross cell membrane in their non-ionized form. Inside the cell, they become ionized again. They block Na+ channels intracellularly, enter into channel when deactivation gate is open and prevent Na+ entry into the cell when the activation gate opens

Question 28

How do general anaesthetics produce hypnosis/amnesia?

Answer 28

Theophylline, Propofol, Etomidate, Midazolam 1) Enhance GABA, more are released 2) GABA binds to GABA receptors which cause a prolonged influx of Cl- 3) Cell hyperpolarises and pain messages are supposed causing hypnosis/amnesia. Ketamine 1) noncompetitive antagonism at the N-methyl-Daspartate (NMDA) receptor Ca2þ channel pore. Reduces Ca2+ influx. 2) In addition, it reduces the presynaptic release of glutamate. Inhibits excitation.

Question 29

How do general anaesthetics produce hypnosis/amnesia?

Answer 29

Thiopentone, Propofol, Etomidate, Midazolam 1) Enhance GABA, more are released 2) GABA binds to GABA receptors which cause a prolonged influx of Cl- 3) Cell hyperpolarises and pain messages are supposed causing hypnosis/amnesia. Ketamine 1) noncompetitive antagonism at the N-methyl-Daspartate (NMDA) receptor Ca2þ channel pore. Reduces Ca2+ influx. 2) In addition, it reduces the presynaptic release of glutamate. Inhibits excitation.

Question 30

Describe the the pharmacokinetics of general anaesthetic agents

Answer 30

Delivered straight to the vessel rich organs, including the brain. Therefore onset is rapid. Offset is mainly not due to metabolism. General plasma concetration falls, especially in the VRG, as the circulation takes the drug to the other tissues where it has no effect- redistribution Then the drug is metabolised.

Question 31

Describe the characteristics of IV anaesthetics: Thiopentone (5)

Answer 31

-Very rapid onset. -Rapidly redistributed. -Metabolised in liver -Cleared slowly (will accumulate) -Barbituate

Question 32

Describe the characteristics of IV anaesthetics: Propofol (5)

Answer 32

-Phenol -Moderately Rapid onset -Rapidly redistributed -Can be infused because of rapid clearance -Metabolised in liver

Question 33

Describe the characteristics of IV anaesthetics: Etiomidate (6)

Answer 33

-Imidazol -Moderate onset -Cardiovascular stability -Rapid clearance -Adrenocortical inhibition (poor recovery) -Myoclonus and epileptogenic

Question 34

What are the 2 types of NMBAs?

Answer 34

Depolarising -Succinylcholine -Agonist of Acetylcholine receptor (biphasic effect) Non-depolarising -Block Acetylcholine receptor (antagonist)

Question 35

How would you treat someone with ALS?

Answer 35

Not a lot you can do Rilozole has shown small beneficial effects

Question 36

What is botox?

Answer 36

Botulism toxins bind to nerve terminals They are internalised by endocytosis and cause proteolysis of several membrane proteins involving in neurotransmitter release Therefore causes weakness of striated and msooth muscles.

Question 37

How do you diagnose Parkinson’s Disease

Answer 37

1) 2 or more motor symptoms 2) Symptoms improve with L-dopa 3) Cannot be explained by other causes

Question 38

(d) Describe how an action potential for discriminative touch and pressure at the level of the hand is transmitted through the dorsal column-medial lemniscus tract. Include the important areas of the spinal cord, brainstem, thalamus, internal capsule, and cortex (10 marks).

Answer 38

1. A myelinated, granule, pseudounipolar primary sensory neuron sends an action potential to the spinal cord through the dorsal root.
2. 25% of fibres will then move to the dorsal funiculus. The other 75% will synapse at laminae III and IV, or VIII and IX.
3. Depending on where the primary neuron originated, it will either move up the spinal cord via the gracile (leg) or cuneate (arm) fasciculi.
4. At the level of the medulla, the gracile and cuneate fasciculi terminate at the gracile and cuneate nuclei. The primary neurons synapse with a secondary neuron here, and decussation occurs.
5. The secondary neurons travel as internal arcuate fibres through the hindbrain in the tegmentum, as a structure called the medial lemniscus. This travels up through the midbrain posterior to the substantia nigra.
6. At the thalamus, the secondary neurons terminate at the ventroposterior l_ateral nucleus, as this is the nucleus that receives information on the body._
7. The secondary neuron synapses with a tertiary neuron, which then travels up through the internal capsule to the primary sensory cortex which is also arranged in a h_omuncular fashion_. The leg and foot is medial while the face and arms are lateral.

Question 39

(c) Describe how an action potential for movement is transmitted through the corticospinal tract in a normal patient. Include the important areas of the cortex, internal capsule, brain stem, and spinal cord during your explanation. (10 marks)

Answer 39

1. The upper motor neurons project their axons down from the primary motor cortex through the internal capsule.
2. The internal capsule passes around the thalamus. The posterior limb carries the body’s information.
3. Once past the thalamus, the corticospinal tract makes up the crus cerebri in the mid brain. T_he foot is found laterally, face medially._
4. At the level of the pons, the corticospinal tract breaks up into the pontine nuclei, to make way for lower motor facial neuronal bodies.
5. Once all of the facial neurons have left, the pons thins out into the medulla.
6. The corticospinal tract forms the medullary pyramids, where decussation occurs for 85% of all fibres.
7. These fibres then become the lateral corticospinal tract, which goes on to form the lateral funiculus in the spinal cord. The l_eg is represented laterally, the arm medially._
8. At the level of the spinal cord of the muscle this neuronal path innervates, the upper motor neuron crosses over to laminae 8 and 9 in the grey matter.
9. The UMN synapses with a lower motor neuron, which leaves the body via the ventral root to innervate the muscle.