Peripheral Neuropathy

Question 1

What is the value of a resting membrane potential

Answer 1

-65mV

Question 2

What are the relative concentrations of Cl, Na and K in a RMP

Answer 2

Cl and Na high outside.

K higher inside.

Question 3

What maintains the RMP, and how?

Answer 3

Na-K transporter (pump) transports 3 Na out to every 2 K in, using ATP.

Question 4

what are the 2 types of channels enabling RMP/APs?

Answer 4

LGIC, VGIC

Question 5

Initial trigger for AP

Answer 5

ligand gated Na channel (ligand it the neurotransmitter), Na starts to move into cell.

Question 6

What causes the fast rising phase of depolarisation?

Answer 6

after some Na has entered through LGICs, VG Na channels open, allowing Na to flood in.

Question 7

what does the membrane potential reach in a full AP?

Answer 7

40mV

Question 8

What causes the fast depolarisation to stop, and repolarisation to begin?

Answer 8

LGIC and VGIC for Na close (depolarisation stops). This level of depolarisation causes VGIC for K to open. Electrochemical gradient causes K to efflux - depolarisation.

Question 9

What is Myelin?

Answer 9

80% lipid, 20% protein.
White matter.
insulates and speeds up APs.

Question 10

pathology of Lambert-Eaton syndrome

Answer 10

Antibodies are generated against calcium channels at the NMJ. This can be due to small cell lung carcinoma. Not enough Ca influx to elicit an AP, but continuous effort may enable a response.

Question 11

What is the course of events to transfer an AP from one neurone to another?

Answer 11

AP arrives and is sensed by a VG Ca channel.
Ca influx onto presynaptic terminal
Vesicles release neurotransmitter into cleft
Neurotransmitter binds to post synaptic receptors.

Question 12

How does the initiation of an AP from an excitatory neurotransmitter differ from an inhibitory neurotransmitter?

Answer 12

Excitatory neurotransmitters allow influx of Ca, whereas inhibitory neurotransmitters open Cl channels.

Question 13

What are the two divisions of the PNS?

Answer 13

Somatic and ANS.

Question 14

From where does the SNS arise?

Answer 14

T1-L2

Question 15

What is the sympathetic chain?

Answer 15

para-vertebral ganglia into which myelinated sympathetic axons enter, and unmyelinated post ganglionic sympathetic axons leave.

Question 16

what do post ganglionic sympathetic neurones release?

Answer 16

NA (onto adrenergic receptors)

Question 17

from where does the PSNS arise?

Answer 17

brainstem and sacrum

Question 18

What neurotransmitter do posts ganglionic parasympathetic neurones release?

Answer 18

ACh (onto muscarinic or nicotinic receptors)

Question 19

What are nicotinic receptors?

Answer 19

excitatory
LGICs
activated by ACh

Question 20

What are muscarinic receptors?

Answer 20

Metabotropic receptors (eg GPCRs)
activated by ACh
on effectors of PSNS

Question 21

What does ACh activate?

Answer 21

Muscarinic and nicotinic receptors.
Initiates all pre ganglionic neurones.
released from PSNS post ganglionic neurones to effectors

Question 22

What does NA activate?

Answer 22

Adrenergic receptors (alpha and beta).
released from SNS post ganglionic neurones.

Question 23

What can CMAP studies show?

Answer 23

Compound Muscle Action Potential
the velocity and the
amplitude of the AP

Question 24

What would be a feature of CMAP study in a demyelinating pathology?

Answer 24

slow conduction velocity, dispersed AP (not all firing at once)

Question 25

What would be a feature of CMAP in an axonal injury?

Answer 25

reduced AP amplitude - not all firing, but ones that are, are fine, so conduction velocity is normal.

Question 26

Explain carpel tunnel syndrome

Answer 26

Compression neuropathy of median nerve at wrist. Index, middle and half of ring finger loss os sensation. Loss of thumb abduction Thenar eminence wasting.

Question 27

what are the symptoms of ulnar nerve compression?

Answer 27

little and half of ring finger loss of sensation/function.

Question 28

Pain, loss of sensation on top of foot. Weakness lifting foot.

Answer 28

Peroneal Nerve (at knee) compression.

Question 29

Wrist drop. Lateral posterior of hand numb.

Answer 29

Radial nerve compression.

Question 30

pain/numbness/burning sensation on outer thigh.

Answer 30

compression of lateral cutaneous nerve.

Question 31

What is the pathology of GBS?

Answer 31

following an infection, autoimmune response causing Wallerian demyelination of PNS neurones. SELF LIMITING

Question 32

``` Weakness: Rapid onset, distal, bilateral following infection. ```

Answer 32

GBS.

Question 33

Treatment for GBS

Answer 33

GBS is self limiting, but pt can be very ill. Reduce autoimmune response: IV Ig, Plasma exchange Reduce risk of DVT - heparin Monitor resp - poss ITU.

Question 34

What is the pathology of LEMS?

Answer 34

Antibodies against VG Ca channels, prevents ACh release at NMJ. 60% of Pts have had lung cancer.

Question 35

Areflexia, proximal muscle weakness - improves as effort is sustained, reflexes may return too.

Answer 35

Lamber Eaton Myasthetnic Syndrome

Question 36

What's the pathology of myasthenia gravis?

Answer 36

Antibodies against ACh receptor. There are fewer receptors to excite - when prolonged excitation occurs, they get saturated rapidly and weakness progresses. There is an association with thymus hyperplasia/atrophy.

Question 37

``` Progressive weakness esp in: Face/mouth: difficulty speaking dysphagia difficulty breathing *symptoms improve is pt relaxes for a while ```

Answer 37

Myasthenia Gravis (ACh receptors become available (unsaturate) upon relaxation and are able to elicit a response again.

Question 38

Treatment for Myasthenia Gravis

Answer 38

Reduce excitation: AChase to reduce ACh in NMJ reduce antibodies: IV Ig, plasma exchange, immunosuppressants. Thymectomy.

Question 39

COPS Maintain myelin. | What is the Mnemonic?

Answer 39

in the CNS - Oligodendrocytes | in the PNS - Schwann cells

Question 40

Child Foot drop Curled toes Loss of sensation - feet, hands.

Answer 40

Charcot-Marie-Tooth

Question 41

What is the pathology of Charcot-Marie-Tooth?

Answer 41

Genetic - peripheral demyelination