Peripheral Neuropathies

Question 0

Carpal tunnel syndrome examination

Answer 0

Sensation in index>little finger, impairment on one side of ring finger
Weakness of thumb abduction and wasting of APB
Tinel and phalen signs

Question 1

Carpal tunnel syndrome history

Answer 1

Pins and needles in fingers
Sensory loss or pain proximally or wrist
Weakness in thumb/fingers
Occurs for a few minutes at night on waking or when gripping

Question 2

Tinel sign

Answer 2

A test for irritated nerves used to diagnose carpal tunnel

Taping on the nerve elicit a ‘pins and needles’ sensation over the distribution of the nerve

Question 3

Phalen manoeuvre

Answer 3

A way to test for carpal tunnel by holding the hands at full forced flexion for 30-60 seconds, or at full extension for 2mins (reverse phalen)
The pressure in the carpal tunnel is raised by the contraction of FDP pulling the lumbricals into it,worsening any symptoms.

Question 4

Pathology of carpal tunnel

Answer 4

Pressure on the nerve> demyelination> slow conduction
If pressure is prolonged > axonal loss > wasting of muscle
Demyelination is reversible, axonal loss much less
In CTS the median nerve conduction is slower than the ulna nerve

Question 5

Carpal tunnel syndrome treatment

Answer 5

Early treatment is occupational
After this splinting
Steroid injections
Surgery

Question 6

Ulnar neuropathy at the elbow

Answer 6

Often history of arthritis or trauma with a palpable ulnar nerve
Pain/tenderness at elbow and sensory loss in the lateral ring and little finger
Weakness and wasting in the small muscles of the hand

Question 7

Common perineal nerve palsy

Answer 7

Foot drop or weakness and numbness
Made worse by compression (bending, squatting, crossing legs)
Often occurs after long periods of compression (flights) and usually recover after a couple of two days

Question 8

Generalised peripheral neuropathies

Answer 8

Can be hereditary or acquired
Axonal or demyelination
Polyneuropathy (single continuous problem) or mononeuritis multiplex (multiple distinct mononeuropathy)

Question 9

Length dependant polyneuropathy

Answer 9

Length dependant, glove and stockings distribution
Symmetrical, distal sensory loss/wasting/areflexia
Check for metabolic cause (glucose, B12, folate, thyroid)
Treat underlying cause and give drugs for pain (gabapentin, pregabalin, amotriptyline)

Question 10

Pathogensis of peripheral neuropathies

Answer 10

Axonal –> muscle wasting, pain, sensory symptoms and signs but only ankle reflexes lost

Demyelinating –> weakness without wasting, motor signs, general loss of reflexes

Question 11

Nerve conduction changes in peripheral neuropathies

Answer 11

Axonal –> small amplitude, Normal velocity/F waves
Needle EMG: denervation
Demyelination –> prolonged distal latency, slow velocity with conduction block, prolonged F waves
Needle EMG: possibly normal

Question 12

F waves

Answer 12

When a nerve is stimulated in an EMG the impulse travels up the nerve to the spine and come back down producing a second wave

Question 13

Diabetic neuropathies

Answer 13

Symmetrical distal length dependant sensory deficits
Proximal neuropathy lumbosacral radiculo-plexus neuropathy
Can also get mononeuropathy

Question 14

Demyelination neuropathies

Answer 14

Hereditary–> Charcot-Marie-tooth disease
Acquired–> acute : Guillain-Barré syndrome
Chronic –> chronic inflammatory demyelinating polyradiculoneuropathy (CIDP)
IgM paraprotein-associated

Question 15

Clinical findings in Guillain-Barré syndrome

Answer 15

Raised CSF protein but normal cells
Reduced conduction velocity/block due to patchy demyelinating neuropathy
Can lead to secondary axonal loss

Question 16

Guillain-Barré syndrome

Answer 16

Acute ascending progressive paralysis, sensory loss and areflexia, often secondary to infection
Worsening progress over 1-3 weeks –> risk of respiratory muscle involvement or cardiac arrhythmias
Recover in 2-6 months

Question 17

Chronic inflammatory demyelinating polyradiculoneuropathy (CIDP)

Answer 17

Chronic form of GBS giving a syndrome similar to peripheral MS, with weakness more Than sensory loss
Usually worst proximal
Areflexia
Raised CSF protein

Question 18

Causes of mononeuritis multiplex

Answer 18

Diabetes
Vasculitis, ANCA associated or secondary rheumatological or due to hepatitis B/C
Multiple nerve compressions

Question 19

Bell’s palsy

Answer 19

Acute unilateral facial nerve weakness
May have pain behind the ear, Loss of taste or hyperacusis
UMN palsy effects all muscles equally, LMN palsy spares forehead
Treat with 10day prednisolone –> 75% improve spontaneuously
25% develop synkinesis/crocodile tears

Question 21

Crocodile tears

Answer 21

A rare consequence of recovery from Bell’s palsy causes faulty regeneration of the nerve such that the patient sheds tears when the eat

Question 22

Motor Neuron Disease - symptoms

Answer 22

MND refers to a collection of 5 syndromes with different presentations and symptoms

Question 23

MND - treatment

Answer 23

No curative treatment but Riluzole (blocks TTX sensitive Na channels which occur in damaged neurons) prolongs survival for 2-3 months

Question 24

MND classification

Answer 24

Amyotrophic lateral sclerosis (ALS)
Primary Lateral sclerosis (PLS)
Progressive muscular Atrophy (PMA)
Progressive bulbar palsy (PBP)
Pseudobulbar palsy

Question 25

Amyotrophic lateral sclerosis (ALS)

Answer 25

Most common form of MND
a mix of UMN and LMN signs. 75% present with limb symptoms, 25% with bulbar symptoms
No sensory deficit
5% frontotemporal dementia and 30-50% show some subtle cognitive decline.

Question 26

Primary Lateral sclerosis (PLS)

Answer 26

A rare form of MND with only UMN symptoms with onset after 50. commonly progressive leg spasticity with pain, but may start in hands or face –> slowly progressive with normal life span unless it progresses to ALS

Question 27

Progressive Muscular atrophy (PMA)

Answer 27

A rare (4%) form of MND only affecting the LMNs with a life expectancy of ~ five years (ALS is less)
presents with atrophy, fasciculations and weakness
may present in just arms or legs, which has a better prognosis

Question 28

Progressive Bulbar Palsy

Answer 28

25% of people diagnosed, affects CN IX,X,XII (LMN)
slow onset at 50-70yrs with 1-3 year prognosis
25% of PBP pts will go on to develop ALS
can show emotional changes if corticobulbar tract is involved

Question 29

Pseudobulbar palsy

Answer 29

UMN damage in the bulbar region/corticobulbar tract of the brainstem. Presents with dysphagia, dysarthria, brisk jaw jerk, spastic tongue and labile affect.often found to have UMN signs in the limbs as well. Can be due to several reason and a form of MND

Question 30

Cauda Equina syndrome

Answer 30

Compression or injury to the cauda equina at the end of the spinal cord (L1/2). Presents with low back pain +-radiation to the legs, LMN signs in the legs, saddle sensory abnormalities and sphincter dysfunction