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Neurology > Neurophysiology and peripheral neuromuscular disease > Flashcards

Neurophysiology and peripheral neuromuscular disease Flashcards

1
Q

What is the result of a nerve cell body lesion/MND?

A

Normal nerve conduction study

Widespread lower motor neuron signs

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2
Q

What is the result of a nerve root lesion?

A

Changes in multiple muscles with the same nerve root

Normal sensation

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3
Q

What is the results of a nerve plexus injury?

A

Changes in multiple peripheral nerves both sensory and motor

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4
Q

What is the result of a peripheral nerve injury?

A

Mononeuropathy
Mononeuropathy multiplex
Polyneuropathy

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5
Q

What is the result of a defect in the neuromuscular junction

A

Repetitive stimulation –> decreased amplitude

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6
Q

What is the result on NCS if demylination is present?

A

Slow conduction velocity
Conduction block –> decay in amplitude
Temporal dispersion of wave
Delayed or absent f waves

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7
Q

What is the result on NCS if axonopathy is present?

A

Reduced amplitude

Relatively normal conduction velocities

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8
Q

At what time can NCS be preformed after a suspected nerve injury?

A

After day 7 post event

Prior to this NCS will not distniguish between demylinating or axonal lesions

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9
Q

Features of carpal tunnel syndrome on NCS?

A

Compare median nerve conduction with ulnar or radial nerves

Sensory nerves affected earliest
Sensory conduction slowed –> reduced sensory amplitude –> slowed motor conduction –> reduced motor ampitude –> denervation

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10
Q

Normal EMG: pattern

A

At rest = silence
Motor unit potentials = triphasic waves
Interference = full pattern = full muscle force

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11
Q

EMG in acute denervation

7days-6 weeks

A

At rest = fibrillation potentials
Motor unit potentials = normal in surviving units
Interference = gaps

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12
Q

EMG in chronic denervation and collateral sprouting

>6 weeks

A

At rest = silence
MUPs= increased amplitude and duration, polyphasic and unstable shape
Interference = big gaps

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13
Q

EMG in myopathy?

Degeneration and regeneration of muscle fibres

A

At rest = can have fibrillation potentials if inflammatory otherwise silent
MUPs = decreased duration and amplitude, polyphasic shape
Interference = small amplitude but full pattern

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14
Q

Characteristics of anterior horn diseases?

A

Progressive, asymmetric
Proximal and distal motor
Mixed upper and lower motor neuron signs

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15
Q

MND epidemiology

A

A disease of motor networks –> loss of motor neurons in the CNS, spinal cord and periphery

Usually sporadic disease
5% AD inherited

Onset 55yrs
Survival 5yrs

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16
Q

MND clinical manifestations

A

Progressive skeletal weakness, atrophy, fasciculations and spasticity

Localised to 1 region initially then spreads over body

Variants:

  • Amyotrophic Lateral sclerosis = UMN and LMN signs
  • Spinal Muscular Atrophy - LMN
  • Primary Lateral Sclerosis - UMN
  • Progressive bulbar palsy

Associated with FTD

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17
Q

MND on EMG

A

Chronic widespread denervation and reinnervation

Fasciculations
Fibrillations
Unstable MUPs

Multiple segments

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18
Q

Treatment of MND

A

Riluzole

  • Inhibits glutamate release from presynaptic terminals and stabilizes voltage dependant sodium channels, inhibits uptake of GABA
  • Improves survival

PEG feeds
NIV

19
Q

What is multifocal motor neuropathy with conduction block?

A

Progressive, asymmetrical, distal, motor LMN pattern with some atrophy

Upper limb > lower limb
Cramps and fasciculations common
Weakness > atrophy
Depressed tendon reflexes

20
Q

Investigations of MMNCB?

A

NCS = partial conduction block proximally with normal distal latencies. Normal sensory nerves

Anti-GM1 antibodies

21
Q

Treatment of MMNCB?

A

IVIG

Cyclophosphamide

22
Q

Causes of brachial plexopathy?

A

Usually unilateral

Upper C5-7

  • Brachial neuritis
  • Radiation
  • Trauma - arm pushed down
  • Hereditary neuropathy
  • Post immunisation

Lower C8-T1

  • Cancer
  • Cervical rib
  • Trauma - arm pushed up
23
Q

Causes of mononeuropathy?

A

Single peripheral nerve

Entrapment - carpal tunnel
Demylinating > axonal

24
Q

Causes of mononeuritis multiplex?

A

Multifocal, random, asymmetric

DM
Leprosy
HIV
Arteritis
Trauma
Sarcoid
Cancer
25
Q

Charcot-Marie-Tooth clinical features

A 
Onset in 1st or 2nd decades
Insidious and slow course
Distal disease
Impaired sensation
Calf atrophy
Pes Cavus
26
Q

Subtypes of CMT

A

CMT 1

  • AD or X -limked
  • Demylinating
  • Duplication of PMP-22

CMT 2
- Axonal

CMT x

  • X linked dominant disease
  • Connexin gene disorder
27
Q

Diagnosis of diabetic neuropathies

A

F-waves in the lower limbs are the most sensitive measure

28
Q

Clinical features of treatment induced neuropathy of diabetes

A

Follows the rapid correction of chronic hyperglycaemia
HbA1c drop >4 in 8 weeks = high risk

Small fibre neuropathy

  • -> pain
  • -> autonomic dysfunction
  • -> Retinopathy
  • -> Nephropathy
29
Q

What is Guillain-Barre syndrome?

A

Acute demylinating autoimmune neuropathy

2/3rd are preceded by symptoms of URTI or GIT infection.
Most often campylobacter jejuni
EBV
CMV
Mycoplasma
30
Q

Clinical features of GBS?

A

Rapidly progressive
Symmetrical weakness - can be proximal or distal
Pain
Hyporeflexia
Autonomic involvement - arrhythmias, hyponatraemia, ileus, urinary retention, labile BP

Plateau for 15 days then slow recovery

31
Q

Clinical variants of GBS

A

Miller-Fisher syndrome - external opthalmoplegia, ataxia and areflexia. Anti- GQ1b antibody

Polyneuritis cranialis
Sensory variant
Pharyngeal-cervical-brachial variant
Acute motor axonal neuropathy

32
Q

GBS investigations

A

CSF = elevated proteins

NCS:

  • Conduction slowing
  • Conduction block
  • Long latencies
  • Delayed F waves

EMG = denervation changes 2 weeks

Autoantibodies:

  • Anti-DQ1b = miller fisher
  • Anti-DM1 and Anti-GalNAc-GD1 = axonal variant
33
Q

GBS treatment and prognosis

A

Monitor FVCs

  • <20 = ICU
  • <15 = intubation

Plasma exchange and IVIG

10-20% need ventilation
5% die
20% residual motor weakness at 1 yr
3% recurrent weakness

34
Q

Chronic inflammatory demylinating neuropathy features

A

Similar to GBS but protracted course and rarely follows illness

Can be secondary to HIV< SLE, MGUS, POEMs, hepatitis, IBD, lymphoma, amyeloid

Treat with steroids, plasma exchange and IVIG

35
Q

Neuropathy and monoclonal gammopathy

A

10% of peripheral neuropathies ass. with monoclonal gammopathy:

  • 2/3rd MGUS
  • 1/3 MM, amyloid, waldenstoms, lymphoma

Antibodies against neural components common
Anti- myelin associated glycoprotein

36
Q

Distal acquired demylinating symmetric neuropathy - DADS-M

A

Elderly males
Distal sensory loss with mild distal weakness
Associated falls

Anti-MAG antibodies

37
Q

Critical illness polyneuropathy

A

Sepsis and trauma –> organ failure
–> Axonal polyneuropathy
–> difficulty weaning off ventilators
Limb weakness, sensory loss and depressed reflexes

Critical illness myopathy:
- Motor only, normal sensory nerves

38
Q

Clinical features of myasthenia gravis

A

Fatiguable weakness
Extra-ocular muscles
Facial and bulbar muscles

50% –> generalised weakness
Neck, shoulders, pelvic girdle, respiratory muscles

Preserved muscle mass and reflexes

75% reach max intensity in 1yr

39
Q

MG association with thymoma

A

Almost all thymomas are associated with MG

10% are malignant

AChR antibodies

Removal associated with better outcomes

40
Q

Investigation of MG

A

EMG normal

NCS:

  • Reduced amplitude with repeated stimulation
  • Jitter

ACh receptor antibodies - 80%

Anti-MuSK antibodies - 70% of ACh receptor antibody negative patients. Higher rates of bulbar involvement and respiratory crises. Thymus less involved –z. no thymectomy

41
Q

Treatment of MG?

A

Pyridostigmine

Prednisone
IVIG
Plasma exchange
Thymectomy - thymoma or AChR Abs
AZA, MMF, cyclosporine
42
Q

Lambert-Eaton myasthenic syndrome

A

Antibody to presynaptic voltage gated calcium channels

Paraneoplastic syndrome - SCLC

Proximal weakness
Ptosis
Dry mouth
Reduced reflexes

Treatment - plasma exchange, prednisone, AZA

43
Q

Statin Myopathy

A

Pain +++

> 80yrs, female, liver or kidney dysfunction, EtOH, surgery = increased risk

More likely with lipophilic statins - simvastatin, atorvastati

3-Hydroxy-3-methylglutaryl-coenzyme A reductase antibodies - HMGGCR Abs = protacted course

Neurology (6 decks)

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