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Muscle weakness [Ix and Mx] Flashcards

1
Q

Where are the ascending tracts on the spinal cord? Give examples of ascending tracts.

A

Look slides

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2
Q

Where are the descending tracts of the spinal cords?

A

Look slides

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3
Q

Main way of subgrouping the descending tracts

A

Pyramidal vs extrapyramidal tracts

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4
Q

What is the origin and function of the pyramidal tracts?

A

Origin: cerebral cortex
Function: responsible for the voluntary control of the musculature of the body and face

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5
Q

What is the origin and function of the extrapyramidal tracts?

A

Origin: brain stem
Function: responsible for the involuntary and automatic control of all musculature such as muscle tone, balance, posture, and locomotion

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6
Q

Where do the pyramidal tracts derive their name from?

A

The medullary pyramids of the medulla oblongata which they pass through

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7
Q

Functionally, how can the pyramidal tracts be subdivided into?

A

Corticospinal tracts: lateral and anterior

Corticobulbar tracts

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8
Q

Which part of the corticospinal tract decussates at the medulla?

A

The lateral corticospinal tract and terminates in the ventral horn [at all segmental levels]

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9
Q

What is the route of the anterior corticospinal tract?

A

Cerebral cortex -> internal capsule -> medulla [remains ipsilateral] -> decussates/terminates in the cervical and upper thoracic segmental levels

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10
Q

Where do the extrapyramidal tracts originate from?

A

Brainstem

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11
Q

What do the extrapyramidal tracts carry?

A

Motor fibres to the spinal cord

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12
Q

How many extrapyramidal tracts are there in total?

A

4 tracts:

  • vestibulospinal [do not decussate, ipsilateral innervation]
  • reitculospinal [also ipsilateral]
  • rubrospinal [decussate, provide contralateral innervation]
  • tectospinal [decussate, provide contralateral innervation]
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13
Q

What are the two parts to the PNS?

A
  • somatic nervous sytem [incl. cranial nerves]

- autonomic nervous system

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14
Q

Why is the PNS more vulnerable to damage than the CNS?

A

PNS not protected by the vertebral column and skull, or by the blood-brain barrier which can leave it exposed to toxins and mechanical injuries

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15
Q

Which cranial nerve is NOT part of the PNS?

A

optic nerve [II]

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16
Q

How many pairs of spinal nerves are there in the somatic nervous system? Divide into bodily areas

A

31 pairs:

  • cervical: 8
  • thoracic: 12
  • lumbar: 5
  • sacral: 5
  • coccygeal: 1
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17
Q

Compare an UMN to a LMN

A

look up

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18
Q

What is in a muscle weakness history?

A

Onset [instant/gradual], distribution [proximal/distal, symmetrical/asymmetrical, mono or local process/poly or diffuse, cranial involvement e.g. bulbar or facial or ophthalmoplegia], variability [fatigueability/relapse remissions], additoonal features [sensory Sx like tingling or pins or loss sensation], context [recent illness/PMH/FH/drugs/alcohol]

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19
Q

Motor system examination for a UMN lesion

A 
Bulk - normal
Tone - increased
Strength - decreased
Fasciculations - absent
Reflexes - increased
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20
Q

Motor system examination for a LMN lesion

A 
Bulk - reduced [wasting
Tone - normal or decreased
Strength - decreased
Fasciculations - may be present
Reflexes - decreased or absent
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21
Q

Go through the 5 parts to the grading of the muscle power system

A

MRC look up

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22
Q

List example causes of weakness

A 
Neuropathies: 
- peripheral neuropathy
- GBS
- myasthenia gravis
- MND
Myopathy
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23
Q

What are the three ways of classifying damage to peripheral nerves?

A

Polyneuropathy [peripheral neuropathy]
Mononeuropathy multiplex [mononeuritis multiplex; at least two nerves]
Mononeuropathy: one single nerve

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24
Q

What does peripheral neuropathy describe? Progression, where does it start, and is it sensory or motor?

A

Essentially, describes disease affecting the peripheral nerves
usually, chronic and slowly progressive
Starts in the legs and longer nerves
Sensory or motor or both

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25
Q

Examples of peripheral neuropathies with predominantly motor loss

A
  • Guillain-Barre Syndrome [GBS]
  • Chronic Inflammatory demyelinating polyneuropathy [CIDP [i.e. chronic version of GBS]]
  • Hereditary sensorimotor neuropathies [HSMN] e.g. Charcot-Marie-Tooth Disease
  • Diptheria
  • Porphyria
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26
Q

Examples of diseases with predominantly sensory loss

A
  • Deficiency states e.g. B12/folate
  • Diabetes
  • Alcohol/toxins/drugs
  • Metabolic abnormalities e.g. uraemia
  • Leprosy
  • Amyloidosis
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27
Q

Is GBS motor or sensory?

28
Q

Diabetic neuropathy motor or snesory?

A

Sensory I think

29
Q

CMT motor or sensory?

30
Q

Define mononeuritis multiplex

A

Painful, asymmetrical sensory and motor neuropathy

31
Q

How does Mononeuritis multiplex present, how is it mediated and what are the causes?

A

Presentation: subacute
Inflammatory/immune mediated
Causes: vasculitides e.g. Churg Strauss, connective tissue disorders

32
Q

What is a mononeuropathy? Common location of presentation. Give 4 examples

A

Individual nerve deficits in isolation
Upper limb nerves most commonly affected at compression points
Median nerve entrapment at the wrist most common [Carpal Tunnel Syndrome]
Ulnar nerve at elbow common also
Radial nerve in axilla common
Common peroneal nerve in leg most common

33
Q

Describe Carpal Tunnel syndrome

A

look up. Essentially, I think flexor reticunalum.

34
Q

Neuropathy investigations

A

History and examination:

  • neuropathy screen
  • vasculitic screen
  • EMG/NCS
  • CSF study
  • imaging/nerve biopsy
35
Q

What does a neuropathy screen involve?

A 
FBC, ESR
U&E, glucose, TFT, CRP, serum electrophoresis
B12 folate
anti-gliadin
TPHA, HIV
36
Q

What does a vasculitic screen involve?

A

FBC, ESR

U+E, Cr, CRp, ANA, ANCA, anti-dsDNA, RhF, complement cryoglobulins

37
Q

Neuropathy treatment

A

20% idiopathic with no Tx
- neuropathic analgesic [gabapentin, pregabalin, amitrptyline]

Treat/remove underlying cause e.g. DM/B12 deficiency

Inflammatory neuropathy [e.g. CIDP - chronic version of GBS]
- prednisolone with steroid sparing agents e.g. azathioprine

Vasculitis neuropathy [e.g. with Wegners]
- prednisolone with immunosupressaant e.g. cyclophosphamide

38
Q

Describe the mechanism of Guillain-Barre syndrome

39
Q

What type of disease is GBS?

A

Autoimmune response causing demyelination

40
Q

Common trigger for GBS?

A

Post-infectious; resp or GI [e.g. campylobacter]

41
Q

progression of GBS

A

Subacute [less than 6w], ascending paralysis/numbness/areflexia

42
Q

What would NCS show?

A

Demyelinating

43
Q

What would LP show?

A

Raised CSF protein

44
Q

How to treat GBS

A

Treat with IVIg or plasmapharesis, support, monitor FVX, ITU review
Recovery may take weeks to years

45
Q

Eyes for people with myasthenia gravis

46
Q

Which NT does myasthenia gravis affect?

A

Autoimmune disorder that effects antibodies against nicotinic acetylcholine receptors

47
Q

How treatable is it, and what is also commonly associated with myasthenia gravis?

A

Common disease itsefl, potentially fatal but treatable
Thymus dysfunction is common
-hyperplasia
- thymoma

48
Q

Dsecribe the pathophysiology of myasthenia gravis

49
Q

Which muscles does MG effect?

A

Generalised:
- fatigueable weakness: proximal limbs, neck and face [head drop, ptosis], extraocular [complex diplopia], bulbar [speech, swallow] particularly elderly

Ocular [10-25%]

At risk of other autoimmune diseases [thyroid, PA etc.]

50
Q

MG investigations

A

Tensilon test [allow accumulation of Ach in the NMJ]
AChR antibodies
EMG: looks at NMJ
CT thorax

51
Q

MG treatment

A

Acetylcholine esterase inhibitors [pyridostigmine] - symptomatic

Immunosuppresants: steroids [start slowly], azathioprine/MTX/mycophenolate

Thymoectomy

52
Q

What is a myasthenic crisis?

A

Severe weakness including respiratory muscles

High risk of death

53
Q

Cause of a myasthenic crisis

A

Infection, natural disease cycle, under dosing or overdosing of medication

54
Q

Action taken during a myasthenic crisis

A
  • Take change in myasthenic condition seriously
  • urgent review by nuerologist
  • think about breathing and monitor
  • anaesthetic review
55
Q

What is MND?

A

Degeneration of motor neurones in the motor cortex and anterior horns of the spinal cord

56
Q

What type of signs does MND present with

A

UMN and LMN signs

57
Q

Investigations done in MND

A

LP, NCS/EMG and MRI [to r/o other conditions]

58
Q

How is MND Dx?

A

Mainly a clinical Dx

59
Q

Clinical signs of MND

A

No sensory, visual or B/B involvement
Asymmetric weakness
Bulbar or limb onset
Survival usually 2-5 years

60
Q

What are the four common muscle disorders?

A

Steroid myopathy
Statin myopathy
Metabolic and endocrine myopathies
Myotonic dystrophy

61
Q

what are some uncommon muscular disorders?

A

Most muscular dystrophies:
- Duchenne, Becker, Facioscapulohumeral muscular dystrophy [FSHD]

Inflammtory muscle disease:
- polymyositis, dermatomyositis

Mitochondrial disorders

62
Q

Which muscles commonly and noticeably affected in muscle disorders? Other muscles less commonly affected?

A

Stairs, chairs and hair muscles
Facial weakness occurs in some e.g. facioscapulohumeral dystrophy

Neck weakness can occur

Contractures can occur

Scoliosis is oftena feature esp. in Duchenne

Eye movement disroders rare [seen mitochondrial]

63
Q

Which muscle condition scioliosis common feature?

64
Q

Eye movement disorders are common or rare muscular disorders?

A

Rare [seen in mitochondrial]

65
Q

Muscle investigations done

A

CK, EMG, ESR/CRP
+/- genetics [DMD/Becker]
+/- biopsy

66
Q

Muscle disorders Tx

A 
Remove causal agent 
Supportive
- OT [aids adaptions]
- physio [prevent contracture]
- back
- renal 
- diet
Immunosuppres if inflammatory
67
Q

Type of weakness comparin gnerve disease to muscle disease

A

nerve disease - distal weakness

muscle disease - proximal weakness

Neurology (13 decks)

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