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Neurology > Muscle weakness [Ix and Mx] > Flashcards

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
Examples of peripheral neuropathies with predominantly motor loss
- 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
26
Examples of diseases with predominantly sensory loss
- Deficiency states e.g. B12/folate - Diabetes - Alcohol/toxins/drugs - Metabolic abnormalities e.g. uraemia - Leprosy - Amyloidosis
27
Is GBS motor or sensory?
Motor
28
Diabetic neuropathy motor or snesory?
Sensory I think
29
CMT motor or sensory?
Look up
30
Define mononeuritis multiplex
Painful, asymmetrical sensory and motor neuropathy
31
How does Mononeuritis multiplex present, how is it mediated and what are the causes?
Presentation: subacute Inflammatory/immune mediated Causes: vasculitides e.g. Churg Strauss, connective tissue disorders
32
What is a mononeuropathy? Common location of presentation. Give 4 examples
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
Describe Carpal Tunnel syndrome
look up. Essentially, I think flexor reticunalum.
34
Neuropathy investigations
History and examination: - neuropathy screen - vasculitic screen - EMG/NCS - CSF study - imaging/nerve biopsy
35
What does a neuropathy screen involve?
``` FBC, ESR U&E, glucose, TFT, CRP, serum electrophoresis B12 folate anti-gliadin TPHA, HIV ```
36
What does a vasculitic screen involve?
FBC, ESR | U+E, Cr, CRp, ANA, ANCA, anti-dsDNA, RhF, complement cryoglobulins
37
Neuropathy treatment
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
Describe the mechanism of Guillain-Barre syndrome
slides
39
What type of disease is GBS?
Autoimmune response causing demyelination
40
Common trigger for GBS?
Post-infectious; resp or GI [e.g. campylobacter]
41
progression of GBS
Subacute [less than 6w], ascending paralysis/numbness/areflexia
42
What would NCS show?
Demyelinating
43
What would LP show?
Raised CSF protein
44
How to treat GBS
Treat with IVIg or plasmapharesis, support, monitor FVX, ITU review Recovery may take weeks to years
45
Eyes for people with myasthenia gravis
look up
46
Which NT does myasthenia gravis affect?
Autoimmune disorder that effects antibodies against nicotinic acetylcholine receptors
47
How treatable is it, and what is also commonly associated with myasthenia gravis?
Common disease itsefl, potentially fatal but treatable Thymus dysfunction is common -hyperplasia - thymoma
48
Dsecribe the pathophysiology of myasthenia gravis
slides
49
Which muscles does MG effect?
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
MG investigations
Tensilon test [allow accumulation of Ach in the NMJ] AChR antibodies EMG: looks at NMJ CT thorax
51
MG treatment
Acetylcholine esterase inhibitors [pyridostigmine] - symptomatic Immunosuppresants: steroids [start slowly], azathioprine/MTX/mycophenolate Thymoectomy
52
What is a myasthenic crisis?
Severe weakness including respiratory muscles | High risk of death
53
Cause of a myasthenic crisis
Infection, natural disease cycle, under dosing or overdosing of medication
54
Action taken during a myasthenic crisis
- Take change in myasthenic condition seriously - urgent review by nuerologist - think about breathing and monitor - anaesthetic review
55
What is MND?
Degeneration of motor neurones in the motor cortex and anterior horns of the spinal cord
56
What type of signs does MND present with
UMN and LMN signs
57
Investigations done in MND
LP, NCS/EMG and MRI [to r/o other conditions]
58
How is MND Dx?
Mainly a clinical Dx
59
Clinical signs of MND
No sensory, visual or B/B involvement Asymmetric weakness Bulbar or limb onset Survival usually 2-5 years
60
What are the four common muscle disorders?
Steroid myopathy Statin myopathy Metabolic and endocrine myopathies Myotonic dystrophy
61
what are some uncommon muscular disorders?
Most muscular dystrophies: - Duchenne, Becker, Facioscapulohumeral muscular dystrophy [FSHD] Inflammtory muscle disease: - polymyositis, dermatomyositis Mitochondrial disorders
62
Which muscles commonly and noticeably affected in muscle disorders? Other muscles less commonly affected?
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
Which muscle condition scioliosis common feature?
Duchenne
64
Eye movement disorders are common or rare muscular disorders?
Rare [seen in mitochondrial]
65
Muscle investigations done
CK, EMG, ESR/CRP +/- genetics [DMD/Becker] +/- biopsy
66
Muscle disorders Tx
``` Remove causal agent Supportive - OT [aids adaptions] - physio [prevent contracture] - back - renal - diet Immunosuppres if inflammatory ```
67
Type of weakness comparin gnerve disease to muscle disease
nerve disease - distal weakness | muscle disease - proximal weakness

Neurology (13 decks)

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