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Jess Nervous > Examination of the motor system > Flashcards

Examination of the motor system Flashcards

1
Q

What would you inspect for in a motor examination?

A

DWAARFSS

Deformities, wasting, asymmetry, atrophy, rashes, fasciculations (muscle twitches), swelling and scars

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2
Q

What would you be looking for in a patient’s gait? Which myotomes are assessed?

A

Walking: watch arm swinging, smooth turning, symmetry and size of steps (watch for pigeon steps)

Tiptopes: S1/S2 myotome
Heels: L4/L5 myotome

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3
Q

Define the following types of gaits

a) Hemiplegic
b) paraplegic
c) cerebellar
d) ataxic
e) high stepping
f) shuffling
g) antalgic

A

a) paralysis on one side of body
b) paralysis of the legs/lower body
c) wide based gait with lateral veering, unsteadiness and irregularity of steps
d) Uncoordinated walking
e) high leg lift with foot drop
f) shuffling
g) a gait that develops as a way to avoid pain while walking (shortened swing phase)

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4
Q

What are some possible causes for an UMN lesion?

A

UMN lesions may be caused by:
Issues with the cerebral cortex such as stroke (or CVA) or traumatic injury.

Issues with the spinal cord such as trauma, cauda equina syndrome, tumour or MS

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5
Q

Name four possible causes for a LMN lesion

A
  1. Trauma to the nerve (i.e carpal tunnel, winged scapula, erb palsy caused by brachial plexus injury following shoulder dystocia at delivery)
  2. Motor neuron disease
  3. Cauda equina
  4. Infection (polio)
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6
Q

What is cauda equina syndrome?

A

Nerve roots of the cauda equina are compressed; disrupting motor and sensory functions to the lower extremities and bladder

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7
Q

Name one potential cause for an issue at the NMJ and two potential causes for a muscular issue

A

NMJ: Myasthenia gravis
Muscular: Duchenne’s muscular dystrophy, myotonic dystrophy (muscle wasting and weakness)

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8
Q

What are three possible signs of an UMN lesion and what are their fundamental causes?

A

An UMN lesion means there is no inhibition of the descending pathways

  1. Spastic paralysis caused by over exaggerated stretch reflex
  2. Increased tendon reflexes/hyperreflexia caused by lack of descending inhibitory pathways
  3. Extensor plantars (positive Babinski sign and clonus) as normally extension is inhibited but UMN damage means this inhibition is blocked - resulting in extension of the great toe

*insert photo of babinski foot

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9
Q

What are four possible signs of a LMN lesion and what are their fundamental causes?

A

Lack of functioning efferent neuron

  1. Flaccid paralysis (or atonia)
  2. Loss of tendon reflexes
  3. Wasting; atrophy of muscles due to damage to alpha motor neurons (lack of trophic fibres needed by muscle fibres)
  4. Fasciculations; damaged alpha neurons can produce spontaneous action potentials which fire the motor unit and cause twitches
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10
Q

Describe a decorticate posture, what is it caused by?

A

The ‘Mummy position’ caused by

  1. disinhibition of the red nucleus resulting in overactivity of the rubrospinal tract - causing flexion in the upper extremities
  2. disruption of the lateral corticospinal tract - results in pontine reticulospinal and medial and lateral vestibulospinal tracts overwhelm causing extension of the lower extremities

*include pic of decorticate position from slide

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11
Q

What are decorticate and decerebrate posturing indicative of?

A

Severe brain injury - very poor prognosis

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12
Q

Describe a decerebrate posture, what is it caused by?

A

Posture: head arched back, arms extended by sides, elbows extended, legs extended and internally rotated

Brainstem damage BELOW the red nucleus

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13
Q

What and where is the red nucleus?

A

Structure in the midbrain involved in motor coordination

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14
Q

How might patients progress in terms of a decorticate and decerebrate posturing? What would this be indicative of?

A

Can progress from decorticate to decerebrate posture which often indicates brain herniation

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15
Q

Name four general clinical features of a motor neurone disease

A
  1. 3 main patterns and all are progressive at different rates
  2. Stiffness/weakness in hands which spreads distal to proximal with fasciculations
  3. Speech and swallowing difficulties
  4. Progressive muscle wasting distal - proximal
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16
Q

What is involved in the pathophysiology of a motor neurone disease?

A

Degeneration of the motor cortex, spinal tracts, anterior horn grey matter and LMNs

50% may also have frontotemporal dementia (personality changes)

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17
Q

What is the aetiology of motor neurone disease? When does prognosis tend to be poor?

A

Unknown, 5% familial

Prognosis tends to be poor in adults >50 yrs

18
Q

Describe the pathophysiology of Myasthenia gravis and name four clinical features

A

Autoimmune condition with antibodies against Ach receptors in synaptic clefts

Clinical features include variable muscle weakness and fatigability in eyes, speech, swallowing and arms

19
Q

What do 65% of patients with Myasthenia gravis have?

A

Thymic hyperplasia (role is unclear)

20
Q

How is myasthenia gravis diagnosed?

A

Antibodies, Electromyography (EMG) - assesses health of muscles and motor neurons, edrophonium test

21
Q

How is myasthenia gravis treated? How is its prognosis?

A

Treated with cholinesterase inhibitors and immunosuppression/thymus removal

Prognosis is a normal life but long term treatment

22
Q

How might a patient with a facial nerve lesion vs a supranuclear lesion present?

A

Facial nerve lesion: Bell’s palsy

Supranuclear lesion: paralysis of the affected side of the face with sparing of the forehead

23
Q

Give an example of a common class of limb motor reflexes routinely examined as part of a medical examination

A

Deep tendon reflexes

24
Q

What is clonus? What is it indicative of and generally accompanied with?

A

Series of rhythmic reflex contractions of a muscle after being stretched. Indicative of an UMN lesion and generally accompanied with hyperreflexia

25
Q

What is the explanation for failure to evoke muscle stretch reflexes in relaxed healthy individuals?

A

Though descending inhibition of the spinal cord is constant, its severity is variable to the individual

26
Q

What would the consequence of a pure lesion of the axon of an alpha motor neuron be both acutely and chronically? What is the usual cause of this kind of scenario?

A

This would result in the nerve dying and the muscle losing its neural innervation, hence all its ability to produce force both acutely and chronically with no chance of recovery. This scenario is usually caused by a complete transection of a peripheral nerve by trauma

27
Q

Study the following image and identify which of the following conditions correlate to lesions at a, b, c, d, e, f and g?

**insert photo

A

a) Stroke
b) Multiple sclerosis
c) Lumbar disc prolapse
d) motor neuron disease
e) peroneal nerve injury
f) myasthenia gravis
g) duchenne’s muscular dystrophy

28
Q

Name three major symptoms of a lumbar disc prolapse

A

Numbness/tingles in one or both arms or legs, pain behind the shoulder blades or buttocks, loss of bladder and/or bowel control in severe cases

29
Q

Name three major symptoms of multiple sclerosis

A

fatigue, vision problems, muscle spasms, stiffness and weakness

30
Q

Name three major symptoms of a peroneal nerve injury

A

Foot drop, numbness and pain

31
Q

Which gene is defective in duchenne’s muscular dystrophy? Name three major symptoms of this condition

A

Defective dystrophin (important in strengthening muscle fibres)

Frequent falls, difficulty rising from a lying or sitting position, waddling gait

32
Q

What is the inheritance pattern of duchenne muscular dystrophy?

A

X linked recessive

33
Q

List five signs that distinguish upper/lower motor neuron lesions :)

A
  1. Muscle Power: Patients complain of muscle weakness because..
    UMN: They’ve lost voluntary control, but muscles are still innervated and contract reflexly
    LMN: Motor units are denervated, the pattern of weakness has the distribution of the ‘final common pathway’, i.e alpha motor neurons
  2. Muscle tone
    UMN: Increased tone due to removed inhibitory effect of the corticospinal tract; Upper limb flexion and lower limb extension
    LMN: Reduced tone which may range from barely noticeable change to complete flaccidity in proportion to the number of motor neurons denervated
  3. Muscle wasting:
    UMN; None
    LMN: depends upon the length of time the affected motor neurons have had to degenerate and the number deneverated. Wasting appears early and is obvious
  4. Reflexes
    UMN: Hyperreflexia; reflexes become exaggerated due to removal of the “dampening” effect of the corticospinal tracts - flexor reflexes are dominant in the upper limb and extensor responses in the lower
    LMN: Hyporeflexia
  5. Plantar Response
    UMN: Positive Babinski sign
    *Bing sign also present: the normal reaction of extending the foot away from a sharp stimulus applied to the dorsum of the food is replaced by flexion that drives the foot towards the stimulus
    LMN: NO babinski sign (plantar response stays normal)

*add photo

34
Q

Where would an UMN lesion be for contralateral vs ipsilateral muscle weakness to occur?

A

Contralateral: above the decussation
Ipsilateral: longer tract lesions due to spinal damage

35
Q

What is cog-wheel and clasp knife rigidity indicative of?

A

UMN lesion

36
Q

How is the plantar response of the foot elicited?

A

A key to the plantar foot to simulate walking on rough ground

37
Q

Which reflexes are lost in an UMN lesion?

A

Loss of cremasteric reflex and abdominal reflex

38
Q

Where might sensory deficits be in an UMN lesion?

A

The quadrants or halves of the body

39
Q

What might occur BEFORE weakness is noted by a patient with an UMN lesion?

A

Drift of limbs; if the eyes are closed and arms outstretched, the arm on the affected side will tend to drift downwards

40
Q

What might occur at the end stage of a LMN deficit and why?

A

Muscle contractures as muscle cells are replaced by fibrous tissue

41
Q

Where might sensory deficits be in an LMN lesion?

A

Likely to have a peripheral nerve pattern

42
Q

What is the sign of Babinski?

A

When the sole of the foot is stoked the normal response is toe curling and plantar flexor, this is replaced by dorsiflexion and fanning of the toes following an UMN lesion

Jess Nervous (16 decks)

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