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PDX 2 > Somato sensory exam > Flashcards

Somato sensory exam Flashcards

1
Q

What are the 4 primary sensory modalities?

A

Pain, touch, vibration and joint position sense.

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2
Q

What is crude touch?

A

When a patient cant tell if the touch is soft or sharp or any other description, but they can tell they were touched.

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3
Q

What part of the spinal cord will pain, light touch,

A

Pain- lateral spinothalamic tract, light touch- anterior

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4
Q

vibration and position sense travel in?

A

spinothalamic tract:

  • Vibration- dorsal columns (gracilis and cuneatus).
  • Position (spinocerebellar tract).
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5
Q

Vibration sense is tested with a ____ tuning fork?

A

128 cps.

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6
Q

Assessing vibrations is used in suspected cases of?

A

Peripheral neuropathy (diabetes, alcoholism) and cord compression

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7
Q

Compression of posterior columns can cause?

A

Subjective vibration/ electrical shock sensation.

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8
Q

Intermittent compression of posterior column:

A

During flexion/extensio, a central disc herniation can induce temp. decrease in dexterity.

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9
Q

L’Hermitte’s sign

A

electrical shock sensation during cervical flexion

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10
Q

Barber chair sign

A

electrical shock sensation during cervical extension.

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11
Q

What is an important observation seen with abnoramal motor exams?

A

Fasciculation, atrophy, hypertrophy or asymmetry

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12
Q

Fasciculations may sometimes be elicited by what?

A

Percussing/tapping the muscle.

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13
Q

Fasciulations in an otherwise strong muscle are usually what?

A

Benign.

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14
Q

Fasciculations in weak muscles could indicate what?

A

Lower motor neuron lesions and anteior horn cell lesions.

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15
Q

What will hypotonicity and spacsticity mean while assessing muscle tone?

A

Hypotonicity is associated with lower motor neurons.

Spasticity is associated with upper motor neuron lesions.

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16
Q

What is spacsticity?

A

hypertonicity.

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17
Q

Clasp knife phenomenon

A

resistance is felt when joint is first moved but the resistance decreases as the joint is opened

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18
Q

Rigidity is usually associated with?

A

Parkinson’s

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19
Q

Cogwheel rigidity

A

gives way in a series of litte jerks

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20
Q

Lead pipe rigidity

A

felt thru entire range of motion

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21
Q

When would you considered repetitive or sustained muscle testing?

A

Indications of weakness, fatigue, abnormalities on sensory exam or DTRs

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22
Q

How should muscle strength tests be done?

A

use 10 repetitions or sustained resistance for 5 seconds.

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23
Q

What is Myopathy

A

A muscle disease that is unrelated to any disorder of innervation or the neuromuscular junction.

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24
Q

What is the classic findings with myopathies?

A

Proximal symmetric weakness without sensory loss.

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25
Q

Does weakness get better with rest with myopathies?

A

no

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26
Q

What are the causes of myopathies?

A

idiopathic, alcoholic, drug-induced (cortisone, statins), endocrinological or infectious in origin.

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27
Q

Are there denervation changes, atrophy or fasciculations with myopathies?

A

no

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28
Q

What is a dystrophic gate like?

A

Waddling wide-based.

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29
Q

What disease will have a dystrophic gate?

A

Duchenne muscular dystrophy.

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30
Q

What drugs can lead to myopathies?

A

cholesterol-lowering drugs like statins.

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31
Q

What is occular myasthenia gravis like?

A

Fluctuating (since fatigability gets better with rest) double vision and or ptosis.

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32
Q

What muscle is commonly affected by occular myasthenia gravis? Which one is affected the second most?

A

superior rectus and medial rectus is second most common

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33
Q

How often will occular myasthenia gravis remain only occular?

A

Only about 16%.

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34
Q

what will the progression of myasthenia gravis be like?

A

goes from mild to severe over weeks to months and spreads from ocular to facial to bulbar and then to limbs

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35
Q

How often will the patients with myasthenia gravis will the disease generalize in a little over a year?

A

83%.

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36
Q

What will bulbar mean?

A

It is an older term for medulla oblongata.

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37
Q

How will pure lower motor neuron lesions present?

A

Motor deficits only.

38
Q

Where will pure lower motor neuron lesions happen at?

A

Anterior horn cells and spinal cord axons of the anterior horn cells.

39
Q

What will mixed lower motor neuron lesions present like?

A

combined motor, sensory and autonomic deficits.

40
Q

Where will mixed lower motor neuron lesions happen at?

A

nerve roots, peripheral nerves.

41
Q

Fasciculations are more likely to be seen with what?

A

LMNL of very slow onset.

42
Q

What is a classic sign of a lower motor neuron lesion?

A

Possible nerve irritability, hyporeflexia, Flaccid parasis/paralysis of specific muscles and marked atrophy

43
Q

What are the classic signs of upper motor neuron lesions?

A

hyperactive DTR, Clonus, spastic paresis, no fasciculations, no gross atrophy or marked trophic changes, pathologic reflexes.

44
Q

How many types of peripheral neuropathy have been identified?

A

More than 100.

45
Q

Peripheral neuropathy usually refers to what?

A

metabolic neuropathy-due to diabetes and chronic alcoholism

46
Q

Mononeuropathy:

A

common peroneal nerve palsy @ the level of the fib head

47
Q

Plexopathy

A

neurogenic thoracic outlet syndrome and brachial plexus

48
Q

Plexopathy Lower extremity

A

steppage gait and numbness or decreased sensation in the antero lateral calf and the dorsum of the foot

49
Q

Plexopathy Painless foot drop and steppage gait is caused by?

A

compression of the common peroneal nerve at the fibular head leading to painless foot drop.

50
Q

Radiculopathy:

A

peripheral neuropathy from nerve root disease

Classic: asymmetric pain, flaccid weakness and sensory deficits

51
Q

Radiculopathy Reality:

A

not all radiculopathies manifest in painà pain is sharp, stabbing, hot or shooting

52
Q

signs of radiculopathy

A
  • Asymmetric flaccid weakness: LMN disease
  • Denervation changes occur in the area served by the nerve rootà atrophy/fasciculations
  • Decreased muscle tone
  • Diminished or absent deep tendon reflexes
53
Q

Sensory abnormalities almost always accompany radiculopathies

A

a. Paresthesias/sensory changes precede any motor changes
b. Sensnory changes are dermatome;
c. Any overt sensory loss tends to involve all four primary sensory modalities: local/focal/limited ANS dysfunction

54
Q

Lumbar/cervical radiculopathy:

A

from nerve root disease and most are asymmetric and dermatomal/myotomal

55
Q

Radiculopathies and gait: the heel walk

A

walk 10 steps on heels and get abnormal foot drop and steppage gait.

56
Q

Radiculopathies and gait: the toe walk

A

patient walks 10 steps on toes and get abnormal heel drop

57
Q

Cervical spine and possible mixed LMNL/UMNL

A

· Cervical spondylosis
· Central cord syndrome
· Cervical radiculopathy
· Potential compression

58
Q

Cervical spondylosis

A

a common cause of cervical nerve root impingement and cervical radiculopathy may lead to LMNL findings.

59
Q

Central cord syndrome LMNL findings in the upper extremity UMNL findings in the lower extremity: associated with?

A

whiplash and cervical spondylosis

60
Q

Cervical radiculopathy:

A

peripheral neuropathy that is due to nerve root disease + pain and or numbness down the course of the involved nerves

61
Q

Potential compression

A

paradoxical or mixed reflexes in the upper extremity

62
Q

Possible end result of Potential compression:presentation.

A

: an incomplete cord lesion and both the nerve root and white matter of the cord leading to mixed LMNL/UMNL

63
Q

Classic: ALS:

A

ALS: slow onset of mixed upper and lower motor neuron lesions

64
Q

UMN lesions of slow onset

A

a. Bulbar symptoms: lesions of cranial nerve and corticobulbar tractsà slurring of words or choking during a meal may be the first clinical indication
b. Corticospinal tract lesions: muscle cramps are common

65
Q

LMN lesions of slow onset

A

a. Wide spread fasciculations may be an early sign (anterior horn cells are not firing properly)
b. Muscle weakness, atrophy and hyporeflexia

66
Q

Cranial nerve lesions categorized

A

-Supranuclear lesions (central lesions)
-Nuclear lesions
(Peripheral lesions)
-Infranuclear lesions
(Peripheral lesions)

67
Q

Hyposmia/ anosmia and conduction deficits:

A

inability to recognize smell: inflamed receptors and makes them dysfunctional

68
Q

Dysomia/parosmia:

A

can notice smell but have trouble identifying from damage to the receptors / neuroepithelium

69
Q

Phantosmia/olfactory hallucination and supra nuclear lesions:

A

think that the smelt something but really there’s no odor present, from olfactory cortex disorder

70
Q

CN VI: lesion to this nerve?

A

trochlear palsy

71
Q

CN III: pupillary reaction to light. Damage can lead to?

A

ptosis/ oculomotor palsy

72
Q

CN VI: lesion

A

abducens palsy

73
Q

Cardinal fields of gaze tests?

A

CN III, IV, VI

74
Q

LMN lesions of CN V lead to?

A

atrophy and flaccid paresis of the chewing muscles.

75
Q

Trigeminal neuralgia/ Tic douloureux/ idiopathic TN

A

Neuro exams are normal!
· Diagnosis based on clinical history and absence of any exam findings
· Onset 60-70
· Patients presents with stabbing, paroxysmal and unilateral facial pain, triggered by chewing or touching affected facial areas. Localized pain. Pain runs along line dividing either mandibular/ maxillay portion or the mandibular/ ophthalmic portion of the nerve.
· Sensory exam is normal
· The one’s who suffer with this disease at the age of 20-40 more likely to suffer from demyelinating lesion in the pons secondary to MS.

76
Q

LMN lesions of CN VII

A

ipsilateral flaccid paresis/ flaccid paralysis

i. Nuclear or infranuclear lesions
ii. Ipsilateral frontalis dysfunction/ orbicularis oculus dysfunction (possibly from dysarthria with lip sounds B,P,M).
iii. Loss function of ipsilateral nasio labial fold
iv. Possible dysfunction of chorda tympani

77
Q

UMN lesions of CN VII: Supra nuclear lesions

A

i. Facial paralysis more on lower face
ii. Able to wrinkle frontalis both sides of forehead
iii. Some spastic paralysis involving eyelids
iv. Nasio labial fold intact
v. Some spastic paralysis involving corner of mouth

78
Q

UMN lesions of CN VII: Contralateral spastic paresis/ spastic paralysis

A

i. Most obvious during lip retraction
ii. Least obvious when patients wrinkle forehead
iii. Nasio labial folds partially intact

79
Q

Bell’s Palsy (Idiopathic facial paralysis) Typical progression

A

recent viral upper respiratory tract infection, next is history of ear and or mastoid discomfort, paresis (weakness) or paralysis then develops over 24-96 hours period, paresis/ paralysis usually lasts 3- 6 weeks.

80
Q

Bell’s Palsy Incomplete recovery

A

Paresis> paralysis lasts longer than 6 weeks

81
Q

Bell’s Palsy Diagnosis criteria:

A

o Sudden onset of paralysis/ paresis of all muscle groups on one side of face
o Absence of CNS disease/ other causes of acute peripheral palsy

82
Q

CN VIII Nuclear or infranuclear lesions

A

sensorineural deafness

83
Q

CN IX and X: Testable functions of these two nerves are not ?

A

entirely separable, therefore must be test together

84
Q

CN XI lesion

A

unilateral weakness and atrophy: shoulder droop, winged scap

· Test traps and SCMs

85
Q

Upper extremities: cerebellar Limb ataxia

A
  1. Decomposition of voluntary movement
  2. Dysmetria/ past pointing
  3. Intention tremor/terminal intention tremor
86
Q

Lower extremities: cerebellar Limb ataxia

A

The findings: failed heel to shin and cerebellar truncal ataxia/ cerebellar sitting posture

87
Q

Other forms of neurologic gait abnormalities:

A
  1. Cerebral palsy:
  2. Spastic hemiplegia/ circumduction gait:
  3. Scissor gait/spastic diplegia:
  4. Parkinsonism
88
Q

Parkinson gait:

A

very advanced Parkinson’s disease:

89
Q

Pathologic reflexes and other signs of UMNLs

A
  1. This term indicates there is an abnormal response to superficial reflex and abnormal response likely due to pyramidal tract lesion
  2. Abnormal responses are highly indicative of UMNLs
  3. Note: atypical response are normally seen in infants up to about age 7 months
90
Q

Babinski response:

A
  1. Normalà flexor response/neg Babinski and big toe is down

2. Abnormalà extensor response/ positive Babinski and big toe is up

91
Q

Other findings that can indicate UMNLs

A
  1. sustained clonus after brisk dorsiflexion of foot or wrist
  2. sustained clonus is clinical indication of hyperreflexia
  3. Pronation sign/ pronator drift: he talked about it in class but not red on the PPT

PDX 2 (6 decks)

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