Somato sensory exam Flashcards
1
Q
What are the 4 primary sensory modalities?
A
Pain, touch, vibration and joint position sense.
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.
3
Q
What part of the spinal cord will pain, light touch,
A
Pain- lateral spinothalamic tract, light touch- anterior
4
Q
vibration and position sense travel in?
A
spinothalamic tract:
- Vibration- dorsal columns (gracilis and cuneatus).
- Position (spinocerebellar tract).
5
Q
Vibration sense is tested with a ____ tuning fork?
A
128 cps.
6
Q
Assessing vibrations is used in suspected cases of?
A
Peripheral neuropathy (diabetes, alcoholism) and cord compression
7
Q
Compression of posterior columns can cause?
A
Subjective vibration/ electrical shock sensation.
8
Q
Intermittent compression of posterior column:
A
During flexion/extensio, a central disc herniation can induce temp. decrease in dexterity.
9
Q
L’Hermitte’s sign
A
electrical shock sensation during cervical flexion
10
Q
Barber chair sign
A
electrical shock sensation during cervical extension.
11
Q
What is an important observation seen with abnoramal motor exams?
A
Fasciculation, atrophy, hypertrophy or asymmetry
12
Q
Fasciculations may sometimes be elicited by what?
A
Percussing/tapping the muscle.
13
Q
Fasciulations in an otherwise strong muscle are usually what?
A
Benign.
14
Q
Fasciculations in weak muscles could indicate what?
A
Lower motor neuron lesions and anteior horn cell lesions.
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.
16
Q
What is spacsticity?
A
hypertonicity.
17
Q
Clasp knife phenomenon
A
resistance is felt when joint is first moved but the resistance decreases as the joint is opened
18
Q
Rigidity is usually associated with?
A
Parkinson’s
19
Q
Cogwheel rigidity
A
gives way in a series of litte jerks
20
Q
Lead pipe rigidity
A
felt thru entire range of motion
21
Q
When would you considered repetitive or sustained muscle testing?
A
Indications of weakness, fatigue, abnormalities on sensory exam or DTRs
22
Q
How should muscle strength tests be done?
A
use 10 repetitions or sustained resistance for 5 seconds.
23
Q
What is Myopathy
A
A muscle disease that is unrelated to any disorder of innervation or the neuromuscular junction.
24
Q
What is the classic findings with myopathies?
A
Proximal symmetric weakness without sensory loss.
25
Does weakness get better with rest with myopathies?
no
26
What are the causes of myopathies?
idiopathic, alcoholic, drug-induced (cortisone, statins), endocrinological or infectious in origin.
27
Are there denervation changes, atrophy or fasciculations with myopathies?
no
28
What is a dystrophic gate like?
Waddling wide-based.
29
What disease will have a dystrophic gate?
Duchenne muscular dystrophy.
30
What drugs can lead to myopathies?
cholesterol-lowering drugs like statins.
31
What is occular myasthenia gravis like?
Fluctuating (since fatigability gets better with rest) double vision and or ptosis.
32
What muscle is commonly affected by occular myasthenia gravis? Which one is affected the second most?
superior rectus and medial rectus is second most common
33
How often will occular myasthenia gravis remain only occular?
Only about 16%.
34
what will the progression of myasthenia gravis be like?
goes from mild to severe over weeks to months and spreads from ocular to facial to bulbar and then to limbs
35
How often will the patients with myasthenia gravis will the disease generalize in a little over a year?
83%.
36
What will bulbar mean?
It is an older term for medulla oblongata.
37
How will pure lower motor neuron lesions present?
Motor deficits only.
38
Where will pure lower motor neuron lesions happen at?
Anterior horn cells and spinal cord axons of the anterior horn cells.
39
What will mixed lower motor neuron lesions present like?
combined motor, sensory and autonomic deficits.
40
Where will mixed lower motor neuron lesions happen at?
nerve roots, peripheral nerves.
41
Fasciculations are more likely to be seen with what?
LMNL of very slow onset.
42
What is a classic sign of a lower motor neuron lesion?
Possible nerve irritability, hyporeflexia, Flaccid parasis/paralysis of specific muscles and marked atrophy
43
What are the classic signs of upper motor neuron lesions?
hyperactive DTR, Clonus, spastic paresis, no fasciculations, no gross atrophy or marked trophic changes, pathologic reflexes.
44
How many types of peripheral neuropathy have been identified?
More than 100.
45
Peripheral neuropathy usually refers to what?
metabolic neuropathy-due to diabetes and chronic alcoholism
46
Mononeuropathy:
common peroneal nerve palsy @ the level of the fib head
47
Plexopathy
neurogenic thoracic outlet syndrome and brachial plexus
48
Plexopathy Lower extremity
steppage gait and numbness or decreased sensation in the antero lateral calf and the dorsum of the foot
49
Plexopathy Painless foot drop and steppage gait is caused by?
compression of the common peroneal nerve at the fibular head leading to painless foot drop.
50
Radiculopathy:
peripheral neuropathy from nerve root disease
| Classic: asymmetric pain, flaccid weakness and sensory deficits
51
Radiculopathy Reality:
not all radiculopathies manifest in painà pain is sharp, stabbing, hot or shooting
52
signs of radiculopathy
- 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
Sensory abnormalities almost always accompany radiculopathies
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
Lumbar/cervical radiculopathy:
from nerve root disease and most are asymmetric and dermatomal/myotomal
55
Radiculopathies and gait: the heel walk
walk 10 steps on heels and get abnormal foot drop and steppage gait.
56
Radiculopathies and gait: the toe walk
patient walks 10 steps on toes and get abnormal heel drop
57
Cervical spine and possible mixed LMNL/UMNL
· Cervical spondylosis
· Central cord syndrome
· Cervical radiculopathy
· Potential compression
58
Cervical spondylosis
a common cause of cervical nerve root impingement and cervical radiculopathy may lead to LMNL findings.
59
Central cord syndrome LMNL findings in the upper extremity UMNL findings in the lower extremity: associated with?
whiplash and cervical spondylosis
60
Cervical radiculopathy:
peripheral neuropathy that is due to nerve root disease + pain and or numbness down the course of the involved nerves
61
Potential compression
paradoxical or mixed reflexes in the upper extremity
62
Possible end result of Potential compression:presentation.
: an incomplete cord lesion and both the nerve root and white matter of the cord leading to mixed LMNL/UMNL
63
Classic: ALS:
ALS: slow onset of mixed upper and lower motor neuron lesions
64
UMN lesions of slow onset
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
LMN lesions of slow onset
a. Wide spread fasciculations may be an early sign (anterior horn cells are not firing properly)
b. Muscle weakness, atrophy and hyporeflexia
66
Cranial nerve lesions categorized
-Supranuclear lesions (central lesions)
-Nuclear lesions
(Peripheral lesions)
-Infranuclear lesions
(Peripheral lesions)
67
Hyposmia/ anosmia and conduction deficits:
inability to recognize smell: inflamed receptors and makes them dysfunctional
68
Dysomia/parosmia:
can notice smell but have trouble identifying from damage to the receptors / neuroepithelium
69
Phantosmia/olfactory hallucination and supra nuclear lesions:
think that the smelt something but really there’s no odor present, from olfactory cortex disorder
70
CN VI: lesion to this nerve?
trochlear palsy
71
CN III: pupillary reaction to light. Damage can lead to?
ptosis/ oculomotor palsy
72
CN VI: lesion
abducens palsy
73
Cardinal fields of gaze tests?
CN III, IV, VI
74
LMN lesions of CN V lead to?
atrophy and flaccid paresis of the chewing muscles.
75
Trigeminal neuralgia/ Tic douloureux/ idiopathic TN
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
LMN lesions of CN VII
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
UMN lesions of CN VII: Supra nuclear lesions
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
UMN lesions of CN VII: Contralateral spastic paresis/ spastic paralysis
i. Most obvious during lip retraction
ii. Least obvious when patients wrinkle forehead
iii. Nasio labial folds partially intact
79
Bell’s Palsy (Idiopathic facial paralysis) Typical progression
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
Bell’s Palsy Incomplete recovery
Paresis> paralysis lasts longer than 6 weeks
81
Bell’s Palsy Diagnosis criteria:
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
CN VIII Nuclear or infranuclear lesions
sensorineural deafness
83
CN IX and X: Testable functions of these two nerves are not ?
entirely separable, therefore must be test together
84
CN XI lesion
unilateral weakness and atrophy: shoulder droop, winged scap
| · Test traps and SCMs
85
Upper extremities: cerebellar Limb ataxia
2. Decomposition of voluntary movement
3. Dysmetria/ past pointing
4. Intention tremor/terminal intention tremor
86
Lower extremities: cerebellar Limb ataxia
The findings: failed heel to shin and cerebellar truncal ataxia/ cerebellar sitting posture
87
Other forms of neurologic gait abnormalities:
1. Cerebral palsy:
2. Spastic hemiplegia/ circumduction gait:
3. Scissor gait/spastic diplegia:
4. Parkinsonism
88
Parkinson gait:
very advanced Parkinson’s disease:
89
Pathologic reflexes and other signs of UMNLs
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
Babinski response:
1. Normalà flexor response/neg Babinski and big toe is down
| 2. Abnormalà extensor response/ positive Babinski and big toe is up
91
Other findings that can indicate UMNLs
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
