Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Brain Power: Adam and Victor's Neurology > Peripheral Nerve > Flashcards

Peripheral Nerve Flashcards

You may prefer our related Brainscape-certified flashcards:
The Brain flashcards
0
Q

What separates bundles of nerve fibers? Epi or Peri NEURIUM

A

Perineurium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
1
Q

What structures are outside the pail membrane but are not member of the peripheral nervous system?

A

Optic nerves and olfactory bulbs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Wallerian or axonal degeneration? Dying backward in metabolic polyneuropathies.

A

Axonal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Wallerian or axonal degeneration? Dying forward in axonal damage

A

Wallerian

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

In wallerian degeneration and axonal degeneration give the histologic picture associated with the neuronal CELL BODY.

A

Chromatolysis: swelling of the cell cytoplasm and margnializaiton and dissolution of the Nissl substance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Match:

  1. GBS
  2. Polyarteritis nodosa
  3. Diptheric polyneuropathy

A. Endoneurial infiltrates of lymphocytes and other mononuclear cells in the nerves, roots and sensory and sympathetic ganglia
B. Demylinative changes around the roots and the sensory ganglia and a LACK OF INFLAMMATORY REACTION
C. Necrotizing panarteritis with thrombotic occlusion of vessels and focal infarction of peripheral nerves

A

1A
2C
3B

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Most axonal polyneuropathies: nutritional, metabolic and toxic neuropathies assume a distal axonal pattern wherein the pathologic process begins in the largest and longest nerves, i.e. those of feet and legs EXCEPT FOR?

A

Porphyrias, mainly proximal weakness at first

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Differentiate axonal polyneuropathies from demyelinating neuropathies in terms of pattern of weakness

A

Demyelinating: weakness of the proximal limb and facial muscles before or at the same time as the distal parts are affected
AP: Distal before proximal, feet before cranial nerves and arms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

T or F, motor neuron or motor axon disease spare muscle bulk

A

F, demyelinating disease spare muscle bulk

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the only CNS disease that will cause areflexia?

A

Spinal shock

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What for of sensory loss usually predominates in axonal polyneuropathies?

A

Small afferent fibbers of pain and temperature

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Which can cause burning type of pain in both feet? DM neuropathy or Partial nerve lesions?

A

BOTH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What kind of tremor arises from polyneuropathy?

A

Fast frequency action tremor much like cerebellar tremor. Look for other cerebellar signs such as nystagmus and scanning speech to differentiate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Give three diseases that causes ataxia without weakness.

A
  1. Tabes dorsalis
  2. DM polyneuropathy
  3. Fisher syndrome
  4. Cerebellar disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

In chronic polyneuropathies, tabes dorsalis and syringomyelia analgesic joints that are chronically traumatised become deformed then disintegrate, what is this process called?

A

Charcot arthropathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Diabetic neuropathy with autonomic dysfunction usually manifests with which 2 symptoms?

A

Anhidrosis and orthostatic hypotension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Fasciculations cramps and spasms are prominent features of which kind of disease?

A

Anterior horn cell disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What can be used to treat myokimia?

A

Carbamazepine or phenytoin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

GBS– What is the most frequently identifiable antecedent infection to GBS?

A

C. jejuni. Also associated are Herpes family of viruses, and Hodgkin lymphoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

GBS– Which muscles are affected first? Proximal or distal?

A

BOTH affected at the same time BUT LE before UE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

GBS– Describe the sensory involvement

A

Burning sensation may occur in feet and hands; Joint and position sense&raquo_space;> pain and temperature

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

GBS- What symptoms are similar to a primary spinal cord disease?

A
  1. Back pain
  2. Motor and sensory problems
  3. Urinary retention occurs in 15 percent of patients needing catheterisation for a few days
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

GBS– Reflexes?

A

Reduced or absent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

GBS– Autonomic dysfunction?

A

Facial flushing, labile BP, HR and sweat pattern

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What variant of GBS?

  1. Abrupt and severe denervating paralysis, atrophy within weeks
  2. Complete ophthalmoplegia with ataxia and areflexia
  3. Severe axonal degeneration with minimal inflammatory changes
  4. Difficulty swallowing and proximal arm weakness occurring as presenting symptoms
A
  1. AMAN
  2. Fisher syndrome
  3. AMAN
  4. Pharyngeal-cervical-brachial muscle variant
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Which GBS variant antibody?

  1. AMAN
  2. Fisher syndrome
A
  1. Antibodies to GM1 ganglioside

2. Anti-GQ1b

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What comes first nerve conduction abnormalities or increase in CSF protein?

A

Nerve conduction abnormalities are early (within days of symptom onset) and dependable dxtic indicators of GBS. CSF protein normal in first few days and peaks at 4-6 weeks.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What are the EMG findings of GBS?

A
  1. Reduction in the amplitude of muscle action potentials
  2. Slowed conduction velocity
  3. Conduction block
  4. Absent F responses
  5. Prolonged distal latencies
  6. H reflex delayed or absent
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

GBS– Pathology

A

Endoneural perivenous lymphocytic infiltrates –> segmental demyelination –> PMNs arrive –> Axon degenerates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

How to differentiate tick paralysis from GBS?

A

CSF protein normal and sensory loss is usually not a feature of tick paralyssi

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

How to differentiate polio from GBS?

A
  1. Fever
  2. Meningoencephalitic sxxs
  3. Asymmetrical areflexic paralysis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What electrolyte abnormality mimics GBS?

A

Hypophosphatemia of hyperalimentation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What characteristics differentiate carcinomatous meningitis from GBS?

A
  1. Weakness is mainly distal
  2. Absence of facial weakness
  3. Appearance of symptoms sequentially in one limb to another
  4. Spinal fluid with malignant cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

How does pupillary examination and reflexes differentiate

  1. GBS
  2. Brainstem infarction
  3. Botulism
A

GBS: Good pupillary response until very late in the disease + Areflexic
Botulism: Early pupillary paralysis + Poor reflexes
Brainstem infarction: Early pupillary paralysis + Lively reflexes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Being able to count to 20 means that once has a vital capacity of how much?

A

1.5L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What percentage of patient parlayed from GBS will develop hypotension from dysautonomia?

A

10%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What is the golden period for the treatment of GBS with plasma exchange?

A

2 weeks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What are the 2 most important predictors of responsiveness to plasma exchange treatment of GBS?

A

Young age and preservation of motor compound muscle action potential

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What subset of patients should not be given IVIg 0.4g/kg for 5 consecutive days?

A

Those with congenital absence of IgA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What are adverse effects of IVIg?

A

Aseptic mengingitis, proteinuria, renal failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

After GBS residual deficits still present for ___ years will probably be permanent.

A

2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Critical illness polyneurpathy usually spares?

A
  1. Cranial nerves

2. Few or no dysautonomic symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

How can one distinguish paresis from critical illness polyneuropathy from GBS?

A

EMG findings are mostly axonal and CSF is normal in CIPN. Difficult to distinguish from acute axonal form of gbs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What is the most common cranial nerve affected in DM neuropathy?

A

3

45
Q

What muscles are frequently affected in DM amyotrophy?

A

Proximal leg muscles

46
Q

What vessels are occluded in those DM neuropathy?

A

Vasavenorum, endoneurial blood vessels

47
Q

What are the tropic changes associated with DM neuropathy?

A

Deep ulceration a and Charcot joints (neuropathic degeneration of joints)

48
Q

What are the 3 most frequently involved nerves in acute diabetic neuropathy? In order.

A
  1. Femoral
  2. Sciatic
  3. Peroneal
49
Q

What does the CSF look like in DM polyneuropathy?

A

CSF may be elevated from 50 to 150mgdl

50
Q

T/F: Segmental demylination and demyelination creating onion bulb formations of Schwann cells and fibroblasts are seen in DM neuropathy.

A

True

51
Q

T/F: Low intramural myoinositol and increased orbital have been purported in the pathophysio of the DM neuropathy

A

True

52
Q

What is the only treatment for diabetic neuropathy?

A

Maintenance of blood glucose concentrations close to normal range

53
Q

Distressing parenthesis of DM neuropathy can be managed by what drug?

A

Amitryptyline or the other new antidepressants

54
Q

What drugs may cause acute sensory neuronopathy?

A
  1. Cisplatin

2. Excessive intake of pyridoxine

55
Q

What is the golden period of institution of antitoxin in Diptheric polyneuropathy to reduce the incidence and severity of neuropathic complications?

A

48 hours

56
Q

What comes first in Diptheric polyneuropathy?

  1. Acute or subacute limb weakness with paraesthesias and loss of vibratory and position sense
  2. Cranial neuropathy involving dysphagia, nasal voice and BOV from failure of accomodation
A
  1. 5 to 8 W after onset of infection

2. Local toxin effect so earlier in 1 to 2 weeks after infection

57
Q

What polyneuropathy is mainly motor, associated with
1. Convulsions
2. Psychosis
3. Abdominal pain
manifesting in late adolescence and early adulthood?

A

Porphyric polyneuropathy– acute intermittent porphyria

58
Q

How is the diagnosis of porphyric polyneuropathy confirmed?

A

Large amounts of porphobilinogen and aminolevulinic acid in the urine– URINE TURNS DARK upon standing

59
Q

Acute toxic polyneuropathy with thallium salts have what 2 striking features that distinguish it from GBS?

A
  1. Complete alopecia

2. Relative preservation of reflexes

60
Q

T/F In contrast to acute polyneuropathies, subacute ones are usually motor and demyelinating in type.

A

False. Inverse is true. Sensory and axonal EXCEPT FOR SUBACUTE INFLAMMATORY DEMYELINATING TYPE

61
Q

What is the most common cancer to cause paraneoplastic polyneuropathy and sensory ganglionopathy?

A

Lung CA 50% total and 75% of those purely sensory

62
Q

Paraneoplastic polyneuropathy is usually what type? Motor or sensory.

A

MIXED. But take note that lung CA is notorious for purely sensory distal to proximal spread. NB: Small cell lung CA associated with anti-Hu antibody.

63
Q

Match:

  1. Arsenic
  2. Lead
  3. Thallium

A. Subacute: Jaundice, Mees lines, anemia
B. Subacute: Motor mononeurpathy in the distribution of the radial nerves: wrist or finger drop, basophilic stippling of rbis
C. Acute: Complete alopecia

A

1A 2B 3C

64
Q

Most chemotherapeutic agents cause only a sensory polyneuropathy impairing vibration and sensation, which among these also cause some degree of weakness?

  1. Vincristine
  2. Docitaxel
  3. Carboplatin
  4. Cisplatin
A

Vincristine. Also the sensory component is mostly paresthesias

65
Q

What anti hypertensive is associate with an INH like peripheral neuropathy manifesting as tingling of toes and feet?

A

Hydralazine

66
Q

What antibiotic usually used in UTI is known to cause pain and tingling paresthesias in the toes and feet?

A

Nitrofurantoin

67
Q

What antiarrythmic is purported to cause motor sensory neuropathy?

A

Amiodarone

68
Q

What dose of pyridoxine is enough to prevent INH neuropathy completely?

A

150-450mg daily

69
Q

What anaesthetic agent has a predilection for 5th cranial nerve?

A

Trichloroethylene

70
Q

What AED causes loss of ankle and patellar reflexes with chronic use?

A

Phenytoin

71
Q

What is the most common cause of vasculitic polyneuropathy according to a series by Said?

A

PAN 75% will involve vasavenorum of nerves by autopsy but only half will manifest

72
Q

Match
1 PAN
2 Churg Strauss

A bowel and renal infarction
B lung and skin

A

1A 2B

73
Q

What kind of polyneuropathy is observed in Churg Strauss disease?

A

PAINFUL MONONEURITIS multiplex

74
Q

Besides the typical angiopathic polyneuropathy how else does wegener granulomatosis present?

A

Lower cranial nerve neuropathy

75
Q

Approximately what percentage of patients exhibit signs and symptoms of peripheral nerve involvement?

A

10 percent will have ascending sensorimotor paralysis

76
Q

All chronic polyneuropathoes are symmetric in patter except for:

A

Leprous neuritis

77
Q

What is the EMG and CSF picture of CIDP?

A

EMG reduced conduction velocity and conduction block like that in demyelinating dz

CSF cytoalbuminologoc dissociation

78
Q

T of F CIDP commonly presents after a mild or moderate type of GBS

A

False

79
Q

T or F Cranial nerve involvement is NOT a usual feature of CIDP

A

True

80
Q

What are the 3 major categories of treatment for CIDP patients?

A

1 Corticosteroids
2 IVIG
3 Plasma exchange

81
Q

Uremic polyneuropathy is usually painless progressive symmetrical sensory loss but may manifest as ______ occurring usually at _________ relieved by ___________.

A

Painful, itching, crawling, burning sensation
Night
Movement

82
Q

Which among the ff will RELIEVE uremic polyneuropathy?

  1. Renal transplant
  2. Long term dialysis
  3. Both
  4. Neither
A

1 only since methyl guanidine and myoinositol, the accumulated neurotoxic substances are not filtered by hemodialysis

83
Q

What type of leprous polyneuritis is described as innocuous appearing skin macule or papule which is often hypo pigmented and lacking in sensation due invasion of cutaneous nerves?

Indeterminate
Tuberculoid
Lepromatous

A

Indeterminate

Tuberculous: Epitheloid granuloma
Lepromatous: Diffuse infiltration of organs due to hematogenous spread

84
Q

What is the most vulnerable motor nerve to leprosy?

A

Ulnar nerve

85
Q

What regions of the body are spared by leprosy?

A

The warm regions usually in the antecubital areas, the buttocks, the palms– colder areas are favored

86
Q

What genetic late chronic polyneuropathy is described by, high arches and distal foreleg atrophy?

A

Charcot Marie Tooth Disease

87
Q

What type of brachial plexus injury results from Pancoast tumours of the lung?

A

Lower brachial plexus paralysis– weakness and wasting of the small muscles of the hand and characteristic claw hand deformity

88
Q

Match which cord is affected
1 weakness of deltoid, extensor a of wrist fingers and upper arm sensory loss
2 weakness of pronation and…
Esupination of the forearm

A

1 posterior cord

2 lateral cord

89
Q

What nerve is most commonly affected by solitary brachial plexus neuritis?

A

Long thoracic nerve of the serratus anterior

90
Q

What radiation dose can cause brachial neuropathy?

A

6000 cGy or more

91
Q

Injury to the long thoracic nerve of bell results in inability to?

A

Raise arms over head and winging of the medial border of the scapula

92
Q

Meat packer’s neuropathy results in inability to?

A

Suprascapular nerve palsy
Supraspinatus first 15 degree abduction
Infraspinatus external rotation of the shoulder

93
Q

What degrees of shoulder abduction is taken care of by the deltoids?

A

15-90 degrees

94
Q

What brachial plexus nerve is susceptible to lead intoxication and is commonly known as CRUTCH palsy?

A

Radial nerve

95
Q

The phalen and tinel tests for carpal tunnel syndrome are more sensitive or more specific?

A

More specific. Sensitivity only at 50%

Phalen you flex the wrist
Tinel you tink the collar aspect of the wrist

96
Q

Why is claw hand deformity worst at the 3rd and fourth digits?

A

Lumbricals supplied by the median nerve counteract the deformity seen at the 2nd and 3rd digits.

CLAW HAND DEFORMITY IS FROM ULNAR NERVE PALSY

97
Q

Differentiate what actions are supported by the upper lumbar plexus compared to the lower lumbar plexus

A

Upper lumbar plexus with femoral nerve ergo for hip flexion and knee extension

Lower lumbar plexus with sciatic nerve (tibial and peroneal) for hip extension, knee flexion and ankle dorsi and plantar flexion

98
Q

While trauma leads the list of etiologies for brachial plexus dysfunction what conditions result in lumbar plexus palsies?

A

Cancer and diabetes

99
Q

What are the treatment options for meralgia paresthetica?

A

Weight loss and position modification – lidocaine block – nerve transection

AKA Lateral cutaneous nerve

100
Q

How to know if the lesion is a femoral one or a third lumbar root lesion?

A

Check thigh adduction. Intact in thigh adduction in femoral nerve lesion but not in L3 because obturator nerve will also be involved L3 L4

101
Q

How differentiate intra pelvis and extra pelvis lesions of the femoral nerve?

A

Intrapelvis with weakness of hip flexion extra pelvis only knee extension

102
Q

T or F The sciatic nerve supplies all muscles below the knee

A

True through its 2 segments the peroneal and the tibial nerve

103
Q

Based on ankle movement how can one differentiate a lesion of the hernitaion of l4 l5 disc with l5 s1 disc?

A

Dorsi flexion is an action of l4 l5 deep peroneal tibialis anterior
Plantar flexion is s1 s2 tibial nerve gastrocnemius

104
Q

What is the most common cause of femoral neuropathy?

A

dm

105
Q

T or F The anterior tibial nerve supplies the dorsiflexors of the foot and toes

A

T, the anterior tibial nerve is the old name for the deep perineal nerve

106
Q

What goes hand in hand with a foot drop due to common perineal nerve palsy? Weakness of:

  1. Inversion
  2. Eversion
A
  1. Eversion
107
Q

What are the most commonly compressed nerves?

A
  1. Median
  2. Ulnar
  3. Peroneal
  4. Tibial
  5. Plantar
108
Q

How long should surgical repair be done for traumatic interruption of nerves?

  1. Sharp clean division
  2. Bluntly severed ragged ends
A
  1. 72 hours

2. 2 to 4 weeks

Brain Power: Adam and Victor's Neurology (19 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions