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IPAP JUNIOR SEM. > Nuero Block I: Diseases Of The Nerve > Flashcards

Nuero Block I: Diseases Of The Nerve Flashcards

1
Q

How many pairs of spinal nerves are there

A

31 pairs

8 cervical 
12 thoracic 
5 lumbar 
5 sacral 
1 coccygeal
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2
Q

What are the basic parts of the neuron

A

The cell body, axon, and dendrites

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3
Q

What is the recieveing portion of the neuron

A

The dendrite

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4
Q

What part of the neuron propagates impulses to other neurons

A

The axon

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5
Q

Where do axons arise from

A

Typically arises from an elevation in the cell body called the axon hillock (= small hill)

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6
Q

Where is the trigger zone on an axon

A

Impulses (action potentials) generally arise in the trigger zone, the junction of the hillock and initial segment

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7
Q

What class of drug is lidocaine and Marcaine

A

NA+ channel blockers

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8
Q

Where are Schwann cells located

A

They are the myelin sheath of the peripheral nerves

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9
Q

Where are oligodendrocytes located

A

They are the myelin sheath of the CNS

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10
Q

What are the three steps to Dz of the spinal cord

A

Identify where the lesion is

Identify the cause

Determine proper Tx

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11
Q

What are the seven key questions for dz of the spinal cord

pt approach

A

What systems are involved

What is the distribution of weakness

What is the nature of sensory involvement

Is there upper neuron involvement

What is the time of S/s

Is there evidence of hereditary neuropathy

Are there associated medical condition s

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12
Q

Wrist drop with weakness in thumb aBduction and finger extension is a sign of neuropathy where

A

The radial nerve

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13
Q

Sensory loss of the dorsal web space betweeen the thumb and index finger is neuropathy where

A

Radial nerve

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14
Q

What is the Tx approach to radial neuropathy

A

Cock up wrist and finger splints

Followed by physical therapy

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15
Q

What is the nerve compression responsible for Carpal Tunnel

A

Median nerve compression

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16
Q

Numbness in the thumb, index, and middle finger, with aching pain in the hand and forarm that is worse at night…

A

Carpal tunnel

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17
Q

What is tinel sign

A

A sing of nerve compression, taping on the nerve leads to tingling sensations through the dermatomes

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18
Q

What is a positive phalens sign

A

A PE sign for carpal tunnel

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19
Q

What is the Tx approach to CTS

A

U/s of the median nerve to assess for swelling

EDX: sensory delay before motor delay

Tx: 
Activity mod. 
NSAIDs
Wrist splint worn at night 
Methylprednisosne injections

And possible surgical decompression

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20
Q

Parasethisa and tingling of the medial hand, and either the 4th or 5th fingers is compression of what nerve

A

Ulnar nerve

cubital tunnel syndrome

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21
Q

What are the S/s of cubital tunnel syndrome

A

decreased sensation in ulnar distribution
Tinel’s sign at the elbow
Froment Sign

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22
Q

postive tinsels sign at the elbow indicates what neuropathy

A

Compression of the ulnar nerve

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23
Q

What is the Tx approach to Cubital tunnel syndrome

(ulnar nerve compression)

A

EDX: slowing of ulna motor NCV across the elbow

U/S: swelling of the ulnar nerve near the elbow

Tx: 
Activity mod 
Elbow pads 
Splints 
Possible surgery
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24
Q

What is meralgia parenthetica

A

Compression of the lateral femoral cutaneous nerve

Common in obese, DM, and pregnant pts
MERICA= Meralgia

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25
Q

What anatomical position relieves meralgia parenthetica

A

Sitting

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26
Q

What is the Tx approach to Meralgia paresthetica

A

Wt loss
Lidoderm patch
NSAIDS
And Neuropathic pain meds

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27
Q

What are the 1st line medication for the Tx of painful sensory neuropathies

A 
Lidoderm 
TCA- amitryptyline or notriptyline 
Gabapentin 
Pregabalin 
Duloxetine
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28
Q

What are 2nd line agents for Tx of painful sensory neuropathies

A

Carbamazepine
Phynetoin
Venlafaxine
Tramadol

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29
Q

What are the S/s of a B12 deficiency

A

Distal symmetric numbness and gait instability with distal weakness

Usually hands numb first
-Harrison’s but Current does not differentiate

GI S/Sx: diarrhea, glossitis, anorexia

PE: Decreased vibratory sensation, hyperreflexia, absent Achilles reflex, gait issue

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30
Q

What is the Tx approach to B12 deficiency

A

IM injection q weekly x 1 month

Then q month

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31
Q

A B12 deficiency deficits permanent?

A

50% of pts with have some perm. Neuro deficit

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32
Q

What is the most common complication of DM

A

Diabetic neuropathies

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33
Q

What is the most common form of DM neuropathy

A

Diabetic distal symmetric sensory and Sensorimotor Polyneuropathy (DSPN)

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34
Q

What is the TX approach to diabetic neuropathy

A 
Tight glycemic control 
Pain control (examples):
Tricyclic antidepressants
Gabapentin
Serotonin/norepinephrine reuptake inhibitor
Capsaicin cream
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35
Q

A pt that presents with a stocking-glove pattern of neuropathy.. suspect

A

DM (DSPN)

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36
Q

A pt with otro static HOTN, sweating disturbances, excercse intolerances, bladder dysfunction of ED, with DM suspect

A

DM neuropathy

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37
Q

What is the number one agent of neuropathies in HIV infected pts

A

CMV

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38
Q

What is the most common S/s of Lyme Dz neuropathy

A

facial neuropathy ( bilateral unlike Belsy palsy)

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39
Q

What are the biopsy result in Lyme disease neuropathy

A

Axon degeneration w/ perivascular inflammation

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40
Q

What is the Tx for Lyme Dz neuropathy

A

Doxy

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41
Q

A pt presents with severe pain along a dermatomes followed by a vesicular rash.. think

A

HVZ ( herpes zoster) - a peripheral neuropathy

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42
Q

What is the Tx approach to shingles

A

Within 72 hours- acyclovir, ect

Reduce pain

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43
Q

What is the most common cause of peripheral neuropathy in Asia, Africa, and South America

A

Leprosy aka Hansens Dz

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44
Q

A pt that presents with tuberculoid and lepromatous lesions… think

A

Hansens/ Leprosy

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45
Q

Where is neuropathy most common in leprosy

A

To the ears and distal limbs

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46
Q

What is the confirmatory lab for leprosy

A

Acid fast bacillus in skin lesions (( biopsy)

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47
Q

What are the complications of leprosy

A

Anesthesia, motor d/o, kidney failure, hepatomegaly, and secondary amyloidosis

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48
Q

WHO ecommended Tx of leprosy/ Hansens Dz

A

Lepromatous: Rifampin 600mg plus Clofazimine 300mg once a month (supervised) AND Dapsone 100mg plus Clofazimine 50mg daily for 1-2 years

Tuberculoid: Rifampin 600mg once a month (supervised) and Dapsone 100mg daily (unsupervised) for 6 months

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49
Q

What is the most common type of hereditary neuropathy

A

Charcot-Marie-tooth

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50
Q

What is the most common presentation of Charcot-Marie-tooth

A

Foot drop

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51
Q

A pt that presents with distal weakness, that defines in the legs then spreads to the hands and forearms, has inverted champagne bottle legs (atrophy), Depressed or absent DTRs.. think

A

Charcot-Marie-tooth

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52
Q

CMT type one distinction

A

Charcot-Marie-Tooth disease

CMT Type 1 (most common): characterized by demyelination on electrodiagnostic

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53
Q

What is the Tx approach to Charcot-Marie-tooth

A

Physical and Occupational Therapy

AFO – foot drop

And in late stages surgical intervention to treat foot deformity if unable to manage conservatively

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54
Q

What is HSAN

A

Hereditary Sensory and Autonomic Neuropathy

Autosomal dominant disease involving progressive degeneration of small myelinated and unmyelinated nerve fibers.

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55
Q

A pt presents with distal sensory loss ( burning, aching, knife like pain) with deep dermal ulcers, recurrent OA, foot and hand deformities, w/ bladder dysfunction and reduced sweating in the feet… think

A

HSAN

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56
Q

What is familial amyloid polyneuropathy

A

Mutation in the genes for transthyretin that leads to

  • Insidious onset of numbness and painful paresthesias
  • Early involvement on the autonomic nervous system
  • Cardiomyopathy leading to cardiac failure
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57
Q

What is the Tx approach to Familial amyloid polyneuropathy

A

Liver transplant

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58
Q

What is refsums Dz

A

Autosomal recessive Dz
With onset in infancy to early adulthood

Earliest s/s night blindness

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59
Q

What is the earliest s/s of refsums dz

A

Night blindness

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60
Q

What is the classic tetrad of Refsums

A

Peripheral neuropathy
Retinitis pigmentosa (Bone spicules in the eye)
Cerebellar ataxia
Elevated CSF protein concentration

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61
Q

What is the Dx criteria for Refsums

A

Elevated levels of phytanic acid in the serum and urine

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62
Q

What is the Tx approach to refsums

A

Avoid dietary sources of phytanic acid

Plasmaphoresis

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63
Q

What is the most common variant of Guillian-barre syndrome

A

Acute Inflammatory Demyelinating Polyradiculoneuropathy

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64
Q

What are the precipitation fxs that lead to Guillian barre syndrome

A

Polyneuropathy 1-3 weeks following an illness (70%; respiratory or GI) or vaccination (H1N1, 1976)

An association with preceding Campylobacter jejuni enteritis.

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65
Q

A pt that complains for variable weakness that starts in the legs and ascends leading to paralysis , following an infection or IMR, and has absent DTRs think. ?

A

Guillian Barre

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66
Q

What are the ADE outcomes of Guillian BArre syndrome

A

Autonomic dysfunction (loss of vasomotor control): tachycardia, dysrhythmias, hypotension, pulmonary dysfunction, loss of sphincter control, sweating, labile BP

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67
Q

What will the CSF be like in a pt with Guillian barre

A

High protein with a NML cell count

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68
Q

What is the Tx approach to Guillian barre

A 
IV immunoglobulin
Plasmapheresis
Hospitalization - ICU admission 
\+/- intubation
Steroids are not helpful
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69
Q

What is the prognosis of Guillian Barre

A

Self limiting

Patient may need rehab to regain lost function
Minor findings may persist (areflexia)
Fatigue is typical persistent symptom

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70
Q

What is chronic inflammatory demyelination g Poly neuropathy

A

Occurs in adults M>F

75% have reasonable function after several years following treatment
Death rare

Clinical presentation:
-Gradual onset
-Initial attack is indistinguishable from GBS
-Consider if (chronic course)
It lasts longer then 9 weeks
Or > then 3 relapses

Sx both motor and sensory.

Symmetric but may be asymmetric in a variant

Considerable variability from case to case

Tremor in 10% of pts

May have cranial nerve findings (external ophthamoplegia)

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71
Q

A pt with external opthomoplegia think..

A

Chronic inflammatory Demyelinating Poly Neuropathy

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72
Q

A CSF that is acellular with elevated protien… think

A

Chronic Inflammatory Demyelinating Polyneuropathy

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73
Q

A Electro Dx of Variable degrees of conduction slowing

Prolonged distal latencies

Temporal dispersion of compound action potentials

Conduction block

Evidence of axonal loss is evident in >50% of patients

Think….

A

Chronic Inflammatory Demyelinating Polyneuropathy

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74
Q

What is the Tx difference of Chronic Inflammatory Demyelinating Polyneuropathy and GBS

A

Responds to glucocorticoids, whereas GBS does not

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75
Q

What is the Tx approach to Chronic Inflammatory Demylenation Poly Neuropathy

A

Initiate when progression is rapid or when walking is compromised

If mild, spontaneous recovery can be expected.

Consider IVIg, Plasma Exchange (PE), glucocorticoids

May need to retreat at 6 week intervals

Up to one third fail to respond to initial tx

consider immunosuppressive agents like azathioprine, methotrexate, cyclosporin, and cyclophosphamide

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76
Q

What is Multiple myeloma

A

Neuropathies with Monoclonal Gammopathy

X-rays will show either lytic or diffuse osteoporotic bone lesions

Effects men more than women

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77
Q

A pt with an elevated ESR in isolation of other systemic disease test.. think

A

Vasculitic Neuropathy

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78
Q

What is the Tx approach to polyarteritis nodosa

A

Treat underlying condition causing the vasculitis and aggressive use of glucocorticoids and other immunosuppressive agents

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79
Q

What are the hallmark features of myasthenia gravis

A

EOMs affected first (diplopia, ptosis)

Dysarthria, dysphagia, and respiratory muscle weakness

Generalized, fluctuating weakness

Symptoms worse towards end of day

Symptoms typically improve with rest and on first arising

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80
Q

If ACh Abs are detected in the blood, think

A

Myasthenia Gravis

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81
Q

How does myasthenia gravis show on CT

A

May reveal thymoma: thymic medullary cells can synthesize anti-acetylcholine receptor antibodies

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82
Q

The ice pack test is for what disorder

A

Myasthenia gravis

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83
Q

What is the tensilon test

A

Administration of edrophonium 2mg IV
-short acting cholinesterase inhibitor (inhibits ACh breakdown at the NMJ)

Reserved for patients with clinical findings c/w MG and negative antibody and electrodiagnostic test results

Positive test - Definite improvement to weakness

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84
Q

What test can be used for patients with clinical findings c/w MG and negative antibody and electrodiagnostic test results

A

Tensilon test

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85
Q

What is the Tx approach to Myasthenia Gravis

A

Anticholinesterase drugs:
-Pyridostigmine 30-60mg 3-4x/day provides symptomatic relief without influencing the course of the disease.
Tailored to the patient’s symptoms

Thymectomy for patients with generalized MG

Cortiosteroids:
-Prednisone can be started at 20 mg orally daily and increased by 10 mg increments weekly to a target of 1 mg/kg/day (maximum daily dose 100 mg).

Plasmapheresis - temporary improvement in rapidly deteriorating cases or to improve condition prior to surgery.

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86
Q

What is myasthenic syndrome

A

Associated w/ small cell carcinoma

Defective release of acetylcholine in response to a nerve impulse
caused by P/Q-type voltage-gated calcium channel antibodies, and this leads to weakness, especially of the proximal muscles of the limbs.

Unlike myasthenia gravis, however, power steadily increases with sustained contraction

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87
Q

What is the Tx approach to myasthenic syndrome

A

Prednisone and azathioprine

88
Q

What are the DDx findings in Myasthenic syndrome vs myasthenia gravis

A

Unlike myasthenia gravis, however, power steadily increases with sustained contraction in myasthenic syndrome

89
Q

How does Botulism work

A

Prevents the release of Ach at NMJ and can cause neuromuscular paralysis

Can be food or wound (rare) borne. Most commonly from home canned foods

90
Q

What are the S/s of botulism

A

Weakness begins 12-72 hrs after ingestion (GI)

  • Double or blurred vision
  • Eye lid lag (ptosis)
  • Facial Weakness
  • Dysphagia
  • Nasal Speech
  • Difficulty w/ respirations
  • Limb weakness last sign
91
Q

A child less than one year that presents with constipation, poor feeding, and failur to thrive ( progressive weakness + impaired RR) think?

A

Botulism

92
Q

What is the Tx approach to botulism

A

Initial management – supportive care

Need to be hospitalized and may require ventilator support and aggressive inpatient care

Botulism Antitoxin Heptavalent (equine-derived)

Botulism Immune Globulin Intravenous (human-derived)

-Avoid aminoglycosides and neuromuscular junction blocking medications (potentiate botulism effects)

93
Q

What medications should be avoided in pts with botulism

A

Avoid aminoglycosides and neuromuscular junction blocking medications (potentiate botulism effects)

94
Q

What medications are C/I in myasthenia gravis and lambert Eaton myasthenic syndrome pts

A

Gentamicin and Strptomycin

95
Q

What effects go gentamicin and streptomycin have on nerve endings

A

Prevents the release of ACH from the nerve endings

May be related to Ca++ channel blockade

96
Q

What is the incubation period for lock jaw

A

5 days to 12 weeks

Ave 8-12 days

97
Q

A pt with trismus, dysphagia, facial muscle contortion (risus sardonicus) think

A

Tetanus: Clostridium tetani

98
Q

What is opisthotonos

A

Hyperextended posturing assoc with tetanus

99
Q

What is the Tx approach to Tetanuc

A

Human tetanus immune globulin, 500 units, should be administered intramuscularly within the first 24 hours of presentation

General Measures:
Cleaning and Debridement of wound is first step

Tetanus toxoid booster if no vaccination in past 5-10 yrs

Hospitalization in ICU to monitor pulmonary and cardiac function

Metronidazole 500mg IV q6h for 7 days (preferred abx)

Heavy sedation with benzodiazepines for muscle spasms

Mortality 10-60% (95% who recover do so without long-term sequelae)
Decreased through early detection

100
Q

What is the perferred ABX in tetanus

A

Metronidazole

101
Q

What is pyridostigmine bromide

A

Nerve agent pretreatment

Increases the amount of nerve agent a person can be exposed to and survive

102
Q

What is the Tx approach to nerve agents

A 
Emergency measures
Supportive measures
Meds: 
-Atropine 2mg 
-2Pam Cl
103
Q

What is pralidoxime

A

Protects acetylcholinesterase from degredation
Irreversible binding by nerve agent
AKA: 2 PAM Chloride

104
Q

Spasticity implies that the lesion originates

A

UMN

105
Q

Rigidity implies

A

Extrapyramidal dysfunction

106
Q

Hypotonia implies

A

LMN lesion or myopathy

107
Q

A pt w/ Spasticity, diffuse weakness, hyperreflexia, positive Babinski; no muscle atrophy until late where is the lesion

A

UMN

108
Q

A pt w/ Flaccidity, focal weakness, hyporeflexia, negative Babinski, wasting of muscles where is the lesion

A

LMN

109
Q

Hyper reflex ismplies what lesion

A

UMN lesion

110
Q

Hypo reflexia implies what lesion

A

LMN

111
Q

When reflexes are asymmetric and lateralized its typically a lesion where?

A

UMN on the brisk side

112
Q

A focal deficit implies

A

A rott/ plexus/ peripheral nerve lesion

113
Q

A pt with loss of distal DTRs yet proximal DTRs remain intact, suspect

A

DM poly neuropathies

114
Q

What are the 5 types of imbalance

A

Imbalance with Cerebellar ataxia

Cerebellar limb ataxia

Imbalance with vestibular dysfunction

Imbalance with sensory ataxia

Sensory limb ataxia

115
Q

Where is the lesion in Hemiparetic gait

A

UMN caused by Brain stem, Cerebral hemisphereStroke, tumor, trauma

The upper extremity adducted and internally rotated
Flexion at elbows, wrist and fingers
Extension at hip, knee and ankle
Forward swing of the spastic leg requires abduction and circumduction
Contralateral tilt of the hip to help with swing phase
The patient will have to “circumduct” or swing the leg around to step forward.

116
Q

A scissor gait is AKA? And is common in what pts

A

Paraparetic or Diplegic gait

And common from stroke
Often from periventricular lesions

The patient has spasticity in the lower extremities greater than the upper extremities.
Hips and knees are flexed and adducted with the ankles extended and internally rotated
The patient circumducts the lower extremities
Upper extremities are held in a mid or low guard position.
Often seen with periventricular lesions.
The legs are more affected than the arms b/c the corticospinal tract axons that are going to the legs are closest to the ventricles.

117
Q

What is a steppage or neuropathic gait associated with

A

Usu. assoc. with L5 lesion if unilateral, however if bilateral consider polyneuropathy or lumbosacral poly radiculopathy

Most often seen in peripheral nerve disease
The distal lower extremity is most affected.
Causes weakness of the foot dorsiflexors
B/C they are weak the pt will have a high stepping gait
This is an attempt to avoid dragging the toe on the ground
Causes: sensory neuropathy; vitamin B12, tabes dorsalis

118
Q

A waddling or myopathic gait is caused by,..

A

Caused by myopathy, NMJ disease, or proximal symmetric spinal muscular weakness

The proximal limb weakness. With weakness of hip flexion the trunk is tilted away from the leg that is being moved

This provides additional distance between the leg and the floor
The pelvis is rotated to forward to assist in forward motion

The patient will not be able to stabilize the pelvis as they lift their leg to step forward

The weakness is normally bilateral causing the typical waddling type gait

119
Q

Describe a parkinsonian gait

A

Forward stoop, modest flexion of hip and knees.

Arms flexed at elbows and adducted at shoulders

4- to 6-Hz resting pill-rolling tremor in his hands.

Bradykinetic gait initiated by a slow lean forward and maintained small, shuffling steps

Gait tends to accelerate

Falls are common due to postural instability and freezing of the gait

Turns en bloc (all together, or as a whole) like a statue

There is decreased facial expression

120
Q

Describe apraxia

A

Found in bilateral frontal lobe disease.
May be accompanied by dementia and incontinence

Caused by an inability to plan and execute sequential movements

Resembles the Parkinsonian gait
-Stoop posture with short shuffling steps

Difference in initiation though
-When patient is asked to step forward while standing, there is a long pause before any attempt is made to flex at the hip and knees

Once started the gait is only maintained for a few steps then patient has to stop for several seconds or longer

121
Q

A gait with a lurching appearance, unpredictable movements, and Intrusion of intermittent, irregular, jerky, involuntary movements in both the upper and lower extremities

A

Choreoathetotic gait

Basal ganglia D/o

122
Q

A gait that is wide based, with truncal instability w/ erect posture, and

A

Irregular lurching steps in which speed and stride vary
Results in lateral veering and if severe, falling.

Cerebellar ataxia gait!

Assoc. with Cerebellar disease.If there is disease of the cerebellar hemispheres, limb ataxia and nystagmus is often present

123
Q

A pt that resembles a cerebellar gait, board stanced with difficulty changing positions yet can maintain balance with eyes open, but falls in the Romberg test has what gait

A

Sensory Ataxia

124
Q

A pt with asymmetric nystagmus, normal proprioception, and normal strength, and tend to fall to one side.. has what type of ataxia

A

Vestibular

125
Q

Describe a stasis-abasia

A

A psychogenic gait disorder

Physical Exam shows normal coordination of leg movement while lying or sitting

Yet patient is unable to stand or walk without assistance

But if distracted they can maintain balance and may be able to take several steps

But this is usually followed by a dramatic demonstration of imbalance with lunge toward support

126
Q

What are the 4 characterizations of MS

A

Inflammation
Demyelination
Gliosis formation
Neuronal loss

127
Q

What is the age of onset fo MS

A

20- 40 years old typically women of European lineage

128
Q

What are the 4 major RSK fxs for MS

A

genetic predisposition

Vitamin D deficiency

Epstein-Barr virus (EBV) exposure after early childhood

Cigarette smoking

129
Q

20-40 year old woman that presents with sensory loss, optic neuritis, and weakness think

A

MS

130
Q

What is Inter nuclear opthalmoplegia

A

Impaired adduction of eye 2ndary to lesion in ipsilateral medial longitudinal fasciculus often seen in MS pts

131
Q

What Nerve palsy is common in MS

A

CN 6 palsy

132
Q

How can you tell the difference between MS and Bell’s palsy

A

Unlike Bell’s palsy, MS not associated w/ ipsilaeral loss of taste or retroauricular pain

133
Q

What are the 3 clinical types of MS

A

Relapsing-Remitting Dz
-Most common (90% of cases)

Secondary progressive Dz
-Always begins as RMS then has steady deterioration

Primary Progressive Dz
-Steady progression from onset

134
Q

What is the D criteria for MS

A

Requires evidence that at least two different regions of central white matter are affected at different times.

Bright lesions in the white matter of the cerebral hemispheres, brain stem, and spinal cord

Contrast (ie gadolinium) enhances the lesions

135
Q

What is the hallmark of Dx for MS

A

Two or more episodes of symptoms and Two or more signs (weakness, fatigue, sensory loss, motor loss, blindness)

Symptoms longer than 24hrs

Involvement of anatomically white matter tracts of the CNS.

Distinct episodes separated by a month or more.

136
Q

How will CSF present with MS

A

oligoclonal banding in the cerebrospinal fluid.

137
Q

What is the Tx approach for acute flare ups of MS

A

Managed with glucocorticoids

  • Methyprednisolone 1g daily IV for 3 days
  • Then oral prednisone 60-80mg/day x 1 wk then tapered
138
Q

What is the Tx approach for long tern immuno modulation for RMS

A

Beta-interferon ie Avonex 30mcg IM q week

Glatiramer acetate 20mg SQ daily

139
Q

What is the DOC from Primary progressive MS

A

Ocrelizumab

140
Q

What are three things that can lead to thinking MS will have a favorable prognosis

A

Optic neuritis or sensory symptoms at onset

<2 relapses in first year

Minimal impairment after 5 years

141
Q

What is the RSK of developing MS if the MRI shows three or more typical T2 weight lesions

A

80 percent at 20 years

142
Q

A pt presents with MS symptoms ( optic neuritis) and behavioral changes and cognitive abnormalities thing..

A

ADEM

Acute Disseminated Encephalomyelitis

143
Q

What is the hallmark of ADEM

A

Hallmark is the presence of widely scattered small foci of perivenular inflammation and demyelination as compared to MS which has large confluent demyelinating lesions.

144
Q

How does the CSF of ADEM present

A

Lymphocytic pleocytosis
Elevated protein
Oligoclonal bands are rarely seen (unlike MS)

145
Q

What is the Tx approach to ADEM

A

Recovery is typically complete

IV corticosteroids often shorten the course and lessens the
severity

146
Q

What is the most common progressive motor neuron Dz

A

ALS

147
Q

What are the S/s of ALS

A

Sx:
Example: LMN – asymmetric weakness

W/ sensory, bowel/bladder, cognition
intact

Dx:
Simultaneous UMN & LMN involvement
w/ progressive weakness

148
Q

What is the Tx approach to MS

A

No Cure

Riluzole, 50mg bid po
-Increased short-term survival

Edaravone 60mg IV
-Slows dz progression in pts w/ mild dz

symptomatic Tx

149
Q

How is polio spread

A

Fecal oral

Enterovirus

150
Q

What part of the spine does polio effect

A

Anterior horn cells

151
Q

How is polio Dx

A

Stool or NP secretions

152
Q

Lesions at T6 result in loss of what reflexes

A

Abdominal reflexes

153
Q

What type of dysfunction results from lesions above the sacral level

A

Bowel and bladder dysfunction

154
Q

Lesions at the right dorsal column at L1 produce what impairment

A

Ipsilateral loss of vibration/position sense generalized below the lesion level

155
Q

What is a common cause of dorsal column lesions at L1

A

Common causes include MS, penetrating injuries, and compression from tumors.

156
Q

Lesion of the right fasciculus cuneatus at C3 produces what impairment?

A

Ipsilateral loss of vibration and position in the right arm and upper trunk.

157
Q

What are common causes of Right fasciculus cuneatus lesions at C3

A

Common causes include MS, penetrating injuries, and compression from tumors.

158
Q

Lesion of the right lateral corticospinal tract at L1 produces what impairment?

A 
Ipsilateral upper motor neurons signs generalized below the lesion level
-UMN signs
	Weakness (Spastic paralysis)
	hyper reflexia 
 (+ Babinski, clonus)
	Hypertonia
159
Q

What are common causes of lateral corticospinal tract lesions

A

Common causes include penetrating injuries, lateral compression from tumors, and MS.

160
Q

lesions of the elateral spinothalamic tract produces what impairment

A

Contralateral loss of pain and temperature sense

161
Q

What are common causes of lateral spinothalamic tract lesions

A

Common causes include MS, penetrating injuries, and compression from tumors.

162
Q

Lesion of the anterior gray and white commissures (Central Cord Syndrome) at C5-C6 produces what impairment?

A

Blanket or cape dermatomes pattern

Impaired pain and temperature
sensation, C5-C6 dermatomes,
bilaterally

163
Q

What is a common cause of central cord lesions

A

Common causes include posttraumatic contusion, syringomyelia, and intrinsic spinal cord tumors.

164
Q

Complete transection of the spinal cord (Transverse Cord Lesion) at L1 would produce what impairments?

A

Bilateral loss of vibration and position sense
( dorsal column lesion)

Bilateral UMN signs
(Lateral corticospinal tracts lesion)

Bilateral Loss of pain and temp sense
(Lateral spinothalamic tract)

165
Q

Complete transection of the dorsal columns, bilaterally, (Posterior Cord Syndrome) in the cervical region would produce what impairments?

A

Bilateral loss vibration and position sense, generalized below lesion level

166
Q

Complete transection of the lateral corticospinal and lateral spinothalamic tracts with sparing of the dorsal columns, bilaterally, (Anterior Cord Syndrome) in the cervical region would produce what impairments?

A

ipsilateral UMN signs
( lateral corticospinal tract lesion)

And Contralateral loss of pain and temp sense
( lateral spinothalamic tract lesion)

167
Q

What are the two types of cord compression tumors

A

Intramedullary – 10%, Ependymomas most common type, Gliomas make up the rest

Extramedullary – 90%, most commonly related to Neurofibromas and Meningiomas.

168
Q

What is the most common Extrapyramydal type of cord tumors

A

Extrapyramidal

-neurofibromas and mengiofibromas

169
Q

How will the CSF present with spinal tumors

A

Xanthochromatic

Greatly elevated protein

Normal or elevated WBC

Normal or depressed glucose elevation

Quenckenstedt Test may reveal a partial or complete block

170
Q

Where are the most common locations for disc prolapse

A

L4-5 and L5-S1

171
Q

A pt presents with specific radicular pain, abnormal posture, and Limited ROM.. suspect

A

Disc prolapse

Loss of DTRE is more suggestive of a root lesion

172
Q

What are the 4 criteria for referral to spine ortho or MRI in Disc prolapse

A

Progressive motor weakness from nerve root injury

Bowel/bladder disturbance or other sign of cord compression (cauda equina)

Incapacitating pain for at least 4 weeks

Recurrent incapacitating pain despite conservative treatment

173
Q

How does Neurogenic Shock present

A

Loss of sympathetic tone
Reduced systemic vascular resistance
Hypotension
No Tachycardia!

174
Q

A lesion at the optic chains presents with what blindness

A

Loss of lateral visual fields

175
Q

Describe the pupillary pathway

A

Light impulse travels up optic nerve, divides at the chiasm, arrives at pretectal nucleus. (Afferent)

Efferent signals sent via CN III to cause direct and consensual constriction

176
Q

Temporary decrease of blow flow to the retina presents as

A

Transient monocular blindness
(Vision loss in one eye, CNII deficit)
Aka: Amaurosis Fugax

177
Q

What is most common cause of Inflamation to the optic nerve

A

MS

178
Q

A pt with subacute unilateral vision loss, that develops over a few days and has low serum vitamin D,… think

A

Optic neuritis associated with MS

179
Q

Pallor of the optic disk is a sign of

A

Late finding in optic neuritis from MS

180
Q

What is the Tx approach to Optic neuritis

A

IV methylprednisolone 1 g daily for 3 days followed by a tapering course of po prednisolone

181
Q

What is the prognosis of Optic neuritis

A

Associated with a 50 percent progression of MS

( optic neuritis and pain with EOM is an early sign of MS)

182
Q

What is giant cell arthritis/ temporal arteritis

A

Inflammation of the external carotid artery at the superficial temporal artery that may lead to blindness

183
Q

A pt with Jaw Claudication, headache, scalp/ temporal tenderness, Visual S/s and throat pain… think

A

Giant cell arteritis

184
Q

What is the Tx approach to Giant Cell Arteritis

A

Prednisone 60 mg PO daily

185
Q

In order to start Tx for Giant cell arteritis what must be done (according to current)

A

Artery Bx

However the teacher says just start on prednisone

186
Q

Marcus Gunn/ swinging light test assess for

A

associated with disease of retina or optic nerve

Sensory system deficit

187
Q

What is papilledema a sign of

A

ICP ( search for the cause)

188
Q

What is the cardinal S/s of papiledema

A

HA esp. when recumbent

189
Q

What CN palsy is apparent in papilledema

A

CN VI palsy

190
Q

A pt with a “down and out” fixed gaze, +diplopia, + ptosis .. think

A

CN III palsy

191
Q

New onset CN III palsy with pupillary involved.. order

A

MRI/ MRA r/o cerebral artery aneurysm

192
Q

Interruption of the cervical sympathetic nerves to the eyes leads to…

A

Ptosis, miosis, and anhidrosis

Horner syndrome

193
Q

What should be r/o in Horner syndrome

A

Lung tumor or Carotid Artery Aneurysm

194
Q

A pt with ptosis of the eyelid on the side of the small pupil =>

A

Horners syndrome

195
Q

A pt with ptosis of the eyelid on the side of the large pupil =>

A

the patient has a partial third nerve lesion on that side

CN III palsy

196
Q

Argyll Robertsons pupil aka prostitutes pupil presents

A

Pupil does accommodate to near vision

Pupil does not react to light, either directly or consensually

Associated with CNS syphilis and other conditions

197
Q

A tonic pupil with parasympathetic denervation that constricts poorly to light but reacts better to accommodation

A

Adies pupil

Benign

198
Q

How does CN IV palsy present

A

Up and In deviation of the eye

199
Q

What is the most common cause of CN IV palsy

A

Head trauma

200
Q

What should be evaluated If a pt has CN VI palsy what should be evaluated

A

MRI! ICP UPO

201
Q

A pt with an adducted eye at rest that can not abduct the eye has what CN palsy

A

VI

202
Q

CN V present how

A

AKA Tic douloureux

Lancinating pain in distribution of one or more branches of CN V – lower 2/3 of face.

203
Q

10/10 pain along the lower 2/3rd of the face is a sign of

A

CN V palsy

204
Q

What is the Tx approach to Trigenminal neuralgia ( CN V)

A

Spontaneous recovery

Treatment options include
-Carbamazepine
Can cause agranulocytosis
Monitor w/ CBC and LFTs

-Oxcarbazepine
Less bone marrow toxicity than carbamazepine

205
Q

CN VII is called what

A

Bell’s palsy, LMN problem

206
Q

What is the most common form of facial paralysis

A

Bell’s palsy ( CNVII)

207
Q

Pain behind ear followed by facial paralysis with an assoc loss of taste is what

A

Bells Palsy ( CN VII LMN)

208
Q

A pt with Bell’s palsy, yet the forehead lesions are intact think..

A

Central lesion

209
Q

What is the Tx approach to Bell’s palsy

A

Prednisone 60 mg x 5 days, then tapered 5 days

210
Q

Herpes Zoster along CN VII is called what

A

Ramsay Hunt Syndrome

Presents with Facial weakness
( like Bell’s palsy)

Vesicular rash, vesicles on the tympanic membrane

Assoc with decrease hearing

211
Q

What is the Tx approach to Ramsay Hunt Syndrome

A

Acyclovir and Famiciclovir with steroids

212
Q

A Weber test that laterlized to one side and the BC is greater than AC conduction on the same side is what kind of hearing loss

A

Conductive

213
Q

A Weber test that lateralizase away from the lesion and the AC > BC on the side of the lesion is what kind of hearing loss

A

Sensorineural hearing loss

214
Q

What is the most common cause of CN VIII dysfunction from a tumor

A

A Schwannoma or meningioma

215
Q

A d/o in the gene tranrythrein is what d/o

A

Familial amyloid

IPAP JUNIOR SEM. (43 decks)

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