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Neurology Module > Motor Disorders - Motor Neuron > Flashcards

Motor Disorders - Motor Neuron Flashcards

1
Q

Movement Disorders

A

Parkinson’s
Benign Essential Tremor
Huntington’s chorea
Restless Leg Syndrome

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2
Q

Drugs that can cause Parkinsonism

A 
ANTIPSYCHOTICS - Haldol
METOCLOPRAMIDE
Amiodarone
Alcohol
Methylphenidate
Lipitor
Carbamazepine
Stimulatants
Corticosteroids
Cocaine
Albuterol
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3
Q

Pathophysiology of Parkinsons

A

Degeneration of the dopaminergic neurons in the substantia nigra

Substantia nigra is located in the midbrain; part of the basal ganglia

Control/modulation of extrapyramidal systems; motor control

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4
Q

Supstantia nigra is located

A

in the midbrain

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5
Q

Parkinsons typically presents after age

A

50

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6
Q

Incidence of Parkinsons

A

1% >60 yo

4% >80 yo

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7
Q

_% with Parkinsons have some type of family history.

A

25%

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8
Q

Parkinsons Disease

Men vs Women

A

Men > Women

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9
Q

Parkinsons Signs and Symptoms

A

Tremor - Rest
Bradykinesia
Rigidity

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10
Q

Parkinsons Tremor

A 
Rest tremor   (may have action tremor too)
“Pill rolling”
Bilateral or asymmetrical
Starts in fingers, extends to elbows
Also affects head, face, tongue

May be absent in up to 20%

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11
Q

Parkinsons Rigidity

A 
"Cogwheeling”
“Lead Pipe resistance”
Posture- stooped
Decreased arm swing
Masked facies
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12
Q

Smaller handwriting

A

Micrographia

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13
Q

Parkinsons Bradykinesia

A 
Affects speech, swallowing, eating
Smaller handwriting; micrographia
Infrequent blinking
Slow, shuffling gait
Difficulty initiating steps but difficulty stopping- festinating gait
Difficulty arising from a chair
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14
Q

Parkinsons - blinking

A

infrequent

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15
Q

Parkinsons - gait

A

slow and shuffling
festinating
difficulty initiating steps

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16
Q

PE Parksinsons - rigidity

A

Lead Pipe Resistance

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17
Q

Parkinsons Faces

A

Masked

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18
Q

Parkinsons Later Symptoms

A 
Cognitive impairment/dementia (60% by 12 y)
Depression
Fatigue (1/3)
Orthostatic hypotension
Decreased olfaction
Dysautonomia
Dysphagia
Drooling
Urinary urgency
Constipation
Sleep disturbance
Daytime somnolence
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19
Q

Parkinsons movement

A

Slow - Bradykinesia

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20
Q

Parkinsons - problems with swallowing

A

Slow! May become an aspiration risk.

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21
Q

Difficult to stop walking

A

festinating gait

Seen in Parkinsons

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22
Q

Parkinsons turning

A

End Block Turns

Can’t pivot

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23
Q

Parkinsons Differential Diagnosis

A 
Dementia with Lewy Body (visual hallucinations)
Vascular Parkinsonism
NPH
Benign essential tremor
Progressive supranuclear palsy
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24
Q

Parkinsons Primary Treatment

A

Sinemet - Levodopa/Carbidopa

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25
Q

Parkinsons Imaging

A

Spect Imaging

can see degeneration

Not routinely done.

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26
Q

Sinemet

A

Sinemet
25/100 mg TID
may increase by one pill every 2 days;
Max - 3 pills TID

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27
Q

Side Effects of Sinemet

A

dyskinesias/choreiform movements

+/- hallucinations

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28
Q

Long term Sinemet therapy issues

A

After 5-10 years: wearing off, “on/off” issues

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29
Q

Parkinsons Adjunctive Treatment

A 
Amantadine (Symmetrel)
Dopamine Agonists
COMT Inhibitors
MAO-B Inhibitors
Anticholinergics
Surgery - deep brain stimulation
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30
Q

What is Amantadine (Symmetrel) used for?

A

Mild symptoms, may help with dyskinesias associated with Levodopa

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31
Q

Dopamine Agonists

A

Pramipexole (Mirapex)
Ropinirole (Requip)
Apomorphine (Apokyn)

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32
Q

COMT Inhibitors

A

Entacapone (Comtan) (decreases metabolism of levodopa and extends half-life)

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33
Q

MAO-B Inhibitors

A

Selegiline (Eldepryl)

Rasagiline (Azilect)

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34
Q

Anticholinergics

A

may alleviate tremor/rigidity but not bradykinesia

Trihexyphenidyl (Artane)
Benztropine mesylate (Cogentin)
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35
Q

Parkinsons Disease

What other things may you have to treat?

A

Constipation- Miralax
Depression
Fatigue- methylphenidate (Ritalin)
Daytime somnolence- modafinil (Provigil)

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36
Q

Parkinsons constipation treatment

A

Miralax

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37
Q

Parkinsons fatigue treatment

A

methylphenidate - Ritalin

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38
Q

Parkinsons daytime somnolence treatment

A

modafinil - Provigil

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39
Q

Onset of benign essential tremor

A

20-60 yo

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40
Q

Benign Essential Tremor is _______ inheritance

A

autosomal dominant

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41
Q

Benign essential tremor is a ________ tremor.

A

Action

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42
Q

Benign essential tremor affects what?

A

Hands (wrists)
Head (flex/extension- “yes” or lateral “no”)

+/- voice, LEs

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43
Q

Where does benign essential tremor increase in amplitude?

A

at end point

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44
Q

BET exacerbating factors

A

Stress/fatigue

Stimulants

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45
Q

BET alleviating factors

A

Alcohol

Rest

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46
Q

Benign Essential Tremor Treatment

A

Beta-blockers (Propranalol - nonselective; Atenalol, Metoprolol)

Anticonvulsant - Primidone (Mysoline)

Other: topirimate, gabapentin, botulinum toxin

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47
Q

BET and occupation

A

Up to 25% need to change careers or retire early due to tremor

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48
Q

Huntington’s Chorea onset

A

Mid-life

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49
Q

Huntington’s Chorea inheritance

A

autosomal dominant

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50
Q

Huntington’s Chorea onset

A

Gradual

Failing memory, restlessness, lack of initiative

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51
Q

Huntington’s Chorea classic symptoms

A

Choreiform movements

mental decline/dementia

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52
Q

Huntington’s Chorea duration

A

20 years

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53
Q

4th leading cause of insomnia

A

restless leg syndrome

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54
Q

Family history of RLS

A

50-60%

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55
Q

Women vs Men RLS

A

Women > Men

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56
Q

RLS ages

A

18 or younger to >65

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57
Q

Uncomfortable sensation in the legs that can range from mild to severe

A

Restless Leg Syndrome

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58
Q

Restless Leg Syndrome is described as

A

Creeping, crawling
Tingling
Pulling or drawing sensation

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59
Q

What temporarily relieves RLS?

A

movement

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60
Q

What worsens RLS?

A

Prolonged sitting/laying down

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61
Q

RLS and sleep

A

Movements continue early in sleep phase.

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62
Q

RLS Pathophysiology

A

Decreased dopamine brainstem
Decreased endogenous opiates
Small fiber neuropathy

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63
Q

RLS Contributing Factors/Causes

A 
Idiopathic
Iron deficiency anemia
Pregnancy
Hypothyroidism
DM
Medications:  SSRIs, others
Caffeine
smoking
64
Q

RLS Treatment

A

Pramipexole (Mirapex)
Ropinirole (Requip)
+/- Sinemet, gabapentin, others

65
Q

Polyneuropathy DDx

A 
Diabetes
Alcoholism induced
HIV/AIDs
Malignancies
Toxins
Metals - arsenics, lead
Medications
Vitamin Deficiencies
Protenemia
Infections
Sarcoid
66
Q

Degenerative Motor Neuron Diseases

A 
Progressive Bulbar Palsy
Pseudobulbar palsy
Progressive Spinal Muscular Atrophy
Primary Lateral Sclerosis
Amyotrophic Lateral Sclerosis
67
Q

Voluntary Movement of the Limbs

A

One of the largest descending tracts. Arises in the motor cortex. The majority (90%) of fibers cross over at the pyramids and descend to the lower spinal levels. The function is voluntary movements of the limbs.

68
Q

Cortex to brainstem/spinal cord

Cortex to spinal cord

A

Upper Neurons

69
Q

Spinal motor neurons

Cranial nerve motor neurons

A

Lower Neurons

70
Q

Upper Motor Neuron Injury casues

A 
MS
CVA
TBI
Cerebral palsy
ALS
71
Q

Lower Motor Neuron Injury causes

A

Progressive Bulbar Palsy
Bell’s Palsy
ALS

72
Q

Characteristics of upper motor neuron diseases

A 
Muscle weakness
Decreased motor control
Spasticity
Hyperreflexia
Babinksi’s (upgoing plantar)
73
Q

Characteristics of lower motor neuron diseases

A

Paralysis
Atrophy
Fasciculations
Loss of all reflex

74
Q

Degenerative Motor Neuron Disease

A 
Progressive Bulbar Palsy
Pseudobulbar palsy
Progressive Spinal Muscular Atrophy
Primary Lateral Sclerosis
Amytrophic Lateral Sclerosis
75
Q

Progressive Bulbar Palsy affects

A

lower motor neurons

cranial nerves

76
Q

Progressive Bulbar Palsy affects CN

A 
V
VII
IX
X
XII
77
Q

Effects of progressive bulbar palsy

A

drooling
chewing
dysphagia
dysarthria

78
Q

Progression of progressive bulbar palsy

A

aspiration pneumonia 1-3 years

79
Q

Pseudobulbar Palsy

A

Similar to Progressive Bulbar Palsy

Crying or laughing outbursts.

80
Q

Progressive Spinal Muscular Atrophy affects

A

lower motor neurons - spinal level

81
Q

Primary Lateral Sclerosis affects

A

Upper motor neurons only

82
Q

Amytrophic Lateral Sclerosis affects

A

Upper and motor neurons

83
Q

Amytrophic Lateral Sclerosis etiology

A

Idiopathic

+/- inheritance?

84
Q

“Lou Gehrigs Disease”

A

Amyotrophic Lateral Sclerosis

85
Q

ALS presentation - age

A

30-60

86
Q

S/S ALS

A

Muscle aches/cramps

Weakness- distal upper limbs and progresses inferiorly

Dysarthria, dysphagia, spasticity, hyperreflexia, muscle fasiculations

87
Q

Diagnosis of ALS

A

EMG

88
Q

Treatment of ALS

A

No Treatment

Riluzole 50mg BID (extends life 3m) $$$$$
10% alive at 1-3 years

89
Q

Who does Multiple Sclerosis affect?

A

White>Black
Female>Male
Higher socioeconomic classes
Northern latitudes

90
Q

MS age of onset

A

15-60

91
Q

MS pathophysiology

A

Demyelination of white matter
Autoimmune
Repeated inflammation causes formation of plaques

92
Q

MS Causes

A

Environmental/toxin exposures?
Familial patterns?
HLA?
Vitamin D deficiency?

93
Q

MS Types

A

Relapsing remitting

Secondary progressive (will occur in 65% of patients with relapsing remitting)

Primary progressive

Progressive relapsing

94
Q

MS Facts

A

Remission after first episode (90%)

Progressive course after onset (10%)

Benign course: 1-2 relapses then recovery (20%)

Progressive course after 5 years (60-90%)

Rapidly progressive course after onset (rare- Marburg)

95
Q

Optic Neuritis presents

A

Usually unilateral

Acuity 20/100 (rather than total blindness)

Onset: hours – days

+/- pain

96
Q

Optic Neuritis Exam

A

Optic nerve pallor
+/- pain with EOM
NORMAL PUPILLARY REFLEX

97
Q

What are patients with optic neuritis at higher risk for?

A

Patients with optic neuritis have a 50% chance of developing MS within 15 years

98
Q

MS Presentation

A

Sensory loss (37%)

Optic neuritis (36%)

Weakness (35%)

Paresthesias (24%)

Other:
Ataxia, diplopia, Lhermitte sign (electrical shock sensation down spine when head is flexed), telegraphic speech, dementia, facial palsies, impotence

99
Q

MS Exam may show

A

Dysarthria

Decreased pain, vibration, position sense

Ataxia

Horizontal nystagmus

Increased DTRs, spasticity, Babinski (up), ankle clonus

100
Q

MS Diagnosis

A

MRI
Spotty, irregular demyelination
Commonly affected areas: brainstem, cerebellum, corpus callosum, white/grey junctions

101
Q

MS Lumbar Puncture will show

A

Oligoclonal bands >75 – 90% patients

Bands of immunoglobulin

102
Q

MS Serum Tests

A

+/- anti-myelin oligodendrate glycoprotein (ant-MOG)

+/- anti-myelin base protein (anti-MBP)

103
Q

MS Acute Exacerbation Treatment

A

Methylprednisone IV
1000mg daily x 3 days

Then…

After the first three days,
Oral prednisone taper 1 – 3 weeks

104
Q

MS Management to slow progression

A 
First line:
Betaseron SC QOD
Avonex  SC Q week
Rebif  SC 3x weekly
Glatiramer (Copaxone) SC daily

Know treatments are SC so pts will have to give themselves shots.

Second line:
Mitoxantrone (Novantrone) IV Q 3 months

Third Line:
Natalizumab (Antegren, Tysabri) IV once monthly $$$

105
Q

MS Other Management

A 
Spasticity: Baclofen 10 – 40 mg TID
Others:  tizanidine, gabapentin
Pain: Amitriptyline, gabapentin, carbamazepine
Urinary
     -Oxybutynin (Ditropan)
     -Tolterodine (Detrol)
Constipation
Fatigue - Modafinil (Provigil)
Depression - SSRIs
Temperature control - heat makes it worse
Education and support
106
Q

MS Prognosis

A 
Most live 30 years from onset
     -5-10 years less than expected
90 % lose independent walking by 10 yrs
Almost all lose the inability to walk by death
Death is often secondary to sequelae
107
Q

What will an MS MRI show?

A

Spotty, irregular demyelination

Commonly affected areas: brainstem, cerebellum, corpus callosum, white/grey junctions.

108
Q

Cause of Guillain Barre

A

Idiopathic

Inflammatory Neuropathy

109
Q

Progression of Guillain Barre

A

Progressive symmetrical weakness
Maximum weakness within 4 weeks
Mild to severe (respiratory failure)

110
Q

Guillain Barre affects…

A

Males > Females

111
Q

What is affected in Guillain Barre?

A

Sensory and Motor Neurons

112
Q

Guillian Barre Pathophysiology

A

Usually follows an infection/exposure- ‘antigen mimicry

113
Q

Types of Guillain Barre

A

Acute Inflammatory Demyelinating Polyradiculoneuropathy (AIDP) 90%
Acute Motor Axonal Neuropathy (AMAN)- Campylobacter jejuni
Other rare forms

114
Q

Guillain Barre is Associated with which infections?

A 
C jejuni
EBV
Mycoplasma
H influenzae
CMV
VZV
115
Q

Guillain Barre is associated with which vaccinations?

A

H1N1 influenza
+/- tetanus
hepatitis

116
Q

Guillain Barre usually follows

A

acute illness

1-3 weeks

117
Q

Guillain Barre Presentation

A 
Proximal muscle weakness (+/- CNs)
Legs then arms
Myalgias:  shoulder, back, thighs
Paresthesias
Decreased DTRs
118
Q

Guillain Barre Diagnosis

A

CSF – elevated protein (NL WBC)
EMG
+/- PFTs, ABGs (if respiratory sxs)

119
Q

Guillain Barre Treatment

A

Supportive

IVIg or plasmapheresis

120
Q

Guillain Barre Prognosis

A

85% will make full recovery
Long term: foot drop, hand weakness
Relapse: 3-5%

121
Q

CIDP

A

Chronic Idiopathic Demyelinating Polyneuropathy

122
Q

What is CIDP?

A

Chronic form of Guillain Barre.

Symptoms >8 weeks.

123
Q

Diagnosis of CIDP

A

CSF, EMG

Nerve biopsy

124
Q

Treatment of CIDP

A

Corticosteroids or immunosuppressants
Plasmapheresis, IVIg
PT

125
Q

What is Myasthenia Gravis?

A

Neuromuscular autoimmune disease where antibodies form to nicotinic acetylcholine receptors.

126
Q

Symptoms of Myasthenia Gravis

A

Proximaly asymmetric limb weakness (85%)

CN weakness:
Lid lag, ptosis, diplopia
Facial weakness, slurred speech
Easy fatiguability

127
Q

Most common form of Guillain Barre

A

Acute Inflammatory Demyelinating Polyradiculoneuropathy

128
Q

Diagnosis of Myasthenia Gravis

A

Blood
Ach receptor antibodies (will not be present in those with isolated eye symptoms)
Anti-MuSK (present in 30-40% of those with neg Ach rec)

EMG

Edrophonium test (Tensilon)- blocks acetylcholinesterase and improves symptoms

129
Q

What autoimmune diseases is Myasthenia Gravis associated with?

A

Hashimoto’s, Grave’s
DM-1
Lupus
RA

130
Q

Drug Induced Myasthenia caused by

A

Tetracycline
Aminoglycosides
Propanolol
Lithium +++++

131
Q

Autoimmune- voltage gated calcium channels at neuromuscular junction

A

Lambert-Eaton Syndrome

Almost the same presentation of MG but not the same. Do not respond to the Tensilon test.

132
Q

60% of pts with Lambert-Eaton Syndrome also have…

A

underlying SCC of the lung.

133
Q

Causes of Cervical Spondylotic Myelopathy

A

Disc herniation
Nerve roots- upper extremity radiculopathy
Cord- LE , ataxia

134
Q

Tumors that can cause Myelopathies

A

Malignant: sarcoma, multiple myeloma

Mets: 25x more common than a primary
Breast, lung, renal, prostate, lymphoma, thyroid

HIV related myelopathies (varicella zoster, lymphoma, T. gondii, CMV)

135
Q

Patients with malignancies to the spine often complain of

A

Pain awakens at night; worse at night laying flat

136
Q

Myesthenia Gravis is worse when…

A

the patient is tired.

137
Q

A rare thymus tumor that occurs in 15% of patients with MG.

A

Thymoma

CT/MRI the neck

138
Q

MG Treatment

A

Anticholisterase inhibitors - Mestinon

Immunosuppression - Prednisone, azathioprine

+/- plasmapheresis, IVIg

+/- thymectomy (if thymoma present)

139
Q

Complications of Myasthenia Gravis

A

“myasthenia crisis”
Paralysis of the respiratory muscles
Aspiration

140
Q

Persistent pain in dermatomal distribution after zoster infection

A

Postherpetic Neuralgia

141
Q

Pathology of postherpetic neuralgia

A

(?) damage to dorsal root ganlion

142
Q

Prevalence of Postherpetic Neuralgia

A

Age > 80 = 30%
Age 60-65 = 20%
Age < 50 = rare

143
Q

Risk Factors of Postherpetic Neuralgia

A

Age
Female
Severe rash, pain at outbreak
Zoster ophthalmicus

144
Q

Postherpetic Neuralgia Treatment

A 
Lidocaine 5% ointment/patches
Capsaicin crm
TCA:  amitriptyline, nortriptyline
SNRI- Cymbalta, Effexor
Anticonvulsants:  gabapentin, pregablin
Pain Mgmt?-  nerve blocks, TENS units

Course: 30 d – 6 months

145
Q

Complex Regional Pain Syndrome is often linked to

A

a previous injury

Needlestick
Sprain/strain
Immobilization- cast

146
Q

Age where complex regional pain syndrome presents.

A

~40

Seen in kids

147
Q

Regional Pain Syndrome is seen in __________ limbs.

A

One or Multiple

148
Q

Complex Regional Pain Syndrome AKA

A

Reflex Sympathetic Dystrophy

149
Q

Symptoms of Complex Regional Pain Syndrome

A

Nerves/Vascular

Skin color changes
Temperature
Swelling
Tremor/movement disorder
Pain out of proportion to anything seen on exam.
Changes in nail/hair growth

Diagnosis of exlcusion.

150
Q

Two types of Complex Regional Pain Syndrome

A

CRPS1

CRPS2 - nerve

151
Q

Treatment of CRPS

A

Symptomatic

Rehab!!!!!!!!!

152
Q

Narcolepsy

A

Uncommon <0.2%

Secondary: head trauma, encephalitis, tumor

Daytime sleepiness- sleep attacks

Cataplexy: (30%)

Sudden loss of voluntary muscle control usually following an emotional trigger

Hallucinations (upon awakening, falling asleep)

Sleep paralysis

153
Q

Diagnosis of Narcolepsy

A

PSG

REM Cycle dysfunction

154
Q

Treatment of Narcolepsy

A

Stimulants
SSRI
SNRI - cataplexy, hallucinations, paralysis

155
Q

Cause of Narcolepsy

A

Idiopathic

HLA-DR2

Neurology Module (7 decks)

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