Movement Disorders Flashcards
1
Q
What are the four cardinal manifestations of Parkinson’s disease?
A
Tremor, bradykinesia, rigidity, postural instability (gait disturbance)
2
Q
Most common presenting symptom of PD
A
Tremor (pill rolling, resting tremor)
3
Q
A pt complains of weakness, tiredness, and decreased manual dexterity of the fingers. What do we call this?
A
Bradykinesia
4
Q
Ratchety pattern of resistance and relaxation as the examiner moves the limb through ROM
A
Cogwheel rigidity
5
Q
What causes cogwheel rigidity?
A
In PD, from tremor superimposed on increased tone
6
Q
Feeling of imbalance and tendency to fall
A
postural instability
7
Q
Least responsive symptom of PD to dopaminergic therapies
A
Postural instability
8
Q
difficulty initiating gait
A
freezing
9
Q
short stepped gait
A
festination
10
Q
A neurotransmitter that is responsible for motor control, motivation, and arousal
A
Dopamine
11
Q
Enzymes that break down dopamine in the synapse
A
MAO and COMT
12
Q
Where are dopamine neurons found?
A
Substantia nigra
Part of the basal ganglia
Part of the midbrain
13
Q
The loss of dopamine _____ (increases, decreases) the excitatory drive in BG and disrupts voluntary motor control causing PD symptoms
A
increases
14
Q
Abnormal proteins that develop inside the neurons of those with PD
A
Lewey Bodies
15
Q
Characterized by visual hallucinations, fluctuating cognition, and parkinsonism
A
Dementia with Lewey Bodies
16
Q
How do you distinguish corticobasal degeneration from PD?
A
Corticobasal degeneration:
- Does not have tremor
- Does not respond to levodopa
17
Q
Presents with parkinsonism, dysautonomia, cerebellar involvement, and pyramidal signs.
No tremor, doesn’t respond to levodopa
A
Multiple System Atrophy
18
Q
What meds are more likely to cause secondary parkinsonism?
A
Antipsychotics
Reglan
19
Q
Most common form of secondary parkinsonism?
A
Drug-induced
20
Q
What drugs cause tardive dyskinesia?
A
Antipsychotic drugs and metoclopramide (reglan)
21
Q
What else can cause secondary parkinsonism besides meds?
A
Toxins Brain lesions Trauma Metabolic disorders Infections Cerebrovascular disease
22
Q
How is PD diagnosed?
A
Gold standard is neuropathologic examination
No physiologic or blood tests exists
23
Q
Most effective drug for symptomatic treatment of PD
A
Levodopa
24
Q
What does the addition of carbidopa prevent when given in combination with levodopa?
A
N/V, orthostatic hypotension
25
What is Sinemet primarily effective for?
Bradykinesia
26
SE of Sinemet
Motor Complications (Dyskinesia, dystonia, freezing episodes)
dry mouth
mood changes
hallucination
27
Sinemet is C/I in who?
narrow angle glaucoma
| Use of MAOIs within the last 2 weeks
28
Sinemet patient education
Take 30 minutes before meals
Don't withdrawal rapidly--risk of neuroleptic malignant syndrome
Don't take if you've taken MAOIs in the last 2 weeks
29
A pt presents with MS change, rigidity, fever, and dysautonomia. What are you worried about?
Neuroleptic malignant syndrome
30
What is the advantage of dopamine agonists over levodopa?
Longer duration of action
| less motor fluctuations
31
SE of dopamine agonists
Impulse control disorder, peripheral edema
| Can be avoided by initiating treatment in small doses
32
C/I of dopamine agonists
Breastfeeding
33
What are the dopamine agonists?
Ropinirole (Requip)
Pramipexole (Mirapex)
Bromocriptine (Cycloset)
34
A patient on dopamine agonists presents to you with anxiety, sweating, nausea, pain, and dizziness. What do you ask them?
Did you stop taking your DAs suddenly?
35
A 70 year old pt is put on a Sinemet for her PD. She shows no improvement. You decide to put her on a DA next. Is this okay?
No
| DAs are ineffective in pts who have shown no response to levodopa
36
May be useful in pts with early PD
| May be neuroprodective
MAOI
Rasagiline (Azilet)
Selegiline (Eldepryl)
37
-giline
MAOI
38
Patient education with rasagiline (Azilect)
C/I in liver disease
| Avoid tyramine containing foods --> high BP
39
Patient education wiht selegiline (Eldepryl)
Can cause insomnia and confusion
| Avoid with TCA or SSRIs
40
Antiviral that may reduce intensity of levodopa-induced dyskinesia and motor fluctuations
Amantadine (Symmetrel)
41
SE of Amantadine
Ankle edema, livedo reticularis, confusion, hallucinations
42
COMT inhibitor
Entacapone (Comtan)
43
Mostly used as an add on to treat patients iwth motor fluctuations who experience end of dose "wearing off"
Entacapone (Comtan)
44
Patient education for Comtan
Ineffective when given alone
Just a levodopa extender.
May cause dyskinesia
45
Non-Pharmocologic Tx for PD
Educations, therapy, nutrition, emotional support
46
Most frequently performed surgical procedure for the treatment of advanced PD
Deep brain stimulation
47
How long is DBS effective after treatment?
3-5 years after electrode implantation
48
How does DBS work?
It blocks the abnormal nerve signals that cuase tremor and PD symptoms
49
Seldom performed procedures except in regions where DBS is unavailable or not affordable. Uses liquid nitrogen to kill nbrain tissue
Thalamotomy and Pallidatomy
50
Place dopamine producing cells in or near sites in the brain where dopamine production is lacking
Neural transplantation
51
Alternating contractions of agonist and antagonist muscles in an oscillating, RHYTHMIC manner.
Tremor
52
Type of tremor in PD
Resting tremor
53
Type of tremor in essential tremor
Postural (ask pt to hold arms out forward, hands shake)
54
Type of cerebellar tremor
Intentional or kinetic tremor (touch finger to nose)
55
Most common movement disorder
Essential tremor
56
High frequency tremor that predominantly affects the upper extremities. Manifests as postural or kinetic tremor.
Essential tremor
57
Essential tremor is typically (bilateral/unilateral) and (symmetric, assymetric)
bilateral and symmetric
58
Essential tremor most often involves what?
the head
59
Tremor that is characteristically improved with alcohol and worse with stress
Essential tremor
60
What is a difference between essential tremor and PD?
ET does not have cogwheel rigidity
61
Treatment of mild cases of ET
reassurance
62
Treatment of severe cases of ET that interfere with eating, writing, ADLs
beta blockers (propanolol) or mysoline (primidone)
63
Vertigo, rash, agranulocytosis, and loss of appetite are side effects of what drug?
Mysoline (Primidone)
64
What drug metabolizes to phenobarbital and raises the seizure threshold?
Mysoline (Primidone)
65
What treatment might be helpful for limb or voice tremor?
Botox
66
Which antiseizure meds may help with tremor?
Topiramate (Topamax) and Gabapentin (neurontin)
67
Sustained or repetitive involuntary muscle contractions frequently associated with twisting or repetitive movements and abnormal posture
Dystonia
68
How is dystonia classified?
Age of onset (childhood, vs adult)
Distribution (focal, multifocal, segmental, general)
Etiology (primary or secondary)
69
Most common forms of dystonia
Facial dystonia.
| Blepharospasm and Oromandibular dystonia
70
Involuntary dystonic contractions of eyelids; blinking that can interfere with daily activities
blepharospasm
71
Dystonic contractions of muscles of the lower face, lips, tongue, and jaw
Oromandibular dystonia
72
Dystonic contractions of the vocal cords causing impaired speech (strained or whispering quality of speech)
Spasmodic dystonia
73
Dystonic contractions of the neck muscles causing head to deviate to one side, forward, or backward
Cervical dystonia
74
Writer's cramp and musician's cramp are examples of this
Limb dystonia
75
Likely a source for some dystonias
Basal ganglia
76
Dopaminergic therapy can (induce, treat) dystonia
both!
77
Treatment of dystonia
Mostly symptomatic
Baclofen
Botox
78
First line treatment for cervical dystonia
Botox
79
What are the three characteristics of Hungtington's disease?
Choreiform movements
Psychiatric problems
Dementia (can't make decisions and multi-task)
80
Rapid, jerky, nonrepetitive or ARRHTYMIC movements involving hte face, trunk, and limbs
Choreiform movements
81
What might you see regarding the eye exam in a HD pt?
Delay in initiation of saccadic eye movements (pt can't follow your finger right and left)
82
Average age of death of HD
60
83
Common symptom of HD that's not in the main 3
Weight loss/cachexia
84
What 3 categories are HD symptoms put in?
Neurologic (movements, reflexes, gait)
Psychiatric (mood, delusions)
Cognitive (thought, concentration, memory)
85
Pathophys of HD
trinucleotide expansion of HTT gene which makes hte huntington protein toxic. Repeat numbers of the expanison >38 is diagnostic for HD
86
Treatment of HD
No known cure
Symptomatic management. PT, OT, ST
(manage chorea, psychosis, and depression)
87
FDA approved treatment for chorea in HD
Tetrabenazine (Xenozine)
| Reduces dopamine transmission
88
Used in HD patient wiht psychosis and chorea
Neuroleptics (Olanzapine, Risperidone, Quitiapine, Arpiprazole, Haldol)
89
Last resort option for chorea in HD
Amantadine
| RIluzole
90
Characterized by multiple motor tics that are often accompanied by vocalizations (phonic tics)
Tourette's
91
Brief, rapid, recurrent and seemingly purposeless stereotyped motor contraction
Tic
92
Blinking, jerking of the neck
Simple motor tic
93
Jumping, sniffing, head banging
Complex motor tic
94
Grunting
Simple vocal tic
95
Repeating other people's words
Echolalia
96
Repeating one's own words
Palilalia
97
Expression of obscene words
Coprolalia
98
Unpleasant focal sensations in the face, head, or neck
Sensory tics
99
What age do tics occur? When do they stop?
between 2 and 15
| stop in adulthood
100
Associated problems with Tourettes
Anxiety, depression, ADHD, OCD, personality disorders, self destructive behaviors
101
Pathophysiology of Tourettes
complex inheritance pattern
102
Treatment of mild tourettes
education and counseling
103
Treatment of tourettes with tics that are disabling/interfering with quality of life
```
Clonidine
Guanfacine
Neuroleptics
Antipsychotics (if neuroleptics don't work)
Botox
(Giggles needs a bigger couch)
```
104
Develops months to years after initiating neuroleptic treatment. Characterized by choreiform movements involving the mouth, lips, and tongue
Tardive dyskinesia
105
Treatment of tardive dyskinesia
Stop the med. 1/3 have remission within 3 months, most improve over years
106
Primary RLS vs Secondary RLS
Primary: genetic, idiopathic, onset at 27
Secondary: associated with pregnancy, anemia, renal failure, peripheral neuropathy
107
What should you always check in someone with suspected restless leg syndrome?
Iron level
108
How will the neuro exam be in someone with restless leg syndrome?
normal
109
Four core symptoms for diagnosis of RLS
1. Urge to move legs
2. Sx begin/worsen with rest
3. Relief with movement
4. Worse during evening
110
Treatment of RLS
Pramipexole (Mirapex) or Ropinirole (Requip)
| ^^Dopamine agonists
111
Non-pharmacologic treatment of RLS
Mental alerting activities
Regular exercise
Leg massage
Heat
112
Gnenetic abnormality inherited in an autosomal recessive manner that leads to impairment of cellular copper transport
Wilson's disease
113
Categories of clinical manifestations of Wilson's disease
Psychiatric
Hepatic
Neurologic
114
Pathophysiology of Wilson's disease
Decreased level of ceruloplasmin (copper carrying protein in the blood)
115
Where does copper accumulate in WIlson's dz?
Liver, brain, and cornea
116
What PE findings would you expect in someone with Wilson's disease?
```
Kayser-Fleischer rings (copper can be seen in eyes)
abdominal pain
Jaundice
Hepatomegaly and splenomegaly
Ascites
Upper GI bleeding
MS changes
```
117
Brownish or gray-green rings that are due to fine pigmented granular deposits of copper in teh cornea.
Kayser-Fleischer rings
