Common Movement disorders - Melanie Flashcards

(64 cards)

1
Q

what is Tremor

A

rhythmical, involuntary and oscillatory movement of body part

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2
Q

what is rhythmic

A

regular and repetitive in timing (though the amplitude may vary)

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3
Q

what is Oscillatory

A

moves about an axis

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4
Q

what is involuntary

A

does not go away (or often enhanced) with distraction

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5
Q

what is the physiology of a tremor

A

arise from an overactive or unchecked basal ganglia system i which neurons with spontaneous oscillatory activity override the normal balance of inhibitory vs excitatory transmission

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6
Q

what is the epidemiology of a tremor

A

most common movement disorder
most common action tremor is essential tremor
most common rest tremor is parkinson’s disease

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7
Q

what are the types of tremors

A

essential, physiologic, dystonic, orthostatic, cerebellar, homes, functional, etc

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8
Q

what is an essential tremor

A

generally bilateral, symmetrical postural/kinetic tremor. mostly seen in hands/arms. it is visible and persistent. can spread to head but less common in the legs

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9
Q

what is a physiologic tremor

A

natural tremor that every person has as a result of several factors including cardiac vibrations transmitted throughout the body, stretch reflexes generated from muscle contraction and natural oscillatory action of neuronal bodies in the brain.

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10
Q

what makes physiologic tremors worse?

A

worse with exercise, anxiety, hyperthyroidism, certain medications

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11
Q

what is the typical history presentation for essential tremors

A

slow, progressive nature of the tremor
+ FH
tremor with action/posture but not at rest
should not have other neurologic signs
tremor can be reduced with alcohol consumption

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12
Q

what are exam findings for essential tremors

A

tremor is usually bilateral and absent at rest. will see mild tremor with postural movements or kinetics
typically not seen in legs (should have normal gait, balance, romberg testing, reflexes)

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13
Q

what are diagnostics for essential tremors

A

spiral drawings with both hands - may see unidirectional tremor axis
handwriting is normal or large, no micrographia

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14
Q

what should patients absolutely NOT have with essential tremors

A

bradykinesia or rigidity on exam

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15
Q

what is a differential diagnosis for essential tremors

A

mild bilateral dystonic tremor or cerebellar tremor

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16
Q

what are labs or diagnostics used for tremor

A

no labs absolutely necessary
MRI/CT
EMG

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17
Q

when might patients obtain labs for tremors and what labs

A

might be indicated depending on history
(B12, renal function, LFTs, Hypocalcemia, hypoatremia, hyperthyroidism, hyperparathyroidism, serum ceruloplasmin, toxicity/exposures)

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18
Q

when are MRI/CT indicated for tremor

A

if there is neurological symptoms exist.

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19
Q

when are EMGs indicated for tremor

A

for difficult to differentiate tremor syndromes

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20
Q

what is the mainstay treatment for tremors

A

propranolol or primidone (level A).

Can be used alone or together.

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21
Q

how is propranolol prescribed and for what

A

for essential tremors
starting at 10mg TID

Not used in patients with severe asthma or COPD

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22
Q

what is primidone used for and how much

A

used to treat tremors - anticonvulsant/barbiturates.
needs to be tapered over 7 weeks and cannot stop suddenly.

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23
Q

what are the primary side effects of primidone

A

sedation, dizziness and CNS depression

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24
Q

what are level B treatments for tremors

A

alprazolam, atenolol, gabapentin, sotalol, topiramate

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25
what is Kayser-fleisher rings
iron metabolism disorder
26
what are red flags for tremors
Kayser-Fleisher rings, any significant nystagmus, ataxia, weakness/hemiparesis, difficulties with EOMI, particularly upward gaze, significant dementia/behavioral issues, hepatic dysfunction
27
what are exacerbating factors for tremors
caffeine, beta-agonists, dopaminergic drugs, stimulants, thyrotoxicosis, psych drugs, SSRIs, valproate, amiodarone and toxicities
28
what do you need to look for in a functional tremor
1. sudden onset 2. static course 3. multiple/mixed tremors 4. changing amplitude/frequency 5. entrainment 6. distractibility 7. sudden remission
29
what can functional tremors be concomitant with
depression/anxiety/somatic disorders and responds to psychotherapy and physical therapy
30
what are physiologic tremors
faster, but lower amplitude than essential tremor. Usually not with intention. can be present in voice/hands but not neck. Neck tremor is always pathologic. Can be seen with anxiety.
31
what is parkinsons disease
progressive, degenerative motor and non-motor neurological disease characterized by the loss of dopaminergic neurons in the substantia nigra pars compacta and the presence of Lewy bodies
32
what are the common associated causes of parkinsons
genetics, environmental toxins, free-radical damage, alpha-synuclein aggregation. Links to melanoma and diabetes (military vets with agent orange and/or burn pits)
33
what are the diagnostic criteria for PD
Bradykinesia and either rigidity or a rest tremor and postural instability
34
what is bradykinesia
slowness of movement AND decrement in amplitude and/or speed of repeated movements
35
what is the Hoehn and Yahr scale
severity of PD on a 0-5 scale
36
what are supportive findings of PD
clear, dramatic response to levadopa olfactory loss
37
what are exclusionary findings of PD
cerebellar abnormalities (ataxia, nystagmus, supranuclear gaze palsy, etc) early, severe dementia or behavioral distubances strictly lower limb involvement >3 years normal DaT imaging
38
what are red flags of ruling out PD
severe autonomic failure in first 5 years of diagnosis rapid gait impairment, early bulbar dysfunction (swallowing/speech), bilateral symmetric Parkinsonism, limited disease progression for 5 years
39
what is important to ask about with PD
presenting symptom? when did it start? how long has it occurred? anosmia, constipation, urinary retention, acting out dreams, restless legs, increased saliva, hypophonia, no strong family history, exposure to pesticides, decreased hand dexterity, depression, sweating, seborrheic dermatitis, slowness, rigidity, dystonia
40
what is the exam for PD
observe the patient.... Masked face, slowed movements, resting tremor, mental status, Romberg/tandem walk, test extremities for rigidity, finger taps, hand opening, RAM, heel/toe taps, decreased decrements, decreased amplitude, standing from chair, gait, arm swing, tremors during walking, freezing of gait, festination, pull test
41
what are DaT scans used for
ruling in or ruling out parkinsonian diseases (not just idiopathic Parkinson's disease)
42
how is PD diagnosed
clinical diagnosis no labs or imaging diagnoses PD
43
what are the mainstay treatments for PD
carbidopa/levodopa
44
what is the best treatment to slow the progression of PD
Exercise and Monitoring symptoms
45
what are other treatment options for PD
MAOB inhibitors Amantadine Dopamine Agnoists Anti-cholinergics COMT inhibitors DBS
46
what are the MAOB inhibitors and how to they work
treatment for PD Selegine, Rasagiline increase dopamine by interfering with dopamine re-uptake good for any age, mild symptoms. can dose once/twice daily
47
what is Amantadine used for
treatment of PD acts as dopamine agnoist - antiviral works well for tremors
48
what are the dopamine agonists that are used to treat PD
Pramipexole, Ropinirole
49
what are anti-cholinergics used to treat PD
Trihexyphenidly (Artane), Benztropine - patients <65yo
50
what COMT inhibitors are used to treat PD
entacapone - taken with levodopa to maintain higher serum levels of dopamine
51
what needs to be watched for with any treatments of PD
hallucinations, impulse control problems or obsessive behaviors, motor fluctuations, dyskinesias, withdrawal (mental status change)
52
what are non-motor complications of PD
autonomic dysfunctions (constipation, urinary retention, sexual dysfunction, rhinorrhea, orthostatic hypotension) depression/apathy/anxiety psychosis memory problems sleep/fatigue
53
what are atypical parkinsonisms
MSA, PSP, CBD Vascular parkinsonism Drug induced parkinsonism
54
what is huntingtons disease
progressive, inherited neurodegenerative disease in an autosomal dominant patter (only need gene from one parent) Caused by CAG trinucleotide repeat expansion
55
when is CAG considered abnormal
36-120 repeats
56
what is the epidemiology of Huntingtons disease
can be found in familial clusters. in US 6 per 100,000
57
what is the presentation of Huntingtons disease
movement, psychiatric and behavioral most common movement is chorea can be unaware of their own movements hypotonia, hyperreflexia and dystonia common along with bradykinesia inability to sustain prolonged muscle movements progresses to spasticity, clonus and rigidity
58
what is chorea movements
dancing movement. may look fidgety or restless and can include limbs, trunk and face
59
what is the psychiatric presentation of Huntingtons
can precede motor symptoms year prior to motor involvement depression, irritability, apathy, withdrawn hallucinations and paranoia OCD and psychosis high risk of suicide among patients as well as carriers
60
what is the cognitive presentations of huntingtons
usually present after motor and psychiatric symptoms most common is executive dysfunction - problem with multi--tasking, making decisions. lack insight into their condition and limitations weight loss
61
what is a typical history presentation of hutningtons disease
unless adopted patient will have family member with known Huntingtons or an unknown movement, psychiatric problem family/caregiver history collaboration vital as patients can lack insight may report restlessness, dysarthria, dyphagia short term memory dysfunction
62
what is seen on exam with Huntington's disease
observation of movements eye movements - delay motor impersistence with tongue protrusion tone reflexes gait tics, myoclonus
63
how is huntingtons disease diagnosed
proven family hisotyr and exam genetic testing for CAG repeats
64
what are the treatments for huntingtons diease
symptomatic management hallucinations/psychosis mood/depression spasticity/hyperkinesia dopamine depleting agens for chorea/ballism