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clin med - neuro > Common Movement disorders - Melanie > Flashcards

Common Movement disorders - Melanie Flashcards

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
Q

what is Kayser-fleisher rings

A

iron metabolism disorder

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26
Q

what are red flags for tremors

A

Kayser-Fleisher rings, any significant nystagmus, ataxia, weakness/hemiparesis, difficulties with EOMI, particularly upward gaze, significant dementia/behavioral issues, hepatic dysfunction

27
Q

what are exacerbating factors for tremors

A

caffeine, beta-agonists, dopaminergic drugs, stimulants, thyrotoxicosis, psych drugs, SSRIs, valproate, amiodarone and toxicities

28
Q

what do you need to look for in a functional tremor

A
  1. sudden onset
  2. static course
  3. multiple/mixed tremors
  4. changing amplitude/frequency
  5. entrainment
  6. distractibility
  7. sudden remission
29
Q

what can functional tremors be concomitant with

A

depression/anxiety/somatic disorders and responds to psychotherapy and physical therapy

30
Q

what are physiologic tremors

A

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
Q

what is parkinsons disease

A

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
Q

what are the common associated causes of parkinsons

A

genetics, environmental toxins, free-radical damage, alpha-synuclein aggregation. Links to melanoma and diabetes
(military vets with agent orange and/or burn pits)

33
Q

what are the diagnostic criteria for PD

A

Bradykinesia and either rigidity or a rest tremor
and postural instability

34
Q

what is bradykinesia

A

slowness of movement AND decrement in amplitude and/or speed of repeated movements

35
Q

what is the Hoehn and Yahr scale

A

severity of PD on a 0-5 scale

36
Q

what are supportive findings of PD

A

clear, dramatic response to levadopa
olfactory loss

37
Q

what are exclusionary findings of PD

A

cerebellar abnormalities (ataxia, nystagmus, supranuclear gaze palsy, etc)
early, severe dementia or behavioral distubances
strictly lower limb involvement >3 years
normal DaT imaging

38
Q

what are red flags of ruling out PD

A

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
Q

what is important to ask about with PD

A

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
Q

what is the exam for PD

A

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
Q

what are DaT scans used for

A

ruling in or ruling out parkinsonian diseases (not just idiopathic Parkinson’s disease)

42
Q

how is PD diagnosed

A

clinical diagnosis
no labs or imaging diagnoses PD

43
Q

what are the mainstay treatments for PD

A

carbidopa/levodopa

44
Q

what is the best treatment to slow the progression of PD

A

Exercise and Monitoring symptoms

45
Q

what are other treatment options for PD

A

MAOB inhibitors
Amantadine
Dopamine Agnoists
Anti-cholinergics
COMT inhibitors
DBS

46
Q

what are the MAOB inhibitors and how to they work

A

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
Q

what is Amantadine used for

A

treatment of PD
acts as dopamine agnoist - antiviral
works well for tremors

48
Q

what are the dopamine agonists that are used to treat PD

A

Pramipexole, Ropinirole

49
Q

what are anti-cholinergics used to treat PD

A

Trihexyphenidly (Artane), Benztropine - patients <65yo

50
Q

what COMT inhibitors are used to treat PD

A

entacapone - taken with levodopa to maintain higher serum levels of dopamine

51
Q

what needs to be watched for with any treatments of PD

A

hallucinations, impulse control problems or obsessive behaviors, motor fluctuations, dyskinesias, withdrawal (mental status change)

52
Q

what are non-motor complications of PD

A

autonomic dysfunctions (constipation, urinary retention, sexual dysfunction, rhinorrhea, orthostatic hypotension)
depression/apathy/anxiety
psychosis
memory problems
sleep/fatigue

53
Q

what are atypical parkinsonisms

A

MSA, PSP, CBD
Vascular parkinsonism
Drug induced parkinsonism

54
Q

what is huntingtons disease

A

progressive, inherited neurodegenerative disease in an autosomal dominant patter (only need gene from one parent)

Caused by CAG trinucleotide repeat expansion

55
Q

when is CAG considered abnormal

A

36-120 repeats

56
Q

what is the epidemiology of Huntingtons disease

A

can be found in familial clusters. in US 6 per 100,000

57
Q

what is the presentation of Huntingtons disease

A

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
Q

what is chorea movements

A

dancing movement.

may look fidgety or restless and can include limbs, trunk and face

59
Q

what is the psychiatric presentation of Huntingtons

A

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
Q

what is the cognitive presentations of huntingtons

A

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
Q

what is a typical history presentation of hutningtons disease

A

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
Q

what is seen on exam with Huntington’s disease

A

observation of movements
eye movements - delay
motor impersistence with tongue protrusion
tone
reflexes
gait
tics, myoclonus

63
Q

how is huntingtons disease diagnosed

A

proven family hisotyr and exam

genetic testing for CAG repeats

64
Q

what are the treatments for huntingtons diease

A

symptomatic management

hallucinations/psychosis
mood/depression
spasticity/hyperkinesia
dopamine depleting agens for chorea/ballism

clin med - neuro (13 decks)

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