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Clin Med - NEURO > Other Neuro topics - Waldron > Flashcards

Other Neuro topics - Waldron Flashcards

1
Q

what are tics

A

repetitive, stereotyped, involuntary movements and vocalizations

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2
Q

what is a simple tic

A

sudden, brief, repetitive movements involving limited number of muscle groups
motor - blinking, eye movements, facial grimace, heads/shoulder jerking
Vocal- throat clearning, grunting, barking, sniffing/snorting

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3
Q

what is a complex tic

A

distinct, coordinated patterns of movements involving several muscle groups, may appear purposeful

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4
Q

what is premonitory urge

A

urge/sensation in muscle prior to onset of tic

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5
Q

what is the epidemiology of Tourette’s syndrome

A

Boys 3-5x > girls
non-hispanic white 2x more likely than hispanic or AA
1/162 children

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6
Q

what is the pathophysiology of Tourette’s syndrome

A

cause unknown

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7
Q

what are possible risk factors for Tourettes syndrome

A

smoking during pregnancy
pregnancy complications
low birthweight
infection - research with mixed results about preceding infection

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8
Q

what are the genetic components of Tourettes syndrome

A

research shows inherited dominant gene
boys with gene 3-4x more likely to display symptoms
may be triggered by abnormal metabolism of dopamine

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9
Q

what is the presentation of TS

A

typically onset between 5-10yo, most commonly 6yo
tics increase in frequency and severity between 8-12yo
tic improvement seen in adolescence, may become tic free

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10
Q

what are the three types of Tic Disorders

A

Tourettes
Persistent
Provisional

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11
Q

what are Tourettes tics

A

both. motor and vocal tics
present for at least 1 year

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12
Q

what are persistent tics

A

Motor OR vocal tics
present at least 1 year

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13
Q

what are provisional tics

A

motor OR vocal OR both
present less than 1 year

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14
Q

what are the diagnostic requirements for TS

A

2+ motor tics
1+ vocal tics
Tics present for at least 1 year
tics onset prior to age 18 years
symptoms are NOT result of medication or other medical condition

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15
Q

what are common associated mental health, behavioral or developmental disorders diagnosis with TS

A

ADHD and Anxiety/OCD

as well as other learning disabilities

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16
Q

what chronic health conditions are also diagnosed with TS

A

asthma, Hearing or vision, bone, joint or muscle conditions or suffered brain injury or concussion

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17
Q

what is the treatment for TS

A

goal is tic suppression - but response highly variable to any tx

Medications: Neuroleptics, alpha adrenergic, stimulants, or SSRIs

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18
Q

what Neuroleptics are used to treat TS

A

Haloperidol, Pimozide, Aripiprazole
can cause sedation, weight gain, cognitive dulling’ tremor, dystonic reactions, parkinsonian - like symptoms
Concern for Tardive dyskinesia - associated with chronic med use

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19
Q

what is Tardive Dyskinesia associated with

A

chronic medication use

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20
Q

what alpha adrenergic medications are used to treat TS

A

Clonidine or guanfacine - usually first line
can cause sedation

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21
Q

what is typically the first line treatment of TS

A

Neuroleptic medications

but neurologist typically use: alpha adrengerics such as clonidine, guafacine

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22
Q

what stimulants are used to treat TS

A

methylphenidate, dextroamphetamine
research shows control concomitant aDHD without worsening tics

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23
Q

what SSRI medications are used to treat TS

A

Fluoxetine, paroxetine, sertraline
best in patients with concomitant OCD/Anxiety

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24
Q

what medications are often used with patients with TS and OCD/Anxiety

A

SSRI such as fluoxetine, paroxetine or sertraline

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25
Q

what are other non-medication treatments for TS

A

deep brain stimulation
medical marijuana
dental orthotic devices liked used for TMJ
behavioral therapies

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26
Q

what behavioral therapies are often used to help with TS

A

Biofeedback, supportive therapies
Habit reversal
cognitive behavioral intervention for tics (CBIT) - NIH funded trial

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27
Q

what is the only medication approved for TS

A

Neuroleptics

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28
Q

what medications are contraindicated in patients with tics

A

Stimulants

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29
Q

How is TS managed

A

in most cases - tics decrease during adolescence/early adulthood and sometimes disappear completely
Genetic screening for future parents

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30
Q

what does ALS stand for and what is another name for it

A

Amyotrophic Lateral Scerlosis
AKA Lou Gehrig’s Disease

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31
Q

what is ALS

A

A RARE neurological disease affecting the control of voluntary muscle movements - DISTALLY TO CENTRALLY
both upper and lower motor neurons degenerate or die
PROGRESSIVE disease involving a gradual onset - muscles gradually weaken, fasciculate and become atrophic

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32
Q

what is lost with ALS

A

brain loses ability to initiate and control voluntary movements
patients lose their strength and ability to eat, speak, move and breathe

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33
Q

what is the cause of ALS

A

unknown but believed both genetics and environment involved

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34
Q

what is the epedimilogy of ALS

A

can strike at any age, but most common between 55 - 75 years old
Caucasians and non-hispanics more common
Military vets 1.5-2x more likely to develop

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35
Q

why do most patients die from ALS

A

die from respiratory failure usually 3-5 years from symptom onset
~10% survive 10+ years

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36
Q

what are genetic connections with ALS

A

mutations discovered suggest changes in RNA processing leads to motor neuron degeneration
other mutations - “protein recycling” - malfunction in how proteins broken down and used again
possible defects in neuron shape/structure increase susceptibility to toxins

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37
Q

what are the environmental connections with ALS

A

toxin exposure during warfare, strenuous physical activity

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38
Q

what ate the different types of ALS

A

Sporadic ALS and Familial (Genetic) ALS (FALS)

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39
Q

what is Sporadic ALS

A

90+% of cases
diagnosis occurs at random, no clearly associated risk factors, no history

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40
Q

what is FALS

A

5-10% of cases
inherited from one parent - autosomal dominant
mutations in > 12 genes responsible

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41
Q

what is the presentation of ALS

A

gradual onset, generally painless, progressive muscle weakness is most common initial symptom
early muscle weakness/stiffness
develops into more obvious weakness or atrophy

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42
Q

what are the symptoms of ALS

A

fasciculations in arms, leg, shoulder or tongue
muscle cramps
spasticity
muscle weakness affecting an arm, leg, neck or diaphragm
slurred and nasal speech, uncontrollable periods laughing/crying
difficulty chewing or swallowing

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43
Q

what is Limb onset of ALS

A

symptoms onset in arms and leg

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44
Q

what is bulbar onset of ALS

A

symptoms onset with speech or swallowing concerns/changes

45
Q

how do symptoms ‘spread’ as the diagnosis progresses

A

varied patterns and severities
problems moving, dysphagia, dysarthria, dyspnea
eventually patient will be unable to stand, walk, use hands and arms

46
Q

what are concerns with ALS patients

A

malnourishment - burn calories at faster rate, concern for weight loss
retain higher mental functions

47
Q

how is ALS diagnosed

A

detailed history and physical exam (only motor neurons affected)
Testing to rule out other concerns

48
Q

what is the treatment of ALS

A

no cure available
treatments used to control symptoms, prevent complications, ease living with diagnosis
medications
PT/OT/Speech therapy
Nutritional support
Breathing support

49
Q

what are the medication therapies used for ALS

A

Riluzole
Edaravone
others used for pain control, depression, sleep disturbances, constipation, neuropathy

50
Q

what is the purpose of Riuzole

A

decreases gluatmate levels which reduces motor nerve damage

51
Q

what is the pupose of Edaravone

A

slows decline in daily functioning, may add several months to survival

52
Q

what are breathing support types

A

non-invasive ventilation (NIV) - delievered via mask
Mechanical cough assist devices
“breath stacking”
Mechanical ventilation- tracheostomy

53
Q

what are ALS patients at a greater risk for

A

High risk for pneumonia/aspiration as respiratory weakens/fails

54
Q

what is one of the most important treatment types for patients with ALS

A

Nutritional support because they burn calories much faster

55
Q

What is MS

A

multiple sclerosis
auto-immune process directed at the CNS
- resulting inflammation damages myelin and myelin producing cells

56
Q

what are the symptoms types and severity based on

A

location of damage - damaged areas scar

57
Q

what is the epidemiology of MS

A

most often appears in young adulthood, with incidence peaking ~30 yo
F>M (3:1)

58
Q

what is the pathophysiology of MS

A

immunological
infectious factors
Environmental
Genetics

59
Q

what are the immunological associations with MS

A

T cell mediated - T regulatory cells - fail to “shut off” inflammation; cytotoxic T cells - target myelin and myelin producing cells
B Cells (from T - cell activation) - produce antibodies and proteins causing further CNS damage

60
Q

what are the infectious factors of MS

A

viral precursor?
Measles, canine distemper, HSV-6, EBV, chlamydia pneumonia

61
Q

what are environmental factors of MS

A

Geographical - more frequent further away from equator
Vitamin D
Smoking
Obesity

62
Q

what are the genetic factors of MS

A

not inherited disease but there is inherited risk
Highest if first degree relative with diagnosis
~200 genes identified as contributing to overall risk

63
Q

what are disproven theories to MS

A

Environmental allergies
Household pets
Heavy metal exposure - mercury, lead or manganses
NutraSweeet (aspartame) use

64
Q

what are the common symptoms of MS

A

Fatigue
bladder problems
parasethesias
vision problems
walking/gait difficulties
spasticity
weakness
cognitive changes
dizziness and vertigo
sexual problems
bowel problems
pain and itching
emotional changes
depression

65
Q

what are less common symptoms of MS

A

speech problems
swallowing problems
tremor
seizures
breathing problems
hearing loss

66
Q

what are secondary concerns with MS

A

repeated UTI
loss of muscle tone causing weakness, poor posture
decreased bone density, increased fracture risk
pressure sores from immobility
social, vocational complications

67
Q

what are the different types of MS

A

clinically isolated syndrome (CIS)
Relapsing-remitting MS (RRMS) - most common
Secondary Progressive MS (SPMS)
Primary progressive MS (PPMS)

Radiologically isolated syndrome (RIS)

68
Q

what is RIS

A

radiologically isolated syndrome
MRI abnormalities of brain/spinal cord consistent with MS lesions not explained by another diagnosis, with no hx neuro symptoms or abnormalities on physical exam

69
Q

What is CIS

A

clinically isolated syndrome
1st episode of symptoms caused by inflammation/demyelination of CNS
symptoms MUST last > 24 hours

70
Q

what is the treatment of CIS

A

FDA approved DMARDs - early treatment shown to delay MS onset

71
Q

if Brain lesions on MRI are consistent with MS what are they likely to have

A

likely to have 2nd episode and have a diagnosis of RRMS

72
Q

what is RRMS

A

Most common
relapses - clearly defined attaches of new/increasing neuro symptoms
Remission-periods of partial/complete recovery

NO APPARENT PROGRESSION DURING REMISSION

73
Q

what is SPMS

A

secondary progressive MS
eventually transition from initial RRMS course
accumulation of disability with or without evidence of disease activity - progressive worsening of neuro function
UNIQUE TO EACH PATIENT when this will develop

74
Q

what is PPMS

A

primary progressive MS - worst of the stages
worsening accumulation of disability from onset of symptoms without early relapses or remission

may have brief periods of diagnosis stable

PERSISTENTLY GETTING WORSE

75
Q

what is the diagnosis of MS

A

no single test, symptoms, of PE findings that make the diagnosis by themselves

history and Physical exam are key

76
Q

what is the common type of medication used for fatigue symptom management in MS

A

stimulants

77
Q

what are the McDonald Criteria

A

diagnosis criteria of MS
dissemination in space (DIS) - 2+ damages in separate areas of CNS
Dissemination in time (DIT) - evidence damage occurred at different points in time

78
Q

what is the treatment of MS

A

disease modification agents (immune modulating medications)
Relapse management
symptom management

79
Q

what is the relapse management for severe MS

A

High dose Prednisone or High dose IV methylprednisolone
ACH

80
Q

what is the prognosis of MS

A

it is NOT a terminal illness
most common cause of death in MS patients are secondary complications- i.e. immobility, chronic UTI, Compromised swallowing and or breathing

81
Q

what are the goals of treatment for MS

A

relieving symptoms of the disease
treating acute relapses and shortening their duration
reducing frequency of relapses
preventing disease progression

82
Q

What is NPH

A

Normal Pressure Hydrocephalus
- simply too much CSF in ventricles - unable to drain/absorb excess CSF, ventricles enlarge to accommodate and press on areas of the brain

83
Q

what is the cause of NPH

A

cause is never known but may follow:
head injury, stroke or cerebral bleeding, meningitis, brain tumor, brain surgery

84
Q

what is the epidemiology for NPH

A

usually occurs in older adults >60yo; developing slowly over time

85
Q

what control areas are often affected by NPH

A

Legs - gait abnormality
Bladder - incontinence (occ. also bowl incontinence)
Cognitive processes (memory, reasoning, problem solving, speaking) - dementia symptoms similar to alzheimers

86
Q

what are the preventative measures for NPH

A

No preventative measures

87
Q

what is the presentation of NPH

A

subtle onset, worsening gradually
dementia symptoms
walking symptoms
urinary symptoms
other symptoms: Nausea, headache, difficulty with vision focus

88
Q

what are the typical dementia symptoms with NPH

A

memory loss, speech problems, apathy/withrawal
difficulties with reasoning, paying attention or judgement

89
Q

what are the typical walking symptoms associated with NPH

A

unsteadiness, sudden falls, shuffling steps, trouble initiating first step
“getting stuck”, “freezing” while walking

90
Q

what are the typical urinary symptoms associated with NPH

A

incontinence urinary/feces, polyuria, urgency

91
Q

how is NPH diagnosed

A

combination of dementia, walking and urinary symptoms should be altering
hx and PE with mental status and gait evaluation
No labs necessary - no imaging needed but may assist
lumbar puncture provides improvements of symptoms - possible benefit of surgical shunt

92
Q

what are the 3 Ws of NPH

A

weird
wet
wobbly

93
Q

what is the treatment of NPH

A

no cure or definitive management but symptoms can be reversed
non surgical - mood and behavioral issues, incontinence management, ambulatory assistance
surgical - shunt vs endoscopic third ventriculostomy

94
Q

what is Myasthenia Gravis

A

muscle weakness that worsens after periods of activity and improves with periods of rest
chronic autoimmune disease causing weakness in skeletal muscles

95
Q

what is the epidemiology of M. Gravis

A

M=W
all racial/ethnic groups
most common in women <40 yo and Men >60yo
not inherited or contagious
neonatal myasthenia
congential myasthenic syndromes (CMS)

96
Q

what is the pathophysiology of M. Gravis

A

Interruption at NMJ - antibodies block/alter/destroy ACh receptors - antibodies to MuSK (muscle specific kinase) further impair signal transmission
Thymus - large (lymphoid hyperplasia) - believed to give incorrect instructions to developing immune cells

97
Q

what are the presentation of M. Gravis

A

muscles controlling eye/eyelid movement, facial expression, swallowing most frequently affected - first noticeable symptom usually weakness of eye muscles
Variable severity
onset may be sudden and therefore misdiagnosed

98
Q

what are common symptoms of M. Gravis

A

Ptosis (drooping of one/both eyelids)
Diplopia
Facial expression changes
Dysphagia (swallowing difficulties)
SOB
Dysarthria(impaired speech)
weakness in arms, hands, fingers, legs and neck

99
Q

how is M. Gravis diagnosed

A

Edrophonium test, blood work, single fiber EMG, Imaging - CT/MRI for thymoma, Pulmonary function testing (PFT)

100
Q

what is edrophonium test

A

drug blocks breakdown of ach and temporarity increases levels
typically used to test ocularmuscle weakness

101
Q

what is seen on bloodwork for M.gravis

A

ach receptor antibodies
anti-MuSK antibodies

102
Q

what is the most sensitive test for M.gravis

A

Single fiber EMG - detects impaired nerve to muscle signal transmission

103
Q

what are the treatment of M. gravis

A

thymectomy - may be cure for some patients -~50% complete remission
Anti-cholinesterase medications
Immunosuppressive agents
plasmapheresis
IV immunoglobulin

104
Q

hat is Mestinon used for

A

slows breakdown of ach at junction for M. gravis patients

105
Q

what are complications of M. gravis

A

myasthenia crisis
MEDICAL EMERGENCY -respiratory muscles so weak require ventilator support

106
Q

what is the treatment of Myasthenia crisis

A

Medical emergency - requires ventilator support
IV immunoglobulin, plasmapheresis effective reversals

107
Q

what can myasthenia crisis be triggered by

A

infection
stress
surgery
adverse reaction to medication

108
Q

what is the prognosis of M. gravis

A

with treatment, most significantly improve muscle weakness, able to live full lives
some cases: remission either temporary or permanent

109
Q

what are patient instructions with M. gravis

A

budget energy, regular rest
rest the eyes or lie down briefly 2-3x/day
keep overall health good: good diet, sleep hygiene
good control of any other medical conditions

Clin Med - NEURO (13 decks)

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