neuro Flashcards

1
Q

What is Multiple Sclerosis

A
  • An immune-mediated disease of the central nervous system
  • A disease of myelin and axons
  • primarily diagnosed clinically
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2
Q

For MS, where are Immune cells are made throughout the body?

A
•	Tonsils
•	Thymus
•	Bone Marrow
•	Spleen
•	Lymphoid tissue of the gut
******EXCEPT the brain and spinal cord******
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3
Q

Tell me about the Nerve Damage and Myelin Loss pathway

A

A. Normally, axons have a protective myelin coating that is necessary for normal conduction of electrical impulses
B. In MS, the immune system destroys myelin, resulting in slowed (not absence) conduction and exposure of axons
C. Exposed axons may then be severed…
D. …leading to permanent loss of the axon
E. The result is permanent loss of nerve function

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4
Q

What are common MS presenting s/s?

A
  • Spasticity
  • Gait, balance, and coordination problems
  • Speech/swallowing problems
  • Tremor
  • *****s/s unpredictable
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5
Q

between ages is MS usually dx?

A

20-50

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6
Q

risk factors with MS

A

risk is higher in any family in which there are several family members with the disease (multiplex families)

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7
Q

What happens with Myelin in Chronic Multiple Sclerosis Lesion?

A

In Early MS lesions as “shadow plaques,” which are areas of thinly remyelinated axons.

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8
Q

What will You Do in the Diagnosing MS?

A
  • The core requirement for the diagnosis →dissemination in time and space: evidence that damage has occurred in at least two separate areas of the CNS at different points in time
  • There must be no other explanation
  • Diagnosis of MS require evidence of plaques that occurred in different places in the CNS at different points in time
  • Clinical findings alone or a combination of clinical and MRI findings
  • Can sometimes take months or even years to confirm the diagnosis
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9
Q

WHAT IS Dissemination in space

A

demonstrated with MRI by one or more T2 lesions in at least two of four MS-typical regions of the central nervous system (periventricular, juxtacortical, infratentorial, or spinal cord) OR by the development of a further clinical attack implicating a different central nervous system site. For patients with brainstem or spinal cord syndromes, symptomatic MRI lesions are excluded from the criteria and do not contribute to lesion count.

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10
Q

WHAT IS Dissemination in time

A

demonstrated with MRI by the simultaneous presence of asymptomatic gadolinium-enhancing and nonenhancing lesions at any time, OR a new T2 and/or gadolinium-enhancing lesion(s) on follow-up MRI, irrespective of its timing with reference to a baseline scan, or by the development of a second clinical attack

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11
Q

What is the test of choice to support the clinical diagnosis of MS

A

MRI

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12
Q

T/F: Most patients with MS have relapsing-

remitting disease

A

TRUE

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13
Q

role of lumbar puncture with MS:

A

not a requirement for the diagnosis of MS in patients with classic MS symptoms and brain MRI appearance- but - it can be used to help rule out the diagnosis in equivocal cases

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14
Q

What is Evoked potential testing

A
    • electrical events generated in the central nervous system by peripheral stimulation of a sensory organ
  • *Used to detect subclinical, abnormal central nervous system function
  • *Detection of a subclinical lesion in a site remote from the region of clinical dysfunction supports a diagnosis of multifocal MS
  • *Evoked potentials also may help define the anatomical site of the lesion in tracts not easily visualized by imaging (eg, optic nerves, dorsal columns).
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15
Q

what is a Clinically Isolated Syndrome (CIS)

A

**A first neurologic event suggestive of demyelination
• pt with CIS are at high risk for developing MS if the neurologic event was accompanied by multiple, clinically silent (asymptomatic) lesions on MRI typical of MS

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16
Q

Name the four stages of MS and describe

A
  • Primary Progessice MS [ppms]- gradual progession of disease since onset without remission/relapse
  • Relapsing/Remitting MS [rrms]- unpredicatable attacks which may or may not leave permanent deficits followed by periods of remission
  • Secondary Progressive MS [spms]- initial rrms that progressed to progessive ms/ sudden steady decline without remission/relapse
  • Progressive relapsing MS [prms]- steady decline since onset with SUPER-imposed attacks
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17
Q

define relapse with ms

A

new symptom or sudden worsening of old symptom lasting at least 24 hours, and usually accompanied by an objective change in neurologic findings

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18
Q

in a pt with rrms, how would the np manage a relapse?

A
  • Treatment with corticosteroids recommended if relapse significantly interferes with everyday functioning
  • 3-5 day course of high-dose intravenous methylprednisolone with or without oral taper
  • High-dose oral steroids may also be used
  • Rehabilitation can help restore function following a relapse
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19
Q

How would the NP medically treat MS?

A

• Baclofen (Lioresal) – oral; intrathecal or procedure with • Baclofen pump

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20
Q

T/F: Temperature Sensitivity is common with pts with MS

A

TRUE: Heat sensitivity is common AND cold sensitivity may occur too

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21
Q

What is pseudoexacerbation

A

When even a slight elevation in core body temperature in MS pt can cause temporary worsening of symptoms

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22
Q

What is Parkinson’s Disease?

A

a chronic, progressive neurodegenerative disorder characterized by any combination of four cardinal signs: rest tremor, rigidity, bradykinesia, and gait disturbance.

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23
Q

what are the 4 cardinal signs of parkinsons diease?

A

rest tremor, rigidity, bradykinesia, and gait disturbance.

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24
Q

what is the patho of parkinson disease?

A

Loss of dopamine in the corpus stratia is the primary defect in Parkinson’s disease. [Destruction of neural cells in the substantia nigra pars compacta (midbrain) that secrete dopamine]

Nerve cells in the substantia nigra send out fibers to the corpus stratia, gray and white bands of tissue located in both sides of the brain.

There the cells release dopamine, an essential neurotransmitter (a chemical messenger in the brain)

25
Q

what is the pathological hallmark of parkinsons?

A

lewy bodies (on autopsy)

26
Q

risk factors for parkinsons

A

increased with older age

decreased risk with smoking cigarettes

27
Q

Motor parkinsonism required traits:

A

Bradykinesia

Rest tremor or rigidity

28
Q

clinical presentation of pt with Parkinson disease

A
  • Bradykinesia
  • Plus Tremor (most common presenting sign)
  • or Rigidity
  • Postural instability (occurs late in disease)
  • Resting tremor
  • Asymmetry (one side more affected than the other)
  • Good response to Levodopa
29
Q

What are the red flags that mean dx is NOT parkinsons

A
  • Falls at presentation or early in the course of the disease
  • Poor response to Levodopa
  • Symmetrical motor signs
  • Lack of tremor
  • Rapid progression
  • Dysautonomia early in the disease (urinary urgency/incontinence, orthostatic hypotension, erectile failure)
  • History of repeated head injury, or encephalitis
  • History of recurrent strokes
30
Q

T/F: There are no tests to diagnose parkinson disease

A

TRUE

31
Q

Pharmacological management for parkinsons

A
  • Levodopa**INITIAL TX
  • Dopamine agonists*****INITIAL TX
  • Monoamine oxidase (MAO) B inhibitors- Rasagiline 5mg once a day (in AM)
  • Anticholinergic agents
  • Amantadine (Symmetrel, Symadine)- Antiviral agent 200-300 mg/day in divided doses [weak antiparkinsonian drug with low toxicity that is most useful in treating patients with early or mild PD]
  • Catechol-O-methyl transferase (COMT) inhibitors
32
Q

Bradykinesia in parkinsons

A

Generalized slowness of movement
• May be described as “weak”, “incoordination”, “tired”, “stiffness”
- Typically starts distally in arms, w/ dec. manual dexterity of fingers

33
Q

Resting tremor

A
  • occurs @ rest
  • seen as a “pill-rolling” action of the hands that may also affect the chin, lips, legs, and trunk, can be markedly increased by stress or emotions.
  • Onset of parkinsonian tremor is generally after age 60. -Movement starts in one limb or on one side of the body and usually progresses to include the other side.
34
Q

caution with pts with tremors

A

the majority of people with tremor do not have PD:

  • essential tremor (Usually B/L and intention),
  • MS (intention),
  • cerebellar dysfunction (Usually intention & w/ other cerebellar signs)
35
Q

rigidity with parkinsons

A
  • Often begins unilaterally, typically same side as tremor
  • “Cogwheel rigidity”- ratchet pattern of resistance and relaxation
  • “Leadpipe rigidity”- present throughout movement
36
Q

Name Craniofacial features with parkinsons:

A
  • Hypomimia (masked facial expression)
  • Decreased spontaneous eye blink (dysarthria)
  • Speech impairment (hypophonia)
  • Sialorrhea (excessive salivation)
37
Q

initial Parkinson tx

A

Levodopa or Dopamine agonists

38
Q

what is is the most effective symptomatic therapy for parkinson s/s

A

Levodopa (combined with a peripheral decarboxylase inhibitor, ie, Sinemet, Madopar, or Prolopa)
-initiate with immediate release

39
Q

anticholinergic use with parkinson disease

A

should be reserved for younger patients in whom tremor is the predominant problem.
-Their use in older or demented individuals and those without tremor is strongly discouraged.

40
Q

T/F: Patients with Parkinson disease (PD) who take levodopa chronically are increasingly likely to develop motor fluctuations and dyskinesia as the disease progresses.

A

TRUE

41
Q

T/F: Younger patients on levodopa can develop motor fluctuations and dyskinesia SOON after starting treatment.

A

TRUE

42
Q

Describe wearing off phenomenon in parkinsons disease pts on Levodopa

A
  • As the disease advances, effect of levodopa begins to wear off approx. 4 hrs. after each dose (1/2 life = 90 min.)
  • Pt’s will begin to be aware of a wearing “off” effect less than 4 hrs after levodopa dose
43
Q

whats is Dyskinesia

A

abnormal involuntary movements

44
Q

how should the np manage wearing off phenomenon with levodopa?

A
  • DO Shorten the dose interval while administering lower doses
    • Add COMT inhibitor
  • DONT Increase dosE = not usually effective = increase SE w/o increasing dose duration
  • DONT take levodopa w/ high protein meals
45
Q

what are Motor fluctuations ?

A

alterations between periods of being “on”= responding to medication, and being “off”= experiencing symptoms of underlying PD

46
Q

What is Myasthenia gravis?

A
  • most common disorder of neuromuscular transmission. -well understood autoimmune disorder
  • HALLMARK: fluctuating /combo of weakness in ocular (eye/eyelid movement- ptosis), bulbar (facial expression, chewing, talking, and swallowing), limb, and respiratory muscles.
  • ***skeletal muscle weakness INCREASES during periods of activity and IMPROVES after periods of rest
47
Q

what is the patho of myasthenia gravis?

A

Weakness is the result of an antibody-mediated, T-cell dependent immunologic attack directed at proteins in the postsynaptic membrane of the neuromuscular junction (acetylcholine receptors or receptor-associated proteins).
****antibodies BLOCK, alter or destroy the receptors for acetylcholine at the neuromuscular junction = PREVENTION of muscle contraction occurring

48
Q

myasthenia gravis s/s

A
  • increase in females in 20s-30s
  • fluctuating skeletal muscle weakness, often with true muscle fatigue.
  • HALLMARK: fluctuating /combo of weakness in ocular (eye/eyelid movement- ptosis), bulbar (facial expression, chewing, talking, and swallowing), limb, and respiratory muscles.
  • ***skeletal muscle weakness INCREASES during periods of activity and IMPROVES after periods of rest
49
Q

What are the bedside tests for myasthenia gravis?

A
  • the edrophonium test and the ice pack test

- sensitive, but many false-positive results

50
Q

how will the np preform the edrophonium test?

A
  • uses the drug Tensilon (edrophonium) to diagnose myasthenia gravis. Tensilon prevents the breaking down of the chemical acetylcholine, which then helps stimulate the muscles.
  • inject iv and then sub q
  • Pt tests positive for myasthenia gravis if their muscles get stronger after being injected with Tensilon.
51
Q

how will the np preform the ice pack test?

A
  • preform in pt with ptosis
  • NOT helpful for those with extraocular muscle weakness.
  • ice pack placed on pt’s closed lid for two minutes.
  • The ice is then removed and the extent of ptosis is immediately assessed.
52
Q

what SEROLOGIC TESTINGshould be preform to confirm dx?

A

Patients with positive AChR-Ab or MuSK-Ab assays (positive antibodies) have seropositive myasthenia gravis (SPMG)= confirmation of myasthenia gravis
-but DONT rely

53
Q

neuro exam should include

A
  • getting up and down from chair
  • crossing and uncrossing legs
  • holding arms overhead until they get tired
  • counting backward from 100 until their voice starts to weaken
54
Q

t/f : Once the diagnosis of myasthenia gravis has been established, a chest CT or MRI scan should be performed to look for a possible associated thymoma

A

TRUE

55
Q

Where is the birthplace of myasthenia gravis

A

thymus

56
Q

Describe the two clinical forms of myasthenia gravis

A
  • ocular myasthenia = weakness limited to the eyelids and extraocular muscles.
  • generalized disease = the weakness commonly affects ocular muscles & combo of bulbar, limb, and respiratory muscles.
57
Q

what antibiotic is contraindicated with MG?

A

Ketolides (telithromycin)

58
Q

what drugs may mask/worsen MG?

A
abx:
-Aminoglycosides* - eg, gentamicin, neomycin, tobramycin
-Clindamycin
-Fluoroquinolones - eg, ciprofloxacin, levofloxacin, 
-Vancomycin
Cardiovascular drugs:
-Beta blockers 
-magnesium 
Anesthetic agents:
-Neuromuscular blocking agents*
59
Q

what drugs are well tolerated with MG:

A

CArdio:
-calcium channel blockers
Abx:
-Antiretroviral agents - eg, ritonavir
-Tetracyclines - eg, doxycycline, tetracycline
-Macrolides - eg, azithromycin, clarithromycin, erythromycin
-Metronidazole
Anesthetic agents:
-Inhalation anesthetics - eg, isoflurane, halothane
-Local anesthetics- bupivacaine, lidocaine, procaine