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Pathophys > Neurologic Disorders > Flashcards

Neurologic Disorders Flashcards

1
Q

What are the lobes of the cerebellum?

A
  • anterior
  • posterior
  • flocculonodular (in-between anterior/posterior)
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2
Q

What does the cerebellum do and what does it control?

A
  • regulates muscle tone & coordinates muscle groups
  • controls stance, gait & posture
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3
Q

What are two possible clinical presentations will you see in a pt who has a lesion or damage to the cerebellum?

A
  • ataxia (due to a dec. in motor activities)
  • dysmetria (overshoot/undershoot of voluntary motor activity)
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4
Q

What is ataxia?

A

uncoordinated gait

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5
Q

Describe the presentation of a pt with ataxia:

A

wide stance, flinging arms/legs out

(“drunk”)

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6
Q

Polyglutamine ataxia is a genetic mutation that causes dysfunction of the cerebellum. Why does this occur?

A

genetic mutation causes excess glutamine

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7
Q

T/F the pathway of excess glutamine in polyglutamine ataxia is known:

A

FALSE - it is unknown

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8
Q

Tentorium cerebelli is the fold of what meningeal layer?

A

fold of the dura mater

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9
Q

In tentorium cerebelli, where does the fold of dura mater occur in the brain?

A

in the fold separating the cerebellum from inferior part of occipital lobe

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10
Q

Supratentorial lesions develop where?

A

superior to the tentorium

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11
Q

Is the manifestations of supratentorial lesions narrow or widespread?

A

narrow (very localized)

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12
Q

If a pt has a supratentorial lesion, what sx are they most likely to have?

A

paresthesias in fingers of one hand (localized)

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13
Q

Infratentorial lesions develop where?

A

below the tentorium

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14
Q

Is the manifestations of infratentorial lesions narrow or widespread?

A

widespread

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15
Q

If a pt has a infratentorial lesions this can also affect what part of the brain?

A

brain stem

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16
Q

What are 3 motor neuron diseases?

A
  1. UMN disease
  2. LMN disease
  3. ALS (amyotrophic lateral sclerosis)
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17
Q

The corticospinal pathway contains what primary tract?

A

the primary voluntary motor tract

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18
Q

The corticospinal tract extends from where to where?

A

cortex to spine

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19
Q

Is the corticospinal pathway longer or shorter than the corticobulbar pathway?

A

longer (goes to spine!)

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20
Q

The corticobulbar tract extends from where to where?

A

cortex to medulla

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21
Q

Is the corticobulbar pathway longer or shorter than the corticospinal pathway?

A

shorter (stops at medulla!)

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22
Q

The upper motor neurons contain what two tracts?

A
  1. corticospinal
  2. corticobulbar
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23
Q

If a pt has damage or a lesion to the upper motor neurons, what sx will they present?

A
  • weakness
  • paralysis
  • hyperreflexia
  • spastic paralysis
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24
Q

Damage or lesions to the upper motor neurons may cause paralysis. Is this paralysis ipsilateral or contralateral?

A

contralateral paralysis = UMN

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25
Q

What is hyperreflexia?

A

increase in muscle tone + reflexes

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26
Q

Why does hyperreflexia occur if there’s damage or lesions to the upper motor neurons?

A

spinal cord is still carrying out reflexes, no inhibition from cortex

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27
Q

Damage to the lower motor neurons in the anterior horns of the spinal cord causes what?

A
  • weakness or paralysis on same side at or below lesion
  • hyporeflexia
  • flaccid paralysis
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28
Q

Does paralysis occur on the same side or contralateral side of a lesion in upper motor neuron disease?

A

contralateral

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29
Q

Damage or lesions to the lower motor neurons may cause weakness and paralysis. Is this paralysis ipsilateral or contralateral?

A

ipsilateral or below lesion = LMN

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30
Q

A pt with ataxia may not always have a lesion or damage to the cerebellum. Polyglutamine ataxia is one etiology that can cause dysfunction of the cerebellum due to degeneration. Why does this happen?

A

cerebellum is degenerating bc of xs glutamine = ataxia

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31
Q

What is hyporeflexia?

A

no muscle tone/little to no reflexes

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32
Q

What does ALS stand for and what’s another name for ALS?

A

ALS = amyotrophic lateral sclerosis
ALS = Lou Gehrig’s disease

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33
Q

What does amyotrophic mean? (hint: ALS)

A

amyotrophic = muscle atrophy

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34
Q

What does “lateral sclerosis” in ALS mean?

A

sclerosis or ‘hardening’ of the lateral corticospinal tracts

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35
Q

T/F ALS is the most common form of motor neuron degenerative disease:

A

TRUE

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36
Q

T/F ALS affect upper and lower motor neurons:

A

TRUE

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37
Q

ALS involves problems with two tracts, what are they?

A

corticospinal & corticobulbar

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38
Q

ALS involves the bulbar muscles. What are these muscles and what function is affected?

A
  • muscles of mouth, neck, throat
  • affects speech/swallowing
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39
Q

In ALS, death usually occurs 3-5 years after diagnosis due to what?

A

respiratory failure

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40
Q

ALS primarily affects who?

A

men 40-60 y/o

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41
Q

Why did Dr. Stephen Hawking live so long with ALS?

A

possibly due to sheer determination and early diagnosis

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42
Q

What is the cause of ALS?

A

unknown but possibly due to glutamate pathway

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43
Q

What percent of ALS cases are familial?

A

10%

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44
Q

What type of neurotransmitter is glutamate?

A

excitatory

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45
Q

Describe the mechanism of glutamate (hint: how does glutamate release calcium?)

A
  1. released from presynaptic terminal
  2. activates ion channels or PLC
  3. uses IP3 as second messenger
  4. causes release of calcium from cytoplasmic reticulum
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46
Q

Increased glutamate causes increased calcium. What does this cause?

A

death of muscle cells

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47
Q

Glutamate should be removed by transport proteins on ______.

A

astrocytes

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48
Q

What happens when astrocytes don’t remove glutamate?

A
  • increase in glutamate
  • glutamate remains in environment
  • neurons begin to die
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49
Q

What is the function of neurofilaments in large motor neurons?

A

structure & transport

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50
Q

What degenerates in ALS?

A

neurofilaments in large motor neurons

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51
Q

Large motor neurons have neurofilaments that degenerate in ALS. What happens as a cause of this? (hint: 4 steps)

A
  1. decrease transport of factors necessary for motor neuron survival
  2. plaques/scleroses develop due to neuron degeneration
  3. neurons can’t innervate muscles
  4. muscle begins to atrophy including respiratory muscles
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52
Q

T/F in ALS cognitive function and the body decline:

A

FALSE - no cognitive decline while body is declining

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53
Q

What are some clinical presentation in ALS?

A
  • hyperreflexia + spastic paralysis (UMN)
  • hyporeflexia + flaccid paralysis (LMN)
  • fasciculations = muscle twitch
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54
Q

ALS has no cure but what medication can be given to slow the progression of this disease?

A

Rilutek - riluzole (glutamate inhibitor)

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55
Q

What can cause ICP?

A

trauma, infection, hemorrhage, tumors

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56
Q

Will ICP cause an increase or decrease in blood flow?

A

decrease

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57
Q

What will the body do to decrease pressure in the skull?

A

shunt CSF down into the spinal cord

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58
Q

In an effort to decrease ICP, will the body increase or decrease venous return?

A

increase

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59
Q

What is autoregulation?

A

where every organ’s blood vessels will take care of own organ

(body will restrict or dilate for own organ)

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60
Q

If a pt has ICP and no medical intervention is taken, brain tissue will eventually start to die. When this happens, the body’s last attempt is to bring more O2 to the brain. What happens to the blood vessels and what does this cause?

A
  • body brings more O2 to brain and blood vessels DILATE
  • dilation increases ICP
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61
Q

How does the body compensate for ICP in an effort to shunt blood to the brain?

A

systemic vasoconstriction

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62
Q

Explain systemic vasoconstriction due to ICP:

A
  • increase BP = increase pulse pressure
  • decrease HR
  • decrease CO2 in blood
  • chemo receptors detect decrease in blood CO2
  • causing a decrease in respiratory rate (less CO2)
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63
Q

If the body cannot compensate for ICP, ischemia can occur. What brain center does this damage?

A

respiratory center in medulla

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64
Q

Some pt’s with increased ICP will develop Cheyenne-Stokes respiration. Explain this:

A

pt’s will breathe deeply, then breathe fast, then breathe slow, then stop

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65
Q

What is it called when a pt stops breathing for a period of time?

A

apnea

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66
Q

What is pulse pressure?

A

systolic - diastolic = pulse pressure

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67
Q

What are the first signs of ICP?

A
  • lethargy
  • papilledema
  • headaches + vomiting
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68
Q

If you suspect a pt has ICP, what quick exam can you do to check for this?

A

eye exam - you’ll see edema of optic nerve from light of ophthalmoscope (papilledema)

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69
Q

Why do some pt’s with increased ICP present with emesis?

A

pressure on brain increases pressure on medulla oblongata (emetic center)

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70
Q

ICP can affect which cranial nerve? What can this lead to?

A
  • CN 3 (oculomotor)
  • ptosis & pupil constriction

(affected eye will be ipsilateral to lesion)

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71
Q

How can you measure CSF?

A

manometer

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72
Q

What is an abnormal ICP level? What is normal? (hint: mmHg)

A

abnormal = >20 mmHg
normal = 9-14 mmHg

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73
Q

What does cloudy, pink, and yellow/light green CSF indicate?

A

cloudy = many WBC
pink = many RBC
yellow/light green = infection

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74
Q

What is Parkinson’s disease and what does it affect?

A

= progressive degenerative disorder

affects motor branch of nervous system & extrapyramidal neurons

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75
Q

What part of the brain is degenerating in Parkinson’s?

A

basal ganglia

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76
Q

Parkinson’s is known as the disease of _______.

A

bradykinesia (slow movement)

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77
Q

Parkinson’s is caused by what?

A

a decrease in dopamine from the substantia nigra

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78
Q

What percent of neurons are lost in the substantia nigra in Parkinson’s?

A

50-70% of neurons

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79
Q

What type of neurotransmitter is dopamine?

A

inhibitory

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80
Q

In Parkinson’s dopamine is decreased. What does this do to muscle?

A

increases muscle tone & muscle activity

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81
Q

What are the clinical presentations of a pt with Parkinson’s disease?

A

resting tremors, muscle rigidity & instability

(dec. dopa = inc. muscle tone/activity = sx)

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82
Q

What nerves will eventually be affected in Parkinson’s?

A

corticospinal nerves

(cortex won’t be able to inhibit impulses from spine)

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83
Q

Who does primary Parkinson’s disease affect?

A

male & female >60 y/o

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84
Q

What percent of primary Parkinson’s is familial?

A

5%

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85
Q

T/F Parkinson’s disease is multifactorial:

A

TRUE but not proven

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86
Q

What are some causes of secondary Parkinson’s disease?

A

trauma & drugs
(happens in young people - Michael J. Fox)

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87
Q

What is found scattered in neurons of pt’s with Parkinson’s?

A

Lewy bodies

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88
Q

What are Lewy bodies composed of?

A

α-synuclein & other proteins

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89
Q

Lewy bodies are also found in what other disease?

A

Lewy body dementia

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90
Q

How is Lewy body dementia diagnosed?

A

autopsy

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91
Q

Failure of what system is a theory of Parkinson’s?

A

failure of UPS (ubiquitin-proteasome system)

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92
Q

What should the ubiquitin-proteasome system (UPS) be doing, but fails to do in Parkinson’s?

A

should be removing damaged/misfolded proteins & amino acids that haven’t folded into proteins

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93
Q

Failure of the ubiquitin-proteasome system (UPS) causes what?

A

aggregation of neurons in brain

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94
Q

What are the sx of Parkinson’s?

A
  • weakness
  • muscle aches
  • facial expressions change
  • tremors in hand
  • pill rolling movement of fingers
  • festination (short shuffling steps)
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95
Q

Festination is seen in pt’s with Parkinson’s disease. Describe this:

A

festination = short shuffling steps that accelerate as pt goes on

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96
Q

Facial expressions change in Parkinson’s disorder. This is known as “Parkinson’s mask”. Describe this:

A

Parkinson’s mask = pt can’t smile/frown bc voluntary motion is lost

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97
Q

Pt’s with Parkinson’s will present with tremors in hands. What does this look like?

A

tremors at rest, tremor stops when reaching for something

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98
Q

There is no cure for Parkinson’s disease but there are several treatments available. What medication is a precursor of dopamine that you can give to pt’s with Parkinson’s?

A

Levodopa (L-dopa) = dopamine precursor

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99
Q

If pt’s with Parkinson’s need dopamine, why can’t we just give them dopamine?

A

dopamine can’t cross the BBB

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100
Q

What are three medications you can give pt’s with Parkinson’s to treat their sx?

A
  • Levodopa (L-dopa)
  • dopamine agonists
  • MOA-B inhibitors (monoamine oxidase)
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101
Q

T/F L-dopa can cross the BBB and treat pt’s with Parkinson’s disease:

A

TRUE

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102
Q

What does L-dopa metabolize to when it crosses the BBB?

A

dopamine

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103
Q

Dopamine agonists are one of the treatments available for pt’s with Parkinson’s. What does a dopamine agonist do?

A

stimulates dopamine receptors

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104
Q

What does the enzyme ‘MAO’ stand for and what does it do?

A

MAO = monoamine oxidase
breaks down dopamine

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105
Q

MAO-B inhibitors are used for the treatment of Parkinson’s disease and prevents the degradation of what neurotransmitter?

A

dopamine (keeps dopamine off receptors longer)

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106
Q

Pt’s with Parkinson’s will benefit from what two kinds of therapies?

A

physical & occupational therapy

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107
Q

Name two MAO inhibitors and their function:

A

Selegiline & Rasagiline
(keeps dopamine off receptors longer)

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108
Q

What is the most common cause of ICP

A

brain tumors (benign or malignant)

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109
Q

What is the most common malignant brain tumor that causes ICP?

A

gliomas

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110
Q

Gliomas are developed from what type of brain cell?

A

glial cell (NOT neurons)

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111
Q

Gliomas are classified as what type of glial tumor?

A

astrocytoma

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112
Q

What is the function of glial cells?

A

they are supporting cells

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113
Q

What is the most abundant and largest glial cell?

A

astrocyte

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114
Q

You are doing an autopsy on a pt who died of a brain tumor and notice flattening of the gyri. What tumor does the pt have?

A

astrocytoma

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115
Q

A tumor that develops from the meninges is called a what?

A

meningioma

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116
Q

What are the meninges?

A

pia mater, arachnoid mater, dura mater

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117
Q

What is an adenoma?

A

a tumor developed from a gland
(e.g. pituitary gland)

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118
Q

What is a secondary brain tumor and give an example:

A

a brain tumor that developed as a RESULT of cancer elsewhere in the body

e.g. = lung/breast cancer that metastasized to brain

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119
Q

The growth of a brain tumor can cause ICP. What can happen to the brain as a result of this pressure?

A

can herniate through foramen magnum due to pressure

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120
Q

What are the two most common brain tumors in children?

A

brain stem & cerebellar

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121
Q

T/F brain tumors in adults are most common than brain tumors in children:

A

FALSE - children are affected the same % as adults

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122
Q

What is the most common brain tumor in adults?

A

cerebral

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123
Q

What are the S&S of a brain tumor?

A
  • headaches
  • lethargy
  • unexplained nausea/vomiting
  • vision problems
  • problems with gait
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124
Q

Name 3 ways to treat a brain tumor:

A
  1. chemo
  2. radiation
  3. drugs to dec. blood to tumor (not many cross BBB)
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125
Q

What is Myasthenia Gravis?

A

an autoimmune disease where the body produces IgG antibodies against own acetylcholine receptors

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126
Q

What is the only neurotransmitter for skeletal muscles?

A

acetylcholine

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127
Q

If your body is destroying Ach receptors, like in pt’s with Myasthenia Gravis, what else is it destroying as a result?

A

skeletal muscles

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128
Q

Pt’s with Myasthenia Gravis have muscle weakness that ______ with exercise/movement and _______ with rest.

A

increases, decreases

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129
Q

What muscles are affected the most in pt’s with Myasthenia Gravis?

A

muscles with small motor units

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130
Q

What is the first sx of Myasthenia Gravis?

A

problems involving the ocular muscles
(e.g. ptosis)

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131
Q

What muscle can be affected in severe cases of Myasthenia Gravis and lead to death?

A

diaphragm (muscle of primary inspiration)

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132
Q

In Myasthenia Gravis, receptors on postsynaptic muscle membranes are decrease by how much?

A

70-90%

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133
Q

T/F pt’s with Myasthenia Gravis have enough acetylcholine:

A

TRUE - Ach is not affected, ONLY Ach receptors

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134
Q

T/F acetylcholine and acetylcholine receptors are destroyed in Myasthenia Gravis:

A

FALSE - ONLY Ach receptors

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135
Q

90% of pt’s with Myasthenia Gravis have antibodies against what?

A

Ach receptors

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136
Q

Who does Myasthenia Gravis affect and what is the onset?

A

women more than men (onset = 20-30 y/o)

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137
Q

What are some sx of Myasthenia Gravis?

A
  • ptosis
  • weakness of skeletal muscles
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138
Q

5% of pt’s with Myasthenia Gravis seem to have multiple autoimmune antibodies. Why is this happening?

A

pts are not only producing Abs against acetylcholine receptors but against other organs too

139
Q

5% of pt’s with Myasthenia Gravis produce antibodies against other organs. What two sx can be a result of this?

A

hyperthyroidism & hyperplasia of thymus

140
Q

What are two tests to diagnose Myasthenia Gravis and what are they checking for?

A
  1. blood tests (check for autoimmune Abs)
  2. EMG’s (check how strong skeletal muscles are)
141
Q

What are two treatments for Myasthenia Gravis?

A
  1. anti-cholinesterase inhibitors
  2. immunosuppressives
142
Q

What is an anti-cholinesterase inhibitor used for the treatment of Myasthenia Gravis? What does it do?

A

Prostigmin - neostigmine
(keeps Ach on receptors for longer)

143
Q

Vascular disorders can be 4 things. What are they?

A
  • hemorrhagic
  • ischemic
  • focal (one part of brain)
  • general (septic shock or MI)
144
Q

What is a TIA and is it permanent?

A

TIA = transient ischemic attack = mini stroke
NOT permanent

145
Q

T/F a TIA can happen in one area of the brain or multiple areas of the brain:

A

TRUE

146
Q

What is the main cause of a TIA and what are two other causes?

A

main cause = atherosclerosis
other causes = small embolus/vascular spasms

147
Q

Why is it important to treat the underlying cause of a TIA?

A

bc pt could have a major stroke later on

148
Q

What are the S&S of a TIA?

A
  • blurred vision or partial loss
  • weakness in 1 limb
  • numbness/paresthesia’s on face
  • confusion
  • aphasia (difficulty speaking)
149
Q

How long will the sx of a TIA last?

A

few min - hours

150
Q

What is a CVA?

A

cerebrovascular accident = MAJOR stroke

151
Q

What are two characteristics of a CVA?

A
  • sudden, localized neurologic defect for 24 hrs+
  • problem with cerebral circulation
152
Q

What 4 things are going to help you determine if a pt had a TIA or a CVA? (mini stroke vs major stroke)

A
  • cholesterol levels
  • atherosclerosis
  • which blood vessel is clotted or bleeding
  • collateral blood flow
153
Q

Occlusions int eh brain occur more often in large blood vessels. Name 3 large blood vessels in the brain:

A

internal carotid, middle cerebral, basilar arteries

154
Q

What are lacunar infractions?

A

multiple little areas of affects in an ischemic stroke

155
Q

What can happen if a pt loses 5 or more minutes of blood flow to the brain?

A

irreversible damage

156
Q

List 3 categories of strokes:

A
  1. atherosclerosis
  2. embolism
  3. hemorrhagic
157
Q

What is an atherosclerotic stroke?

A

stroke of the large artery like the carotids

158
Q

What develops in an atherosclerotic stroke?

A

atheromas/plaques in arteries

159
Q

What is the cause of an atherosclerotic stroke?

A

unsure but possibly due to prior damage to blood vessel

160
Q

What is the new theory of the cause of atherosclerotic strokes?

A

prior endothelial damage to blood vessels possibly from high BP

161
Q

How does high BP cause damage to the blood vessels?

A
  • inflammation and WBCs attach to area
  • fibroblasts & smooth muscle cells multiply
  • circulating lips attach
  • start of lipid attachment causes plaque to stick
  • plaque dec. diameter of blood vessels
  • blood flow is decreased
  • ischemia
162
Q

What is an embolic stroke?

A

a thromus/clot that break away and flows in blood to brain = stroke

163
Q

Atherosclerotic and embolic are classified as what type of stroke?

A

ischemic stroke

164
Q

What is a hemorrhagic stroke?

A

intracerebral hemorrhage due to rupture of cerebral artery/blood vessel

165
Q

A ruptured blood vessel in a hemorrhagic stroke is most likely the cause of what?

A

HTN & ICP

166
Q

Besides a ruptured blood vessel, what else could cause a hemorrhagic stroke?

A

trauma

167
Q

What do you need to do in the first 24-48 hours of your pt having a hemorrhagic stroke?

A

take care of the inflammation and pressure ASAP

(if not taken care of, more damage is done)

168
Q

Why do you need to treat a hemorrhagic stroke quickly?

A

CNS neurons don’t regenerate

  • as brain tissue dies, neurons can’t regenerate
  • fibrous tissue comes in and causes scar tissue
  • connective tissue regenerates and leaves cyst openings in brain
169
Q

What are risk factors for ALL strokes?

A
  • HTN
  • atherosclerosis
  • high cholest.
  • diabetes
  • systemic lupus
  • young women - smoking + oral contraceptives
170
Q

Strokes are the ___ leading cause of death in the US:

A

3rd

171
Q

What are sx for an occlusion of the larger arteries?

A

aphasia, hemiparesis. coma, death

172
Q

What are sx for an occlusion of the anterior cerebral artery in the frontal lobe:

A

contralateral weakness + sensory loss

173
Q

What are sx for an occlusion in the posterior cerebral occipital lobe?

A

loss or partial loss of vision

174
Q

In some pt’s having a stroke you’ll see flaccid paralysis. What will develop in the next few weeks?

A

spastic paralysis

175
Q

What is the treatment for a stroke?

A

depends on the cause

for mini stroke = TPA = tissue plasminogen activator (Alteplase IV)

176
Q

TPA is given intravenously for pt’s having a mini stroke. What is the name of this medication and when should it be administered?

A

Alteplase IV - must be given within 3 hours of TIA

177
Q

What percentage of stroke are ischemic?

A

87%

178
Q

What is the treatment for an ischemic stroke?

A

endovascular procedure/medical thrombectomy

179
Q

Explain the process of a medical thrombectomy?

A
  • thread a catheter in blood vessel of groin up to brain
  • grab clot, pit in “wire basket”, pull clot out
180
Q

When should a medical thrombectomy be done for pt’s having an ischemic stroke?

A

within 6 hours of onset

181
Q

What is the treatment for a hemorrhagic stroke?

A

surgery to do thrombectomy

(can’t give TPA bc it will cause more bleeding)

182
Q

Why can’t you give TPA to pt’s having a hemorrhagic stroke?

A

causes more bleeding

183
Q

What does F.A.S.T. stand for? (hint: act FAST)

A

F- facial drooping
A- arm weakness
S- speech changes
T- time

184
Q

What is an aneurysm?

A

weakness of a vessel wall (localized dilation)

185
Q

Are aneurysms asymptomatic?

A

they can be until they get large

186
Q

T/F pt’s having an aneurysm don’t lose consciousness

A

FALSE - they can lose consciousness

187
Q

What is the most common cause of a subarachnoid hemorrhage?

A

rupture of blood vessel

188
Q

The rupture of a ‘berry’ aneurysm will cause what?

A

ICP

189
Q

Chronic HTN can result in multiple little aneurysms called what?

A

Charcot-Bouchard aneurysms

190
Q

What are the sx of an aneurysms?

A
  • HA
  • photophobia
  • nuchal rigidity
  • confusion = small leak
  • emesis
  • seizures
  • LOC = rupture of blood vessel (can lead to death)
191
Q

What is the treatment for an aneurysm? (hint: old & new method)

A

old = surgical clipping
new = endovascular coiling

192
Q

What is the endovascular coiling treatment for a stroke?

A

metal coil through groin to brain = seal blood vessels

193
Q

What is epilepsy?

A

uncontrolled, abnormal depolarization of cortical neurons

194
Q

If neurons have a lower threshold are the depolarizing faster or slower?

A

faster

195
Q

What percent of epilepsy is idiopathic?

A

75%

196
Q

What percent of epilepsy is due to trauma, infection, or brain tumors?

A

25%

197
Q

T/F not all seizures are epilepsy;

A

TRUE

198
Q

Describe the presentation of a pt having an epileptic seizure:

A

last a few seconds without loss of posture (pt stares for a while)

199
Q

If you are newly diagnosing a pt with epilepsy, what do you need to find out?

A

if there is a trigger

200
Q

What are a few things that could trigger a pt to have an epileptic seizure?

A

stress, hypoglycemia, loud noises

201
Q

What are two types of seizures?

A

partial/focal or generalized

202
Q

When talking about seizures, what does ‘generalized’ mean?

A

location on both side of brain

203
Q

Do absence, or petit mal, seizures primarily occur in adulthood or childhood?

A

childhood

204
Q

Will children who have absence/petit mal seizures suffer from seizure in adulthood?

A

no

205
Q

Describe what it would look like if a child was having a absence/petit mal seizure:

A

lasts a few seconds, doesn’t lose posture, staring straight ahead then resumes regular activity

206
Q

An absence/petit mal seizure can be an autosomal dominant trait with incomplete ______.

A

penetrance

207
Q

What are two types of generalized seizures?

A

absence/petit mal & tonic-clonic

208
Q

Tonic-clonic, or grand mal, seizures occur in who?

A

children and adults

209
Q

Tonic-clonic seizures follow a prodromal sign. What does this mean?

A

prodromal sign = follows a pattern

210
Q

What are some prodromal signs pt’s will have before a tonic-clonic, or grand mal, seizure?

A
  • auditory sensation
  • nausea
  • muscle twitching (hrs before seizures)
  • an aura before LOC
211
Q

What are two phases of loss of consciousness in tonic-clonic seizures?

A

tonic phase (or ictal phase)
clonic phase

212
Q

Explain the tonic, or ictal phase, of a tonic-clonic seizure:

A

powerful muscle contractions
(arch back and extends limbs 10-30 sec)

213
Q

How long does the tonic phase last in tonic-clonic seizures?

A

10-30 sec

214
Q

Explain the clonic phase of a tonic-clonic seizure:

A

jerking of limbs (1-several min)

215
Q

How long does the clonic phase last in tonic-clonic seizures?

A

1 to several minutes

216
Q

What is the phase called after a pt has a tonic-clonic seizure?

A

postictal phase

217
Q

After a pt has a grand mal seizure, they enter a poetical phase. Describe this phase:

A

when pt regains consciousness after seizure - they are very tired/confused and want to sleep

218
Q

Partial or focal seizures affect how many areas of the brain?

A

one area of the brain

219
Q

Describe the presentation of a pt having a partial or focal seizure:

A
  • one arm jerking
  • head/neck jerking
  • VERY localized
  • pt is conscious
220
Q

How do you treat a pt with seizure disorder?

A
  • try to identify triggers
  • anticonvulsant drugs
221
Q

What is the most common anticonvulsant drug?

A

Dilantin

222
Q

Dilantin is a common anticonvulsant drug that may give pt’s what kind of gun disease?

A

gingival hyperplasia

223
Q

What does Dilantin, an anticonvulsant, do?

A

raises threshold for neurostimualtion

224
Q

What are some side effects of anticonvulsant drugs?

A

dec WBCs, platelets, clotting factors

225
Q

T/F meningococcus in the nasopharynx can cross the mucus membranes:

A

TRUE

226
Q

If meningococcus enters the nasopharynx and crosses the mucus membranes, what can happen?

A

can affect choroid plexus (produced CSF) and can lead to ICP

227
Q

What is the choroid plexus?

A

network of capillaries that produce CSF

228
Q

What are two etiologies of meningitis in children and your adults?

A

Neissseria meningitides
Haemophilus influenzae

229
Q

What is the etiology of meningitis in elderly and very young people?

A

Streptococcus pneumoniae

230
Q

What are 3 sx of meningitis?

A

HA, photophobia, nuchal rigidity

231
Q

What are two physical exams to test for meningitis and explain them:

A
  1. Kernig’s sign - flex hips + knees at right angles and try to extend leg (pain = positive)
  2. Brudzinski’s sign - pt is supine, flex head to neck, pt flexes knees = positive
232
Q

How do you confirm meningitis?

A

test CSF for pathogens

233
Q

What is the treatment for meningitis?

A

antibiotics

234
Q

What are 3 ways a pt could develop a brain abscess

A
  1. ear infection
  2. nose/throat infection
  3. bacterial endocarditis via teeth cleaning in vulnerable pts
235
Q

Encephalitis is the infection of what?

A

connectie tissue + membranes of CNS

236
Q

What are the signs of encephalitis?

A

stiff neck, lethargy, HA, fever

237
Q

T/F encephalitis is bacterial:

A

FALSE - it’s viral

238
Q

Who contracts Western equine encephalitis and how?

A

children via mosquitos

239
Q

Who does St. Louis encephalitis primarily affect?

A

in elderly people across the US

240
Q

What are sx of West Nile encephalitis:

A

flu like sx, HA, fever, can get into nervous system

241
Q

West Nile encephalitis is widespread across what two countries and how is it transmitted?

A

US/Canada via mosquitos

242
Q

What is another name for Lyme disease and what is the bacteria called that is transferred from ticks?

A

Lyme disease = neuroborreliosis
bacteria = Borrelia burgdorferi

243
Q

What are sx of Lyme disease and what is the hallmark sign?

A

sx = flu-like, pain and paresthesia’s on face, severe arthritis

hallmark sign = bulls eye lesion (red lesion w central area)

244
Q

How do you treat Lyme disease?

A

with tetracyclines (doxycycline = Monodox)
MONTHS of antibiotics

245
Q

What nerve can herpes simplex encephalitis (HSV1) travel through?

A

trigeminal nerve - CN 5

246
Q

How do you treat herpes simplex encephalitis (HSV1)?

A

acyclovir (Zovirax)

247
Q

What are some infections that can also affect the nervous system?

A
  • meningitis
  • brain abscess
  • encephalitis
  • Lyme disease
  • herpes simplex encephalitis
248
Q

What are some other infections that can affect the nervous system?

A

rabies, tetanus, poliomyelitis

249
Q

Rabies enters the PNS and travels to the CNS and affects what two brain structure?

A

brain stem + basal ganglia

250
Q

Tetanus is also called what? What does it cause?

A

lockjaw - Clostridium tetani (causes muscle stiffness)

251
Q

What is the treatment for tetanus and what’s the mortality rate?

A

antitoxin (mortality = 50%)

252
Q

Poliomyelitis is a virus that multiplies in what tissue that travels to the CNS? What does it cause?

A

lymphoid tissue (causes severe paralysis)

253
Q

Describe what shingles looks like:

A

erythematous vesicular linear rash

254
Q

T/F shingles affects 1 cranial nerve or 1 dermatome on 1 side of the body

A

TRUE

255
Q

What are two vaccines for herpes zoster?

A

zostrix (65+) & shingrix (2 doses)

256
Q

Pt’s with Guillian-Barre syndrome will have post-infectious ______.

A

polyneuritis

257
Q

Guillian-Barre syndrome is a viral infection that produces what?

A

abnormal immune responses

258
Q

Why do pt’s with Gillian-Barre syndrome get decreased nerve conduction of the legs?

A

because of demyelination of the nerves
(inflammation = axons are destroyed)

259
Q

In Guillian-Barre syndrome, loss of nerve conduction starts where? Which direction does it travel?

A

starts = ankles + feet, knees, legs, diaphragm = fatal
MOVES UPWARDS

260
Q

In Gullian-Barre syndrome, inflammation of the PNS resolves in what direction?

A

opposite direction as it starts (legs, knees, feet + ankles)

261
Q

What is dementia?

A

acquired, progressive, chronic disease of cortical degeneration

262
Q

What are the sx of dementia?

A
  • loss of motor coordination
  • loss of short term and long term memory over time
  • personality changes
263
Q

How many defective genes are found in Alzheimer’s disease?

A

4

264
Q

What do we think causes Alzheimer’s disease?

A
  • dec. Ach
  • plaques & neurofibrillary tangles
265
Q

What do the plaque proteins contain in Alzheimer’s disease?

A

amyloid B-peptide

266
Q

Neurofibrillary tangles in Alzheimer’s disease is a defect in what protein?

A

tau protein

267
Q

What is the treatment for Alzheimer’s disease? What does it inhibit?

A

Aricept (donzepezil) = anticholinesterase inhibitor

268
Q

What are some causes of brain injuries?

A

skill fx, hemorrhage, edema, etc.

269
Q

What is another name for a concussion?

A

mild traumatic brain injury

270
Q

What is a concussion?

A

mild injury to head (movement of brain within skull)

271
Q

Describe some S&S of a concussion. Does permanent brain damage occur?

A
  • temporary amnesia
  • LOC
  • HA
  • no permanent damage (recovery in 24 hrs)
272
Q

What is a countercoup brain injury?

A

where brain bounces from back to front

273
Q

What is an open head injury?

A

skull fx or penetration of brain (ex: bullet wound)

274
Q

What is a basilar skull fracture? What can it cause?

A

fx at base of skull (causes CSF to leak out of brain)

275
Q

What is a head injury due to trauma in babies is called what?

A

shaken baby syndrome

276
Q

List some brain injury sx:

A
  • ICP sx + seizures
  • ottorhea (CSF leaking from ears)
  • otorrhagia (blood leaking from ears)
  • rhinorrhea (CSF leaking from nose)
277
Q

Name one treatment for brain injuries. What does it decrease?

A

steroid medications (dexomethazon) - decreases edema

278
Q

What is a contusion?

A

bruising of brain w rupture of small blood vessels

279
Q

What is the difference between a concussion and a concussion?

A

concussion = mild injury to head where brain moves w/in skull

contusion = bruising of brain w small blood vessel rupture

280
Q

What type of head injury can a concussion and contusion be classified as?

A

closed head injury

281
Q

What is a primary brain injury?

A

direct injury to brain tissue, blood vessels, nerves, etc.

282
Q

Pt’s with a primary brain injury will present with 3 things that start with “I”, what are they?

A

inflammation, ICP, ischemia

283
Q

What is a secondary brain injury?

A

effects of something else causing brain injury

(what is the effect of edema, hemorrhage, hematoma, etc)
(what is happening from that effect?)

284
Q

Where would you see an epidural hematoma in the brain?

A

hemorrhage is between dura & skull
(usually by meningeal artery)

285
Q

Where would you see a subdural hematoma?

A

between dura and arachnoid (cortical veins bleeding into space)

286
Q

What is a common cause of a subarachnoid hemorrhage?

A

rupture of aneurysm

287
Q

Will you see a hematoma on an MRI of a pt who has a subarachnoid hemorrhage?

A

no hematoma bc blood is mixing with CSF

288
Q

What is an intracerebral hematoma

A

a hematoma within brain itself

289
Q

What type of injury can cause vertebrae damage?

A

spinal cord injury

290
Q

What can rip the spinal cord and its ligaments?

A

hyperextension nd hypoflexion

291
Q

How can the spinal cord be damaged?

A
  • penetrating wounds
  • dislocated vertebrae
  • compression fx (fall from height)
  • severing the s.c.
292
Q

What will happen if the spinal cord is severed at T10?

A

irreversible loss of sensory and motor functions inferior to the injury

293
Q

What is spina bifida and what region does it usually occur?

A

defects in the formation of the spine and spinal cord
= common in lumbar region

294
Q

What category of defects does spina bifida fall under?

A

neural tube defects

295
Q

What week of life does the neural tube open into anterior and posterior ends?

A

4th week

296
Q

T/F your entire nervous system is developed from the neural tube

A

TRUE

297
Q

Name 3 types of spina bifida:

A
  1. spina bifida occulta (hidden)
  2. meningocele
  3. myelomeningocele (worst case)
298
Q

What happens in spina bifida occulta? Is there neurological damage?

A

some posterior spinous processed don’t fuse
(no neurological damage)

299
Q

What happens in meningocele spina bifida?

A

meninges herniate through area taking CSF w it

300
Q

In meningocele spina bifida, what does not fuse to form a sac?

A

the vertebrae

301
Q

Within how many days can you do surgery to repair the meninges in meningocele spina bifida? Will there be neurological damage?

A

3 days (neurological damage will be low)

302
Q

What is the worst case of spina bifida?

A

myelomeningocele

303
Q

Describe myelomeningocele spina bifida:

A

open, with meninges - CSF & spinal nerves herniated through unfused vertebrae

304
Q

In myelomeningocele, the spinal process of the vertebra lack fusion. What happens to the spinal nerves in this case?

A

it takes nerves out of vertebrae with it

305
Q

Pt’s with myelomeningocele will experience what sx? Can surgery help this type of spina bifida?

A
  • muscle weakness, possible paralysis, incontinence
  • surgery doesn’t have much benefit (very controversial)
306
Q

The risk of spina bifida increases in babies if the pregnant mother has what deficiency?

A

folic acid

307
Q

Besides mothers with a folic acid deficiency, what other risk factors can cause spina bifida?

A
  • women with uncontrolled diabetes
  • women on anti seizure medication
  • AFP (a-fetoprotein)
308
Q

High levels of AFP (a-fetoprotein) in a mom can cause the baby to develop what?

A

neural tube defects

309
Q

High levels of AFP (a-fetoprotein) in a mom can cause the baby to develop a neural tube defect. How does this happen?

A

produced by fetus’s liver and some enter’s mother’s blood

310
Q

What is cerebral palsy?

A

a non-progressive neurological disorder

311
Q

What is cerebral palsy a result of?

A

genetic mutations that leads to abnormal brain development

312
Q

Cerebral palsy is a result of a generic mutation. How is this genetic mutation caused?

A

possible infectious process of mother

(germinal/rubella, herpes simplex, lack of o2 during delivery)

313
Q

The level of severity of cerebral palsy I can be determined how?

A

if the entire brain is affected or if its just small areas of the brain

314
Q

Cerebral palsy is classified according to what?

A

according to motor disability

315
Q

What are 3 classifications of motor disabilities in cerebral palsy?

A
  1. spastic paralysis
  2. dyskinetic disease
  3. ataxic cerebral palsy
316
Q

What fraction of people who have cerebral palsy have normal cognitive abilities and why?

A

1/3 bc disease is NONPROGRESSIVE

317
Q

What motor disability is most commonly seen in pt’s with cerebral palsy?

A

spastic paralysis

318
Q

What is spastic paralysis and how do pt’s with cerebral plays walk if they have spastic paralysis?

A
  • damage to motor cortex or corticospinal tracts (hyperreflexia)
  • walk on toes and scissors type of gate
319
Q

Dyskinetic disease is a motor disability in pt’s with cerebral palsy. What does dyskinetic disease damage?

A

basal nuclei (or extrapyramidal tracts)

320
Q

You’ll see choreiform movements in pt’s with cerebral palsy. What are chloreiform movements?

A

rapid jerky involuntary movements

321
Q

You’ll see athetoid movements in pt’s with cerebral palsy. Wha are athetoid movements?

A

snake moving, facial expression = grimace or frown

322
Q

Some pt’s with cerebral palsy will have dyskinetic motor disease. What are two types of movements that you may see in these pt’s?

A
  • choreiform movements
  • athetoid movements
323
Q

Ataxic cerebral palsy is a result of damage to the cerebellum in pt’s with cerebral palsy. What other sx may you see if a pt has ataxic CP?

A

seizures, visual problems, hearing problems

324
Q

What is the treatment for cerebral palsy? (hint: not a medication)

A

PT/OT, supportive care

325
Q

What is multiple sclerosis?

A

a progressive neurological disorder

326
Q

Multiple sclerosis is caused by what?

A

myelination of brain and spinal cord neurons

327
Q

Multiple sclerosis is a possibly autoimmune disease of what type of cell?

A

T cells

328
Q

How do T cells in multiple sclerosis begin to degree myelin on nerves?

A

T cells cross BBB in MS

329
Q

How do T cells get through the BBB in multiple sclerosis?

A

an infectious process made BBB more permeable

330
Q

In MS, as nerves are destroyed, myelin develops lesions known as what?

A

plaques or scleroses

331
Q

What virus could be a possible cause of multiple sclerosis?

A

EBV (Epstein-Barr virus)

332
Q

Who does MS affect and at what age?

A

women 2x as much as men (20-40 y/o)

333
Q

What are early S&S of MS?

A
  • blurred vision
  • muscle weakness
  • paresthesia (depends where CNS is being attacked)
  • periods of remission (end up in wheelchair as pt becomes paralyzed)
334
Q

What are two treatments for MS?

A
  • interferon beta-1b (Betaseron - immunosuppressive)
  • steroids (prednisone to decrease inflammation)
335
Q

Huntington’s disease is also known as what?

A

huntingtons chorea

336
Q

What does chorea refer to in Huntington’s chorea?

A

chorea = choreiform movements = rapid jerky involuntary motions

337
Q

Is Huntington’s disease autosomal dominant or autosomal recessive?

A

autosomal dominant

338
Q

Huntington’s disease is a genetic disease carried on what chromosome?

A

chromosome 4

339
Q

When does Huntington’s disease manifest?

A

in adulthood

340
Q

What causes the brain to progressively atrophy in Huntington’s disease?

A

aggregation of proteins

341
Q

What two structures of the brain are affected in Huntington’s chorea?

A

basal ganglia + frontal lobe

342
Q

What two neurotransmitters are decreased in Huntington’s disease and what is a result of this?

A
  • decrease in Ach/GABA
  • increased motor function & decreased cognitive function
343
Q

What is the treatment for Huntington’s disease? What does it do? Is this treatment a cure?

A

Tetrabenazine = decreases chorea/rapid movements
NO CURE

Pathophys (6 decks)

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