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JCNUR172 > NEURO PATHOLOGY > Flashcards

NEURO PATHOLOGY Flashcards

1
Q

3 Classifications of headaches

A

Primary headache, secondary headache, & crania neuralgia/other headache

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2
Q

What are the 3 types of primary headaches?

A

Migraine, tension-type & cluster

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3
Q

What is the definition of a migraine headache?

A

Repeated, episodic headache lasting 4-72 hours

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4
Q

Migraine without aura

A

85% of migraines
lasts 1-3 days
N/V

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5
Q

Migraine with aura

A

Reversible visual symptoms
Reversible sensory symptoms
Aura present

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6
Q

What is required for diagnosis of a migraine?

A 
2 OF THE FOLLOWING:
*unilateral head pain
*throbbing pain
*pain worse with activity
*Mod - severe in intensity
1 OF THE FOLLOWING
*Nausea
*Photophobia
*Phonophobia
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7
Q

Which sex is affected more with migraines?

A

Female

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8
Q

What are the 4 phase of a migraine headache?

A
  • Premonitory Phase (1-2 days prior)
  • Aura phase (20-60 mins)
  • Headache phase
  • Recovery phase
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9
Q

What happens during the aura phase?

A
  • CSD- cortical spreading depression (tingling in occipital lobe=Neurons become depolarized and reduce blood flow occurs
  • Increased cerebral perfusion
  • Decreased electrical activity
  • Decreased blood flow
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10
Q

What happens during the headache phase?

A
  • Decrease in serotonin levels
  • Increase in Substance P=Increase in pain
  • Activation of trigeminovascular system (BV becomes inflammed)
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11
Q

Treatment for migraines

A
  • Nursing Interventions-Environmental, pain assessment/control
  • Education-Triggers
  • Prevention meds-Beta blockers & ACE inhibitors
  • Abortive therapy- Excedrin, Acetaminophen & aspirin
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12
Q

What happens during the recovery phase?

A

Patient experiences lethargy and fatigue

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13
Q

What are the manifestations of cluster headaches?

A
  • Weeks/months then remission
  • severe, unrelenting, unilateral pain
  • rapid onset that lasts 30-90 minutes
  • several times a day
  • eye pain that radiates
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14
Q

What is the pathophysiology of cluster headaches?

A
  • Trigeminal activation
  • Neurologic inflammation
  • Interplay of
    • ANS response
    • Hypothalamus imbalances
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15
Q

Which sex experiences cluster headaches more?

A

Male

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16
Q

What are the associated symptoms of a cluster headache?

A
  • agitation
  • Conjunctival redness
  • Lacrimation
  • Rhinorrhea
  • Sweating
  • Pupil constricton
  • Ptosis (drooping of eyelid)
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17
Q

What are the clinical manifestations of tension headaches?

A
  • less severe, dull, aching diffuse
  • No N/V
  • not affected by activity
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18
Q

What are some theories associated with tension headaches?

A
  • Hypersensitivity of trigeminal nerve
  • Sustained tension
  • Transformed migraine
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19
Q

What can cause a tension headache?

A
  • Psychogenic
    • Anxiety
    • Depression
  • Muscle stress
  • Overuse/withdrawal
    • caffeine
    • analgesics
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20
Q

What are some red flags associated with headaches?

A
  • Sudden onset
  • Progressively worse
  • Occurring with increased CO
  • Associated with
    • change in cognition
    • blurred vision
    • altered vision
    • any other neurological variation
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21
Q

What is normal intracranial pressure?

A

5-15mm HG

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22
Q

What is involved in cerebral blood volume autoregulation?

A
  • CSF (1st)
  • Blood volume adjustments (2nd)
  • Tissue adjustments (3rd)
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23
Q

What is the Monroe-Kellie Hypothesis?

A

If the volume of any of the three compartments increases within crania vault and the volume of the other compartments is displaced , the total intracranial pressure will not change.

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24
Q

What is cerebral oxygenation

A

Measure of oxygen in the internal jugular vein

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25
Q

How is stage 1 of ICP alterations defined?

A
  • CSF forced out
  • Compression of intra-cerebral veins
  • increase in venous vasoconstriction
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26
Q

What are the signs and symptom of Stage 1 ICP alterations?

A

No signs or symptoms.

  • A&0, PERRLA present
  • Eupnea
  • BP & Pulse normal
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27
Q

How is stage 2 of ICP alterations defined?

A
  • arterial BV constrict which lead to decrease in O2 supply to neurons
  • Systemic vessels constrict which lead to an elevation in BP in an attempt to maintain CPP
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28
Q

How is stage 3 of ICP alterations defined?

A
  • ICP approaching CPP
  • Intracranial hypertension
  • tissue hypoxia
  • Hypercapnia
  • acidosis
  • loss of autoregulation
  • additional small volume changes results in dramatic IICP
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29
Q

What are the manifestations of stage 3 ICP (early & late)

A

Early

  • H/A
  • changes in LOC
  • pupils unresponsive/sluggish

Late
*cushings triad
breathing changes

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30
Q

What happens during Stage 4 of ICP?

A
  • lethal with little compliance
  • herniation of brain tissue
  • further ischemia, hypoxia,hemorrhage of tissue
  • systolic BP=ICP=cease of brain blood flow=DEATH
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31
Q

Cingulate Herniation

A

herniation into the falx cerebi

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32
Q

Central Herniation

A

Herniation through the tentorial notch

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33
Q

Uncal Heriation

A

herniation through the tentorial cerebelli

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34
Q

Cerebellar tonsil herniation

A

Herniation towards the tonsils

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35
Q

what is cushings triad?

A
  • hypertension with widening BP
  • Bradycardia
  • Irregular respirations
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36
Q

What are the manifestations of IICP?

A

*Change in LOC
*VS
-RESP
bradypnea, tachypnea, irregular
-TEMP
hyperthermia
-Cushings triad

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37
Q

total brain death

A

Irreversible cessation of function of the entire brain including the brain stem and cerebellum
*coma, no motor, no reflexes, no spont. respirations, isoelectric EEG

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38
Q

Cerebral brain death

A

Death of cerebral hemispheres, brain stem and cerebellum functioning

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39
Q

Types of Cerebral brain death

A
  • PVS- persistent vegetative state
  • MCS - minimally conscious state
  • Locked in syndrome
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40
Q

PVS-Persistent vegetative state

A

no speech, with out cognitive function.

Unresponsive to stimuli

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41
Q

MCS- minimally conscious state

A

Can blink, smile

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42
Q

Locked in syndrome

A

no motor skills
Cognitive use
Eyes function

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43
Q

Hydrocephalus Cause

A
  • overproduction of CSF
  • impaired reabsorption of CSF
  • Obstruction of CSF
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44
Q

Types of hydrocephalus

A 
Noncommunicating
-obstruction of ventricular system
Communicating
-impaired reabsorption
-normal pressure hydrocephalus
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45
Q

Primary/ Direct mechanism of injury r/t hydrocephalus

A

due to impact itself

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46
Q

Secondary mechanism of injury r/t hydrocephalus

A

subsequent cellular and molecular events

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47
Q

Tertiary mechanism of injury r/t hydrocephalus

A

day & months later

consequences and systemic complications

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48
Q

What are the pathogenic patterns associated with hydrocephalus

A
  • enlarged cerebral hemispheres
  • dilated ventricles
  • flattened shallow sulci
  • reduced white matter volume
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49
Q

Considerations with hydrocephalus onset r/t age

A
  • in utero-prior to sutures closing

* adults-sutures closed

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50
Q

Normal pressure hydrocephalus

A

Seen in the elderly
brain atrophy
increased pressure
*reduced cognition, incontinence, unsteady gait

51
Q

Traumatic brain injury (TBI)

A

any structural damage to the head

52
Q

Causes of traumatic brain injury (TBI)

A

MVA #1

53
Q

Ages at risk for traumatic brain injury (TBI)

A

65

54
Q

Types of traumatic brain injury (TBI)

A

Focal-localized

diffused-generalized, damage not localized to one area of the brain

55
Q

signs and symptoms of focal TBI

A

depending on the area and doesn’t usually affect LOC

56
Q

2 Types of Focal TBI’s

A

Lacerations

Contusion

57
Q

Contusion

A

Focal injury
bruising of the brain tissue
associated with closed head injuries
May include: hemorrhage, infarction, necrosis, & edema

58
Q

Hematoma

A 
Focal
2 types 
Venous
Arterial
Escape of blood into the cranium
59
Q

Venous origin hematoma

A

slow bleed, if unrecognized can be ominous

60
Q

Arterial origin hematoma

A

rapid, acute condition with immediate S/S

61
Q

Epidural Hematoma

A

bleeding between dura and skull
can be arterial or venous
Foca

62
Q

signs and symptoms of epidural hematoma

A 
Lucid interval (defining characteristic)
ipsilateral pupil dilation 
contralateral hemiparesis
HA
N/V
Focal symptoms
63
Q

Subdural hematoma

A

Between dura and arachnoid
Venous
classified by timing of symptoms

64
Q

Acute subdural hematoma

A

between dura and arachnoid

presents 24-48 hours

65
Q

S/S of acute subdural hematoma

A

Change in LOC
NO LUCID INTERVAL
HA
Ipsilateral pupil dilation or fixed if IICP

66
Q

Subacute subdural hematoma

A

between dura and arachnoid

presents 2-14 days

67
Q

S/S of Subacute subdural hematoma

A

altered mental status

68
Q

Chronic subdural hematoma

A

between dura and arachnoid

presents weeks to months

69
Q

S/S of chronic subdural hematoma

A

Altered mental status

70
Q

traumatic intracerebral hematoma

A

bleeding within the brain
most common in frontal lobe
elderly & alcoholics

71
Q

S/S of intracerebral hematomas

A

varies d/t size and location

72
Q

Skull fractures

A

identified by the type and the location

73
Q

What are the 5 types of skull fractures

A 
Linear
Depressed
simple
comminuted
compound
74
Q

basilar fracture

A

Linear fracture

s/s over several hours and varies

75
Q

basilar fracture s/s

A 
battle sign- postauriclar ecchymosis
raccoon eyes- peiorbital ecchymosis
Rhinorrhea- tear in the dura and CSF leaking out
otorrhea
CSF drainage
76
Q

how can you test for CSF presence ?

A

Dextrostix

Halo sign

77
Q

diffuse head injury

A

generalized, damage cannot be localized t one area of the brain
axon injury

78
Q

s/s of a diffused head injury

A

alteration in sensory, motor, & cognitive functions & changes to LOC

79
Q

Types of diffuse head injuries

A

concussion

diffuse axon injury

80
Q

concussion

A

a sudden transient mechanical head injury with disruption of neural activity and a change in LOC

81
Q

concussion manifestations

A 
retrograde amnesia
microscopic changes to the brain
neg xray images
"seeing stars"
change in LOC
HA
gait change
loss of reflexes
82
Q

post concussion syndrome

A 
irritability
H/A 
nervousness
insomnia
poor concentration
impaired memory
83
Q

diffuse axonal injury

A
  • widespread axonal injury of subcortical white matter, basal ganglia, thalamus or brainstem
  • trauma causes axon swelling and disconnection
84
Q

S/S of diffuse axonal injury

A

develop over 12/24 hours but persist longer

  • decreased LOC
  • IICP
  • global cerebral edema
  • 90% will remain in a vegetative state
85
Q

intracranial (brain) tumors

A 
collections of neoplasms
each with own 
*histology
*site of origin
*prognosis
*treatment
86
Q

malignant brain tumors

A

cells lack differentiation, invasive and has the ability to metastasize

87
Q

benign brain tumors

A

well differentiated and histological benign BUT can grow and cause death because of their location

88
Q

spinal cord injury

A

damage to the neural element spinal cord with impaired communication (sensory) to the cns and or motor function out of the cns

89
Q

etiology of spinal cord injury

A

high risk

90
Q

sensory ascending - afferent pathways

A

dorsal discriminating pathway

91
Q

dorsal discriminative pathway carries

A

ipsilateral
discriminative touch
light touch
conscious proprioception

92
Q

dorsal discriminative pathway neuron order

A

ipsilateral

93
Q

spinothalamic/anteriolateral tract

A

afferent pathway

94
Q

three concentric subdivisions of cord

A

archilayer
paleolater
neolayer

95
Q

archilayer

A

inner-primitive layer
most developed at birth
RAS reflexes (coma/quickening)

96
Q

paleolayer

A

middle layer
contains spinothalamic tract (sensory info)
fast communication
startle reflex, swallowing

97
Q

neolayer

A

newest- last to develop
highly coordinated movement
contains cortiospinal tracts
bladder training, fine motor movements

98
Q

collateral communication

A

archilayer and paleolayer = bypass damage return of function

99
Q

level of injury dynamic injury

A

spreads two levels

100
Q

cervical damage

A

respiratory

101
Q

damage above t6

A

automatic dysreflexia neurogenic shock risks

102
Q

damage to t12

A

changes to LMN injury

103
Q

primary injury spinal cord injury

A 
irreversible 
initial disruption of axons
within 1 hour
-small hemorrhages in gray matter
-edema of white matter
-necrosis
104
Q

secondary injury of spinal cord injury

A

due to hemorrhage and edema 1-72hr
promotes spread of injury
vascular damage->ischemia
neuronal injury-> spinal shock

105
Q

spinal shock

A 
>t6
immediate 
50% will experience 
last hour, days or weeks
temporary loss of below level of injury
-reflexes
-sensations
-bowel and bladder
-sympathetic vasomotor tone
106
Q

neurogenic(systemic) shock

A 
dt loss of vasomotor control
-hypotension
-bradycardia
dt loss of sympathetic innervation 
-peripheral vasodilation
-venous pooling 
-decreased CO
-hypothermia
107
Q

c6 function

A

adds wrist dorsiflexion

108
Q

spinal cord reflexes

A

spinal reflexes function independently from brain input

alternation depend of injury

109
Q

UMN injury @ T12 or above

A

spinal reflexes intact below level of injury
but no brain communication
spastic paralysis
involuntary muscle movements

110
Q

LMN injury @ T12 or below

A

decreased or absent spinal reflexes
flaccid paralysis
flaccid bladder and bowel

111
Q

automatic dysreflexia

A

acute episode of exaggerated
t6 or higher
stimuli below of injury

112
Q

stimuli below level of injury

A

vasoconstriction

113
Q

stimuli above level of injury

A

parasympathetic response

114
Q

long term complications of spinal cord injury

A

temperature regulation
DVT - first 2-3 weeks
edema
skin integrity

115
Q

define a motor unit

A

1 unit that all muscles stimulate

116
Q

disuse atrophy

A

atrophy due to disuse of muscle- wastes away

117
Q

degenerative atrophy

A

muscle wastes away and is replaced with fiberous tissue

118
Q

myasthenia gravis

A

autoimmune disease-disorder of NMJ
antibody-mediated loss of acetylcholine
-IgG antibodies against AcH receptors block the receptor sites

119
Q

clinical manifestations of myasthenia gravis

A 
muscle weakness
fatigue
diplopia 
ptosis
dysphagia 
speech impairments
120
Q

Myasthenic crisis

A

worsened by certain events

  • illness
  • emotional issue
  • pregnancy
121
Q

monoeuropathies

A

localized condition such as trauma, compression or infection that affects a single nerve, plexus or peripheral nerve trunk

122
Q

trigeminal neuralgia

A

damage to CN V-afferent pathway only

  • compression
  • viral
  • irritation
  • excessive firing
123
Q

clinical manifestations

A

stabbing pain 2-3 minutes and clustering
-knife life
tics/spasms

JCNUR172 (2 decks)

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