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JCNUR172 > NEURO PATHOLOGY > Flashcards

NEURO PATHOLOGY Flashcards

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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
How is stage 1 of ICP alterations defined?
* CSF forced out * Compression of intra-cerebral veins * increase in venous vasoconstriction
26
What are the signs and symptom of Stage 1 ICP alterations?
No signs or symptoms. * A&0, PERRLA present * Eupnea * BP & Pulse normal
27
How is stage 2 of ICP alterations defined?
* 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
28
How is stage 3 of ICP alterations defined?
* ICP approaching CPP * Intracranial hypertension * tissue hypoxia * Hypercapnia * acidosis * loss of autoregulation * additional small volume changes results in dramatic IICP
29
What are the manifestations of stage 3 ICP (early & late)
Early * H/A * changes in LOC * pupils unresponsive/sluggish Late *cushings triad breathing changes
30
What happens during Stage 4 of ICP?
* lethal with little compliance * herniation of brain tissue * further ischemia, hypoxia,hemorrhage of tissue * systolic BP=ICP=cease of brain blood flow=DEATH
31
Cingulate Herniation
herniation into the falx cerebi
32
Central Herniation
Herniation through the tentorial notch
33
Uncal Heriation
herniation through the tentorial cerebelli
34
Cerebellar tonsil herniation
Herniation towards the tonsils
35
what is cushings triad?
* hypertension with widening BP * Bradycardia * Irregular respirations
36
What are the manifestations of IICP?
*Change in LOC *VS -RESP bradypnea, tachypnea, irregular -TEMP hyperthermia -Cushings triad
37
total brain death
Irreversible cessation of function of the entire brain including the brain stem and cerebellum *coma, no motor, no reflexes, no spont. respirations, isoelectric EEG
38
Cerebral brain death
Death of cerebral hemispheres, brain stem and cerebellum functioning
39
Types of Cerebral brain death
* PVS- persistent vegetative state * MCS - minimally conscious state * Locked in syndrome
40
PVS-Persistent vegetative state
no speech, with out cognitive function. | Unresponsive to stimuli
41
MCS- minimally conscious state
Can blink, smile
42
Locked in syndrome
no motor skills Cognitive use Eyes function
43
Hydrocephalus Cause
* overproduction of CSF * impaired reabsorption of CSF * Obstruction of CSF
44
Types of hydrocephalus
``` Noncommunicating -obstruction of ventricular system Communicating -impaired reabsorption -normal pressure hydrocephalus ```
45
Primary/ Direct mechanism of injury r/t hydrocephalus
due to impact itself
46
Secondary mechanism of injury r/t hydrocephalus
subsequent cellular and molecular events
47
Tertiary mechanism of injury r/t hydrocephalus
day & months later | consequences and systemic complications
48
What are the pathogenic patterns associated with hydrocephalus
* enlarged cerebral hemispheres * dilated ventricles * flattened shallow sulci * reduced white matter volume
49
Considerations with hydrocephalus onset r/t age
* in utero-prior to sutures closing | * adults-sutures closed
50
Normal pressure hydrocephalus
Seen in the elderly brain atrophy increased pressure *reduced cognition, incontinence, unsteady gait
51
Traumatic brain injury (TBI)
any structural damage to the head
52
Causes of traumatic brain injury (TBI)
MVA #1
53
Ages at risk for traumatic brain injury (TBI)
65
54
Types of traumatic brain injury (TBI)
Focal-localized | diffused-generalized, damage not localized to one area of the brain
55
signs and symptoms of focal TBI
depending on the area and doesn't usually affect LOC
56
2 Types of Focal TBI's
Lacerations | Contusion
57
Contusion
Focal injury bruising of the brain tissue associated with closed head injuries May include: hemorrhage, infarction, necrosis, & edema
58
Hematoma
``` Focal 2 types Venous Arterial Escape of blood into the cranium ```
59
Venous origin hematoma
slow bleed, if unrecognized can be ominous
60
Arterial origin hematoma
rapid, acute condition with immediate S/S
61
Epidural Hematoma
bleeding between dura and skull can be arterial or venous Foca
62
signs and symptoms of epidural hematoma
``` Lucid interval (defining characteristic) ipsilateral pupil dilation contralateral hemiparesis HA N/V Focal symptoms ```
63
Subdural hematoma
Between dura and arachnoid Venous classified by timing of symptoms
64
Acute subdural hematoma
between dura and arachnoid | presents 24-48 hours
65
S/S of acute subdural hematoma
Change in LOC NO LUCID INTERVAL HA Ipsilateral pupil dilation or fixed if IICP
66
Subacute subdural hematoma
between dura and arachnoid | presents 2-14 days
67
S/S of Subacute subdural hematoma
altered mental status
68
Chronic subdural hematoma
between dura and arachnoid | presents weeks to months
69
S/S of chronic subdural hematoma
Altered mental status
70
traumatic intracerebral hematoma
bleeding within the brain most common in frontal lobe elderly & alcoholics
71
S/S of intracerebral hematomas
varies d/t size and location
72
Skull fractures
identified by the type and the location
73
What are the 5 types of skull fractures
``` Linear Depressed simple comminuted compound ```
74
basilar fracture
Linear fracture | s/s over several hours and varies
75
basilar fracture s/s
``` battle sign- postauriclar ecchymosis raccoon eyes- peiorbital ecchymosis Rhinorrhea- tear in the dura and CSF leaking out otorrhea CSF drainage ```
76
how can you test for CSF presence ?
Dextrostix | Halo sign
77
diffuse head injury
generalized, damage cannot be localized t one area of the brain axon injury
78
s/s of a diffused head injury
alteration in sensory, motor, & cognitive functions & changes to LOC
79
Types of diffuse head injuries
concussion | diffuse axon injury
80
concussion
a sudden transient mechanical head injury with disruption of neural activity and a change in LOC
81
concussion manifestations
``` retrograde amnesia microscopic changes to the brain neg xray images "seeing stars" change in LOC HA gait change loss of reflexes ```
82
post concussion syndrome
``` irritability H/A nervousness insomnia poor concentration impaired memory ```
83
diffuse axonal injury
* widespread axonal injury of subcortical white matter, basal ganglia, thalamus or brainstem * trauma causes axon swelling and disconnection
84
S/S of diffuse axonal injury
develop over 12/24 hours but persist longer * decreased LOC * IICP * global cerebral edema * 90% will remain in a vegetative state
85
intracranial (brain) tumors
``` collections of neoplasms each with own *histology *site of origin *prognosis *treatment ```
86
malignant brain tumors
cells lack differentiation, invasive and has the ability to metastasize
87
benign brain tumors
well differentiated and histological benign BUT can grow and cause death because of their location
88
spinal cord injury
damage to the neural element spinal cord with impaired communication (sensory) to the cns and or motor function out of the cns
89
etiology of spinal cord injury
high risk
90
sensory ascending - afferent pathways
dorsal discriminating pathway
91
dorsal discriminative pathway carries
ipsilateral discriminative touch light touch conscious proprioception
92
dorsal discriminative pathway neuron order
ipsilateral
93
spinothalamic/anteriolateral tract
afferent pathway
94
three concentric subdivisions of cord
archilayer paleolater neolayer
95
archilayer
inner-primitive layer most developed at birth RAS reflexes (coma/quickening)
96
paleolayer
middle layer contains spinothalamic tract (sensory info) fast communication startle reflex, swallowing
97
neolayer
newest- last to develop highly coordinated movement contains cortiospinal tracts bladder training, fine motor movements
98
collateral communication
archilayer and paleolayer = bypass damage return of function
99
level of injury dynamic injury
spreads two levels
100
cervical damage
respiratory
101
damage above t6
automatic dysreflexia neurogenic shock risks
102
damage to t12
changes to LMN injury
103
primary injury spinal cord injury
``` irreversible initial disruption of axons within 1 hour -small hemorrhages in gray matter -edema of white matter -necrosis ```
104
secondary injury of spinal cord injury
due to hemorrhage and edema 1-72hr promotes spread of injury vascular damage->ischemia neuronal injury-> spinal shock
105
spinal shock
``` >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
neurogenic(systemic) shock
``` dt loss of vasomotor control -hypotension -bradycardia dt loss of sympathetic innervation -peripheral vasodilation -venous pooling -decreased CO -hypothermia ```
107
c6 function
adds wrist dorsiflexion
108
spinal cord reflexes
spinal reflexes function independently from brain input | alternation depend of injury
109
UMN injury @ T12 or above
spinal reflexes intact below level of injury but no brain communication spastic paralysis involuntary muscle movements
110
LMN injury @ T12 or below
decreased or absent spinal reflexes flaccid paralysis flaccid bladder and bowel
111
automatic dysreflexia
acute episode of exaggerated t6 or higher stimuli below of injury
112
stimuli below level of injury
vasoconstriction
113
stimuli above level of injury
parasympathetic response
114
long term complications of spinal cord injury
temperature regulation DVT - first 2-3 weeks edema skin integrity
115
define a motor unit
1 unit that all muscles stimulate
116
disuse atrophy
atrophy due to disuse of muscle- wastes away
117
degenerative atrophy
muscle wastes away and is replaced with fiberous tissue
118
myasthenia gravis
autoimmune disease-disorder of NMJ antibody-mediated loss of acetylcholine -IgG antibodies against AcH receptors block the receptor sites
119
clinical manifestations of myasthenia gravis
``` muscle weakness fatigue diplopia ptosis dysphagia speech impairments ```
120
Myasthenic crisis
worsened by certain events - illness - emotional issue - pregnancy
121
monoeuropathies
localized condition such as trauma, compression or infection that affects a single nerve, plexus or peripheral nerve trunk
122
trigeminal neuralgia
damage to CN V-afferent pathway only - compression - viral - irritation - excessive firing
123
clinical manifestations
stabbing pain 2-3 minutes and clustering -knife life tics/spasms

JCNUR172 (2 decks)

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