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CV487 > Class 6: Neurological > Flashcards

Class 6: Neurological Flashcards

1
Q

Primary motor area

A

-Precenteral gyrus; motor control & movement on the opposite side of the body

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2
Q

Supplemental motor area

A

-Anterior to precenteral gyrus; proximal muscle activity, stance, gait, spontaneous movement & coordination

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3
Q

Somatic sensory area

A

Postcentral gyrus; process sensory response from opposite side of the body

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4
Q

Association sensory areas (PAPA)

A

-Parietal lobe; integrates somatic & sensory inputs
-Posterior temporal lobe; integrates visual & auditory language comprehension
-Anterior temporal lobe; integrates past experiences
-Anterior frontal lobe; controls higher-order processes

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5
Q

Basal ganglia

A

-Near lateral ventricles of both hemispheres; control & facilitate autonomic movements

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6
Q

Thalamus

A

-Below basal ganglia
-Relays sensory & motor inputs to the cortex

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7
Q

Hypothalamus

A

Regulates endocrine & autonomic functions

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8
Q

Limbic system

A

-Lateral to hypothalamus
-Influences affective behaviour & basic drives (feeding & sexual behaviour)

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9
Q

Slide 8

A
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10
Q

LOC + disorientation

A

Beginning loss of consciousness; first to time then place, then memory and finally to self recognition

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11
Q

LOC + lethargy

A

Limited spontaneous movement or speech; easy arousal with normal speech or touch; possibly a&o x3

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12
Q

LOC + obtundation

A

Mild to moderate reduction in arousal with limited response to environment, falls asleep unless stimulated, answers questions with minimal response

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13
Q

LOC + Stupor

A

Condition of deep sleep or unresponsiveness unless vigorous & repeated stimulation; response is often withdrawal or grabbing at stimulus (withdrawal better than grabbing)

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14
Q

LOC + Coma

A

No verbal response to any stimuli; noxious stimuli such as deep pain or suctioning do not yield movement

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15
Q

LOC + Light coma

A

Associated with purposeful movement on stimulation

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16
Q

LOC + coma

A

Associated with nonpurposeful movement only on stimulation

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17
Q

LOC + Deep coma

A

Associated with unresponsiveness or no response to any stimuli

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18
Q

Neurological assessment

A

-GCS
-NIH stroke scale
-Orientation/NVS
-Spinal signs
-Pupils & LOC always

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19
Q

Neuro assessment steps

A
  1. NOD, assess A&O x3 (skip to 2 if unconscious)
  2. Vitals
  3. NVS
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20
Q

NVS

A

-Eye opening (spontaneous, to speech, to pain or none)
-Best verbal response (A&O x3, confused? Innapropriate words, incomprehensible sounds, none)
-Best motor response (obeys command, localizes pain, flexion withdrawal, flexion abnormal, extension abnormal, none)

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21
Q

Slide 18 & 19

A
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22
Q

Pupillary response + metabolic imbalance

A

Small, reactive & regular

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23
Q

Pupillary response in dysfunction of tectum (roof) of the midbrain

A

Large “fixed” hippus

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24
Q

Pupillary response + pontine dysfunction

A

Pinpoint

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25
Q

Pupillary response + midbrain dysfunction

A

Midposition and fixed

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26
Q

Pupillary response + dysfunction of third cranial nerve

A

Sluggish, dilated, and fixed

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27
Q

Pupillary response + diencephalic dysfunction

A

Small & reactive

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28
Q

Abnormal posturing

A

Abnormal response to pain, limb goes into extension

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29
Q

Abnormal motor responses with decreased responsiveness (decorticate & decerebrate)

A

-Decorticate; hemispheric damage above the midbrain releasing medullary and pontine reticulospinal systems
-Decerebrate; opisthotonos (associated with severe damage involving midbrain or upper pons), acute brain injury (causes limb extension regardless of location)

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30
Q

Abnormal motor responses with decreased responsiveness (others)

A

-Extensor responses in upper extremities accompanied by flexion in lower extremities; pons
-Flaccid state with little or no motor response to stimuli; lower pons & upper medulla

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31
Q

Slide 22, is decerebrate or decorticate worse?

A

-Note plantar flexion in both
-Decerebrate is worse

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32
Q

NVS/CNS

A

-LOC (GCS), PERRLA, lightheadedness, dizzy
-Pain, sedation/analgesic/sleep
-ICP, external ventricular drain, cerebrospinal drainage, C-spine traction/braces
-Halo sign, otorrhea & battle sign

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33
Q

Apneusis

A

-Prolonged inspiratory cramp (pause at full inspiration); common variant is a brief end-inspiratory pause of 2 or 3 seconds often alternating with an end-expiratory pause
-Damage to respiratory control mechanism at the pontine level; pontine infarction but documented with hypoglycemia, anoxia & meningitis

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34
Q

Central neurogenic hyperventilation

A

-Sustained deep, rapid, but regular pattern (hyperpnea) occurs, with a decreased PaCO2 and a corresponding increase in pH & PO2
-Result of CNS damage or disease involving the midbrain & upper pons; seen after IICP and blunt head trauma

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35
Q

Cheyne-stokes respirations

A

Smooth increasing breathing pattern (crescendo) in rate and depth of breathing (hyperpnea), which peaks and is followed by a gradual smooth decrease (decrescendo) in rate and depth of breathing to the point of apnea. The hyperpneic phase lasts longer than the apneic phase

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36
Q

Cheyne-stoke respirations location of injury

A

Bilateral dysfunction of deep cerebral or diencephalic structures; seen with supraentorial injury and metabolically induced coma states

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37
Q

Cluster breathing

A

-Cluster of breaths with irregular pauses between breaths
-Dyfunction in lower pontine and high medullary areas

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38
Q

Ataxic breathing

A

-Irregular breathing occurs, random shallow & deep breaths and irregular pauses, rate is often slow
-Primary dysfunction of medullary neurons that control breathing
-Reticular formation of the medulla

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39
Q

Abnormal oculomotor responses

A

-Slide 27
-Dolls eyes
-Cold water test; brain dead pt will not respond
-Eyes move with the head and do not deviate

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40
Q

Mechanisms in the lower brainstem

A

-Hiccuping, vomiting and yawning are r/t the medulla
-Projectile vomiting w/o nausea represents a compression of the medulla
-Vomiting w/o nausea indicates a neuro problem

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41
Q

Pain, sensation & dermatomes

A

-Assess from bottom up
-Slide 29

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42
Q

Alterations in cerebral hemodynamics

A

-Brain reacts to an injury through aCerebral blood flow, ICP and O2 delivery
-Changes in cerebral blood flow d/t :
-Inadequate cerebral perfusion, normal cerebral perfusion, or elevated ICP

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43
Q

IICP pathophysiology

A

-If the pressure is able to be displaced to a cranial vault, the pressure is unchanged
-If the pressure is unable to be displaced to another area then IICP

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44
Q

Etiology of IICP

A

-Increased in intracranial content; tumor
-Edema, excess CSF
-Intracranial hematomas or Hemorrhage
-Metabolic and physiological factors; C02, 02, fever, pain
-Vascular anomalies; Arteriovenous malformations (spider web; cluster of thin walled arteries & vein, increased risk for hemorrhage)

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45
Q

Increased breathing + IICP

A

-Increased breathing increases ICP

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46
Q

Fever + IICP

A

Fever increases metabolic rate resulting in an IICP

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47
Q

Nursing management of IICP

A

Head of bed at 30 degrees, lights low, calm

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48
Q

Progression of IICP: Stage 1

A

-Stage 1: Intracranial HTN; little change in ICP, no manifestations except through ICP monitoring, vasoconstriction and external compression of the venous system compensates

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49
Q

Progression of IICP: Stage 2

A

-Intracranial HTN; IICP, O2 changes, systemic arterial vasoconstriction occurs to elevate the systemic BP to overcome IICP
-Manifestations: Confusion, restless, drowsy, aPupillary & breathing

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50
Q

Progression of IICP: Stage 3

A

-Intracranial HTN; hypoxia & hypercapnia, dramatic changes to condition, cushing’s triad presents
-Manifestations; aArousal or central neurogenic hyperventilation, widened pulse pressure, bradycardia, small sluggish pupils

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51
Q

Progression of IICP: Stage 4

A

-Intracranial HTN; brain shifts & herniates, compromised blood supply causing ischemia & hypoxia, increased pressure leads to small hemorrhages, obstructive hydrocephalus

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52
Q

IICP priority assessments

A

LOC & pupillary changes

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53
Q

Pressure on ocular nerve

A

aVision, dizzy, affects RAS

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54
Q

Cerebral edema types

A

Vasogenic cerebral edema; caused by increased permeability of the capillary endothelium
Cytotoxic cerebral edema; increment in total brain water produced, cells swell
Interstitial cerebral edema

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55
Q

IICP manifestations

A

-aLOC & VS
-Cushing’s Triad (widening pulse pressure, bradycardia, irregular respirations
-Ocular signs
-Decreased motor function; abnormal posturing
-Headache, vomiting

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56
Q

Nursing assessment of IICP

A

-Pupils, VS, gait, movement, posturing & headache

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57
Q

Early signs of IICP

A

-Compensatory mechanisms intact
-aLOC, unilateral pupil change in PERRLA
-aResp
-Unilateral hemiparesis

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58
Q

Early variable signs of IICP

A

-Focal findings (aSpeech & vision)
-Papilledema
-Vomiting, headache & seizures

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59
Q

Late signs of IICP

A

-Compensatory mechanisms failing
-Decreased LOC
-Unilateral/bilateral PERRLA
-Ineffective breathing (cheyne-stokes)
-aMotor response (decorticate or decerebrate)

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60
Q

Late/terminal variable signs of IICP

A

-HTN with widened pulse pressure
-Bradycardia
-Hyperthermia

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61
Q

Terminal signs of IICP

A

-Coma
-Bilateral fixed & dilated pupils
-Respiratory arrest
-Absence of motor response (flaccid)

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62
Q

At 41 degrees

A

More prone to seizures

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63
Q

At 43 degrees

A

w/o correction will lead to death

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64
Q

IICP assessment (neuro)

A

-aLOC, monitor for deterioration to worst case
-Coma & unresponsive
-Pupillary changes unilaterally & bilaterally, equal, abnormal in shape, size, reactivity
-Does the patient follow commands, MP weak/strong, equal upper/lower; abnormal posturing, flaccid
-Headache, aVision

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65
Q

IICP assessment (CV)

A

-Bradycardia, widening pulse pressure (sign of Cushing’s triad), HTN
-Are there any changes in perfusion, cap refill, pulses

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66
Q

IICP assessment (resp)

A

-Monitor for changes in respirations: Bradypnea, tachypnea, irregular, Cheyne’s stoke present or absent

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67
Q

IICP assessment (renal)

A

-Urine output, is it > or < 30 cc/hr, colour, consistency, frequency, 24 hour fluid balance

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68
Q

Slide 40

A
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69
Q

Traumatic brain injury

A

-Alteration in brain function
-Caused by an external force; falls are most common
-Classified as primary or secondary

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70
Q

Primary brain injury (focal brain injury) + closed

A

-Coup/ contrecoup, contusions
-Epidural & subdural hematomas
-Subarachnoid hemorrhage

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71
Q

Primary brain injury (focal brain injury) + open

A

-Compound fracture (diffuse axonal injury can occur with a focal injury)

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72
Q

Secondary brain injury

A

Cell death

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73
Q

Primary injury (focal brain injury)

A

-Scalp laceration, skull fracture, contusions
-Epidural subdural, intracerebral and subarachnoid hemorrhages

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74
Q

Diffuse (acceleration/deceleration rotation)

A

-Concussion
-Diffuse axonal injury: Mild to severe over widespread area

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75
Q

Secondary brain injuries

A

-Hypotension, hypoxia, cerebral ischemia, cerebral edema
-Impaired autoregulation of blood flow
-IICP, inflammation, neuronal death
-Excitotoxicity, oxidative stress
-Vascular injury and blood brain dysfunction

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76
Q

Traumatic brain injury definition

A

-Any trauma to the scalp, the skull or the brain
-High potential for a poor outcome

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77
Q

Types of traumatic brain injuries

A

-Scalp lacerations (focal/open)
-Skull fractures (focal/open):
-Linear or depressed
-Simple, comminuted or compound
-Open or closed

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78
Q

Comminuted skull fracture

A

Multiple linear fractures with bone fragmentation (direct high momentum impact)

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79
Q

Compound skull fracture

A

Depressed skull fracture and scalp laceration with communicating pathway to intracranial cavity

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80
Q

Diffuse brain injury

A

-Involves widespread areas of the brain
-Acceleration & deceleration, such as whiplash and rotation causes shearing of axonal fibers and white matter tracts
-Not immediately associated with intracranial HTN but brain swelling caused by increased blood flow, vasodilation, and increased blood volume can result in death

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81
Q

DAI can…

A

Breaks capillaries in their eyelids

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82
Q

Hemotomas & types

A

-Collection of blood
-Epidural
-Subdural: acute, subacute & chronic
-Intracerebral: Intracranial & subarachnoid

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83
Q

Epidural hematoma

A

Collection of blood from bleeding between the dura and the inner surface of the skull

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84
Q

Subdural hematoma

A

Collection of blood that results from bleeding between the dura mater and the arachnoid layer of the meningeal covering of the brain

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85
Q

Subdural hematoma acute stage

A

-Manifest within 48 hours

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86
Q

Subdural hematoma subacute stage

A

2-14 days

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87
Q

Chronic subdural hematoma

A

Develops over weeks or months after a seemingly minor head injury

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88
Q

In a right sided fall, look for

A

Right pupillary changes

89
Q

Intracerebral (intracranial) hematoma

A

-Collection of blood within the parenchyma that results from bleeding within the brain tissue
-Occurs in the frontal and temporal lobes
-Blood cannot be evacuated

90
Q

Traumatic subarachnoid hematoma

A

-Hemorrhage d/t traumatic forces that damage the vascular structure in the subarachnoid space
-May predispose the patient to cerebral vasospasm and diminished cerebral blood flow, increasing the risk of ischemic damage

91
Q

Nursing assessment of hematomas

A

Monitor for signs of IICP, GCS, NVS, Kernig sign and Brudzinski sign (SAH) & airway compromise

92
Q

In concussions time is most important

A
93
Q

Mild concussion

A

-Loss of consciousness may last >30 min , usually caused by blunt force
-GCS= 13-15, confusional state last 1 to several minutes
-Headache, N/V, difficulty concetrating & sleeping for a few days
-May need a CT

94
Q

Moderate concussion

A

-Loss of consciousness >30mins>6 hours
-GCS= 9-12
-Possible skull fracture, no brainstem injury
-Transitory decerebration or decorticate posturing may occur
-Amnesia may last >24 hrs
-Abnormal brain imaging

95
Q

Moderate concussion problems

A

-Permanent deficits in selective attention, vigilance, detection, working memory, data processing, vision or perception and language, may also be mood and affect changes ranging from mild to severe

96
Q

Basal skull fracture

A

-Fracture to the base of skull
-‘Battle sign’, bruising behind the ear
-CSF may drain from the nose (rhinorrhea) and ear (otorrhea)
-Halo sign (blood encircled with yellowish CSF)

97
Q

Severe concussion

A

-Loss of consciousness for > 6 hrs
-GCS= 3-8
-Permanent neurological deficits

98
Q

Severe concussion + learning

A

Inability to learn and reason, inability to modulate behavior

99
Q

Severe concussion + coordination & communication

A

Compromised coordination and verbal and written communication

100
Q

Severe concussion + pulmonary

A

Pulmonary complications occur with severe sensorimotor and cognitive system deficits

101
Q

Severe concussion manifestations

A

Pupillary changes, cardiac and respiratory symptoms, decorticate or decerebrate posturing, and abnormal reflexes

102
Q

Severe concussion + IICP

A

IICP appears 4 to 6 days after injury

103
Q

Cerebral laceration means…

A

There is a tearing of the brain associated with DAI

104
Q

Cognitive deficits associated with TBIs

A

-Hydrocephalus
-Sensory-motor disorders, including pain, paresis, and paralysis
-Loss of coordination

105
Q

Post concussion syndrome

A

-Weeks to months
-Headache, dizziness, fatigue, nervousness/anxiety, irritability, insomnia, depression, inability to concentrate and forgetfulness
Careful monitoring for first 24 hrs to ensure no bleeding

106
Q

Post traumatic seizures

A

-Most often in open brain injuries
-Occurs within days of event and up to 2-5 years

107
Q

Chronic traumatic encephalopathy

A

-Progressive and dementing disease that develops with repeated brain injury
-Leads to violent displays of behaviors

108
Q

Monitor which levels in TBIs

A

Na+

109
Q

Traumatic brain injury assessment (neuro)

A

-LOC, monitor for deterioration to worst case, coma & unresponsive, pupillary changes unilaterally and bilaterally, equal, abnormal in shape, size, reactivity
-Does the patient follow commands, MP weak/strong, equal upper/lower; abnormal posturing, flaccid
-Headache, aVision

110
Q

TBI CV assessment

A

bradycardia & widening pulse pressure (sign of Cushing’s triad), HTN, aPerfusion, cap refill, pulses

111
Q

TBI resp assessment

A

Monitor for changes in respirations: Bradypnea, tachypnea, irregular, Cheyne’s stoke present or absent

112
Q

TBI renal assessment

A

Urine output, is it > or < 30 cc/hr, colour, consistency, frequency, 24 hour fluid balance

113
Q

Spinal cord injury (SCI) common causes

A

Common causes include MVCs, falls, work place related injuries, sports injuries, medical conditions and violence

114
Q

Pathophysiology of SCIs

A

-Initial injury; primary & secondary injuries
-Spinal and neurogenic shock

115
Q

SCI + initial injury + primary vs secondary injuries

A

-Occurs d/t compression by bone displacement, tumor or abscess or from interruption of blood supply to the cord
-Primary injury: Occurs with a fracture of dislocation of the spinal cord column
-Secondary injury: Involves vascular dysfunction, edema, ischemia, electrolyte shifts, inflammation, free radical production and apoptotic cell death

116
Q

Spinal shock

A

-Characterized by decreased reflexes, loss of sensation and flaccid paralysis below the level of injury; lasts days to months
-Pt can recover from spinal shock

117
Q

Neurogenic shock

A

Caused by loss of vasomotor tone and manifested by HYPOTENSION, BRADYCARDIA, and hypothermia.. All other forms of shock result in tachycardia

118
Q

MOA of SCI

A

Flexion, hyperextension, flexion-rotation, extension-rotation and compression

119
Q

Flexion SCI

A

Forward dislocation resulting in damage to the spinal cord & ruptured posterior ligaments

120
Q

Hyperextension SCI

A

Ruptured anterior ligament and compressed posterior ligaments

121
Q

Compression fracture SCI

A

Compression of spinal cord & fractured vertebrae

122
Q

Flexion-rotation SCI

A

Displacement of vertebrae

123
Q

Tool used to assess spinal cord injuries

A

Association impairment scale, r/t sensory & motor function

124
Q

Injury below T6

A

Paraplegic

125
Q

Injury above T6

A

Quadraplegic

126
Q

T6 is where

A

At the nipple line

127
Q

SCI degree of injury

A

-Central cord syndrome
-Anterior cord syndrome
-Posterior cord syndrome
-Brown-Sequard syndrome

128
Q

Central cord syndrome

A

-Complete loss of arm movement, partial leg function & sensation remains
-GI/GU are partially spared
-Recover motor & sensory slowly in legs & trunk

129
Q

Anterior cord syndrome

A

-Complete loss of movement, partial or complete loss of sensation except to pressure & vibration which remains intact

130
Q

Posterior cord syndrome

A

-Movement & sensation preserved
-Difficulty walking

131
Q

Brown-Sequard syndrome

A

-MP impaired on injured side, pain and temperature sensation remain normal.
-MP normal on unaffected side, pain and temperature sensation are reduced or absent.
-Having 1 leg that functions is very helpful in ADLs

132
Q

SCI resp manifestations

A

> T6; PE, difficulty coughing

133
Q

SCI CV manifestations

A

->T6; bradycardia & hypotension d/t peripheral vasodilation, hypovolemia, & ortho hypotension

134
Q

SCI GU/GI manifestations

A

-GU; retention
-GI; >T5; hypomotility causing paralytic ileus, gastric distention, may need to disimpact

135
Q

SCI thermoregulation

A

Cannot regulate temp in high cervical injuries

136
Q

SCI peripheral vascular conditions

A

Virchow’s triad, DVT

137
Q

Autonomic dysreflexia/hyperreflexia

A

-EMERGENCY HTN event
-Caused by noxious stimuli; once stimuli is removed the problem is resolved
-Sudden HTN (240/12 or higher than usual ie. 100/70 to 140/90)
-Management is to remove stimuli

138
Q

Manifestations of autonomic dysreflexia/hyperreflexia

A

-Severe headache
-Flush face & neck with upper chest perspiration
-Appears anxious, cold & goose bumps on lower extremities

139
Q

Slide 66

A
140
Q

CVA pathophysiology

A

-Interruption of blood flow in the brain
-Classified as global hypo-perfusion, ischemic or hemorrhagic stroke
-Caused by: Impairment in autoregulation, changes in blood flow, increased CO2 & ICP, low arterial levels, & aBP

141
Q

Types of CVA

A

-Ischemic, hemorrhagic, r/t hypoperfusion

142
Q

TIA is a..

A

-Precursor to stroke
-Last less than an hour, unable to move

143
Q

Ischemic stroke

A

-Classified as a TIA
-Transient episode of neurological dysfunction
-Acute infarction of the brain
-Symptoms last less than 1 hour, most resolve on their own
-Result of a micro-emboli

144
Q

Manifestations of an ischemic stroke

A

Temporary loss of vision, transient hemiparesis, numbness or loss of sensation, or a sudden inability to speak

145
Q

Types of ischemic strokes

A

-Thrombotic; occurs from injury to a blood vessel and formation of a clot, most commonly the result of atherosclerosis
-Embolic stroke; occurs when an embolus lodges in an occluded cerebral artery

146
Q

Thrombotic stroke pathophysiology

A

-Blood vessel becomes narrowed or occluded causing primary injury (no flow) and secondary injury (low flow)
-Lacunar stroke refers to a stroke from an occlusion of a small penetrating artery

147
Q

Thrombotic stroke manifestations

A

-Motor hemiplegia, sensory stroke, contralateral leg and face weakness with arm and leg ataxia, & isolated motor or sensory stroke

148
Q

Embolic stroke associated conditions

A

Heart conditions

149
Q

Hemorrhagic stroke pathophysiology

A

-Result of bleeding into the brain tissue (intracerebral hemorrhage) or into the subarachnoid space (subarachnoid hemorrhage-SAH)
-Ischemic strokes can lead to hemorrhagic strokes

150
Q

CVA manifestations

A

-Motor function; swallowing, respiratory, gait
-Communication; broca’s (expressive) & Wernicke’s (receptive) aphasia, amnesia and global aphasia
-Affect & intellectual Function
-Spatial-Perceptual Alterations; anosognosia, homonymous hemianopia, agnosia, apraxia

151
Q

Anosognosia

A

Know they have a problem but deny it

152
Q

Homonymous hemianopia

A

Visual changes

153
Q

Agnosia

A

Cannot recognize an object by sight, touch or hearing

154
Q

Apraxia

A

Cannot complete a task with sequential events

155
Q

Left hemisphere is…

A

Most dominant for language in those that are right handed and some that are left handed

156
Q

Amnesia in terms of speech

A

Cannot find the correct word

157
Q

Global aphasia

A

Expressive & receptive issues combined

158
Q

Dysarthria

A

Impaired muscles used when speaking

159
Q

Post CVA manifestations

A

Depression & impaired memory

160
Q

Left brain stroke

A

Impaired memory, language & tend to be cautious when doing things

161
Q

Right brain stroke

A

Impulsive nature

162
Q

Slide 75

A
163
Q

CVA neuro assessment

A

LOC, Canadian Neurological Scale, cognition, motor abilities (unilateral, contralateral sensory and motor weakness)
-Cranial nerve function, sensation, proprioception, cerebellar function
-NVS, pupillary changes, slurred speech, spasticity, seizures

164
Q

CVA CV assessment

A

hypertension, tachycardia, bruit, aPerfusion

165
Q

CVA resp assessment

A

Monitor airway protection; dysphagia, aspiration pneumonia, loss of cough reflex, labored, apnea

166
Q

CVA GI/GU assessment

A

-GI: Loss of gag reflex, decreased or absent bowel sounds, nutritional intake
-GU: Urine output (monitor for dehydration if unable to swallow), frequency, incontinence

167
Q

Canadian neurological scale

A

-Slide 77
-For stroke patients

168
Q

Anterior cerebral artery causes which conditions when occluded?

A

-Hemiplegia on the contralateral side of the body, greater in the lower than upper extremities

169
Q

Occlusion of the middle cerebral artery causes

A

Aphasia dominant hemisphere & contralateral hemiplegia

170
Q

Posterior cerebral artery occlusion causes

A

Visual & sensory loss and contralateral hemiplegia if the cerebral peduncle is affected

171
Q

Slide 79

A
172
Q

Pathophysiology of cerebral aneurysms

A

-Sac like out pouching of a cerebral artery
-Large number of people have intracranial aneurysms which are innocuous and do not bleed
-More often in women than men (ratio 3:2)
-If ruptures, usually results in SAH
-Outcome of ruptured aneurysm is poor, only 1/3 who have SAH recover without a major disability

173
Q

Where cerebral aneurysms form

A

-Located at bifurcations and branches of arteries at base of the brain and circle of Willis
-85% develop at the anterior part of the circle of Willis

174
Q

Classification of cerebral aneurysms

A

Classified by size & shape (small to 15mm & giant from 25 to 50 mm)

175
Q

Shape classifications of cerebral aneurysms

A

-Berry, saccular
-Traumatic, myotic (infectious)
-Dissecting

176
Q

Cerebral aneurysm manifestations before rupture

A

-Dilated pupils, ptosis (eye droop), diplopia, pain above and behind left eye
-Localized headache, N/V

177
Q

Cerebral aneurysm manifestations after rupturing

A

-Violent/explosive headache
-Immediate loss of consciousness
-Vomiting
-SAH (subarachnoid hemorrhage) related deficits

178
Q

Vasopasm + cerebral aneurysm

A

-Narrowing of a cerebral blood vessel
-30% of patients experience vasospasm post rupture
-Spasm causes decreased cerebral perfusion further causing ischemia and/or infarct
-Unknown etiology

179
Q

Manifestations of vasospasms in cerebral aneurysms

A

aLOC, paresis/paralysis, cranial nerve deficits & aphasia

180
Q

Early signs of cerebral aneurysms

A

-aLOC and pupillary responses/ocular movements
-Weakness on one side of the body or in one extremity
-Constant headache that increases in intensity with movement or straining

181
Q

Later signs of cerebral aneurysm: IICP

A

-LOC diminishes to point of comatose
-HR, resps, temp, & BP rise. Pulse pressure widens (distance between the diastolic and systolic), pulse fluctuates between bradycardia and tachycardia within minutes
-Cheyne-stoke respirations

182
Q

Pathophysiology of meningitis

A

-Caused by bacteria, viruses, fungi, parasites or toxins
-May be acute, subacute, or chronic
-Meningococcus can reside in nasopharynx and throat, asymptomatic
-Bacterial organisms grow/replicate in the CSF releasing endotoxins or cells wall fragments; CSF circulation spreads it
-Contact droplet precautions

183
Q

Incidence of meningitis

A

Highest incidence among children and young adults

184
Q

Dx & tx of meningitis

A

-Diagnose using lumbar puncture (LP)
-Prophylactic antibiotics

185
Q

Bacterial meningitis manifestations in children <2 years old

A

-Fever, anorexia, vomiting, diarrhea
-Listlessness, pale, look disinterested
-Bulging fontanels & high pitch cry

186
Q

Manifestations of bacterial meningitis in children & young adults

A

-Headache, stiff neck, pain with knee and neck movement
-Fever, LOC deterioration, generalized convulsions,IICP & cranial nerve dysfunction

187
Q

Nursing assessment of bacterial meningitis

A

-Nutrition, fluid and electrolyte imbalances, transmission
-Brudzinski sign; chin to chest, kernels sign; hamstring pain

188
Q

Brudzinski & kernigs sign assess for

A

Subarachnoid involvement

189
Q

Encephalitis pathophysiology

A

-Acute febrile illness, usually viral in origin
-Most common form associated with mosquitos born viruses or herpes simplex type 1, may follow vaccinations with a live vaccine
-Edema, necrosis with or without -Hemorrhage & IICP develops

190
Q

Clinical manifestations of encephalitis

A

Fever, headache, stiff neck, aLOC (from disorientation to coma)

191
Q

Nursing assessment of encephalitis

A

Full neuro assessment, VS, aLOC, gait & speech

192
Q

General aspects in a neuro assessment + paediatrics

A

-Gain info about infants/toddlers by observing reflexes
-As they age they develop increasingly complex gross and fine motor skills and develop communicative behavior.
-Delayed developmental milestones helps identify at risk children

193
Q

Physical neuro assessment + paediatrics

A

-Size and shape of the head, sensory responses, symmetry in movement
-Inability to suck or swallow, asymmetrical smile, abnormal eye movement, twitching & crying

194
Q

Major features associated with neurological abnormalities + pediatrics

A

-Decreased LOC
-IICP
-Seizures, hypotonia, abnormal head size

195
Q

Moderate features associated with neurological abnormalities + pediatrics

A

-Persistent deviation of head and eyes
-Asymmetrical posture or movement

196
Q

Minor features associated with neurological dysfunction in pediatrics

A

-Jitteriness, poor feeding & abnormal head shape

197
Q

IICP in pediatrics

A

-Often caused by a TBI
-Also occurs in hydrocephalus, brain tumors, & intracranial infections
-Therapy should be directed at both reducing ICP & reversing its underlying causes

198
Q

Intracranial volume is made up of

A

-Brain, CSF & blood; these volumes must remain ~ the same at all times

199
Q

Symptoms of IICP

A

-Headache (earliest symptom)
-Decreased LOC
-Vomiting & pain coming in waves
-aVision, focal physical weakness or loss of coordination

200
Q

Signs of IICP

A

-Papilledema, retinal hemorrhage, scratching head
-Infants; split sutures or bulging fontanel
-Dilated pupil, unilateral on the same side as the lesion
-LOC can range from irritability to coma
-Hyperreflexia, hypertonia, bradycardia & respiratory depression are late signs

201
Q

Nursing assessment of IICP

A

-GCS & pediatric coma scales
-PERRLA
-Spontaneous activity, posture & response to pain
-Posturing (flexion/extension)

202
Q

Investigations for IICP

A

-CT & lumbar puncture

203
Q

Hydrocephalus

A

-Syndrome resulting from CSF disturbances
-Fluid accumulation causes enlargement and dilation of the ventricles of the brain & IICP

204
Q

If left untreated, hydrocephalus can

A

Lead to severe brain damage.

205
Q

Tx of hydrocephalus

A

Surgical shunting procedure to drain CSF

206
Q

Causes of hydrocephalus

A

Congenital defects (e.g. spina bifida), secondary to infection (e.g. meningitis), or trauma

207
Q

Nursing assessment of hydrocephalus

A

-Increased head circumference, veins
-Bulging fontanels & crying
-“Setting sun” sign (eyes look like a setting sun)
-Delayed development, reflexes & poor feeding

208
Q

Causes of pediatric seizures

A

-Structural: Trauma, malformation, intracranial hemorrhage
-Ingestion/drug withdrawal
-Metabolic: Hypoxemia, hypoglycemia, hypo-hypernatremia, hypocalcemia, & hypomagnesemia
-Infections & familial

209
Q

Nursing interventions for seizures

A

-Monitor length, ABC, reps, pulse, diaphoretic or dry, what type, evacuated bladder/bowel
-Cannot protect own airway for >5 minutes (intubation required)

210
Q

Atastic seizure

A

Sudden loss of muscle tone that may be focal (eg. head nod), hemibody or generalized (fall or drop attack)

211
Q

Behavioural seizure

A

Abrupt change in behaviour w/o other overt features (quiet-hyper motor), occasionally autonomic signs (pallor, cyanosis)

212
Q

Clonic seizure

A

Clonic jerking of extremeties or eyelids, occasionally followed by tonic posturing

213
Q

Infantile spasms

A

May be myoclonic or brief tonic flexor or extensor spasms. Often occur in clusters

214
Q

Tonic seizure

A

Symmetric or assymetric posturing (occasional fencer posture), may be followed by focal or generalized clonic activity

215
Q

Versive seizure

A

Forced & sustained tonic deviaton of the eyes that is associated with ipsilateral turning of the head & rotation of the trunk

216
Q

Benign febrile seizure epidemiology

A

-Most common cause of seizures in children
-6 months - 5 years
-Twice as common in boys
-Possibly genetic

217
Q

Etiology of benign febrile seizures

A

-Unknown
-Transient problems occur exclusively in the presence of high spiked fevers

218
Q

Manifestations of benign febrile seizures

A

-Rapid rise in temp
-No neurological or developmental delay before or after seizure
-No hx of non-febrile seizures, no infection before or after
-<15 minutes
-Generalized tonic-clonic, symmetric
-Does not recur in a 24hr period

219
Q

Investigation of benign febrile seizures

A

-Clinical diagnosis
-Septic work up including LP if meningitis is suspected

CV487 (15 decks)

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