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Elsa AACN > Ch 23 CNS infections > Flashcards

Ch 23 CNS infections Flashcards

1
Q

Meningitis

A

infection or inflammation that is confined to the meninges

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2
Q

common causes of meningitis

A

bacteria or virus

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3
Q

which outcome is worse in meningitis? bacterial or virus?

A

bacteria etiology is worse than viral

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4
Q

3 bacterial forms of meningitis (accounts for 95% of bacterial forms of meningitis)

A

haemopilus meningitis
meningococcal meningitis - 2nd most common cause
pneumococcal meningitis - most common cause

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5
Q

how is bacteria spread to meninges

A

can be spread from an adjacent infected area (eg ears or sinuses), from the environment (e.g. congenital defect, penetrating injury) through the bloodstream

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6
Q

primary cause of bacterial meningitis

A

inflammation
- leads to tissue and vascular injury, septic thrombosis, smaller infarcts

TB can also develop meningitis

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7
Q

complications of bacterial meningitis

A

brain edema and increased ICP - hypoxic ischemic encephalopathy (HIE)

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8
Q

what happens when there is bacterial meningitis in children

A

cranial nerve defects (reversible)

- mostly in children (5-11 % cases)

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9
Q

which cranial nerve is most affected by bacterial meningitis?

A

cranial nerve 8 (auditory)
- results in sensorineural hearing loss

Cranial nerve 6 (abducens)

  • longest intracranial route
  • most vulnerable to compression

CN 3, 4, 7 may also be affected

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10
Q

how does TB bacteria spread?

A

to brain and spine from lung

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11
Q

rates of bacterial meningitis

A

0.6-4/100,000 annually

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12
Q

rates of neonatal bacterial meningitis

A

0.25-1/1000

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13
Q

rate of TB meningitis?

A

rare, only in poor regions

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14
Q

bacterial meningitis mortality rate

A

5-10%
significantly improved
highest in 1st year of life, decline mid life, then increase in older adults

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15
Q

mortality rate highest in which type of meningitis?

A

pneumococcal (10-30%)

TB (15-30%)

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16
Q

mortality rate lowest in which type of meningitist?

A

meningococcal (4-5%)

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17
Q

% of people with long term consequences of bacterial meningitis

A

15-25%

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18
Q

common consequences of bacterial meningitis

A

hearing loss 11%
ID 4%
spasticity 4%
seizure disorders 4%

cognitive impairment/ADHD in 50% of childhood survivors

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19
Q

determinants of severity - age

A

most cases happen in children <5 years or > 60 years

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20
Q

medical risk factor for bacterial meningitis

A

immunosuppression - increased risk for infections

e.g. HIV, autoimmune etiology, cystic fibroids, DM, hypoarathyroidism

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21
Q

SES risk factors

A

resources

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22
Q

Types of bacterial meningitis and NP outcomes

A

pneumococal meningitis show greater cognitive impairments than meningococcal meningitis

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23
Q

viral or bacterial meningitis have better outcomes?

A

viral

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24
Q

other medical risk factors for bacterial meningitis

A

complications (prolonged seizures, hemiparesis, b/l hearing loss)
Low CSF glucose level
strep pneumonia infection
younger age - worse language outcome

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25
Q

male or female worse behavioral outcome for bacterial meningitis

A

MALES

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26
Q

acute vs gradual presentation

A

acute:
sudden fever
severe HA
stiff neck

gradual:
non specific flu like symptoms

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27
Q

common presenting sx in children of bacterial meningitis

A 
hyperthermia
lethargy
anorexia
vomiting
respiratory distress
convulsion
irritability
jaundice
diarrhea
stiff neck
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28
Q

assessment of bacterial meningitis

A

lumbar puncture - diagnostic, check CSF to see if there’s blood or white blood cells, protein levels, low glucose

brain imaging - CT/MRI do NOT help with diagnosis!
even if scans do not show meningeal enhancement, it does not r/o diagnosis

MRI is used for TB meningitis

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29
Q

treatment for bacterial meningitis

A 
antibiotics
vaccine
corticosteroids
- inflammation and swelling,
- prevents hearing loss

TB meningitis
- anti TB drugs

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30
Q

NP outcomes overall in bacterial meningitis

A

MORE cognitive impairments than physical impairments

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31
Q

NP IQ in bacterial meningitis

A

adults - average IQ

peds - low average to average IQ

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32
Q

NP academic in bacterial meningitis

A

2x more likely to need special ed, grade retention

no consistent academic deficit in certain domains

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33
Q

NP attention in bacterial meningitis

A

adults - trails B and stroop

peds - ADHD rates higher than average

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34
Q

NP processing speed in bacterial meningitis

A

adults - simple reaction time slower

MAIN DEFICIT

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35
Q

NP language in bacterial meningitis

A

adults - no problem

peds - kids dx before age 1 have impairment

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36
Q

NP visuospatial in bacterial meningitis

A

no consistent finding

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37
Q

NP memory in bacterial meningitis

A

adults - mixed

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38
Q

NP Executive function in bacterial meningitis

A

adults - problems more common

peds - not severe impaired but below expectation

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39
Q

NP sensorimotor in bacterial meningitis

A

hearing loss - consistent finding (usually in pneumococcal than meningococcal)

hemiparesis
cortical blindness
ataxia
spasticity

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40
Q

Meningitis is the cause of ?% of deaf and hard of hearing in youth in USA?

A

3-6%

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41
Q

NP mood in bacterial meningitis

A

peds - ADHD, behavioral changes and other MH issues in adolescence

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42
Q

NP work in bacterial meningitis

A

adults - can work normally

peds - in peds onset, lower economic sufficiency in adulthood

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43
Q

Aseptic Forms of meningitis - aseptic means?

A

non bacterial forms of bacterial meningitis

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44
Q

Cause of aseptic meningitis?

A

virus
fungi
parasite
enterovirus (through intestine)

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45
Q

most common cause of aseptic meningitis

A

enterovirus

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46
Q

examples of fungi that can cause aseptic meningitis

A 
crytococcus
histoplasma
blastomyces
coccidioides
candida - acquired usually in hospital
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47
Q

which one is more common? viral or bacterial forms of meningitis

A

viral forms

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48
Q

how many cases of viral aseptic meningitis

A

10,000 reported

possibly 75,000

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49
Q

fungal meningitis happens in which population?

A

rare

usually in immunocompromised eg HIV positive

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50
Q

most common form of fungal meningitis

A

crytococcus

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51
Q

mortality of viral meningitis

A

< 1%

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52
Q

morbidity of viral meningitis

A

less common long term neurological consequences than bacterial meningitis, usually benign outcomes

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53
Q

recovery of viral meningitis?

A

7-10 days
no residual effects
persistent effects are mild

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54
Q

presenting problem in viral meningitis?

A

headache - most common sx

fever
irritability
nausea and vomiting
stiff neck
rash
fatigue
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55
Q

assessment and dx of viral meningitis

A

lumbar puncture - examine blood and CSF to isolate viral pathogen

CT, MRI, EEG - clarify dx

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56
Q

treatment of viral meningitis

A

antibiotics - USELESS
mostly supportive - rest, fluids, anti inflammatory meds
some antiviral meds

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57
Q

treatment of fungal meningitis

A

antifungal meds

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58
Q

NP in fungal meningitis

A

mostly mild

but long lasting deficits can be seen in motor speed, gross motor, and EF

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59
Q

Definition of Encephalitis

A

infection of the brain tissue/parenchyma

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60
Q

most common cause of Encephalitis

A

virus

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61
Q

other causes of Encephalitis

A

(besides virus #1)
bacteria, fungi, parasites
autoimmune

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62
Q

two types of Encephalitis

A

primary Encephalitis = acute viral Encephalitis

secondary Encephalitis = post-infective Encephalitis

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63
Q

what is primary Encephalitis / acute viral Encephalitis

A

direct infection of brain through direct invasion of pathogen

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64
Q

what is secondary Encephalitis/post-infective Encephalitis

A

results from previous viral infection (e.g. chickenpox, mumps, measles) or immunization (measles vaccine)

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65
Q

how many viruses are these associated with Encephalitis?

A

> 100

66
Q

most common Encephalitis?

A 
herpes simplex virus
varicella zoster virus
epstein barr virus
adenovirus
enterovirus
arbovirus
67
Q

how does virus work to lead to Encephalitis?

A

most virus reach CNS via bloodstream

some virus travel to CNS along cranial nerves

68
Q

how does herpes simplex virus travel and reach the brain?

A

it is dormant in trigeminal ganglia

when activated, it travels along trigeminal nerve into brain

69
Q

rates of Encephalitis

A

7.3/100,000

70
Q

incidence of Encephalitis per year

A

20,000 cases per year, mostly mild

71
Q

highest incidence rate of Encephalitis in which age group?

A

children < 1 year

72
Q

most common cause of Encephalitis in children?

A

Herpes simplex Encephalitis

73
Q

did incidence rate increase or decrease in children?

A

increase

74
Q

mortality rate for Encephalitis

A

5% overall (3% in children)

75
Q

factors predicting mortality rate of Encephalitis

A

age (some types have higher mortality rates in elderly)

type (rabies virus Encephalitis and untreated HSV)

76
Q

morbidity

A

1/3 have some form of neuro and cog difficulties when discharged
6-12 mos full recovery

77
Q

age and severity of Encephalitis

A

most severe in infants and elderly

78
Q

risk factors for Encephalitis and NP

A

HSV Encephalitis has the most impairments compared to other types of Encephalitis (2-4x)

bilateral temporal lesions have worse outcomes than unilateral lesions

79
Q

what predicts severity in children

A

length of hospital stay
neuroimaging
HSV type Encephalitis

80
Q

risk of seizure in Encephalitis

A

20% for those with early seizures

10% without early seizures

81
Q

presentation of Encephalitis

A 
acute (hours to days)
- severe HA and fever
altered consciousness
disorientation
behavioral and speech disturbances
neurological signs

subacute (weeks)
seizures
speech disturbances

chronic
occasional acute sx (as in HIV orl lyme disease)

82
Q

behavioral presentation of Encephalitis

A

behavior or psychotic disorder in HSV
- delusion, hallucination, mood disorder

some develop Kluver Bucy syndrome with b/l damage to amygdala

83
Q

Kluver Bucy syndrome

A

related to amygdala

inappropriate sexual behaviors and mouthing of objects.

84
Q

Assessment of Encephalitis

A

lumbar puncture/blood work
EEG - to detect seizures (usually non specific)
CT MRI - edema, localized infection, mass, inflammatory

85
Q

Treatment of Encephalitis

A

antiviral drugs
anticonvulsant
corticosteroid
hemispherectomy - for Rasmussen Encephalitis

86
Q

IQ and Encephalitis

A

adults - low average to average

peds - low average to average, learning problems

87
Q

attention and Encephalitis

A

higher prevalence in kids

88
Q

processing speed in Encephalitis

A

affected in all

89
Q

language in Encephalitis

A

unaffected

some naming problems in HSV Encephalitis

90
Q

visuospatial in Encephalitis

A

no consistent findings

91
Q

memory in Encephalitis

A

HSV Encephalitis has memory problems

92
Q

EF in Encephalitis

A

common problem

40% EF problems in HSV Encephalitis

93
Q

sensorimotor in Encephalitis

A

no consistent findings

west nile Encephalitis - motor problems

94
Q

mood in Encephalitis

A

behavior, mood, attention (kids)

HSV with more personality changes

95
Q

work in Encephalitis

A

can work with good outcomes

HSV Encephalitis has more difficulty

96
Q

NP impact of Chronic Herpes simplex complex (HSV)

A

lower IQ
lower overall cognitive scores
increased risk for AD

97
Q

Autoimmune and paraneoplastic Encephalitis definition?

A

autoimmune syndrome associated with attack of antibodies on neuronal cell surface or synaptic receptors with or without cancer associated

98
Q

paraneoplastic Encephalitis disorder (PND)

A

cancer related

99
Q

2 groups of Autoimmune Encephalitis

A

intracellular antibody disorders (PND)

synpatic and neuronal surface autoantibody disorders

100
Q

intracellular antibody disorders

A

PND falls in this group
autoimmune reaction initiated in response to tumor, which expresses neuronal antigens, mediated by cytotoxic t cell responses

paraneoplastic limbic encephalitis (PLE)

  • inflammatory process related to cancer (small cell lung)
  • localized to limbic system
101
Q

synaptic and neuronal surface autoantibody disorders

A

antibodies disrupt the neuronal receptor or synaptic protein

prevents post synaptic electrical impulse causing nerve cell and brain to stop working

102
Q

most common form of autoimmune encephalitis

A

2 is ADEM

Anti NMDA receptor encephalitis( anti NMDARE)

103
Q

what is NMDARE - anti NMDA receptor encephalitis?

A

involves antibodies that decrease number of cell surface NMDA receptors and NMDA receptor clusters in postsynaptic dendrites

104
Q

where are NMDA receptors located or concentrated?

A

hippocampus
forebrain
limbic system

play a primary role in synaptic excitatory transmission of glutamate

105
Q

anti NMDARE associated with

A

tumors

106
Q

Classic PND

A

rare

usually in older adults

107
Q

anti NMDARE age?

A

23 mos - 76 years

median age 19 years

108
Q

autoimmune encephalitis gender ratio?

A

females more in NMDARE

109
Q

race of NMDARE

A

blacks more than whites

110
Q

mortality rates of Autoimmune encephalitis and Paraneoplastic encephalitis

A

paraneoplastic higher than autoimmune

autoimmune encephalitis is at 6%

111
Q

morbidity PND and Autoimmune encephalitis

A

PND and AE both have significant morbidity

  • seizures
  • infection
  • cog deficits
112
Q

IQ and anti NMDARE

A

adults - IQ generally average long term

kids - improves over time, poor academic performance in 36%

113
Q

attention and anti NMDARE

A

deficits in attention and working memory

114
Q

processing speed in anti NMDARE

A

improves over time

deficits in some

115
Q

language anti NMDARE

A

no consistent impairment in adults

some verbal fluency problems in small % of kids

116
Q

visuospatial and anti NMDARE

A

adults - worse than average but improves

kids - visuomotor integration impaired in 1/3, but improves

117
Q

memory and anti NMDARE

A

episodic memory core deficit
cannot consolidate
verbal memory more affected, visual memory bad too

118
Q

EF and anti NMDARE

A

persistent deficits in 50% of people

119
Q

mood in anti NMDARE

A

anxiety but not depression

behavioral changes in kids, but improves

120
Q

social of PND and Auto immune encephalitis

A

impaired social cognition and relationships in some groups

121
Q

what affects outcome in anti NMDARE

A

delayed initiation of immunotherapy
age or gender or seizure do NOT correlate with outcomes
removal of tumor - better outcome

122
Q

what affects outcome in paraneoplastic limbic encephalitis

A

sleep disturbance
impairment of cognition
psych sx ( depression, anxiety, agitation, hallucination)

123
Q

paraneoplastic limbic encephalitis presentation?

A

subacute onset of up to 12 weeks

124
Q

paraneoplastic syndromes presentation

A 
altered consciousness
behavior and mood disturbance
sensory changes
cranial nerve palsy
ridigity
cerebellar dysfunction
125
Q

Anti NMDARE phases in symptom presentation

A

prodromal phase
- flu like sx with fever, malaise, HA, fatigue

psychotic phase
- acute psychosis or schizophrenia

unresponsiveness phase

  • stop responding toverbal commands
  • mute, akinetic, fixed gaze, sterotyped athetotic movement

hyperkinetic phase
- autonomic instability (hypo/hypertension, cardiac arrhythmia)

126
Q

anti NMDARE in children presentation

A 
behavioral problems
irritability
agitation
hyperactivity
temper tantrums
127
Q

assessment of autoimmune and paraneoplastic encephalitis

A

lumbar puncture
- look for antibodies in blood, CSF can confirm autoimmune or cancer related (CSF better sensitivity), inflammatory markers
neuroimaging
- CT MRI (T2 flair in anti NMDARE)
EEG
- slowing and epileptoform activity in anti NMDARE although normal in a few months after onset

128
Q

treatment Anti NMDARE

A

cancer treatment - removal of tumor, chemo, steroid, immunotherapy

target anti bodies

129
Q

recovery in paraneoplastic limbic encephalitis PLE

A

seizure and behavior problem improve with tx
persistent deficit in memory and learning

anti nMDARE

  • recovery is slow, hospitalized for few months than rehab
  • most show residual cognitive deficits
  • some with relapse (those without tumor or immunotherapy more at risk)
130
Q

other infection and causes of encephalitis

A

intracranial abscess
intrauterine and intranatal infection
HIV
progressive multifocal leukoencephalopathy (PML)
cerebral toxoplasmosis
acute disseminated encephalomyelitis (ADEM)

131
Q

intracranial abscess

A

infectious pus collections in the brain or surrounding area

can originate in nearby area and spread through blood

can occur after depressed skull fracture, penetrating brain injury, neurosurgery, meningitis

cause brain damage by increasing ICP and mass effect on brain

132
Q

two types of intracranial abscess

A

subdural or epidural empyema

brain abscess

133
Q

intracranial abscess

- subdural or epidural empyema

A

found between inner surface of dura and outer surface of arachnoid (subarachnoid) or in space between dura and skull (epidural)

epidural abscesses more common in spinal cord than brain

134
Q

intracranial abscess

- brain abscess

A

cavity filled with pus in brain parenchyma

135
Q

Intrauterine and intranatal infections

A

TORCH!

toxoplasmosis
other infection
rubella
cytomegalovirus
herpes simplex virus 2

Prion disease

136
Q

prion disease

A

caused by infectious proteins called prions

137
Q

examples of prion dieases

A

CJD,
Gerstmann Straussler Scheinker syndrome,(GSS)
fatal familial insomnia (FFI)

138
Q

CJD

A

belongs to transmissible spongiform encephalopathy
brain tissue develops holes that gives it sponge like appearance
rapidly progressive and fatal
rapidly progressive dementia (memory issues, personality changes, hallucinations, physical problems)

139
Q

Human Immunodeficiency Virus (HIV)

A

neurons NOT directly impacted by HIV infection

infection leads macrophages and microglia to cause gradual destruction of neuronal integrity

140
Q

MRI findings of HIV

A

small areas of bilateral, subcortical signal hyperintensity
volume loss and metabolic changes in basal ganglia
large hyperintensity (showing lesions)
global and diffuse atrophy
ventricular enlargement
reduced white matter
isolated focal lesions

141
Q

2 key syndromes in HIV

A

HIV associated neurocognitive disorder (HAND)

  • common in up to 50% of people
  • deficits in attention, EF, fluency, memory, psychomotor speed
  • decreases in brain activation, L frontal attentional networks
142
Q

HIV1 AIDS dementia complex

HIV associated dementia

A 
severe form of cog impairment
subcortical dementia
- mimics parkinsons
- disruption of cortical connection (fronto-striatal-thalamo cortico loop) leads to attention deficits, working memory, EF, learning
- memory impairment
- psychomotor slowing, motor impairment
143
Q

HIV 1 associated minor cognitive/motor disorder

A

less severe of cog impairment
- similar subcortical profile as HIV dementia
2% in people with HIV
0.5-1 SD below mean on cog impairment at least 2 domains
- deficits in processing speed, attention, psychomotor functioning

144
Q

perinatally acquired HIV infection

A

children and adolescents

  • poor working memory, slow processing, EF
  • poor VS skills, VS memory, language
  • conductive hearing problems 20-30%
  • mental health problems 25%
145
Q

treatment of HIV associated dementia

A

ART - antiretroviral treatment

  • decreased prevalence of HIV assoicated dementia
  • only 28% of children have started it
146
Q

problems with not being treated for HIV?

A

access to care

not disclosing to doctors

147
Q

Progressive multifocal leukoencephalopathy (PML)

A

rare and fatal viral disease
causes progressive and multifocal damage of white matter
affects people who are immunocompromised (e.g. transplant, HIV)

148
Q

what causes PML

A

JC virus

149
Q

Cerebral Toxoplasmosis

A

infection in brain caused by parasite called toxoplasma

leads to brain abscess in HIV patients

150
Q

acute disseminated encephalomyelitis (ADEM)

A

inflammatory demyelinating condition of CNS (brain and spinal cord)
looks like MS
single occurrence or multiphasic (MDEM)

151
Q

cause of ADEM

A

postinfectious or post vaccination (1-2 weeks after)

152
Q

highest incidence of ADEM

A

early childhood 5-8 years

153
Q

presentation of ADEM

A

confusion
cog impairment
neurological deficits
psyc sx - mood lability, agitation, personality, delusion, hallucination (can appear before neurological signs)

154
Q

what does brain MRI show for ADEM

A 
white matter hyperintensities in 
both hemispheres
subcortical region, 
cerebellum, 
spinal cord
155
Q

MRI used to differentiate between ADEM and what?

A

MS

156
Q

some people have ADEM later being reclassified as having

A

MS

157
Q

treatment of ADEM

A

high dose steroids

plasmapheresis

158
Q

mortality of ADEM

A

rare - most recover with treatment

159
Q

NP of ADEM

A

better than pediatric MS

some subtle deficits in attention, processing, EF

160
Q

rasumussen encephalitis

A

frequent and severe seizure
loss of speech and motor skills
hemiparesis
cog deficits

Elsa AACN (35 decks)

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