Infections of the Nervous System Flashcards

1
Q

What is meningitis?

A

Inflammation/infection of the meninges

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2
Q

What is encephalitis?

A

Inflammation/infection of brain substance

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3
Q

What is myelitis?

A

Inflammation/infection of the spinal cord

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4
Q

What is the classic triad of meningitis?

A

Fever
Neck Stiffness
Headache

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5
Q

What are the classic signs of meningitis?

A
Fever 
Neck stiffness
Photophobia 
Nausea 
Vomiting 
Headache
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6
Q

How is neck stiffness examined?

A

By passively bending the neck forward

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7
Q

Describe GCS in meningitis patients

A

Often a little lower than normal

<14 in 69%

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8
Q

What type of rash is seen in meningitis?

A

Petechial rash

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9
Q

What test should be done on a petechial skin rash in suspected meningitis?

A

Tumbler test

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10
Q

What is non-blanching petechial skin rash a hallmark sign of?

A

Meningococcal meningitis

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11
Q

What are the common bacterial causes of meningitis?

A
  • Neisseria meningititis (meningococcus)

- Streptococcus pneumoniae (pneumococcus)

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12
Q

What do viral causes of meningitis include?

A

Enterioviruses

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13
Q

What are the clinical features of encephalitis?

A
Flu like prodrome 
Progressive headaches with fever
\+/- meningism 
Cerebral dysfunction 
Altered brain function - confusion, abnormal behaviour, memory disturbance, depressed conscious level 
Seizures 
Focal symptoms
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14
Q

What is a distinguishing feature between encephalitis and meningitis?

A

Onset of encephalitis is generally slower than for bacterial meningitis and cerebral dysfunction is a more prominent feauture

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15
Q

What investigations should be carried out for meningitis?

A

Blood cultures
Lumbar puncture
No need for imaging if no contraindications to LP

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16
Q

What investigations should be carried out for encephalitis?

A

Blood cultures
Imaging (CT scan+/- MRI)
LP
EEG

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17
Q

What are the contraindications for a lumbar puncture?

A

Focal symptoms or signs that suggest a focal brain mass
Reduced conscious levels suggesting raised ICP
GCS <10
Severely immunocompromised state
New onset seizures

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18
Q

What is opening pressure?

A

The pressure of CSF that is detected just after a needle is placed into the spinal canal

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19
Q

Describe opening pressure in meningitis and encephalitis

A

Meningitis - increased

Encephalitis - normal/increased

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20
Q

Describe cell count in meningitis and encephalitis

A

Meningitis - high, mainly neutrophils

Encephalitis - high, mainly lymphocytes

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21
Q

Describe glucose in meningitis and encephalitis

A

Meningitis - reduced

Encephalitis - normal

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22
Q

Why is glucose reduced in meningitis?

A

Because the bacteria consume the glucose 1

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23
Q

What do you have to do when testing glucose in encephalitis and meningitis?

A

Have to take a 3rd blood sample to compare to the red of the body cannot compare to a ‘normal’ figure

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24
Q

What is the first line of treatment in suspected meningitis?

A

IV ceftriaxone

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25
Q

What should you do if the patient is presenting clinically septic or pyrexial?

A

Do a LP

But do not do a blood culture

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26
Q

What is the commonest cause of encephalitis in europe?

A

Herpex simplex encephalitis

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27
Q

What investigation should you do for HSV encephalitis?

A

LP

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28
Q

What is the lab diagnosis for HSV encephalitis?

A

PCR of CSF for viral DNA

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29
Q

What is the Rx for HSV encephalitis?

A

AciclovirIV

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30
Q

When should aciclovir be given in HSV encephalitis?

A

On clinical suspicion - don’t wait for lab confirmation

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31
Q

What general things does herpes simplex cause?

A

Cold sores

Genital herpes

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32
Q

Where does herpes simplex virus lay dormant?

A

Dorsal route ganglion

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33
Q

What type of HSV causes encephalitis?

A

Nearly all caused by type 1 other than in neonates

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34
Q

What common virus can encephalitis be a rare complication of?

A

HSV

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35
Q

What is meant by neurotropic?

A

a virus, toxin, or chemical) tending to attack or affect the nervous system preferentially.

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36
Q

What do enteroviruses tend to attack?

A

Nervous system

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37
Q

How are enteroviruses spread?

A

Faecal-oral route

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38
Q

What are examples of enteroviruses?

A

Polioviruses, coxsackieviruses, echoviruses

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39
Q

What is a brain abscess?

A

Localised area of pus within the brain

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40
Q

What is a subdural empyema?

A

Thin layer of pus between the dura and arachnoid membranes over the surface of the brain

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41
Q

How does subdural empyema present?

A

With a high pressure headachw

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42
Q

What can be the features of an underlying source of subdural empyema?

A

Dental, sinus or ear infection

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43
Q

What are the differential diagnosis for brain abscess?

A

An focal lesion
More commonly a tumour
Subdural haeatoma

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44
Q

What are the causes for brain abscess and empyema?

A

Penetrating head injury
Spread from adjacent infection (dental, sinusitis, otitis media)
Blood borne infection
Neurosurgical procedure

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45
Q

How is diagnosis for brain abscess and empyema made?

A

CT or MRI
Investigating source
Blood cultures
Biopsy

46
Q

What is the most common organisms present in a brain abscess?

A

Often a mixture of organisms present

Streptococci in 70% of cases

47
Q

What is the management of brain abscess?

A

Surgical drainage if possible

Penicillin of ceftriaxone AB

48
Q

Why are HIV positive patients susceptible to infection?

A

Because their immune system is compromised

49
Q

What is the suspicion when a patient presents with cerebral toxoplasmosis?

A

That they have HIV

50
Q

What is the most common cause of brain abscess in patients with HIV?

A

Cerebral toxoplasmosis

51
Q

What is the diagnosis for HIV brain infection?

A

LP

52
Q

What does toxoplasmosis serology IgG suggest?

A

Past infection

53
Q

What does toxoplasmosis serology IgE suggest?

A

Acute infection

54
Q

What does borrelia burgoferi cause?

A

Lyme disease

55
Q

Which organisms causes syphilis?

A

Trepomena pallidum

56
Q

What is the vector for lyme disease?

A

Tick

57
Q

What are the 3 spirochaetes in the CNS?

A

Lyme Disease (Borrelia burgorferi)

Syphilis (Trepomena pallidum)

Leptospirosis (Leptospira interrogans)

58
Q

Describe stage 1 of lyme disease?

A
Early localised infection 
Characteristic rash at the site of the tick bite 
50% flu like symptoms 
fatigue 
myalgia 
Arthralgia 
Headache 
Fever
Chills 
Neck stiffness
59
Q

Describe stage 2 of lyme disease infection

A

Early disseminated infection (weeks – months)
One or more organ systems become involved
Haematologic or lymphatic spread
Musculoskeletal and neurologic involvement most common

60
Q

Describe stage 3 lyme disease

A
Chronic infection 
Occurring after a period of latency
Musculoskeletal and neurological involvement most common 
Subacute encephalopathy 
Encephalomyelitis
61
Q

Does lyme disease cause chronic fatigue syndrome?

A

No

62
Q

What s the investigation for lyme disease?

A
Complex range of serology tests
CSF lymphocytosis 
PCR of CSF 
MRI brain/spine
Nerve conduction studies
EMG if there is PNS involvement
63
Q

What is the treatment for lyme disease?

A

Prolonged AB treatment
IV ceftriaxone
Oral doxycycline

64
Q

What are the 3 stages of neurosyphilis?

A

Primary
Secondary
Latent

65
Q

In which stage of neurosyphilis is there neuro involvement?

A

Tertiary

66
Q

How is neurosyphilis diagnosed?

A

Serology

67
Q

Which antibody tests should be carried out for neurosyphilis?

A

Treponema - specific

Non specific treponemal

68
Q

What is the treatment for neurosyphilis?

A

High dose penicillin

69
Q

What type of virus are poliovirus?

A

Enterovirus

70
Q

What are the 3 types of poliovirus?

A

Types 1,2,3

71
Q

Where does poliovirus infect in poliomyelitis?

A

Anterior horn cells of lower motor neurons

72
Q

What are the motor features of poliomyelitis?

A

Asymmetric, flaccid paralysis esp in the legs

73
Q

What % of polio viruses are asymptomatic?

A

99%

74
Q

What are the sensory features of poliomyelitis?

A

No sensory features

75
Q

What does the polio vaccination contain?

A

All 3 types of polio

76
Q

What is rabies?

A

Acute infectious disease of CNS affecting almost all mammals

77
Q

How is rabies transmitted?

A

By bite or salivary contamination of open lesions

78
Q

What type of virus is rabies?

A

Neurotropic

79
Q

How does the rabies virus progress?

A

Enters PNS and migrates to CNS

80
Q

What are the symptoms of rabies?

A

Paraesthesiae at the site of origin

Ascending paralysis and encephalitis

81
Q

Who is at risk of rabies in the UK?

A

Bat handlers

82
Q

How is rabies diagnosed?

A

Culture
Detection
Serology

83
Q

What are important sources of human infection of rabies?

A

Dogs in africa/asia

84
Q

What is pre-exposure prevention of rabies?

A

Active immunisation with killed vaccine

85
Q

What is the post-exposure treatment for rabies?

A

Wash wound
Give active rabies immunisation
Give human rabies immunoglobulin if high risk

86
Q

What is tetanus infection with?

A

Clostridium tetanis

87
Q

Where do toxins in tetanus act?

A

The the neuromuscular junction

88
Q

How do toxins in tetanus affect the neuro-muscular junction?

A

Blocks the inhibition of motor neurons

Keep firing

89
Q

What is the signs of tetanus

A

Rigidity and spasms

90
Q

How is tetanus prevented?

A

Immunisation

91
Q

Which organisms causes botulism?

A

Clostridium botulinum

92
Q

How does botulism act as a neurotoxin?

A

Binds irreversibly to the presynaptic membranes of peripheral neuromuscular and autonomic nerve junctions
Toxin binding blocks Ach release

93
Q

How is there recovery from botulism?

A

Sprouting new axons

94
Q

What is the clinical presentation of botulism?

A

Incubation period of 4-14 days
Descending symmetrical flaccid paralysis
Pure motor
Respiratory failure
Autonomic dysfunction (usually pupil dilation)

95
Q

What is the diagnosis for botulism?

A

Nerve conduction studies

Culture from debrided wound

96
Q

What is the treatment for botulism?

A

anti-toxin (A,B,E)
Penicillin
Radical wound debridement

97
Q

What is CJD?

A

rare, degenerative, invariably fatal brain disorder.

98
Q

Forms of CJD

A

Sporadic
New variant
Familial CJD
Acquired

99
Q

Who should sporadic CJD be considered in?

A

Rapidly progressing dementia

100
Q

What are the clinical features of sporadic CJD?

A

Insidious onset
Early behavioural abnormalities
Rapidly progressing dementia
Myoclonus

101
Q

What signs suggest global neurological decline in CJD?

A
Motor abnormalities 
Cerebellar ataxia 
Extrapyramidal: tremor, rigidity, bradykinesis, dystoinia 
Pyramidal: weakness, spaciticity
Cortical blindness 
Seizures may occur
102
Q

What is the progression for sporadic CJD?

A

Rapid progression

Death often within 6 months

103
Q

What is the onset age for new variant CJD?

A

<40

Younger onset

104
Q

What are the investigations for new variant CJD?

A

MRI
EEG
CSF

105
Q

What can be seen in MRI in new onset CJD?

A

Pulvinar sign

106
Q

What can be seen on MRI in sporadic CJD?

A

Often no specific changes are seen

107
Q

What is seen on CSF in new variant CJD?

A

normal or raised protein

108
Q

What is the most common form of CJD?

A

Sporadic

109
Q

What protein can be detected in CJD that is not specific but is very helpful in correct clinical context of CJD?

A

Immunoassay 14-3-3 brain protein

110
Q

What is the treatment for CJD?

A

There is no treatment that can control or cure CJD

111
Q

What is there an infiltration of in CJD?

A

Prions