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N - C > Infections of the Nervous System > Flashcards

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 spinal cord

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4
Q

How strong is the destinction of meningitis, encephalitis and myelitis?

A

In reality the distinction is artificial and patients often have a mixture

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5
Q

What are the clinical features of meningitis

A
  • “Classical triad”
  • Present with short history of progressive headache associated with fever and meningism
  • Cerebral dysfunction
  • Cranial nerve palsy, seizures, focal neurological deficits may also occur
  • Patechial skin rash
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6
Q

What is the “classical triad” in meningitis?

A

Fever
Neck stiffness
Altered mental status

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7
Q

What is meningism?

A

Neck stiffness
Photophobia
Nausea and Vomiting

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8
Q

How is neck stiffness examined?

A

Passively bendng the neck forward

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9
Q

Describe cerebral dysfunction in meningitis

A

Confusion, delirium, declining conscious level

Common

GCS

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10
Q

How many patients with meningitis have cranial nerve palsy?

A

30%

Cranial nerves pass through meninges so may be effected

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11
Q

How many patients with meningitis have seizures?

A

30%

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12
Q

How many patients with meningitis have focal neurological deficits?

A

10-20%

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13
Q

You should always look out for a skin rash in meningitis.

Give more information about this

A

Tumbler test

Hallmark of meningococcal meningitis, but cal also occur in viral meningitis

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14
Q

What is the differential diagnosis of meningitis?

A

Infective
-Bacterial, viral , fungal

Inflammatory
- Sarcoidosis

Drug induced
-NSAIDs, IVIG

Malignant

  • Metastatic
  • Haematological (e.g. leukaemia, lymphoma, meyloma)
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15
Q

What do the bacterial causes of meningitis include?

A

Neisseria meningitidis
(Meningococcus)

Streptococcus pneumoniae
(pneumococcus)

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16
Q

What do the viral causes of meningitis include?

A

Enterovirus

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17
Q

What are the clinical features of encephalitis?

A

Flu-like prodrome (4-10 days)

Progressive Headache associated with fever

  • +/- meningism
  • Progressive cerebral dysfunction
  • Seizures
  • Focal symptoms / signs
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18
Q

Describe progressive cerebral dysfunction in encephalitis

A

Confusion
Abnormal behaviour
Memory disturbance
Depressed conscious level

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19
Q

How does viral encaphalitis differ to bacterial meningitis in its presentation?

A

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

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20
Q

What is a prodrome?

A

An early symptom that might indicate the start of a disease before specific symptoms occur

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21
Q

What is the differential diagnosis for encephalitis?

A

Infective
-Viral (most common is HSV)

Inflammatory

  • Limbic encephalitis
  • ADEM

Metabolic
-Hepatic, Uraemic, Hyperglycaemic

Malignant
-Metastatic, Paraneoplastic

Migraine

Post ictal (after seizure)

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22
Q

What antibodies are involved with limbic encephalitis?

A

Anti VGKC (voltage gated potassium channels)

Anti NMDA

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23
Q

What is ADEM?

A

Acute Disseminated Encephalomyelitis

The disorder manifests as an acute-onset encephalopathy associated with polyfocal neurologic deficits and is typically self-limiting.
Bears a striking clinical and pathological resemblance to other acute demyelinating syndromes of childhood, including multiple sclerosis (MS).

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24
Q

Describe anti-VGKC Auto-immune encephalitis

A

Frequent seizures

Amnesia (not able to retain new memories)

Altered mental state

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25
Q

Decribe anti-NMDA receptor auto-immune encephalitis

A

Flu like prodrome

Prominent psychiatric features

Altered mental state and seizures

Progressing to a movement disorder and come

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26
Q

What is the priority in meningitis and encephalitis?

A

Treat infection

Then try to exclude infection with investigation

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27
Q

What are the investigations for meningitis?

A

Blood cultures (bacteraemia)

Lumbar puncture (CSF culture/ microscopy)

No need for imaging if no contraindications to lumbar puncture

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28
Q

What are the investigations for encephalitis?

A

Blood cultures

Imaging (CT scan +/- MRI)

Lumbar Puncture

EEG

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29
Q

What are the indications for CT scanning before a lumbar puncture?

A

Focal neurological deficit, not including cranial nerve palsies
-Raised ICP

New-onset seizures

Papilloedema
-Raised ICP

Abnormal level of consiousness, interfering with proper neurological examination (GCS

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30
Q

What are the CSF findings in bacterial meningitis?

A

Opening pressure
-Increased

Cell count

  • High
  • Mainly Neutrophils

Glucose
-Reduced

Protein
-High

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31
Q

What are the CSF findings in Viral meningitis and encephalitis?

A

Opening pressure
-Normal/ increased

Cell count

  • High
  • Mainly leukocytes

Glucose
-Normal (60% of blood glucose)

Protein
-Slightly increased

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32
Q

What should be looked at with the CSF extracted from a lumbar puncture?

A
  • Opening pressure
  • Cell count
  • Glucose
  • Protein
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33
Q

What is the most common cause of bacterial meningitis?

A

Streptococcus Pneumoniae

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34
Q

How common is herpes simplex virus as a cause of encephalitis?

A

Relatively rare, but commonest cause of encephalitis is europe

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35
Q

How do you diagnose HSV?

A

Lab diagnosis by PCR of CSF for viral DNA

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36
Q

How do you treat HSV?

A

Treat with aciclovir on clinical suspicion

Treat as soon as you suspect

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37
Q

What is the result if HSV encephalitis is missed?

A

Over 70% mortality and high morbidity if untreated

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38
Q

What are the two types of herpes simplex virus?

A

HSV types 1 and 2

  • Cold sores (type 1&raquo_space; 2)
  • Genital herpes (type 1&2)
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39
Q

What is the herpes group of viruses?

A

Herpes simplex
Varicella Zoster Virus
Epstein Barr Virus
Cytomegalovirus

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40
Q

What happens to the herpes simplex virus after initial infection?

A

Virus remains latent in the trigeminal or sacral ganglion after primary infection

(as with all herpes viruses, once infected, always infected)

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41
Q

How does HSV cause encephalitis?

A

Its a rare complication of HSV

-Other than neonates, nearly all caused by type 1

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42
Q

What are enteroviruses?

A

Large family of RNA viruses

Tendency to cause CNS infections (Neurotropic)

Human infections, no animal reservoir
-Fecal oral route

Many can cause non-paralytic meningitis

43
Q

What is included in the family of enteroviruses?

A

Polioviruses
Coxsackieviruses
Echoviruses

44
Q

Enteroviruses cause gastroenteritis.

True or false?

A

False

Found in gut but DO NOT cause gastroenteritis.
Diarrhoea wont be enterovirus

45
Q

How common is Arbovirus Encephalitides?

A

Common cause of encephalitis in other parts of the world

46
Q

What is included in Arbovirus encephalitides?

A

Variety of virus groups?

Transmitted to man by vector (mosquito or tick) from non-human host e.g.:

  • West nile Virus
  • St Louis Encephalitis
  • Western Equine Encephalitis
  • Tick Borne Encephalitis
  • Japanese B Encephalitis
47
Q

How does the place name of Arbovirus encephalitis relate to where its geographic location is?

A

Generally relate to where first described and NOT to current geographical distribution

48
Q

What is a brain abscess?

A

Localised area of pus within the brain

49
Q

What is a subdural empyema?

A

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

50
Q

What are the clinical features of Brain abscess or subdural empyema?

A

Fever, Headache

Focal symptoms/ signs
-Seizures, dysphasia, hemiparesis etc

Signs of raised intracranial pressure

  • Papilloedema, false localising signs
  • Depressed conscious level

Meningism may be present (particularly with empyema)

Features of underlying source
-e.g. dental, sinus or ear infection

51
Q

What are the differential diagnosis for brain abscess and empyema?

A

Any focal lesion, but most commonly tumour

Subdural haematoma

52
Q

What are the causes of brain abscess and empyema?

A

Penetrating head injury

Spread from adjacent infection (dental, sinusitis, otitis media)

Blood borne infection
-e.g. Bacterial endocarditis

Neurological procedure

53
Q

How do you diagnose brain abscess and empyema?

A

Imaging: CT or MRI

Investigate source

Blood cultures

Biopsy (drainage of pus)

54
Q

What do you need to consider in biopsy of brain abscess and empyema?

A

Risk vs benefits

Need to consider the location (base may be risky)

55
Q

Describe the organisms involved in brain abscess

A

Often mixtures of organisms present:
-Depend on predisposing condition

Streptococci in 70% of cases, esp penicillin-sensitive “Strep milleri” group

Anaerobes in 40-100% of cases
-Bacteroides, Prevotella

56
Q

What is the management for brain abscess?

A

Surgical drainage if possible

-Penicillin or CEFTRIAXONE to cover streps
-METRONIDAZOLE for anaerobes
(high doses required for penetration)

Culture and sensitivity tests on aspirate provide useful guidance

High mortality without appropriate treatment

57
Q

What conditions should you consider HIV testing?

A
  • Cerebral toxoplasmosis
  • Aseptic meningitis/ encephalitis
  • Primary cerebral lymphoma
  • Cerebral abscess
  • Cryptococcal meningitis
  • Space occupying lesion of unknown cause
  • Dementia
  • Leucoencephalopathy
58
Q

What brain infections can occur in HIV patients with low CD4 counts?

A
  • Cryptococcus neoformans
  • Toxoplasma gondii
  • Progressive multifocal leukoencephalopathy (PML)
  • Cytomegalovirus (CMV)
  • HIV-ENCEPHALOPATHY (HIV- ASSOCIATED DEMENTIA
59
Q

How can you diagnose HIV related neurological infections?

A

India Ink, Cryptococcal antigen

Toxoplasmosis serology (IgG)

JC virus PCR

CMV PCR

HIV PCR

60
Q

What Spirochaete infections effect CNS?

A

Lyme disease (Borrelia Burgorferi)

Syphilis (Trepomena Pallidum)

Leptospirosis (Leptospira Interrogans)

61
Q

How does lyme disease spread

A

Spirochaete (Borrelia Burgdorferi) spreads by Tick vector

Common in inverness and moray areas

Has 3 stages

62
Q

What is Lyme disease?

A

Has 3 stages

Multi-system:

  • Skin,
  • Rheumatological,
  • Neurological/ neuropsychiatric
  • Cardiac
  • Opthalmological involvement

Untreated 80% will develop multi-system disseminated disease

63
Q

What is stage 1 of lyme disease?

lasts 1-30 days

A

Early localised infection

Characteristic expanding rash at the site of the tick bite: erythema migrans

50% flu like symptoms for 1 day to a week
-Fatigue, myalgia, arthralgia, headache, fever, chills, neck stiffness

64
Q

What is stage 2 lyme disease?

lasts weeks to months

A

Early disseminated infection

One or more organ systems become involved
-Haematologic or lymphatic spread

Musculoskeletal involvement most common

65
Q

Describe the neurologic involvement in stage 2 lyme disease

A

10-15% untreated patients

  • Mononeuropathy
  • Mononeuritis multiplex
  • Painful radiculoneuropathy
  • Cranial neuropathy
  • Myelitis
  • Meningo-encephalitis
66
Q

Describe stage 3 lyme disease

months to years

A

Chronic infection:
-Occuring after a period of latency

Musculoskeletal and neurologic involvement most common

67
Q

Describe the neurologic involvement in stage 3 lyme disease

A

As described for stage 2

Subacute encephalopathy

Encephalomyelitis

68
Q

What is the relationship of lyme disease and chronic fatigue syndrome?

A

Lyme disease does NOT cause a chronic fatigue syndrome

69
Q

What is the investigation for lymes disease?

A

Complex range of serelogical tests

CSF lymphocytes

PCR of CSF

MRI brain/ spine (if CNS involvement)

Nerve conduction studies/ EMG (if PNS involvement)

70
Q

What is the treatment for lyme disease?

A

Prolonged antibiotic treatment:

  • Intravenous ceftriaxone
  • Oral doxycycline

Stage 1 doxycycline
Late stage IV ceftriaxone

71
Q

Describe neurosyphilis

A

Syphilis (Treponema pallidum) has a similar 3 stage presentation to lyme disease
(Primary -> secondary -> tertiary)

Tertiary disease occurs years/ decades after primary infection (not common)

72
Q

How do you investigate neurosyphilis?

A

Treponema specific and non-treponemal specific (VDRL) antibody tests

CSF lymphocytes increased, evidence of inthrathecal antibody production, PCR

73
Q

How do you treat neurosyphilis?

A

High dose penicillin

74
Q

What is poliomyelitis?

A

Caused by poliovirus types 1, 2 or 3
-all enteroviruses

99% of infections are asymptomatic

Paralytic disease in about 1%
-infects anterior horn cells of lower motor neurones

Asymmetric, flaccid paralysis, esp legs

No sensory features

75
Q

What is rabies?

A

Acute infectious disease of CNS affecting almost all mammals

Transmitted to human by bite or slivary contamination of open lesion

Neurotropic - virus enters peripheral nerves and migrates to CNS

Parasthesiae at site of original lesion

Ascending paralysis and encephalitis

76
Q

How do you diagnose rabies encephalitis?

A

No useful diagnostic tests before clinical disease apparent

Diagnosis:

  • Culture
  • Detection
  • Serology
77
Q

How do you manage rabies encephalitis?

A

Sedation
Intensive care
Death

78
Q

What are important sources of human infection in rabies?

A

Dogs in Africa/ Asia

Bats in the developed world (even UK…)

79
Q

What is the rabies pre-exposure prevention?

A

Active immunisation with killed vaccine

Given to:

  • Bat handlers
  • Regular handlers of imported animals
  • Selected travellers to enzootic areas
80
Q

What is the rabies post-exposure treatment?

A

Wash wound

Give active rabies immunisation

Give human rabies immunoglobin (passive immunisation) if high risk

81
Q

What is tetanus?

A

Infection with Clostridium tetani

Wound may not be apparent

Toxin acts at NMJ

  • Blocks inhibition of motor neurones
  • Rigidity and spasm (risus sardonicus)
82
Q

What type of bacteria is clostridium tetani?

A

Anaerobic Gram positive bacillus

-Spore forming

83
Q

How do you prevent tetanus?

A

Immunisation (toxoid)

Given combined with other antigens (DTap)

Penicillin and immunoglobulin for high risk wounds/ patients

84
Q

What is clostridium botulinum?

A

Anaerobic spore producing gram positive bacillus

Naturally present in soil, dust and aquatic environments

85
Q

Describe the botulinum neurotoxin

A

Binds irreversibly to the presynaptic membranes of peripheral neuromuscular an autonomic nerve junctions

Toxin binding blocks acetylcholine release

Recovery is by sprouting new axons

86
Q

What are the 3 modes of infection for clostridium botulinum?

A

Infantile (intestinal colonisation)

Food-borne (outbreaks)

Wound: almost exclusively injecting or “popping” drug users

87
Q

What is the clinical presentation for botulism?

A

Incubation period 4-14 days

Descending symmetrical flaccid paralysis

Pure motor

Respiratory failure

Autonomic dysfunction
(usually pupil dilation)
88
Q

How do you diagnose botulism?

A

Nerve conduction studies

Mouse neutralisation bioassay for toxin in blood

Culture from debrided wound

89
Q

What is the treatment for botulism?

A

Anti-toxin (A, B, E)
-Fight toxin

Penicillin/ Metronidazole (prolongued treatment)
-Fight infection

Radical wound debridement

90
Q

What should you suspect in an IVDA patient with pure motor descending paralysis?

A

Botulism until proven otherwise

91
Q

What post infective inflammatory syndromes should you watch outfor after a neurological infection?

A

Preceding infection (viral, bacterial) or immunisation

  • “Molecular mimicry”
  • Latent interval between the precipitating infection and onset of neurological symptoms
  • Autoimmune

Central nervous system
-Acute disseminated encephalomyelitis (ADEM)

Peripheral nervous system
-Guillain Barre Syndrome (GBS)

92
Q

What is Guillain Barre Syndrome?

A

Rapid-onset muscle weakness after damage to the peripheral nervous system.
Many experience changes in sensation or develop pain, followed by muscle weakness beginning in the feet and hands.
The symptoms develop over 1/2 day to 2 weeks.

Acute phase -> disorder can be life-threatening
-About 25% developing weakness of the breathing muscles and requiring mechanical ventilation.

Some affected by changes in function of the autonomic nervous system -> dangerous abnormalities in heart rate and blood pressure.

93
Q

What is Creutzfeldt-Jakob Disease (CJD)?

A

Transmissable Proteinaceous Particle (Prion)

94
Q

What is the aetiology of Creutzfeldt-Jakob Disease?

A

Sporadic CJD (most common)

New variant CJD

Familial CJD (10-15%)

Acquired CJD (

95
Q

How can you get acquired CJD?

A

Cadeveric Growth Hormone

Dura mater grafts

Blood transfusion

96
Q

What is the incidence of Creutzfeldt-Jakob Disease?

A

Very Rare

Sporadic = 1 per million per year

97
Q

When should you consider sporadic CJD?

A

Consider in any rapidly progressive dementia

98
Q

What are the clinical features of Sporadic CJD?

A
  • Insidious onset (usually over 60)
  • Early behavioural abnormalities
  • Rapidly progressive dementia
  • Myoclonus
  • Progressing to global neurological decline
  • Motor abnormalities
  • Cortical blindness
  • Seizures may occur
99
Q

What motor abnormalities may occur in sporadic CJD?

A

Cerebellar ataxia

Extrapyramidal:
-tremor, rigidity, bradykinesis, dystonia

Pyramidal:
-weakness, spacticity, hyper-reflexia

100
Q

What is the differential diagnosis of sporadic CJD?

A

Alzheimer’s disease with myoclonus
-Usually more prolonged

Subacute sclerosing panencephalitis (SSPE)
-Very rare, chronic infection with defective measles virus

CNS vasculitis

Inflammatory encephalopathies

101
Q

What is the prognosis in sporadic CJD?

A

Rapid progression

Death often within 6 months

102
Q

How does new varient CJD differ to sporadic CJD?

A

Younger onset

103
Q

How do you investigate CJD?

A

MRI

  • Pulvinar sign in varient CJD
  • Often no specific changes in sporadic CJD

EEG

  • Generalised periodic complexes typical
  • Often normal/ non-specific in initial stages

CSF

  • Normal or raised protein
  • Immunoassay 14-3-3 brain protein (non-specific, but very helpful in correct clinical context)

N - C (35 decks)

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