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year 2 neuro - Robbie > Infections of the Nervous System > Flashcards

Infections of the Nervous System Flashcards

1
Q

What is the definition of meningitis?

A

inflammation/infection of the meninges

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2
Q

What is the definition of encephalitis?

A

inflammation/infection of brain substance

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3
Q

What is the definition of myelitis?

A

inflammation/infection of the spinal cord

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4
Q

What is the classic triad of features of meningitis?

A

fever, neck stiffness and altered mental status

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5
Q

What is the common histroy of meningitis like?

A

Present with a short history of progressive headache associated with:

  • Fever (>38º) and
  • Meningism (neck stiffness, photophobia, nausea and vomiting)

Neck stiffness is examined by passively bending the neck forward

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6
Q

What part of the brain may be dysfunctioning in 69% of >14?

A

Cerebral dysfunction (confusion, delirium, declining conscious level)

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7
Q

What other less common things may be a result of meningitis?

A

Cranial nerve palsy (30%)

seizures (30%)

focal neurological deficits (10-20%)

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8
Q

Look skin rash using a tmbler test in cases of meningitis, what is this a sign of?

A

hallmark of meningococcal meningitis, but can also occur in viral meningitis

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9
Q

What are some differential diagnosis of meningitis?

A

Infective: Bacterial, Viral, Fungal

Inflammatory: Sarcoidosis

Drug induced: NSAIDs, IVIG

Malignant: Metastatic and Haematological

e.g. Leukaemia, Lymphoma, Myeloma

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10
Q

What are some bacterial causes of meningitis?

A

Neisseria meningitidis (meningococcus)

Streptococcus pneumoniae (pneumococcus)

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11
Q

What is the commenest viral cause of meningitis?

A

enteroviruses

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12
Q

What are the clinical features of encephalitis?

A

Flu-like prodrome (4-10days)

Progressive Headache associated with fever:

  • +/- meningism
  • Progressive cerebral dysfunction - confusion, abnormal behaviour, memory disturbance, depressed conscious level
  • Seizures
  • Focal symptoms/signs
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13
Q

How is viral encephalitis different from bacterial meningitis?

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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14
Q

What are some differential diagnosis of encephalitis?

A

Infective: Viral (most common is HSV)

Inflammatory: Limbic encephalitis (Anti VGKC, Anti NMDA receptor), ADEM

Metabolic: Hepatic, Uraemic, Hyperglycaemic

Malignant: Metastatic, Paraneoplastic

Migraine

Post ictal (after seizure)

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15
Q

Is auto-immune encephalitis as common as viral encephalitis?

A

May be as common as viral encephalitis

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16
Q

What are 2 important antibodies in auto-immune encephalitis?

A

Anti-VGKC (Voltage Gated Potassium Channel)

Anti-NMDA receptor

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17
Q

What Investigations of Meningitis?

A

Priority is to exclude (and treat) infection

Blood cultures (bacteraemia)

Lumbar puncture (CSF culture/microscopy)

No need for imaging if no contraindications to LP

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18
Q

What Investigations for Encephalitis?

A

Priority is to exclude (and treat) infection

Blood cultures

Imaging (CT scan +/- MRI)

Lumbar puncture

EEG

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19
Q

What do focal symptoms or signs suggest

What does reduced conscious level suggest

A

Focal symptoms or signs suggest a focal brain mass

Reduced conscious level suggests raised intracranial pressure

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20
Q

What are some contra-indicatiosn for a lumbar puncture?

A

focal neurological deficit, not including cranial nerve palsies

new-onset sezuires

papllioedema

abnormal level of consciousness, interfering with proper neurological examination

severe immunocomprimised state

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21
Q

Describe the CSF finding differences in bacterial meningitis and viral meningitis/encephalitis:

opening pressure

cell count

glucose

protein

A

Bacteria use glucose so lower in bacterial

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22
Q

Herpes simplex (HSV) encephalitis - is it rare or common?

A

Relatively rare, but commonest cause of encephalitis in Europe

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23
Q

What is the diagnosis of Herpes simplex (HSV) encephalitis?

A

Lab diagnosis by PCR of CSF for viral DNA

(opposed to growing bacteria as this is viral)

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24
Q

What is the treatment of herpes simplex (HSV) encephalitis?

A

Treat with aciclovir on clinical suspicion

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25
Q

What is the prognosis of herpes simplex (HSV) encephalitis if left untreated?

A

Over 70% mortality and high morbidity if untreated

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26
Q

Herpes simplex is one of what groups?

A

One of the herpes group of viruses

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27
Q

What are the different types of HSV and what do they cause

A

HSV types 1 & 2 cause:

cold sores (type 1 >> 2)

genital herpes (type 1 & 2 (more so in type 2))

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28
Q

How does HSV present?

A

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

(as with all herpesviruses, once infected, always infected)

Virus never leaves the body – causes acute infection then the virus disappears in the ganglia and lies dormant and if the patient goes under any stress, physical or emotional and then the virus gets reactivated and another re-infection happens and the symptoms come

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29
Q

How does HSV cause encephalitis?

A

Encephalitis is a rare complication of HSV

other than neonates, nearly all caused by type 1

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30
Q

What do enteroviruses (large family of RNA viruses) cause?

A

viral meningitis

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31
Q

What do enteroviruses have a tendency to cause?

A

CNS infection

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32
Q

Who do enteroviruses effect?

A

humans only

no animal reservoir

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33
Q

How are enteroviruses spread?

A

faecal oral route

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34
Q

Enterovirus are _____ virus which is different form herpes which is _____ virus

A

Enterovirus are RNA virus which is different form herpes which is DNA virus

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35
Q

What is an arbovirus and can it cause encephalitis

A

yes it causes arbovirus encephalitides

Inflammation of the brain (encephalitis) caused by infection with an arbovirus, a virus transmitted by a mosquito, tick or another arthropod

36
Q

How is arbovirus encephalitides transmitted?

A

Transmitted to man by vector (mosquito or tick) from non-human host

37
Q

WHat is important to do when someone present that may have a arbovirus encephalitides

A

Relevant to travel so a travel history important and some preventable by immunisation

38
Q

What is a brain abscess?

A

localized area of pus within the brain

39
Q

What is subdural empyema?

A

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

40
Q

What are the clinical features of a brain abscess and empyema?

A

Fever, Headache

Focal symptoms/signs - seizures, dysphasia, hemiparesis, etc

Signs of raised intracranial pressure - Papilloedema, false localizing signs, depressed conscious level

Meningism may be present, particularly with empyema

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

41
Q

What are some 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

Neurosurgical procedure

42
Q

What is the diagnosis of brain abscess and empyema

A

Imaging: CT or MRI

investigate source

blood cultures

Biopsy (drainage of pus)

43
Q

What organisms tend to be present in a brain abscess?

A

Often mixtures of organisms present (polymicrobial) - depend on predisposing condition

Streptococci in 70% of cases - Strep anginosus, Strep intermedius, Strep constellatus

Anaerobes (any organism that does not require oxygen for growth) in 40 - 100% of cases

44
Q

What is the management of a 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 guide
  • High mortality without appropriate treatment
45
Q

WHat conditions seen in patients would make you suspect HIV

A
  • Cerebral toxoplasmosis
  • Aseptic meningitis/encephalitis
  • Primary cerebral lymphoma
  • Cerebral abscess
  • Cryptococcal meningitis
  • Space occupying lesion of unknown cause
  • Dementia
  • Leucoencephalopathy
46
Q

Spirochaetes in the CNS may cause what diseases?

A
  • Lyme Disease (Borrelia burgdorferi)
  • Syphilis (Trepomena pallidum)
  • Leptospirosis (Leptospira interrogans)
47
Q

How is lyme disease transmitted?

A

Vector borne: Tick (wooded areas)

Spirochaete: Borrelia burgdorferi

48
Q

How many stages of lyme disease is there?

A

3

49
Q

Where does lyme disease affect in the body?

A

it is multi-system

Skin, rheumatological, neurological/neuropsychiatric, cardiac and ophthalmological involvement

Untreated 80% will develop multi-system disseminated disease

50
Q

What symptoms is there in stage 1 lyme disease?

A
  • Early localized infection (1-30d)
  • Characteristic expanding rash at the site of the tick bite: erythema migrans
  • 50% flu like symptoms (days – 1 week)

Fatigue, myalgia, arthralgia, headache, fever, chills, neck stiffness

51
Q

What is seen in stage 2 lyme disease?

A

Early disseminated infection (weeks – months)

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

Musculoskeletal and neurologic involvement most common

Neurologic involvement (10-15%) untreated patients

PNS > CNS

52
Q

What is seen in stage 3 lyme disease?

A

similar to stage 2 but further down the line

Chronic infection - months to years

occuring after a period of latency

Musculoskeletal and neurologic involvement most common

Neurologic involvement

Does NOT cause a chronic fatigue syndrome

53
Q

What is the investigtion of lyme disease?

A

Complex range of serological tests

CSF lymphocytosis - higher-than-normal amount of lymphocytes

MRI brain/spine (if CNS involvement)

Nerve conduction studies/EMG (if PNS involvement)

54
Q

What is the treatment of lyme disease?

A

• Prolonged antibiotic treatment

intravenous ceftriaxone

oral doxycycline

55
Q

How does neurosyphilis present?

A

syphilis has a similar 3 stage presentation

primary - secondary - latent

tertiary disease (neurosyphilis) years/decades after primary disease - not common

56
Q

How do you investiage syphilis?

A

antibody tests

CSF lymphocytes increased

57
Q

What is the trestment of neurosyphilis?

A

high dose penicillin

58
Q

moving onto important vaccines

A
59
Q

What causes Poliomyelitis?

A

Caused by poliovirus types 1, 2 or 3

all enteroviruses

60
Q

What does polimyelitis cause?

A
  • 99% of infections are asymptomatic
  • Paralytic disease in ~1%

infects anterior horn cells of lower motor neurones

Asymmetric, flaccid paralysis, esp legs

No sensory features

61
Q

What is the polio immunisation?

A

In UK, both contain all three poliovirus types

UK 2004 changed from oral to injected vaccine

62
Q

What is rabies?

A

Acute infectious disease of CNS affecting almost all mammals

63
Q

How is rabies transmitted?

A

Transmitted to human by bite or salivary contamination of open lesion

64
Q

Rabies is neurotropic, what does this mean?

A

virus enters peripheral nerves and migrates to CNS

65
Q

WHat are the symptoms of rabies?

A
  • Paraesthesiae (an abnormal sensation, typically tingling or pricking (‘pins and needles’)) at site of original lesion
  • Ascending paralysis and encephalitis
66
Q

What is the diagnosis of rabies encephalitis?

A

No useful diagnostic tests before clinical disease apparent

Diagnosis: PCR and Serology

67
Q

WHat is the pre-exposure prevention of rabies?

A

active immunisation with killed vaccine

68
Q

What is the post-exposure treatment of rabies?

A

Wash wound

Give active rabies immunisation

Give human rabies immunoglobulin (passive immunisation) if high risk

69
Q

What is tetanus an infection of?

A

infection with Clostridium tetani

anaerobic Gram positive bacillus, spore forming

70
Q

How does tetanus cause infection?

A

wound may not be apparent

toxin acts at neuro-muscular junction

blocks inhibition of motor neurones

71
Q

What does tetanus cause?

A

rigidity and spasm (risus sardonicus)

72
Q

How is tetanus prevented?

A

Immunisation (toxoid)

given combined with other antigens (DTaP)

Penicillin and immunoglobulin for high risk wounds/patients

73
Q

What is botulism?

A

a serious illness caused by the botulinum toxin. The toxin causes paralysis

Anaerobic spore producing gram positive bacillus

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

Toxin binding blocks acetylcholine release

Recovery is by sprouting new axons

Naturally present in soil, dust and aquatic environments

74
Q

What are the modes of botulism infection?

A

Infantile (intestinal colonization)

Food-borne (outbreaks)

Wound: Almost exclusively injecting or “popping” drug users

75
Q

What is the clinical presentation of botulism?

A

Incubation period 4-14 days

Descending symmetrical flaccid paralysis

Pure motor

Respiratory failure

Autonomic dysfunction - Usually pupil dilation

76
Q

What is the diagnosis of botulism?

A

Nerve conduction studies

Mouse neutralisation bioassay for toxin in blood

Culture from debrided wound

77
Q

What is the treatment of botulism?

A

Anti-toxin (A,B,E)

Penicillin/Metronidazole (prolonged treatment)

Radical wound debridement

78
Q

Creutzfeldt-Jakob Disease (CJD) is what type of disease?

A

Prion

prion is a type of protein that can trigger normal proteins in the brain to fold abnormally

79
Q

What is the aetiology of CJD?

A

Sporadic CJD

New variant CJD

Familial CJD (10-15%)

Acquired CJD (<5%)

• Cadeveric Growth Hormone

• Dura matter grafts

• Blood transfusion

80
Q

How common is CJD?

A

Very rare: sporadic 1 per million per year (incidence)

81
Q

When would you consider sporadic CJD in a patient?

A

Consider in any rapidly progressive dementia

82
Q

What are the clinical features of sporadic CJD?

A

Insidious onset (usually older than 60)

Early behavioural abnormalities

Rapidly progressive dementia

Myoclonus

Progressing to global neurological decline

Motor abnormalities

• Cerebellar ataxia

• Extrapyramidal: tremor, rigidity, bradykinesis, dystonia

• Pyramidal: weakness, spacticity, hyper-refexia

Cortical blindness

Seizures may occur

83
Q

What is the prognosis of sporadic CJD?

A

rapid progession

death often within 6 months

84
Q

What age does new varient CJD present at?

A

Younger onset <40

85
Q

What is more prominent in new varient CJD?

A

Early behavioural changes more prominent

86
Q

What investigations can be used for CJD?

A

MRI - Often no specific changes in sporadic CJD

EEG

CSF - Normal or raised protein

year 2 neuro - Robbie (48 decks)

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