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systems- neuro- oc > Infections of the Nervous System > Flashcards

Infections of the Nervous System Flashcards

1
Q

definition of meningitis

A

inflammation / infection of meninges

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2
Q

definition of encephalitis

A

inflammation / infection of brain substance

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3
Q

definition of myelitis

A

inflammation / infection of spinal cord

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4
Q

clinical features of meningitis

A

“classical triad” – fever, neck stiffness and altered mental status

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

Cerebral dysfunction (confusion, delirium, declining conscious level) is common and GCS is <14 in 69%

Cranial nerve palsy (30%), seizures (30%), focal neurological deficits (10-20%) may also occur

Look for a petechial skin rash (Tumbler test)
hallmark of meningococcal meningitis, but can also occur in viral meningitis

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5
Q

what are differential diagnosis of meningitis?

A

Infective: Bacterial, Viral, Fungal

Inflammatory: Sarcoidosis

Drug induced: NSAIDs, IVIG

Malignant: Metastatic
Haematological
e.g. Leukaemia, Lymphoma, Myeloma

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6
Q

what are the bacterial causes of meningitis?

A 
Neisseria meningitidis (meningococcus)
Streptococcus pneumoniae (pneumococcus)
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7
Q

what are the viral causes of meningitis?

A

enteroviruses

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8
Q

what are 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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9
Q

what are the 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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10
Q

what are the two antibodies involved in auto-immune encephalitis?

A

Anti-VGKC (Voltage Gated Potassium Channel)
Frequent seizures
amnesia (not able to retain new memories)
Altered mental state

Anti-NMDA receptor
Flue like prodrome
Prominent psychiatric features
Altered mental state and seizures
Progressing to a movement disorder and coma
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11
Q

what are the investigations for meningitis?

A 
Blood cultures (bacteraemia)
Lumbar puncture (CSF culture/microscopy)
No need for imaging if no contraindications to LP
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12
Q

what are the investigations for encephalitis?

A

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

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13
Q

what are the indications for CT brain scanning before lumbar puncture?

A

focal neurological deficit, not including cranial nerve palsies

new onset seizures

papilloedema

abnormal level of consciousness, interfering with proper neurological examination

severe immunnocomprimised state

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14
Q

what do focal symptoms or signs suggest on a CT?

A

focal brain mass

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15
Q

what does reduced conscious level suggest on a CT?

A

raised intracranial pressure

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16
Q

what is the cell count in bacterial meningitis?

A

high, mainly neutrophils

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17
Q

what is the cell count in viral meningitis or encephalitis?

A

high, mainly lymphocytes

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18
Q

what is the levels of glucose in bacterial meningitis?

A

reduced

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19
Q

what are the glucose levels in viral meningitis and encephalitis?

A

normal 60% of blood glucose

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20
Q

what are the protein levels in bacterial meningitis?

A

high

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21
Q

what are the protein levels in viral meningitis and encephalitis

A

slightly increased

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22
Q

what would the result of a blood culture gram stain be?

A

gram positive cocci in chains- looks like streptococci

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23
Q

what is the commonest cause of encephalitis in europe?

A

herpes simplex (HSV) encephalitis

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24
Q

how would you treat HSV encephalitis?

A

aciclovir

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25
Q

what are the results of HSV type 1 and 2?

A

cold sores and genital herpes

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26
Q

how are enteroviruses spread?

A

faecal-oral route

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27
Q

what can enteroviruses cause?

A

non-paralytic meningitis

28
Q

do enteroviruses cause gastroenteritis?

A

no

29
Q

how is arbovirus encephalitis transmitted?

A

to man by vector form non-human host

30
Q

what part of a history is related to arbovirus encephalitedes?

A

travel history- can be prevented by immunisation

31
Q

what is a subdural empyema?

A

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

32
Q

what are clinical features of 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

33
Q

differential diagnosis of brain abscess and empyema

A

Any focal lesion, but most commonly tumour

Subdural haematoma

34
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
Neurosurgical procedure
35
Q

how would you diagnose brain abscess and empyema?

A

Imaging: CT or MRI

investigate source

blood cultures

Biopsy (drainage of pus)

36
Q

how do you manage 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

37
Q

what are HIV indicators (brain)

A 
Cerebral toxoplasmosis 
Aseptic meningitis /encephalitis
Primary cerebral lymphoma 
Cerebral abscess
Cryptococcal meningitis 
Space occupying lesion of unknown cause
Dementia
Leucoencephalopathy
38
Q

diagnostics of brain infections in HIV

A

Cryptococcal antigen
Toxoplasmosis serology
CMV PCR
HIV PCR

39
Q

what are the spirochaetes in the CNS?

A 
Lyme Disease (Borrelia burgdorferi)
Syphilis (Trepomena pallidum)
Leptospirosis (Leptospira interrogans)
40
Q

what is the vector invoolved in lyme disease?

A

tick

41
Q

what are the stage 1 signs of 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

42
Q

what are the stage 2 signs of 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

43
Q

what are the stage 3 signs of lyme disease?

A

Chronic infection
months to years
occuring after a period of latency

Musculoskeletal and neurologic involvement most common

Neurologic involvement
As described for stage 2
Subacute encephalopathy
Encephalomyelitis

44
Q

what are the investigations for lyme disease?

A

Complex range of serological tests
CSF lymphocytosis
MRI brain / spine (if CNS involvement)
Nerve conduction studies / EMG (if PNS involvement)

Prolonged antibiotic treatment
intravenous ceftriaxone
oral doxycycline

45
Q

what are the three stages of syphillis?

A

primary, secondary, latent

46
Q

what are the antibody tests involved in syphillis?

A

Treponema specific and non-treponemal specific antibody tests

47
Q

what causes poliomyelitis?

A

poliovirus types 1, 2 or 3

48
Q

how is rabies transmitted to a human?

A

by bite or salivary contamination of open lesion

49
Q

how would you diagnosoe rabies encephalitis?

A

PCR and Serology

50
Q

what is the tetanus infection?

A

Clostridium tetani

51
Q

what type of bacillus is tetanus?

A

anaerobic Gram positive bacillus, spore forming

52
Q

what does tetanus do?

A

blocks inhibition of motor neurones

rigidity and spasm (risus sardonicus)

53
Q

how is tetanus preventable?

A

immunisation

54
Q

what are the three modes of infection of botulism?

A

Infantile (intestinal colonization)
Food-borne (outbreaks)
Wound: Almost exclusively
injecting or “popping” drug users

55
Q

what is the botulism infection?

A

Clostridium botulinum

56
Q

how does botulism (Neurotoxin) work?

A

Binds irreversibly to the presynaptic membranes of peripheral neuromuscular and autonomic nerve junctions
Toxin binding blocks acetylcholine release
Recovery is by sprouting new axons

57
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
58
Q

how would you diagnose botulism?

A

Nerve conduction studies
Mouse neutralisation bioassay for toxin in blood
Culture from debrided wound

59
Q

what is the treatment of botulism?

A

Anti-toxin (A,B,E)
Penicillin / Metronidazole (prolonged treatment)
Radical wound debridement

60
Q

what are some post infective inflammatory syndromes?

A

“Molecular mimicry”Acute disseminated encephalomyelitis (ADEM)
Guillain Barre Syndrome (GBS)

61
Q

what is the aetiology of creutzfeldt-jakob disease?

A 
Sporadic CJD
New variant CJD
Familial CJD (10-15%)
Acquired CJD (<5%)
Cadeveric Growth Hormone
Dura matter grafts
Blood transfusion
62
Q

clinicl 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

63
Q

what are 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

64
Q

what is the prognosis of sporadic CJD?

A

Rapid progression

Death often within 6 months

65
Q

investigations of CJD?

A

MRI
EEG
CSF

systems- neuro- oc (51 decks)

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