Infections of the Nervous System Flashcards

(76 cards)

1
Q

Clinical features of encephalitis

A
Flu-like symptoms for 4-10 days 
Fever and progressive headache 
Progressive cerebral dysfunction - confusion, abnormal behaviour, memory disturbance, depressed conscious level 
Seizures 
Focal signs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Differential diagnoses for encephalitis

A
Infective e.g. viral 
Inflammatory e.g. limbic encephalitis 
Metabolic e.g. uraemic 
Malignancy e.g. metastases 
Migraine 
Post-ictal
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Antibodies present in autoimmune encephalitis

A

Anti-VGKC and anti-NMDA receptor antibodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Features of Anti-VGKC autoimmune encephalitis

A

Frequent seizures
Amnesia
Altered mental state

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Features of Anti-NMDA receptor autoimmune encephalitis

A
Flu-like prodrome 
Prominent psychiatric features 
Altered mental state 
Seizures 
Progression to movement disorder and coma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How is encephalitis caused by HSV (herpes simplex virus) diagnosed?

A

Lab diagnosis by PCR of CSF for viral DNA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Treatment of encephalitis caused by HSV

A

Acyclovir on strong clinical suspicion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Morbidity/mortality rate of encephalitis caused by HSV

A

over 70% mortality and high morbidity if untreated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Where does the HSV lie latent after primary infection and what does this mean there is a risk of?

A

Lies latent in trigeminal or sacral ganglion after primary infection, risk of reactivation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Investigation of encephalitis

A

Blood cultures
Imaging - CT, MRI
LP
EEG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Encephalitis treatment

A

Acyclovir

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is a brain abscess?

A

Localised area of pus within the brain which causes high-pressure symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

When would a fever be present in brain abscess?

A

If there was systemic infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Clinical features of brain abscess

A
Fever 
Headache 
Seizures 
Dysphasia 
Hemiparesis 
Papilloedema 
False localising signs 
Depressed conscious level 
Meningism 
Features of underlying source of infection e.g. poor dentition
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Differential diagnoses for brain abscess

A

Any focal lesion, most commonly a tumour

Subdural haematoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Causes of brain abscess

A

Penetrating head injury
Spread from adjacent infection e.g. dental, sinusitis
Blood borne infection e.g. bacterial endocarditis
Neurosurgical procedure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Brain abscess investigation

A

MRI, CT
Investigate source
Blood cultures
Biopsy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is the risk of a biopsy of a brain abscess?

A

Drainage of pus and removal of needle puts patient at risk of spread of infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Infective organisms in brain abscess

A

Streptococci - 70%, especially streptococcus Milleri group

Anaerobes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Treatment of brain abscess

A

Surgical drainage if possible
Penicillin or ceftriaxone to cover strep infection
Metrondiazole for anaerobe infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is meningitis?

A

Inflammation/infection of the meninges

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Clinical features of meningitis

A
Fever, neck stiffness, altered mental status 
Short history of progressive headache 
May be associated with fever and meningism 
Cerebral dysfunction 
Cranial nerve palsy 
Seizures 
Focal neurological deficits 
Petechial skin rash
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Differential diagnoses of meningitis

A

Infective - bacterial, viral or fungal
Inflammatory - sarcoidosis
Drug induces - NSAIDs, IVIG
Malignant - metastatic, haematological

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Causes of meningitis

A

Bacterial

Viral (enteroviruses)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Bacterial organisms that cause meningitis
Neisseria meningitidis | Streptococcus pneumoniae
26
Investigation of meningitis
Blood cultures | Lumbar puncture
27
Opening pressure in LP of bacterial meningitis
Increased
28
Opening pressure in LP of viral meningitis and encephalitis
Normal or increased
29
Cell count in LP of bacterial menignitis
High, mainly neutrophils
30
Cell count in LP of viral meningitis
High, mainly lymphocytes
31
Glucose in LP of bacterial meningitis
Reduced
32
Glucose in LP of viral meningitis
Normal
33
Protein in LP of bacterial meningitis
High
34
Protein in LP of viral meningitis
Slightly increased
35
HIV indicator illnesses in the brain
``` Cerebral toxoplasmosis Aseptic meningitis/encephalitis Primary cerebral lymphoma Cerebral abscess Cryptococcal meningitis Space occupying lesion of unknown cause Dementia Leukoencephalopathy ```
36
Brain infections in HIV patients with low CD4 counts
``` Cryptococcur neoformans Toxoplasma gondii Progressive multifocal Leukoencephalopathy Cytomegalovirus HIV encephalopathy ```
37
How are cryptococcal infections established?
Following inhalation of airborne organisms into the lungs
38
How do most cases of cryptococcal infections present?
With meningoencephalitis | Most patients will have defects in immune function
39
Spirochaete infections in the CNS
Lyme disease Syphilis Leptospirosis
40
Causative organism of Lyme disease
Borrelia burgdorferi
41
How is Lyme disease transmitted
Vector borne via ticks
42
What parts of the body are affected by Lyme disease?
``` Multi-system involvement Skin Rheumatological Neurological/neuropsychiatric Cardiac Opthalmological ```
43
Consequence of untreated Lyme disease
80% will develop disseminated disease
44
Describe stage 1 Lyme disease
Early localised infection 1-30 days Expanding rash at site of tick bite - erythema migrans Flu-like symptoms (50%) - fatigue, myalgia, arthralgia, headache, fever, chills, neck stiffness
45
Treatment of stage 1 Lyme disease
doxycycline
46
Describe stage 2 Lyme disease
Early disseminated infection (weeks-months) One or more organ systems become involved - haematological or lymphatic spread Musculoskeletal and neurological involvement most common
47
Possible presentations of neurological involvement in Lyme disease
``` Meningo-encephalitis Cranial neuropathy Painful radiculopathy Plexopathy Diffuse or focal mononeuritis multiplex Mononeuropathy Myelitis ```
48
Describe stage 3 Lyme disease
Chronic infection months - years, occurring after a period of latency Musculoskeletal and neurological involvement most common Neurological involvement - subacute encephalopathy, encephalomyelitis
49
Investigation of Lyme disease
``` Serological tests CSF lymphocytosis PCR of CSF MRI brain/spine if CNS involvement Nerve conduction studies/EMG if PNS involvement ```
50
Lyme disease treatment
Prolonged antibiotic treatment IV, 3 weeks-1 month IV ceftriaxone Oral doxycyclin
51
Treatment of neurosyphilis
High dose penicillin
52
Aetiologies of Creutzfeldt-Jakob disease (CJD)
Sporadic New variant Familial Acquired
53
Clinical features of sporadic CJD
``` Rapidly progressive dementia Insidious onset, usually over 60s Behavioural abnormalities Myoclonus Global neurological decline Motor abnormalities Cortical blindness Seizures ```
54
Sporadic CJD differential diagnoses
``` Alzheimer's disease with myoclonus Subacute sclerosing panencephalitis CNS vasculitis Non-convulsive status Toxic/metabolic encephalopathies ```
55
Sporadic CJD prognosis
Rapid progression | Death, often within 6 months
56
Features of new variant CJD
Younger onset (< 40) Linked to bovine spongiform encephalopathy in cattle - eating infected material Early behavioural changes more prominent Longer course, around 13 months
57
Investigation of CJD
MRI - Pulvinar sign present in variant CJD, often no specific signs in sporadic CJD EEG - generalised periodic complexes typical, often normal/non-specific in early stages CSF - normal or raised protein
58
Cause of poliomyelitis
Polioviruses type 1, 2 and 3 (enteroviruses)
59
What percentage of poliomyelitis will result in paralytic disease?
1%, 99% are asymptomatic
60
Features of poliomyelitis
Infects anterior horn cells of lower motor neurones Asymmetric, flaccid paralysis, especially of the legs No sensory features
61
Transmission of rabies
By bite or salivary contamination of an open lesion
62
Features of rabies
Virus enters peripheral nerves and migrates to CNS Paraesthesiae at the site of the original lesion Ascending paralysis and encephalitis
63
Diagnosis of rabies encephalitis
Culture Detection Serology
64
Treatment of rabies encephalitis
Condition has 100% mortality, sedation and intensive care
65
Main sources of rabies encephalitis
Dogs and bats
66
How is rabies pre-exposure prevention carried out?
Active immunisation with killed vaccine
67
Rabies post-exposure treatment
Wash wound Give active rabies immunisation Give human rabies immunoglobulin if high risk
68
Organism causing tetanus
Clostridium tetani | Anaerobic gram-positive bacillus, spore forming
69
Clinical features of tetanus
Rigidity and spasm
70
Treatment of tetanus
Immunisation combined with other antigens | Penicillin and immunoglobulin for high risk wounds/patients
71
Infective organism causing botulism
Clostridium botulinum | Anaerobic sporre producing gram positive bacillus
72
How does clostridium botulinum work?
Neurotoxin, binds irreversibly to the presynaptic membranes of peripheral neuromuscular and autonomic nerve junctions Toxin binding block ACh release
73
Modes of infection of clostridium botulinum
Infantile Food-borne Wound
74
Clinical presentation of botulism
``` Incubation period 4-14 days Descending symmetrical flaccid paralysis Pure motor Respiratory failure Autonomic dysfunction ```
75
Botulism diagnosis
Nerve conduction studies Mouse neutralisation bioassay for toxin in blood Culture for debrided wound
76
Botulism treatment
Anti-toxin Penicillin/metronidazole Radical wound debridement