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Infections of the nervous system Flashcards

1
Q

what is meningitis?

A

inflammation / infection of 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

what are 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 is the classid triad of symptoms for meningitis?

A

fever, neck stiffness and altered mental status

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6
Q

what test is used to check for a rash in meningitis?

A

Tumbler test

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7
Q

what typpe of rash is seen in meningitis?

A

petechial skin rash

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8
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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9
Q

what are bacterial causes of meningitis?

A

Neisseria meningitidis (meningococcus)
Streptococcus pneumoniae (pneumococcus)

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10
Q

what are viral causes of meningitis?

A

enteroviruses

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11
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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12
Q

how does the onset of viral encephalitis compare to 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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13
Q

what are 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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14
Q

what is auto-immune encephalitis?

A

acute to subacute, progressive inflammation of the brain associated with antibodies against neuronal cell surface and synaptic protein, most commonly being anti - NMDA receptor encephalitis

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15
Q

what is anti-VGKC auto-immune encephalitis?

A

Anti-VGKC-complex encephalitis are caused by antibodies against the voltage gated potassium channel-complex (VGKC-complex) and are implicated in several autoimmune conditions including limbic encephalitis, epilepsy and neuromyotonia (i.e. Isaacs’ Syndrome).

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16
Q

symptoms of Anti-VGKC (Voltage Gated Potassium Channel) autoimmune encephalitis?

A

Frequent seizures
amnesia (not able to retain new memories)
Altered mental state

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17
Q

what is anti-NMDA receptor encephalitis?

A

Anti-NMDA receptor encephalitis is a neurologic disease first identified by Dr. Josep Dalmau and colleagues at the University of Pennsylvania in 2007. It is an autoimmune disease, where the body creates antibodies against the NMDA receptors in the brain.

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18
Q

what are symptoms of Anti-NMDA receptor
auto–immune encephalitis?

A

Flue like prodrome
Prominent psychiatric features
Altered mental state and seizures
Progressing to a movement disorder and coma

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19
Q

what are 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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20
Q

what are investigations for encephalitis?

A

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

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21
Q

what are indications for CT brainscanning before lumbar puncture?

A

focal neurological deficit (cranial N palsies)
new onset seizures
abnormal levek conciousness
severe immunocomprimised state

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22
Q

what do Focal symptoms or signs suggest?

A

focal brain mass

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23
Q

what do reduced conciousness levels suggest?

A

raised intracranial pressure

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24
Q

describe the opening pressure, cell count, glucose and protein of CSF in bacterial meningitis?

A

increased
High - mainly neutrophils
reduced
high

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25
describe the opening pressure, cell count, glucose and protein of CSF in viral meningitis and encephalitis?
normal/increased High mainly lymphocytes normal slightly increased
26
which gram stains and cultures do you do for bacterial meningitis?
Blood culture Gram stain: Gram positive cocci in chains - looks like streptococci Culture streptococcus pneumoniae sensitive to penicillin
27
what is herpes simplex encephalitis?
Relatively rare, but commonest cause of encephalitis in Europe Lab diagnosis by PCR of CSF for viral DNA
28
how is herpes simplex virus encephalitis treated?
Treat with aciclovir on clinical suspicion
29
if HSV is left untreated what is the mortality rate?
Over 70% mortality and high morbidity if untreated
30
what is herpes simplex virus?
One of the herpes group of viruses (VZV, EBV, CMV) HSV types 1 & 2 cause cold sores (type 1 >> 2) genital herpes (type 1 & 2) Virus remains latent in the trigeminal or sacral ganglion after primary infection (as with all herpesviruses, once infected, always infected)
31
which types of herpes is cold sores?
(type 1 >> 2)
31
which type of herpes is genital herpes?
(type 1 & 2)
32
what is a rare complication of HSV?
Encephalitis is a rare complication of HSV other than neonates, nearly all caused by type 1
33
what do enteroviruses have a tendency of causing?
Tendency to cause CNS infections (neurotropic) Human infections, no animal reservoir
34
how do enteroviruses spread?
faecal-oral route
35
what conditions do enteroviruses cause?
Many can cause non-paralytic meningitis They do NOT cause gastroenteritis Include polioviruses, coxsackieviruses and echoviruses
36
what is arbovirus encephalitides?
Common in other parts of the world 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
37
by what mechanism is arbovirus encephalitides formed?
Called Arbo as arthropod borne Relevant to travel travel history important some preventable by immunisation Place names of organisms generally relate to where first described and NOT to current geographical distribution
38
what is a brain abscess?
localized area of pus within the brain
39
what is subdural empyema?
thin layer of pus between the dura and arachnoid membranes over the surface of the brain
40
what are clinical features of brain abscess and empyema?
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
what is a differential diagnosis of brain abscess and empyema?
Any focal lesion, but most commonly tumour Subdural haematoma
42
what are causes of brain abcess and empyema?
Penetrating head injury Spread from adjacent infection Dental, Sinusitis, Otitis media Blood borne infection e.g. Bacterial endocarditis Neurosurgical procedure
43
how is brain abscess and empyema diagnosed?
imaging: CT or MRI investigate source blood cultures Biopsy (drainage of pus)
44
what organisms are ussually present in a brain abscess?
Streptococci in 70% of cases, especially the penicillin-sensitive “Strep milleri” group Strep anginosus, Strep intermedius, Strep constellatus Anaerobes in 40 - 100% of cases Bacteroides, Prevotella
45
what is management of brain abscess?
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
46
what are indicator illnesses for HIV?
Cerebral toxoplasmosis Aseptic meningitis /encephalitis Primary cerebral lymphoma Cerebral abscess
47
what are you looking for in HIV patients with low CD4 counts?
Cryptococcus neoformans Toxoplasma gondii Progressive multifocal leukoencephalopathy (PML) Cytomegalovirus (CMV) HIV-encephalopathy (HIV-associated dementia)
48
how do you diagnose HIV indicator illness patients?
Cryptococcal antigen Toxoplasmosis serology CMV PCR HIV PCR
49
how is spirochaetes in the CNS spread?
Lyme Disease (Borrelia burgdorferi) Syphilis (Trepomena pallidum) Leptospirosis (Leptospira interrogans)
50
how is lyme disease borne?
Vector borne: Tick (wooded areas)
51
what is the spirochate og lymes disease?
Borrelia burgdorferi
52
what systems are involved in llymes diseaae?
Skin, rheumatological, neurological / neuropsychiatric, cardiac and ophthalmological involvement Untreated 80% will develop multi-system disseminated disease
53
what is stage one of lymes disease?
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
54
what is stage 2 of lymes disease?
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 Mononeuropathy Mononeuritis multiplex Painful radiculoneuropathy PNS > CNS Cranial neuropathy Myelitis Meningo-encephalitis
55
what is stage 3 of lymes disease?
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
56
how is lymes disease investigated?
Complex range of serological tests CSF lymphocytosis MRI brain / spine (if CNS involvement) Nerve conduction studies / EMG (if PNS involvement)
57
how is lymes disease treated?
Prolonged antibiotic treatment intravenous ceftriaxone oral doxycycline
58
what three stages does neurosyphilis present as?
(Treponema pallidum) primary secondary tertiary
59
what tests are done for neurosyphilis?
Treponema specific and non-treponemal specific antibody tests CSF lymphocytes increased, evidence of intrathecal antibody production
60
how is neurosyphylis treated?
High dose penicillin
61
what are causes of encephalitis?
Herpes Simplex Enteroviruses Arbovirus encephalitides Brain Abscess and Empyema HIV indicator illnesses (brain) Lyme disease Neurosyphilis
62
what is poliomyelitis?
Caused by poliovirus types 1, 2 or 3 all enteroviruses 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
63
describe the polio immunisation?
In UK, both contain all three poliovirus types UK 2004 changed from oral to injected vaccine because of risk of vaccine-associated polio from oral vaccine because indigenous polio due to wild (ie non-vaccine) polio eliminated from UK given combined with other antigens (IPV)
64
what is rabies?
Acute infectious disease of CNS affecting almost all mammals Transmitted to human by bite or salivary contamination of open lesion Neurotropic - virus enters peripheral nerves and migrates to CNS Paraesthesiae at site of original lesion Ascending paralysis and encephalitis
65
what is rabies encephalitis?
No useful diagnostic tests before clinical disease apparent Diagnosis: PCR and Serology Sedation/intensive care/death ~ 40,000 - 50,000 deaths/year, mostly Asia Important sources of human infection: Dogs in Africa/Asia Bats in the developed world. 2002: 1st indigenous case in UK since 1902 – bat handler.
66
what is rpre exposure prevention for rabies?
Active immunisation with killed vaccine In UK give to:- bat handlers regular handlers of imported animals selected travellers to enzootic areas
67
what is post exposure treatment for rabies?
Wash wound Give active rabies immunisation Give human rabies immunoglobulin (passive immunisation) if high risk
68
what is tetanus?
infection with Clostridium tetani anaerobic Gram positive bacillus, spore forming wound may not be apparent toxin acts at neuro-muscular junction blocks inhibition of motor neurones rigidity and spasm (risus sardonicus)
69
how is tetanus prevented?
Immunisation (toxoid) given combined with other antigens (DTaP)
70
what is given to patients at high risk of teanus?
Penicillin and immunoglobulin for high risk wounds/patients
71
what is botulism?
Anaerobic spore producing gram positive bacillus Neurotoxin 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
72
what are the three modes of infection or botulism?
Infantile (intestinal colonization) Food-borne (outbreaks) Wound: Almost exclusively injecting or “popping” drug users
73
what is the clinical presentation for botulism?
Incubation period 4-14 days Descending symmetrical flaccid paralysis Pure motor Respiratory failure Autonomic dysfunction Usually pupil dilation
74
how is botulism diagnosied?
Nerve conduction studies Mouse neutralisation bioassay for toxin in blood Culture from debrided wound
75
how is botylism treated?
Anti-toxin (A,B,E) Penicillin / Metronidazole (prolonged treatment) Radical wound debridement
76
what are post infective inflammatory syndromes?
Central nervous system Acute disseminated encephalomyelitis (ADEM) Peripheral nervous system Guillain Barre Syndrome (GBS)
77
what is Creutzfeldt-Jakob Disease (CJD)?
Aetiology Sporadic CJD New variant CJD Familial CJD (10-15%) Acquired CJD (<5%) Cadeveric Growth Hormone Dura matter grafts Blood transfusion
78
what are clinical features of CJD?
Clinical features 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
79
what are differential diagnosis of sporadic CJD?
Alzheimer’s disease with myoclonus Usually more prolonged Subacute sclerosing panencephalitis (SSPE) Very rare, chronic infection with defective measles virus CNS vasculitis Inflammatory encephalopathies
80
what is prognosis of sporadic CJD?
Rapid progression Death often within 6 months
81
what are investigations for CJD?
MRI Pulvinar sign in variant 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)

Nervous System (40 decks)

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