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Conditions + definitions > Neuro 3 > Flashcards

Neuro 3 Flashcards

1
Q

What is the difference between primary and secondary headaches?

A

Primary - no abnormality behind, just occur
>Tension type, cluster + migraines
Secondary - some sort of pathology behind it
>Not all are sinister

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2
Q

What are tension type headaches?

A

Most frequent type, but not disabling

Mild, bilateral headache - often pressing or tightening in quality

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3
Q

What is the abortive treatment for tension type headaches?

A

Aspirin or paracetamol
NSAIDs
Limit to 10 days per month (~2 days per week) to avoid the development of medication overuse headache

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4
Q

What is the preventative treatment of tension type headaches?

A

Rarely required
Tricyclic antidepressants
>amitriptyline, dothiepin, nortriptyline

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5
Q

What is a migraine?

A

Most common disabling primary headache
Chronic disorder with episodic attacks - complex changes in the brain
Normal life events can trigger or associated with migraines (stress, period, hunger, dehydration diet)

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6
Q

What are the symptoms of migraine?

A 
During attacks 
>Headache
>Nausea, photophobia, phonophobia
>Functional disability
In-between attacks 
>Enduring predisposition to future attacks
>Anticipatory anxiety
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7
Q

What are the stages of a migraine?

A

Premonitory
Early headache
Advanced headache
Prodrome

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8
Q

What is the premonitory phase of a migraine?

A 
Mood + cognitive changes
Fatigue
Muscle pain
Food craving
Some get an aura - 33% 15-60 minutes long normally
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9
Q

What is the early headache phase of a migraine?

A

best place to treat
Dull
Nasal congestion
Muscle pain

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10
Q

What is the early headache phase of a migraine?

A

Unilateral
Throbbing
Nausea
Photo/osma/phono phobia

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11
Q

What is the prodrome phase of a migraine?

A

Fatigue
Cognitive changes
Muscle pain

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12
Q

What is a chronic migraine?

A

Headache >=15 days/month, of which >=8 must be migraine for more than 3 months

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13
Q

What is a transformed migraine?

A

History of episodic migraine
Increasing frequency of headaches
>over weeks / months / years
>symptoms become less frequent and less severe
Some have severe migraines with daily lesser headaches

> can occur with or without escalation in medication use

In patients with medication overuse, discontinuing the overused medication often (but not always) dramatically improves headache frequency

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14
Q

What is a medication overuse headache?

A

Headache present on ≥15 days / month which has developed or worsened whilst taking regular symptomatic medication
Can occur in primary headaches

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15
Q

What can cause a medication overuse headache?

A

Migraineurs taking pain medication for another reason can develop chronic headache
Use of triptans, ergots, opiods and combination analgesics >10 days / month
Use of simple analgesics > 15 days per month
Caffeine overuse: coffee, tea, cola, irn brew

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16
Q

What is the abortive treatment for a migraine?

A

Aspirin or NSAIDs
Triptans
Limit to 10 days per month (~2 days per week) to avoid the development of medication overuse headache

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17
Q

What is the prophylactic treatment for a migraine?

A 
Propranolol, Candesartan
Anti-epileptics
>Topiramate, Valproate, Gabapentin
Tricyclic antidepressants
>amitriptyline, dothiepin, nortriptyline 
Venlafaxine
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18
Q

How do you treat a migraine during pregnancy?

A

Avoid antiepileptics
Acute attack - use paracetoamol
Prevent with propranolol or amitriptyline

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19
Q

What are the causes of trigeminal autonomic cephalagias?

A

Cluster headache
Paraxoysmal hemicrania
SUNCT/SUNA (short lasting unliateral neuralgiform headache)
>Conjunctibital injection + tearing /autonomic symptoms

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20
Q

What is trigeminal autonomic cephalagias?

A

Unilateral head pain - very severe
Attack frequency +duration differs
Get cranial autonomic symptoms

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21
Q

What is a cluster headache attack?

A 
Rapid onset + severe unilateral attacks
>Mainly orbital + temporal pain - 
Last 15mis - 3hrs
>Rapid cessation of pain
Patients restless during an attack
Prominent ipsilateral autonomic symptoms                                  
Migrainous symptoms often present
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22
Q

What are the migrainous symptoms often present in a TAC?

A

Premonitory symptoms: tiredness, yawning
Associated symptoms: nausea, vomiting, photophobia, phonophobia
Typical aura (often under recognised)

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23
Q

How can the TAC attacks present (what frequency/length)?

A

Either bouts that last 1-3 months or chronic clusters

Bouts
>1-8 a day
>At roughly same time each day

Chronic
>Last a year without remission
>Or remission for a month and then restart

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24
Q

What are the cutaneous triggers for headaches?

A

Wind
Cold
Touch
Chewing

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25
Q

What is paroxysmal hemicrania?

A 
Excrutiatingly severe unilateral episodes with acute onset
>Mainly orbital and temporal
Duration: 2-30 mins
Rapid cessation of pain
50% are restless and agitated during an attack
Prominent ipsilateral autonomic symptoms
Migrainous symptoms may be present
Background cutaneous pain
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26
Q

What is the frequency of paroxysmal hemicrania?

A

2-40 attacks a day

With no circadian rhythm

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27
Q

What is a SUNT headache?

A

Unilateral orbital, supraorbital or temporal pain
Stabbing or pulsating pain
10-240 seconds duration
Cutaneous triggers
Pain is accompanied by conjunctival injection and lacrimation

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28
Q

What is the attack frequency for a SUNT headache?

A

Attack frequency from 3-200/day,

>no refractory period

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29
Q

What is trigeminal neuralgia?

A 
Unilateral maxillary or mandibular division pain > ophthalmic division
Stabbing pain
5 - 10 seconds duration
Cutaneous triggers
Autonomic features are uncommon
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30
Q

What is the attack frequency for tirgeminal neuralgia?

A

Attack frequency from 3-200/day,

>refractory period

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31
Q

What is the abortive treatment for a cluster headache?

A

Subcutaneous sumatriptan
nasal zolmatriptan
100% oxygen

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32
Q

What is the abortive treatment for a cluster headache bout?

A

Occipital depomedrone injection (same side as the headache)

Or tapering course of oral prednisone

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33
Q

What is the preventative treatment for a cluster headache?

A

Verapamil (high doses may be required)
Lithium
Methysergide (risk of retroperitoneal fibrosis)
Topiramate

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34
Q

What is the treatment for tirgeminal neuralgia?

A 
No abortive treatment
Prophylaxis:
>Carbamazepine
>Oxcarbazepine
Surgical intervention can be considered (decompression)
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35
Q

What is the treatment for SUNCT/SUNA headaches?

A 
No abortive treatment
Prophylaxis:
>Lamotrigine
>Topiramate
>Gabapentin
>Carbamazepine / Oxcarbazepine
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36
Q

What presentations are more likely to have a sinister cause?

A 
Associated head trauma
First or worst
Sudden (thunderclap) onset
New daily persistent headache
Change in headache pattern or type
Returning patient
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37
Q

What are the main sinister headache risk factors?

A 
Over 50
New or change in headache
Focal symptoms or non-focal neurological symptoms
Abnormal neurological exam
Neck stiffness
High/low pressure
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38
Q

What is a thunderclap headache?

A

A high intensity headache reaching maximum intensity in less than 1 minute
Majority peak instantaneously
May be primary or secondary
No reliable differentiating features!

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39
Q

What are the differentials of a thunderclap headache?

A 
Primary 
>migraine, 
>primary thunderclap headache, 
>primary exertional headache, 
>primary headache associated with sexual activity
Subarachnoid haemorrhage
Intracerebral haemorrhage
TIA / stroke
Carotid / vertebral dissection
Cerebral venous sinus thrombosis
Meningitis / encephalitis
Pituitary apoplexy
Spontaneous intracranial hypotension
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40
Q

Who should be suspected of an SAH?

A

All patients presenting with a sudden severe headache that peaks within a few minutes and lasts for at least 1 hour
Examination is often normal!
Never consider a patient ‘too well’ for SAH

41
Q

How do you manage a suspected SAH?

A

SAME DAY hospital assessment
To check for SAH
CT brain (some false negative)
LP (must be done >12hrs after headache onset)
CT +/- LP is unreliable beyond 2 weeks and angiography is required beyond this time

42
Q

What are the features of a riased ICP?

A

Progressive headache with associated symptoms and signs

Headache is a common 1st presenting feature, but other symptoms and signs are usually present

43
Q

What are the warning features of raised ICP?

A

Headache worse in morning or wakes patient from sleep
Headache worse lying flat or brought on by valsalva (cough, stooping, straining)
Focal symptoms or signs
Non-focal symptoms e.g. cognitive or personality change, drowsiness
Seizures
Visual obscurations and pulsatile tinnitus

44
Q

What are the features of intracranial hypotension headache?

A

Dural CSF leak
Spontaneous or iatrogenic (post lumbar puncture)
Clear postural component to the headache
>Worsens on upright posture
>Gets better lying down
>Chronic headache often loses postural component

45
Q

How do you investigate intracranial hypotension?

A

MRI Brain

MRI spine

46
Q

How do you treat intracranial hypostension?

A 
Bed rest
Fluids
Analgesia
Caffeine
IV caffiene if required
Epidural blood patch
47
Q

What is a giant cell arteritis headache?

A

Consider in patient over 50 with new headache
Diffuse, persistant maybe severe headache
Systemically unwell potentially
Scalp tenderness, jaw claudication + visual disturbance
Prominent temporal arteries may be present
Elevated ESR supports diagnosis

48
Q

What are the eye scores for the glasgow coma scale?

A

Open spontaneously (4)
Open to verbal command (3)
Open to pain (2)
Does not open eyes (1)

49
Q

What is the verbal scores for the glasgow coma scale?

A 
Orientated (5)
Confused speech (4)
Inappropriate words (3)
Incomprehensible sounds (2)
No speech (1)
50
Q

What is the motor response for the glasgow coma scale?

A 
Obeys commands (6)
Localises to pain (5)
Normal flexion to pain (4)
Abnormal flexion to pain (3)
Extension to pain (2)
No movement (1)
51
Q

What is the pathophysiology process of haemorrhage?

A

Haemorrhage – ‘mass effect’
Disruption of blood brain barrier - ↑ECF (vasogenic oedema)
Membrane failure – influx of Ca – cellular swelling (cytotoxic oedema)
Influx of inflammatory mediators
>Brain swelling
>Raised ICP

52
Q

What are the secondary effects of raised ICP?

A

Herniation syndrome

Decreased cerebral perfusion

53
Q

How is cerebral blood flow regulated?

A 
Autoregulation (myogenic)
>vascular smooth muscle constricts in response to an increase in wall tension
Cerebral metabolism
Carbon dioxide + oxygen levels
Neurohumoral factors
54
Q

What are the types of herniation syndrome?

A 
Subfalcine herniation
>medial motor cortex
Uncal herniation 
>IIIrd CN, ipsilateral corticospinal tracts 
Foramen magnum herniation
>brain stem centres
55
Q

What are the surgical interventions to reduce ICP?

A

Craniotomy and evacuation of clot
External ventricular drainage
Decompressive craniectomy

56
Q

What are the main infections of the spinal cord?

A 
Meningitis
encephalitis
cerebral abscess
Post infectious encephalitis
prion diseases
57
Q

What is meningitis?

A

Inflammation or infection of meninges

58
Q

What is encephalitis?

A

Inflammation or infection of Brain substance

59
Q

What is myelitis?

A

Inflammation or infection of spinal-cord

60
Q

What are the differentials of meningitis?

A

Infective: bacterial, viral, fungal
inflammatory: sarcoidosis
drug induced: NSAIDs, IVIG
malignant: metastatic, haematological

61
Q

What are the clinical features of encephalitis?

A 
Flulike prodrome
progressive headache associated with fever +/- meningism
progressive cerebral dysfunction
>confusion
>abnormal behaviour
>memory disturbance
>depressed conscious level
>seizures
line focal symptoms/signs
62
Q

What are the antibodies that cause autoimmune encephalitis?

A

Anti-VGKC (voltage-gated potassium channel)

anti – NMDA receptor

63
Q

What are the symptoms of anti – NMDA receptor encephalitis?

A

flu like prodrome
prominent psychiatric features
altered mental state and seizures
progressing to a movement disorder and coma

64
Q

What are the symptoms of Anti-VGKC (voltage-gated potassium channel) encephalitis?

A

results in frequent seizures
amnesia
altered mental state

65
Q

How do you investigate encephalitis?

A

blood cultures
imaging (CT scan +/- MRI)
lumbar puncture
EEG

66
Q

What are the contraindications to lumbar puncture?

A

vocal symptoms or signs – suggest focal brain mass
reduce conscious level – suggest raised intracranial pressure
new onset seizures
papilloedema
severe immunocompromised state

67
Q

What are enteroviruses?

A

A large family of RNA viruses with a tendency to cause CNS infections
spread by faecal oral route
many cause non-paralytic meningitis
do not cause gastroenteritis
include polio viruses Coxsackieviruses and echo viruses

68
Q

What are arboviruses?

A

Common other parts the world
transmitted to man by vector (mosquito) from nonhuman host
Called Arbo as arthropod borne
relevant to travel (travel history important some preventable by immunisation)

69
Q

What is a brain abscess?

A

localised area of pus within brain

70
Q

what is sub dural empyema

A

thin layer of pus between Dura and arachnoid membranes over surface of brain

71
Q

Were the clinical features of the brain abscess

A

fever, headache
physical symptoms/signs – seizures, dysphasia, hemi paresis
signs of raised intracranial pressure – depressed conscious level, papilloedema, false localising signs
meninges may be present particularly with empyema
features of underlying source – dental, sinus or ear infection

72
Q

What are the causes of brain abscess/empyema?

A 
any focal lesion but most commonly tumour, subdural haematoma
penetrating head injury
grateful adjacent infection
blood-borne infection
neurosurgical procedure
73
Q

How do you diagnose a brain abscess/empyema?

A

imaging CT or MRI
investigate source
blood culture
biopsy

74
Q

How do you manage a brain abscess?

A

surgical drainage of 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

75
Q

What are the spirochaetes infections of the CNS?

A 
Lyme disease (Borrelia burgorferi)
	syphilis (Treponema pallidum)
leptospirosis (Leptospira interrogans)
76
Q

What is lyme disease?

A

vectorborne tick in wooded areas
caused by Borrelia burgdorferi
3 stages
multisystem – skin, rhuematological, neurological, cardiac and ophthalmological involvement

77
Q

What is the first stage of lyme disease?

A

early localised infection
characteristic expanding Russian state of tick bite: arrhythmia migrans
50% flulike symptoms in days to one week

78
Q

What is the second stage of lyme disease?

A

early disseminated infection weeks to months
1 or more organ systems involved
muskets greater neurological involvement most common

79
Q

What is the third stage of lyme disease?

A

chronic infection months to years occurring after period of latency

80
Q

What are the types of neurological involmenet in lyme disease?

A 
Mononeuropathy
	mononeuritis  multiplex
	painful radiculoneuropathy
	cranial neuropathy
	myelitis
	Meningo-encephalitis
	subacute encephalopathy
	encephalomyelitis
81
Q

How do you investigate lyme disease?

A 
complex range of serological tests
		CSF lymphocytosis
		PCR of CSF
		MRI brain/spine CMS involvement
brain conduction studies/EMG if PNS involvement
82
Q

How do you treat lyme disease?

A

prolonged antibiotic treatment –
>IV ceftriaxone,
>oral doxycycline

83
Q

What is neuro syphillis?

A

Causative agent Treponema pallidum
3 stage presentation primary, secondary, latent
Tertiary disease years or decades after primary disease – not common
Treated with high dose penicillin

84
Q

What is poliomyelitis?

A

caused by polio virus types 1 and 2 or 3 – all enteroviruses
paralytic disease in 1% rest asymptomatic
asymmetric flaccid paralysis especially in legs
no sensory features
polio immunisation contains all 3 poliovirus types
>Changed to oral after 2004

85
Q

What is Rabies?

A

an acute infectious disease of CNS affecting almost all mammals
transmitted to humans by bite or slavery contamination of open lesion
neurotrophic – virus and his peripheral nerves and migrate to CNS
paraesthesia at site of original lesion

86
Q

What is tetanus?

A

infection with Clostridium tetani – anaerobic gram-positive bacilli
wound may not be apparent
acts at neurological junctions; blocks inhibition of motor neurons
results in rigidity and (risus sardonicus)

87
Q

How do you prevent tetanus?

A

immunisation (toxoid)
given combined with other antigens (DTaP)
penicillin and immunoglobulin for high risk wounds/patients

88
Q

What is botulism?

A

causative agent Clostridium botulinum
an anaerobic spore producing gram-positive bacilli produces neurotoxin
binds irreversibly to pre-synaptic membranes of peripheral neuromuscular and autonomic nerve junctions
>toxin binding blocks ACH release
>recovery both sprouting new axons
motor infection, infantile (intestinal colonisation), foodborne, wound (almost exclusively injecting or popping drug users)

89
Q

How does botulism present?

A

incubation period 4 to 14 days
descending symmetrical flaccid paralysis
Julie motor, respiratory failure, autonomic dysfunction (usually pupil dilation)

90
Q

How do you diagnose botulism?

A

nerve conduction studies, mouse neutralisation bioassy for toxin and blood
culture from the provided wound

91
Q

How do you treat botulism?

A

antitoxin (A, B, E)
penicillin/Metronidazole (prolonged treatment)
radical wound debridement

92
Q

What is post-infective inflammatory syndrome?

A 
proceeding infection (viral, bacterial) or immunisation
latent interval between precipitating infection and onset of neurological
93
Q

What are the symptoms of post-infective inflammatory syndrome?

A 
autoimmune
Central nervous system
>acute disseminated encephalomyelitis my latest
peripheral nervous system
>Gillian Barre syndrome (GBS)
94
Q

What are the clinical features of Jakob disease CJD?

A 
insidious onset (usually Auden 60)
early behavioural abnormalities
rapidly progressive dementia
myoclonus
progression to global neurological decline
motor abnormalities – cerebellar ataxia, extra pyramidial, pyramidial
cortical blindness
seizures may occur
95
Q

What are the differential diagnoses of CJD

A

Alzheimer’s disease is myoclonus – usually more prolonged
subacute sclerosing panencephalitis– very rare chronic infection with defective measles virus
CNS vasculitis
inflammatory encephalitis

96
Q

What is the prognosis of CJD?

A

rapid progression, death often within 6 months

97
Q

What is new variant CJD?

A

Young onset less than 40
linked to bovine spongiform encephalopathy in cattle
eating infected material, less cases than predicted
new cases last few years
early behavioural changes more comments
longer course (average 13 months)

98
Q

How do you investigate CJD?

A

MRI
EEG
CSF

Conditions + definitions (68 decks)

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