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NEURO > headache > Flashcards

headache Flashcards

1
Q

15 mins to 2 hours headache

A

cluster headache

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2
Q

2s - 3mins headache

A

trigeminal neuralgia

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3
Q

4-72hrs

A

migraines

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4
Q

triggers of cluster headahe

A

more common in men (3:1)
smokers
Alcohol may trigger an attack and there also appears to be a relation to nocturnal sleep.

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5
Q

examples of primary headache

A

TTH
Migraine
Cluster Headache
Others

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6
Q

examples of secondary headache

A 
Vascular
Infective
Neoplasia
Drugs 
Inflammation
RICP
Trauma
Metabolic
Toxins
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7
Q

examples of drugs causing chronic headache

A

paracetamol, aspirin or NSAIDs used for 15 days per month or more

triptans, opioids or ergot preparations for 10 days a month or more

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8
Q

red flag signs for headache

A 
Thunderclap Headache
Neck Stiffness
Rash
Photophobia
Focal Neurology
Nausea/ Vomiting
Characteristics of RICP headache
- Present on waking 
- Worse if lying
- Exacerbated by valsalva/ bending/ cough
- Papillodema
Fever
Recent Onset or Change in character
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9
Q

causes of raised ICP

A
  • SOL
  • Idiopathic Intracranial Hypertension
  • Venous S§inus Thrombosis
  • Hydrocephalus
  • infection - meningitis
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10
Q

Symptoms of raised ICP

A

papilloedema

Cushing’s triad - HTN, bradycardia, irregular respiration

Headache – worst on waking, inc. or ass with visual obscurations with valsalva, bending, coughing etc

vomiting

If severe, bradycardia and ↑BP

Respiratory changes – periodic breathing, apnoea

False localising signs eg VI palsy - abducen

If fever, leucocytosis look for ear, nose infection preceeding headache

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11
Q

SOL in the cerebellum signs

A 
Dysdiadochokinesis
ataxia
nystagmus
intention tremor
slurred speech
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12
Q

SOL in the temporal lobe

A

depersonalisation
deja vu - hallucinations of smell, taste, sound and sight.

visual field defects - inferior fibres so upper quadrant

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13
Q

SOL in the frontal lobe

A

anosmia
change in personality, dishonesty
dysphasia
hemiparaesis

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14
Q

SOL in the parietal lobe

A

hemisensory loss

decreased 2 point discrimination

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15
Q

features of cerebellopontine angle

A 
ipsilateral deafness.
Tinnitus.
Nystagmus.
Reduced corneal reflex.
Facial and trigeminal nerve palsies.
Ipsilateral cerebellar signs.
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16
Q

features of midbrain lesion

A

Unequal pupils.
Inability to direct the eyes up or down.
Amnesia for recent events, with confabulation.
Somnolence.

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17
Q

risk factors of idiopathic intracranial hypertension

A

obese females
recent weight gain
hypertension
menstrual irregularity

pregnancy

drugs*: oral contraceptive pill, steroids, tetracycline, high vitamin A, lithium

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18
Q

aetiology of idiopathic intracranial hypertension

A
  • obstruction to CSF
  • excess CSF production
  • increased cerebral oedema

endocrine - adrenal insufficiency, dushings, thyroid

medication - cimetidine, steroids

PCV
Iron deficiency anaemia
CKD
SLE

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19
Q

presentation of idiopathic intracranial hypertension

A

generalised throbbing - worst morning and night

relieved on standing

aggravated by straining, coughing or change in position

blurred vision

enlarged blind spot

NV

CNVI PALSY - diplopia

papilloedema

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20
Q

treatment for idiopathic intracranial hypertension

A

Weight loss

Acetazolamide - reduces rate of CSF production by choroid (diuretics)

Topiramate - cause weight loss

repeated LP

amitryptilline - headache

Urgent LP
Optic nerve sheath fenestration
Shunts

surgery: optic nerve sheath decompression and fenestration may be needed to prevent damage to the optic nerve. A lumboperitoneal or ventriculoperitoneal shunt may also be performed to reduce intracranial pressure

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21
Q

prognosis of idiopathic intracranial HTN

A

not really ass with death

relapse and remission are common

significant threat to sight

upto 50% visual loss

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22
Q

what is GCA

A

type of chronic vasculitis characterized by granulomatous inflammation in the walls of medium and large arteries. The extracranial branches of the carotid artery and branches of the ophthalmic artery, such as short ciliary branches, are preferentially involved,

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23
Q

complications of GCA

A

visual loss

Large artery complications

  • aortic aneurysm
  • aortic dissection
  • large artery stenosis
  • aortic regurgitation

CVS

  • MI
  • Heart failure
  • stroke
  • PAD

Peripheral neuropathy.
Depression.
Confusion and encephalopathy (in about 30% of people).
Deafness.

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24
Q

prognosis of GCA

A

Relapses are common and can occur if corticosteroid treatment is reduced or withdrawn too quickly

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25
Q

clinical manifestations of GCA

A

above 50
-new onset localized headache that is usually unilateral, in the temporal area

  • temporal artery - tender, thick or nodule

Systemic features (fever, fatigue, anorexia, weight loss, and depression

Features of polymyalgia rheumatica (bilateral upper arm stiffness, aching, and tenderness; and pelvic girdle pain

scalp tenderness

intermittent jaw claudication

visual disturbances - shade in one eye

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26
Q

DD of GCA

A

herpes zoster

cluster headache

acute angle galucoma

TIA

Temporomandibular joint pain, sinus disease, and ear problems.

Cervical spondylosis or other upper cervical spine disease.

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27
Q

Tx for GCA

A

For people with visual symptoms — 60–100 mg as a one-off dose (they should be seen by an ophthalmologist the same day) IVmethyl prednisolone prior to oral0,5-1.0g daily for 3/7.

For people without visual symptoms — 40–60 mg daily (minimum 0.75 mg/kg).

Reduce the dose of prednisolone to zero over 12–18 months providing there are no signs and symptoms or laboratory markers of inflammation.

Consider the need for a proton pump inhibitor for gastroprotection in people at high risk of gastrointestinal bleeding or dyspepsia

every 2-8 weeks for first 6 months

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28
Q

Ix for GCA

A

LFTs - ALP esp

CRP

ESR

FBC - normochromic normocytic anaemia and an elevated platelet count are common.

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29
Q

DD for papilloedema

A

tilted optic disc

myelinated nerve fibres

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30
Q

Ix for idiopathic intracranial HTN

A

MRI or MR/CT venography to exclude

  • hydrocephalus
  • mass lesion
  • venous thrombosis
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31
Q

triggers for migraine

A 
Ch – chocolate
O – Oral contraceptive
C – caffeine (or withdrawal)
O- orgasm
L - lack of sleep
A – alcohol
T – travel
E – exercise

irregular 💤

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32
Q

prognosis of migraine

A

improves with increasing age

pregnancy - improvement in frequency and severity of attacks the second and third trimesters

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33
Q

complications of migraine

A

Reduced functional ability and quality of life

Medication overuse headache

progression to chronic migraine

Status migrainosus — debilitating migraine attack lasting for more than 72 hours.

Migrainous infarction — symptoms of aura lasting for more than 60 minutes with evidence of an ischaemic brain lesion on neuroimaging.

Persistent aura without infarction — aura symptoms lasting for more than 1 week, with no radiographic evidence of infarction.

increased risk of stroke

  • infarction
  • haemorrhagic
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34
Q

features of migraine without aura

A

Headache lasting 4–72 hours in adults or 2–72 hours in adolescents.

Headache with at least two of the following characteristics:

  • UNILATERAL location (more commonly bilateral in children).
  • PULSATING quality — may be described as ‘throbbing’ or ‘banging’ in young people.
  • MODERATE/SEVERE intensity.
  • AGGRAVATION by, or causing avoidance of, routine activities of daily life (for example walking or climbing stairs).

Headache with associated symptoms including at least one of:

  • N/V
  • PHOTOPHOBIA (sensitivity to light) and PHONOPHOBIA (sensitivity to sound)
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35
Q

migraine with aura symptoms

A

One or more typical fully reversible aura symptoms including:

  • VISUAL - zigzag lines / scotoma
  • transient hemianopic disturbance
  • spreading scintillating scotoma (‘jagged crescent’).
  • SENSORY -> symptoms such as unilateral pins and needles or numbness.
  • SPEECH and/or language symptoms such as dysphasia.

At least three of the following:

  • At least one aura symptom spreads gradually over at least 5 minutes.
  • Two or more aura symptoms occur in succession.
  • Each individual aura symptom lasts 5-60 minutes.
  • At least one aura symptom is unilateral.
  • At least one aura symptom is positive.
  • The aura is accompanied, or followed within 60 minutes, by headache.
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36
Q

acute management for migraine

A
  • simple analgesia
  • oral sumatripatan (50-100mg)
    fails - intra-nasal or subcutaneous
  • antiemetic - such as metoclopramide 10mg or prochlorperazine 10mg even in the absence of N/V
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37
Q

when to consider preventative treatments for migraine

A
  • significant impact on quality of life and daily function
  • acute treatment is shit
  • at risk of medication overuse headache
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38
Q

what medical preventative treatment for migraines are available

A

the aim of treatment is to reduce the frequency and severity of migraine symptoms and not complete remission or cure of migraine.

  • Propranolol (80–160 mg daily, in divided doses) or
  • Topiramate (50–100 mg daily, in divided doses [contraindicated in pregnancy — highly effective contraception is required prior to initiation]) or
  • Amitriptyline (25–75 mg at night).
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39
Q

what nonmedical preventative treatment for migraines are available

A
  • Behavioural interventions (such as relaxation techniques [for example mindfulness or meditation] or cognitive behavioural therapy).
  • Acupuncture (up to 10 sessions over 5–8 weeks) if both topiramate and propranolol are unsuitable or ineffective.
  • Riboflavin 400 mg once a day — may be effective in reducing migraine frequency and intensity for some people (avoid if planning a pregnancy or pregnant).
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40
Q

preventative drug Tx for menstrual migraine

A

Frovatriptan (2.5 mg twice daily) on the days migraine is expected or from two days before until three days after bleeding starts.

Zolmitriptan (2.5 mg twice or three times daily) on the days migraine is expected or from two days before until three days after bleeding starts.

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41
Q

risk factors of subarachnoid haemorrhage

A 
HTN
smoking
cocaine
alcohol
genetic - D polycystic kidney disease, EDS, neurofibromatosis

marfans - berry

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42
Q

what are berry anuerysms

A

circle of willis

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43
Q

clinical manifestations of SAH

A

sudden explosive headache - thunderclap

vomiting

confusion/altered level of consciousness

neck stiffness and other signs of meningism 6 hours after onset of SAH

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44
Q

DD of SAH

A

Other causes of stroke.
Meningitis (rarely features thunderclap headache).
Trauma.
Thunderclap headache of other aetiology.
Primary sexual headache.
Cerebral venous sinus thrombosis.
Cervical artery dissection.
Carotid artery dissection.
Hypertensive emergency (severely raised blood pressure).
Pituitary apoplexy (infarction or haemorrhage of the pituitary gland).

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45
Q

Ix for SAH

A

first line CT scanning without contrast

FAILS
lumbar puncture should be undertaken over 12 hourse after the onset for xanthochromia to be detected by spectrophotometry

46
Q

what is cerebral panangiography

A

gold standard for detection, demonstration and localisation of ruptured aneurysms

47
Q

how to determine the origin of the bleed of SAH

A

cerebral angiography

CT angiography

48
Q

ECG changes for SAH

A

QT prolongation
Q waves
dysrhythmias
ST elevation.

49
Q

aim of Tx for SAH

A

prevent further bleeding or rebleeding

50
Q

complications of SAH

A

death

rebleeding - endovascular coiling/neurovascular clipping

vasospasm - nimodipine 60mg

hydrocephalus - CSF shunt

epilepsy

cognitive dysfunction

Stroke/poor cerebral perfusion -> maintain hydration/control BP

51
Q

MAIN red flags of headache

A
  • Vomiting more than once with no other cause.
  • New neurological deficit (motor or sensory).
  • Reduction in conscious level (as measured by the Glasgow coma score).
  • Valsalva (associated with coughing or sneezing) or positional headaches.
  • Progressive headache with a fever.
52
Q

what is post traumatic headache

A

within one week after an injury or when they regain consciousness

features are similar to a migraine

53
Q

features of post LP headache

A

usually develops within 24-48 hours following LP but may occur up to one week later
may last several days
worsens with upright position
improves with recumbent position

54
Q

tx for post LP headache

A

analgesia rest
caffeine and fluids

usually develops within 24-48 hours following LP but may occur up to one week later
may last several days
worsens with upright position
improves with recumbent position

55
Q

migraine criteria

A

A- At least 5 attacks fulfilling criteria B-D

B Headache attacks lasting 4-72 hours* (untreated or unsuccessfully treated)

C Headache has at least two of the following characteristics:

  1. unilateral location*
  2. pulsating quality (i.e., varying with the heartbeat)
  3. moderate or severe pain intensity
  4. aggravation by or causing avoidance of routine physical activity (e.g., walking or climbing stairs)

D During headache at least one of the following:

  1. nausea and/or vomiting*
  2. photophobia and phonophobia

E Not attributed to another disorder (history and examination do not suggest a secondary headache disorder or, if they do, it is ruled out by appropriate investigations or headache attacks do not occur for the first time in close temporal relation to the other disorder)

56
Q

children with migraine features

A

attacks are shorter lasting

more commonlu bilateral

GI distubrance is more prominent

57
Q

features of auras

A
  • are fully reversible
  • develop over at least 5 minutes
  • last 5-60 minutes
58
Q

atypical aura symptoms that may prompt further investigation/referral

A
  • motor weakness
  • double vision
  • visual symptoms
  • affecting only one eye
  • poor balance
  • decreased level of consciousness.
59
Q

Ix for raised ICP

A

CT/MRI scanning to determine any underlying lesion.

Check and monitor blood glucose, renal function, electrolytes and osmolality.

60
Q

who do we monitor ICP in

A
  • management of severe closed head injury.
  • Appropriate in patients with severe head injury (GCS between 3 and 8 after CPR) and an abnormal CT scan (haematomas, contusions, oedema or compressed basal cisterns).
  • Appropriate in patients with severe head injury and a normal CT scan if two or more of the following features are noted on admission
  • – age over 40 years
  • – unilateral or bilateral motor posturing
  • – systolic blood pressure <90 mm Hg.
  • Subarachnoid haemorrhage with associated hydrocephalus: ventriculostomy allows therapeutic drainage and ICP monitoring.
  • Reye’s syndrome: active treatment of raised ICP decreases mortality.
  • Brain tumours: may be of value in selected patients deemed at high risk of swelling or obstructive hydrocephalus - eg, following posterior fossa surgery.
  • Normal pressure hydrocephalus.
  • Decompensated hydrocephalus: can be a valuable diagnostic tool in complex cases.
  • Idiopathic intracranial hypertension
  • — diagnostic test
  • — monitor response to treatment

Other potential indications include hypoxic brain swelling after drowning, meningitis, encephalitis, venous sinus thrombosis and hepatic encephalopathy.

61
Q

what is raised ICP the values

A

above 20mmHg

62
Q

Mx of ICP

A
  1. head elevation to 30° improves jugular venous outflow and lowers intracranial pressure

mannitol osmotic diuretic

  • > controlled hyperventilation
  • aim is to reduce pCO2 → vasoconstriction of the cerebral arteries → reduced ICP
  • leads to rapid, temporary lowering of ICP. However, caution needed as may reduce blood flow to already ischaemic parts of the brain
-> removal of CSF, different techniques include:
drain from intraventricular monitor (see above)
repeated lumbar puncture (e.g. idiopathic intracranial hypertension)
ventriculoperitoneal shunt (for hydrocephalus)
63
Q

what is tension-type headache and classification

A

primary headache disorder

infrequent - <1 day per month
frequent - at least 10 episodes of headache

chronic TTH - >15 per month for 3 months

64
Q

clinical manifestations of Tension headache
Sx
Signs

A

bilateral
Quality - pressing or tightening (non-pulsating)
intensity - mild to moderate
duration - lasting minutes to days.

no aggravating factors or ass Sx

pericranial tenderness on manual palpation may be present.

65
Q

DD for tension type headache

A

migraine
trigeminal neuralgia
trauma

66
Q

treatment for tension type headache

A

analgesia
sleep hygiene

chronic TTH
- A course of up to 10 sessions of acupuncture over 5–8 weeks.

  • low dose amitryptilline 10-75 mg
67
Q

triggers for tension headache

A

stress
tiredness
squint

68
Q

Prognosis of TTH

A
  • > Infrequent episodic tension-type headache (TTH) occurs in a large proportion of the population. It is self-limiting and simple analgesia is usually effective.
  • > Chronic TTH can evolve from frequent episodic TTH, with daily or very frequent episodes of headache. It is a serious condition which decreases quality of life and leads to high disability.
69
Q

complications of TTH

A
  • > Frequent episodic tension-type headache (TTH) and chronic TTH can be associated with considerable disability and loss of quality of life.
  • > Self-medication is common in TTH and may lead to medication overuse headache.
70
Q

prodromal and postdromal Sx of migraine

A

Prodromal

  • fatigue
  • poor concentration
  • neck stiffness
  • yawning
  • occur hours or 1–2 days before onset of other symptoms of migraine.

Postdromal

  • fatigue
  • elated
  • depressed mood
  • may occur after resolution of the headache and last up to 48 hours.
71
Q

DDx for migraine

A
  • > Tension-type headache.
  • > Trigeminal autonomic cephalgias for example cluster headache and paroxysmal hemicranias.
  • > Other primary headache disorders such as primary cough headache and cold-stimulus headache.
72
Q

prognosis of medication overuse headache

A

improve after discontinuation of the overused medication

73
Q

Mx of medication overuse headache

A

Drugs such as triptans and simple analgesics (such as NSAIDS and paracetamol) can generally be stopped abruptly.

Advise the person to stop taking all overused acute headache medications for at least 1 month.

Warn the person that withdrawal may initially worsen symptoms and that headache improvement may not occur for weeks after discontinuation.

Advise the person to keep a diary recording symptoms and medication use during withdrawal and to maintain good hydration.

74
Q

classification of cluster headache

A

Episodic cluster headache — attacks occur in periods lasting from 7 days to 1 year and are separated by pain-free periods lasting at least 1 month.

Chronic cluster headache — attacks occur for more than 1 year without remission, or with remission periods lasting less than 1 month.

75
Q

prognosis of cluster headache

A

lifelong disorder - periods of remission may lengthen with increasing age.

76
Q

features of cluster headache

A

unilateral peri-orbital pain associated with ipsilateral cranial autonomic symptoms (such as conjunctival injection, lacrimation and eyelid oedema).

rhinorrhoea

  • pulsating, boring, burning, or pressure-like.
  • 15 and 180 minutes.
  • characteristically restless or agitated, cannot lie still and may pace the floor.
77
Q

International Classification of Headache Disorders (ICHD)

diagnostic criteria

A
  • At least five attacks of severe or very severe unilateral orbital, supraorbital and/or temporal pain lasting 15–180 minutes and
  • Headache associated with at least one of: ipsilateral conjunctival injection and/or lacrimation; nasal congestion and/or rhinorrhoea; eyelid oedema; forehead and facial sweating or flushing; a sensation of fullness in the ear; or miosis and/or ptosis; and/or a sense of restlessness or agitation.
  • Attacks occur between one every other day and eight per day for more than half of the time when the disorder is active.
78
Q

acute treatment for cluster headache

A
  • Sumatriptan by subcutaneous injection (for adult) - 6mg for one dose contraindicated in pts w CAD have potential to cause coronary vasospasm
  • Sumatriptan by intranasal administration (for adult aged 18–65 years - 10-20mg
  • provide 100% oxygen at a flow rate of 12–15 litres per minute via a non-rebreather face mask for 15 to 20 minutes.
79
Q

preventative treatment for cluster

A

verapamil

80
Q

what is meningitis

A

inflammation of the two inner meninges (the pia and arachnoid mater) of the brain and spinal cord.

81
Q

causative organisms of meningitis

A

bacterial -> Neisseria meningitidis (meningococcus), Streptococcus pneumoniae (pneumococcus), and Haemophilus influenzae type b

viral -> enteroviruses

mycobacterium TB

82
Q

incubation period of neisserria and strep pnuemonia

A

neisseria - 3/5 days

strep - 1-3 days

83
Q

risk factor of meningitis

A 
young age
winter
absent or non-functioning spleen
immunocompromised 
cancer
organ dysfunction
smoking
84
Q

complications of meningitis

A 
hearing loss
brain abscess 
seizures
visual impairment
distal limb loss in septicaemia 
hemi and quadraparaesis
cognitive impairment
hydrocephalus
reduced QOL
anciety
learning difficulties
85
Q

poor prognosis of meningitis in adults

A

Low Glasgow Coma Scale score on admission (low level of consciousness).
Tachycardia.
Absence of rash.
Thrombocytopenia.
Elevated erythrocyte sedimentation rate (ESR).
Positive blood culture.
Cerebrospinal fluid leucocyte count of less than 1000 x 109 cells per mL.

86
Q

specific symptoms of meningitis

A
  • Non-blanching rash.
  • Stiff neck.
  • Capillary refill time of more than 2 seconds, cold hands and feet.
  • Unusual skin colour.
  • Shock and hypotension.
  • Leg pain.
  • Back rigidity.
  • Bulging fontanelle.
  • Photophobia.
  • Kernig’s sign (person unable to fully extend at the knee when hip is flexed).
  • Brudzinski’s sign (person’s knees and hips flex when neck is flexed).
87
Q

DD for meningitis

A

viral - conservative management - enteroviruses, HSV

fungal - life threatening

TB meningitis

sepsis

pneumonia

encephalitis

88
Q

Management of meningitis

A

single dose of parenteral benzylpenicillin (intravenously or intramuscularly)

Children younger than 1 year of age — 300 mg.
Children 1–9 years of age — 600 mg.
Adults and children 10 years of age or older — 1200 mg.

89
Q

after discharge what happens meningitis

A

All children should have a review with a paediatrician 4–6 weeks after hospital discharge to assess their recovery.

90
Q

what is encephalitis

A

inflammation of the brain parenchyma - caused by viral infections

HSV1

91
Q

presentation of encepahlitis

A 
acute
TRIAD 
Fever
headache
altered mental status
Viral - may begin flu or headached
altered consciousness
confusion
drowsiness
seizures
coma

increased ICP Sx

92
Q

DDx of encephalitis

A 
meningitis
behcet
SLE
stroke
MS
syphillis
leukaemia
93
Q

Ix foe encephalitis

A

CSF - lymphocytosis, elevated protein
PCR test for HSV, VXV and enteroviruses
- Elevated protein
- elevated CSF specific antibody levels

FBC and blood film - leukocytosis

CT scan - rule out SOL, strokes and basilar fractures
- identify ICP

EEG

94
Q

Mx for encephalitis

A
  • urgent hospital admission
  • immediate parentral ABx
  • IV aciclovir
  • no specific Mx for other causes
  • role of steroids
95
Q

complications of encephalitis

A

inappropriate antidiuretic hormone secretion

DIC

cardiac and respiratory arrest

epilepsy

96
Q

clinical manifestations of acute sinusitis

examination

chronic

A
  • nasal blockage (obstruction/congestion) or nasal discharge (anterior/posterior nasal drip)
  • facial pain/pressure (or headache)
  • loss) of the sense of smell.
  • Altered speech indicating nasal obstruction.
  • Tenderness, swelling, or redness over the cheekbone or periorbital areas.
  • Cough.

Inspecting and palpating the maxillofacial area to elicit swelling and tenderness.
Performing anterior rhinoscopy (using the largest speculum of an otoscope, or a head light and nasal speculum) to identify:
Signs which support a diagnosis of acute sinusitis such as nasal inflammation, mucosal oedema, and purulent nasal discharge.
Associated pathology such as nasal polyps, or anatomical abnormalities such as septal deviation.

more than 12 weeks

97
Q

DDx for sinusitis

A 
URTI
allergic rhinits
nasal foreign body
adenoiditis/tonsillitis
sinonasal tumour
turbinate hypertrophy
98
Q

Mx for acute sinusitis

A

more than 10 days

high dose nasal corticosteroid for 14 days

99
Q

bacterial meningitis CSF findings

A

Appearance: cloudy and turbid

Opening pressure: elevated (>25 cm H₂O)

WBC: elevated >100 cell/µL (primarily polymorphonuclear leukocytes (>90%))

Glucose level: low (<40% of serum glucose)

Protein level: elevated (>50 mg/dL)

100
Q

viral meningitis CSF findings

A

Appearance: clear

Opening pressure: normal or elevated

WBC: elevated (50 – 1000 cells/µL, primarily lymphocytes, can be PMN early on)

Glucose level: normal (>60% serum glucose, however, may be low in HSV infection)

Protein level: elevated (>50 mg/dL)

101
Q

TB meningitis CSF findings

A

Appearance: opaque, if left to settle it forms a fibrin web

Opening pressure: elevated

WBC: elevated (10 – 1000 cells/µL, early PMNs then mononuclear)

Glucose level: low

Protein level: elevated (1-5 g/L)

102
Q

SAH CSF findings

A

Appearance: blood-stained initially, then xanthochromia (yellowish) >12 hours later

Opening pressure: elevated

WBC: elevated (WBC to RBC ratio of approx 1:1000)

RBC: elevated

Glucose level: normal

Protein level: elevated

103
Q

GBS CSF findings

A

Appearance: clear or xanthochromia

Opening pressure: normal or elevated

WBC: normal

Glucose level: normal

Protein level: elevated (>5.5 g/L)

104
Q

when might CSF maybe

A
  1. Suspected subarachnoid haemorrhage
  2. Suspected meningitis/encephalitis
  3. Immunological disorders such as multiple sclerosis or Guillain-Barré Syndrome
105
Q

migraine and menstruation

A

mefanamic acid or a combination of aspirin, paracetamol and caffeine. Triptans are also recommended in the acute situation

106
Q

what do u do if someone comes in with sudden headache confusion

A 
full set of obs including BM
Full neuro examination including fundoscopy
CT scan
NBM 
cannulate
107
Q

DDx of subdural haematoma

A 
stroke
intoxicated/drug overdose
metabolic imbalance - hypoglycaeamia
septicaemia
acute bleed into a brain tumour
108
Q

RFs fo subdural haematoma

Mx

A 
increasing age - brain shrinkage occurs
chronic alcoholism
epilepsy
long term anticoagulation
falls

surgical evaluation of the haematoma thru burr holes

109
Q

Triggers of trigeminal neuralgia

A 
washing
shaving
touching
brushing teeth
brushing hair
cold wind
eating
110
Q

causes if trigeminal neuralgia

A

MS
lesions of the cerebellopontine angle
atrioventricular malformation
tumors of CNV

111
Q

Mx of post herpetic neuralgia

A

amitryptilline

NEURO (30 decks)

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