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Neuro and geriatrics > Headache > Flashcards

Headache Flashcards

1
Q

How common are headaches?

A

One of the most common symptoms

Symptoms are unpleasant, disabling and common worldwide and have substantial economic impact due to time lost from work

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2
Q

What is a primary headache?

A

No underlying cause relevant to headache

Migraine, cluster, tension

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3
Q

What is a secondary headache?

A

A headache with underlying cause

Need to identify underlying cause eg giant cell arteritis

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4
Q

What are the red flags for secondary headache?

A 
HIV/immunosuppressed
Fever
Thunderclap headache
Seizure and new headache
Suspected meningitis
Suspected encephalitis
Red eye - acute glaucoma
Headache + new focal neurology eg papilloedema
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5
Q

Give an example of a secondary cause of secondary headache?

A

Meningitis
SAH
GCA
Medication overuse headache

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6
Q

Name another type of headache

A

Trigeminal neuralgia

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7
Q

What is a cluster headache?

A

Most disabling of primary headache disorders

Headache causing excruciating pain around one eye, temple or forehead

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8
Q

How common are cluster headaches?

A 
Distinct from migraines
Much rarer than migraines 1 per 1000
More common in men
Affects adults between 20-40
Commoner in smokers
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9
Q

What can increase your risk of getting cluster headaches?

A

Smoker
Male
Autosomal dominant gene has role

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10
Q

What is the pathology of cluster headache?

A

Unknown
Superficial temporal artery smooth muscle hyper-reactivity to serotonin
Hypothalamic grey matter abnormalities

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11
Q

How do cluster headaches present?

A

Sudden onset of excruciating pain around on eye, temple or forehead
Ipsilateral cranial autonomic features
- Eye may become watery and bloodshot with lid swelling and lacrimation
- Facial flushing
- Rhinorrhoea
- Miosis +/- ptosis
Pain unilateral and almost always affects same side
Rises to crescendo over minutes lasts 15-160 mins, one/twice per day - usually at same time
Nocturnal/early morning
+/- vomiting
Episodic - clusters last 4-12 weeks and followed by pain-free periods of months or even 1-2 years before next
Can be chronic (last for more than 1 year without remission)

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12
Q

What could be a differential diagnosis of cluster headaches?

A

Migraine

SAH

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13
Q

How are cluster headaches diagnosed?

A

Clinical diagnosis
Rule out differentials
At least 5 headache attacks fulfilling above criteria

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14
Q

How can you treat an acute attack of cluster headaches?

A

Analgesics don’t help
100% 15L for 15mins via non-rebreathable mask
Triptan

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15
Q

How can you prevent cluster headaches?

A

CCB eg verapamil first line
Avoid alcohol
Corticosteroids can help

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16
Q

What is a migraine?

A

Recurrent throbbing headache often preceded by aura and associated N&V, and visual changes

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17
Q

What might you get in a migraine aura?

A 
Fortification spectra (zig-zag lines)
Shimmering
Scotomas (black holes in visual field)
Results in pins and needles
Dysphasia
Weakness of limbs and motor function
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18
Q

How common is migraine?

A

Most common cause of episodic recurrent headache
More common in women
90% onset before 40
If > 50 then pathology sought
Usually severity decreases with advancing age

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19
Q

What can trigger a migraine?

A 
CHOCOLATE
Chocolate
Hangovers
Orgasms
Cheese
Oral contraceptives
Lie-ins
Alcohol
Tumult - loud noise
Exercise
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20
Q

What might cause a migraine?

A

Brain chemical imbalance

Changes in brainstem and interactions with trigeminal nerve

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21
Q

What can increase your risk of migraine?

A

Strong genetic component - FHx
Female
Age - can occur at any age but majority have first migraine in adolescence

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22
Q

What is the pathology of migraine?

A

Genetic and environmental factors play role
Genetics - neuronal hyper-excitability
Changes in brainstem blood flow lead to unstable trigeminal nerve nucleus and nuclei in basal thalamus
Cortical spreading depression - self-propagating wave of neuronal and glial depolarisation spreading across cerebral cortex thought to cause aura of migraine and leads to release of inflammatory mediators impacting on trigeminal nerve nucleus
Results in release of vasoactive neuropeptides including calcitonin gene related peptide and substance P - results in process of neurogenic inflammation - vasodilation and plasma protein extravasation leading to pain the propagates all over cerebral cortex

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23
Q

What might you get before a migraine and what might it entail?

A

Prodrome hours/days before - yawning, cravings, mood/sleep changes
Aura
- Visual - chaotic cascading, jumbling, distorting lines, dots, zigzags, scotoma, hemianopia
Somatosensory
- Paraesthesia spreading from fingers to toes

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24
Q

How does a migraine present?

A 
Attacks lasting 4-72 hours
Two of the following
- Unilateral 
- Pulsing
- Moderate/severe pain
- Aggravated by routine physical activity
During headache at least one of
- Nausea and/or vomiting 
- Photophobia and phonophobia
Not attributable to another disorder
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25
Q

How might a migraine with aura present?

A

At least 2 attacks
Aura precedes attack by minutes and may persist during it
Unilateral, pulsatile headache

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26
Q

What could be a differential diagnosis of migraine?

A 
Tension headache
Cluster headache
Medication over-use headache
Meningitis/SAH if sudden
Thromboembolic TIA
Brain tumour
Temporal arteritis
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27
Q

How do you diagnose migraine?

A

Clinical diagnosis

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28
Q

What might you examine to rule out other differentials?

A

Eyes - papilloedema and other eye issues
BP
Head and neck (scalp, neck muscle and temporal arteries)

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29
Q

What tests might you do to rule out other differentials?

A

CRP and ESR
MRI/CT if red flags
LP

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30
Q

When would you do an LP?

A

Worst headache of life
Severe rapid onset headache
Progressive headache
Unresponsive headache

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31
Q

How do you treat migraine?

A 
Reduce triggers
Acute
- Triptans
- NSAIDs
- +/- anti-emetic
Prevention
- Beta-blocker/tricyclic antidepressant/anti-convulsant if > 2 attacks per month or acute treatment required > 2x per week
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32
Q

What are the side effects of triptans?

A

Arrhythmias
Angina
MI

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33
Q

When are triptans CI?

A

IHD
Coronary spasm
Uncontrolled high BP

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34
Q

What is a tension headache?

A

Most chronic daily and recurrent headaches are tension headaches

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35
Q

How common are tension headaches?

A

Commonest primary headache
Can be episodic < 15 days/month or chronic > 15 days/month for at least 3 months
No organic cause

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36
Q

What can cause tension headaches?

A 
Stress
Sleep deprivation
Bad posture
Hunger
Eyestrain
Anxiety
Noise
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37
Q

How do tension headaches present?

A 
Usually has one of the following - bilateral, pressing/tight non-pulsatile, mild/moderate pain, +/- scalp muscle tenderness
No vomiting/sensitivity to head movement
No aura
Not aggravated by physical activity
Tight band-like sensation
Pressure behind eyes
Last from 30 mins to 7 days
Not attributed to another disorder
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38
Q

What could be a differential diagnosis for tension headaches?

A

Migraine
Cluster
GCA
Drug-induced

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39
Q

How are tension headaches diagnosed?

A

Clinical

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40
Q

How can you treat tension headaches?

A 
Reassurance and lifestyle advice
Stress relief
Symptomatic treatment
- Aspirin/paracetamol/NSAIDs
Limit analgesia to prevent medication overuse
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41
Q

When might you get medication over-use headaches?

A

Worsens whilst on regular analgesics espec opioids

Other causes are mixed analgesics

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42
Q

What is trigeminal neuralgia?

A

Chronic, debilitating condition resulting in intense and extreme episodes of pain

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43
Q

What are the branches of the trigeminal nerve?

A

1 - ophthalmic
2 - maxillary
3 - mandibular

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44
Q

How common is trigeminal neuralgia?

A 
Peak incidence between 50-60
More common in women
Prevalence increases with age
May be due to genetic predisposition
Almost always unilateral
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45
Q

What is the cause of trigeminal neuralgia?

A

Compression of trigeminal nerve by a loop of vein or artery
Local pathology - aneurysms, meningeal inflammation, tumours eg vestibular schwannoma - local pathology more common in younger people as cause of compression
5th nerve lesion due to pathology
- With brainstem - tumour, multiple sclerosis, infarction
- At cerebellopontine angle - acoustic neuroma, another tumour
- Within petrous bone - spreading middle ear infection
- Within cavernous sinus - aneurysm of internal carotid, tumour or thrombosis of cavernous sinus

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46
Q

What can increase your risk of trigeminal neuralgia?

A

Hypertension

Triggers - washing affected area, shaving, eating, talking, dental prothesis

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47
Q

What happens when the nerve is compressed in trigeminal neuralgia?

A

Demyelination and excitation of nerve resulting in erratic pain signalling

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48
Q

How does trigeminal neuralgia present?

A

Almost always unilateral
At least 3 attacks of unilateral facial pain
Facial pain occurring in one or more distribution of trigeminal nerve, with no radiation beyond trigeminal distribution
Pain has at least 3 of the following
- Reoccurring in paroxysmal (sudden and frequent) attacks from a fraction of a second to 2 minutes
- Severe intensity
- Electric shock like, shooting, stabbing, or knife-like
- Precipitated by innocuous stimuli by affected side of face eg washing or shaving

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49
Q

What are the differential diagnoses of trigeminal neuralgia?

A 
GCA/temporal arteritis
Dental pathology
Temporomandibular joint dysfunction
Migraine
Cluster headaches
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50
Q

What is the diagnosis of trigeminal neuralgia?

A

Needs to be at least 3 attacks with unilateral facial pain
Clinical diagnosis based on above criteria and based on history
MRI to exclude secondary causes or other pathologies
Not attributed to another disorder

51
Q

What is the treatment of trigeminal neuralgia?

A

Typical analgesics and opioids don’t work
Anticonvulstants eg oral carbamazepine
Less effective - phenytoin, gabapentin, lamotrigine
May spontaneously remit after 6-12 months
If drugs fail then surgery
- Microvascular decompression - anomalous vessels separated from trigeminal root
- Gamma knife surgery - directly at trigeminal nerve ganglion or nerve root
- Stereotactic radiosurgery

52
Q

What can cause temporal arteritis?

A

Giant cell arteritis

53
Q

What is giant cell arteritis?

A

Inflammatory granulomatous arteritis of large cerebral arteries as well as other large vessels

54
Q

How common is GCA?

A

Primarily in those over 50
Incidence increases with age
More common in women

55
Q

What can increase your risk of GCA?

A

Over 50
Female
RA, SLE, scleroderma

56
Q

What is the pathology of GCA?

A

Arteries become inflamed, thickened and can obstruct blood flow

57
Q

What arteries are most likely to be affected in GCA?

A

Cerebral arteries

  • Temporal artery
  • Ophthalmic artery
58
Q

How does GCA present?

A 
Severe headaches (temporal pulsating)
Tenderness of scalp or temple
Claudication of jaw when eating
Tenderness and swelling of one or more temporal or occipital arteries
Sudden painless vision loss - emergency
Malaise
Lethargy
Fever
Dyspnoea
Morning stiffness
Unequal or weak pulses
59
Q

What could be a differential diagnosis of GCA?

A

Migraine
Tension headache
Trigeminal neuralgia
Polyarteritis nodosa

60
Q

How do you diagnose GCA?

A 
3 or more of
- Over 50
- New headache
- Temporal artery tenderness/decreased pulsation
- ESR raised
- Abnormal artery biopsy - inflammation infiltrates present
Normochromic, normocytic anaemia
Raised ESR
ANCA very high
CRP very high
Serum alkaline phosphatase raised
Temporal artery biopsy
61
Q

How do you treat GCA?

A

High dose steroid - prednisolone to prevent vision loss - gradual reduction of steroids over 12-18 months
Used long term so GI and bone protection
Monitor treatment by ESR/CRP

62
Q

What can cause raised intracranial pressure?

A 
Bleeds
Tumour
Stroke - oedema/haematoma
Aneurysm
Hypertension
Brain infection
Idiopathic intracranial hypertension
Meningitis or encephalitis
Abnormal blood vessel - arteriovenous fistula or arteriovenous malformation
Venous sinus thrombosis
Chiari malformation
Vasculitis
63
Q

How does raised intracranial pressure present?

A 
Headache
Blurred or temporary loss of vision
Feeling less alert than usual
N&V
Fatigue
Irritability
Changes in behaviour
Weakness/problems with moving or talking
Present on waking - worse in morning, may improve on standing up
Made worse by coughing, sneezing, straining
Papilloedema
64
Q

How is raise ICP diagnosed?

A

Neuroimaging - to rule out mass lesions, venous sinus thrombosis, hydrocephalus
LP - measure opening pressure

65
Q

How do you treat raised ICP?

A

Treat underlying cause
Diuretics
Carbonic anhydrase inhibitors - acetazolamide (reduces CSF production)
LP
Surgery - shunts, protection of optic nerve

66
Q

What is idiopathic intracranial hypertension?

A

Build up of pressure around brain that is attributed to no other cause

67
Q

What can increase your risk of getting IIH?

A 
Young, overweight, female
Polycystic ovary disease
Cushing's
Hypoparathyroidism
Hypo/hyperthyroidism
Medications - some antibiotics, steroids, combined OCP
Iron deficiency anaemia
Polycythaemia
Lupus
68
Q

What causes IIH?

A

Reduced CSF resorption

69
Q

How does IIH present?

A 
Headaches
Transient visual obscuration due to papilloedema
6th nerve palsy
CSF pressure elevated
Brain imaging normal
70
Q

What must you do when someone presents with symptoms of raised ICP?

A

Look at eyes
CT/MRI
THEN LP

71
Q

How is IIH diagnosed?

A

Rule out other differentials

72
Q

How can you treat IIH?

A

Weight loss
Stop medications causing symptoms
Diuretics
Carbonic anhydrase inhibitors eg acetazolamide
Short course steroids
Regular LP
Surgery - shunts, protection of optic nerve

73
Q

What is hydrocephalus?

A

Build up of fluid in brain causing extra pressure to be exerted on brain which can cause damage

74
Q

What is normal pressure hydrocephalus?

A

Triad of symptoms

  • Difficulty walking
  • Urinary frequency urgency, incontinence
  • Mental slowing (mild dementia)
75
Q

What can cause hydrocephalus?

A 
Haemorrhage
Thrombosis
Meningitis (particularly TB)
Brain tumours - posterior fossa and brainstem obstructing aqueduct or 4th ventricle outflow
Head injury
Stroke
Idiopathic
3rd ventricle colloid cyst
Choroid plexus papilloma - rare but secretes CSF
76
Q

How does hydrocephalus present?

A 
Headache
Neck pain
N&V
Sleepiness - can progress to coma
Changes in mental state such as confusion
Blurred or double vision
Difficulty walking
Urinary and bowel incontinence
Ataxia
77
Q

How can you diagnose hydrocephalus?

A 
CT/MRI
Assessment of gait/mental ability
LP
Lumbar drainage test
Lumbar infusion test
78
Q

How is hydrocephalus treated?

A

Shunt surgery

Endoscopic third ventriculostomy

79
Q

What is meningitis?

A

Inflammation of the meninges of the brain

Often implies infection

80
Q

How common is meningitis?

A

Occurs in people of all age groups but more common in infants, young children, and the elderly
Meningococcal disease is a notifiable disease

81
Q

What are the main causes of meningitis in adults and children?

A

Neisseria meningitides - gram negative diplococci - droplet spread
Strep pneumoniae or pneumococcus
Less common - H influenzae due to vaccine

82
Q

What is the main cause of meningitis in pregnant women/older adults?

A

Listeria monocytogenes - found in cheese

83
Q

What are the most common causes of meningitis in neonates?

A

E coli

Group B haemolytic strep eg streptococcus agalacticae

84
Q

What is the most common cause of meningitis in the immunocompromised?

A 
Cytomegalovirus
Cryptococcus neoformans (fungi)
TB
HIV
HSV
85
Q

What bacteria can cause meningitis?

A 
Neisseria meningitides
Strep pneumoniae
Strep aureus
Group B strep
Listeria monocytogenes
Gram negative bacilli eg E coli
TB
Teponema pallidum
86
Q

What viruses can cause meningitis?

A 
Enterovirus - ECHO, coxsackie
Mumps
HSV
HIV
EBV
87
Q

What fungi can cause meningitis?

A

Cryptococcus neoformans

Candida albicans

88
Q

What are the non-infective causes of meningitis?

A

Malignant meningitis
Intrathecal drugs
Blood following SAH

89
Q

What can increase your risk of getting meningitis?

A 
Intrathecal drug administration
Immunocompromised
Elderly
Pregnant
Bacterial endocarditis
Crowding eg military base, university students
Diabetes
Malignancy
IVDU
90
Q

How can microorganisms reach the meninges?

A

Direct extension - from ears, nasopharynx, cranial injury, congenital meningeal defect
Bloodstream

91
Q

How do you get meningococcal septicaemia?

A

Bacteria invade into blood
Presence of endotoxin on bacteria leads to inflammatory cascade
Petechial rash + signs of sepsis

92
Q

What does the pia arachnoid look like?

A

Congested with polymorphs (neutrophils)

Layer of pus forms which may organise to form adhesions leading to cranial nerve palsies and hydrocephalus

93
Q

What does chronic meningitis with TB look like?

A

Brain covered in viscous grey-green exudate with numerous meningeal tubercles

94
Q

What does viral meningitis look like?

A

Predominantly lymphocytic inflammatory CSF reaction without pus formation
Little or no cerebral oedema unless encephalitis develops

95
Q

What is the triad of symptoms of meningitis?

A

Headache
Neck stiffness
Fever

96
Q

What is the clinical presentation of acute bacterial infection causing meningitis?

A

Onset sudden
Papilloedema usually bilateral can occur over hours to weeks due to raised ICP
Intense malaise, fever, rigors, severe headache, photophobia, vomiting
Irritable and preferring to lie still
Neck stiffness, positive Kernig’s and Brundzinski’s sign
Septicaemia - non-blanching petechial and purpuric skin rash
Altered mental state and GCS
Seizures and focal CVS signs
Progressive drowsiness, materialising signs and cranial nerve lesions indicated complications

97
Q

What complications can you get in meningitis?

A 
Venous sinus thrombosis
Severe cerebral oedema
Cerebral abscess
Hearing loss
Seizures
Developmental problems
98
Q

What is viral meningitis?

A

Benign self-limiting condition lasting 4-10 days

Headache may follow for some months

99
Q

What can cause chronic meningitis and what are the symptoms?

A

TB
Long history of vague symptoms - headache, anorexia, vomiting
Signs of meningeal triad often absent/late

100
Q

What could be a differential diagnosis for meningitis?

A

Aseptic meningitis (due to tumour)
SAH
Encephalitis

101
Q

How do you diagnosed meningitis?

A 
Blood cultures before LP
Bloods - FBC, U&E, CRP, glucose
LP - if unable to perform within 30 mins give empirical antibiotics
- Send for microscopy and sensitivity
CT head - exclude lesions
Throat swabs
Pneumococcal and meningococcal serum PCR
Don't do LP with non-blanching rash
102
Q

What would the LP for bacterial meningitis look like?

A

Neutrophils, raised protein, low glucose, turbid colour

103
Q

What would the LP for viral meningitis look like?

A

Lymphocytes, normal protein and glucose

104
Q

What would the LP for TB meningitis look like?

A

Lymphocytes, raised protein, low/normal glucose

105
Q

What are the indications for CT before LP in suspected meningitis?

A 
Age > 60
Immunocompromised
Hx of CNS disease
New onset/recent seizures
Decreased conscious level
Focal neurological signs
Papilloedema
106
Q

How do you treat meningitis?

A

If suspect bacterial start antibiotics before tests come back
IV benzylpenicillin/cefotaxime if septicaemia
IV cefotaxime/ceftriaxone - 3rd gen cephalosporins
IV chloramphenicol if severe anaphylaxis to penicillin
Over 50/immunocompromised - add IV amoxicillin to treat listeria
Consider steroids to reduce cerebral oedema
IV vancomycin if recently travelled

107
Q

What prophylaxis do you give to contacts?

A

Oral ciprofloxacin stat

Oral rifampicin - can’t give to pregnant women

108
Q

What is encephalitis?

A

Infection and inflammation of brain parenchyma

109
Q

How common is encephalitis?

A

Most frequent in children and elderly - mainly viral cause

More common in immunocompromised

110
Q

What are the viral causes of encephalitis?

A 
HSV 1 and 2
Varicella zoster
EBV
Cytomegalovirus
HIV
Mumps
Measles
Enteroviruses
Adenoviruses
111
Q

What are the non-viral causes of encephalitis?

A

Bacterial meningitis
TB
Malaria

112
Q

What are the causes of autoimmune encephalitis?

A

Paraneoplastic limbic encephalitis
Voltage-gated potassium channel limbic encephalitis
Anti-NMDA receptor anti-body encephalitis

113
Q

What can increase your risk of encephalitis?

A

Extremes of age

Immunocompromised

114
Q

What is the pathology of encephalitis?

A

Disease mostly affecting the frontal and temporal lobes resulting in decreased consciousness, confusion, and focal signs

115
Q

How does encephalitis present?

A

Whole brain affected - problems with consciousness
Insidious onset over days or can be abrupt
Triad - fever, headache, altered mental status
Begins with features of viral infection - fever, headaches, myalgia, fatigue, nausea
Progresses to personality and behavioural changes, decreased consciousness, drowsiness and confusion
Focal neurological deficit - hemiparesis, dysphasia, seizures, raised ICP, midline shifting = coning, coma
Hx of travel and/or animal bites

116
Q

What are the differentials of encephalitis?

A

Meningitis
Stroke
Tumour

117
Q

What investigations should you do in suspected encephalitis?

A

MRI - areas of inflammation and swelling, generally in temporal lobes in HSV encephalitis, midline shifting
EEG - period sharp and slow wave complexes
LP - high lymphocytes, PCR
Blood and CSF serology

118
Q

How is encephalitis treated?

A

If viral - acyclovir before investigation results 10mg/kg TDS for 14-21 days
Early treatment can reduce mortality and long term damage
Anti-seizure medication eg primidone

119
Q

What are the complications of encephalitis?

A

Memory impairment
Personality change
Epilepsy

120
Q

What are the symptoms of limbic encephalitis?

A

Facio-branchial dystonic seizures, confusion, agitation, hyponatraemia

121
Q

What is paraneoplastic limbic encephalitis?

A

Seen with small cell lung cancer and testicular tumours
Associated with variety of antibodies inclu anti-Hu and anti-Ma2
MRI - high hippocampal signal
Precedes diagnosis of cancer in most cases and should prompt investigations

122
Q

What is voltage-gated potassium channel limbic encephalitis?

A 
Produce a variety of disorders
Usually occurs in patients over 50
Can be associated with thymoma (v rare)
Treatment - high dose steroids
Neuromyotoninand peripheral nerve hyperexcitability syndromes seen with antibodies to VGKC
123
Q

What is anti-NMDA receptor antibody encephalitis?

A

Limbic encephalitis followed by coma and status epilepticus
Orofacial dyskinesias characteristic
Patients usually younger and most have teratomas eg ovarian
May respond to immunotherapy - IV Ig or plasma exchange initially, followed by steroids, rituximab or cyclophosphamide

Neuro and geriatrics (21 decks)

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