Headaches Flashcards
1
Q
Differential diagnosis for headache…
A
- Primary Headache: Migraine, cluster headache, tension-type headache
- ICP: Space-occupying lesion (tumour, haematoma) , idiopathic intracranial hypertension, low pressure headache
- Vascular: stroke, SAH, cerebral venous sinus thrombosis
- Infection: meningitis, encephalitis, sinusitis
- Rheumatological: temporal arteritis, cervical arthritis
- Visual: straining from poor visual acuity, acute angle closure glaucoma
- Other: CO poisoning, trigeminal neuralgia
2
Q
Red flags for headache…
A
- Change in pattern of headache
- New onset headache at >50 y/o
- Systemic illness with the headache
- Sx suggesting raised ICP (papilloedema)
- Meningism
- Seizures
- Acute onset worst headache ever
- Vomiting >1
- Reduced GCS
3
Q
What are the main types of migraine?
A
- Migraine with aura
- Migraine without aura
- Aura without headache
4
Q
Presentation of migraine…
A
Prodromal phase: feeling unwell in days before
Aura preceding the migraine develops over 20 mins - symptoms include:
- Visual disturbances e.g. spectra, homonymous blurring
- Numbness, paraesthesia
- Speech problems e.g. dysphasia
Symptoms of migraine:
- Severe unilateral pulsatile pain - disabling, lasting 4-72 hours
- Nausea and vomiting
- Photophobia
- Phonophobia
5
Q
Management of migraine…
A
Avoidance of potential triggers: stress, exercise, lack of sleep
Acute attacks:
- First line = oral triptan + NSAID/simple analgesic
- Second line = add non-oral metoclopramide/ prochlorperazine
Prophylaxis of migraines (when >2 per month):
- First line = B blocker e.g. propranalol or anti-epileptic e.g. topiramate - depending on pt comorbidities e.g. pregnant women should have B blocker
- Second line = TCA/ SSRI
- Acupuncture sessions - 10 over 5-8 weeks
- Botox
6
Q
What are the contraindications of triptans?
A
- Vascular disease
- Ischaemic heart disease
- Pregnancy
7
Q
Two different types of TTH…
A
- Episodic TTH= <15 days per month
2. Chronic TTH= >15 days per month
8
Q
Presentation of tension type headache…
A
- Tight, pressure -like pain in distribution of band around forehead
- Associated neck, back, jaw pain
- NO VISUAL SX
- Typically occurs near end of the day - almost every day, for a few hours
9
Q
Management of tension type headaches…
A
Conservative = physiotherapy to relieve neck tension
Medical management:
- Epsiodic TTH= simple analgesics e.g. NSAIDs, paracetamol
- Chronic TTH= TCA is first line e.g. nortryptyline
- Acupuncture = prophylactic for chronic disease
10
Q
What is the definition of medication overuse headache?
A
Headache present for > 15 days per month alongside overuse for at least 3 months of following medications:
- Triptans, opioids for at least 10 days per month
- Paracetamol/ NSAIDs for at least 15 days per month
11
Q
What is the treatment for medication overuse headache?
A
- Headache medication should be STOPPED for at least 1 month
- Advise patient about rebound worsening headaches occurring for 2-4 weeks - need willpower!!
- 3 week course of ibuprofen can be used to break cycle of medication use
12
Q
Characteristic features of cluster headaches…
A
- Severe, unilateral pain centred around eye, temple, forehead
- Rapid onset
- Lasting 15- 180 minutes, multiple times per day
- Occur in clusters lasting a few weeks
- Autonomic sx= lacrimation, rhinnorhoea, sweating, eyelid oedema
- Mostly affecting young men, smokers
13
Q
Management of cluster headaches…
A
Acute attack: high flow oxygen + 6mg sumatriptan neb/SC
Prophylaxis:
- First line = Verapamil 40mg BD
- Second line= Prednisolone 60mg, titrated down over 2-3 weeks- can break the cluster of headaches
14
Q
What are the different causes of increased intracranial pressure?
A
Different components of ICP:
- Increased arterial BP: malignant HTN, pre-eclampsia, hypercapnia
- Increased venous BP: cerebral venous sinus thrombosis
- Increased CSF pressure: overproduction e.g. IIH, failure of reabsorption e.g. meningitis, obstruction of flow e.g. intracerebral mass
- Increased brain pressure: space occupying lesion e.g. malignancy, abscess
15
Q
How can increased ICP present?
A
- Classic triad of symptoms= headache, papilloedema, intractable vomiting:
- Headache worse on lying flat, on coughing, and when lying forward
- Fundoscopy will show blurred optic disc margins, loss of venous pulsation, venous engorgement
- Vomiting is hard to control
*Additional focal neurological signs and seizures may be present
16
Q
Features of papilloedema…
A
- Venous engorgement (usually first sign)
- Blurring of optic disc margins
- Loss of venous pulsation
- Elevated optic disc
17
Q
Red flag physical examination signs for raised ICP…
A
- Visual field defects e.g. bitemporal hemianopia (tunnel vision) caused by optic chiasm compression
- Cranial nerve abnormalities e.g. diplopia
- Abnormal gait
- Torticollis ( stiff, asymmetrical head/ neck position)
- Cranial bruits - caused by AVM
- Bradycardia
18
Q
What is Cushing’s response in increased ICP?
A
- Hypertension
- Bradycardia
- Reduced respiratory rate
19
Q
What is the normal CSF pressure?
A
100-180 mm of H2O (8-15 mmHg)
20
Q
Risk factors for IIH…
A
- Obesity
- Female sex
- Pregnancy
- Medications: OCP, steroids, antibiotics
21
Q
Features of IIH…
A
- Headache
- Blurred vision
- Papilloedema
- Enlarged blind spot
- CN VI palsy (LR6 = affected eye cannot move laterally)
22
Q
Diagnosis of IIH…
A
Presence of:
- Papilloedema
- Raised CSF opening pressure
- NORMAL head imaging
- NORMAL CSF biochemical analysis
*Features of increased intracranial pressure present, but no obvious cause can be identified
23
Q
Management of IIH…
A
Conservative:
- Weight loss
- Removal of precipitating agents e.g. drugs
Medical:
- First line = diuretics e.g. acetazolamide
- Second line = steroids to reduce cerebral oedema
- Topiramate - also helps with weight loss
Surgial:
- Repeated LP
- Optic nerve sheath fenestration
- Lumboperitoneal shunt: device attached to lumbar spine to drain CSF into peritoneal cavity
24
Q
What are the ,most common infectious agents of sinusitis?
A
- Strep pneumoniae
- Haemophilus influenzae
- Rhinovirus
25
Risk factors for developing acute sinusitis...
- Nasal obstruction e.g. polyps
- Recent local infection e.g. rhinitis, URTI
- Swimming/ diving
- Smoking
26
Features of acute sinusitis...
- Facial pain - frontal pressure pain which is worse on bending forward
- Nasal discharge - thick and purulent
- Nasal obstruction
27
Management of acute sinusitis...
Sx present for <10 days:
- Simple analgesics - most likely viral illness that will self resolve
Limited evidence for:
- Intranasal decongestants / nasal saline
- Antihistamines
Sx present for >10 days:
- Intranasal corticosteroids 14 day course
Systemically unwell:
- First line: Pen V
28
Risk factors for SAH...
- Polycystic kidney disease
- EDS
- Marfan's syndrome
- AVM
- Arterial dissection
29
Presentation of SAH...
- Very severe, thunderclap headache - 10/10 severity within a few minutes
- Nausea and vomiting
- Meningism: neck stiffness, photophobia
- Reduced consciousness
- Seizures
- Focal neurological deficit e.g 3rd/6th nerve palsy
30
Investigations in SAH...
In any case of thunderclap headache, it should be treated as SAH until proven otherwise.
- CT imaging: Acute bleed will show as hyperdense/ bright on CT scan - but will not show on 7% of cases
- LP should be done >12hrs after onset if CT is normal but still suspect SAH (xanthachromia will not be present <12h).
When SAH is confirmed - need to find cause and determine site of bleed:
- CT intracranial angiogram
- Digital subtraction angiography
31
Management of SAH...
- Endovascular coiling - most intracranial aneurysms
- Craniotomy and surgical clipping
* Patient should follow strict bed rest until aneurysm repair to prevent risk of rebleed
- Nimodipine 60mg every 4 hours - 21d course- to prevent cerebral ischaemia from vasospasm
- Mannitol if there is increased ICP
32
What are some complications from SAH?
- Re-bleeding in 30%
- Vasospasm due to irritant blood by-products causing vessels to spasm and narrow- may cause cerebral infarct
- Hponatraemia due to SIADH
- Seizures
- Hydrocephalus
33
Risk factors for developing cerebral venous sinus thrombosis...
- Infection e.g. meningitis, abscess
- Hypercoaguability: pregnancy, OCP, antiphospholipid syndrome
- Rheumatological conditions: SLE, vasculitis
34
What is the presentation of cerebral venous sinus thrombosis?
Symptoms develop over days-weeks:
- Headache - may be sudden (thunderclap)
- Focal neurological signs e.g. limb weakness - mimic stroke
- Signs of increased ICP: papilloedema
- Seizures develop in many patients
35
Investigations for cerebral venous sinus thrombosis...
Bloods:
- FBC: elevated Hb/ platelets, raised WCC in infection
- Thrombophilia screen
Imaging:
- CT/MRI to rule out SAH if thunderclap headache present
- Venography may show absent sinuses
36
Management of cerebral venous sinus thrombosis...
Anticoagulation is mainstay of tx:
- LMWH followed by warfarin - aimed at keeping INR between 2-3
If sx deteriorate despite anticoagulation:
- Endovascular thrombolysis
If imminent transtentorial herniation:
- Emergency surgery - decompressive hemicraniectomy
37
How does temporal arteritis present?
* Usually >50 years old
- Headache
- Scalp tenderness - tender palpable temporal artery
- Jaw claudication - due to decreased perfusion of muscles of mastication
- Visual disturbances (due to inflammation of temporal artery - causing ischaemic optic neuropathy)
- Fever
- Weight loss
- Depression
- Proximal muscle weakness
38
What condition is temporal arteritis associated with and what symptoms may be seen due to this?
Polymyaligia rheumatica (PMR) - symptoms include:
- proximal muscle weakness
- morning stiffness/ aches
39
Investigation findings in temporal arteritis...
Bloods:
- FBC: anaemia
- ESR: raised >50mm/hr
- CRP: raised
Biopsy:
- Temporal artery biopsy may be diagnostic but has poor sensitivity due to skip lesions
40
Management of temporal arteritis...
- High dose steroids: 40-60mg OD Prednisolone - should be dramatic response.
* Gradually titrated down over 1-2 years to 1mg OD
- Urgent ophtalmology review to look for visual disturbances - need to be admitted for IV steroids as vision damage may be irreversible
41
Presentation of trigeminal neuralgia...
Unilateral sharp/ shooting pains distributed along one or more branches of CN V:
- Episodic, sudden onset pain
- Pain can be precipitated by light touch e.g. washing, shaving, bushing teeth
42
Red flags symptoms and signs for trigeminal neuralgia...
- Sensory changes
- Deafness
- Bilateral pain / only in ophthalmic divison
- Optic neuritis
- Family history of MS
- Onset before 40 y/o
43
Why do most trigeminal neuralgia patients have an MRI scan?
To exclude extracranial and intracranial masses along the course of CN V, or lesions affecting the trigeminal nerve brainstem pathway.
44
Management of trigeminal neuralgia...
First line = Carbamazepine - dose titrated to provide adequate pain control
Failure to respond to treatment: glycerol injection/ microvascular nerve decompression
45
Risk factors for meningitis...
- Extremities of age: very young and elderly
- Diabetes
- Immunosuppression
- Splenectomy
- Alcoholism
- IVDU
- Malignancy
46
Causes of meningitis...
BACTERIAL:
- Commonly s.pneumoniae and n.meningitides
- Patients> 60 y/o: L. monocytogenes
- Patient has had recent surgery: S. aureus
NON_BACTERIAL:
- Viruses: enterovirus, mumps, HSV, HZV, HIV
- Fungal infection
- Parasitic infection: spirochetes, protozoa
47
Presentation of meningitis...
Symptoms:
- General sx: fever, vomiting
- Meningism: neck stiffness, photophobia, headache
- Altered mental state, seizure
Signs:
- Kernig's sign: painful knee extension when knee and hip are flexed at 90deg
- Brudzinksi's sign: neck flexion causes hip flexion
- Non-blanching purpuric rash, skin mottling (in invasive meningococcal disease)
48
How may TB meningitis present?
Insidious onset:
- Often presents with mild persistent headache
- CN III, IV, VI affected - ocular muscles
- Papilloedema
49
Investigations for meningitis...
Bloods:
- FBC: raised WCC
- CRP: raised in infection
- Coagulaiton screen: before LP
- Blood culture
- Blood glucose
- Blood gas
Imaging:
- CT scan if focal neurological deficit / low GCS: will appear normal in meningitis
- MRI: temporal lobe changes in viral encephalitis, and ring-enhancing lesion in cerebral abscess
Biopsy:
- LP is most sensitive test- needs to be performed rapidly when raised ICP ruled out
50
CSF analysis for meningitis...
Bacterial meningitis:
- Cloudy appearance
- Very raised polymorphs
- High protein
- Low glucose
Viral meningitis:
- Clear appearance
- Raised lymphocytes
- Normal protein
- Normal glucose
TB meningitis:
- Cloudy/ fibrin web appearance
- Raised lymphocytes
- High protein
- Low glucose
51
Management of meningitis...
BACTERIAL:
- In pre-hospital setting if meningococcal disease suspected: give 1.2g benzylpenicillin IM/IV
- Hospital: take blood cultures, LP and treat bacterial meningitis according to trust abx guidelines
- Meningococcal = IV cefotaxime/ benzylpenicillin
- Pneumococcal = IV cefotaxime
- Dexamethasone given if meningism present
- Household contacts require prophylaxis: 1 dose of ciprofloxacin
VIRAL:
Supportive treatment: antipyretics and rest
TB MENINGITIS:
2 months of RIPE (rifampicin, isoniazid, pyrazinamide, ethambutol) + 10 months of PE (pyrazinamide and ethambutol)
52
Features of encephalitis...
Classic triad: fever, headache, psychiatric symptoms
| Other features: convulsions, focal neurological deficit, vomiting, seizures
53
What is the main causative agent of encephalitis ?
HSV-1 causes 95% of adult cases
54
Investigations for encephalitis...
Bloods:
- Routine bloods to look for infection
- Autoimmune assay to look for auto-antibodies
Biopsy:
- LP will show raised lymphocytes and protein
- CSF used for PCR analysis for HSV, VZV, enteroviruses
Imaging:
- EEG shows diffuse slowing of conduction
- CT - shows temporal and frontal changes e.g. petechial haemorrhage and rules out space-occupying lesion
- MRI
55
Management of encephalitis...
IV acyclovir to be started immediately
56
Name two types of autoimmune encephalitis, and how do they present?
- Anti-NMDA encephalitis: causing psychiatric sx e.g. hallucinations/delusions, seizures, movement disorders
- Limbic encephalitis: antibodies attacking limbic system leading to: subacute amnesia, confusion, seizures, SIADH
57
How is autoimmune encephalitis managed?
- IV steroids and IV Ig with plasma exchange
- Full body CT scan is normally taken as autoimmune encephalitis tends to be a paraneoplastic syndrome so primary tumour must be located
58
Presentation of hypertension headahces...
- Usually occur when person has a blood pressure of 200/100 or higher
- Dull, occipital headache
- Associated sx= throbbing noise in ears, confusion, blurred vision
59
Management of hypertension headaches...
Patients with headache need BP measurement promptly.
- Identify precipitating cause e.g. medication review and ask about recreational drugs like cocaine and amphetamines
- Treat the hypertension - lifestyle changes and optimal medical management
60
What are the categories of hypertension headaches?
1. Phaeochromacytoma
2. Hypertensive crisis without encephalopathy
3. Hypertensive crisis with encephalopathy
4. Pre-eclampsia and eclampsia
5. Acute pressure response to exogenous agent
61
What is a low pressure headache and how is it caused?
Low CSF pressure leads to brain sagging downward when patient is upright which stretches meninges and nerves causing a headache.
Causes:
- Head/ neck injury causes tear in dura
- Iatrogenic: LP/ spinal surgery/ anaesthesia
- Connective tissue disorder e.g. EDS
62
What are the features of a low pressure headache?
- Headache worse on standing or sitting
- Relieved by lying flat
- Mild in the morning, and worsens throughout the day
- Commonly occipital in region
63
Investigations carried out in low pressure headaches...
- Brain MRI with contrast dye - may show brain sagging
- CT myelogram - may show leak directly
- LP may show reduced opening pressure but may worsen sx temporarily
64
Treatment of low pressure headaches...
- Conservative: bed rest, increased fluid intake, caffeine
| - Surgery: epidural blood patch, glueing of hole
65
Risk factors for acute angle-closure glaucoma
Impairment in aqueous flow:
- Narrow angle due to pupillary dilatation
- Increased age
- Cataracts
- Hypermetropia
66
Presentation of acute angle-closure glaucoma
- Severe ocular pain / headache
- Decreased visual acuity
- Red eye
- Haloes around lights
- Semi-dilated non-reacting pupil
- Visual field defects - nasal step
- Systemic sx = nausea and vomiting
67
Management of acute angle-closure glaucoma...
- Acetazolamide 500mg IV stat - reduce aqueous secretions
- Pilocarpine - pupillary constriction
- Steroid drops for pain
- Laser iridotomy
68
What is the pathophysiology behind carbon monoxide poisoning?
CO irreversibly binds to haemoglobin to form carboxyhaemoglobin which decreases the oxygen-carrying capacity of the blood. This eventually leads to severe tissue hypoxia.
69
What are the features of carbon monoxide poisoning?
```
Early/ symptomatic phase:
- Headache
- Nausea an vomiting
- Vertigo
- Confusion
Severe toxicity (>30%) causes:
- Hyperventilation
- Hypotension
- Hyperreflexia
- 'pink' skin
```
70
What investigations are used in carbon monoxide poisoning?
- VBG/ ABG to show accurate Hb
| - ECG to look for signs of cardiac ischaemia
71
Why is pulse oximetry not reliabe in diagnosing carbon monoxide poisoning?
Structurally, oxyhaemoglobin and carboxyhaemoglobin are very similar therefore it may provide a falsely normal Hb level.
72
What are normal carboxyhaemoglobin levels?
<3% in non smokers
<10% in smokers
10-30% = symptomatic: headache, vomiting
>30% = severe toxicity
73
Management of carbon monoxide poisoning...
- Remove patient from exposure
- As high conc of O2 as possible - 100% via non-rebreathe or IPPV if unconscious
- Check ABG for metabolic acidosis from tissue hypoxia - correct with O2
- Hyperbaric O2 indicated in patients: CoHB>25%, LoC, neuro signs, myocardial ischaemia, pregancy
