Headaches Flashcards
Why are headaches important?
- Headaches can be a warning symptom:
- Cerebral tumours
- Raised intracranial pressure
- Intracranial haemorrhage
- Aneurysms
- Meningitis, encephalitis
- Giant cell arteritis (temporal arteritis)
- Headaches themselves can cause significant morbidity:
- Tension headaches
- Migraine
- Other headache sub-types
- ~40% of individuals report ≥1 severe disabling headache per year
- Headaches are also common as a nonspecific epiphenomenon:
- Many febrile illnesses, malaise
- Ischaemic stroke
List sources of head pain
- Blood vessels, especially meningeal arteries, also large veins
- Meninges
- Supratentorial dura (trigeminal nerve)
- Posterior fossa, (cervical roots C1-3, vagal nerve, glossopharyngeal n)
- Scalp – skin, muscles
- Skull – bone, periosteum
- Face – trigeminal nerve
- Neck – muscles, spine, ligaments
- Sensory nerves – direct activation as well as true nociception => pain in regions shown
- NOT the brain itself – no pain receptors
- But, experimentally, stimulation of midbrain dorsal raphe may cause headache
- Migraines probably originate in brainstem structures, with secondary activation of trigeminal system
What are some ddx considerations for headache?
This depends on the chronological course and clinical setting:
- Acute, severe headache
- Subacute headache
- Recurrent headache or facial pain
- Chronic headache
- Progressive headache
- Also spatial and temporal distribution
(See lists at end of lecture)
The diagnosis is usually apparent from the history and examination. As in any pain syndrome, the history needs to focus on the site, nature, course, triggering and relieving factors, etc of the pain. Follow it up with a careful neurological examination, including funduscopy, and assessment of the neck.
Differential Diagnosis of Headache
First priority is to detect serious underlying causes. Important issues to resolve are:
- Is there meningism (stiff neck, photophobia)?
- Is there evidence of raised intracranial pressure (postural headache- raised ICP relieved when patient supine, visual change)?
- Was the onset sudden (over seconds)?
- Is the headache progressive (over weeks or months)?
- Are there associated neurological deficits?
- Could it be giant cell arteritis?
Any of these might indicate a sinister or dangerous cause.
Describe meningism
- ‘Meningism’ refers to a cluster of signs and symptoms indicating meningeal irritation or inflammation
- Neck rigidity is the hallmark
- Photophobia is common
- Pain may be increased with stretch of meninges
- Kernig’s sign (pain on straightening legs with hips flexed)
- Brudzinksi’s sign (active flexion of hips/knees on passive flexion of neck)
- Always a serious symptom, demands further investigation
- Important causes are:
- Subarachnoid blood
- Meningitis (bacterial, viral)
- Mild cases may be confused with migraine or cervicogenic headache
Discuss raised ICP and associated signs
- The skull is a closed, rigid container
- Small changes in volume of intracranial contents can cause large changes in pressure, especially if rapid, with stretch of meninges and blood vessels, causing headache
- The extra volume can come from:
- a ‘mass’ lesion (tumour, abscess, haematoma)
- bleeding
- oedema (around a mass lesion, with inflammation, or following a stroke)
- increased cereberospinal fluid (CSF), from increased CSF production, blockage to flow, or impaired absorption
- Slowly progressive mass lesions may produce few signs or symptoms, often with no headache at all, especially in older patients who have relatively atrophic brains and increased CSF spaces
Evolution of raised ICP
Initial compensation for a volume/pressure challenge involves the compression of CSF spaces, but once these are compressed the brain parenchyma shifts, intracranial pressure rises steeply, and cerebral perfusion falls.
Is there evidence of raised intracranial pressure?
- The hallmark of raised ICP, on history, is a headache worse on lying flat, (though this can also come from scalp tenderness or neck discomfort)
- Raised pressure may also compress the optic nerves, producing papilloedema, but this is a relatively late sign
- Papilloedema is often subtle, and requires careful examination by the most experienced doctor available. Absence of papilloedema is not proof of normal ICP.
What are consequences of raised ICP?
- Optic nerve compression, with serious threat to vision
- Raised ICP reduces cerebral perfusion pressure (arterial pressure – intracranial pressure), which may cause drowsiness (a fall in the Glascow Coma Score, or GCS), coma and death.
- Patient may respond to raised ICP with hypertension and bradycardia (the Cushing response), but this is a late and inconsistent sign. Coupled with respiratory depression, usually from brainstem compression, this is known as Cushing’s triad.
- Severely raised pressure may cause compression or herniation of the brainstem or cerebellum, which is a major, life-threatening emergency – signs can include unconsciousness, the Cushing response, cranial nerve abnormalities (particularly dilated or ‘blown’ pupils), hemiparesis, or quadriparesis
- A raised ICP may be confirmed by doing a lumbar puncture, but this is unsafe in the presence of raised ICP due to a mass lesion – a pressure gradient can develop and increase the risk of herniation
List types of cerebral herniation
1) Subfalcine herniation – left <-> right, under the falx
2) Central herniation – longitudinal compression/kinking of brainstem, or herniation of brainstem relative to temporal lobe
3) Uncal/transtentorial herniation – temporal lobe –> posterior fossa
4) Tonsillar herniation – cerebellar tonsils through foramen magnum
The brainstem may also be compressed laterally against the tentorial edge without herniation
What is the approach for suspected ICP?
Suspicion of raised ICP mandates an urgent imaging study (CT brain, usually with CT venogram) – look for a mass, compression of ventricles, midline shift, sulcal effacement. SOL unless proven otherwise
- If no mass lesion – consider:
- obstructive hydrocephalus – check size of ventricles
- venous thrombosis, including sagittal sinus thrombosis
- “benign” (idiopathic) intracranial hypertension (BIH/IIH) – see later
- REMEMBER: Intracranial pressure can often be checked and treated by lumbar puncture, but this is unsafe in the presence of a mass lesion
Describe sagittal sinus thrombosis
- Often misdiagnosed, or diagnosed late
- May cause chronic headache, with symptoms of raised ICP
- Postural headache
- Visual changes
- Papilloedema
- May progress to venous infarction/bleed
- Ischaemic stoke due to engorgement, with high risk of haemorrhage
- May be bilateral
- May cause seizures
- May be an underlying hypercoaguable state
- Treat with anticoagulation, even in the presence of a bleed
- Best diagnosed on CT venogram or MR venogram, but can be seen on contrast CT Empty delta sign – failure of contrast to fill the sagittal sinus
Describe raised ICP management
Treatment:
- Shrinkage or removal of mass lesion (chemo/radiation for tumours, antibiotics/drainage for abscess, neurosurgical removal of masses)
- Anticoagulants for venous thrombosis
- Treatment of oedema with corticosteroids
- Lumbar puncture and removal of CSF (if raised CSF volume is the cause) – record pressure (normal is ~5-20 cm CSF)
- Neurosurgical drainage device (temporary or permanent CSF shunt)
- Rarely, craniectomy to decompress the skull (“malignant” infarction)
- For urgent reduction in ICP, especially if falling conscious state or imminent herniation/coning, use mannitol and forced hyperventilation on a ventilator
Describe subarachnoid haemorrhage, likely causes and precipitants, and course of action
- Most often secondary to aneurysms, which are balloon-like swellings of the medium or large blood vessels, often at branch points. May be due to other vascular malformations, or rarely traumatic.
Subarachnoid Haemorrhage
- Often due to aneurysms (in Asia, more likely due to angiomas)
- May follow exertion
- Headache onset often described as “a blow to the head”
- Unilateral headache rapidly spreading to become generalised, and then causing meningism
- May be impaired consciousness, or focal neurological signs due to:
- the aneurysm compressing cranial nerves
- cerebral herniation
- ischaemia secondary to vasospasm
- 10-15% of patients die before reaching hospital, ~50% mortality overall, high risk of long-term disability in survivors
- About one third have a prior history of sudden, severe ‘sentinel’ headaches, probably due to stretching of the aneurysm – if investigated early, the later SAH could have been prevented
Subarachnoid Haemorrhage
- Investigate suspected SAH with urgent CT, looking for blood
- If CT normal and still suspicious, do LP after 12 hrs (allow time for blood to spread through CSF), looking for xanthochromia (yellowness from old, lysed blood); need for this step has been questioned recently, if very good CT available
- Red blood cells may be in all 3 CSF tubes in equal numbers (c.f. “Traumatic tap”, with less blood in 3rd bottle)
- Follow-up with CT/MR angiography, or invasive angiography, to find the aneurysm
- Anti-vasospasm treatment e.g. CCBs?, control of ICP, in neurosurgical intensive care unit
- Aneurysm treated radiologically or neurosurgically (clip or coil)
Discuss intraparenchymal bleed
Typically occurs in elderly
- Consider this in a patient who has:
- a progressive or slow-onset stroke
- focal neurological signs
- often declining conscious state if large
- with headache
- with risk factors (HT, coagulopathy; if no HTN consider amyloid angiopathy)
- May mimic an ischaemic stroke, or arise from secondary haemorrhagic transformation of an ischaemic stroke
- Headache often a major complaint but focal neurological signs or reduced conscious state usually make it clear that this is not a benign headache
- Easily seen on CT – fresh blood looks white
Describe giant cell arteritis
- Usually age>50
- Headache often localised, with arterial tenderness or visible/palpable swelling
- Not confined to the temporal artery (hence the name change from “temporal arteritis” to GCA) - occurs in medium and large vessels
- Risk of stroke
- Involvement of ophthalmic artery can lead to transient visual obscurations or blindness. Prompt diagnosis is needed to save vision.
- Jaw claudication from ischaemia (“angina”) of chewing muscles
- Often accompanied by polymyalgia
- Rarely oculomotor nerve palsies
- Raised ESR/CRP in many patients
- Dx by biopsy and Rx with steroids +/- methotrexate or azathioprine as steroid sparing agents
Discuss warning signs and symptoms of ‘dangerous’ headaches
- Sudden and severe – SAH, or other bleed, aneurysmal ‘sentinel’ headache
- Febrile, with meningism – meningitis or meningoecephalitis
- Focal neurology – bleed, aneurysm, infarction (but focal neurology may also be due to migraine)
- Chronic, progressive – tumour
- Postural (raised ICP) – tumour, sinus thrombosis, IIH, chronic subdural
- Visual symptoms, polymyalgia, jaw claudication, temporal artery tenderness – giant cell arteritis (screen with ESR, CRP, biopsy if suspicious)
Describe migraine
- A common condition with a complex, poorly understood pathophysiology
- Classically produces episodic, unilateral, throbbing headache, associated with nausea and photophobia – but may cause no headache at all
- Probably due to abnormal neural firing in brainstem structures that project to the cerebral vasculature, leading to altered serotinergic tone, altered vascular reactivity and spasm, inflammatory changes, autonomic features and (usually) resulting in vascular pain
Migraine
- Focal deficits in migraine (“auras”)
- May precede, accompany or follow headache
- May be almost any central, focal deficit, often positive rather than negative features cv stroke
- Vertigo
- Dysphasia
- Hemiparesis
- Hemisensory change, especially migrating paraesthesia
- Classically, and most commonly, patients report visual changes
- Zig-zag lines (“fortification spectra”)
- Dots/blobs
- Often moving or shimmering or shiny in nature (positive)
- Classically become more extensive during the migraine…
