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30th July 2024

Headache

Meningitis

Background

Meningitis describes inflammation of the meninges covering the brain and spinal cord. It is a potentially life-threatening neurological emergency requiring urgent treatment and assessment in secondary care. In addition to headache, symptoms also include neck stiffness, fever, photophobia, nausea and vomiting. The key diagnostic investigations are blood cultures and analysis of cerebrospinal fluid taken by lumbar puncture. Cases of meningitis with negative bacterial culture results (for example, viral, fungal and tuberculous meningitis) are referred to as aseptic meningitis. Empirical treatment is initiated on presentation with further treatment being tailored to investigation results.

Bacterial meningitis

Bacterial meningitis is a rare but life-threatening condition which is more common in very young and elderly people. The most common causative organisms include Streptococcus pneumoniae, Neisseria meningitidis, Haemophilus influenzae and Listeria monocytogenes. The most severe symptoms are typically seen in meningococcal infection, with patients presenting with septic shock and the characteristic non-blanching rash (Figure 1). Listeria monocytogenes usually affects those who are at the extremes of age, immunocompromised or pregnant.

Treatment of bacterial meningitis

  • In suspected bacterial meningitis, empirical antibiotic treatment should be initiated immediately.
  • Due to the severity of the infection, cases of suspected meningococcal meningitis in the community should be treated with benzylpenicillin before transfer to hospital.
  • For adults <50 years, empirical antibiotic treatment in the hospital consists of cefotaxime or ceftriaxone.
  • For those >50 years, amoxicillin should be added to cover for Listeria.
  • In suspected pneumococcal meningitis, dexamethasone should be started no later than 12 hours after the 1st antibiotic dose, as it has been shown to reduce mortality.
  • The antimicrobial regime should then be reviewed with the CSF results and adjusted accordingly.
  • Antimicrobial chemoprophylaxis is indicated for close contacts of those with confirmed meningococcal meningitis. Close contacts include household members, intimate contacts and anyone who has spent more than 8 hours less than 3 feet away from the person from 7 days before the onset of their symptoms to 24 hours after starting antibiotics. It also includes those who have had direct exposure to the patient’s oral secretions (for example, during intubation or suctioning) during this period.

Viral meningitis

Viral infections are the most common cause of meningitis and are usually self limiting. Common causes include human enteroviruses (most common), herpes simplex virus, varicella zoster virus and influenza.

Tuberculous meningitis

Tuberculous meningitis can occur in primary infection or reactivation. The onset of symptoms is typically slower than in other types of meningitis. Treatment is with anti-tuberculosis medications.

Fungal meningitis

Fungal infection is rare but life threatening. It is predominantly seen in those who are immunocompromised and is most commonly caused by infection with the cryptococcus species.

Aseptic meningitis

There are many other causes of aseptic meningitis, a small number of which will be outlined in this section:

  • Primary HIV infection can present as meningitis which often resolves without treatment. It is, therefore, important to routinely screen for HIV in cases of meningitis.
  • Mollaret’s meningitis is a recurrent meningitis which is defined as more than 3 episodes of meningism which resolve spontaneously. It is a rare condition and is usually caused by HSV (Herpes simplex virus)-2.
  • Aseptic meningitis is a possible complication of mumps infection. Prior to the introduction of the mumps vaccine this was a very common cause of aseptic meningitis.
  • Secondary syphilis, caused by the spherocyte Treponema pallidum, can present with meningism and a widespread rash.
  • Acute lyme disease can present with a meningitic picture. It is a vector-borne disease caused by infection with Borrelia species which is spread by ticks. Cranial nerve palsies can be present, especially bilateral facial nerve palsy, which is characteristic of this disease. Another classical sign which would point towards this diagnosis is the presence of an erythema migrans rash.
  • Rarely, aseptic meningitis can occur in response to a drug reaction. A variety of medications have been associated with this condition including NSAIDs, antibiotics and anti-epileptics.
  • Malignant meningitis can occur with invasion by solid tumours or when haematological malignancies spread to the CNS.

Interpretation of cerebrospinal fluid results

Correct interpretation of cerebrospinal fluid (CSF) characteristics can indicate the diagnosis before culture results are available and, therefore, guide management decisions.

CSF appearance Opening pressure (cmH₂O) WBC (per mm³) Protein

(g/litre)

 Glucose

(mmol/Litre)
Normal Clear 5-20 0-5 (lymphocytes) 0.2-0.45 75% of blood glucose
Viral Clear normal/↑ 15-1,000 (lymphocytes) ↑ Normal
Bacterial Turbid ↑ 100-60,000

(predominantly neutrophils)

 ↑ ↓
TB Opaque ↑ 10-500 (neutrophils initially, then lymphocytes) ↑ ↓
Fungal Clear/cloudy ↑ 25-500 (mainly lymphocytes) ↑ ↓

MRCP Part 2 - Non-blanching meningococcal rash

Image Source: James Heilman, M.D. Own work. CC BY-SA 3.0. Wikimedia Commons (2010). Vasculitis, Licensed under a creative commons licence. Available for free at: https://commons.wikimedia.org/wiki/File:Vasculitis.JPG (Accessed: 16 January 2024)

MRCP Part 2 - Turbid CSF seen in bacterial meningitis

Image Source: James Heilman, M.D. Own work. CC-BY-SA-4.0. Image Source: Wikimedia Commons (2019). MenigitisCSF2019, Licensed under a creative commons licence. Available for free at: https://commons.wikimedia.org/wiki/File:MenigitisCSF2019.jpg (Accessed: 16 January 2024)

References

Primary headache syndromes

Overview

Headache is a common symptom which usually has a benign cause. Those which are not a symptom of underlying disease are known as primary headaches. In this section, we will cover tension headaches, migraines, cluster headaches and trigeminal neuralgia. The full diagnostic criteria for all headache disorders can be found in the International Classification of Headache Disorders (ICHD) Criteria, which is in the references section.

Tension-type headaches

Tension headaches are commonly triggered by stress. The patient usually reports a mild, bilateral, constricting pain as if a tight band is being stretched around their head. The course can be episodic or chronic. They usually respond well to simple analgesia and non-pharmacological treatments such as relaxation techniques and cognitive behavioural therapy. In cases of chronic tension-type headaches, where headaches are occurring on more than 15 days per month, prophylaxis with a low-dose tricyclic antidepressant can be initiated.

Migraine

Migraine is a common neurovascular disorder affecting around 1 in 6 people. It commonly occurs in young to middle-aged females. There is a strong genetic component to the disorder with around half of migraine sufferers reporting a family history. Migraines are thought to be caused by an inflammatory process in the brain resulting in non-painful stimuli being perceived as painful, for example sound and light.

  • The headache follows a chronic, episodic course with each episode lasting approximately 4-72 hours.
  • It is described as a severe throbbing pain which is made worse by normal daily activities and associated with photophobia, phonophobia and nausea.
  • Migraine can be split into two types: migraine with aura and migraine without aura. Auras typically consist of temporary unilateral sensory or visual disturbances, however they can also include motor symptoms in cases of hemiplegic migraine.
  • Acute symptomatic treatment options include combination therapy with an oral triptan and NSAID or oral triptan and paracetamol. Alternatively, monotherapy with paracetamol, aspirin, NSAIDs or a triptan can be offered. Antiemetics should also be offered if needed. Triptans should be avoided in migraine with hemiplegic aura as they may increase the chance of stroke.
  • Preventative measures include trigger avoidance and pharmacological therapies. In those patients who wish to start preventative medication, topiramate or propranolol should be offered. Topiramate is teratogenic and, therefore, should be avoided in females of childbearing age.  Other preventative options include amitriptyline, venlafaxine and verapamil.
  • It is also important to ensure that those who experience migraine with aura are not taking a combined oral contraceptive pill as this will increase their risk of stroke.
  • Migraines can be disabling, however the majority of patients respond well to treatment and the frequency of episodes generally decreases with age.

Cluster headaches

Cluster headaches are characterised by severe unilateral pain around the eye and side of the face associated with autonomic features including nasal congestion, ptosis and lacrimation. Patients are generally agitated during an attack and move around a lot. Males are more likely to be affected than females.

Episodes last 15-180 minutes and occur in clusters lasting from a few weeks to 3 months with an attack-free period of at least 3 months. There is also a chronic form of the disorder where the clusters last for 1 year or more or the remission period is less than 3 months.

Cluster headaches are classified as a subtype of trigeminal autonomic cephalalgia in the ICHD-3 criteria. The other subtypes are listed in the table below.

Paroxysmal hemicraniaSigns and symptoms are very similar to cluster headaches however the acute attacks are shorter (2-30 mins) and more frequent (occurring up to 40 times per day). Attacks respond completely to indomethacin.Short-lasting unilateral neuralgiform headache attacks with conjunctival injection and tearing (SUNCT)Moderate to severe unilateral stabbing/saw-tooth pain lasting from seconds to minutes. Associated with ipsilateral redness of the eye and lacrimation.Short-lasting unilateral neuralgiform headache attacks with autonomic features (SUNA)Similar to SUNCT, however these patients experience only one or neither of conjunctival injection and lacrimation.Hemicrania continuaUnilateral headache associated with autonomic features lasting for at least 3 months. This headache also responds to indomethacin.

      • Acute attacks are treated with high flow oxygen and/or subcutaneous or nasal triptans. Intranasal lidocaine can be used instead of triptans, for example in those with coronary artery disease where triptans are contraindicated.
      • First line prophylactic treatment is verapamil.
      • As preventative treatments can take a few weeks to work, corticosteroids can be started at the same time as verapamil as a bridging therapy. High-dose prednisolone has been shown to induce remission quickly, however it should be weaned after 5 days due to the risks of long-term steroid use.

Trigeminal neuralgia

Trigeminal neuralgia describes neuropathic facial pain along at least one division of the trigeminal nerve. The pain usually lasts a few seconds and the attacks can be triggered by stimuli such as touch and the cold. The majority of cases are caused by compression of the nerve root, however it is also seen in multiple sclerosis, head injury, cerebellopontine angle tumour, arteriovenous malformations or herpes zoster infection. The presence of sensory loss, bilateral symptoms, optic neuritis or presentation under the age of 40 are concerning for a secondary cause of trigeminal neuralgia such as multiple sclerosis. These cases would need further investigation with MRI.

The first line treatment is with carbamazepine which is started at a dose of 100-200 mg twice a day and gradually uptitrated. If medical treatment fails, then surgical options such as microvascular decompression or ablative procedures can be considered.

Other primary headache disorders

There are a number of other primary headache disorders described in ICHD. These headaches are generally poorly understood and can mimic secondary headache disorders. The table below briefly outlines some of these conditions.

Primary headache disorder Clinical features Differentials to rule out
Primary cough headache Precipitated by coughing and other valsalva manoeuvres Structural intracranial lesions
Primary exercise headache Precipitated by exercise Structural intracranial abnormalities, ICH, migraine
Primary headache associated with sexual activity Precipitated by sexual activity with increased intensity at orgasm ICH (particularly SAH), arterial dissection, reversible cerebral vasoconstriction syndrome, CVST
Primary thunderclap headache Sudden onset, high intensity headache ICH (particularly SAH), arterial dissection, reversible cerebral vasoconstriction syndrome, CVST, unruptured aneurysmal malformation
Nummular headache Pain in a small circumscribed area of the scalp Cranial bone lesions, dermatological scalp lesions

References

Secondary headache syndromes

Overview

Secondary headaches occur as a symptom of underlying disease. It is a common symptom therefore the list of causes is extensive. This section will focus on: medication overuse headache, idiopathic intracranial hypertension, subarachnoid haemorrhage, cerebral venous sinus thrombosis, giant cell arteritis, intracranial neoplasia and head injury. A full list can be found in the International Classification of Headache Disorders-3.

Medication overuse headache

Medication overuse headache occurs in patients with a pre-existing headache disorder who overuse analgesia on a regular basis. It presents as a change in their usual headache. Patients will report having a headache most days (at least 15 days/month). It should be considered in those who regularly take paracetamol, aspirin, NSAIDs, triptans, opioids or ergots. The treatment is to stop the overused medications.

Idiopathic intracranial hypertension (IIH)

IIH is a disorder of raised intracranial pressure in patients with a normal ventricular system. The cause remains unknown, however we do know that it predominantly occurs in overweight females of childbearing age.

      • Symptoms include a throbbing headache, transient loss of vision, blurring of vision, pulse -synchronous tinnitus, photophobia and nausea.
      • Cranial nerve exam may show signs of raised intracranial pressure including papilloedema, visual field deficits and cranial nerve VI paresis.
      • The Modified Frisen Scale is used to grade papilledema. Those with grade 3 to 5 papilloedema are at high risk of visual loss. The major criteria for each grade are shown below:
Grade Key feature
Grade 0 Normal optic disc
Grade 1 C-shaped halo with a temporal gap obscuring the retinal details
Grade 2 A circumferential halo
Grade 3 Obscuration of 1 or more segments of major blood vessels leaving the disc
Grade 4 Total obscuration of a segment of a major blood vessel on the disc
Grade 5 Obscuration of all vessels both on the disc and leaving the disc
      • The modified Dandy criteria states that CSF pressure must be >25 cmH2O on lumbar puncture for a diagnosis of IIH to be made.
      • MRI brain may show an empty sella or flattening of the posterior globe.

MRCP Part 2 - Retinal photograph demonstrating severe papilloedema

Image Source: Wikimedia Commons (2011). Papilledema, Licensed under a creative commons licence. Available for free at: https://commons.wikimedia.org/wiki/File:Papilledema.jpg (Accessed: 16 January 2024)

MRCP Part 2 - MRI brain showing empty sella sign

Image Source: Wikimedia Commons (2011). Empty SellaMRT T2 sag 002, Licensed under a creative commons licence. Available for free at: https://commons.wikimedia.org/wiki/File:Empty_Sella_MRT_T2_sag_002.jpg (Accessed: 16 January 2024)

      • Initial treatment is with weight reduction, a low salt diet, fluid restriction, analgesia and stopping any medications which are known to increase intracranial pressure (for example, tetracyclines, retinoids and vitamin A). In patients with moderate papilloedema, acetazolamide or furosemide may also be started.
      • If symptoms do not respond to medical treatment then optic nerve sheath fenestration or CSF shunting may be performed. The prognosis varies and symptoms can be transient or chronic. Evidence shows that with treatment about half of patients have significant improvement in their vision.

Subarachnoid haemorrhage

SAH refers to bleeding into the subarachnoid space, usually as the result of a ruptured intracranial aneurysm. Those with hypertension, autosomal dominant polycystic kidney disease, a smoking history or a family history of SAH are at increased risk of developing SAH.

      • Patients report a severe, sudden ‘thunderclap’ headache associated with vomiting and meningism. In severe cases, it can present with coma or sudden death.
      • A diagnosis can be confirmed by CT brain or lumbar puncture. Studies have shown that a CT performed within 6 hours of symptom onset can detect almost all cases, showing hyperdensity in the subarachnoid space. This sensitivity decreases over time, therefore in the majority of cases a lumbar puncture should also be performed if the scan is negative. This should be done at least 12 hours after the onset of a headache so that the xanthochromia can be accurately detected.
      • Patients should be warned about the risk of developing a headache post lumbar puncture. The risk of this can be reduced by replacing the stylet before removing the LP needle.
      • Note that hyponatraemia and hyperglycaemia can be features of SAH.
      • All cases of confirmed SAH should immediately be discussed with the neurosurgery team. The use of nimodipine has been shown to improve outcomes.
      • Around 30% of patients die within 30 days of a SAH and many survivors experience cognitive impairment.

MRCP Part 2 - Subarachnoid haemorrhage

Image Source: Wikimedia Commons (2010). SubarachnoidP, Licensed under a creative commons licence. Available for free at: https://commons.wikimedia.org/wiki/File:SubarachnoidP.png (Accessed: 16 January 2024)

A condition that presents similarly to SAH is reversible cerebral vasoconstriction syndrome. This condition is caused by reversible constriction of the cerebral arteries and presents with recurrent thunderclap headaches. Some people also experience focal neurological deficits. Triggers such as stress, valsalva manoeuvres or exertion are often reported. The characteristic neuroimaging finding is multifocal segmental cerebral artery vasoconstriction on cerebral angiography. There may also be evidence of subarachnoid haemorrhage or ischaemia on imaging.

Cerebral venous sinus thrombosis

The pathophysiology of CVST (cerebral venous sinus thrombosis) is not fully understood, however it is thought to be caused by the thrombosis of cerebral veins or dural sinuses leading to blockages in the drainage of blood in the brain. Reduced CSF absorption in the brain is also thought to play a role. These mechanisms ultimately lead to an increase in intracranial pressure.

Risk factors are female sex, prothrombotic conditions, pregnancy and the puerperium, oral contraceptives, cancer, ENT infections and head injury.

It can be difficult to diagnose as it can present in a variety of ways. The headache can be acute, subacute or chronic and does not follow a specific pattern. Diagnosis relies on an MRI brain and MR venogram or CT brain and venogram.

The three key clinical presentations to look for are:

      1. Intracranial hypertensive syndrome: headache, visual changes and papilloedema.
      2. Focal neurological deficits: seizures, hemiparesis or dysphasia.
      3. Encephalopathy: delirium, multiple neurological deficits or coma.

It should also be noted that isolated thrombosis of the different sinuses or veins will present differently:

      • Cavernous sinus thrombosis presents with ocular signs and is generally preceded by an ear, sinus or tooth infection.
      • Lateral sinus thrombosis, a rare complication of untreated otitis media, usually presents with a headache or isolated intracranial hypertension but focal neurological deficits can be present (usually CN [cranial nerve] VI palsy).
      • Sagittal sinus thrombosis presents with motor deficits or seizures. It is associated with the use of oral contraceptives and is also a rare complication of meningitis.

After diagnosis, antithrombotic treatment with low molecular weight heparin is started. Most patients are then given dabigatran or warfarin for a minimum of 3 months.

With treatment, the prognosis is usually quite good, with studies reporting a complete recovery in around 80% of patients. However about 5% unfortunately die during the acute phase of the disease.

Giant cell arteritis (GCA)

GCA is a vasculitis which affects medium and large vessels, especially branches of the external carotid artery. It is more common in those aged over 50 years.

Symptoms include headache, scalp tenderness, jaw claudication, fever and loss of vision. It is also commonly associated with polymyalgia rheumatica. In severe cases, patients can develop permanent loss of vision.

Blood tests will show raised CRP and ESR. Diagnosis is confirmed with vascular ultrasonography and/or temporal artery biopsy, however temporal biopsy has been shown to give a high number of false negative results.  The ultrasound finding which is most suggestive of  GCA is a circumferential hypoechoic vessel wall thickening which does not disappear on compression. This is known as the halo sign.

Treatment is with high-dose steroids, which should be started on suspicion of the diagnosis, rather than awaiting a temporal artery biopsy.

Intracranial neoplasia

Brain tumours can occur as primary intracranial neoplasms or as a result of metastatic malignancies.

Around 20% of those with a brain tumour experience headache. This headache is generally progressive, worse in the mornings, exacerbated by valsalva manoeuvres and associated with nausea and vomiting.

On examination, neurological deficits may be present, which are usually progressive.

CT brain with contrast will identify the site and size of the tumour. A biopsy is usually required to confirm the diagnosis.

Management will depend on the patient and the nature of the tumour. Dexamethasone is used to manage symptomatic oedema.

The most common primary brain tumours are gliomas, meningiomas and pituitary adenomas and the most common cause of brain metastases are lung and breast cancer. The typical neuroimaging findings of these tumours are described below:

Tumour Imaging findings
High-grade glioma Hypointense masses on T1-weighted MRI, which enhance heterogeneously with contrast
Low-grade glioma Hyperintense lesions on T2-weighted MRI. Most are non-enhancing
Meningioma Extra-axial lesions which are hypointense (on T1 MRI) and enhance with contrast
Pituitary adenoma Pituitary lesion which is isointense to grey matter. May extend into the suprasellar cistern and compress the optic chiasm
Brain metastases Rounded, well circumscribed masses which enhance with contrast

MRCP Part 2 - MRI image of a meningioma

Image Source: Wikimedia Commons (2016). MRIMeningioma, Licensed under a creative commons licence. Available for free at: https://en.wikipedia.org/wiki/Meningioma#/media/File:MRIMeningioma.png (Accessed: 16 January 2024)

MRCP Part 2 - MRI image of lung metastases

Image Source: Wikimedia Commons (2012). Brain MRI 131716 T2, Licensed under a creative commons licence. Available for free at: https://commons.wikimedia.org/wiki/File:Brain_MRI_131716_T2.png (Accessed: 16 January 2024)

It should be noted that pituitary adenomas can also present with a thunderclap headache in cases of pituitary apoplexy. This is when a bleed or infarction occurs in the pituitary gland, usually in the context of a pituitary adenoma. The possible complications include adrenal insufficiency, which should be treated with urgent corticosteroid replacement. The case should be urgently discussed with neurosurgery as transsphenoidal decompression should be considered.

Head injury

Head injuries are an extremely common A&E presentation, especially in teenagers, young adults and the elderly. Possible consequences of head injury include concussion, intracerebral haemorrhage, contusion, axonal injuries and skull fracture. Patients presenting with head injuries should be assessed using the ATLS (advanced trauma life support) guidelines. CT brain will identify most injuries. The guidelines as to when a CT head is indicated is shown in the table below.

CT head to be performed within 1 hour if any of the following risk factors are present: CT head to be performed within 8 hours if the patient has experienced some loss of consciousness or amnesia since the head injury and any of the:
GCS <13 on initial assessment or <15 2h post injury Over 65 years old
Suspected opened or depressed skull fracture History of bleeding or clotting disorders
Any sign of basal skull fracture Those on anticoagulation therapy
Post-traumatic seizure More than 30 minutes of retrograde amnesia
Focal neurological deficit Dangerous mechanism of injury
More than 1 episode of vomiting

Concussion is the most common injury seen in head trauma, however these microscopic changes cannot be seen on CT. The diagnosis is therefore clinical and symptoms include headache, dizziness and confusion.

Subdural haematomas usually occur in motor-vehicle accidents or falls. They are more common in those with cerebral atrophy or coagulopathies. Patients may develop confusion or focal neurological deficits (Figure 8).

Extradural haematomas usually occur after direct force to the skull and can be associated with fractures of the temporal bone. Patients may experience a lucid interval before a subsequent deterioration in GCS (Figure 9).

MRCP Part 2 - Classical subdural haematoma: crescent-shaped subdural fluid collection which crosses the suture line

Image Source: Wikimedia Commons (2012). Subduralandherniation, Licensed under a creative commons licence. Available for free at: https://en.wikipedia.org/wiki/Subdural_hematoma#/media/File:Subduralandherniation.PNG (Accessed: 16 January 2024)

MRCP Part 2 - Classical extradural haematoma: lentiform collection which does not cross the suture lines

Image Source: Wikimedia Commons (2012). Traumatic acute epidual hematoma, Licensed under a creative commons licence. Available for free at: https://en.wikipedia.org/wiki/Epidural_hematoma#/media/File:Traumatic_acute_epidual_hematoma.jpg (Accessed: 16 January 2024)

Notable differentials

There are many conditions that can present with headache. Below are a few differentials to consider.

Condition Presentation and key information
Sinusitis Nasal congestion and sinus tenderness.
Temporomandibular joint (TMJ) dysfunction TMJ pain, TMJ click and limited mandibular movement.
Dental caries Pain on consumption of sweet, hot or cold food or drink. Caries may be visible.
Otitis media Ear pain. A bulging tympanic membrane may be present on otoscopy.
Acute angle-closure glaucoma Eye pain, blurred vision, redness of the sclera and vomiting.
Hypertensive encephalopathy Headache, nausea, change in mental status or visual changes in the context of a raised blood pressure. There may be evidence of end-organ damage on examination.
Pre-eclampsia Usually presents after 20 weeks gestation. Patients will have a raised BP and proteinuria. The presence of a headache is suggestive of severe disease. If not treated the patient can develop eclampsia.
Carbon monoxide poisoning Morning headaches, dizziness, ataxia and nausea. Oxygen saturations are usually normal but ABG will show raised carboxyhaemoglobin levels.
Malaria Malaria and other vector-borne infections such as Dengue fever, Chikungunya and Zika virus can present with headache.
Stroke Very rarely strokes can present with headache.

References

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