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The head 

The head
The head

Mike Perry

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Common presentations

  • Blackouts/fits (seizures)/faints

  • Headaches (bilateral/generalized)

  • Headaches (unilateral/focal)

  • Trauma

  • Loss of smell (see The head Chapter 7)

  • Vertigo/loss of balance (see also The head Chapter 6)

  • Visual disturbance.

Common problems and their causes

Blackouts/fits (seizures)/faints

Headaches (bilateral/generalized)

Headaches (unilateral)


Loss of smell

(See The head Chapter 7.)

Vertigo/loss of balance

(See also The head Chapter 6.)

Useful questions and what to look for

Blackouts/fits (seizures)/faints

Headaches (all types)


Loss of smell

(See The head Chapter 7.)

Vertigo/loss of balance

(See also The head Chapter 6.)

Examination of the head

This is tailored according to the suspected pathology (injuries, infections, neurological). Various elements make up a comprehensive examination. Neurological examination cannot be considered in total isolation from the rest of the body. The following should all be considered.

Conscious level: the Glasgow Coma Scale

The GCS has three components (Table 3.1). A fully alert and orientated person has a GCS score of 15. A dead body has a GCS score of 3 (not zero).

Table 3.1 Components of the Glasgow Coma Scale (corresponding score in brackets)

Eye opening (EO)

EO spontaneously


EO to speech


EO to pain*


EO none


* Do not test with supraorbital pressure as patient will instinctively close their eyes.

Verbal response





Inappropriate words


Incomprehensible sounds




Best motor response

Obeys commands


Localizes pain


Flexion to pain


Abnormal (spastic) flexion*


Extension to pain




Adapted from The Lancet, Volume 304, Issue 7872, Graham Teasdale and Bryan Jennett, Assessment of coma and impaired consciousness: a practical scale, pp. 81–84, Copyright (1974), with permission from Elsevier.

Cranial nerve examination

This should be undertaken routinely. With practice, a ‘quick cranial nerve survey’ can be undertaken in just a few minutes (see Table 3.2).

Table 3.2 Cranial nerve functions and their examination









Various smell bottles, e.g. coffee, lemon (test each nostril separately)

Loss of small (anosmia)




Visual acuity, visual fields, pupillary responses, fundoscopy, colour vision

Blind eye, visual field defect or loss of acuity



Eye movements

Eye movement in all directions, pupillary responses

Ptosis, eye deviated down and outwards, unreactive dilated pupil



Eye movements

Eye movement down when looking medially

Inability to look down when looking medially



Facial sensation

Muscles of mastication

Sensation in 3 trigeminal divisions, corneal reflex, jaw movement

Loss of facial sensation, loss of corneal reflex

Jaw weak & deviates to side of lesion on opening, wasting of mastication muscles (chronic)



Eye movements

Eye movement laterally

Inability to look laterally



Facial movements

Taste to anterior tongue

Facial movements

Sweet, bitter, salt taste substances

  • Loss of facial movement

  • UMN: forehead spared

  • LMN: forehead affected

  • Loss of taste



  • Hearing

  • Equilibrium

Hearing, Weber’s & Rinne’s tests, balance & equilibrium


Nystagmus, loss of equilibrium



  • Pharyngeal & posterior tongue sensation & taste

  • Motor to upper pharynx

Pharyngeal sensation, gag reflex

  • Loss of gag reflex & pharyngeal sensation

  • Deviation of the uvula.



  • Visceral parasympathetic supply (extensive)

  • Larynx & pharynx motor function

  • Pharyngeal movement, gag reflex

  • Laryngoscopy

  • Loss of gag reflex & pharyngeal movement

  • Hoarse voice, vocal cord paralysis



Trapezius & sternomastoid motor function

Trapezius & sternomastoid power

Weakness of trapezius & sternomastoid



Tongue movements

Tongue movements

Tongue deviates to side of lesion

Peripheral neurological examination

This should also be undertaken routinely as part of the evaluation of the central nervous system (CNS). Deficits in the limb may also occur with spinal cord and peripheral nerve injuries (see also The head Chapter 4).

  • Limb function:

    • Appearance (deformity, wasting, abnormal movement, fasciculations)

    • Muscle tone

    • Power in each muscle group

    • Limb reflexes

    • Sensation in each dermatome (touch, pain, vibration, temperature, proprioception).

  • Coordination:

    • Romberg’s test for equilibrium

    • Gait

    • Finger-nose/heel shin test

    • Cerebellar signs (dysdiadochokinesia).

Higher functions

  • Language ability: expressive, receptive, and nominal dysphasia

  • Reading ability: dyslexia

  • Writing ability: dysgraphia

  • Calculation ability: dyscalculia

  • Object recognition: agnosia

  • Ability to perform specific tasks: dressing, geographical (follow route), and constructional (copy drawing) apraxia.

  • Memory test: immediate, short-term, long-term, verbal and visual memory (cannot be tested if confused or dysphasic).

  • Reasoning and problem-solving ability.

  • Mental state: degree of anxiety, mood, emotional behaviour, inhibition, speed of thought and response.

External examination of the head

Be methodical. Your examination will be guided by the suspected problem (trauma, sinusitis, headache, subarachnoid haemorrhage (SAH)):

  • Inspection. Standing at a distance from the patient, take a general look at the head and neck. Note any asymmetry, lumps, trauma, scars, discolouration, and obvious neurological deficit.

  • Function. Check eye movements, vision, and the cranial nerves.

  • Palpation of the head. Depending on the presenting complaint, a thorough palpation of any visual findings is performed:

    • Scalp

    • Forehead. Percussion over the frontal sinus may elicit tenderness if there is sinusitis

    • Supraorbital ridges

    • Nasal bridge

    • Occiput

    • Neck.

Feel for tenderness, fluctuation, steps in bony continuity, and enlarged lymph nodes or swellings in the neck. If there is an obvious exposed skull fracture do not manipulate it. Cover with a sterile dressing

  • Auscultation. Can be considered for vascularized lumps (e.g. haemangioma, arteriovenous malformation (AVM)) or following trauma (surgical emphysema/carotid bruit). A carotid cavernous fistula can cause an orbital bruit along with proptosis, chemosis, ophthalmoplegia and loss of vision

  • Don’t forget to check for papilloedema.

Some useful signs

Facial nerve palsy

Following a head injury this can indicate a fractured base of skull. Often with associated hearing loss.

Intercanthal distance

If greater than 30–32 mm (female) or 32–34 mm (male) the patient may have detached canthi secondary to an underlying NOE fracture. Check for CSF leakage


Loss of smell can occur due to tearing or infiltration of the olfactory nerves (anterior cranial fossa fracture or tumour). It is common after head injury as the olfactory nerves are vulnerable to injury as they run across the skull base anteriorly.

Racoon (panda) eyes

Bilateral, well-defined ‘black eyes’—fractured base of skull (anterior cranial fossa), Le Fort II/III, or NOE fracture.

Third nerve palsy

Dilated pupil, the eye looks down and out, and there is ptosis. In severe head injuries this represents third nerve compression from an expanding intracranial lesion. The patient may have a reduced GCS.

Superior orbital fissure (SOF) syndrome

Ophthalmoplegia, fixed dilated pupil and ipsilateral forehead numbness—fracture extending into the SOF, or possible carotid aneurysm. This is usually part of a significant injury.

Orbital apex syndrome

As in the SOF syndrome but here the patient also has reduced visual acuity.


Blood visualized behind the ear drum. Indicative of a fracture of the middle cranial fossa.

Battle’s sign

Bruising around the mastoid region—fractured base of skull (Figure 3.1).

Figure 3.1 Battle’s sign.

Figure 3.1 Battle’s sign.

Reproduced with permission from Johnson, C., Anderson S. R., Dallimore J., et al., Oxford Handbook of Expedition and Wilderness Medicine, Second Edition, Plate 22, Copyright © 2015 with permission from Oxford University Press.

CSF rhinorrhoea/otorrhoea

‘Tramlining’—fractured base of skull (Figures 3.2 and 3.3).

Bleeding from the ear

May indicate a fractured base of skull or mandibular condyle.

Useful investigations

Laboratory tests

  • A white cell count (WCC) should be taken in all suspected infections and patients presenting with severe headaches (for underlying infections).

  • C-reactive protein (CRP) or erythrocyte sedimentation rate (ESR) are usually very high in temporal arteritis and should prompt administration of steroids and urgent referral.

  • Lumbar puncture (LP) may be required for CSF analysis.

  • Blood cultures in suspected meningitis/encephalitis.

CT/MRI scanning

These are now the investigation of choice in the assessment of most head-related problems, especially trauma and suspected space-occupying lesions. CT scanning is the mainstay of imaging in head trauma. Often the cervical spine is imaged simultaneously as there is a 5% risk of cervical spine fracture with a serious head injury.

Fresh blood can be seen on CT and therefore it is often a preliminary investigation in the assessment of suspected SAH.

CT angiography may be considered in carotid dissection or penetrating injury and CT venography for suspected cerebral venous thrombosis.

Head trauma: introduction

Head injuries are a common reason for attendance at the emergency department, particularly at night and weekends. A wide spectrum of severity is seen and it is important not to overlook the patient with a potentially serious intracranial injury. However, there are also other causes of an altered conscious level, in addition to head injuries. Alcohol excess, drugs, hypoxia, hypotension, hypoglycaemia, and other metabolic disturbances should always be considered. A systematic approach to trauma patients should be followed with airway, breathing, and circulation remaining the priority, even in patients with an apparently isolated head injury.


‘Primary’ brain injury occurs at the time of the trauma. As clinicians there is nothing we can do about this. Prevention is the only way to reduce this. ‘Secondary’ brain injury occurs after the initial event and is due to complications such as hypoxia, hypercarbia, hypotension, raised ICP (haematomas or cerebral oedema), cerebral herniation, or infection. One way or another, these all result in either hypoxia or inadequate cerebral perfusion.

The aim of head injury management is to prevent secondary brain injury by regular observation and rapid correction if any deterioration occurs. This helps promote a physiological milieu that encourages natural recovery from the primary injury.

Primary brain injury

Primary brain injury can take the form of:

Cortical lacerations (burst lobe)

This also usually results in an acute subdural haematoma together with a cerebral haematoma and surrounding contusions. The affected brain usually swells markedly. A craniotomy is often necessary for evacuation of the subdural haematoma and debridement of the damaged brain. Prognosis is usually poor due to the extent of the primary brain damage.

Cerebral contusions

This is discussed under ‘Intracranial haematomas’ in ‘Classification and common types of head (brain) injuries’ topic later in this chapter, and occurs when the brain strikes the inner table of the skull.

Diffuse axonal injury

This consists of widespread disruption and shearing of axon sheaths following a high-energy impact. It is particularly associated with a rotational or deceleration element to the force. Concussion is a transient impairment of consciousness following a minor or moderate head injury is probably a mild form of diffuse axonal injury. The CT scan in diffuse axonal injuries can be normal, but more often shows a tight, swollen brain, with or without petechial haemorrhages. The degree of brain swelling usually increases over the first 48 hours post injury. The prognosis for diffuse axonal injury is poor and surgical options are limited.

Head injuries: pathophysiology

The brain is the most sensitive organ in the body to hypoxia and ischaemia. Therefore it is essential to maintain an adequate supply of well-oxygenated blood to the injured brain.


This maintains a constant supply of blood to the brain between a mean arterial pressure of 50 and 160 mmHg. However, this mechanism can be impaired following head injury. The cerebral perfusion pressure (CPP) is the force driving blood through the brain and is normally over 70 mmHg. It is related to the mean arterial pressure (MAP) and intracranial pressure (ICP) by:


The effects of intracranial swelling and bleeding

Any developing intracranial mass lesion will initially be compensated for by displacement of venous blood and CSF, so the ICP will not rise. When this compensatory mechanism has been exhausted, the ICP will rise and the CPP will fall. The Cushing reflex then comes into play, increasing the systemic BP to maintain cerebral blood flow. The pulse rate falls due to a vagal reflex. When this compensatory reflex fails, progressive cerebral ischaemia will occur leading to cerebral infarction and brain death. A vicious circle becomes established with hypoxia, hypotension, and cell breakdown products, which worsen the cerebral oedema, contributing to further deterioration (Figure 3.4).

Figure 3.4 Pathophysiology of raised ICP.

Figure 3.4 Pathophysiology of raised ICP.

Brain herniation

Three main types of herniation are commonly seen when a mass lesion develops intracranially (Figure 3.5).

Figure 3.5 Brain herniation. (1) Subfalcine ‘midline’ herniation. (2) Tentorial herniation. (3) Tonsillar herniation.

Figure 3.5 Brain herniation. (1) Subfalcine ‘midline’ herniation. (2) Tentorial herniation. (3) Tonsillar herniation.

Reproduced with permission from Smith J., Greaves I. and Porter K., Oxford Desk Reference: Major Trauma, Figure 8.11, p. 132, Copyright © 2010 with permission from Oxford University Press.

Subfalcine herniation

One hemisphere is displaced beneath the falx, which is seen as midline shift on a CT scan. This can obstruct the foramen of Monro anteriorly, causing unilateral ventricular dilatation. It can also compress the posterior cerebral artery against the falx posteriorly, causing a posterior cerebral infarction.

Transtentorial herniation

The uncus of the medial temporal lobe herniates through the tentorial notch. This compresses the oculomotor nerve (dilated pupil), and the midbrain.

Tonsillar herniation

The cerebellar tonsils herniate through the foremen magnum causing brainstem compression (coning).

Assessment of head injuries


The following are important and should be determined in all cases:

  • When it occurred.

  • Mechanism of injury—suddenly stopping (a deceleration injury) will transfer more energy to the brain than a stationary person struck by a moving object (an acceleration injury).

  • Loss of consciousness or seizure—any delayed loss of consciousness implies complications are developing. With children, was a cry heard immediately? This reduces the likelihood that there was loss of consciousness.

  • Progression of symptoms since injury.

  • Alcohol or drug use.

  • PMH.

  • Medications, especially anticoagulants.

  • Preceding headache or other symptoms such as collapse leading to a fall.

  • Period of retrograde or antegrade post-traumatic amnesia.

  • Other injuries.


  • Airway, breathing, and circulation status.

  • Always consider cervical spine injury with airway assessment.

  • Glasgow Coma Scale.

  • Pupil responses: unequal but reactive pupils occur in 20% of normal individuals. A dilated unreactive pupil is usually on the side of a mass lesion (a true localizing sign). The usual sequence is initial pupillary constriction as CN III is irritated followed by dilatation as a palsy occurs.

  • Focal neurology: cranial nerve and limbs. A hemiparesis can be caused by a mass lesion pressing on the opposite motor cortex, or a mass on the same side compressing the opposite cerebral peduncle against the edge of the tentorium (Kernohan’s notch). Thus, a hemiparesis does not help in determining the side of a mass lesion and is considered a false localizing sign.

  • Local signs of injury:

    • CSF rhinorrhoea or otorrhoea, bleeding from the ear: an open (compound) skull base fracture.

    • Battle’s sign (bruising over the mastoid): a fractured petrous bone.

    • Panda eyes or periorbital haematoma (well-circumscribed periorbital bruising): an anterior fossa skull base fracture.

    • Scalp lacerations, abrasions, swelling.

  • Examination for other injuries: this should be repeated when the patient has been stabilized (notably neck/scalp/facial/ocular).


CT scanning is the mainstay of imaging in head trauma. Often the cervical spine is imaged simultaneously as there is a 5% risk of cervical spine fracture with a serious head injury. Today, skull X-rays have little role in current investigation of head injuries.

Classification and common types of head (brain) injuries

Head injuries are usually classified for management, epidemiological, and research purposes into minor, moderate, and severe, based upon the GCS score.

The headConcussion

This is a temporary disturbance in brain function following relatively minor head injuries. Macroscopically, the brain structure remains undamaged. Typically the patient is ‘knocked out’ for several minutes. Prolonged episodes of unconsciousness are rare. In any event, the patient rapidly wakes up and makes a full recovery. So long as there are no other complicating medical or social factors such patients can go home providing they can be carefully observed. They should avoid a second concussion/head injury (if due to sports). Documented advice should be provided, including risks of complications and when they might need to return. ‘Return to play’ protocols are now widely used in contact sports.

The headIntracranial haematomas

The risk of harbouring an intracranial haematoma is related to the patient’s level of consciousness and the presence of a skull fracture. One of several different types of haematoma might develop.

The headCerebral contusions and haematomas

In cerebral contusions, blood is interspersed between the neurons and glia, whereas with cerebral haematomas, the bleeding forms a cavity within the brain. However, cerebral contusions can enlarge and result in a haematoma (Figure 3.6).

Contusions often occur at the poles of the brain due to a contrecoup injury, i.e. the contusion is in an area of the brain opposite the site of impact. These can be associated with marked oedema and a greatly raised ICP. Contusions are usually treated conservatively, but a lobectomy (or evacuation of an intracerebral haematoma) can be performed if the ICP cannot be controlled.

The headExtradural haematomas

Extradural haematomas are usually associated with a skull fracture or suture diastasis. The commonest site is temporal, due to a tear of the middle meningeal artery, but they can also occur in the frontal and occipital regions. They are rare in young children, as the skull fractures are not sharp enough to damage the artery, and in the elderly, as the dura is usually adherent to the skull. They classically present with delayed deterioration due to the dura being only slowly stripped from the skull. However, only a minority of patients are completely asymptomatic during this ‘lucid interval’.

Extradural haematomas are biconvex (lens) shaped on CT scans and are mostly high density (Figure 3.7). Low-density areas within them are due to active bleeding.

The prognosis is very good if they are treated early enough. Very small extradural haematomas with minimal symptoms can often be left alone (although they should be discussed with the local neurosurgical unit).

The headAcute subdural haematomas

Acute subdural haematomas may occur due to tearing of bridging veins between the brain and skull. In such cases the prognosis is good with prompt treatment. Alternatively a laceration of the brain surface (burst lobe) may occur. This has a worse prognosis. There need not be a skull fracture with subdural haematomas. They are more common than extradural haematomas and can extend over a wide area of the lateral cortical surface. They are crescent shaped on CT scans as the blood follows the surface of the brain (Figure 3.8).

Thin acute subdural haematomas can be treated conservatively with close observation, but significant ones need a craniotomy as the clotted blood is too viscous to drain via burr holes.

The headChronic subdural haematomas

Chronic subdural haematomas are thought to be due to minor venous bleeding following a minor head injury several weeks previously. The head injury is often so trivial that it cannot be remembered in 50% of cases. They usually occur in the elderly who have a degree of brain atrophy and stretching of the bridging cortical veins, but can also occur in babies due to non-accidental injuries. They are often associated with coagulopathies and alcohol excess.

Chronic subdural haematomas can cause a wide variety of symptoms, including headaches, reduced consciousness, and focal neurology. Therefore, consider this diagnosis in all elderly patients with intermittent confusion or transient ischaemic attack (TIA)-like symptoms after trauma. Chronic subdural haematomas can be treated by burr hole drainage as the blood is liquid. They have a good prognosis but might recur, especially with a persistent coagulopathy.

The headPenetrating head injury

A penetrating head injury is an open injury in which the dura mater has been breached. These are often caused by high-velocity projectiles but can also occur from objects such as knives, or bone fragments from an overlying skull fracture. Penetrating injuries are similar to closed head injuries (such as contusion or ICH) but have an increased incidence of infection. Haemorrhage may be harder to control. Initial management is the same as closed injuries although antibiotics should also be given.

Take care if exploring penetrating or open head wounds overlying a skull fracture, especially those in the midline. This can result in massive blood loss if a venous sinus has been torn.

Head injuries: initial management

The headScalp lacerations

Scalp lacerations should be thoroughly cleansed and closed urgently, in two layers if possible. The use of tissue glue may be acceptable for small lacerations. The possibility of foreign bodies or an underlying fracture should be considered and imaging may be necessary to confirm this. Also remember anti-tetanus prophylaxis. Scalp sutures can usually be removed after 7 days. Haemorrhage can be significant from these and can result in haemodynamic instability if neglected.

Potentially significant head injuries

Observations should be performed hourly initially, and half-hourly in higher-risk patients. Make sure the nursing staff know when to call for a medical review. Most patients can be discharged the following day if asymptomatic. Stable patients who need longer admission can have their observation frequency reduced to 2-hourly. Patients not admitted should receive written guidelines of when to return to hospital and should only be discharged with a responsible adult who can call for assistance if required.

Transferring patients

  • Fully resuscitate in all patients before transfer—this may include a laparotomy/pelvic fixation etc. to stop bleeding as per ATLS® protocol.

  • Intubate and ventilate comatose patients.

  • If patients are being transferred for observation only, avoid intubation and sedation if safe to do so (discuss with neurosurgeons). This allows their conscious level to be assessed.

  • Rapidly reverse anticoagulant medication to prevent further bleeding.

  • IV mannitol can be given to buy time by reducing ICP. Maximum dose is 1 g/kg—in a 70 kg adult, this is 350 mL of 20% mannitol.

  • Hypertonic saline is also increasingly used to reduce ICP, but always seek advice from ICU/neurosurgery before prescribing.

  • Transfer promptly with an experienced anaesthetist.

The headHead injuries in children

These can be difficult to assess. Many of the clinical features which would lead to concern in adults are often present, even following minor injuries (vomiting, drowsy, headaches, etc.). An infant can become haemodynamically unstable due to bleeding into a scalp haematoma. Consider the mechanism of injury, other injuries present, and whether the parents are capable of taking the child home for close observations. Interpretation of skull X-rays can be difficult as large fractures may be confused with wide sutures or vascular markings. If in doubt, refer or admit. Non-accidental injury is the second most common cause of ICH in a child. This should be considered if the history is inconsistent with the mechanism of injury, or if the child has had multiple attendances with injuries at different hospitals. Retinal haemorrhages, multiple old fractures, and cigarette burns are other signs.

Other issues

Post-concussion headache

This may have features of a tension-type headache but is often associated with dizziness and loss of concentration.


A significant head injury will often result in a restriction from driving for at least 6 months.

CSF leaks

CSF can leak from the nose (rhinorrhoea) or from the ear (otorrhoea). Clear CSF tends to mix with blood and presents as a heavily blood-stained, watery discharge. This trickles down the side of the face, where peripherally the blood tends to clot while the non-clotted blood in the centre is washed away by CSF. This creates two parallel lines referred to as ‘tramlining’. One bedside test for CSF is the ‘ring test’ (allow drops to fall on blotting paper: blood clots centrally, and the CSF diffuses outwards to form a target sign). Tell the patient not to blow their nose for 3 weeks. If they do, the increased pressure can force air intracranially through the tear, which then cannot escape. This is the neurosurgical equivalent of a tension pneumothorax and results in tension pneumocephalus. CSF should test positive for glucose. Beta-2 transferrin is a more specific test for CSF.

Post-traumatic seizures

Risk factors include intracerebral haematoma, open depressed fractures with dural laceration, and focal neurological signs.

The headHeadache

Headache is a symptom, not a diagnosis. It can arise from a number of different conditions involving the head, neck, and beyond. These include the periosteum of the skull, muscles, nerves, arteries and veins, subcutaneous tissues, eyes, ears, sinuses, and mucous membranes. There are a number of different classification systems for headaches. A useful one is from the International Headache Society. Treatment of a headache depends on the underlying cause. Take headaches seriously. Although most cases are benign and self-limiting, a few are due to serious pathology. The key is awareness of important causes and eliminating them from the differential diagnosis clinically and by investigation.

Classification of headaches

The International Classification of Headache Disorders (ICHD) is a useful guide to the causes of headache and is accepted by the World Health Organization. It contains diagnostic criteria. Several groups are listed.

Primary headaches

These are the most common types and include tension-type headache and migraine. They have typical features. Rarer types include cluster headache (severe pains that occur in bouts), and hemicrania continua (a continuous headache on one side of the head).

Secondary headaches

These are classified based on their aetiology and not symptoms. There are more than 200 types. Causes include:

  • Head or neck trauma

  • ICH:

    • SAH

  • Post craniotomy

  • Ischaemic stroke or TIA

  • Vascular malformations

  • Arteritis:

    • Temporal arteritis

  • Cerebral venous thrombosis:

    • Cavernous sinus or sagittal sinus thrombosis

  • Low or high pressures of the CSF pressure:

    • Hydrocephalus

    • Benign/idiopathic intracranial hypertension

    • Post-LP headache

  • Non-infectious inflammatory disease

  • Intracranial neoplasm

  • Substance ingestion or its withdrawal

  • Intracranial infections: meningitis, brain abscess, subdural empyema

  • Systemic infections

  • Dialysis

  • High BP

  • Fasting

  • Injury to facial structures including teeth, jaws, or TMJ.

This list is not complete but illustrates the diverse nature and potential seriousness of any patient you may encounter who has a headache. In the absence of identifiable pathology, management of headache is the treatment of its symptoms. Analgesia is often the initial treatment.

Assessing a patient with a headache

Ask about the following:


  • Severe, pulsatile headache is typical of common migraine.

  • Throbbing, sharp, headache is described in classic migraine.

  • Stabbing or burning pain is described in cluster headache.

  • Pressure, or a ‘band-like’ tightness that varies in intensity, frequency, and duration is consistent with tension headache.


Headaches that are worst on wakening are typical of raised ICP. It can also occur with caffeine withdrawal.


Headaches at night for 1–3 weeks are features of cluster headaches.

Exacerbating or precipitating factors

  • Straining, coughing, or sneezing can worsen headaches associated with raised ICP. Cough impulse headache is common in Chiari malformation.

  • Stress, diet (chocolate, cheese, red wine), hormonal state (pre-menstrual, oral contraceptive pill), emotions, and barometric changes are associated with migraine. Caffeine withdrawal can cause severe symptoms, which are quickly relieved by ingestion of caffeine.


Sudden-onset headache is often termed thunderclap headache. The most concerning cause of this is a SAH.

Preceding symptoms

  • Flu-like illness can precede temporal arteritis.

  • Impending sense of ill health is a feature of classic migraine.

  • Visual aura can precede migraine.

Other associated factors

Family history

Often seen in migraine.


Temporal arteritis is seen in patients over 60. Migraine is more often seen in puberty.


Females are more likely to have SAH, migraine, venous sinus thrombosis, and tension headache; men tend to get cluster headaches.

Associated medical problems

Depression and anxiety often relate to tension headache; smoking and hypertension are risk factors for SAH and stroke. Pregnancy predisposes to thrombosis or pre-eclampsia.

Headaches: associated symptoms

Reduced level of consciousness

This is concerning when it is associated with a headache. It may reflect raised ICP. Urgent investigation and treatment are required. SAH, ICH, tumour, or intracranial infection are all possible diagnoses.

Visual disturbance

  • Sudden irreversible loss of sight may occur within weeks of the onset of temporal arteritis. Often the presenting feature is of a visual field disturbance, which becomes progressively worse. Blindness is thought to occur as a result of ischaemic optic neuritis caused by arteritis of the ophthalmic arteries. Cavernous sinus thrombosis can also cause loss of vision as can pituitary apoplexy.

  • Visual aura, such as flashing lights, are a feature of classic migraine.

  • Loss of visual acuity or field constriction can be a feature of raised ICP and benign/idiopathic intracranial hypertension.

  • Ophthalmoplegia can occur in pituitary apoplexy, cavernous sinus thrombosis, or in a cavernous carotid fistula.

Nausea and vomiting

These are often present in migraine but are seen with raised ICP.

Autonomic symptoms

Such as rhinorrhoea, unilateral nasal obstruction, a red eye (conjunctival injection), and lacrimation. These are often seen in trigeminal autonomic cephalalgias.


This is often seen in classic migraine but if seen with thunderclap headache, SAH must be considered. It also occurs in meningitis.

Neck stiffness

This can be due to meningism in meningitis and SAH.

Focal neurological deficit

Such as dysphasia, hemiparesis, or sensory disturbance, in association with a headache is a concerning finding. A brain tumour, SAH, or a stroke could be the cause. However, some migraines can cause temporary hemiparesis or hemisensory loss.

Jaw claudication

Pain on chewing due to temporal arteritis of the facial artery (rare).


May be seen in brain tumours, SAH, or intracranial infection.

Systemic symptoms

Weight loss, arthralgia, and fever can occur in temporal arteritis.

The headIntracranial infections

The headMeningitis

Patients with meningitis can deteriorate extremely rapidly, so immediate attention is necessary. Consider this in any irritable child with a non-blanching petechial rash. Meningitis is inflammation of the linings of the brain and spinal cord (the meninges) with infection of the CSF. Most frequently, the pathogen is viral and may vary with age and social environment. Bacterial pathogens need urgent treatment.

Clinical features

  • Pyrexia

  • Tachycardia/tachypnoea/shock

  • Headache

  • Photophobia

  • Irritability

  • Seizures

  • Vomiting

  • Neck stiffness

  • Positive Kernig’s sign (a strong sign of meningeal irritation)—pain occurs with attempts at passive knee extension with the hips fully flexed

  • Maculopapular rash (meningococcal meningitis)

  • Deteriorating conscious level in late cases.


  • Resuscitation, IV fluids.

  • Antibiotics should be given as soon as the diagnosis is suspected and continued until the CSF WCC is normal. Discuss choice with microbiologist/neurologist.

  • Take throat swabs and blood for polymerase chain reaction (PCR).

  • Blood cultures.

  • CT scan to determine safety of LP and rule out other pathology.

  • LP for CSF analysis.

  • Contact tracing (local public health department)—for single cases treat close contacts only (‘kissing contacts’). Usual regimens: rifampicin 600 mg twice daily for 2 days, ciprofloxacin 500 mg single dose.

The headSubdural empyema

Most cases of subdural empyema are secondary to sinusitis or middle ear infection. Patients initially present with an illness similar to meningitis, but can develop a hemiparesis due to cortical venous thrombosis. Seizures are common.

Investigations and management

This should follow the same pathway as for meningitis, but a LP should be avoided due to the risk of coning. A CT scan will usually show a thin subdural collection, and pus can accumulate along the falx. The size of the collections is much less than with symptomatic chronic subdural haematomas.

Patients should be resuscitated and referred for prompt neurosurgical drainage of the pus, usually via a craniotomy. Efforts should be made to look for a source of infection and to treat it accordingly. Investigations such as an echocardiogram may be required.

The headBrain abscess

Sinusitis and middle ear infections are common causes of brain abscesses, following direct spread intracranially. Haematogenous spread of infection can also occur. Well-recognized causes include infective endocarditis and dental caries. However, in some cases the cause is never determined.

Clinical features

  • Headache

  • Vomiting

  • Focal neurology

  • Epileptic fits

  • Deteriorating conscious level in late cases

  • Pyrexia is often absent.


  • The WCC and CRP are often normal.

  • CT scans show a ring-enhancing lesion with surrounding oedema. In contrast to gliomas, abscesses are usually perfectly circular with a wall of uniform thickness. Abscesses may be multiple.

  • MRI—diffusion-weighted sequence can help differentiate from other pathology, such as tumour.

  • LP should not be performed due to the risk of coning.

The diagnosis is usually suspected on the basis of an enhancing circular lesion on a CT scan of a patient with an infection elsewhere.


Patients should be referred for prompt neurosurgical drainage. If their consciousness is deteriorating, patients should be fully resuscitated and consider administering steroids and mannitol prior to transfer.

The headEncephalitis

This is an acute inflammation of the brain and has both infective and non-infective causes. Encephalitis which is associated with meningitis is referred to as meningoencephalitis. Herpes simplex virus, poliovirus, and measles virus are common pathogens. Others rare types of encephalitis include Japanese encephalitis and equine encephalitis. Bacterial encephalitis may occur following spread of meningitis. Parasitic or protozoal infestations, such as toxoplasmosis, malaria, or amoebic infection, can also cause encephalitis. Cryptococcus neoformans causes fungal encephalitis in immunocompromised patients.

Clinical features

Whatever the cause, common symptoms include:

  • Headache

  • Fever

  • Confusion

  • Drowsiness, and fatigue

  • Seizures, tremors, hallucinations, and memory problems may indicate advanced disease.

Children or infants may present with non-specific symptoms such as irritability, drowsiness, and fever.

Always check for a stiff neck—this indicates meningitis or meningoencephalitis.


  • CT scan is initially undertaken to exclude brain swelling. If there is no swelling a LP can be undertaken.

  • CSF analysis usually shows increased amounts of protein and white blood cells with normal glucose. Specific diagnosis is made with detection of antibodies on PCR.

  • Serological tests may show high antibody titres.


  • Patients should be resuscitated and referred urgently. Supportive treatment (IV fluids/sedation/mechanical ventilation) may be required.

  • Antiviral agents (e.g. aciclovir for herpes simplex virus).

  • Corticosteroids may be used to reduce brain swelling but this is controversial in the presence of infection.

The headIntracranial bleeding (non-traumatic)

The headSubarachnoid haemorrhage

Aetiology of spontaneous SAH

  • 80% are from intracranial saccular (Berry) aneurysm. These often remain asymptomatic and are found in 2–3% of routine post-mortems.

  • 15% have no identifiable cause

  • 5% from other causes (e.g. AVM).

Up to 50% of aneurysmal SAH patients die within a month of the initial bleed. Untreated, the re-bleed rate over the first month approaches 50% and 80% of these patients die or become dependent. It is therefore vital not to delay the diagnosis, as patients are at risk of re-bleeding and death.

The risk of re-bleeding in AVMs is much less at around 6% in the first year and 3% for each subsequent year, so treatment can often be delayed.

Clinical features

  • ‘Thunderclap’ headache—a sudden, severe occipital headache radiating over the head and down the neck

  • Impaired conscious level

  • Neck stiffness

  • Photophobia

  • Nausea or vomiting

  • Seizure.

Unfortunately ‘thunderclap’ is a non-specific symptom and less than 25% of patients presenting with this symptom will actually have a SAH. The differential diagnosis is wide. All patients with a sudden-onset headache should therefore be investigated for SAH, even if the headache has eased within a few hours.


A CT scan should be performed as soon as possible after the bleed. Delay in performing the scan reduces its diagnostic rate as the blood lyses. A normal CT scan does not rule out a SAH. LP and CSF spectrophotometry for bilirubin is required in all suspected cases if the CT scan is normal, but if performed too soon, the CSF can be normal, as bilirubin has not yet been produced from the blood breakdown products. The LP should not therefore be performed within 12 hours from the onset of headache.

Once SAH has been diagnosed, CT angiography or cerebral catheter angiography is performed to determine the cause (Figure3.9).

Figure 3.9 Angiogram showing berry aneurysm.

Figure 3.9 Angiogram showing berry aneurysm.

Often CT angiography is performed as the first-line test.


  • Resuscitation, IV fluids, routine bloods including clotting studies.

  • Analgesics, antiemetics.

  • Oral nimodipine. This improves outcome by reducing the risk of ischaemic complications. It limits the normal surrounding vasoconstrictor response that occurs following a bleed.

  • Aneurysms are secured by either surgical clipping or endovascular embolization. In many centres, practice has moved towards endovascular coiling as the mainstay of aneurysm treatment.

  • AVMs can be excised, embolized, or treated with extremely high-dose, finely localized radiation (stereotactic radiosurgery), which leads to gradual obliteration over a 2-year period.

  • If no structural cause is found on detailed angiography, the patient can be reassured that they are not at increased risk of further bleeds.

The prognosis for recovery from a SAH is closely associated with the GCS. A lower GCS will likely result in a worse outcome.

Complications of SAH

  • Vasospasm—this results in stroke/death in 15% of patients with SAH. At day 7, up to 70% will have angiographic vasospasm, although this is only clinically manifest in 20–30%. The pathophysiology is poorly understood but the risk is increased with a heavy blood load. In patients who develop vasospasm, hypertensive therapy is often instituted when the aneurysm is secured. This involves transfer to level 3 care and an inotrope infusion. Direct angioplasty by intra-arterial nimodipine can also be tried.

  • Hydrocephalus occurs in 25% of patients. This is often communicating and can usually be managed with LPs or an external ventricular drain. A shunt may be required.

  • Seizures have been reported in 5–10% of SAH patients.

  • Electrolyte problems—this is usually low sodium and often due to ‘cerebral salt wasting’. It is treated with adding sodium orally or intravenously using 1.8% saline. Fluid restriction is dangerous as it may precipitate vasospasm.

  • ECG/cardiac rhythm changes occur in >50% of SAH patients.

  • Pulmonary oedema and pneumonia are common.

The headSpontaneous intracerebral haemorrhage

ICH, a form of stroke, is most commonly due to hypertension. Bleeding disorders, AVMs, aneurysms, tumours, and venous hypertension secondary to central venous thrombosis can also be responsible.

Clinical features

These include the following, but not all need to be present:

  • Headache

  • Loss of consciousness

  • Focal neurological deficit.


  • Resuscitation, IV fluids, clotting studies.

  • CT scan. This should be performed as soon as possible after the onset of symptoms, especially if the patient is unconscious or an aneurysmal SAH is a possibility.

  • An LP is unnecessary and potentially dangerous.

  • An angiogram should be considered, especially if the clot is close to the circle of Willis or Sylvian fissure (possible aneurysmal cause) in younger non-hypertensive patients (possible AVM), or if surgical evacuation is being considered.

  • Neurosurgeons may consider ICH evacuation if the patient is deteriorating due to raised ICP and the clot is superficial.

  • Stroke rehabilitation. This will be necessary in the majority of patients.

The headHydrocephalus and raised intracranial pressure

The headHydrocephalus

  • Communicating: there is free flow of CSF from the ventricular system to the subarachnoid space.

  • Non-communicating (or obstructive): there is an obstruction within the ventricular system so that the CSF cannot reach the subarachnoid space. It is not safe to perform a LP in this group.

Clinical features

  • Headache

  • Vomiting

  • Visual disturbance/loss of upgaze

  • Deterioration in consciousness.


A CT scan will typically show ventricular dilatation. The fourth ventricle is usually dilated in communicating hydrocephalus, but may be small in non-communicating hydrocephalus. A MRI scan might be necessary, particularly if a third ventriculostomy is being considered, to visualize the basal cisterns.


  • Shunts: divert CSF into the peritoneum, or less commonly the right atrium or pleura.

  • Third ventriculostomy: creates an internal bypass by forming a stoma between the floor of the third ventricle and the basal cisterns.

  • External ventricular drainage: the CSF drains via a manometer to an external collecting system. This is usually performed if there is infection or bloodstained CSF preventing shunt insertion, or in an emergency when there is insufficient time to insert a shunt.

The headRaised intracranial pressure (intracranial hypertension)

Causes include:

  • Masses (tumour, infarction with oedema, contusions, haematoma, or abscesses)

  • Generalized swelling (ischaemia, acute liver failure, hypertensive encephalopathy, hypercarbia, and Reye’s syndrome)

  • Increase in venous pressure (venous sinus thrombosis, heart failure, or mediastinal obstruction)

  • Obstructed CSF (aqueduct stenosis, Chiari malformation, meningeal disease)

  • Increased CSF production (choroid plexus tumour)

  • Craniosynostosis

  • Idiopathic

  • Management is directed at the cause. CSF diversion may be required.

The headShunts and shunt complications

These are devices used in the management of hydrocephalus. They divert CSF into the peritoneum (or less commonly the right atrium or pleura) and maintain the ICP at the correct level. If a shunt fails to function correctly the ICP is affected. Total obstruction can result in rapid onset of symptoms and deterioration in consciousness. Shunts consist of:

  • A ventricular catheter.

  • A subcutaneous reservoir—for sampling CSF.

  • A valve—this may have an incorporated reservoir, depending upon the type.

  • A distal catheter—most commonly to the peritoneum (ventriculoperitoneal (VP) shunt), but occasionally to the right atrium via the internal jugular vein (ventriculoatrial (VA) shunt) or pleura.

Shunt assessment

  • CT scan: to look at the ventricular size. It is most useful to compare the scan with a previous scan taken when the shunt was known to be functioning.

  • However, in patients who have had multiple-shunt revisions, the ventricular wall can become stiff and the ventricles may not dilate.

  • Shunt series: plain X-rays of the whole of the shunt to look for breakages, disconnections, or migration of the shunt from its usual location.

  • Shunt tap: a needle is inserted into the subcutaneous reservoir under aseptic technique. This can exclude infection, reduce ICP by removing CSF, and also assess ventricular catheter patency.

The headShunt obstruction

The commonest site of a blocked shunt is the ventricular catheter (due to choroid plexus), followed by the valve (due to CSF debris) and the distal catheter (due to omentum in VP shunts and clot in VA shunts). A blocked shunt usually presents with similar symptoms to the patient’s initial presentation, but the symptoms often progress more rapidly.

CT scan usually confirms the diagnosis but if there is doubt, symptomatic patients should be admitted for observation until their symptoms have settled. If symptoms persist, the obstructed component, or the whole shunt, will need to be replaced. Attempts to clear the obstruction usually fail.

The headShunt infection

Shunt infections usually develop within a few weeks of the last shunt operation and are due to contamination from skin bacteria. Patients can present with symptoms of a blocked shunt accompanied by a fever. They usually do not have meningism. An infected VA shunt will usually not block and so the infection may continue undetected for a long period.

The symptoms of an infected VA shunt usually consist of vague ill health and a low-grade temperature. Diagnosis is by a shunt tap, with CSF microscopy and culture. The CSF WCC might be normal, as CSF flow flushes the bacteria away from the ventricles. Antibiotics alone are usually insufficient to clear a shunt infection. Removal of the shunt and external ventricular drainage are often necessary, with a new shunt being inserted when the CSF is sterile.

Prophylactic antibiotics have not been shown to prevent shunt infections. New antibiotic impregnated or silver-lined shunt catheters are available.

The headShunt overdrainage

Occasionally a shunt will drain excessive CSF, so that the patient develops low-pressure headaches, which are worse when upright and are eased by lying down. If the ventricles are very large, the low pressure can cause them to collapse, tearing cortical bridging veins and causing subdural haematomas. These patients can have symptoms of raised ICP with a hemiparesis.

Low-pressure headaches are treated with reassurance and advising a high fluid intake. Caffeine can also be helpful. The shunt can be revised if the symptoms persist.

The headIntracranial thrombosis

The headVenous sinus thrombosis

Venous sinus thrombosis can affect any age and either sex, but most commonly affects young and middle-aged females. It can be caused by trauma with depressed fractures overlying the sinus, tumours invading the sinus, and post neurosurgery.

Clinical features

  • Headaches, especially in the morning

  • Visual disturbance

  • Papilloedema.


CT or MRI scans might show brain swelling. The ‘delta’ sign is a triangular filling defect in the sinus on a contrast CT scan. An occluded sinus is usually visible on MRI scans. Infarction or haemorrhage due to venous hypertension might also be visible.


  • Anticoagulation.

  • Thrombolytic therapy may be given if the patient is deteriorating.

  • CSF diversion: may be necessary later if intracranial hypertension results.

The headCavernous sinus thrombosis

Often fatal in the pre-antibiotic era, cavernous sinus thrombosis is essentially a septic thrombosis within the cavernous sinus. It usually arises from an infection in the face (hence the advice not to squeeze spots!), most commonly the periorbital region, but it can also arise from paranasal sinus infection.

Propagation of an infected thrombus to the cavernous sinus occurs against venous flow, because of the absence of valves in the facial, angular, ophthalmic, and pterygoid plexus of veins. Thrombosis might spread to other venous sinuses and the infection may spread to cause subdural empyema or meningitis. Infective endocarditis and thrombosis of the internal carotid artery can also occur.

Clinical features

  • Systemic upset: swinging pyrexia/tachycardia/rigors/sweats.

  • Facial or periorbital pain.

  • Venous obstruction: eyelid oedema/dilated facial veins.

  • ‘Pulsating exophthalmos’: a transmitted carotid pulse with periorbital oedema.

  • Blindness with papilloedema and retinal haemorrhages.

  • Ophthalmoplegia: classically CN VI first followed by CNs III and IV.

  • Obvious site of infection: usually unilateral initially; most commonly a periorbital cellulitis.

  • Central signs: developing evidence of meningeal irritation.

  • Bilateral signs develop with contralateral extension of thrombus.


  • CT or MRI scans: usually show brain swelling and possible local infection. An occluded sinus might be visible on MRI scans.

  • Bloods including inflammatory markers and coagulation studies.

  • Cerebral angiogram, with venous phase (if diagnosis uncertain).

  • Investigations into the cause of the infection.


  • Antibiotics and drainage of any collection of pus.

  • Anticoagulation.

  • Thrombolytic therapy might be considered if the patient is deteriorating.

The headCerebral tumours

There are a large number of different brain tumours and cysts, both benign and malignant. Commonly they present with one of three syndromes (or a combination of them):

  • Raised ICP

  • Progressive neurological deficit

  • Epileptic fits.


MRI scan is now the investigation of choice and will invariably be required before surgery, but a CT scan, without and with contrast, is usually the first-line investigation. Malignant tumours are seen as irregular enhancing lesions that might be cystic or solid, with mass effect and surrounding oedema. The three commonest tumours are:

  • Metastases, which can be small, round ‘cannon ball’ lesions, usually multiple, at the grey–white mater junction and most commonly in the middle cerebral artery territory; if suspicious, a CT chest/abdomen/pelvis can be performed to search for a primary source.

  • Gliomas, which are usually large irregular lesions with indistinct margins.

  • Meningiomas, which have a dural attachment and homogeneous contrast enhancement.


  • Steroids to reduce vasogenic oedema—typically dexamethasone 4 mg four times daily. This is usually given with a proton pump inhibitor for gastric protection.

  • Anticonvulsants should be given if the patient has had fits. Some neurosurgeons use prophylactic anticonvulsants.

  • Neurosurgical referral. Excision of the tumour is the preferred treatment, but might not be possible due to the site of the tumour, the extent or nature of the lesion, or the frailty of the patient, in which case a biopsy or debulking may be performed or a palliative course of management without surgery.

In high-grade malignant tumours, patients will proceed to adjuvant therapy with radiotherapy with or without chemotherapy. There are advances in this field based on molecular profiling of tumours.

Emergency treatment

Rarely, if the patient is deteriorating rapidly, IV mannitol and a massive dose of dexamethasone should be given pending neurosurgical transfer and emergency surgery.

The headExtracranial causes of headache

The headTemporal arteritis

Temporal arteritis (giant cell arteritis) is a vasculitic disease predominantly affecting patients over 60 years of age. It is an important diagnosis in the elderly patient who presents with severe headache because of the potential for blindness if left untreated.

Clinical features

Patients present with a headache that is either a generalized ‘tension’ type or severe and well localized over the temporal arteries, often with burning or tenderness of the scalp. Jaw claudication on chewing can be another feature, thought to be due to involvement of the facial artery. There may also be weight loss, arthralgia, and fever.

Of great importance is the risk of sudden irreversible loss of sight which may occur within weeks of the onset of symptoms. Often the presenting feature is of a visual field disturbance, which becomes progressively worse. Blindness is thought to occur as a result of ischaemic optic neuritis caused by arteritis of the ophthalmic arteries.

Temporal arteritis generally affects medium and large sized arteries. Branches of the carotid arteries are the commonest sites of involvement, but the vertebral, meningeal, and intracerebral vessels can be involved leading to hemiplegia or epilepsy.


  • ESR is usually markedly raised in excess of 90 mm/hour in these patients.

  • Temporal artery biopsy will help to confirm the diagnosis. However, the disease generally shows ‘skip lesions’ and therefore a negative biopsy does not exclude a diagnosis.


The aims of management are to reduce the pain and prevent complications, particularly blindness. High-dose steroids are given urgently. Dosage can be titrated against the ESR, and clinical response, but it may be necessary to continue treatment for 2–3 years with a gradually reducing dose.

The headPolymyalgia rheumatica

Polymyalgia rheumatica (PMR) is a condition of middle-aged/elderly patients which is associated with temporal/giant cell arteritis. It is characterized by

  • Systemic upset—weight loss, fever, fatigue.

  • Severe arthralgia with stiffness—usually bilateral and symmetrical.

  • Elevated ESR.

  • A rapid response to small doses of corticosteroids.

Around 50% of patients with temporal arteritis have symptoms of PMR, whereas 15–50% of patients with PMR have giant cell arteritis.


(See The head Chapter 10, pp. [link][link].) Patients may complain of pain in and around the eyes. It is important to consider ophthalmic conditions, especially glaucoma.

The headFrontal sinusitis

This is potentially serious due to the risk of intracranial infection. The frontal sinuses make up one of the four paranasal sinuses. They are formed by extension of the ethmoidal air cells, into which they drain. These sinuses are absent at birth, but become reasonably well developed by the age of 7, reaching their full size after puberty. In up to 4% of the population they can be absent. The right and left sinuses form a cavity within the frontal bone, which is highly variable in size and shape and rarely symmetrical. A midline septum separates the two. The average sinus volume is approximately 6–8 mL.

Each sinus is lined with ciliated mucus-secreting epithelium. Mucus drains into the middle meatus of the nose via the frontonasal ducts (or frontal sinus drainage pathways (FSDP)). The ducts pass through the ethmoid sinuses taking a variable pathway. (This is an important point to remember when managing apparently isolated NOE fractures. It is around the drainage of the frontal sinus that classification, management, and complications of these injuries are based.)

If free drainage of mucus from the frontal sinus is impaired, infection can occur, resulting in frontal sinusitis. Patients complain of frontal headache, which is tender to percussion. Untreated, the infection can spread intracranially or spread into the orbit (orbital cellulitis).

The headEthmoid sinusitis

This usually occurs with other sinus infections. Patients complain of deep-seated throbbing pain, deep to the bridge of the nose. The medial orbital walls are paper thin, so orbital cellulitis can rapidly develop.

Clinical presentation of frontal/ethmoid sinusitis

  • Headache/facial pain.

  • Sensation of dull, constant pressure over the affected sinus.

  • Symptoms are usually localized over the involved sinus and are often made worse on bending, straining, or lying down.

  • Nasal discharge.

  • Halitosis.

  • Post-nasal drip.

  • Pott’s puffy tumour is a rare clinical entity characterized by subperiosteal abscess associated with osteomyelitis. It is usually seen as a complication of frontal sinusitis or trauma predominantly in the adolescent age group.

Management of sinusitis

Antibiotics and in some cases, sinus washout with opening of the middle meatus, using functional endoscopic sinus surgery. Ephedrine nasal drops and menthol inhalations may help reduce congestion and improve sinus drainage.

The headDrug/medication-induced headache

Many drugs can cause headaches among their side effects. Caffeine can result in severe pain sometimes on waking. Migraine sufferers are particularly vulnerable to a vicious cycle of pain requiring increasing medication, which then triggers more pain. Medication should be slowly withdrawn. In some cases prednisone may help control pain during this period.

The headIce-cream headache

Some patients are prone to develop sudden, sharp head pain within a few seconds of eating or drinking anything cold, which stimulates the palate. The pain usually lasts less than a minute and resolves completely. It is believed to result from either rapid constriction and swelling of the anterior cerebral arteries, or as a result of referred pain from the roof of the mouth to the head. Treatment is preventative measures (eat slowly).

The headPrimary sexual headache (coital cephalalgia)

In this condition, the pattern of headaches can be variable. Some appear suddenly and stop abruptly; others occur on a regular basis for a long period of time. Attacks may be mild or severe. The differential diagnosis is SAH as this has been precipitated by coitus in patients. Management includes avoiding/reducing activities which precipitate symptoms. Propranolol, indometacin, and calcium-channel blockers (e.g. diltiazem) may help.

Remember that carbon monoxide poisoning can also present with a headache.

The headPrimary headaches

These are not emergency conditions but are included as they are within the differential diagnosis of headache.

The headMigraine

Migraine is a severe headache that may present as a facial pain affecting the cheek, orbit, or forehead. However, classical migraine with preceding visual disturbances and an aura rarely affects the face.

  • ‘Common’ migraine is ten times more frequent and is described as a severe pulsatile headache invariably associated with nausea. Migraine is episodic in nature and is thought to affect approximately 10% of the population. It is more common in females (3:1), usually begins around puberty and continues into middle age, and there may also be a family history.

  • Classic migraine is described as starting with an impending sense of ill health and a visual aura (e.g. flashing lights). The throbbing, severe, sharp unilateral headache is associated with anorexia, nausea and vomiting, photophobia. and withdrawal—the patient often wants to just go into a darkened room and sleep.

Associations have been made with such trigger factors as stress, diet (chocolate, cheese, red wine), hormonal state (pre-menstrual, oral contraceptive pill), emotions (anger, excitement), and barometric changes.

Some migraines can cause temporary hemiparesis (hemiplegic migraine) or hemisensory loss. This can result in diagnostic confusion.


Recognizing and removing precipitating causes, and simple analgesics in the first instance. Antiemetics may also be used to reduce nausea. If attacks are frequent and affect routine daily activities then prophylactic treatment can be considered with, e.g. oral pizotifen at night, or daily beta-blockers. In severe cases, patients may be prescribed sumatriptan to use in the prodrome state. Avoid narcotics.

The headCluster headaches

Attacks generally occur in clusters, usually at night for 1–3 weeks, every 12–18 months. More common in men between 20 and 40 years it may be precipitated by alcohol. Typically the patient is woken at night by a severe unilateral stabbing or burning pain which may be frontal temporal, around the eye or over the cheek. Nausea is not a common feature but there is frequently rhinorrhoea, unilateral nasal obstruction, and the eye may be red (conjunctival injection) with lacrimation.

Cluster headaches often respond to ergotamine. Other prescribed drugs include verapamil, topiramate, and lithium.

The headTension headaches

Tension headaches are described as a feeling of pressure, or a ‘band-like’ tightness that varies in intensity, frequency, and duration. It is often felt bilaterally over the forehead or temples but may affect the vertex, occiput, or eyes. Commonest in middle-aged women with associated stress or depression, it may be chronic or episodic and is only occasionally helped with simple analgesics (NSAIDs).

The headHemicrania continua

This is a persistent unilateral headache that is usually unremitting. The pain is usually moderately severe, unilateral, and continuous, without pain-free periods. There may also be lacrimation, nasal congestion, or ptosis. The cause of hemicrania continua is unknown and there is no definitive diagnostic test for it. However, it generally responds only to indomethacin, which must be continued long term.