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CHAP TER3 Thehead
Investigation
A CT scan should be per formed as soon as possible after the bleed.
Delay in performing the scan reduces its diagnostic rate as the blood
lyses. Anormal C T scan does not r ule out a SAH. LP and CSF spectrophotometr y 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 hour s from the onset
of headache.
Once SAH has been diagnosed, CT angiography or cerebral catheter angiography is performed to determine the cause (Figure3.9).
Often CT angiography is per formed as the rst- linetest.
Management
• Resuscitation, IV uids, 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 ableed.
• Aneur ysms 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, nely localized radiation (stereotactic radiosurgery), which
leads to gradual obliteration over a 2- year period.
• If no structural cause is found on detailed angiogr aphy, the patient
can be reassured that they are not at increased risk of further bleeds.
Figure3.9 Angiogram showing berry aneurysm.
INTRACRANIAL BLEEDING (NON-TRAUMATIC)
The prognosis for recovery from a SAH is closely associated with the
GCS. A lower GCS will likely result in a worse outcome.
ComplicationsofSAH
• 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 heav y blood load.
In patients who develop vasospasm, hypertensive therapy is often
instituted when the aneur ysm is secured. This involves transfer to
level 3 care and an inotrope infusion. Direct angioplasty by intraarterial nimodipine can also betried.
• Hydrocephalus occur s in 25% of patients. This is often
communicating and can usually be managed with LPs or an external
ventr icular drain. Ashunt may be required.
• Seizures have been repor ted in 5– 10% of SAH patients.
• Electrolyte problems— this is usually low sodium and of ten 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 precipit ate vasospasm.
• ECG/ cardiac rhythm changes occur in >50% of SAH patients.
• Pulmonary oedema and pneumonia are common.
eSpontaneous intracerebral haemorrhage
ICH, a form of stroke, is most commonly due to hyper tension. 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 decit.
Investigation/ management
• Resuscitation, IV uids, 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 ssure (possible aneurysmal cause)
in younger non- hyper tensive 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 supercial.
• Stroke rehabilitation. This will be necessary in the majority of
patients.
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CHAP TER3 Thehead
eHydrocephalus and raised
intracranial pressure
eHydrocephalus
• Communicating:there is free ow of CSF from the ventricular system
to the subarachnoidspace.
• 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 thisgroup.
Clinical features
• Headache
• Vomiting
• Visual disturbance/loss of upgaze
• Deterioration in consciousness.
Investigations
A CT scan will t ypically show ventricular dilatation. The four th ventricle
is usually dilated in communicating hydrocephalus, but may be small in
non- communicating hydrocephalus. AMRI scan might be necessar y, particularly if a third ventriculostomy is being considered, to visualize the
basal cisterns.
Management
• 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 oor 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 per formed if there is
infection or bloodstained CSF preventing shunt insertion, or in an
emer genc y when there is insucient time to insert ashunt.
eRaised intracranial pressure (intracranial
hypertension)
Causes include:
• Ma sses (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.
SHUNTS AND SHUNT COMPLICATIONS
eShunts and shunt complications
These are devices used in the management of hydrocephalus. T hey 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 aected. Total obstruction can result in r apid onset of
symptoms and deterior ation in consciousness. Shunt s consistof:
• Aventricular catheter.
• Asubcutaneous reservoir— for samplingCSF.
• Avalve— this may have an incorporated reservoir, depending upon
thetype.
• Adistal 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
ventr icular wall can become sti 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 it s usual
location.
• Shunt tap:a needle is inserted into the subcut aneous reservoir
under aseptic technique. This can exclude infection, reduce ICP by
removing CSF, and also assess ventricular catheter patency.
eShunt 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). Ablocked
shunt usually presents with similar symptoms to the patient’s initial presentation, but the symptoms of ten progress more rapidly.
CT scan usually conrms the diagnosis but if there is doubt , symptom-
atic patient s 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
usuallyfail.
eShunt infection
Shunt infections usually develop within a few week s of the last shunt
operation and are due to contamination from skin bacter ia. 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
ow ushes the bacteria away from the ventricles. Antibiotics alone are
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CHAP TER3 Thehead
usually insucient to clear a shunt infection. Removal of the shunt and
external ventr icular 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.
eShunt 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 cor tical 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 uid intake. Caeine can also be helpful. The shunt can be revised if
the symptoms persist.
eIntracranial thrombosis
eVenous sinus thrombosis
Venous sinus thrombosis can aect any age and either sex, but most
commonly aects 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.
Investigations
CT or MRI scans might show brain swelling. The ‘delta’ sign is a triangular
lling defect in the sinus on a contrast CT scan. An occluded sinus is
usually visible on MRI scans. Infarc tion or haemorrhage due to venous
hyper tension might also be visible.
Management
• Anticoagulation.
• Thrombolytic therapy may be given if the patient is deteriorating.
• CSF diversion:may be necessary later if intracranial hypertension
results.
eCavernous 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 parana sal
sinus infection.
Propagation of an infected thrombus to the cavernous sinus occurs
against venous ow, because of the absence of valves in the facial,
CEREBRAL TUMOURS
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 alsooccur.
Clinical features
• Systemic upset:swinging pyrexia/ tachycardia/ rigors/ sweats.
• Facial or periorbitalpain.
• Venous obstruction:eyelid oedema/ dilated facialveins.
• ‘Pulsating exophthalmos’:a transmitted carotid pulse with periorbital
oedema.
• Blindness with papilloedema and retinal haemorrhages.
• Ophthalmoplegia:classically CN VI rst followed by CNs III andIV.
• 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.
Investigations
• CT or MRI scans:usually show br ain swelling and possible local
infection. An occluded sinus might be visible on MRIscans.
• Bloods including inammatory markers and coagulation studies.
• Cerebral angiogram, with venous phase (if diagnosis uncertain).
• Investigations into the cause of the infection.
Management
• Antibiotics and drainage of any collection ofpus.
• Anticoagulation.
• Thrombolytic therapy might be considered if the patient is
deteriorating.
cCerebral tumours
There are a large number of dierent brain tumour s and cysts, both
benign and malignant. Commonly they present with one of three syndromes (or a combination ofthem):
• RaisedICP
• Progressive neurological decit
• Epilepticts.
Investigations
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
rst- line investigation. Malignant tumours are seen as irregular enhancing lesions that might be cystic or solid, with mass eect and surrounding
oedema. The three commonest tumoursare:
• 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 terr itory; if suspicious, a CT chest/ abdomen/
pelvis can be performed to search for a primary source.
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CHAP TER3 Thehead
• Gliomas, which are usually large irregular lesions with indistinct
margins.
• Meningiomas, which have a dural at tachment and homogeneous
contrast enhancement.
Management
• Steroids to reduce vasogenic oedema— t ypically dexametha sone
4 mg four timesdaily. This is usually given with a proton pump
inhibitor for gastric protection.
• Anticonvulsants should be given if the patient has had ts. 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 per for med or a palliative
course of management without surgery.
In high- gr ade malignant tumours, patients will proceed to adjuvant
therapy with radiotherapy with or without chemotherapy. There are
advances in this eld based on molecular proling of tumours.
Emergency treatment
Rarely, if the patient is deterior ating rapidly, IV mannitol and a ma ssive
dose of dexamethasone should be given pending neurosurgical transfer
and emergency surgery.
eExtracranial causes ofheadache
eTemporal arteritis
Temporal arteritis (giant cell arteritis) is a vasculitic disease predominantly aecting patients over 60years 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, andfever.
Of great importance is the risk of sudden ir reversible loss of sight
which may occur within weeks of the onset of symptoms. Often the presenting feature is of a visual eld 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 aects medium and large sized ar teries.
Branches of the carotid arteries are the commonest sites of involvement,
but the vertebr al, meningeal, and intr acerebral vessels can be involved
leading to hemiplegia or epilepsy.
EXTRACRANIAL CAUSES OF HEADACHE
Investigations
• ES R is usually markedly raised in excess of 90mm/ hour in these
patients.
• Temporal ar tery biopsy will help to conrm the diagnosis. However,
the disease gener ally shows ‘sk ip lesions’ and therefore a negative
biopsy does not exclude a diagnosis.
Management
The aims of management are to reduce the pain and prevent complications, particular ly 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– 3years with a gradually
reducingdose.
cPolymyalgia rheumatica
Polymyalgia rheumatica (PMR) is a condition of middle- aged/ elderly
patients which is associated with temporal/ giant cell arteritis. It is
characterizedby
• Systemic upset— weight loss, fever, fatigue.
• Severe arthralgia with stiness— usually bilateral and symmetrical.
• ElevatedESR.
• Arapid response to small doses of cor ticosteroids.
Around 50% of patients with temporal arteritis have symptoms of PMR,
whereas 15– 50% of patients with PMR have giant cell arteritis.
Glaucoma
(See E Chapter 10, pp. 303–5.) Patients may complain of pain in and
around the eyes. It is impor tant to consider ophthalmic conditions, especially glaucoma.
cFrontal sinusitis
This is potentially serious due to the r isk of intracranial infection. The
front al 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 pubert y. 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 aver age
sinus volume is approximately 6 – 8mL.
Each sinus is lined with ciliated mucus- secreting epithelium. Mucus
drains into the middle meatus of the nose via the frontonasal ducts (or
front al 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 fr actures. It is
around the drainage of the front al sinus that classication, 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).
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CHAP TER3 Thehead
cEthmoid 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 offrontal/ ethmoid sinusitis
• Headache/ facialpain.
• Sensation of dull, constant pressure over the aectedsinus.
• Symptoms are usually localized over the involved sinus and are of ten
made worse on bending, straining, or lyingdown.
• Nasal discharge.
• Halitosis.
• Post- nasaldr ip.
• Pott’s puy tumour is a rare clinical entit y char acterized by
subperiosteal abscess associated with osteomyelitis. It is usually seen
as a complication of frontal sinusitis or trauma predominantly in the
adolescent agegroup.
Management ofsinusitis
Antibiotics and in some cases, sinus washout with opening of the middle meatus, using functional endoscopic sinus surger y. Ephedrine nasal
drops and menthol inhalations may help reduce congestion and improve
sinus drainage.
bDrug/ medication- induced headache
Many dr ugs can cause headaches among their side eects. Caeine
can result in severe pain sometimes on waking. Migraine suerers are
particularly vulnerable to a vicious c ycle of pain requiring increasing
medication, which then trig gers more pain. Medication should be slowly
withdrawn. In some cases prednisone may help control pain during this
period.
bIce- 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 cerebr al ar teries, or as a result of referred pain from the roof of
the mouth to the head. Treatment is preventative measures (eat slowly).
bPrimary sexual headache (coital cephalalgia)
In this condition, the pattern of headaches can be variable. Some appear
suddenly and stop abruptly; other s occur on a regular basis for a long
period of time. Attacks may be mild or severe. The dierential 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)
mayhelp.
Remember that carbon monoxide poisoning can also present with a
headache.
PRIMARY HEADACHES
bPrimary headaches
These are not emergency conditions but are included as they are within the
dierential diagnosis of headache.
bMigraine
Migraine is a severe headache that may present as a facial pain aecting
the cheek, orbit, or forehead. However, classical migraine with preceding visual distur bances and an aura rarely aects theface.
• ‘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 aect 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 a s starting with an impending sense of
ill health and a visual aura (e.g. ashing 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 andsleep.
Associations have been made with such trigger factors a s stress, diet
(chocolate, cheese, red wine), hormonal state (pre- menstr ual, 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.
Management
Recognizing and removing precipitating causes, and simple analgesics
in the rst instance. Antiemetics may also be used to reduce nausea. If
attacks are frequent and aect routine daily ac tivities 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.
bCluster headaches
Attacks generally occur in clusters, usually at night for 1– 3 weeks, every
12– 18 months. More common in men bet ween 20 and 40years 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 rhinor rhoea, unilateral nasal obstr uction, and the eye
may be red (conjunctival injection) with lacrimation.
Cluster headaches often respond to ergotamine. Other prescribed
drugs include verapamil, topiramate, and lithium.
bTension headaches
Tension headaches are described as a feeling of pressure, or a ‘bandlike’ tightness that varies in intensity, frequency, and duration. It is often
felt bilaterally over the forehead or temples but may aect the vertex,
occiput, or eyes. Commonest in middle- aged women with a ssociated
stress or depression, it may be chronic or episodic and is only occasionally helped with simple analgesics (NSAIDs).
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