Hospital Based Practice – Acute Severe Headache.

• Headache is the most common neurological symptoms.

o About 4.1% have chronic daily headaches.
• Patients get very worried about ones that persist.
• Cause of significant morbidity.

• History.
o Normal SOCRATES questions.
o Tempo of onset
o Signs of meningism
o Rhythm
o Time of day it comes one
o Affect of coughing/ position

• Causes.
Pattern Causes
Solitary acute episode Infection.
• Meningitis
• Encephalitis
• Abscess
Vascular events
• Intracranial haemorrhage (especially
subarachnoid)
• Venous sinus thrombosis
• Occasionally infarction due to arterial
dissection.
Trauma
First presentation of other types.
Progressive headache Raised intracranial pressure
(including benign intracranial hypertension)
Giant cell arteritis
Tumour
Hydrocephalus
Episodic headache/ facial pain Migraine
Cluster headache
Trigeminal neuralgia
Coital cephalgia
Chronic headache/ facial pain Tension headache/ analgesic rebound headache.
Postherpetic neuralgia
Post head injury
Paget’s disease of the skull
Other causes of facial pain Dental problems
Temporomandibular joint
Ears/ nose/ sinuses
Cervical spine
Eye
MI (rarely)
Examination
• Raised intracranial pressure.
o Worsened by.
 Coughing
 Sneezing
 Leaning down
o Worse in the morning
o Visual disturbances.
 Papilloedema
o Nausea & Vomiting
o Diplopia.
 False localizing CN VI palsy.
o Altered level of consciousness
o Bradycardia
o Hypertension.
 Mainly if acute or severe
o Decebrate posturing
o Death.
• Meningism
o Irritability.
o Neck stiffness
o Kernig’s sign.
 Hamstring spasm & pain on knee extension
o Brudzinski’s sign.
 Neck flexion causes leg flexion
o Signs of infective meningitis
 Delerium
 Fever
 Petechial rash.
o Signs of sub – arachnoid haemorrhage
 Retinal (subhyaloid) haemorrhage
 Arteriovenous malformation bruit
 CN III palsy
• Direct pressure from posterior communicating artery aneurysm.
• Signs of temporal arteritis.
o Temporal artery tenderness
o Loss of temporal artery pulsation.
 May be overlying erythema
o Optic atrophy
o Low – grade pyrexia.
Investigations.
• If history suggestive of temporal arteritis.
o ESR
o Temporal artery biopsy
• If history suggests some other diagnosis, treat as appropriate.
o Migraine
o Tension headache
o Coital cephalgia
o Cluster headache
o Temporomandibular joint pain.
• If diagnosis not clear, or suggests intracranial pathology.
o CT head scan.
 May show
• Blood
• Tumour
• Abscess
• Hydrocephalus
o If CT normal, perform lumbar puncture.
 CSF leucocytosis.
• Meningitis
 High CSF pressure.
• Benign intracranial hypertension
• Dural sinus thrombus.
 Xanthochromia
• Subarachnoid haemorrhage.
o If SAH suspected, do angiography, which may show.
 Berry aneurysm
 Arteriovenous malformation.

• FBC.
o Normocytic normochromic anaemia suggests chronic pathology.
 Temporal arteritis
 Tuberculous meningitis
o Leucocytosis seen in infection
• ESR.
o High in temporal arteritis
o Also raised in.
 Chronic infection
 Pregnancy
• Temporal artery biopsy.
o 100% specific.
o Due to patchy nature of inflammation, not very sensitive.
• CT or MRI.
o Will show blood, tumour, abscess and hydrocephalus.
o If tumour is suspected, use contrast enhancement to better define the extent.
 • Lumbar puncture.
o Never perform if raised ICP possible.
 Causes coning.
o CSF should be sent to lab for assessment for meningitis and SAH.
 Glucose
 Protien
 MC&S
 Cytology.
 Xanthrochromia

• Cerebral angiography.
o Perform if surgery is being considered for SAH.
o Identifies and locates berry aneurysms and arteriovenous malformations.
• Visual fields.
o Serial measure in patients with benign intracranial hypertension
o Monitors due to the risk of optic nerve infarction.
• Electroencephalography.
o Herpes simplex will give characteristic features

Tension headache
• Defined as headaches that occur.
o On 15 or more days a month
o Pain is.
 Bilateral pressing or tightening
 Non – pulsating
 Mild or moderate intensity
 Doesn’t worsen with physical activity.
o No more than one feature of.
 Mild nausea
 Photophobia
 Phonophobia
• Pain can last minutes – days.
• Main differential diagnosis is migraine.
o Many experts dispute that the extra features of photphobia, phonophobia and nausea
should be included in definition of tension headache.
• Other differentials include.
o New daily, persistant headache
o Medication overuse headache.
o Chronic migraine
o Hemicrania continua
• Neurologically normal

Incidence
• About 2 – 2.5% suffer tension headaches.
• About 2:1 Female to male ratio
• Symptoms start before age of 10 in 1.5% of patients.
• Prevelence decreases with age
• Family history of some form of chronic headache in 40%.
o Similar rates in identical and non – identical twins.
Management
• Amitriptyline.
o Reduces symptom
 Duration
 Frequency.
o Side effects.
 Dry mouth
 Drowsiness
 Weight gain
• Mitarzapine.
o Reduces symptom.
 Duration
 Frequency
 Intensity
o RCT found similar effects with mitarzapine and amitriptyline.
 Mitarzapine has less side effects.
o Side effects.
 Dizziness
 Drowsiness
 Increased appetite & weight
• Serotonin reuptake inhibitors.
o Similar effect to amitriptyline
o Less side effects than amitriptyline.
o Side effects.
 Transient nausea
 Anorexia
 Irritability
• Benzodiazipines.
o Some possible effects.
o Side effects.
 Altered mental state
 Poisoning
 Depression
 Dependence
• Botox.
o Can improve symptoms.
o Side effects.
 Facial weakness
 Difficulty with swallowing
  Disturbed local sensation
 Vertigo
 Pain at injection site
 Muscle cramps
 Flu – like symptoms
 Subjective feeling of.
• Neck weakness & pain
• Temporomandibular joint pain.
• Conventional acute analgesia has no effects, and can cause analgesia – induced headache.
o Can convert an acute headache into a chronic one
o Caffeine can relieve an acute headache, but perpetuate a chronic headache.

Non – drug therapy.

• Cognitive behavioural therapy.
o Effective by 6 months.
o About as effective as amitriptyline
o No side effects
• Acupuncture.
o Laser acupuncture can improve headache
 Duration
 Frequency
 Intensity
• Indian head massage.
o No effect
• Relaxation and electromyographic biofeedback.
o No effect
o Requires expensive equipment and staff.

Migraine.
• Many people with migraine or analgesia – induced headaches can also have background headaches,
which resemble tension headaches.
o Very important to take a good history to look for alternative diagnosis and elicit
 Features
 Prodrome
 Accompanying feature
• Clinical features.
o Unilateral headache
o Pulsating character
o Photphobia
o Reccurrent nature
o Last up to 30 hours.
o Aura
 Visual chaos
 Hemianopia
 Hemiparesis
 Dysphasia
 Dysarthria
 Ataxia.
 • With basilar migraine.
o Can cause tenderness all over the face and head.
o Diagnostic criteria in absence of aura.
 > 5 headaches
 Lasting 4 – 72 hours
 With either.
• Nausea
• Vomiting
• Photophobia
• Phonophobia
 And 2 or more of:
• Unilateral
• Pulsating
• Interference with normal life
• Worsened by routine activity.

• Pathogenesis
o Old theory
 Cerebral oligaemia leading to the aura.
 Cerebral and extracranial hyperaemia leading to the headache.
 Undelrying cause of vascular abnormalities may be dysfunction of sensory
modulation of craniovascular afferent nerves.
 Attacks are associated with changes in plasma serotonin.
o MRI evidence shows cerebral oedema, dilatation of intracerebral vessels and reduced
water diffusion are not associated with vascular territories.
 Primary event may be neurological after all.

• Triggers.
o CHOCOLATE.
 CHocolate or CHeese.
 Oral contraceptive pill
 Caffeine (or caffeine withdrawal)
 alcohOL
 Anxiety
 Travel
 Exercise
o In 50%, no trigger is found
o In only a few does avoiding triggers prevent all attacks

• Associations.
o Obesity
o Patent foramen ovale
 Catheter closure may help.

• Differentials.
o Cluster or tension headaches
o Cervical spondylosis
o Hypertension
 o Intercranial pathology
o Sinisitis/ Otitis media
o Tooth caries
o TIA

o Migraine is rarely a sign of serious pathology

o Don’t expend too much time looking for.
 Antiphospholipid antibody
 Microemboli
 Vascular malformations
o However, these factors are important in some.

• Prophylaxis.
o Mainly used if frequency > 2 times in a month.
o If one drug doesn’t work after 3 months, try another.
o > 65% will achieve an attack frequency reduction of 50%

o Pizotifen.
 Serotonin antagonist.
 0.5 – 1 mg TDS
• or 3 mg OD at night
 Side effects.
• Drowsiness
• Weight gain
• Increased effects of alcohol
• Increased glaucoma risk
o Propanolol
 40 – 120 mg BD PO
o Amitriptyline.
 25 – 75 mg nocte
 Side effects.
• Drowsiness
• Dry mouth
• Blurred vision

o Second line prophylaxis include.

 Valproate
• 400 – 600 mg BD
 NSAIDs
 Gabapentin
  Topiramate

• Treatment
o Dispersible, high dose aspirin.
 600 mg QDS PO
o Paracetamol & Metoclopramide
 1 g QDS & 5 mg TDS
 Give metoclopramide 10 minutes before paracetamol
 Beware extrapyramidal side effects.
o Ketoprofen.
 100 mg stat PO

o No evidence of any difference between ergotamine, NSAIDs and triptans/

 In terms of QUALYs Rizatriptain is better than sumatriptain, which is better
than Cafergot.
 Rizatriptain is fastest acting.
 Rizatriptan and xolmitripan are available as fast dissolving wafers for buccal
administration
 Imigrain recover is available over the counter


o Triptans.
 Serotonin agonists
 Constrict cranial arteries
 Rare side effects include.
• Arrythmias
• Angian
• MI
 Contraindications.
• Previous IHD
• Coronary spasm
• Uncontrolled hypertension
• Recent lithium
• SSRIs
• Ergot use.

o Ergotamine
 Serotonin agonist
 Constricts cranial arteries
 1 mg PO as headache starts.
 Repeated every half an hour.
  Maximum of 3 mg in a day
 Maximum of 6 mg in a week.
 Can be more effectively given as suppositories.
• 2 mg ergotamine + 100 mg caffeine
• Up to 2 in 24 hours
• After use, have to have a break for > 4 days.
 Emphasise risk of.
• Gangrene
• Vascular damage
 Contraindicated in.
• COCP use
• Peripheral vascular disease
• IHD
• Pregnancy
• Breast feeding
• Hemiplegic migraine
• Raynaud’s disease
• Liver or renal impairment.
• Hypertension.

Cluster Headaches.
• Prevelence of 1%
• Peak onset of 20 – 40 years.
o Sometimes remit with increasing age.
• Risk factors.
o Head or facial trauma
o Smoking
 85% of sufferers are smokers
 Stopping smoking once you have cluster headaches doesn’t improve condition
o Family history
 May be autosomal dominant, autosomal recessive or multifactorial inheritance
o Male gender

• Features.
o Last 15 – 180 minutes
o Unilateral
o Severe pain
o Occur up to 8 times a day
o Episodic in 80 – 90% of patients.
 Clusters and remission
o Autonomic symptoms in 97%
 Horner’s sydrome
 Ptosis
  Miosis
 Eye watering or bloodshot
 Runny or blocked nose
 Sweating
 Flushing

 Occur during the attack.

 Occur on same side as pain
 Ptosis and miosis may be constant, but intensified during attacks.
o Circadian rhythm
o Symptoms can shift to other side.
 Some paitients can have their pain shift, but their autonomic disfuctnion remain
on the original side.

• Episodic cluster headaches.

o 80 - 90% of patients have this type.
o Headaches occur daily few a few weeks, then period of remission.
o During active periods, patients can suffer up to 8 attacks a day
o Active periods can last anything from a week to a year.
o When in a bout, headaches can be triggered by.
 Alcohol
 Vasoactive substances
o When in remission, alcohol has no effect on headaches and patients are asymptomatic.
• Chronic cluster headaches.
o No remissions, or remissions lasting less than 30 days.
o Can be primary
o Can be secondary as an evolution from the episodic form.

Examination.
• No neurological abnormalities.
o If abnormalities found, investigate patient for secondary cause.
• Some patients develop persistant miosis and ptosis.

• CT/MRI to exclude abnormalities

o Mid line mass lesions or malformations are associated with cluster headaches.
 Especially in older patients.

Treatment
• Divided into abortion of the acute attack and prophylaxis to prevent recurrence.

• Acute therapy.
o Oxyegn
 100% oxygen in non – rebreath mask is effective in stoping attacks.
 Flow rate of 7 – 10 L/min
 Give for at least 20 minutes in upright position.
 60% of patients respond within 20 – 30 patients.
 Be careful of the possibility of hypoxic drive patients.
o Triptans.
  SC sumtriptan can relieve pain within 20 minutes in about 75% of patients.
 Oral triptans are inneffecitve due to the slowness of their action
 Few side effects in most patients, but can cause.
• Chest pain
• Distal parasthesia.
 Contraindicated in.
• Vascular disease
• Hypertension
• Patients taking MAOI or ergotamine.
o Lignocaine.
 Nasal lignocaine effective in about a third of patients.
 Dosage of 1 ml of 4 – 10% given on same side as pain.
 Lie patient back and to the side with pain to allow the drug to drain back to the
painful area.
 All patients should be tried on lignocaine at least once as can be effective and
has no systemic effects when not injected.
o Ergotamines have been used in the past, but little evidence to support their use.

• Prevention.
o Important to try and prevent attacks.
 If management purely based around aborting attacks, patient may become over
medicated.
o Once prophylaxis is effective, gradually reduce and withdraw medications when cluster
period is over.
o For chronic form, gradually withdraw and reduce medication every other month to assess
whether it is still needed

o Verapamil.
 First line prophylaxis for all types of cluster headache.
 Both normal preparation and modified release have been shown to be effective.
 Comparable to lithium, but acts faster once levels established.
• Can take 2 – 3 weeks until dose is titrated to effective levels.
 Not licenced for cluster headaches, but suggested dose is 240 – 320 mg.
 Side effects.
• Bradycardia
• Oedema
 • Constipation
• Dull headache
• Second line prevention.
o Lithium.
 78% of chronic cluster headache patients report benefit with lithium
prophylaxis.
• No reported benefit for episodic patients.
 Monitor blood levels and keep them between 0.6 – 1.2 mmol/L
• Recommended dose is 600 – 1500 mg OD
• Ideally given as sustained release.
 Also monitor.
• Liver function
• Renal function
• Thyroid function
 Side effects.
• Thyroid dysfunction
• Tremor
• Renal dysfucntion
 Due to danger and side effects, lithium only recommended in chronic cluster
headaches, and only when other drugs contraindicated or ineffective.
 Lots of drugs interact with lithium.
• Normally be increasing renal excretion
o Methysergide.
 Evidence of benefit is limited.
 Seems to be more effective in episodic headaches than chronic.
 Normal dose is 4 – 8 mg OD.
 Use caution when giving with triptans or other ergotamine derivatives
 Side effects.
• Nausea
• Muscle cramps
• Abdominal pain
• Pedal oedema
 Do not use continuously for > 6 months.
• High risk of pulmonary or retroperitoneal fibrosis with long term use.

o Corticosteroids.
 Used to rapidly suppress attacks whilst longer acting agents take effect.
 Medication of choice in periods of cluster activity of less than 2 months.
 Up to 80% of patients will respond to steroid therapy.
 Some patients will only respond to steroids, and so will need to take them
continuously.
 Start dosage at 60 – 100 mg prednislone OD for 5 days.
• After the 5 days, try and reduce dosage by 10 mg a day.

• Third line prevention

o 10 – 20% of patients don’t respond to previous lines of prophylaxis, or the headaches
become resistant.
o Following drugs have limited evidence supporting their use.

o Pizotifen.
  Antiserotonergic drug.
 3 mg per day have been effective in trails
 Only have modest effects
 Side effects.
• Tiredness
• Weight gain
o Valproate.
 5 – 20 mg/kg per day.
o Topiramate.
 Effective therapy.
 Recommended dose is at least 100 mg
• Titrating up from 25 mg daily.
 Side effects.
• Cognitive disturbances
• Paresthesia
• Weightloss
 Contraindicated in renal stones.
o Capsaicin.
 Effective in two thirds of patients.
 3 times a day nasally for 6 days on side that pain is.

o Many patients do better on combination therapies, rather than high dose of a single drug.
o A good starting point is
 Verapamil at 240 – 480 mg + another drug.

• Future treatments and those lacking evidence base

o Antiepileptics
 Pregabalin
 Levetiracetam
 Zonisamide
o Vanilloid/ cannaboid receptor agonists.
o SC octrrotide.

o Surgery.
 Consider if all drugs are ineffective, and secondary cause of headaches have
been ruled out.
 Be cautious, as little data on long term effect.

 Blocking the greater occipital nerve can be effective.

• Should be tried first.
 If patient has episodic headaches, be very careful when considering surgery near
the trigeminal structures as can cause:
• Trigeminal neuralgia.
• Anaesthesia dolorosa
o Sensation to that part of the face is lost, but pain remains.
  Deep brain stimulation of posterior inferior hypothalamus can be effective.
• Procedure reversible
• Normally well tolerated.
• Still experimental.

Trigeminal neuralgia.
• Clinical picture.
o Paroxysms of intense, stabbing pain
o Lasts seconds
o Unilateral
o In trigeminal nerve distribution
 Typically maxillary or mandibular branches.
o Face screws up in pain.
 “Tic Doloureux”
o Aggrevated by.
 Washing face
 Shaving
 Eating
 Taling
 Dental prostheses
• Typical patient.
o Male
 In Asians, 2:1 Female:Male ratio
o Over 50 years
• Causes.
o Anomalous intracranial vessels compressing trigeminal root.
o Secondary causes (14%)
 Aneurysm
 Tumour
 Chronic meningeal inflammation
 MS
 Herpes zoster
 Skull base malformation.
• Eg. Chiari
• Investigations.
o MRI to rule out secondary causes.

• Treatment.
o Carbamazepine.
 Start at 100mg BD PO
 Titrate up to a maximum of 400 mg QDS
o Phenytoin
 200 – 400 mg OD PO
o Gabapentin.
 300 mg on day 1
 1300 mg BD on day 2
  2800 mg TDS on day 3
 Side effects.
• Diarrhoea
• Dry mouth
• Dyspepsia
• Vomiting
• Peripherla oedema
• Dizziness
o Lamotrigine.

o If drugs fail, surgical microvascular decompression may be needed.

 Can be performed on the.
• Peripherl nerve
• Trigeminal ganglion
• Nerve root.
 Anomalous vessels are separated from the trigeminal root.
 Stereotactic gamma knife surgery can work.
• Limited by.
o Length of pain relief
o Time taken to get response to treatment.

Subarachnoid haemorrhage,.
• Spontaneous bleeding into the subarachnoid space is often catastrophic.
• Incidence.
o 8/100000 per year.
o Typically aged 35 – 65 years.
• Caused by.
o 80% due to rupture of berry aneurysms
o 15% due to AV malformations
o <15% no cause is found.
• Risk factors.
o Smoking
o Alcohol misuse
o Hypertension
o Bleeding disorders
o Mycotic aneurysm post – SBE
o Post – menopausal
 Possibly due to oestrogen deficiency.
o Family history.
 Close relatives of SAH patients have a 3 – 5 fold risk

• Berry aneurysms.
o Common sites.
 Junction of posterior communicating and internal carotid arteries
 Junction of anterior communicating and anterior cerebral arteries
 Bifurcation of middle cerebral artery.
o 15% are multiple
 o Some are hereditary.
o Associations.
 Polycystic kidneys
 Coarctation of aorta
 Ehlers – Danlos syndrome

• Symptoms.
o 10% have sudden death.
o Headache.
 Onset within seconds.
 Maximal within minutes.
 Meningism
o Vomiting
o Collapse
o Seizures
o Coma/ drowsiness.
 May last for days.
• Signs.
o Neck stiffness
o Kernig’s sign.
 Takes about 6 hours to develop.
o Retinal and subhyaloid haemorrhage
o Focal neurology,.
 At presentation suggests sit of aneurysm or intracerebral haematoma.
• Eg. Pupil changes suggest CN III palsy and posterior communicating
artery aneurysm.
 Later on suggests
• Ischemia from re – bleeding or vasospasm
• Hydrocephalus.
• Differentials.
o Only 25% of patients with “thunderclap headache” in primary care have SAH.
 In 50 – 60% no cause is found.
o The others have.
 Meningitis
 Migraine
 Intracerberal bleeds
 Cerebral venous thrombosis.

• Sentinal headaches.
o 6% of SAH patients have lesser headaches before their SAH.
 Probably due to warning bleeds.
o Not a reliable sign as recall bias clouds the picture.
o As surgery outcomes are now good for patients with few symptoms, be suspicious of any
severe, sudden onset headache. Particularly if associated with.
 Neck pain
 Back pain.

• Investigations.
o Modern CT scanners can pick up > 90% of SAH within 48 hours of onset.
o Older ones may miss small bleeds.
  If clinical suspicion high, but CT –ve, send for LP at 12 hours.
o CSF in SAH is uniformly bloody.
 Becomes yellow and xanthochromic after a few hours.
o Supernatant from spun CSF is examined for breakdown products of haemoglobin.
 Finding bilirubin in CSF is diagnostic.

• Management.
o Get immediate neurosurgical help if.
 Reduced GCS
 Progressive focal deficit
 Suspected cerebellar haematoma
o Bed rest
o Closely monitor.
 BP
 Pupils
 Coma level
 Neurology
o Repeat CT if deteriorating
o Prevent straining with stool softeners.

o Surgery.
 Craiotomy and clipping of aneurysms can stop rebleeds.
• Best option in those with few or no symptoms (Grade II or less)
• If surgery likely, do prompt angiography.
• Side effects.
o Intra – operative rupture
o Post – op epilepsy
 Endoscopic Platinum coil insertion is an alternative.
• Less invasive
• Slightly higher rebleed rate
 Intracranial stents and ballon remodelling allow treatment of wide – necked
aneurysms.
 Microcatheters can now pass through tortuous vessels to treat previously
unreachable aneurysms
 AV malformations and fistulae may also benefit from endoscopic surgery.
o Medical.
 Cautiously control severe hypertension
 Analgesia for headache.
 Best rest ± sedation for 4 weeks
 Keep well hydrated.
• “running dry” so as not to increase ICP causes more vasospasm.
 Nimodipine.
• 60 mg every 4 hours PO/ 1 mg/h IV
• Treat for 3 weeks.
• Calcium channel blocker
• Reduces vasospasm.
• Give to all patients who’s blood pressure allows it.
 • Prognosis
o Death often occurs following re – bleeding
 Occurs in 30%
 Often in the first few days.
o Almost all death occurs in the first month.
o Oif those who survive the first month, 90% are still alive at 1 year.
o Vascular spasm following a bleed often causes ischemia and permenant CNS deficit.
 Surgery is not useful at the time if this happens, but may be so later.

Grade Signs Mortality (%)

I None 0
II Neck stiffness and cranial nerve palsies 11
III Drowsiness 37
IV Drowsy with hemiplegia 71
V Prolonged Coma 100

• Prevention.
o Risk of surgery normally outweighs benefit of prophylactic surgery.
o Except, possibly, in young patients with
 Aneurysms > 7 mm in diameter.
 Aneurysms at junction of internal carotid and posterior communicating arteries.
 Aneurysms at rostral basilar bifurcation
 Uncontrolled hypertension
 History of bleeds
o Surgery twice as risky if > 45 years.
o Relative risk of rupture for aneurysm > 7 mm across is 3.3.
o Relative risk of rupture for aneurysm > 12 mm across is 56

o Should screen patients with previous SAH who are also:

 Smokers
 Hypertensives
 Multiple aneurysms

Benign coital headache.

• Also known as coital cephalgia.
• Experienced as an explosive headache.
o Symptoms can be indistinguishable from SAH.
• Can only make the diagnosis after excluding SAH.
• May recur during subsequent orgasms
• Will not cause persistant neurological disability.
Meningitis
• Presentation.
o Headahce
o Fever
o Neck stiffness
 Absent in 18% of patients
o Photophobia
 May take hours – days to develop.
o Rash.
 Associated with macular rash that progresses to petechiae or purpura.
o Confusion & psychiatric disturbances or altered GCS.
 Particularly in elderly with co – morbidities
 In immunocompromised.or neutropaenic, the only sign could be confusion.
o Focal neurological signs.
 Complicate meningitis in about 15%
 Can suggest.
• Cerebral damage.
o Eg. Hemiparesis following venous infarction or arteritis.
• Cranial nerve and brainstem involvement
o Basal exudation and inflammation
o Eg. Listeria monocytogenes meningitis.
• Brain shift secondary to raised ICP
 If focal signs or seizures are prominent, consider possibility of:
• Brain abscess
• Encephalitis
 If papilloedema present, consider alternative diagnosis.
• Complicates only 1% of meningitis.
 Siezures are the presenting sign in > 30%
• Predisposing factors.
o Usually none.
o Otitis media
o Mastoiditis
o Pneumonia
o Head injury
o Sickle cell disease
o Alcoholism
o Immunocompromise.
• Causes in adults.
o Common.
 Neisseria meningitides
 Strep. pneumoniae
o Rarer.
 Tend to affect elderly
 Gram negative bacilli
 Listeria
• Assessment of severity.
o Mortality increases as consciousness decreases.
 About 55% for comatose adults.
 o However, can proceed quickly in alert patients as well.

• Management.
o Stabalize and resuscitate.
o Give oxygen
o CT scan.
 Rule out raised ICP
 Safest to use CT to determine safety of doing LP
• Argument to say that this is only needed if.
o Decreased GCS
o Focal signs
o Papilloedema
o Signs suggesting impending cerebral herniation.
• Discuss with senior collegue.
o Give empirical antibiotics.
 Take blood cultures and LP before starting.
 Don’t wait for results before starting.
o Make definitive diagnosis with LP
o Review antibiotic treatemtn in light of LP result.
 Consider Corticosteroid adjunct.
o Arrange for contacts tracing (including nursing and medical staff)
 Give prophylactic antibiotics.
o Notify public health consultant
o Observe for and treat complications.

• Antibiotic therapy.
o Follow hospital guidelines.
o Adult patients with typical meningococcal rash.
 IV benzylpenicillin 2.4 mg every 4 hours.
o Adults < 50 without rash.
 Cefotaxime 2g TDS
 Ceftriaxone
• 2g BD
o Adults > 50 without rash.
 Add 2g ampicillin every 4 hours to cover Listeria.
o If patient from are where penicillin and cephalosporin – resistant pneumococci are
common (eg. Mediterranean countries).
 Add IV vancomycin 500 mg QDS.
o If penicillin allergic.
 IV chloramphenicol 25 mg/kg + Vancomycin 500 mg QDS
 If > 50, add co – trimoxazole.
 Discuss case with microbiologist.
 • Lumbar puncture.
o Measure operating pressure.
 Often raised to > 14 cm CSF in meningitis.
 Very few reports of coning following procedure.
 If pressure is raised.
• Observations every 15 minutes.
• Send for CT if not already done.
o Complications of meningitis
o Space occupying lesion, eg. Cerebral abscess.
o Analysis of CSF.
Bacterial Viral TB
Appearance Turbid Clear Clear
Cells per mm3 5 – 2000 5 – 500 5 – 1000
Main cell type Neutrophil Lymphocyte Lymphocyte
Glucose (mM) Very low Normal Low
Protein (g/L) Often > 1 0.5 – 0.9 Often > 1
Other tests Gram stain PCR Ziehl - Neelsen
Bacterial antigen Fluorescent test
PCR

o WCC.
 Bacterial meningitis typically causes high WCC with predominance of
neutrophils.
 Low CSF WCC (0 –20/mm3) with high bacterial count on Gram stain is
associated with poor prognosis.
o Glucose.
 CSF: blood ratio < 3.1 in 70%
 May be normal.
o Protien
 Usually elevated
o Gram stain.
 Positive in 60 – 90%
 May be negative if there has been a delay between starting antibiotics and
lumbar puncture.
 Early antibiotics will also cause CSF culture yield to drop from 70 – 80% to
< 50%.
o A bacterial CSF profile may appear in early stages of viral or TB meningitis.
 Repeat CSF analysis will show transformation to luymphocytic predominance.
o Patients with CSF profile suggesting bacterial meningitis should be treated as such until
proven otherwise.
• Review of antiobiotics.
o If Gram –ve diplococci are present.
 Continue with benzylpenicillin or ampicillin.
o If Gram +ve cocci diplococci present, change to:
 2 g cefotaxime IV QDS
 Consider Vancomycin 500 mg QDS
o If Gram +ve cocco – bacilli present.
 Suggests Listeria.
 Ampicillin 2 mg every 4 hours + gentamycin 5 mg/kg/day as single dose or split
into TDS.
o Adjuvant corticosteroids.
 Reduces incidence of neurological sequelae.
• Especially in pneumococcal meningitis.
 Give in patients with.
• Raised ICP
• Stupor
• Impaired mental status
 Dose.
• 10 mg dexamethosome IV loading dose
• 4 – 6 mg PO QDS maintenance.

• Prophylaxis for contacts.

o Give immediately.
o Adult contacts.
 Rifampicin 600 mg BD for 2 days.
 Ciprofloxacin 750 mg as single dose
o Children > 1 year.
 Rifampicin 10 mg/kg BD for 2 days.
o Children 3 months – 1 year.
 Rifampicin 5 mg/kg BD for 2 days.

o Inform public health services when diagnosis made.

 Can recommend on current best practice for prophylaxis.
 Can assist with contact tracing.
• Complications.
o Raised ICP
 Steroids
 If evidence of brain shift or imending coning.
• Mannitol
o 1g/kg IV over 10 – 15 minutes.
o 250 ml of 20% solution for average adult.
• Elevated head of bed to 30o.
• Consider oral glycerol.
o Hydrocephalus.
 Diagnosed by CT.
 May require intraventricular shunt.
 Discuss urgently with neurologists.
 Can occur due to
• Thickened meninges obstructing CSF flow.
• Adherence of inflamed lining of aqueduct of Sylvius or 4th ventricular
outflow.
 Papilloedema may not be present.
o Seizures.
 Treat as normal.
o Persistant pyrexia.
 Suggest occult source of infection.
 Carefully re – examine patient.
• Check oral cavity and ears.
o Focal neurological deficit.
 May occur due to.
• Arterial or venous infarction.
o Don’t respond to anti – coagulants.
• Space occupying lesion
o Eg. Subdural empyema.
• Inflammation at base of skull can cause cranial nerve palsies.
 Request CT scan if hasn’t already been performed.
o Subdural empyema.
 Rare complication.
 Can cause.
• Focal signs
• Seizures
 • Papilloedmea
 Requires urgent surgical drainage.
o DIC.
 Ominous sign.
 May require .
• Platelets.
• Fresh frozen plasma
 Discuss heparin use with neurologist and haematologist.
o SIADH.
 Regularly check
• Fluid balance
• Electrolytes.

Lymphocytic CSF
• Due to viral or TB meningitis.
• Viral meningitis
o Clinically indistinguishable from acute bacterial meningitis.
o Normally self limiting.
• TB meningitis.
o Usually preceded by history of malaise and systemic illness.
 Can last days – weeks.
o May present very acutely.
o Associated with.
 Basal archnoditis
 Vasculitis
 Infarctions causing focal sings
• Cranial nerve palsies
• Hydrocephalus with papilloedema
o Cryptococcal and syphilitis meningitis in the immunocompromised can present like TB
meningitis.

• Causes.
o Viral.
 Coxsackie
 Echo
 Mumps
 Herpes simplex I
 Varicella zoster
 HIV
 Lymphocytic choriomeningitis virus
o Non – viral.
 TB
 Cryptococcus
 Leptospirosis
 Lyme disease
 Syphilis
 Brucellosis
  Parameningeal infection with CSF reaction.

• CSF findings.
o Usually demonstrates lymphocytosis.
 Can start as demonstrating neutrophils
o Important not to dismiss possibility of TB meningitis if CSF glucose is normal.
 May be in 20% of cases.
o Tuberculin may be negative in 20%
o M. Tuberculosis is seen in the initial CSF in 40% of patients with TB meningitis.
o Send SCF for viral and TB PCR.

• Treatment.
o Viral meningitis normally requires only supportive measures.
o TB meningitis.
 Dual therapy.
• Pyrazinamide 30 mg/kg/day
• Isoniazid 10 mg/kg/day
o Maximum isoniazid does of 600 mg/day.
o Give pyridoxine 10 mg/day to prevent isoniazid neuropathy.
 Good CSF penetration.
 If patient is conscious, for the first 3 months add.
• Rifampicin
o 450 mg/day if weight < 50 kg
o 600 mg/day if weight > 50 kg.
• Ethambutol
o 25 mg/kg/day
 For the next 7 – 10 months give.
• Rifampicin
o 450 mg/day if weight < 50 kg
o 600 mg/day if weight > 50 kg.
• Isoniazid.
o 300 mg/day
 Consult local respiratory/ infectious disease specialist for advice.

 Different mycobacteria require different drug copmbinations.

 Give corticosteroids if.
• Raised ICP
• Very high CSF protein levels.
o Cryptococcal meningitis.
 Several regimens are used.
 Two common ones last 6 weeks.
• Amphotericin B as monotherpay.
 o 0.6 – 1 mg/kg/day
• Amphotericin B and Flucytosine dual therapy.
o Amp: 0.5 mg/kg/day
o Fluc: 150 mg/kg/day
 Alternative in AIDS patients is Fluconazole.
• 400 mg/day initially
• 200 – 400 mg/day for 6 – 8 weeks.

Giant Cell arteritis

• Commenest primary large vessel vasculitis.
o Oincidence of 1: 10000
• Typically disorder of the elderly.
o Mean age of 70 years.
o Female: Male ratio of 2:1
• Diagnosis is clinical, but supported by raised acute response proteins and temporal artery histology
o ESR
o CRP
o Thrombocytosis
• Classical pathological discription is a segmented, granulomatous pan – arteritis
• Early stage changes may be simply
o Thickening of internal elastic lamina.
o Mononuclear cell infiltrate of wall.

• Clinical features.
o Headache 90%
o Temporal artery tenderness 85%
o Scalp tenderness 75%
o Jaw claudication 70%
o Pulseless temporal artery 40%
o Visual symptoms (including blindness) 40%
o Polymyalgic symptoms 40%
 Proximal muscle stiffness without weakness or wasting

o Systemic features 40%

o Thickened/ nodular temporal artery 35%
o CVA or MI Rare
 • Investigations.
o FBC
 Normochromic anaemia
 Thrombocytosis
o LFTs
 Elevated alkaline phophatase
o ESR
 > 50 mm in first hour.
 95% sensitive
o CRP
 Elevated
o CXR
 To exclude underlying CA bronchus
o Urinalysis.
 To exclude haematuria and protienuria
o Temporal artery biopsy.

• Management.
o Immediate high dose prednisolone.
 Prevents blindness.
 40 mg OD is normally sufficient.
 60 – 80 mg may be used if patient already has visual symptoms.
o All patients should have temporal artery biopsy within 48 hours of starting steroids to try
and confirm diagnosis.
 May be negative due to “skip lesion” nature of disease.
• Differential diagnosis is spondylisis.
Sinusitis
• Symptoms.
o Blocked/ runny nose
o Frontal headache.
 Worse on bending
o Chronic.
 Post nasal drip
 Cough
 Frontal headache
 Facial pain
 Blcoked nose
 Nasal polyps
 History of allergic rhinitis
• Signs.
o Tender over sinuses.
 Above medial eyebrow
 Bridge of nose
 Below eyes
o Pyrexia
• Management.
o Saline nebulizers.
 5 ml/ 2 – 4 hours.
o Beclamethosome nasal spray.
 2 sprays to each nostril BD
o Ephidrine nasal drops.
 1 – 2 drops to each nostril QDS
  Maximum of 7 days of therapy.
o If severe give Amoxycillin 500 mg TDS PO
 Purulence mucus
 Systemically unwell.
• Complications.
o Local spread of infection.

Temperomandibular joint dysfunction

• Caused by inflammation of TMJ
• Can cause significant pain and dysfunction.
• Can be caused by any joint problems.
o Ankylosis
o Arthritis
o Trauma
o Dislocation
o Developmental abnormalities
o Neoplasia
• Presentation
o Variable as can be due to any part of the joint.
 Muscles
•
 Nerves
 Tendons
 Ligaments
 Bone
 Connective tissue
 Teeth
o Commonly causes ear pain due to swelling of proximal tissues.
• Signs and symptoms.
o Jaw pain
 o Reduced jaw opening.
o Jaw “clicking” or “popping”
o Pressure on “trigger points”
o Toothache
o Ear ache
• Causes.
o Overuse of muscles of mastication.
 Chewing gum continuously
 Clenching teeth
o Infection
o Over opening mouth.
• Treatment.
o Referral to a dentist.
o Repairing any damage to teeth.
o Simple pain relief.
 May only give initial relief.
o Low dose tricyclic antidepressants.
 Due to anti – muscarinci effect.
 Nortriptyline
 Amitriptyline.
o Correction of poor jaw action
 Non – repositioning stabilization splint may be helpful.
 Biting on this too hard may worsen condition.
• Anterior splint, which only has contact with front teeth, may help this
problem.
o If these methods don’t work, consider.
 Arthrocentesis
 Surgical reposition to correct congential abnormalities.
 Replacement of the joints.