Headache for Medical Finals (based on Newcastle university learning outcomes)

8/14/2019 Headache for Medical Finals (based on Newcastle university learning outcomes)

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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 neuralgiaPost head injury

Pagets disease of the skull

Other causes of facial pain Dental problems

Temporomandibular joint

Ears/ nose/ sinusesCervical spine

Eye

MI (rarely)


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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 Kernigs sign.

Hamstring spasm & pain on knee extensiono Brudzinskis 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.


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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.


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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

Doesnt 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.


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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


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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 natureo Last up to 30 hours.

o Aura

Visual chaos

Hemianopia

Hemiparesis

Dysphasia

Dysarthria

Ataxia.


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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.

Pathogenesiso 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 orCHeese.

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


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o Intercranial pathology

o Sinisitis/ Otitis media

o Tooth caries

o TIA

o Migraine is rarely a sign of serious pathology

o Dont expend too much time looking for. Antiphospholipid antibody

Microemboli

Vascular malformationso However, these factors are important in some.

Prophylaxis.

o Mainly used if frequency > 2 times in a month.

o If one drug doesnt 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 POo Amitriptyline.

25 75 mg nocte

Side effects.

Drowsiness

Dry mouth

Blurred vision

o Second line prophylaxis include.

Valproate

400 600 mg BD

NSAIDs

Gabapentin


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Topiramate

Treatment

o Dispersible, high dose aspirin.

600 mg QDS POo 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.


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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

Raynauds 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 doesnt improve condition

o Family history

May be autosomal dominant, autosomal recessive or multifactorial inheritance

o Male gender

Features.

o Last 15 180 minuteso 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%

Horners sydrome

Ptosis


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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.


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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 dont respond to previous lines of prophylaxis, or the headaches

become resistant.

o Following drugs have limited evidence supporting their use.

o Pizotifen.


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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.


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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 POo Gabapentin.

300 mg on day 1

1300 mg BD on day 2


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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 reliefo 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


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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 stiffnesso Kernigs 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.


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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

Neurologyo 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 neckedaneurysms.

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 whos blood pressure allows it.


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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.


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Meningitis

Presentation.

o Headahce

o Fevero 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.


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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.

Dont 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.


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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

Bacterial antigen

PCR Ziehl - Neelsen

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.


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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.


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Complications.

o Raised ICP

Steroids

If evidence of brain shift or imending coning.

Mannitolo 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 Dont respond to anti coagulants.

Space occupying lesiono Eg. Subdural empyema.

Inflammation at base of skull can cause cranial nerve palsies.

Request CT scan if hasnt already been performed.

o Subdural empyema.

Rare complication.

Can cause.

Focal signs

Seizures


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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


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Parameningeal infection with CSF reaction.

CSF findings.

o Usually demonstrates lymphocytosis.

Can start as demonstrating neutrophilso 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.

Rifampicino 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.


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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


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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 eyeso Pyrexia

Management.

o Saline nebulizers.

5 ml/ 2 4 hours.

o Beclamethosome nasal spray.

2 sprays to each nostril BDo Ephidrine nasal drops.

1 2 drops to each nostril QDS


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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


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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 teetho 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 dont work, consider.

Arthrocentesis

Surgical reposition to correct congential abnormalities.

Replacement of the joints.

Headache for Medical Finals (based on Newcastle university learning outcomes)

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