HEADACHE

ALI ABDIRAHMAN MOHAMED

221-083011-22882
 HEADACHE
✓ Introduction
✓ Etiology
✓ epidemiology
✓ Symptoms and clinical evaluation
✓ Types of headache
✓ Clinical features
✓ Management.
 Introduction
■ Headache is the symptom of pain anywhere in the
region of the face, neck or head caused by any
irritation, agitation or stimulation of blood vessels
of the dura mater or trigeminal nerve or muscles of
the head and neck.
Classification:
according to international headache society;
1) Primary headache
2) Secondary headache
Etiology
■ Dehydration
■ Fatigue
■ Sleep deprivation
■ Stress
■ The effects of medication
■ Viral infection
■ Infections
■ Loud noises
■ Common cold
■ Head injury
Epidemiology
■ About half of the adults have a headache in a given
year.
■ Tension headaches are the most common,
affecting about 1.6billion (21.8% of the population)
followed by migraine (11.7%)
■
primary headaches
■ Migraines
■ Cluster
■ Tension
 Migraine Tension Cluster

Pain description Throbbing, Pressure, Abrupt onset,

moderate to tightness, waxes deep, continous,
severe, worse and wanes excruciating,
w/exertion explosive

Associated Photo/phono- none Tearing,

symptoms phobia, N/V, aura congeston,
rhinorrhea, pallor,
sweating

Location 60-70% unilateral Bilateral Unilateral

Migraine headache
■ Migraine headache is usually severe and throbbing pain
on one side of your head with photophobia, phonophobia
and vomiting lasting from 4 to 72 hours.
■ Movement makes the pain worse and patients prefer to
lie in a quiet, dark room.
■ it affects about 20% of females and 6% of males at some
point in life.

Causes
■ The cause is unknown but thought to be linked to:
■ Familial factors
■ Craniovascular disorders, which can be precipitated by:
stress, anxiety, menstruation, flashing lights, hunger,
 Pathophysiology

❖ The cause of migraine is unknown but there is

increasing evidence that the aura is due:
I. dysfunction of ion channels causing a spreading frontal
cortical depolarisation (excitation)
II. followed by hyperpolarisation (depression of activity).
❖ This process (the ‘spreading depression of Leão’)
spreads over the cortex at a rate of about
➢ 3 mm/min, corresponding to the aura’s symptomatic
spread.
Clinical features
prodrome of malaise, irritability or behavioural change for
some hours or days.
i. Around 20% of pt experience: migraine with aura
(classical migraine)
ii. The 80% of patients with characteristic headache
lbut no ‘aura’ are said to have migraine without aura
(previously called ‘common’ migraine).
➢ Pulsatile, Photophobia, phonophobia
➢ One day in duration
➢ Unilateral
➢ Nausea and vomiting
➢ Disability plus worsen with excertion
Management
➢ Avoidance of identified triggers or exacerbating
factors (such as the combined contraceptive pill)
may prevent attacks.
➢ Treatment of an acute attack consists of simple
analgesia with aspirin, paracetamol or
nonsteroidal anti-inflammatory agents.
➢ Nausea may require an antiemetic such as
metoclopramide or domperidone.
 Cluster headaches
■ Cluster headaches (also known as migrainous
neuralgia)
■ Males predominate 5:1, and onset is usually in the third
decade.
■ The syndrome comprises runs of severe, unilateral
periorbital pain accompanied by unilateral lacrimation,
nasal congestion and conjunctival injection, lasting 30–
90 mins.
Pathophysiology
■ The cause is unknown but this type of headache
differs from migraine in many ways, suggesting a
different pathophysiological basis.
CONTINUATION
• Although uncommon, it is the most common of
the trigeminal autonomic cephalalgia
syndromes.
• Functional imaging studies have suggested
abnormal hypothalamic activity.
• Patients are more often smokers.
CLINICAL PRESENTATION
Cluster headache is strikingly periodic, featuring
runs of identical headaches beginning at the same
time for weeks at a stretch (the ‘cluster’).
Clinical features continuation:
➢ Patients may experience either one or several attacks within
a 24-hour period, and typically are awoken from sleep by
symptoms (‘alarm clock headache’).
Cluster headache causes severe, unilateral periorbital pain with
autonomic features, such as :
• ipsilateral tearing,
• nasal congestion
• conjunctival injection (occasionally with the other features of a
Horner’s syndrome).
The pain, though severe, is characteristically brief (30–90
minutes). In contrast to the behaviour of those with migraine,
patients are highly agitated during the headache phase.
Management
■ Acute attacks can usually be halted by subcutaneous
injections of sumatriptan or inhalation of 100%
oxygen.
■ The brevity of the attack probably prevents other
migraine therapies from being effective. Migraine
prophylaxis is often ineffective too but attacks can be
prevented in some patients by verapamil, sodium
valproate, or short courses of oral glucocorticoids.
■ Patients with severe debilitating clusters can be
helped with lithium therapy, although this requires
monitoring
Tension type headache
This is the most common type of headache and is experienced to some degree
by the majority of the population.
Pathophysiology
• Tension-type headache is incompletely understood, and some consider that it
is simply a milder version of migraine;
• The original notion that it is due primarily to muscle tension (hence the
unsatisfactory name)
• Anxiety about the headache itself may lead to continuation of symptoms, and
patients may become convinced of a serious underlying condition.
Clinical features
• The pain of tension headache is characterised as ‘dull’, ‘tight’ or like a
‘pressure’, and there may be a sensation of a band round the head
• It is of constant character and generalised, but often radiates forwards from
the occipital region.
• It may be episodic or persistent, although the severity may vary, and there is
no associated vomiting or photophobia.
Management
Most benefit is derived from a careful assessment, followed by discussion
of likely precipitants and reassurance that the prognosis is good.
• The concept of medication overuse headache needs careful
explanation.

❑ An important therapeutic step is to allow patients to realise that their

problem has been taken seriously and rigorously assessed.
• Physiotherapy (with muscle relaxation and stress management) may
help and low-dose amitriptyline can provide benefit.
Red flag signs.
■ Systemic signs:
fever, Weight loss, Myalgia , Arthralgie
■ Neurological deficits: hemiparesis
■ Onset of headache: acute/ abrupt
■ Old >= 50y/o
■ Papillaedema
■ Position: worse lying down, better sitting up
■ Pattern change
■ Precipitation by valsalva maneuver:
Decrease venous drainage
Increase ICP
Secondary headache
■ May be caused by problems in the head and neck e.g. due to
harmful substances like medication overdose, cervicogenic
headache
❖ Mass Occupying lesion
• Increase blood: trauma
• Increase CSF: hydrocephalus
• Mass: pituitary adenoma
• Brain abscess: 3 signs, H/F/Nd
• Brain tumor: GBM, meningioma, metastasis

❖ Meningitis/encephalitis: 3 signs plus meningeal signs

❖ Cerebral sinus thrombosis
❖ Carotid. Vertebral artery dissection
❖ Sinusitis
❖ Acute angular glaucoma
Trigeminal neuralgia
This is characterised by unilateral lancinating, stabbing and lightening
facial pain, most commonly involving the second and/or third divisions of
the trigeminal nerve territory, due to compression by superior cerebellar
artery
➢ usually in patients over the age of 50 years.
Clinical features
• The pain is repetitive, severe and very brief (seconds or less).
• It may be triggered by touch, a cold wind or eating.
• Physical signs are usually absent, although the spasms may make
the patient wince and sit silently (tic douloureux).
• There is a tendency for the condition to remit and relapse over many
years.
• Rarely, there may be combined features of trigeminal neuralgia and
cluster headache (‘cluster–tic’).
 Management
➢ The pain often responds to carbamazepine.
• It is wise to start with a low dose and increase gradually, according
to effect.
■ In patients who cannot tolerate carbamazepine:., oxcarbazepine,
gabapentin, pregabalin, amitriptyline or glucocorticoids may be
effective alternatives,
■ If medication is ineffective or poorly tolerated, surgical treatment
should be considered.
■ Otherwise, localised injection of alcohol or phenol into a peripheral
branch of the nerve may be effective.
Sign and symptoms

SIGN OR SYMPTOM POSSIBLE CAUSE

Recent trauma to the head Intracranial bleeding

Head injury
High fever Malaria
Meningitis
Other infections
Acute onset, severe Intracranial bleeding
Chronic worsening Tumours, hypertension
headache
Altered consciousness Tumour, intracranial
and/or focal neurological bleeding, intracranial
symptoms and/or seizure infection
■ Any patient who presents with headache and the following
should be considered to have a secondary headache
syndrome:
■ • “Worst headache of my life”
■ • Worsening symptoms over days to weeks
■ • Abnormal neurologic exam
■ • Fever
■ • Vomiting preceding the headache
■ • Headache induced by coughing, bending, lifting; or onset
age >55
■ a headache that is described as “the worst headache of my
life” and/or “thunderclap” at onset, and is accompanied by
nuchal rigidity without fever, suggests an intracranial
hemorrhage as the underlying cause.
■ Patients with brain tumors will present complaining of
headache that is described as a deep, dull, aching pain that
disturbs sleep.
■ The history of vomiting that precedes the onset of headache
by a number of weeks, or a history of headache induced by
coughing, lifting, or bending, is typical of posterior fossa brain
tumors.
■ Patients with temporal arteritis complain of a unilateral
pounding headache associated with visual changes,
described as dull and boring with superimposed lancinating
Added management for
migraines
■ Pharmacologic treatment for migraine headaches
can be divided into management of an acute
episode and prophylaxis.
■ Initially, for a mild migraine—which is defined as
headache in the absence of nausea or vomiting—
NSAIDs may be used.
■ Acutely, abortive therapy consists of sumatriptan,
which acts as a serotonin receptor agonist.
Dihydroergotamine is the alternative to the triptans.
Ergotamine can be used in combination with
caffeine. The triptans are contraindicated in
patients with known cardiovascular disease,
uncontrolled hypertension, or pregnancy.
continuation

■ These medications can be given orally, intranasally,

or even subcutaneously, depending on the severity
of the headache.
■ Dopamine antagonists such as metoclopramide
can be given acutely as oral formulations to aid in
the absorption of other abortive medications.
■ Prophylactic treatment for migraine therapy should
be initiated when patients have acute migraine
headaches >3–4/month. And the best prophylactic
drug used is a beta blocker eg propranolol and this
drug takes 2 to 6 weeks to have an effect and
discontinue their use gradually over 6 months.
■ Other prophylactic drug include:verapamil, valproic
acid,
Clinical assessment
■ The most important question that has to be
answered in any patient who presents complaining
of a headache is whether there exists a serious
underlying cause for the symptoms.
■ By taking a thorough history and performing an
adequate physical examination, it is possible to
make this differentiation.
■ An essential point in the history is to determine
whether this is the first episode of headache that
the patient has experienced
■ . A history of recurrent symptoms makes the
diagnosis of a primary headache disorder more
likely.
■ A history of a first-time headache, especially when
severe and rapidly peaking, speaks strongly for
serious underlying pathology
References

1. Hutchison's 23rd edition

2. Davidson’s principle.
3. Kaplan internal medicine usmle step 2.