PRINCIPLES OF HEADACHE DIAGNOSIS (4)
- Chronic headaches rarely need more than a good Hx & physical examination for a diagnosis to be made.
2. Which headaches need to be investigated? • Recent onset • Consistently focal • Post traumatic • HA's beginning after 30
- Skull X-rays are only useful when:
• Considering abnormalities of the base of the brain (eg sellar/suprasellar lesions)
• Immediately following head trauma - Diagnostic lumbar puncture should be used when an acute headache is:
• accompanied by fever (e.g. bacterial meningitis)
• explosive in onset (e.g. acute subarachnoid haemorrhage)
• described as the most severe headache experienced by the patient (e.g. acute subarachnoid haemorrhage)
VASCULAR HEADACHES TYPICAL
CHARACTERISTICS (6)
- Recurring attacks (over months and years)
- Unilateral
- Throbbing quality
- Precipitated by identifiable environmental or psychological factors
- Tenderness of affected arteries during the attack
- Carotid artery compression may result in temporary pain relief
MIGRAINE WITHOUT AURA:
EPIDEMIOLOGY
AKA Common Migraine
Begins in childhood
Females > males
Familial
Specific to WITHOUT AURA
- related to menstrual cycle
- considered a neurobiological disorder (attacks probably originate in the CNS tissue rather than the blood vessels)
- no signs of cortical spreading depression
MIGRAINE WITHOUT AURA:
CLINICAL MANIFESTATIONS (6)
- Recurrent
- Attacks last 4-72 hours
- Unilateral location
- Pulsating quality
- Moderate or severe intensity
- Aggravated by physical activity
Often associated with:
- Nausea
- Malaise
- Photophobia
- Phonophobia
MIGRAINE WITHOUT AURA:
PRECIPITATING FACTORS (5)
• Holidays/weekends • Menstruation • Foods (e.g. chocolate, nuts, aged cheese) • Alcohol (esp. Red wine) • Environmental stimuli e.g. - bright sunlight - too much sleep - emotional stress - other medical conditions - drugs e.g. vasodilators, reserpine, oestrogens etc.
MIGRAINE WITHOUT AURA:
DIAGNOSTIC CRITERIA (5)
At least 5 attacks fulfilling the following criteria are needed for a dx:
- HA lasts 4-72 hours (untreated or unsuccessfully treated)
- HA has at least 2 of the following characteristics:
• unilateral location
• pulsating quality
• moderate or severe pain intensity - HA aggravation by or causing avoidance of routine physical activity (e.g., walking or climbing stairs)
- During headache at least one of the following occurs:
• nausea and/or vomiting
• photophobia and phonophobia - HA not attributed to another disorder
CORTICAL SPREADING DEPRESSION DEFINITION, OUTCOMES
DEFINITION
CSD is a short-lasting depolarization wave that moves across the cortex at a rate of 3–5 mm/min.
In CSD, a slow-moving wave of K+ ions travels through the brain causing large numbers of neurons to fire at once.
This is followed by a wave of inhibition during which normal neuronal activity in that region is halted.
OUTCOMES
• Temporary INCREASE in local blood flow
• Small regions of short-term local hypoxia resulting in:
– neuronal swelling
– temporary loss of dendritic spines (i.e. tiny projections on neurons that form synapses with other neurons)
• Multiple, repeated CSD waves could result in permanent hypoxic neuronal damage
- Excess K+ levels must be returned to normal (process requires a lot of energy)
- blood flow in the CSD affected region is temporarily increased as the brain attempts to ↓[K+]’s
- Most of the oxygen is used by the neurons closest to the dilated blood vessels
- Pockets of relatively ischemic neurons which are distant to the blood vessels
MIGRAINE WITH AURA AKA
CLASSIC MIGRAINE
MIGRAINE WITH AURA
CLINICAL MANIFESTATIONS:
Aura - thought to be a clinical manifestation of CSD. Aura often starts in the visual or somatosensory cortex, hence the aura is often visual or tactile in nature.
• Recurrent disorder
• Attacks of reversible focal neurological symptoms
- usually develop gradually over 5-20 mins
- last <60 mins
• Exhaustion following the HA
MIGRAINE WITH AURA
AETIOLOGY:
Before or simultaneously with the onset of aura symptoms, regional cerebral blood flow is decreased in the cortical areas corresponding to the clinically affected area.
Blood flow reduction usually starts posteriorly and spreads anteriorly and is usually above the ischaemic threshold.
After one to several hours, gradual transition into hyperaemia occurs in the same region.
MIGRAINE WITH AURA
FOCAL NEUROLOGICAL SSX: (5)
- Visual (usually) eg bright flashing lights
- Unilateral Paraesthesia (hand, periorally)
- Aphasia
- Hemiparesis
- Hemisensory defects
MIGRAINE WITH AURA
DIAGNOSTIC CRITERIA:
At least 2 attacks fulfilling the following criteria:
– Presence of an aura
– Not attributable to another disorder (e.g. stroke, MS etc)
CLUSTER HEADACHES
Classifications
• Episodic cluster headache
Attacks occur in periods lasting 7 days to 1 year separated by pain-free periods lasting 1 month or longer
• Chronic cluster headache
Clusters occur more than once a year without remission, or the cluster-free interval is shorter than 1 month
CLUSTER HEADACHES
Epidemiology (4)
- Age at onset is usually 20-40 years
- Prevalence is 3-4 times higher in men than in women
- 5% of cases are inherited
- typically occur in spring and autumn
CLUSTER HEADACHES
Aetiology
Activation of posterior hypothalamic gray matter
- leads to central disinhibition of the trigeminal nociceptive pathways.
The intense pain that typically occurs in this condition is caused by the dilation of blood vessels which compress the trigeminal nerve (central sensitisation of this area)
CLUSTER HEADACHES
Definition
short-lived paroxysms of extremely severe, unilateral head pain, which occurs in clusters e.g. several times a day.
CLUSTER HEADACHES
Typical Clinical manifestations (9)
- Pain is of rapid onset, and knife-like
- Strictly unilateral
- Pain is orbital, supraorbital, temporal or in any combination of these sites
- Pain then spreads to involve the forehead
- The headache disappears as abruptly as it appeared
- The ipsilateral nostril waters and the affected eye may tear (associated autonomic manifestations)
- 20% of patients develop homolateral Horner’s syndrome
- Each attack lasts 15mins-3hrs hours
- Clusters typically last 3 – 8 weeks
CLUSTER HEADACHES
Provoking Factors
Alcohol
Histamine
Nitroglycerine
CLUSTER HEADACHES
Diagnostic criteria
At least 5 attacks fulfilling the following criteria:
• Severe unilateral pain
- Orbital, supraorbital and/or temporal pain lasting 15mins to 3hrs if untreated
- Attacks have a frequency from one every other day to 8/day
HA is accompanied by at least one of the following:
• ipsilateral conjunctival injection and/or lacrimation
• ipsilateral nasal congestion and/or rhinorrhoea
• ipsilateral eyelid oedema
• ipsilateral forehead and facial sweating
• 20% have ipsilateral miosis &/or ptosis (ie Horner’s)
• a sense of restlessness or agitation
TENSION TYPE HEADACHE
Classification
• Episodic TTH
There are two subtypes:
– Infrequent subtype:
HA episodes 15 episodes per month
• Probable TTH
TTH
Epidemiology
- Most common type of primary headache
- Lifetime prevalence in the general population ranges in different studies from 30-78%
- Thought to account for ≈ 90% of all headaches
TTH
Aetiology
Peripheral pain mechanisms likely in episodic TTH
Central pain mechanisms likely in chronic TTH
TTH
Clinical Picture: PAIN per classification
Episodic:
- occurs randomly
- shorter duration
- usually triggered by
- stress
- anxiety
- anger
- fatigue
Chronic:
- daily and continuous (always present)
- pain intensity may vary during 24 hour cycle
- can result from either anxiety or depression
TTH
Clinical features of Pain general (7)
- Steady
- Non-pulsatile
- Unilateral/bilateral
- Aching
- Vice-like
- Usually begins occipitally but often involves frontal and temporal
- Recurrent
- Tenderness of pericranial mm
- Commonly:
- dizziness
- blurred vision
- tinnitus
