HEADACHE TOOLS
HANDOUT
DIAGNOSIS : International Headache Society Criteria (u sed loosely)
PRIMARY HEADACHE: No other pathological cause
Tend to be paroxysmal, episodic, and nonprogressive with recovery
in between
Positive family history, especially for migraine
MIGRAINE: Five similar attacks lasting 4 – 72 hours with the following:
2 of 4 :
1 of 2 :
Unilateral
Photo and Phonophobia
Throbbing
Nausea / Vomiting
Mod / Severe
Worsens with activity
Note 5 stages: Prodrome, Aura, Pain/HA, Resolution, Postdrome
CLUSTER: Flurries of daily headaches for 2 – 8 weeks with the following features:
Unilateral / periorbital
And > 1 of these ipsilateral autonomic features:
Non-throbbing
Miosis
Ptosis
Severe / excruciating
Lacrimation Conjuctival
erythema
Clockwork periodicity
Rhinorrhea Congestion
TENSION-TYPE: Five similar attacks lasting up to 7 days with the following tendencies:
Bilateral
Nonthrobbing
Moderate severity
Does not interfere with daily activities
CHRONIC DAILY HEADACHE
Often arises from a background of episodic migraine
Overly frequent analgesic use is often contributory
SECONDARY HEADACHE:
ACUTE
CHRONIC
First / Worst headache of my life
Insidious onset but never fully recovering
Sudden “thunderclap” onset
Side-locked / stereotypical
location
Meningismus
Progressively worsening
History of trauma
Weight loss
BOTH
Evidence of focal neurologic, behavioral or cognitive deficit
Evidence of systemic illness (fever)
Papilledema
TREATMENT OF HEADACHE
NONPHARMACOLOGIC
EDUCATION
| Migraine
pathophysiology : Genetically hypersensitive nervous system ( à not weakness of character) prone to episodic “overload” ( à triggers) leading to reversible impairment of neuronal function ( à prodrome, aura, and other associated symptoms) and inflammation of meninges and cranial vessels ( à pain) via the trigeminal nerve through neurotransmitters (such as serotonin) |
| Cluster pathophysiology
: Less well known. Now there is evidence of genetic link Hypothalamic association explains periodicity ( à relaxation, sleep) Trigeminal / sphenopalatine association explains pain, autonomic features |
| Tension-type headache
pathophysiology : Also not as well known. Decreased ability to release nerve-firing in certain tests of muscular activity. Clinically the episodic variety is not usually significant. |
| Chronic Daily
Headache Discuss “rebound” as a function of brain's “pain control mechanism” becoming dependent on exogenous analgesics, having to “relearn” how to control pain. Meanwhile, withdrawal headache occurs. “You have to get sick first to get better”. Scientific explanation: downregulation of neurotransmitter (opiate and other) receptors takes time to upregulate / normalize. |
| **Important to remember this is the case for many (perhaps ~50%) but not all. For the rest, pathophysiology is unclear why the brain loses the ability to modulate sensory input and it becomes painful. |
STRESS MANAGEMENT
Biofeedback and Autogenics
Cognitive psychotherapy
LIFESTYLE CHANGES
Avoidance of triggers
Diet, exercise, sleep hygiene
PHYSICAL MEASURES
Physical therapy, chiropractic, massage, ice
Acupuncture, others
Most
probably work by “calming down” a hypersensitive nervous system via various
mechanisms, |