Headache is the 4th most common symptom of outpatient visits.

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description

 Pain-sensitive structure ◦ Arteries of the circle of Willis, meningeal arteries ◦ Dural venous sinus ◦ Dura ◦ Scalp, neck muscle ◦ Cervical n. ◦ Mucosa of sinus, teeth

Transcript of Headache is the 4th most common symptom of outpatient visits.

Page 1: Headache is the 4th most common symptom of outpatient visits.
Page 2: Headache is the 4th most common symptom of outpatient visits.

Headache is the 4th most common symptom of outpatient visits

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Pain-sensitive structure◦ Arteries of the circle of Willis, meningeal arteries◦ Dural venous sinus◦ Dura◦ Scalp, neck muscle◦ Cervical n. ◦ Mucosa of sinus, teeth

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Disturbance of pain-sensitive structures◦ Inflammation◦ Traction◦ Compression◦ Malignant infiltration

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Important points in the headache history1.The tempo of onset2. The time of day of onset of maximal pain3. The effect of posture, coughing and straining4. The location of pain5. Any associate symptoms

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Migraine-primary Tension Type-primary Cluster-primary Raised intracranial pressure

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Headache of Raised Intracranial Pressure

•Worse in morning, improve through the day•Associated with morning vomiting•Worse bending forward•Worse with cough and straining•Relieved by analgesia•Dull ache, often mild

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F>M Idiopathic, recurring HA disorder manifesting

in attacks lasting 4 to 72 hrs, develops over minuutes to hours

Typically - Unilateral (may be bilateral), pulsating (progresses from dull ache to pulsating pain), moderate or severe intensity, aggravated by routine physical activity and associated w/ nausea, photo & phonophobia,

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Usually begins in frontotemporal region and radiates to occiput and neck

Alleviated by relaxation in dark room and sleep, Complicated migraine - less common,

neurologic symptoms are more pronounced or disabling◦ Aura symptoms may outlast the migraine

Permanent neurologic sequelae not common with migraine

Subclassified to Aura or No Aura

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Occurs with Migraine about 30% of cases Complex of focal neurologic symptoms

◦ alterations in vision or sensation Usually begin 10 minutes to 1 hr prior to onset of

head pain Light headedness and photophopsia (unformed

flashes of light) Scotoma- Isolated area within the visual field where

vision is absent (30% of cases) Scintillating scotoma- looks like silvery kaliedoscope

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Reassurance Avoidance of trigger factors :

- excessive caffeine intake - smoking - alcohol intake - irregular sleep habits - food containing nitrites (hotdog), monosodium glutamate (Chinese dishes, canned)- chocolate, red wine, fermented items

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Pharmacotherapy Symptomatic treatment

- as early as possible before pain begins - rest in a dark, quiet room with an ice pack on the head

Prophylactic treatment

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Lifetime prevalence of 88% (F) and 69% (M) Highest prevalence in women, age 30-39, with

higher education Dull, persistent HA Bilateral “hatband” distribution Usually NOT debilitating and intensity may

fluctuate throughout the day Usually intermittent, however can have Chronic

TTHA(2% of population), Continuos HA for months or years

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Often occur during or after stress Skeletal muscle overcontraction, depression,

and nausea may accompany HA No prodrome May be associated with depression, repressed

hostility, resentment Patients with recurrent TTHA may not

experience more stressful events than those without TTHA, but may have less effective coping strategies

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Pathophysiology elusive◦ was felt to be caused by excessive muscle

contraction with constriction of pain-sensitive extracranial structures However, no correlation between muscle contraction

and presence of TTHA◦ Vascular reactivity felt to play a role

However, temporal muscle flow is unaltered compared to controls

◦ Platelet 5HT is lower in patient with TTHA some overlap with pathophysiology of migraine

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Promote relaxation Aspirin, acetaminophen, NSAIDsMuscle relaxants,major/minor tranquilizer : ineffective

Prophylactic treatment : amitriptyline 50-150 mg daily , Valproic acid

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Associated with trauma, vascular disorders, Central Nervous System (CNS) infections, HIV, metabolic disorders

>300 disorders can produce HA Watch out for HA especially if

◦ New for patient and Severe in nature, may be sudden onset (Acute HA) or over days to months (subacute HA) may be a sign of destructive cause for HA

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May be symptomatic of ◦ subarachnoid hemorrhage (SAH), stroke, meningitis,

intracranial mass lesion (e.g. brain tumor, hematoma, abscess)

SAH HA - “worst HA of my life”, may also see alteration in mental status and focal neurologic signs

Meningitis HA - usually bilateral, develops over hrs to days, may also see fever, photophobia, positive meningeal signs (Kernigs’s Brudzinski)

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May be symptomatic of ◦ increased intracranial pressure, intracranial mass

lesion, temporal arteritis, sinusitis or trigeminal neuralgia

Trigeminal neuralgia - >40, F>M, characterized by sudden intense pain that recurs paroxysmally, occurs along the second or third division of trigeminal nerve and lasts only moments, triggered by talking, chewing, shaving , etc.

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Brain itself is insensitive to pain HA Pain can be produced by nociceptors

(peripheral pain receptors), injury to CNS or peripheral nervous system, or displacement of pain sensitive structure below

Pain sensitive structures◦ proximal portions of cerebral arteries, large veins,

and venous sinuses ◦ Also may be referred pain from inflammation of

frontal or maxillary sinus or refractive error of the eye

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Issues in older people Headache

•Headache are less common in those aged over 60 years than in younger people•Common causes of Headache which occur in old age, and either rarely or not at all younger patients, include trigeminal neuralgia, temporal arteritis and post –herpetic neuralgia•Migraine and tension headache are much less common than in younger people•Raised intracranial pressure is not always associated with Headache, vomiting or papilloedma•Intracranial mass lesions can often reach larger sizes before presentation as the involutional process that occurs in most ageing brains allows the accommodation of an expanding lesions more easily than in younger patients

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Abortive Therapy◦ relief during an acute attack

Prophylactic Therapy◦ prevent or reduce severity of recurrent HA

Infrequent tension-type HA - just need abortive therapy with OTC analgesics

Migraine and Cluster HA- may need prophylactic therapy ◦ HA that impact patients life despite abortive therapy

(>2xmonth), disabling HA unresponsive to abortive tx, pts in whom abortive agents contraindicated, migraines which are severe in nature

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Abortive◦ Ergot alkaloids (ergotamine& dihydroergotamine)

used to be popular for migraine/cluster HA◦ Triptans (sumatriptan, zolmitriptan, naratriptan,

rizatriptan, almotriptan, frovatriptan, eletriptan) more favored, efficacious and fewer ADR

Prophylactic for migraine◦ Antidepressants (e.g. amitriptyline), Beta blockers (e.g.

propranolol), valproate, calcium channel blockers (e.g. verapamil), NSAIDs

Prophylactic for cluster - verapamil, prednisone, valproate