Chapter 39 Tension-Type Headache, Chronic Tension-Type Headache, and Other Headache Flashcards

KEY POINTS 1. Chronic tension-type headaches are frequently caused by analgesic overuse, that is, using analgesic medication 10 or more times per month. 2. Prophylactic medication usually does not work in the setting of analgesic overuse headache. 3. “Sinus headaches” are rarely that; they usually represent analgesic overuse or parasympathetic symptoms of a milder migraine. 4. Sleep-disordered breathing can cause headaches, particularly in patients whose sleep architecture is disrupted or s

1
Q

The pain of a TTH

A

duller, less intense, and less
localized than that of a migraine or a cluster attack. The
pain usually lasts several hours to a day, but it may continue
for days or weeks.

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2
Q

During a severe TTH patients can experience

A

photophobia, phonophobia, nausea, and occasionally
emesis. Pain referred to the neck is common; patients
also frequently complain of “a knot in the neck,” but the
neurologic examination should be normal.

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3
Q

major variants of TTH

A

those with disorder of the
pericranial muscles, those without disorder of the pericranial muscles, and chronic TTH (CTTH) (with or without disorder of the pericranial muscles).

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4
Q

Those with disorder of
the pericranial muscles are characterized by

A

tenderness on palpation of those muscles, increased activity on electromyography
(EMG), or both

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5
Q

CTTH, previously
called chronic daily headache, is diagnosed

A

in a patient with a headache frequency of 15 days per month or 180 headaches per year averaged over a 6-month period.

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6
Q

If patient require analgesics

A

It stands to reason that patients should be advised against using analgesics more than twice per week over a prolonged period of time. If they require analgesics at least twice per week, they should be offered
a prophylactic regimen.

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7
Q

In adolescents (age 12 to 14 at the time of diagnosis), the
cause and prognosis of CDH

A

Many of these children seem to have personal or
family history of migraine.

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8
Q

The mainstay of treatment for MOH

A

total withdrawal
from analgesics for a period of time not shorter than
2 months.

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9
Q

The initial several
days to 2 weeks following analgesic withdrawal might be
the most difficult and are frequently punctuated with

A

a severe rebound headache; antiemetics and maintaining
hydration, as well as patience, are effective

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10
Q

characteristic of patients with MOH is that drugs
administered with prophylactic intent tend

A

to not work unless analgesics are discontinued. Patients whose MOH is typified by the regular use of narcotics or barbiturates may require a controlled tapering off of the drugs as well as management of potential withdrawal symptoms

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11
Q

temporal arteritis

A

should be
considered in an elderly patient with a persistent headache of recent onset whether or not other typical elements are present in the history and physical examination.

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12
Q

temporal arteritis diagnosis and treatment

A

In these
patients an erythrocyte sedimentation rate (ESR) or a
sensitive C-reactive protein (s-CRP) should be ordered
immediately, and consideration should be given to treatment
with a corticosteroid and to a temporal artery biopsy

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13
Q

Idiopathic intracranial hypertension (previously
called pseudotumor cerebri) usually presents

A

in overweight young women with chronic headaches, a normal examination, a normal scan, and papillede —although a subset of these patients do not have papilledema. The diagnosis is made when a lumbar puncture reveals an otherwise normal fluid under high pressure (at least 20 to 25 cm H2O).

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14
Q

The muscle contraction
theory of TTH

A

relates pain to prolonged contraction, or spasm, of cervical or pericranial muscles

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15
Q

Most patients with a headache,
migrainous or TTH, have

A

pericranial muscle tenderness
or sore spots;

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16
Q

Cervical pain can be referred to the head from

A

intervertebral discs, interspinous ligaments, zygapophyseal joints, the periosteum, paracervical muscles, carotid and vertebral arteries, and from irritation of the C1, C2, and C3 nerve roots.

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17
Q

The dorsal rami of the first three cervical nerve roots supply the sensory innervation to the

A

neck and
to the scalp caudal to the innervation of the trigeminal
nerve, and to the meninges and arteries of the posterior
fossa.

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18
Q

Headache also can arise from pathology in the area
of the foramen magnum examples

A

Chiari I malformation, the Dandy-Walker syndrome, atlantoaxial dislocation (e.g., from rheumatoid arthritis), Paget’s disease of the bone, and basilar invagination.

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19
Q

Abortive Treatment Strategies

A

For the occasional TTH, an over-the-counter (OTC)
analgesic preparation is all that is required.

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20
Q

OTC analgesic preparations

A

Several OTC
analgesic preparations involve combinations of drugs
(e.g., aspirin plus acetaminophen) and may contain caffeine.
Caffeine combined with analgesics such as aspirin,
acetaminophen, and ibuprofen enhances their analgesic
effectiveness.

21
Q

Stronger headaches may require an analgesic

A

(aspirin, acetaminophen, or ibuprofen) in combination
with either codeine or butalbital.

22
Q

If aspirin or acetaminophen, with or without codeine,
butalbital, or caffeine, is ineffective in controlling the
headache, the choice of an alternative analgesic should
proceed

A

in an orderly fashion by testing in turn members
of different NSAID chemical categories at adequate doses. Indomethacin is reported to be more effective than
alternative NSAIDs for pain of cephalic origin; it is particularly
effective in treating hemicrania

23
Q

The major chemical
categories of NSAIDs include

A
  • Carboxylic acids—includes aspirin, which is an acetylated
    acid, as well as salsalate and choline magnesium trisalicylate, which are nonacetylated
  • Propionic acids—ibuprofen, naproxen, ketoprofen, and
    fenoprofen
  • Aryl and heterocyclic acids—indomethacin, diclofenac,
    sulindac, and tolmetin
  • Fenamic acids—mefenamic acid and meclofenamate
  • Enolic acids—piroxicam and phenylbutazone
  • Pyrrolo-pyrrole—ketorolac
  • Cyclooxygenase 2 (COX-2) inhibitors—celecoxib
24
Q

Prophylactic Treatment Strategies

A

Antidepressants, particularly amitriptyline or nortriptylene
at a starting dose of 10 to 25 mg at bedtime, are
active prophylactic drugs.16 Most patients who respond to
tricyclic antidepressants (amitriptyline, nortriptyline,
imipramine, or desipramine) usually do so at doses of 25 to
200 mg at bedtime;

25
Q

How does Tricyclics help?

A

induce sleep, which may constitute
one of the mechanisms by which they help.

26
Q

The major side effects from tricyclics relate to

A

their anticholinergic effects
and include a dry mouth, excessive daytime sleepiness, dizziness,
urinary retention, glaucoma, cardiac arrhythmias,and photosensitization; they can also cause weight gain.

27
Q

The specific serotonin reuptake inhibitors (SSRIs) and
specific serotonin-norepinephrine reuptake inhibitors

A

(SNRIs) might be tried in patients who do not respond or who develop intolerable side effects from tricyclic drugs.

28
Q

The major side effects of the SSRIs and SNRIs include

A

jitteriness, tremors, gastrointestinal distress, decreased libido,
and occasionally headaches

29
Q

SSRIs and SNRIs are relatively contraindicated in patients who

A

use triptans, as they may suffer from excessive serotonin stimulation (serotonin syndrome).

30
Q

Beta-blockers,

A

propranolol, metoprolol, atenolol, timolol, and nadolol, can be tried and sometimes prove effective. In most healthy people, 60 to 80 mg once per day of a long-acting propranolol preparation can be started and the dosage can be adjusted as necessary.

31
Q

Beta-blockers Side effects

A

dizziness from bradycardia or hypotension, fatigue,
depression, worsening of symptoms in patients with
asthma or chronic obstructive pulmonary disease, gastrointestinal distress, blunting of hypoglycemic symptoms in patients with diabetes, and vivid dreams.

32
Q

Anticonvulsants

A

valproic acid (Depakote and
Depakote ER) are sometimes worth a try to prophylax
against frequent TTH. The usual starting dose for
Depakote ER is 500 mg/day; the dose should be adjusted
as necessary at 2- to 6-week intervals.

33
Q

Valproic acid can cause

A

weight gain, hair
loss, tremor, and abdominal distress.

34
Q

botulinum toxin A

A

injection into the most tender pericranial muscle(s) or directly
into a trigger point

35
Q

“sinus headaches

A

Most patients complain of
periorbital pain and might also experience a sensation of nasal stuffiness.

36
Q

True sinus pain occurs when

A

the ability of the sinus to drain is impaired by an acute blockage of the osteum (e.g., following an upper respiratory infection or for some anatomic reason), a bacterial infection takes hold, the mucosa becomes inflamed, and pressure builds in the sinus.

37
Q

true sinus or nasal inflammation can be a trigger for

A

migraine.

38
Q

Habitual snoring is increasingly being recognized as
a cause of

A

chronic daily headache

39
Q

Sleep-disordered
breathing such as that caused by sleep apnea may precipitate
headaches from

A

the resultant hypoxemia and
hypercapnia (which causes cerebral vasodilation)

40
Q

Hypnic headaches

A

represent another
syndrome of recurring head pain that awakens patients
from REM sleep. This headache
responds best to treatment with either indomethacin
or lithium.

41
Q

Post-traumatic headache

A

occurs frequently following
mild to moderate closed head injury or a whiplash injury
(rapid flexion and extension trauma of the neck); loss of
consciousness need not have occurred

42
Q

Post-traumatic headache symptoms

A

include pain in the neck or
shoulders, dizziness, cognitive complaints, and disturbances
of sleep, mood, and/or personality. The syndrome
should begin within 2 weeks of the injury; it is considered
acute if it lasts 8 weeks or less and chronic if it lasts longer,
although this distinction is arbitrary

43
Q

Post-traumatic headache Etiology

A

reflect underlying brain injury relating to the trauma and
also injury to the head, face, jaw, and neck

44
Q

Post-traumatic headache treatment

A

treated in accord with the general principles mentioned
above but with additional consideration being given to
addition of physical therapy and to identification and
treatment of a possible contributing occipital nerve neuralgia.

45
Q

occipital neuralgia (also called “cervicogenic” headache)

A

can arise from injury around the area of the C2–C3 zygapophyseal joint, which is common in whiplash;
the pain, paresthesiae, or dysesthesiae usually are
referred to the occipital scalp. On examination, the nerve
is tender to palpation or percussion along the course of
the dorsal ramus of C2, particularly around the cranial
insertion of the trapezius muscle, lateral to the occipital protuberance.

46
Q

occipital neuralgia treatment

A

is a nerve
block with or without adding a drug useful in the treatment
of neuropathic pain such as gabapentin.

47
Q

Trauma can also result in a chronic cerebrospinal fluid
(CSF) leak with consequent CSF hypotension and a
chronic low-pressure headache.

A

This headache, usually
associated with an opening CSF pressure of 90 mm
of water or less, typically manifests when the patient
assumes a sitting or standing position and improves
when the patient lies down. Most post-traumatic leaks
arise around the cervico-thoracic junction.

48
Q

chronic low-pressure headache. treatment

A

Treatment is similar to that of a postlumbar puncture (post-LP)
headache.