248 Headaches
peripheral vascular abnormalities once thought to be the key
causal factor, research has shown that biochemical imbal-
ances, neurotransmitter/receptor dysfunction, and neuronal
suppression play pivotal roles as well (Olesen & Goadsby,
2000).
Tension-type headache has received a number of labels
over the years (muscle contraction headache, psychogenic
headache, depression headache, stress headache, conversion
headache, psychomyogenic headache, and the like), which
re”ect the varied views and confusion about its etiology. The
IHS classi“cation committee proposed a four -group scheme
to help investigators and clinicians sort out the role of various
causative factors. Tension-type sufferers are now grouped
on the basis of chronicity (episodic versus chronic), as this
has been found to have a direct bearing on outcome, and the
presence of identi“able muscle involvement (evidence of
pericranial muscle tenderness upon palpation or elevated
electromyographic readings versus the absence of this
evidence), as the role of muscle contraction in this headache
type has been questioned, resulting in a 2 2 classi“cation
table. This more expanded coding format asks diagnosticians
to identify the most likely causative factors by specifying
whether one or more of the following factors are present:
oromandibular dysfunction, psychosocial stress, anxiety,
depression, delusion, muscular stress, drug overuse, or other
headache condition. Unfortunately, researchers have rarely
used this level of precision when investigating pathophysiol-
ogy of tension-type headache so progress has been slow at
partialing out the role of the numerous suspected causes.
A new diagnostic entity that had not been formally recog-
nized previously concerns •headaches associated with sub-
stances or their withdrawal.Ž Although it had long been
suspected that two types of medication commonly prescribed
for headache patients, namely analgesics and ergotamine
preparations, could lead to •reboundŽ headaches if overused
(Horton & Macy, 1946), it was not until the 1980s that
researchers began to take serious note of this fact (Kudrow,
1982; Saper, 1987). The term reboundrefers both to the
gradual worsening of the headache as the medication wears
off and the extreme exacerbation that often accompanies
abrupt discontinuation of the medication (withdrawal-like
phenomenon). This sequence •seducesŽ patients into taking
ever-increasing amounts of medication, establishing a
vicious cycle (Saper, 1987).
Kudrow (1982) “rst described this condition for tension-
type headache patients. He noted that such patients gradually
take increasing amounts of analgesics, which subsequently
increase pain symptomatology and then renders the headache
refractory to treatments that formerly would have been of
bene“t. Kudrow conducted one of the few empirical tests of
this concept by assigning analgesic abusers to one of four
conditions. Patients were either withdrawn from or allowed
to continue analgesics and simultaneously were assigned
either to placebo or amitriptyline (the most commonly pre-
scribed prophylactic drug for this form of headache at that
time). He found that mere withdrawal from analgesics led to
measurable improvement (approximately 40%), withdrawal
combined with a proven medication led to the greatest
improvement (nearly 75%), and, perhaps most importantly,
that allowing patients to continue analgesics at an abusively
high level markedly interfered with the effectiveness of the
medication (effectiveness was reduced by approximately
two-thirds, or from 72% to 30%). More recent research has
con“rmed these “ndings regarding medication overuse and
its interference potential (Blanchard, Taylor, & Dentinger,
1992; Mathew, Kurman, & Perez, 1990; Michultka,
Blanchard, Appelbaum, Jaccard, & Dentinger, 1989).
Clinicians working with headache patients need to be fa-
miliar with criteria for medication abuse, to inquire carefully
about current and past medication consumption, and to
arrange, in close collaboration with a physician, a medica-
tion reduction/detoxi“cation plan for patients suspected of
experiencing medication rebound headache. Ergotamine
withdrawal can be especially dif“cult to accomplish on an
outpatient basis and may require a brief hospital stay. Saper
(1987) reports that within 72 hours of ergotamine withdrawal
patients may experience their most intense headache, which
may last up to 72 hours (often necessitating a 6 to 7 day hos-
pital stay). Saper believes that dosage days per week are the
more critical variable in determining if ergotamine is being
abused. He suggests that any patient consuming ergotamine
on more than two days per week should be considered as a
candidate for medication withdrawal (when taking ergota-
mine three or more days per week, signi“cant enough
amounts remain in the body to perpetuate the problem). More
recent criteria for diagnosing drug-induced headache give
primary emphasis to days of consumption, rather than quan-
tity of consumption (Diener & Wilkinson, 1988). Lake
(2001) identi“es a number of behavioral patterns to look for
that are suggestive of drug misuse and abuse.
Patients often “nd it dif “cult to discontinue the of fending
medications. Kudrow (1982) required his patients to with-
draw abruptly on their own and encountered high rates of
dropout in the process. Regular therapist contact and support,
concurrent provision of appropriate prophylactic medication
as necessary, and beginning instruction in behavioral coping
skills may help patients to be more successful in completing
a needed medication washout period (Worz, 1983). Grazzi
et al. (2001) found it necessary to hospitalize a group of re-
fractory drug-induced headache patients in order to withdraw