Cluster Headache
台北榮總神經內科 傅中玲醫師
Cluster
headaches are among the most painful of all headaches. The signature
is a pattern of periodic cycles of headache attacks, which may be one
of the following: Episodic (occurring regularly for weeks to months,
followed by long pain-free periods), or Chronic (occurring without
sustained breaks).
Cluster
symptoms tend to occur during spring, autumn or both and they most
often occur at night. Over half of cluster headache patients
experience warning symptoms, long before an attack. They are called prodromal, or premonitory, symptoms. They include the
following: strange tingling sensations around the eye, nose, or neck,
nasal congestion or runny nose, excessive tearing, feeling restless or
depressed. When the actual attack occurs, symptoms typically escalate
rapidly (within about 15 minutes) to intense levels. The pain is
typically described as severe, stabbing or boring. It is virtually
always on one side, although it may occur on the opposite side in
other attacks or even within the same attack. Pain does not worsen
with movement (as it often does with migraine headaches). Other
symptoms include the following: excessive tearing, feelings of intense
restlessness and agitation, facial sweating, and nausea.
Headache attacks tend to occur
with great regularity at the same time of day. About 75% occur between
9 at night and 10 in the morning. Peaks have also been reported
between 1 PM and 3 PM. A single cluster attack is usually brief but
extremely painful, lasting about one to three hours. During an active
cycle, sufferers can experience these attacks as infrequently as one
every other day to several attacks a day. Cycles of such daily or near
daily attacks typically occur over the course of a week to a
year--most often in spring and autumn. Usually a patient has one or
two cycles per year that each last one to three months.
Evidence now strongly suggests
that abnormalities in the hypothalamus, a complex structure
located deep in the brain, may play a major role in cluster headaches.
Advanced imaging techniques have revealed that a specific area in the
hypothalamus is asymmetrical in these patients and is activated during
a cluster headache attack. The most important nervous cluster is the suprachiasmatic nuclei (SCN), which appears to help coordinate
the body's activities (sleep/wake) with the environment (dark/light).
Some studies support the idea that some failure in this biologic
pacemaker may impair the pain control system and cause these terrible
attacks.
Lifestyle factors, including
smoking, alcohol abuse, and stress (in particular stressful work
situations), appear to play a very strong role in this headache.
Alcohol, in fact, can trigger an attack. A particularly high
association exists between smoking and cluster headaches. Quitting
smoking, however, is not associated with any fewer or less severe
attacks.
The most effective treatments
for a cluster attack are the following: oxygen inhalation and triptan
drugs (injections of sumatriptan). Relief can occur in five to 10
minutes. Prevention of attacks during a cluster cycle is extremely
important. The following are the most commonly used preventive agents:
calcium-channel blockers (most often used for preventing cluster
headaches), corticosteroids, lithium and antiepileptic medications.
Surgical intervention may
be considered for patients with chronic cluster headaches that do not
respond to treatments at all or when they have not gone into remission
for at least a year. To date, surgery has limited success and can have
distressing side effects. Deep brain electrical stimulation is showing
promise, however.
Pathophysiology of Tension-type Headache
新光醫院神經科 陳威宏醫師
Tension type headache (TTH) is the most frequent
primary headache, with a lifetime prevalence of 74% in general
population. Despite its tremendous socioeconomic impact in modern
society little is known about the underlying pathophysiology and
treatment. For decades, it has been debated if the pain in TTH
originates from myofascial tissues or from central mechanisms in the
brain. The increased tenderness in TTH represents the activation of
peripheral nociceptors. Decreased pain, thermal and electrical
thresholds have been reported in chronic TTH patients, which probably
represents a central misinterpretation of the incoming signals. Nitric
oxide (NO) might play a role in the pathophysiology of chronic TTH. It
has been demonstrated that NO synthetase inhibitor reduces headache
and muscle hardness, whereas the NO donor glycerol trinitrate causes
headache in patients with chronic TTH. Myofascial factors and
peripheral sensitization of nociceptors play an important role in the
episodic form, and central sensitization has been demonstrated in the
chronic form. As chronic tension-type headache usually evolves from
the episodic form, prevention and reversal of this central
sensitization may be an important target for future pathophysiological
studies and drug development.
Nonpharmacologic Treatments for Primary Chronic Headache
高雄長庚神經內科 李連輝醫師
As the mechanisms of chronic headache are so
complicated with multiple factors. Edogeneous and exogeneous factors,
environmental and genetic predisportions. So the treatment of chronic
headache need to be multyiplicity: acute and prophylactic with
pharmacologic and nonpharmacologic treatments.
I. Classification
and causes of primary chronic hedacahe
II. Pathogenesis of chronic headache(multiple factors)
III.Treatments of Chronic headache: 1)Acute treatment
2) Prophylactics treatments 3) Pharmacologic treatments 4)
Nonpharmacologic treatments
IV.Nonpharmacologic
treamnents:
1. Migraine:
1) Common
provacational triggers for migraine
2) Evidence-
based guideline of nonpharmacologic treatments in migraine
2. Tension
headache:
1) Conventional
nonpharmacologic treatments: Psychologic, physical treatments
2) Unconventional
nonpharmacologic treatments: Local therapy, manipulation of the neck,
acupuncture, hypnosis, others
V. Demonstration
of nonpharmacologic treatments(digital)
1) Biofeedback 2)
Relaxation 3) Walking 4) Jogging 5) Taichi chikon(with tree)
VI. Strategy of
chronic headache treatments in future
1) Pharmacoliogic and nonpharnacologic treatments
2) Team work for
treat chronic headache patients
3) Research
Migrainous Infarction
台北榮總神經內科 國立陽明大學醫學院醫學系神經科 王署君醫師
The diagnosis of migrainous infarction is based on the
association of the abrupt onset of a neurologic deficit during a
migraine attack with evidence of cerebral infarction on neuroimaging.
Other causes of stroke must be excluded. Strict criteria for the
diagnosis of migrainous infarction must be applied because migraine is
common and patients with migraine may suffer from other causes of
stroke. The diagnosis of migrainous infarction should be made only
when patients with an established history of migraine suffer a
cerebral infarction during a typical migraine attack (Rothrock et al
1988).
The diagnostic criteria of migrainous infarction were
just revised by the International Classification of Headache
Disorders, second edition, as follows (coded as 1.5.4): (1) the
present attack in a patient with 1.2 migraine with aura is typical of
previous attacks except that 1 or more aura symptoms persists for more
than 60 minutes; (2) neuroimaging demonstrates ischemic infarction in
a relevant area; (3) the headache is not attributable to another
disorder (Headache Classification Subcommittee of the International
Headache Society, 2004).
The exact cause of migrainous infarction is still not
certain. Based on studies using cerebral angiography during attacks,
the most important underlying mechanism for the stroke is believed to
be carotid or vertebral arterial spasm resulting in a critical degree
of cerebral hypoperfusion (Featherstone 1986; Rothrock et al 1988;
Sanin and Mathew 1993). However, this may not always be true, so other
factors should be considered. The incidence of migrainous infarction
is rare, according to the strict diagnosis proposed by International
Headache Society. Henrich and colleagues reported that the incidence
rate of first migrainous infarction was 3.36 per 100,000 per year (Henrich
et al 1986). However, in the absence of other stroke risk factors,
this estimate was reduced to 1.44 per 100,000 people per year. In a
recent study of the Barcelona Stroke Registry, Arboix and colleagues
reported that the group of patients with migrainous infarction
accounted for only 0.6% of all first-ever acute strokes, 0.8% of
ischemic strokes, 12.8% of ischemic strokes of unusual etiology, and
13.7% of ischemic strokes in young adults 45 years of age or younger (Arboix
et al 2003). Because distinct diagnostic criteria are lacking,
migrainous infarction should be considered a diagnosis by exclusion.
The diagnosis demands a well established history of
migraine and exclusion of other conditions that cause stroke. Computed
tomography, MRI (including diffusion-weighted image,
perfusion-weighted image, magnetic resonance spectroscopy, and MRA),
cerebral arteriography, transcranial Doppler evaluations, and
transesophageal echocardiography evaluations should be performed when
possible. Lumbar puncture and blood studies to help exclude vasculitis
should also be carried out. Prophylactic treatment of migrainous
infarction in patients with prolonged aura includes platelet
antiaggregants or calcium channel blockers. Aspirin administration
should be considered as a prophylactic treatment against migrainous
infarction. Patients who have anticardiolipin syndrome may need
anticoagulants. Calcium channel blockers are recommended for patients
at risk for migrainous infarction. Nimodipine reduces cerebral
vasoconstriction, and several studies have demonstrated the potential
effectiveness of calcium channel blockers in the prophylactic
treatment of migraine headaches (Meyer 1985).Ergotamine, triptans, and
serotonergic medications may initiate or worsen intracranial vasospasm
and dysautoregulation in patients with migrainous infarction. These
drugs should be withheld in patients with prolonged aura. Peripheral
beta-blockers, such as propranolol, should also be withheld, since
they may worsen intracranial vasoconstriction.
In general, the long-term prognosis in patients with
migrainous infarction is good. Milhaud and colleagues, in a
prospective stroke registry, found that the outcome at 1 month was
favorable in more than 70% of migraineurs with ischemic stroke (Milhaud
et al 2001). Arboix and colleagues reported the mean length of
hospital stay of 9 consecutive patients with migrainous infarction was
9.75±6.2 days. No patients died during hospital stay, and 67% were
symptom-free at discharge (Arboix et al 2003).
Cases Demonstration
活水神經內科診所 王博仁醫師
The classification and diagnostic criteria of Migraine with aura, Persistent aura without infarction and Migrainous infarction have some changes in ICHD-II. There are 6
subforms of Migraine with aura. The identification of the
symptom of motor weakness is the first step in their differentiation.
The past history of Migraine with aura is essential in
diagnosis of Persistent aura without infarction and Migrainous infarction. Similar aura, but lasting more than one
week, is mandatory in Persistent aura without infarction. On
the other hand, when the similar aura symptom persisted more than 60
minutes with a relevant positive finding in neuroimaging, then we can
therefore consider the diagnosis of Migrainous infarction. Clinical cases were demonstrated for the audience to practice these
criteria. |