Headache and Facial Pain 2 Flashcards

1
Q

Episodic tension-type headache criteria

A
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2
Q

Tension-type headache clinical findings

A
  • “band-like” head pain without significant accompanying autonomic phenomenology
  • Pain can be described as “constricting” or “nonpulsatile” and may involve the frontal or occipital regions, or commonly the pain is holocephalic
  • The headache episodes may be short- or long-lasting.
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3
Q

Tension-type headache treatment

A
  • Most acute episodic tension-type headaches respond to simple analgesics such as ibuprofen or naproxen.
  • In patients with chronic headaches, the possibility of underlying depression and sources of secondary headaches should be explored.
    Medications including tricyclic antidepressants such as amitriptyline or nortriptyline have shown some benefit in patients with tension-type headaches who also suffer from depression.
    Venlafaxine and mirtazapine also have some efficacy in chronic tension-type headaches.
  • Some headaches may respond to centrally active muscle relaxants such as tizanidine.
  • Physiotherapy, biofeedback, mindfulness, and acupuncture, as well as supraorbital or occipital nerve blocks, appear to be useful in some chronic tension-type headache sufferers.
    Myofascial trigger point injections should also be considered in patients with known tenderness of the neck and shoulder muscles.
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4
Q

Cluster headache: which sex is mostly affected

A

It occurs predominantly in men, with a 4:1 male-to-female ratio

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5
Q

Cluster headache diagnostic criteria

A
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6
Q

Cluster headache hallmark

A

Circadian periodicity

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7
Q

Cluster headache pathogenesis

A

The most widely accepted theory is that primary cluster headache is characterized by hypothalamic activation with secondary activation of the trigeminal-autonomic reflex, probably via a trigeminal-hypothalamic pathway

This finding is not surprising, considering the striking rhythmicity of cluster attacks and the role of the hypothalamus in mediating circadian rhythms

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8
Q

Cluster headache characteristics

A
  • Attacks tend to cluster over time
  • Onset of attacks is more rapid than with migraine, reaching full intensity over minutes, but not seconds.
  • The pain is always unilateral and often affects the same side with recurrent attacks.
  • Drinking alcohol during cluster period nearly always triggers an attack.
  • Unlike migraineurs, who seek dark, quiet environments and prefer to keep still during attacks, patients who experience cluster headaches often pace relentlessly, seeking cold and other distractions.
  • Attacks are commonly nocturnal, rendering sufferers sleep deprived as they awaken patients from sleep.
  • The quality of the pain is described as “boring” and “knifelike.”
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9
Q

Cluster headache acute treatment

A

Symptomatic management of acute attacks includes:

1) administration of inhaled high flow oxygen through a nonrebreather mask (8–12 L/min until the attacks resolve).

2) Injectable sumatriptan, 2–6 mg, is highly effective, but its use is limited to a maximum of 12 mg daily.
Because these attacks are more rapid in onset but shorter in duration than migraines, no other form of sumatriptan or other triptan tends to be effective.

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10
Q

Cluster headache preventive treatment

A

*Patients with frequent and/or longer cluster periods: For patients with chronic cluster headache (ie, continuous headaches or remission intervals of <3 months) and those with episodic cluster headache with relatively long-lasting active periods (ie, four weeks or longer), we use combination therapy.

-We suggest preventive therapy with verapamil rather than other agents.
The starting dose is usually 240 mg daily in three divided doses. Most patients respond to a total dose of 240 to 480 mg daily. Titration to a total dose of up to 960 mg daily may be necessary for some patients to obtain full prophylactic benefit.

-We also suggest a short course of glucocorticoids to provide rapid benefit during the initial titration of verapamil. We use oral prednisone 100 mg once a day for at least three days and then tapering by decreasing the dose 10 mg every third day.
Patients who experience good relief with symptomatic treatment and those with relative contraindications to glucocorticoids may choose to forego such treatment.

*Patients with infrequent and shorter cluster periods – For patients with episodic cluster headache who have active cluster periods that are infrequent and last less than four weeks, we suggest initial preventive therapy with glucocorticoids alone.
We prefer oral prednisone 100 mg once a day for at least three days, followed by a taper with a dose reduction of 10 mg every three days

*Alternative options – We reserve galcanezumab for patients with prior cluster headache periods lasting longer than one month when first-line preventive medications are ineffective, poorly tolerated, or contraindicated.

Alternative medications such as lithium, topiramate, and interventional procedures may be useful for some patients who do not respond to initial preventive therapies.

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11
Q

Chronic paroxysmal hemicrania diagnostic criteria

A
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12
Q

Differences between paroxysmal hemicrania and cluster headache

A
  • Most patients with CPH are female.
  • Attacks are short-lived but frequent, and the headaches respond dramatically to indomethacin
  • Patients may experience a first attack at any age.
  • Positive family histories are not seen.
  • circannual periodicity does not appear to be a feature of CPH
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13
Q

Chronic paroxysmal hemicrania treatment

A

Indomethacin, usually 75–150 mg daily, administered in divided doses.

In patients with gastric ulcers, or in patients where indomethacin is otherwise contraindicated, preventive therapy with verapamil may provide some benefit.

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14
Q

A concerning adverse effect from chronic indomethacin use

A

Peptic ulcer

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15
Q

Hemicrania continua diagnostic criteria

A
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16
Q

Hemicrania continua treatment

A

Indomethacin is usually administered at doses of 75–150 mg/day
(treatment may be life-long)

17
Q

SUNCT diagnostic criteria

A
18
Q

SUNCT acute treatment

A
  • Initial therapy with an intravenous lidocaine infusion.
    Continuous electrocardiogram monitoring is required during intravenous lidocaine administration, along with close observation for adverse effects.
  • For patients unresponsive or unable to tolerate lidocaine, acute treatments used for other trigeminal autonomic cephalalgias, including oxygen, oral and intramuscular indomethacin, and occipital nerve blocks may be tried but have not been consistently effective for SUNCT or SUNA
19
Q

SUNCT preventive treatment

A

For patients with less severe pain during attacks, those with very brief attacks with long (months) interictal intervals, and those with interictal pain between attacks, we treat with a preventive medication.

For most patients with SUNCT or SUNA, we suggest initial preventive therapy with lamotrigine

*For patients who do not respond to or are unable to tolerate lamotrigine, we use an alternative medication such as oxcarbazepine, topiramate, carbamazepine, duloxetine, or gabapentin

*We reserve invasive procedures for patients who do not achieve satisfactory results with acute and preventive oral medications.
Several invasive procedures have been attempted to alleviate SUNCT or SUNA symptoms.
These take the form either of local blockades, surgical procedures involving the trigeminal nerve, or neuromodulatory procedures

20
Q

Which are the trigeminal autonomic cephalalgias?

A
  • cluster headache
  • paroxysmal hemicrania
  • short-lasting unilateral neuralgiform headache attacks (SUNCT + SUNA)
  • hemicrania continua
21
Q

Medication overuse headache diagnostic criteria

A
22
Q

New daily persistent headache diagnostic criteria

A
23
Q

Trigeminal neuralgia diagnostic criteria

A
24
Q

Trigeminal neuralgia pain distribution

A

The pain is usually unilateral and typically involves the second, third, or both of these trigeminal nerve distributions.
Involvement of the first division is exceedingly rare.

25
Q

Trigeminal neuralgia causes

A

Most cases are associated with pathologic processes located at the trigeminal root entry zone, the junction of central and peripheral myelin.
Most commonly, an ectatic vascular loop, often of the superior cerebellar artery, compresses and demyelinates the trigeminal nerve.
Because ectatic loops occur rarely in young patients, cases involving patients younger than 40 years are unusual.
Should a younger person develop trigeminal neuralgia, multiple sclerosis or a neoplasm is a common cause.

26
Q

Trigeminal neuralgia treatment

A

A) Pharmacotherapy:
Carbamazepine or oxcarbazepine, phenytoin, and divalproex are the most commonly employed.
Clonazepam, gabapentin, lamotrigine, and topiramate can also provide relief.
Tizanidine or baclofen, although marketed as centrally acting muscle relaxants, can also be effective in trigeminal neuralgia.

B) Surgical treatment:
In cases refractory to medical management, surgical intervention should be considered.

One approach involves a selective injury of the appropriate trigeminal root; accomplished with a gamma knife, balloon compression, radiofrequency probe, or glycerol.
These procedures almost always cause some degree of numbness and carry the risk of anesthesia dolorosa.

Microvascular decompression of the trigeminal nerve has higher serious risks related to the surgery itself (eg, complications from the craniotomy, injury to other neighboring nerves), but the results are often more satisfactory because there is no numbness and less risk of developing dysesthetic facial pain.
In rare cases involving V1 where the development of corneal anesthesia with these blocking procedures would be problematic, microvascular decompression is always favored in those refractory to medical therapy.

27
Q

Glossopharyngeal neuralgia A) Epidemiology B) Clinical findings C) Diagnosis + DD
D) treatment

A

A)
- it is more prevalent in the elderly
- it is less likely to have a benign origin

B) Sharp, repetitive pains are experienced in the throat, tongue, ear, and tonsillar fossa.
Swallowing commonly triggers these severe paroxysms of pain.
Syncope and even sudden death have been reported.

C) Evaluation of the brain by MRI scan is essential to identify the presence of a vascular loop or neoplasm cross-compressing the glossopharyngeal nerve, evidence of multiple sclerosis, or a malignancy or infection of the peritonsillar region.

D) Is more refractory to treatment than trigeminal neuralgia, although the same medications are used, and surgical procedures include a microvascular decompression of the ninth cranial nerve.

28
Q

Yawning headache 1) primary 2) secondary

A

1) Primary yawning headache consists of retroauricular, submandibular, or facial pain felt exclusively upon yawning

2) patients with temporomandibular joint dysfunction and with trigeminal or glossopharyngeal neuralgia

29
Q

Eagle syndrome 1) Cause 2) Clinical findings 3) Diagnosis 4) Treatment

A

1) The cause is an elongation of the styloid process or calcification of the stylohyoid ligament

2) The pain of Eagle syndrome is experienced in the pharynx and, similar to glossopharyngeal neuralgia, radiates to the ear.
Some individuals complain of a foreign body sensation in the throat.

3) Radiographs of the skull can assist in diagnosing this syndrome, which may be confused with glossopharyngeal neuralgia.

4) Medical management can include anticonvulsants or antidepressants, or local injection of steroids to the area.
In severe cases, surgical management involves styloidectomy

30
Q

Red ear syndrome

A
  • often migraineurs
  • recurrent attacks of unilateral pain in the ear, which becomes red and burns.
  • Attacks tend to be triggered by chewing, drinking, sneezing, or exposure to heat or cold.
  • The treatment is uncertain, but attacks can respond to other migraine therapies.
31
Q

Temporomandibular joint disorder

A
  • frequently accompanies chronic tension-type headache.
  • Pain may reflect either spasm of the temporalis and masseter muscles or primary pathology of the temporomandibular joint, such as rheumatoid arthritis.
  • chewing triggers pain; clicking and pain are experienced over the joints during jaw movement, and reduced or uneven movements occur upon opening the jaw.
  • Muscle relaxants and NSAIDs can be helpful.
    If the syndrome becomes chronic, a dental evaluation is indicated.
32
Q

Primary stabbing headache

A
  • Patients experience a sharp pain in the eye or temple that frequently changes locations.
  • Idiopathic stabbing headache often occurs in migraineurs, primarily women, and sometimes interictally to their migraine attacks.
  • Primary stabbing headaches also often accompany other primary headache syndromes, such as hemicrania continua, SUNCT syndrome, and cluster headache.
  • Other than reassurance, treatment is usually not warranted. Periodic attacks are frequent and troublesome. In that setting, indomethacin or aspirin may be effective.
33
Q

Difference between trigeminal neuralgia and primary stabbing headache

A

The pain differs from that of trigeminal neuralgia because
1) it usually involves the first division of the trigeminal nerve (rare in trigeminal neuralgia) and
2) is not triggered by cutaneous stimuli