71. Headache

**TABLE 71-1** Danger signals in headache
From Reddy MJ: Headache. In Rakel RE, editor: *Saunders manual of medical practice,* Philadelphia, 1996, WB Saunders, with permission.© WB Saunders1996
Danger signal	Possible cause
Headache during exertion/straining	Increased intracranial pressure
Headache during exertion/straining	Leaking berry aneurysm
Headache with fever	Encephalitis
Headache with fever	Meningitis
Headache when neck is not perfectly supple	Encephalitis
Headache when neck is not perfectly supple	Meningitis
Headache in a drowsy, confused patient	Increased intracranial pressure (ICP) (encephalitis, meningitis, metabolic)
Headache with abnormal examination (pupil size, fundus, extraocular movement reactivity, facial asymmetry, reflexes)	Subdural
Headache in a patient who looks ill	Critical causes

J. Critical causes of acute headache (Table 71-2)

**TABLE 71-2** Critical causes of acute headache
From Reddy MJ: Headache. In Rakel RE, editor: *Saunders manual of medical practice,* Philadelphia, 1996, WB Saunders, with permission.© WB Saunders1996
Cause	Adverse outcomes	Signs	Diagnostic tests
Acute angle-closure glaucoma	Blindness	Ocular hypertension Dilated pupils Eye pain	Ocular hypertension Cup-to-disk ratio in fundus
Acute sinusitis	Intracranial extension	Fever, toxic, sinus tenderness	Sinus radiographs CT scan
Central nervous system mass lesion: tumor, abscess	Mortality, neurologic deficits	Papilledema, mental status change	CT scan/MRI
Cerebrovascular accident	Mortality, neurologic deficits	Neurologic signs	Clinical or radiologic
HIV	Increased morbidity	HIV risks, opportunistic infections: cryptosporidiosis, cytomegalovirus, toxoplasmosis	HIV test Lumbar puncture CT/MRI
Malignant hypertension	End-organ damage	Papilledema Elevated blood pressure (systolic over 210, diastolic over 120 mm Hg)	Vital signs Funduscopy Urinalysis micro Electrocardiogram Cardiologic examination
Meningitis	Increased morbidity and mortality	Nuchal rigidity, fever, Kernig’s and Brudzinsky’s signs	Lumbar puncture Rapid antibiotic therapy
Pheochromocytoma	End-organ damage	Classic presentation	CT scan of adrenals, urinary metanephrines
Subarachnoid hemorrhage	Mortality, neurologic deficits	Worst ever	CT scan Lumbar puncture
Temporal arteritis	Blindness	Tenderness, temporal area	Sedimentation rate (over 50)
		Patient older than age 50	Temporal arteritis biopsy, at least
		Signs of polymyalgia	5 cm required
Toxic exposure		Confusion Nausea	See env/occ chart

K. Management of subarachnoid hemorrhage (Table 71-3)

**TABLE 71-3** Summary of subarachnoid hemorrhage
From Keiser MM: Neurologic disorders. In Gawlinski A, Hamwi D, editors: *Acute care nurse practitioner: clinical curriculum and certification review,* Philadelphia, 1999, WB Saunders, with permission.© WB Saunders1999
aPTT, Activated partial thromboplastin time; BUN, blood urea nitrogen; CBC, complete blood count; CT, computed tomography; OTC, over-the-counter; PT, prothrombin time; SAH, subarachnoid hemorrhage; SBP, systolic blood pressure.
Origin	Craniocerebral trauma
	Cerebral aneurysm rupture
	Cerebral arteriovenous malformation
	Clotting abnormalities
Signs and symptoms	“Worst headache of my life” with sudden onset, no precipitating factors, no relief with OTC analgesia
	Altered consciousness
	Mental status changes
	Stiff neck
	Nausea and vomiting
	Photophobia
	Seizures
	Cranial nerve abnormalities
	Motor or sensory deficits
Diagnosis	If you suspect SAH, first obtain a CT scan of the brain. If negative, a lumbar puncture must be performed to look for the presence of blood
	Routine serum blood work includes CBC, BUN, creatinine, glucose, electrolytes, PT, and aPTT
	Upon diagnosis of SAH and in the absence of cranial trauma, a cerebral angiogram is required to ascertain the source of the bleeding
Treatment	The goals of treatment are to prevent rebleeding along with secondary complications (most commonly, hydrocephalus and cerebral vasospasm)
	“Triple H therapy” to prevent vasospasm: ▪ Hypertension to SBP =150 ▪ Hemodilution to hematocrit 31 to 33 ml/dl ▪ Hypervolemia, which aids in maintaining blood pressure and hematocrit in desired ranges
	Routine medications include the following: ▪ Colace, 100 mg PO twice daily ▪ Codeine, 30-60 mg subcutaneously every 4 hours as needed ▪ Nimodipine (Nimotop), 60 mg PO every 4 hours for 21 days ▪ Phenobarbital, 30-60 mg PO or subcutaneously every 6 hours as needed for sedation ▪ Dilantin, 100 mg PO 3 times a day (although use of anticonvulsants as seizure prophylaxis is controversial)
	SAH precautions include the following: ▪ Dimly lit, quiet, private room ▪ No stress, and limited visitors ▪ Complete bed rest ▪ Avoidance of Valsalva maneuver

L. International Headache Society Classification of Headaches (Table 71-4)

**TABLE 71-4** The International Classification of Headache Disorders (ICHD-II)
Data from International Headache Society: The International Classification of Headache Disorders, second edition, *Cephalalgia* 24(suppl 1):2004, Oxford, UK, 2004, Blackwell Publishing, with permission.© Blackwell Publishing2004
Primary code	Headache type
1	Migraine
2	Tension-type headache (TTH)
3	Cluster headache and other trigeminal autonomic cephalalgias
4	Other primary headaches
5	Headache attributed to head or neck trauma
6	Headache attributed to cranial or cervical vascular disorder
7	Headache attributed to nonvascular intracranial disorder
8	Headache attributed to a substance or its withdrawal
9	Headache attributed to infection
10	Headache attributed to disorder of homeostasis
11	Headache or facial pain attributed to disorder of cranium, neck, eyes, ears, nose, sinuses, teeth, mouth, or other facial or cranial structures
12	Headache attributed to psychiatric disorder
13	Cranial neuralgias and central causes of facial pain
14	Other headache, cranial neuralgia, central or primary facial pain

III. Subjective findings

A. Obtain the individual’s headache attack profile

1. Prodromal symptoms (preceding the headache)

2. Time of peak severity of symptoms

3. Duration of symptoms

4. Precipitating factors

5. Associated symptoms

6. Alleviating symptoms

7. Review of history that predisposes to QT-interval prolongation:

a. History of unexplained syncopal episodes

b. Structural heart disease on a variety of cardioactive medications

c. Renal or liver disease–related altered drug clearance

B. Obtain the history of prior headaches.

1. Variables (as in the headache attack profile)

2. Family history of headaches or sudden death in family members

3. Correlation or relationship of headaches to particular events/activities

C. See Table 71-5 for comparison of major headache syndrome characteristics

**TABLE 71-5** Characteristics of major headache syndromes
From Lehne RA: *Pharmacology for nursing care,* ed 5, St. Louis, 2004, Elsevier Saunders, with permission.© Elsevier Saunders2004
	Migraine	Cluster headache	Tension headache
^*Headaches occur in clusters that typically consist of one or more headaches, lasting 15 minutes to 2 hours every day for 2 to 3 months, with a headache-free interval (months to years) between each cluster.
^†Chronic tension headaches occur at least 15 days/month for 6 months or longer.
Pain location	Unilateral (60%)	Unilateral	Bilateral
	Bilateral (40%)	Behind the right or left eye	“Head band” configuration
Pain quality	Throbbing	Throbbing Sometimes piercing	Nonthrobbing
Pain severity	Moderate to severe	Severe	Mild to moderate
Duration	4 hours to 3 days	15 minutes to 2 hours^*	30 minutes to 7 days^†
Impact of activity	Worsens pain	None	None
Associated symptoms	Nausea, vomiting, photophobia, phonophobia	Conjunctival redness, lacrimation, nasal congestion, rhinorrhea, ptosis, miosis—all on the same side as the headache	Uncommon
Usual time of onset	Early morning	Nighttime	Daytime
Preceded by aura	Yes, in 30%	No	No
Triggers	Many; see Table 71-10	Usually unidentified	Tension, anxiety
Gender prevalence	More common in females (3:1)	More common in males (5:1)	Slightly (10%) more common in females
Family history	Likely	Unlikely	Unlikely
Impact on daily life	Often substantial	Usually substantial	Minimal