Headache

Question 1

2 Categories of Headaches

Answer 1

Primary: accounts for 90%
Secondary: identifiable distinct pathological process in which head pain is the presenting symptom

Question 2

3 examples of primary headache

Answer 2

Migraine
Cluster
Tension

Question 3

3 examples of secondary headache

Answer 3

Tumors
Aneurysms
Meningitis

Question 4

Pain may originate from (extra cranial) 4

Answer 4

Skin
Blood vessels
Muscles
Bone

Question 5

Pain may originate from (intracellular) 5

Answer 5

Venous sinuses
Dura at the base of the skull
Dural arteries
Falx cerebri
Large arteries at the base of the brain

Question 6

What 4 structures in the head have no pain fibers?

Answer 6

Brain parenchyma, majority of dura, arachnoid & pia mater have no pain fibers

Question 7

High Risk Exam findings– Ophthalmologic Findings

Answer 7

Papilledema – detected by blurring of optic disks … increased ICP, malignant hypertension
Retinal or subhyaloid hemorrhage – SAH, malignant hypertension
Decline or loss of vision – temporal arteritis, carotid dissection, increased intraocular pressures

Question 8

Evaluation of High Risk patients– neuroimaging

Answer 8

Yield is very low if no high risk historical feature is present
CT & MRI abnormalities present in only 2.4% of patients with normal neuro exam
Non-contrast head CT most helpful in identifying IC lesions or bleed & skull fracture

Question 9

Evaluation of High Risk patients— LP

Answer 9

Should always be performed in patients with suspected SAH in whom CT scan is normal

Patients with SAH may present with minimal symptoms but may decompensate rapidly

Presence of yellowish discoloration of fluid raises concern for SAH

Measure opening pressures of LP if > 200 mmH2O consistent with idiopathic intracranial hypertension & other conditions that may increase ICP such as meningitis

First test for patients with suspected CNS infection, however low risk of herniation leads many providers to get CT first

Question 10

Evaluation of High Risk patients–Labs

Answer 10

May include CBC, lytes, BUN/CR, glucose, ESR, CRP, coags, ABG’s, & carboxyhemoglobin

Question 11

Criteria for low risk patients? (6)

Answer 11

Previous h/o HA
Present with failure to standard therapy regimen & meet the following criteria:
No substantial change in typical HA pattern
No new concerning historical features (seizure, trauma, fever)
No focal neurological symptoms or abnormal neuro findings
No high risk comorbity

Question 12

Treatment of low risk patients?

Answer 12

May be treated with analgesics & antiemetics

No neuroimaging or CSF evaluation is indicated

Question 13

SAH

Answer 13

Subarachnoid Hemorrhage (SAH) presents with abrupt onset of excruciating pain

Question 14

What are SAH caused by?

Answer 14

are caused by ruptured saccular aneurysms, others include trauma, AV malformation/fistula, intracranial arterial dissections, amyloid angiopathy, bleeding diatheses, & illicit drug use

Question 15

Risk Factors of SAH

Answer 15

Most SAH are caused by ruptured aneurysm
Cigarette smoking is the most preventable risk factor for SAH
Hypertension
Alcohol
Genetics – family h/o SAH increases risk
Phenylpropanolamine (appetite suppressant & cold remedies)
Cocaine use
Estrogen deficiency – 54-61% of intracranial aneurysms are found in women
Antithrombotic therapy

Question 16

Carotid Artery Dissection

Answer 16

Cause is multifactorial including blunt or high impact trauma & underlying arteriopathies either alone or in combination

Arteriopathies may be caused by connective tissue disorders, Marfans syndrome, polycystic kidney disease, hypertension, oral contraceptive use, smoking, & respiratory tract infections

Common cause of ischemic stroke in patients < 50 y/o

Question 17

Signs and symptoms of carotid artery dissection?

Answer 17

HA including neck & facial pain that is constant & severe
Amaurosis fugax – transient episodic blindness caused by decreased blood flow to the retina
Ptosis with miosis that is painful (partial Horner Syndrome)
Neck swelling, hematoma or ecchymosis
Pulsatile tinnitus occurs in up to 25% of patients
Decreased taste sensation
Focal weakness

Question 18

Diagnosis of Carotid Artery Dissection?

Answer 18

Helical CT Angiography (CTA) – hallmark sign is change in the caliber of the vessel
MR Angiography (MRA) – used at many Level I Trauma Centers
Bedside ultrasound

Question 19

Vertebral Artery Dissection

Answer 19

Usually a very young person with severe occipital headache & posterior nuchal pain following a recent, relatively minor, head or neck injury
Focal neurologic signs attributable to ischemia of the brainstem or cerebellum develop within 3 days of onset of pain
Most patients only present with the development of neurologic symptoms

Question 20

Signs and Symptoms of Vertebral Artery Dissection

Answer 20

Ipsilateral facial pain & numbness is the most common symptom
Dysarthria or hoarseness (CN IX & X)
Contralateral loss of pain & temperature sensation in the trunk & limbs
Ipsilateral loss of taste
Hiccups
Vertigo
Nausea & vomiting
Diplopia

Question 21

Diagnosis of Vertebral Artery Dissection?

Answer 21

CT Cerebral Angiography
MRI/MRA identify vessel disturbances
Duplex Ultrasonography

Question 22

Treatment for HTN emergency

Answer 22

Oral agents are indicated if the BP is > 180/110
Diltiazem 10 mg po
Lisinopril 10 mg po
Hydrochlorathiazide 25 mg po
Nitropaste 1 inch (may give the patient a headache)

Discharge on antihypertensive or continue with current regimen if already on meds

Follow up within 72 hours

Return to the ED if symptoms worsen

Question 23

Labs and Imaging for HTN

Answer 23

Toxicology, pregnancy test
CBC, BUN, SCr
UA

Question 24

Management of HTN

Answer 24

Primary goal is to determine which patients are exhibiting signs of end organ damage & require IV meds
Acutely lowering BP with IV meds in the ED in patients with no signs of end organ damage is controversial
Treatment goal is the immediate reduction of mean arterial pressure (MAP)

Question 25

Acute angle closure glaucoma

Answer 25

Usually in elderly with no h/o glaucoma
Presents with periorbital pain & visual deficits
Pain is boring in nature & associated with an ipsilateral headache
Patients describe blurred vision with halos around objects
On exam visual deficts include inability to read eye chart & only able to see hand movements
Cornea is cloudy obscuring fundoscopic exam
Intraoccular pressure (IOP) is increased (normal 10-20 mmHg)
Eye pain on movement
Mid-dilated non-reactive pupil & a firm globe

Question 26

Treatment of Acute angle glaucoma

Answer 26

Goal is to decrease IOP
Have the patient lie in a flat supine position
Avoid eye patches or masks
Timoptic 0.5% 1 drop
Pred Forte 1% 1 drop every 15 minutes x 4 doses then hourly
Acetazolamide 500 mg IV or po (IV preferred because of associated nausea)
Mannitol 1-2 g/kg IV as adjunct to reduce IOP
Recheck IOP hourly
Pilocarpine 1% or 2% 1 drop 4 times daily to constrict pupil when IOP < 40 mmHg
STAT Opthamology consult

Question 27

Giant Cell Arteritis

Answer 27

Also known as Temporal Arteritis
Systemic inflammatory, vascular syndrome that affects the temporal arteries
Commonly associated with polymyalgia rheumatica.
Occurs almost exclusively in patients > 50 y/o
HA is the most common symptom & is severe & throbbing usually located in the frontotemporal region
Temporal artery may be non-pulsatile, tender to palpation, or have a diminished pulse.
Most serious complication is loss of vision due to optic neuritis

Question 28

Diagnosis of Giant Cell Arteritis

Answer 28

Must fulfill at least 3 of 5 criteria
Age > 50 y/o
New onset localized HA
Tenderness over temporal artery or decreased pulse
ESR > 50
Abnormal arterial biopsy findings

Question 29

Treatment of Giant Cell Arteritis

Answer 29

In order to prevent loss of vision treatment should begin immediately with 40-60 mg of Prednisone daily when dx is suspected
Prompt referral to rheumatology

Question 30

Meningitis

Answer 30

Inflammation of the meninges due to virus, bacteria, other microorganisms, or certain drugs
Can be life threatening due to the proximity to the brain & spinal cord
Most common symptoms are headache, fever, altered mental status, nausea, vomiting, & photophobia
Nuchal rigidity, Kernig sign (neck pain with knee extension) & Brudzinski sign ( involuntary LE flexion elicited with passive neck flexion) are only helpful if positive

Question 31

Diagnosis and Labs for MEningitis

Answer 31

LP is the gold standard for diagnosis & should be performed whenever meningitis is suspected
CBC, electrolytes, BUN, creatinine, glucose, blood & urine cultures should be obtained prior to the LP
CSF from LP should be obtained for culture & sensitivity, protein & glucose levels, cell count & gram stain
CSF leukocytosis with a predominance of PMN’s, protein > 100 mg/mL, & glucose level < 50 % are considered a positive LP for bacterial meningitis
Aseptic meningitis is more common & refers to meningeal inflammation with a negative LP

Question 32

Treatment for Meningitis

Answer 32

Empirical antibiotic therapy directed at the suspected pathogen should be initiated empirically
S. pneumoniae & N. meningitidis are the most common
IV steroid therapy is helpful to decrease neurological complications due to Hib if given before or with IV antibiotics
Cefotaxime or Ceftriaxone 1-2 g IV daily along with Vancomycin 1g IV is the standard for initial treatment for patients with normal creatinine levels, otherwise dosing is based on creatinine clearance
IV fluids & oxygen supplementation to maintain hydration & O2 sat levels > 95% are standard
Admission with isolation
All close contacts & medical personnel caring for the patient should be treated prophylactically as well

Question 33

Migraine H/A

Answer 33

Common with onset usually in teens
Females > Males
HA is generally slow in onset & lasts 4 – 72 hours
Typically unilateral & pulsating, worsens with activity
Nausea, vomiting, photophobia, & phonophobia frequently accompany the HA
May or may not be preceded by an aura prior to the onset of HA
Certain triggers may cause the HA
Suspicion for other more serious causes should be suspected when HA is worse or different than usual

Question 34

Treatment for Migraines

Answer 34

Pain relief in primary headaches includes:
NSAID’s – Ketorolac 15 - 30 mg IV with
Antiemetics – Onadesteron, Prochlorphenazine, Metoclopramide
Pretreatment with Diphenhydramine 12.5 mg IV for akathisia & dystonic reactions
If unresponsive to treatment combination Dihydroergotamine (DHE) 1 mg IV may be effective

Question 35

Tension H/A

Answer 35

Usually bilateral, not worsened by activity, & not associated with nausea or vomiting
Treatment is usually with NSAIDs &/or mild analgesics
Muscle relaxants may be helpful – Flexeril, Soma
In severe cases treatment is similar to migraine
May also be caused by cervical spine abnormalities

Question 36

Cluster H/A

Answer 36

Rare
More common in men
Onset is usually after 20 y/o
Dysfunction of the trigeminal nerve is believed to be the cause
Characterized by severe unilateral orbital, supraorbital, or temporal pain lasting 15-180 minutes
Pain is such that the patient cannot lie still & most are pacing & restless
Associated with at least one of the following on the ipsilateral side: conjunctival injection, lacrimination, nasal congestion, rhinorrhea, facial swelling, miosis, or ptosis
Tend to occur in clusters ie. Multiple daily HA on the same side of the face for several weeks before remitting for weeks to years

Question 37

Treatment for Cluster H/A

Answer 37

High flow O2 is effective treatment in up to 70% of patients
DHE & Sumatriptan IV/IM have also been shown to be rapidly effective
Narcotics may be indicated in severe cases
Oral agents are usually ineffective due to the long time for absorption
NSAIDs may be effective in reducing the frequency & severity of future attacks
Referral to neurology for further management is indicated for recurrent episodes