Transcript Headache and Facial Pain

Headache
&
Facial Pain
Headache & Facial Pain:
Definition;
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Headache: Pain in the head: From the orbit back to the
sub-occipital region.
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Facial pain: Pain elsewhere in the face.
Mechanism; Traction or distention of pain sensitive structures
Headache & Facial Pain:
Pain sensitive structures
1. Dura of skull base
2. Cerebral arteries
3. Venous sinuses
4. Nerves
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Cranial nerves; 5, 9, 10
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Cervical nerves; C2,3
Background
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Headache is the 4th most common symptom of outpatient
visits
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99% of women and 93% of men have had headache during
their lifetime
12.6 % prevalence (18% women, 6.5% men)
Prevalence is highest between age 25 – 55 years
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25% of women and 8% of men have had migraine
headache
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Approximately 50% remain undiagnosed
Headaches: Pathophysiology
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Where does the pain arise
from?
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Blood vessels
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Scalp
Dura mater
Blood vessels
Cervical & cranial nerves
Dilate
Become congested  Pain
Headache Classification
IHS Classification
Primary Headaches
( The headache is the disease )
Benign Headache disorders
 Migraine (with or without aura)
 Tension-type headaches
 Cluster headaches
 Drug rebound headaches-Medication overuse headache
 Chronic daily headache
Secondary Headaches
Headaches that are symptoms of organic disease
Characters of Primary Headache
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Benign, Recurrent
NOT associated with underlying pathology
The headache is the disease
Recurrent attacks
Symptoms free between the attacks
Clinical syndromes
Normal physical examination
No organic causes
Exception: drug-abuse headache
Diagnosis is based on exclusion
Characters of Secondary Headache
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Sudden, progressive Course
Symptoms persist
Pain select to anatomical lesions
Physical examination usually abnormal
Associated with pathology
May require immediate action
Secondary Headache
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Aneurysms, AVMs
and SAH
Thunderclap
Headache
Meningitis
Stroke
SOL
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Trigeminal Neuralgia
Temporal Arteritis
Hypertension
Benign Intracranial
Hypertension
Lumbar Puncture
Headache
Sinus Headache
Secondary Headache
Warning Signs and Signals
 Sudden
 Onset
onset
after age 50 years
 Systemic
signs (fever, myalgias, weight loss)
 Systemic
disease (Malignancy, AIDS)
 Change
in headache pattern
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Progressive headache with loss of headache-free periods
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Change in frequency or severity
 Neurologic
symptoms or abnormal physical findings
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Cognitive changes
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Asymetry
Clues for Secondary Headache
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Focal neurological deficits
Slowly progressive course
Sudden severe headache
Appearance at old age
Systemic manifestation
Secondary Headache Paracranial Structure
Areas responsible for pain: Sinus, Eye, Dental, Ear,
Skull and base of skull, Vascular, Soft tissue of
head and neck
 Character of headache
1. Small focal area of refered pain
2. Localized tenderness
3. Local symptoms of the affected organ
4. Persistent pain
Three Types of HA Onsets
Acute
1)
Time: onset w/I – 2 Days ( 3 dys max )
Intensity: severe
Examples
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Subacute
2)
Time: onset wks-mnths, may be an acute presentation
Intensity: not as severe
Examples
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3)
Chronic/Recurrent
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Time: onset usually years
Intensity: varied
Examples
History of Presenting Complaint
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How recent in onset?
Abrupt onset?
How frequent?
Episodic or constant?
How long lasting?
Intensity of pain?
Quality of pain?
Site of pain?
Radiation?
Eye pain?
Aura?
Photophobia?
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Phonophobia?
Associated vomiting?
Diurnal variation?
Snoring?
Neck stiffness?
Trigger factors?
Aggravating factors?
Relieving factors?
Family history?
What does the patient do
during headache?
What medication used?
Physical Examination
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Fever?
Pulse/BP
Neck stiffness?
Purpuric rash?
Pupils?
Neurologic exam
GCS score
Scalp tenderness?
Examine eardrum
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Thickened temporal
arteries?
Fundoscopy –
papilloedema?
Sinus tenderness?
Cervical
tenderness/ROM?
Obese?
Facial plethora?
Localization & Characterization of HA
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Location: Unilateral or Bilateral
Characteristics
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Pulsating, Tightness, Dull & Steady, Sharp/Lancinating, Ice
Pick
Associated Symptoms
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Weight Loss
Fever/Chills
Dyspnea
Visual Disturbances
Nausea/Vomiting
Photophobia
Location of pain
Forehead : Primary > Secondary
 Occipital area : Primary > Secondary
 Face : Secondary > Primary
 Neck : primary = Secondary
 Unilateral pain:
- Large area intracranial structure ( Diffuse )
- Meningeal pain
- Increased intracranial pressure
- Low intracranial pressure
- Toxic vascular headache
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In Summary….
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To what extend should each patient be evaluated?
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Absolute clinical indications
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Worst headache ever
Onset associated with exertion
Depressed cognition or neurologic deficit on exam
Nuchal signs
Deterioration during observation
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Conservative approach acceptable in patients
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Lack the above findings with normal VS
Improvement during observation
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Investigations
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FBC
ESR
Capillary blood glucose
Plasma Alkaline phosphatase
Arterial blood gas
Skull radiograph
Cervical spine radiographs
CT Brain
Lumbar puncture
CSF manometry
MR angiogram
Temporal artery biopsy
Sinus radiographs
Sleep studies
Differential Diagnosis
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Tension headache
Cluster headache
Trauma
Vascular
Migraine
Subarachnoid haemorrhage
Arteriovenous malformation
Subdural haematoma
Hypertensive encephalopathy
Temporal arteritis
Skull disease
Sinusitis
Skull fracture
Mastoiditis
Paget’s disease of bone
Acute mountain sickness
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Medications
Nitrates
Sildenafil
OCP
Metabolic
Sepsis
CO2 retention
Hypoxia
Obstructive sleep apnoea
Hypoglycaemia
Alcohol withdrawal
Raised intracranial pressure
Cerebral tumour
Meningitis
Otitis media
Acute angle-closure glaucoma
Hyperviscosity
Tension-Type Headache
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Most common headache syndrome
Episodic < 15 days per month
Chronic > 15 days per month (2% of population)
Lifetime prevalence of 88% (F) and 69% (M)
Highest prevalence in women, age 30-39, with
higher education
TTH - Characteristics
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30 minutes to 7 days
Dull, persistent HA ( Pressing or tightening )
Mild to moderate pain (Usually NOT debilitating
and intensity may fluctuate throughout the day )
Variable location, often bilateral
Nausea and vomiting rare
TTH - Characteristics
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Often occur during or after stress
Skeletal muscle overcontraction, depression, and
nausea may accompany HA
No prodrome
May be associated with depression, repressed
hostility, resentment
Patients with recurrent TTHA may not experience
more stressful events than those without TTHA, but
may have less effective coping strategies
TTH - Treatment
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Stress management
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Biofeedback
Stress reduction
Posture correction
Medication rarely needed
in ETTH
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Benzodiazepines
amitriptyline
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CTTH
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Abortive
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NSAIDs
ASA-caffeine-butalbital
Phenacetin
Preventative
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Antidepressants
Muscle relaxants
NSAIDs
Migraine
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17% of females, 6% of males ( F > M )
Moderate to severe pain
Unilateral, pulsating
4 to 72 hours
Typically - Unilateral (may be bilateral), pulsating
(progresses from dull ache to pulsating pain)
Moderate or severe intensity, aggravated by routine physical
activity and associated w/ nausea, photo & phonophobia
Subclassified to Aura or No Aura
Aura
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Occurs with Migraine about 30% of cases
Complex of focal neurologic symptoms
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alterations in vision or sensation
Usually begin 10 minutes to 1 hr prior to onset of
head pain
Light headedness and photophopsia (unformed
flashes of light)
Scotoma- Isolated area within the visual field where
vision is absent (30% of cases)
Scintillating scotoma- looks like silvery kaliedoscope
Migraines - Causation
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Sterile inflammation of
intracranial vessels trigeminovascular system
Serotonin (5hydroxytryptamine)
receptors
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Triggering factors
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Stress
Menses
OCP
Infection
Trauma
Vasodilators
Aged cheeses
Migraine - Treatment
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Abortive
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5-hydroxytryptamine
receptor agonists
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Imitrex
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Oral, SQ, nasal spray
Maxalt
Zomig
Amerge
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Ergotamine
Butorphanol
Midrin
NSAIDs
Lidocaine
Migraine - Treatment
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Symptomatic
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Prochlorperazine
Dihydroergotamine
Chlorpromazine
Haloperidol
Lorazepam
BOTOX?
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Preventative
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Antidepressants
Bellergal (ergotamine)
NSAIDs
-blockers
Calcium channel blockers
Cluster Headache
Cluster Headaches (HA)
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M>F (5:1), usually 20-40 years old
Recurrent HA separated by periods of remission (months
to yrs)
During the “cluster”time -HA occur >1/day
Unilateral, occurs behind eye, reaches MAX intensity over
few minutes, lasts for <3hrs
Unilateral lacrimation, rhinorrhea, and facial flushing may
accompany cluster
HA is commonly precipitated by alcohol, stress, missed
meals and vasodilating drugs - (Avoid during cluster period)
No Aura
Cluster Headache
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Intensely severe pain
Unilateral
Periorbital
15 to 180 minutes
Nausea and vomiting
uncommon
No aura
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Alcohol intolerance
Male predominance
Autonomic hyperactivity
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Conjunctival injection
Lacrimation
Nasal congestion
Ptosis
Cluster Headache
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Episodic
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Two episodes per year to
one every two or more
years 7 days to a year
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Chronic
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Remission phases less
than 14 days
Prolonged remission
absent for > one year
Cluster Headache - Treatment
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Preventative
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Calcium channel blockers
Bellergal
Lithium
Methysergide
Steroids
Valproate
Antihistamines
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Abortive
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Oxygen
5-HT receptor agonists
Intranasal lidocaine
Chronic Headaches
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Analgesic/Caffeine Withdrawal Headaches
Associated with intake of high doses of caffeine
and/or analgesics
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Pathophysiology
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Serum level drop
Clinical Presentation
Constant
 Atypical
 Afternoon
 Hx key
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Chronic Daily Headache
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6 days a week for 6 months
Bilateral, frontal or occipital
Non-throbbing
Moderately severe
Due to overuse of analgesics
? Transformation of migraine or TTH
CDH - Treatment
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Patient understanding
Remove causative medication
Avoid substitution
Antidepressants
Adjuvant therapy
Treatment of withdrawal
Acute Headache (HA)
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May be symptomatic of
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Subarachnoid hemorrhage (SAH), stroke, Meningitis,
Intracranial mass lesion (e.g. brain tumor, hematoma,
abscess)
SAH headache - “worst HA of my life”, may also
see alteration in mental status and focal neurologic
signs
Meningitis HA - usually bilateral, develops over hrs
to days, may also see fever, photophobia, positive
meningeal signs (Kernigs’s Brudzinski)
Headaches of Acute Onset
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Subarachnoid Hemorrhage (SAH)
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Background
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Aneurysms & AVM’s
Clinical Presentation
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Signs & Symptoms
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Lab Findings
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CT & Lumbar Puncture
Complications
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NEW, Sudden onset, LOC frequent, Vomiting & stiff neck
Reoccurnance doubles mortality rate
Prognosis
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20% DOA
25% die from initial bleed; 20% from reoccurance
Survival
Clinical Features of SAH
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Sudden “thunderclap”
headache
Can be associated with
exertional activities
Nausea/vomitng-75%
Neck stiffness-25%
Seizures-10%
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Meningismus-50%
Subhyloid or retinal
hemorrhages
Oculomotor nerve pulsy
with dilated pupil
Restlessness and altered
level of consciousness
Headaches of Acute Onset
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Infectious Headaches
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Background
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Meningitis and Encephalitis
Clinical Presentation
Classic: HA, Fever, Stiff Neck, & Altered Level of Consciousness
 S/S can vary depending on age
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Neonate, Children & Adults, Adults, Older generation
Headache Presentation
Diagnosis & Management:
CSF analysis
 Neurologist
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Intracranial Infection
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HA is common complaint in Meningitis
meningitis, brain abscess,
encephalitis or AIDS
Encephalitis
Diagnostic tools include CT
of head and LP
Severe HA, nuchal
rigidity, meningismus
HA, confusion, fever,
change of mental
status, seizures
Brain
Abscess
HA, vomiting, focal
neurological signs,
depressed level of
consciousness
AIDS
Toxoplasmosis, CMV,
Cryptococcus
Headaches of Acute Onset
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Headaches Following Lumbar Puncture
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Background
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Low Pressure Headache
MC is lumbar puncture
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Headache Presentation
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Clinical Pearl:
Worse with sitting or standing
Vertex or occipital, pulling, steady
Usually resolve spontaneously (Blood patch for resistant cases )
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The more severe the HA, the more frequent it is assoc. w/ vertigo,
nausea/vomiting, & tinnitus
The longer the pt is upright, the longer it takes for the HA to subside
Headaches of Acute Onset
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Coital Headaches
Three Types: Types I, II, III
 Clinical Presentation
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Type I:
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Type II: AKA Vascular or Explosive
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Occurs @ orgasm
Severe, throbbing, frontal or occipital, min-hrs
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Clinical Pearl
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Occurs as sexual excitement inc
Dull ache, Occipital or Diffuse, Sever @ orgasm
Type III:
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Occurs after coitus resembling a low pressure HA
Subacute Headache (HA)
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May be symptomatic of
Increased intracranial pressure
 Intracranial mass lesion
 Temporal arteritis
 Sinusitis or
 Trigeminal neuralgia
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Temporal Arteritis = Giant Cell Arteritis
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Classic presentation is a 50 plus year old female with
unilateral HA that is causing unilateral visual disturbance.
Intensity is moderate to severe and will be insidious in onset.
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Moderate to severe, unilateral pain
Patients over 65
Tortuous scalp vessels
ESR elevated
Biopsy for definitive diagnosis
Treat with steroids
Untreated complicated by vision loss
 Other findings:
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Jaw claudication
Bruits over temporal artery
Blindness
May be accompanied by polymyalgia rheumatica.
Trigeminal Neuralgia= Tic Douloureux
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Paroxysmal pain – seconds to < 2 min
Distributed along 5th cranial nerve ( V2 & V3 )
Asymptomatic between attacks
Trigger points ( triggered by talking, chewing,
shaving)
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Intense burning
Face may distort = tic
>40, F>M,
Characterized by sudden intense pain that
recurs paroxysmally, occurs along the second
or third division of trigeminal nerve and lasts
only moments,
Trigeminal Neuralgia - Treatment
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Carbamazepine
Gabapentin
Baclofen
Phenytoin
Valproate
Chlorphenesin
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Adjuvant
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TCAs
NSAIDs
Surgery for refractory
cases
Herpes zoster Facial pain
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Herpetic eruption in territory of nerve in distribution of
nerve (10 – 15% the trigeminal ganglion and 80% the
ophthalmic division)
Geniculate ganglion causes eruption in the EAM.
Upper cervical nerve roots affects soft palate.
Pain precedes herpetic eruption by <7 days
Pain resolves within 3 months
Postherpetic Neuralgia
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Neuralgia of the trigeminal nerve following herpes infection.
Most commonly affects V1 as well as V2 & V3
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This is the KEY difference between post-herpetic and trigeminal neuralgia.
Post-Herpetic Neuralgia
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Persistent neuritic pain for > 2 months after
acute eruption
Treatment
Anticonvulsants
 TCAs
 Baclofen
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Glossopharyngeal Neuralgia
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Severe (Unilateral pain )
Transient stabbing pain in the ear, base of tongue,
tonsillar fossa, or beneath the angle of the jaw.
(auricular and pharyngeal branches of the vagus
nerve and glossopharyngeal nerve)
Evoked by swallowing, talking, or coughing
Treatment as for Trigeminal Neuralgia
Occipital Neuralgia
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Paroxysmal jabbing pain in the distribution of the
greater and lesser occipital nerves or the third occipital
nerve
Sometimes diminished sensation
Pain is eased by local anaesthetic block
Must be distinguished from occipital referral of pain
from the atlantoaxial or upper zygoapophyseal joint or
trigger points in suboccipital muscles
Posttraumatic Headache(PTHA)
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Estimated that 30-50% of 2
million closed head injuries
per year develop headache.
Associated with dizziness,
fatigue, insomnia, irritability,
memory loss, and difficulty
with concentration.
Acute PTHA develops hours
to days after injury and may
last up to 8 weeks.
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Chronic PTHA may last
from several months to years.
Patients have normal
neurological examination and
imaging
Treatment for acute PTHA is
symptomatic while for
chronic PTHA, adjunct
therapies include betablockers and antidepressants.
Atypical Facial Pain
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Diagnosis of exclusion
? Psychogenic facial pain
Location and description inconsistent
Women, 30 – 50 years old
Usually accompanies psychiatric diagnosis
Treat with antidepressants
Temporomandibular Disorders
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Symptoms
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Temporal headache
Earache
Facial pain
Trismus
Joint noise
60% spontaneous
Tenderness to palpation
Pain with movement
Audible click
Degenerative Joint Disease
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Pain with joint movement
Crepitus over joint
Flattened condyle
Osteophyte formation
Myofascial Pain
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Most common 60% - 70%
Muscle pain dominates
Tenderness to palpation of masticatory muscles
TMD - Treatment
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NSAIDs
Physical therapy
Biofeedback
Trigger point injection
Benzodiazepines
TCAs or SSRIs for chronic muscle pain
Pseudotumor Cerebri
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Intermittent headache
Variable intensity
Normal exam except papilledema
Normal imaging
CSF pressures > 200 cm H2O
Pseudotumor Cerebri - Associated History
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Mastoid or ear infection
Menstrual irregularity
Steroid exposure
Retro-orbital or vertex
headache
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Vision fluctuation
Unilateral or bilateral
tinnitus
Constriction of visual
fields
Weight gain
Idiopathic Intracranial
Hypertension(IIP)
Treatment
-Stop offending med
-Lower CSF production with
acetazolomide and
furosemide.
-Steroids
-Repeat LPs
-Ventricular shunt if with
impending visual loss.
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Diagnostic Criteria for IIP
Increased intracranial
pressure(>200mmHg) measured by
lumbar puncture
Signs and symptoms of increased
ICP, without localizing signs
No mass lesions or hydrocephalus
on imaging
Normal or low CSF protein
No clinical or neuroimaging suspicion
of venous sinus thrombosis
Mass Lesion - Brain Tumor
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Children - 75% Infratentorial
Adults - 75% Supratentorial
Metastatic tumor most common mid-life
Symptoms due to increased intracerebral pressure, tissue
destruction, irritation
Depends on growth rate and location
Headache ( 30 % ) - steady, non-throbbing, dull, worse in
AM. May be intermittent initially.
Headache worse with bending over, Valsalva maneuvers
Hx of IV drug abuse - abscess
Subdural Hematoma
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History of trauma
Fluctuating level of consciousness
Pain lateralized
Tenderness to percussion over hematoma
Trauma may be remote in chronic SDH
Hypertension
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Usually with diastolic pressures > 115 mm Hg
Throbbing
Nausea
Sinus Headache
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Acute sinusitis accepted
Chronic sinusitis controversial
Constant, dull, aching
Worsened with stooping or leaning forward
Referred pain possible
“ RED FLAG “ Headaches
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Headache with altered mental status
Headache with focal neurological findings
Headache with papillidema
Headache with meningeal signs
The “worst headache of life”
Headache in the patient with AIDS
Conclusion
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Headache & facial pain are common complaints
History most important in making accurate
diagnosis
Recognize psychological aspects of pain