HEENT Week 1 Flashcards
GENERAL APPROACH TO PATIENT
- History
- Physical Exam
- Laboratory (as indicated)
- Imaging/Procedure (as indicated)
- Referral (as indicated)
What is the approximate percentage of HEAD TRAUMA results in mortality?
What types of damage do we see and what general Sx may appear?
~ 50% with severe injury (more deaths & disability than other neuro cause in >50 yo)
- Damage to nerve tissue, blood vessels and meninges can result in neural disruption,
ischemia, hemorrhage and edema
Open head injuries: (emergency)
Piercing of the skull, direct trauma e.g. GSW (gun shot wound)
–> direct effects from the tissue damage and shock waves
Closed head injuries (emergency or urgency)
Eg. acceleration-deceleration injury (whiplash)- local injury and opposite side of skull
“contra-coup injury”
- severity based on:
i) loss of consciousness or not
ii) presence or absence of neurologic signs
Questions appropriate for History Taking in the case of Head pain.
- Full history with presentation of head pain
- Accompanying symptoms (eg. eye, ears, cranial nerves, neurologic, GI, temperature, etc)
- History of head injury?
- Follow-up Q: Any loss of consciousness?
- Lesions, tumors, scalp hair loss, rashes?
Physical Exam for Head Pain.
- Observation: ex. cranial size → hormonal issues
- Vitals: height and weight every time (weight: chronic disease, particular with wasting; kids, elderly; height: kids, elderly)
- Palpation of head and scalp: lesions, masses, tenderness; On infants, examine fontanelles
- Full exam of Ears, Eyes, Nose, Sinus, Throat, Neck
- Appropriate neurological exams (CN, peripheral, orientation, cognitive) *Review of cranial nerves 1-12
Laboratory for Head Pain
as indicated.
examples: ESR, CRP, CBC, CMP
Imaging/Procedure for Head Pain
(as indicated) – mass, bleeding, ruptured layers or blood vessel
- MRI (vasculature)
- CT (gen structures)
- angiography
- lumbar puncture
- CSF analysis
Referral for Head Pain
as indicated
Emergency, Neurology, Dermatology
What is the approximate mortality percentage for Head Trauma with severe injury? What type of damage does it cause?
Mortality ~ 50% with severe injury (more deaths & disability than other neuro cause in >50 yo)
–> Damage to nerve tissue, blood vessels and meninges can result in neural disruption, ischemia, hemorrhage and edema
Categories of Head Injury
Open Head Injury
Closed Head Injury
Migraine HA
- Sex
- Age of Onset
- Location
- Pain Intensity
- Pain Quality
Sex: 1:3 M:F Age: before 30 Location: unilateral Intensity: Moderate - Severe Pain Quality: Pulsating
Migraine HA
- Triggers
- Frequency
- Duration
- Concomitants:
Triggers: stress, food, disrupted homeostasis
Frequency: 2-6/mo
Duration: 4-72 hours
Concomitants: nausea, vomiting, photophobia, aura
Tension HA
- Sex
- Age of Onset
- Location
- Pain Intensity
- Pain Quality
- Sex: 1:2 M:F
- Age of Onset: anyone
- Location: bilateral, occiput
- Pain Intensity: mild to moderate
- Pain Quality: tightening, steady
Tension HA
- Triggers
- Frequency
- Duration
- Concomitants:
- Triggers: mental stress, eye strain, posture
- Frequency: -
- Duration: variable
- Concomitants: pericranial tenderness
Cluster HA
- Sex
- Age of Onset
- Location
- Pain Intensity
- Pain Quality
- Sex: 4.3:1::M:F
- Age of Onset: 30 for men, later for women
- Location: unilateral, temple V1 V2
- Pain Intensity: severe
- Pain Quality: boring, searing
Cluster HA
- Triggers
- Frequency
- Duration
- Concomitants
- Triggers: season, cigarettes
- Frequency: 1-3 per day
- Duration: 30 min-3hr
- Concomitants: miosis, eyelid edema, conjuctival injection, congestion, lacrimation, ptosis, facial swelling, rhinorrhea
Trigeminal Neuralgia
- Sex
- Age of Onset
- Location
- Pain Intensity
- Pain Quality
- Sex: 1:1.5::M:F
- Age of Onset: after 40 yrs, few pediatric
- Location: Unilateral, V3
- Pain Intensity: severe
- Pain Quality: lightning, burning
Trigeminal Neuralgia
- Triggers
- Frequency
- Duration
- Concomitants
- Triggers: movement or contact, unique per person
- Frequency: -
- Duration: 1-120 seconds
- Concomitants: increased risk of suicide
Hemicrania continua
- Sex: 1:2 M:F
- Age of Onset: -
- Location: Unilateral, V1 V2
- Pain Intensity: moderate with spikes
- Pain Quality: jabbing
Hemicrania Continua
- Triggers
- Frequency
- Duration
- Concomitants
- Triggers: unknown
- Frequency: daily for >3mo
- Duration: Daily or continuous
- Concomitants: conjectival injection, lacrimation, congestion, rhinorrhea, ptosis, miosis Indomethacin is effective treatment
SUNCT Syndrome
- Sex
- Age of Onset
- Location
- Pain Intensity
- Pain Quality
- Sex: Rare
- Age of Onset: -
- Location: unilateral Orbital, periobital, temporal
- Pain Intensity: unilateral Orbital, periobital, temporal
- Pain Quality:severe
SUNCT Stymdrome:
- Triggers
- Frequency
- Duration
- Concomitants
- Standout Features
- Triggers: touching the area: the face, bathing, washing/brushing hair, shaving, chewing, coughing
- Frequency: 3-200 a day
- Duration: 5-240 sec, 1-2 bouts a year
- Concomitants: Automonic symptoms;
- Standout Features: High frequency per day
Medication overuse HA
- Sex
- Age of Onset
- Location
- Pain Intensity
- Pain Quality
- Sex: 1:5::M:F
- Age of Onset: 30-40 with hx of HA
- Location: -
- Pain Intensity: like migraine or tension
- Pain Quality
Medication overuse HA
- Triggers
- Frequency
- Duration
- Concomitants
- Standout Features
- Triggers: overusing analgesic
- Frequency: HA>15day/mo
- Duration: -
- Concomitants: Worse upon waking, with exercise. N/V, cramps, other GI distress, anxiety, restlessness, sweating, sleep problems
- Standout Features: HA worse than before overusing anagesic, overuse> 3mo.
Dietary Related HA
COME BACK
HA from inflammation in skull
- Sex
- Age of Onset
- Location
- Pain Intensity
- Pain Quality
- Sex: -
- Age of Onset: often young
- Location: generalized, worst in occiput
- Pain Intensity: very severe
- Pain Quality: Throbbing
HA from inflammation in skull
- Triggers
- Frequency
- Duration
- Concomitants
- Standout Features
- Triggers: -
- Frequency: 1x
- Duration:
- Concomitants: Triad: Nuchal rigidity, change in mental status, fever.
- Standout Features: Rash on legs; Kernig’s and brudzinski’s sign positive
HTN HA
Concomitants
Standout Features
Concomitants: epistaxis, bruits in carotids
Standout Features: Sudden severe increase in BP
Intracranial hypertension
- Pain Intensity
- Pain Quality
- Triggers
- Duration
- Standout Feature
- Pain Intensity: mild, but becomes worse
- Pain Quality: deep, aching
- Triggers: posture change, laying down
- Duration: up to 3 hours
- Standout Feature: Worse upon laying, abrupt posture change
Intracranial hypotension
- Age of Onset
- Triggers
- Stand Out Features
- Age of Onset: after lumbar pucture or dural tear
- Triggers : Sitting upright
- Stand Out Features: Better laying down than sitting upright
Giant cell (temporal) arteritis
- Sex
- Age of Onset
- Location
- Pain Intensity
- Pain Quality
- Sex
- Age of Onset: 72 yo
- Location: temporal, occipital, orfFrontal-occipital
- Pain Intensity: variable
- Pain Quality: not throbbing
Giant cell (temporal) arteritis
- Triggers
- Concomitants
- Standout Features
- Triggers: aging, heavy smoking, northern European
- Concomitants: fever, anorexia, weight loss, declining visual acuity, jaw and arm claudication, polymyalgia rheumatica
- Standout Features: Better sitting upright than laying down, palpable nodules over artery, superficial tenderness
Subarachnoid hemorrhage
- Sex
- Age of Onset
- Location
- Pain Intensity
- Pain Quality
- Sex
- Age of Onset
- Location: generalized, worst in occiput
- Pain Intensity: sudden; worst and worsening
- Pain Quality: Throbbing
Subarachnoid Hemorrhage
- Triggers
- Frequency
- Duration
- Concomitants
- Standout Features
- Triggers: head trauma, spontaneous
- Frequency: 1x
- Duration: continuous
- Concomitants: personality changes, hemiparesis, and altered consciousness if subdural*
- Standout Features: Similar to meningitis
Temporomandibular joint syndrome
- Sex
- Age of Onset
- Location
- Concomitants
- Standout Feature
mal-position, inflammation or arthritis in TMJ, post-whiplash injury
- Sex: usu F
- Age of Onset: young
- Location: unilateral, TMJ radiating to ear
- Concomitants; bruxism
- Standout Feature: limited ROM, tenderness in area, popping or clicking
Depressive HA
- Location
- Concomitants
- Location: generalized, vague
- Concomitants: Other somatic complaints
Eye Pain HA
- Concomitants
- Concomitants: Glaucoma, conjuctivitis, iritis, uveitis, strabismus, errors of refraction causing eye strain
Types of Primary Head Injuries
- Mild Traumatic Brain Injury (Simple Concussion)
- Moderate diffuse TBI
- Severe diffuse TBI (traumatic brain injury)
How many grades of severity categorize Mild Traumatic Brain Injury (Simple Concussion)?
Differentiate between the grades.
3 grades of severity (Grading scale: American Academy of Neurology guidelines)
GRADE I: Confusion, sx last < 15 min, no LOC
GRADE II: Symptoms last >15 min, no LOC
GRADE III: LOC for seconds to minutes
What Signs and Sx point to Mild TBI (simple concussion)?
What PEs need to be done?
- Signs & Sxs: none-to-brief loss of consciousness, dilated pupils, breathing stops, muscles flaccid, heart slows. Recovery in seconds to minutes- may have days to weeks of giddiness, anxiety, poor concentration, headaches, sleep disturbance
- PE: perform neuro exam; CT scan may be needed if persistent symptoms
What is Moderate diffuse TBI?
Unconsciousness for up to an hour with slower recovery of orientation and behavior. Wider area of the brain involved.
What are the signs and Sxs for moderate diffuse TBI?
- Signs & Sxs: Lethargic for 1-7 days. Many have agitation or anxiety
What type of imaging can be used for moderate diffuse TBI and what will it show?
- Imaging: CT may be normal or may show scattered petechiae or contusion in brain. May show hematoma at contra-coup position
Tx for moderate diffuse TBI?
Prognosis?
- Tx: hospitalization to watch for complications; rest (physical & cognitive), NO alcohol or drugs
- Prognosis: complete recovery in days to weeks in those under 40yrs. Those > 40 may have permanent intellectual and psychological effects. Worse prognosis in alcohol/drug abusers.
Red Flag Sx for moderate diffuse TBI?
- unconsciousness
- altered mental status
- convulsions
- persistent HA (constant or intermittent)
- extremity weakness
- bleeding from ear(s)
- loss of hearing
What is Severe diffuse TBI (traumatic brain injury)?
What is the Tx?
categorized by patient response rather than the injury.
- Severe brain edema, ischemic infarction, hemorrhages-immediate or delayed several hours (20%)
- usu. deep unconsciousness from the start
- Respiratory obstruction due to aspiration of vomit or saliva
- Brain stem damage shown by bilateral pupillary fixation, slow responses to light, or anisocoria
Tx: emergency hospitalization required
Post-concussion syndrome: What type of Sxs and how long do Sx persist?
Sx can include: HA (headache), fatigue, anxiety, dizziness, memory problems, attention problems, sleep disturbance, irritability, nausea, vomiting.
Duration: weeks to years.
What is a secondary injury?
after primary injury: further brain swelling and can lead to secondary brainstem damage and death—from hypotension, hypoxia, infection, hematoma
What is a headache?
How common is it?
Where does the pain come from?
head or neck pain; may be a disorder in its own right or caused by underlying medical condition
Common! 5 -10% US population seek medical help for headache, 20% kids have significant HA
Brain tissue itself does not have sensory nerves, so headache pain comes from outside the brain (meninges, scalp, blood vessels and muscles)
What classifications are used to explain HAs?
- Primary or secondary
2. Vascular or nonvascular
What is a primary HA? Examples?
not caused by underlying medical diagnosis
90% of all HAs
Examples: migraine (with or without aura) – primary and vascular; tension-type (episodic or chronic) – primary and non-vascular; cluster
What is a secondary HA? Examples/Causes?
caused by/accompany underlying medical condition
- Head and neck trauma – eg. post-concussion syndrome
- Cranial or cervical vascular disorders – eg. temporal arteritis, hematoma, hemorrhage
- Nonvascular intracranial disorders - either high CSF pressure (e.g., secondary to tumors) or low CSF pressure; benign intracranial hypertension
- Infection – eg meningitis or systemic infection
- Disorders of the cranium, neck, eyes, ears, nose, sinuses, teeth, mouth, etc
- Disorders of homeostasis - diving, high altitude, hypoxia, hypertension, hypothyroidism, fasting, heat stroke, “sphenopalantine ganglioneuralgia”
- Substance use or its withdrawal – i. Acute substance use (e.g., nitric oxide, alcohol, food additives, cocaine, cannabis, histamine). ii. Medication overuse headache (e.g., from triptans, analgesics, opioids, combinations). iii Substance withdrawal headaches (e.g., from caffeine, opioids)
- Psychiatric conditions – eg depression, anxiety disorders, somatization disorders
- Cranial neuralgia - both trigeminal and glossopharyngeal neuralgias
- Iatrogenic: lumbar puncture, manipulation, physiotherapy
Name of a brain freeze?
“Sphenopalantine ganglioneuralgia”
What defines a Vascular headache? Examples?
What is the quality of pain?
various triggers lead to rapid changes in artery size; from spasm/ constriction. Other arteries in the brain and scalp then dilate, and throbbing pain is perceived in the head
- Examples: migraine with or without aura, cluster, fever, hypertension, exertion, hangover
- quality of pain: throbbing or pounding, sharp)
What is the quality of pain for a Non-vascular headache? Examples?
quality of pain: steady, constant, dull
- Examples: tension-type, TMJ, brain tumor, sinus or dental infection, inner or middle ear
RED FLAGS on HA History
- Onset after age 50: temporal arteritis, intercranial mass
- Incr. frequency and severity: subdural hematoma, mass, medication overuse
- Sudden onset of headache: subarachnoid hemorrhage, vascular malformation, mass
- Pain moves to lower neck and thoracic spine: meningial irritation
- First or worst headache: intercranial hemorrhage, CNS infection
- History of head trauma: intracranial hemorrhage, subdural hematoma, epidural hematoma
- History of HIV or cancer: meningitis, brain abscess, metastasis, opportunistic infx
- Any change in mental status, personality, level of consciousness
D. Physical examination for headache
vital signs (BP, temp)
head and neck – carotid and temporal artery pulsations
cervical ROM
tenderness of muscles of head and neck
palpate cranium, jaw, neck, sinus
perform oral and ear exam
neurological exam (cranial nerves, motor/sensory, reflexes, coordination)
HEENT exam (opthalmascopic/fundoscopic exam extremely important, to check for papilledema)
Red Flags on PE for HA
- Fever: intercranial, systemic or local infection
- Neck stiffness/rigidity: meningitis
- Papilledema: meningitis, mass, pseudotumor cerebri, increased intracranial pressure
- Focal neurological signs
- Signs of systemic illness or infection: meningitis, encephalitis, lyme dz, systemic infx,
- collagen vascular disease
Describe a Migraine HA.
Often familial. Recurrent attacks, variable in intensity, frequency, duration. Usually unilateral and associated with anorexia, nausea and vomiting. Photophobia Aura may or may not occur
What are the classifications of Migraine HAs?
- Migraine without aura
- Migraine with aura
- Subtypes of Migraine with Aura
Impact of Migraine HAs
Patient: decreased energy and vitality; decreased social functioning
- 50% of pts miss at least 2 workdays/mo; avg at least 6 days of impaired ability/mo; 43% reduction in performance effectiveness
Family: negative impact on family and partner, eg missed activities
Theories/Pathophysiology of Migraine HAs
neurovascular, vasoactive neuropeptides (substance P), cortical spreading depression, role of serotonin? genetics? Combination
Poly-factoral means multiple vectors of treatment approaches!
Diagnosis of Migraines
Mainly through the Medical History—get clear picture and chronology of symptoms –> HA DIARY
Record: Date(s) of attack, what time the attack began, what time the attack ended, any warning signs?, previous few days (activity, triggers), medications/dose taken, symptoms including aura, if present
Screening Test for Migraine
Self administered 3 question test has >90% accuracy at detecting migraine.
- Has a headache limited your activities for a day or more in the last 3 months?
- Are you nauseated or sick to your stomach when you have a headache?
- Does light bother you when you have a headache?
Other Work-up possible: (only to exclude secondary causes)
EEG CT and/or MRI EMG TMJ radiography Cervical spine films CMP Psychometric testing
Diagnostic Criteria for Migraine without Aura (previously termed “common migraine”)
at least 5 attacks with the following:
•HA lasting 4-72 hr. (untreated or unsuccessfully treated)
•At least 2 of the following characteristics:
- unilateral location
- pulsating quality
- moderate to severe pain
- worse with routine activity
•During headache at least one of the following occurs:
- nausea and/or vomiting
- photophobia and phonophobia
•History, physical exam, and neuro exam show no evidence of organic dz.
Diagnostic Criteria for Migraine with Aura (previously termed “classic migraine”)
at least two attacks of: Aura includes at least 1 of the following (reversible sx) •visual - scintillating scotoma (area of loss of vision, irregular luminous patch) - photopsia (flashing lights) •sensory –paresthesia on face - numbness - unilateral weakness - olfactory hallucinations •dysphasic- speech disturbance (aphasia)
Aura develops over 5-20 min, usu lasting < 60 min.
HA follows during or after aura, lasts 4-72 hr
History, physical exam, and neuro exam show no evidence of organic dz.
May also be prodromal symptoms occurring hours/day before migraine: hyperactivity, lethargy, depression, cravings, frequent yawning
Headache has similar features to above migraine, starting during the aura or w/in 60 min
TENSION-TYPE HEADACHE (TTH) Classifications
- Infrequent episodic TTH—headache episodes less than one day a month (30-80% of pop)
- Frequent episodic TTH—headache episodes 1-14 days a month
- Chronic TTH—headaches 15 or more days a month (3% of pop)
TTH Pathophysiology
- multifactorial
Heightened sensitivity of pain pathways in CNS and peripheral nervous system.
Sensitization of dorsal horn neurons due to increases nociceptive imputs from pericranial myofascial tissue. Innocuous stimuli misinterpreted as pain.
Nitric oxide and genetics may play a role.
TTH Diagnostic criteria (ICHD-2)
At least 2 of the following 4 features:
• bilateral in head or neck
• Quality of the pain is steady (pressing/tightening), nonthrobbing
• Intensity is mild to moderate
• HA pain not aggravated by normal physical activity
- Duration of pain between 30 minutes to 7 days
- No evidence of organic dz.
- may be associated pericranial (neck, shoulder) tenderness
Work-up on TTH (steps you will do to evaluate the situation):
- Assess triggers/stressors
* Neurologic and Mskel PE- typically all findings will be normal
What is a CLUSTER HEADACHE?
neurovascular headache with severe pain attacks which recur daily for prolonged periods
Pathophysiology of Cluster HA: Proposed Mechanisms
not well understood, some proposed mechanisms include:
a. Hemodynamic: Vascular dilatation may play a role
b. Trigeminal nerve: may be responsible for neuronal discharge causing cluster headaches. Substance P neurons carry sensory and motor impulses in the maxillary and ophthalmic divisions of the nerve.
c. Autonomic nervous system: Sympathetic (e.g., Horner syndrome, forehead sweating) and parasympathetic (e.g., lacrimation, rhinorrhea, nasal congestion) effects occur.
d. Circadian rhythm: often recur at the same time every day, suggesting that the hypothalamus, which controls circadian rhythms, may be the site of activation.
e. Mast cells: Increased numbers of mast cells have been found (inconsistently) in the skin of painful areas of some patients (quercitin is good for this)
Diagnostic criteria for Cluster HA from ICHD-2
Episodic cluster headache:
- at least 2 cluster periods lasting 7 days to 1 year
- separated by pain-free periods lasting ≥ 1 month
Chronic cluster headache:
- attacks occur for >1yr without remission or with remission for <1mo
Cluster Headache characteristics:
• Onset: sudden - peaks in 10-15 minutes; typically awakens a person from sleep 1 to 2 hours after going to bed. “alarm clock headaches” often awaken the person at the same time at night. These nocturnal attacks can be more severe than the daytime attacks.
Cluster HA
At least 1 of the following on ipsilateral side: anisoria • conjunctival injection • lacrimation (84-91%) • miosis • ptosis • eyelid edema • facial sweating (26%) • nasal congestion (48-75%) • rhinorrhea
Cluster HA Course, Work-Up, DDX.
Course: Remission - long symptom-free intervals occur in some patients. Avg 2 yrs, but can range
from 2 mos to 20 yrs.
Work-up: initial diagnosis, CT or MRI - warranted to rule out brain or pituitary pathology
DDX: paroxysmal hemicrania, trigeminal neuralgia, HA with intracranial lesion, SUNCT (Short-lasting unilateral neuralgiform headache with conjunctival injection and tearing) syndrome
Pathogenesis of TRIGEMINAL NEURALGIA (Tic Douloureux)
Paroxysmal (comes and goes), severe attacks of lightning-like pain in the branches of the trigeminal nerve
Pathogenesis: compression of trigeminal nerve root by aberrant loop of an artery or vein (80-90%), acoustic neuroma, meningioma, cyst, AV malformation. Compressed area demyelinates, setting up ectopic impulse generation
Diagnostic criteria of Trigeminal Neuralgia (Tic Douloureux) by the International Headache Society:
• Paroxysmal attacks of facial or frontal pain occur, lasting a fraction of a second to 2 minutes.
• Pain has at least one of the following characteristics:
- sudden, intense, sharp, superficial, stabbing, or burning in quality
- precipitation from trigger areas or by trigger factors
• Attacks are stereotypical for each individual patient
• Not attributed to another disorder
Work-Up and DDX of Trigeminal Neuralgia
head CT or MRI is indicated in:
- Patients with trigeminal sensory loss (light touch)
- Patients with bilateral symptoms
- Patients under the age of 40
Electrophysiologic trigeminal reflex testing
DDX: SUNCT syndrome, cluster-tic syndrome, jabs and jolts syndrome, post-herpetic neuralgia (varicella zoster virus) and other neuralgias
Describe HEMICRANIA CONTINUA
(a type of trigeminal autonomic cephalagia)
Headache of unknown origin. Different from cluster HA in higher frequency/shorter duration of attacks; higher incidence in women, 2:1; indomethacin is effective treatment (COX 1&2 inhibitor)
Diagnostic Criteria and Work-Up for Hemicrania Continua
- Daily headache for > 3 mos with 3 other criteria
- All of the following features:
unilateral pain without side-shift
daily or continuous, without pain-free periods
moderate intensity, with some exacerbations of severe pain (short, “jabbing” pain) - At least one of the following occurring on ipsilateral side:
• conjuntival injection and/or lacrimation
• nasal congestion and/or rhinorrhea
• ptosis and/or miosis - treatment with indomethacin is effective
Other SSX can include: eyelid edema, forehead sweating, nausea, vomiting, photophobia
Work-up may include head CT to rule out other causes
Describe SUNCT syndrome
(Short lasting, unilateral neuralgiform headache attacks with conjuctival injection and tearing)
Rare. Unknown cause. A type of trigeminal autonomic cephalagia
Sudden brief attacks of severe unilateral head pain in orbital, periorbital, or temporal areas, with concomitant ipsilateral cranial automonic symptoms
Attacks last 5-240 seconds, with 3-200 attacks a day; 1-2 bouts a year, with remissions lasting mos
Triggers: touching the area: the face, bathing, washing/brushing hair, shaving, chewing, coughing
Workup may include head CT or MRI to rule out other causes
Definition and characterists of MEDICATION OVERUSE HEADACHE (“Rebound headache”)
Diagnostic Criteria for Med Overuse HA
worsening of head pain in chronic HA sufferers due to frequent and excessive use of analgesics
Criteria:
- HA > 15 days/mo
- regular overuse of > 3 mos: ergotamine, triptans, opioids, combination analgesics > 10d a month for > 3 mos
- HA has developed or worsened during medication overuse
Characteristics and DDx for Medication Overuse HAs
3) Characteristics of medication overuse headache:
• Daily or almost daily headache, with daily use of analgesic medication (possible multiple drugs)
• Headache is often worst on waking and often increased after physical exertion.
• The history may begin with episodic headache months or years earlier.
• Sx often include N/V, abd. cramps, diarrhea, restlessness, anxiety, sleeplessness, sweating
• depression and sleep disturbances frequently co-exist.
4) DDx: migraine, tension-type headache, chronic rhinosinusitis, intracranial pathology and space occupying lesions.
DIETARY RELATED HEADACHES: Nitrates/Nitrites:
flushed face
DIETARY RELATED HEADACHES: MSG
tightness of skin on head, GI problems
DIETARY RELATED HEADACHES: NutraSweet
no Sx
DIETARY RELATED HEADACHES: Hangover
alcohol w/d with dehydration and general toxicity; fine tremor in extremities; mild nausea or stomach pain; mental dullness with mild in-coordination
DIETARY RELATED HEADACHES: Hypoglycemia
variable HA, similar to tension-type HA, relieved by eating, worse fasting or after foods (i.e. 2 hours or less after sugar)
HEADACHE FROM INFLAMMATION and INFECTION in skull/brain
Meningitis
Other causes: Sinus headache, dental pain (more later)
Etiology of Meningitis
Causing Organisms
Onset and Signs and Sx - Triad!
Etiology: microbial infx/ inflam. of pain sensitive structures around the brain. Often in young folks
Organisms: Streptococcus pneumoniae, Neisseria meningitides (Meningococcal meningitis), staphylococci
• Haemophilus influenza type B (in those not vaccinated), Mycobacterium tuberculosis
• Viral, fungal, parasitic, and non-infectious cases
Onset: rapid or gradual (occiput)
Signs & Sxs: generalized HA (may be worse in occiput), throbbing, very severe
Triad: nuchal rigidity (neck stiffness); change in mental status, fever. (not all have 3!) LOOK SICK (later sign = rash, often on their legs)
Physical Examination for Meningitis
Diagnosis
- Kernig’s sign –positive= guarding in hamstrings to prevent traction of spinal cord
- Brudzinski’s sign – positive = involuntary flexion of hip/ knee and neck pain
- fundoscopic exam to check for papilledema
- Mental status exam
- dermatologic exam to assess for rash (later sign)
Associated sx and signs: seizure, collapse, loss of consciousness, vomiting, petechial rash
Diagnosis by lumbar puncture, blood culture/gram stain
INTRACRANIAL MASSES
Eg: Pituitary tumor: (compressing on sella turcica)
Signs & Sxs: pain is referred to frontal and temporal regions (bilateral), or vertex or occiput
• as tumor gets larger, it compresses optic chiasm or nerves & hypothalamus leading to visual field defects bilateral or unilateral
• Associated signs of pituitary hormone deficits
Dx by CT or MRI of cranium
A mass that is found incidentally: incidentiloma.
GIANT CELL (temporal) ARTERITIS
Chronic inflammation of large and medium sized vessels; thrombosis may develop at sites of active inflammation– temporal, occipital or frontal-occipital head pain
Signs & Sxs: unilateral or bilateral
- usu superficial tenderness (temple area), not throbbing, variable intensity.
- Pain worse brushing hair, pressure, when lying, possibly on exposure to cold
Associated symptoms:
o fever, anorexia, weight loss
o declining visual acuity (occlusion of retinal artery), ptosis, diplopia
o jaw and arm claudication
o may have polymyalgia rheumatica (muscle and joint-shoulder,hip- pain/stiffness)
o chronic nonproductive cough
GIANT CELL (temporal) ARTERITIS PE and Labs:
PE: palpable nodules over the artery, temporal artery tenderness, pulse often absent
Lab: marked increase in ESR (erythrocyte sedimentation rate) , Elevated CRP
CBC: May be leukocytosis and mild normochromic anemia
Elevated liver enzymes, decreased serum albumin
Procedure: Arterial biopsy is diagnostic.
Complications:
permanent blindness, stroke, aortic aneurism and dissection, MI, peripheral arterial insufficiency
SUBARACHNOID HEMORRHAGE (artery?)
Bleeding due to head trauma or spontaneous rupture of a congenital intracranial aneurysm
Onset: sudden, followed by chronic, persistent intense HA (worst and worsening)
Signs & Sxs: see meningitis
Subdural hematoma: onset gradual, steady aching, gradual personality changes, altered consciousness, hemiparesis (vein?)
Nose and Sinus PE
Physical Exam:
- Nose: use nasal illuminator or otoscope to examine nasal vestibule and turbinates
- Sinus: palpate or percuss for tenderness. Transilluminate for patency
Describe Anosmia
loss of sense of smell.
Consider CN I abnormality if unilateral, with accompanying visual problems, behavior change;
Consider local problem if bilateral, with concomitant nasal symptoms.
Also seen in neurological conditions (eg Alzheimer’s disease or Parkinson’s disease
Etiology of Epistaxis (nosebleed)
i. Anterior → ( Kiesselbach plexus) most common in children and young adults
Risk factors: winter weather: low temps and exposure to dry air, irritants; following URI (nose blowing), acute rhinitis, chronic sinusitis, allergies, trauma, nose-picking
ii. Posterior → (Woodruff’s plexus) more likely in older adults; More prolonged bleeding and difficult to control
Risk factors: HTN , arteriosclerosis, cocaine use, liver disease, alcoholism, blood thinners (coumadin, ASA)
Also consider: bleeding disorders- hemophilia, cancer, anemia
Describe RHINITIS
infection of mucus membranes of nose with stuffy, obstructed, runny nose
DEscribe Allergic rhinitis, its Signs and Sx and PE.
bilateral, chronic, recurrent, very common!
Etiology: Ag triggers IgE on mast cells which releases histamine cascade
seasonal: usu pollens of trees, grass, weeds
perennial (year-round)–animal dander, dust, mold
Signs & Sxs: itchy nose and eyes, watery lacrimation
episodic nasal obstruction, sneezing, nasal voice
allergic salute (crease above bridge of nose)
allergic shiners - bluish discoloration under eyes 2° to obstruction of venous drainage of nasal and sinus congestion; halitosis from mouth breathing
PE: red mucosa (paler than bacteria; rhinitis), if chronic - pale, bluish mucosa, enlarged adenoids, may also have atopic dermatitis (eczema), asthma
DEscribe acute rhinitis, s&s, and PE.
bilateral; common cause—Rhinovirus; usually self-limiting to 7 days
Signs & Sxs: watery, profuse discharge with sneezing, clear and later yellow or green, malaise, mouth breathing
PE: erythematous, swelling of mucosa, low fever
DEscribe Atrophic rhinitis, etiology, S&S and PE.
bilateral, Nasal mucous membrane to stratified squamous epithelium
Etiology: unknown, although bacterial infection frequently plays a role.
Signs & Sxs: anosmia or hyposmia and epistaxis may be recurrent and severe, nasal congestion, unpleasant smell (ozoena) resulting from a progressive atrophy of the nasal mucosa and underlying bone, painful nasal passage, may be foul smelling d/c
PE: membranes dry & shiny, atrophy of tissues; yellow and green crusts that bleed when removed
DEscribe Vasomotor rhinitis, S&S, Triggers, PE and Labs
bilateral; Non-allergic, non-infectious syndrome caused by parasympathetic dominance.—leading to vasodilation and edema of nasal vasculature
Signs & Sxs: similar to allergic rhinitis with rhinorrhea: sneezing, pruritus, congestion. May alternate sides
Triggers: emotions, smoke, weather changes (very common)
cold air strong odors stress
inhaled irritants recumbency trauma
spicy foods alcohol
rates of anxiety and depression are higher in women with vasomotor rhinitis
PE: swollen inferior nasal turbinates, dark red to bluish mucosa
Labs: all allergy tests negative, nasal smear negative for organisms
DEscribe S&S and PE for cocaine use
Signs & Sxs: constant runny nose; watery d/c when drug affected, congested when not, chronic sore throats, hoarseness
PE: may see chemical burns, septal perforation
Name some bilateral rhinitis examples
Acute, allergic, atrophic, vasomotor, cocaine use
Name unilateral types of rhinitis
a. Trauma- ominous sign for possible skull fracture if trauma involved; may be CS fluid (blood-
tinged) ; check with Benedict’s solution—should remain clear if no sugar (CSF has sugar in it)
b. Choanal Atresia- congenital defect in septal development Test: infant will become distressed if block unaffected nares c. Foreign body- discharge, odor d. Neoplasm- bloody discharge
trauma (rhinitis)
a. Trauma- ominous sign for possible skull fracture if trauma involved; may be CS fluid (blood-tinged); check with Benedict’s solution—should remain clear if no sugar (CSF has sugar in it)
Choanal Atresia (Rhinitis)
- congenital defect in septal development
Test: infant will become distressed if block unaffected nares
Foreign body (Rhinitis)
Look for discharge, odor
Neoplasm (Rhinitis)
bloody discharge
DEscribe Polyps, their etiology, S&S concomitants
Soft, pedunculated lesions that emanate from any portion of the nasal mucosa or paranasal sinuses
Linked to chronic inflammation, ANS dysfunction, genetic predisposition, chronic infection or allergy predispose
M:F incidence 2 - 4:1 in adults - more common in pts > 40 years
Conditions associated with multiple benign polyps:
bronchial asthma
cystic fibrosis
allergic rhinitis
allergic fungal sinusitis
chronic rhino-sinusitis
Signs and Sxs: (depends on the size of the polyp) no sx to nasal obstruction, postnasal drainage, Dull headaches, snoring, rhinorrhea, epistaxis, hyposmia or anosmia
Often surgically removed and then return unless real cause is managed
Nasal septum problems:
Deviation from trauma- eg. boxers
Perforation from chronic infection, crusting, nasal surgery, TB, syphilis, cocaine use
Abscess - rare, dangerous, may lead to cavernous sinus thrombosis
Rhinophyma;
Enlarged, bulbous, reddened nose; may obstruct breathing or vision
Granulomatous infiltration/hypertrophy of sebaceous glands
Associated with untreated acne rosacea, worsened by (but not caused by) alcoholism
More common in men >50; significant psychological toll
RHINOSINUSITIS: (paranasal sinuses) (previous term: Sinusitis)
What predisposing factors are there?
> 30 million pts in the US have sinus disease
Organisms: Viral (common, less severe); Bacterial (Staph, Strep, H. flu; more severe); Fungal (Mucor, Aspergillis)
Predisposing factors: decongestants, fatigue, dental problems, food sensitivities, GI issues, septal deviation, large adenoids, foreign bodies
Types of Rhinosinusitis
Acute and Chronic supperative sinusitis
Acute suppurative rhinosinusitis , S&S and PE
Signs & Sxs: >1 week, but < 3 weeks
duration (most improve within 7-10 days so the complaint of persistent or worsening symptoms may indicate a developing bacterial sinusitis.)
nasal congestion, purulent drainage, and facial pain with headache
pain is often exacerbated by leaning forward or any head movement
may have dental pain or altered smell
Kids: may complain of a daytime cough and persistent nasal discharge
Symptoms by involved sinus:
i. Maxillary: dull, throbbing pain in cheek, tender, painful max. teeth, tenderness over maxilla
DDX infected tooth
ii. Frontal: tenderness over forehead area, swelling of eyelids, frontal h/a
iii. Ethmoid: pain more medial to eye, feels deep in head or eye, splitting h/a on one side, swelling of eyelids
iv. Sphenoid: pain behind eye or in occiput or vertex, deeper pain, not local tenderness
PE: purulent secretions in the middle meatus (highly predictive of maxillary sinusitis) fever is rare unless bacterial cause. (usu no fever if viral), facial tenderness to palpation or percussion, complete opacification of sinus on transillumination—sinus not patent
partial opacification is a nonspecific finding, and it is not as reliable.
Chronic suppurative rhinosinusitis:
approximately 32 million cases/ year
Etiology: Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis > 70% of cases
Osteo-meatal obstruction, allergies, polyps, immunodeficiency states, and dental problems
Signs and Sxs:
manifests more subtly than acute sinusitis; typical sx of acute sinusitis (facial pain and fever) are usually absent.
nasal stuffiness, nasal discharge, postnasal drip, facial fullness headache, hyposmia, sore throat, chronic unproductive cough, fetid breath, malaise, exacerbation of asthma, unpleasant taste, dental pain, visual disturbances, sneezing stuffy ears
PE: tenderness on palpation over frontal or maxillary sinuses
- transillumination of maxillary or frontal sinuses shows little opacity
- oropharyngeal erythema, purulent secretions check for dental caries
Endoscopic (rhinoscopic) examination:
Nasal mucosal erythema, edema, purulent secretions; check for nasal obstruction from deviated nasal septum or hypertrophied turbinates, check for nasal polyps
Eye examination: conjunctival congestion, lacrimation, Check extraocular movements
What are some Serious complications of rhinosinusitis
i) orbital or periorbital cellulitis- edema, pain moving the eye, chemosis (conj. edema) - very sick pt.
ii) cavernous sinus thrombosis - very dangerous, mortality 50%
- high fever, chills, prostrated, comatose, change in mental status
- arly signs - have deep eye pain, ocular palsy (III, IV, VI), diplopia
- late sign- both eyes involved, edema, death within 2-3 days.
Upper Airway Cough Syndrome SSX and PE
common sequellae to rhinosinusitis, “post-nasal drip”
SSX: cough, rhinorrhea, frequent swallowing, halitosis, frequent spitting, tickling in throat, constant clearing of throat, chronic sore throat
PE: may see tonsilloliths, cobblestoning of oropharyneal mucosa, tenderness of sinuses
