Head Nose Sinus Flashcards
• What are the 5 general approaches to seeing a patient?
o History, physical exam, laboratory (as indicated), imaging/procedure (as indicated), referral (as indicated)
• What are some hx question?
o Head pain? (get full history with presentation of head pain)
o Accompanying symptoms (eg. eye, ears, cranial nerves, neurologic, GI, temperature, etc)
o History of head injury? Any loss of consciousness?
o Lesions, tumors, scalp hair loss?
• What are some things involved in the PE?
o Observation: normocephalic (microcephalic, macrocephalic)
o Vitals
o Palpation of head and scalp: lesions, masses, tenderness; On infants, examine fontanelles
o Full exam of Ears, Eyes, Nose, Sinus, Throat, Neck
o Appropriate neurological exams (CN, peripheral, orientation, cognitive)
• What are some common labs?
o ESR, CRP, CBC, CMP
• What are some common imaging/procedures?
o MRI, CT, angiography, lumbar puncture and CSF analysis
• What are some common referrals?
o Emergency, Neurology, Dermatology
• What is the mortality of a head trauma?
o ~ 50% with severe injury (more deaths & disability than other neuro cause in >50 yo)
o Damage to nerve tissue, blood vessels and meninges can result in neural disruption, ischemia, hemorrhage and edema
• What are the 2 types of head traumas?
o Open and closed head injuries
• What may be the effects of an open head injury?
o Emergency
o Piercing of the skull, direct trauma e.g. GSW (gunshot wound)
o direct effects from the tissue damage and shock waves
• How may closed head injuries occur? Emergency?
o Emergency or urgency
o Eg. acceleration-deceleration injury (whiplash)- local injury and opposite side of skull
o “contra-coup injury”
• How is the severity of closed head injuries based?
o loss of consciousness or not
o presence or absence of neurologic signs
• What are the 2 classes of closed head injuries?
o Primary and secondary injuries
• What are the 3 types of primary head injuries?
o Mild traumatic brain injury (TBI)-simple concussion
o Moderate diffuse TBI
o Severe diffuse TBI
• What are the grades of severity of mild TBI?
o American Academy of Neurology guidelines
o Grade 1- Confusion, sx last < 15 min, no LOC
o Grade 2- Symptoms last >15 min, no LOC
o Grade 3- LOC for seconds to minutes
• What are the signs and symptoms of mild TBI?
o No to brief loss of consciousness, dilated pupils, breathing stops, muscles flaccid heart slows.
o Recovery in seconds to minutes- may have days to weeks of giddiness, anxiety, poor concentration, headaches, sleep disturbance
• What PE should be done for mild TBI?
o perform neuro exam; CT scan may be needed if persistent symptoms
• What is characteristic of a moderate diffuse TBI?
o Unconsciousness for up to an hour with slower recovery of orientation and behavior.
• What are the signs and symptoms for moderate diffuse TBI?
o Lethargic for 1-7 days. Many have agitation or anxiety
o Imaging: CT may be normal or may show scattered petechiae or contusion in brain. May show hematoma at contra-coup position
• What is the treatment for moderate diffuse TBI?
o hospitalization to watch for complications; rest (physical & cognitive), NO alcohol or drugs
• What are red flag symptoms in moderate diffuse TBI?
o unconsciousness, altered mental status, convulsions, persistent HA, extremity weakness, bleeding from ear(s), loss of hearing
• What is the prognosis for moderate diffuse TBI?
o 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.
• How is severe diffuse TBI categorized?
o by patient response rather than the injury
• What are the signs and symptoms of severe diffuse TBI?
o Severe brain edema, ischemic infarction, hemorrhages-immediate or delayed several hours (20%)
o usu. deep unconsciousness from the start
o Respiratory obstruction due to aspiration of vomit or saliva
o Brain stem damage shown by bilateral pupillary fixation, slow responses to light, or anisocoria
• What is the treatment for severe diffuse TBI?
o emergency hospitalization required
• What is post-concussion syndrome?
o In some individuals, symptoms of mild TBI persist for weeks to years.
o Sx can include: HA, fatigue, anxiety, dizziness, memory problems, attention problems, sleep disturbance, irritability
• What is a secondary head injury?
o Requires careful monitoring in pts with TBI
o after primary injury: further brain swelling and can lead to secondary brainstem damage and death—from hypotension, hypoxia, infection, hematoma
• Generally, what may cause headaches? How common are they? Where does the pain come from?
o head or neck pain may be a disorder in its own right or caused by underlying medical condition
o Common! 5 -10% US population seek medical help for headache, 20% kids have significant HA
o Brain tissue itself does not have sensory nerves, so headache pain comes from outside the brain (meninges, scalp, blood vessels and muscles)
• What are the classifications of HA?
o International Headache Society (HIS)
o Primary or secondary
o Vascular or nonvascular
• What is a primary HA? How common? Examples?
o not caused by underlying medical diagnosis
o 90% of all Has
Main examples: migraine (with or without aura), tension-type (episodic or chronic), cluster
What is a secondary HA?
o caused by underlying medical condition
• What are 10 examples of a secondary HA?
o Head and neck trauma – eg. post-concussion syndrome
o Cranial or cervical vascular disorders – eg. temporal arteritis, hematoma, hemorrhage
o Nonvascular intracranial disorders - either high CSF pressure (e.g., secondary to tumors) or low CSF pressure; benign intracranial hypertension
o Infection – eg meningitis or systemic infection
o Disorders of the cranium, neck, eyes, ears, nose, sinuses, teeth, mouth, etc
o Disorders of homeostasis - diving, high altitude, hypoxia, hypertension, hypothyroidism, fasting, heat stroke, “sphenopalantine ganglioneuralgia”
o Substance use or its withdrawal: Acute substance use (e.g., nitric oxide, alcohol, food additives, cocaine, cannabis, histamine); Medication overuse headache (e.g., from triptans, analgesics, opioids, combinations); Substance withdrawal headaches (e.g., from caffeine, opioids)
o Psychiatric conditions – eg depression, anxiety disorders, somatization disorders
o Cranial neuralgia - both trigeminal and glossopharyngeal neuralgias
o Iatrogenic: lumbar puncture, manipulation, physiotherapy
• What are 3 types of features or concomitant symptoms suggestive of secondary HAs?
o Change in typical HA
o Following head trauma
o Associated with systemic condition
• What may be considered changes in the typical HA?
o Sudden onset of new HA, “Worst HA ever”(Consider subarachnoid hemorrhage)
o Drowsiness, confusion, memory loss (infection, mass, subdural hematoma)
o Progressive vision loss (tumor, inc ICP, MS, Lyme, glaucoma, arteritis)
o High blood pressure
• What features may present with a HA may follow a head trauma?
o Progressively worsening HA
o Metabolic imbalance eg Hypoglycemia, thyroid problem
o Fever (common sign of infection)
o Focal neurological signs
• What features associated with systemic conditions may present with a HA?
o Onset with exertion, coughing, straining, sexual activity, Valsalva (mass, subarachnoid hemorrhage)
o Chronic malaise, myalgia, arthralgia (temporal arteritis, collagen vasc dz, Lyme dz)
o Weakness, clumsiness, postural instability (focal brain dz)
o CSF rhinorrhea
• What is a vascular HA? Examples?
o quality of pain: throbbing or pounding, sharp
o Various triggers lead to rapid changes in artery size; from spasm/ constriction.
o Other arteries in the brain and scalp then dilate, and throbbing pain is perceived in the head
o Examples: migraine with or without aura, cluster, fever, hypertension, exertion, hangover
• What is a non-vascular HA? Examples?
o quality of pain: steady, constant, dull
o Examples: tension-type, TMJ, brain tumor, sinus or dental infection, inner or middle ear
• Why is a hx important? Letters?
o 99% of information needed to make diagnosis!
o L, M, N, O, P, Q, R, S, T, concomitants
• What are common questions in a hx of HA?
o When and how (sudden, gradual) did HA begin?
o First or Worst HA?
o Worsening HA? (often organic)
o Effect of activity on pain
o Location of HA, does it move? Is it always on the same side? (changeable less likely organic)
o Age of first HA? (90% migraines in <40 yo)
o Is THIS HA similar to prior ones?
o Frequency, pattern of HA (episodic, daily)
o Duration of HA
o Family history of HA (migraine, cluster)
o Medications (change in method of birth control)
o Any prodromal symptoms?
o Any recent change in vision?
o Known triggers and aggravations (light, sound)
o Stressors: home, work, relationships
o Association to recent trauma
o Any association to environmental factors
o Relationship to food/alcohol
o Any recent change in sleep, exercise, weight
o Response to previous treatment
o PMHx: any concurrent medical problem
o General health status
• What are the red flags of a HA hx?
o Onset after age 50: temporal arteritis, intracranial mass
o Incr. frequency and severity: subdural hematoma, mass, medication overuse
o Sudden onset of headache: subarachnoid hemorrhage, vascular malformation, mass
o Pain moves to lower neck and thoracic spine: meningeal irritation
o First or worst headache: intracranial hemorrhage, CNS infection
o History of head trauma: intracranial hemorrhage, subdural hematoma, epidural hematoma
o History of HIV or cancer: meningitis, brain abscess, metastasis, opportunistic infection
o Any change in mental status, personality, level of consciousness
• What is done for a PE for a HA?
o vital signs (BP, temp)
o 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
o neurological exam (cranial nerves, motor/sensory, reflexes, coordination)
o HEENT (fundoscopic exam extremely important, to check for papilledema)
• What are the red flags for PE of a HA?
o Fever: intracranial, systemic or local infection
o Neck stiffness/rigidity: meningitis
o Papilledema: meningitis, mass, pseudotumor cerebri, increased intracranial pressure
o Focal neurological signs
Signs of systemic illness or infection: meningitis, encephalitis, Lyme dz, systemic infx, collagen vascular disease
What are the 16 types/causes of HA (more and less common)?
o Most common: Migraine; Tension-type headache (TTH); Cluster; Trigeminal neuralgia
o Less common: Hemicrania continua; SUNCT syndrome; Medication overuse; Dietary related; Inflammation/infection in skull/brain; Related to BP; Intracranial masses; Giant cell (temporal) arteritis; Subarachnoid hemorrhage; TMJ syndrome; Depressive; Eye pain
• What are some general characteristics of a migraine HA?
o Often familial.
o Recurrent attacks, variable in intensity, frequency, duration
o Usually unilateral and associated with anorexia, nausea and vomiting
o Photophobia Aura may or may not occur
• What are the frequency, sex, age features of migraine?
o ~10-20% of the US population suffers from migraines; second most common type of headache (tension-type the most common)
o F:M 3:1
o First attack often is in childhood, incidence increases in adolescence; > 80% of patients have a first attack by age 30; less common > age 50. (less frequent and less severe)
o Note: Age of onset > 55 years is a strong predictor for intracranial pathology
• What is the impact of migraine on the patient and their family?
o 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
o Family: negative impact on family and partner, eg missed activities
• What are some theories on the pathophysiology of migraine?
o Neurovascular, vasoactive neuropeptides (substance P), cortical spreading depression, role of serotonin? Genetics? Combination
• What does poly-factoral mean?
o Multiple vectors of treatment approaches!
• What are 12 co-existing/commonly associated medical conditions?
o Epilepsy; asthma; sleep disorders; hemorrhagic telangiectasia; Tourette syndrome; Raynaud’s; familial dyslipoproteinemias; chronic fatigue syndrome; depression and anxiety; ischemic stroke (migraine c aura risk); hypertension; atrial septal defect
• How is info gathered for migraine diagnosis?
o Medical History: get clear picture and chronology of symptoms
o Headache diary: date(s) of attack; medications/dose taken; what time the attack began; what time the attack ended; any warning signs? symptoms including aura, if present; previous few days (activity, triggers)
• What are some common precipitating factors/trigger for migraine?
o emotional and physical STRESS (strongest trigger in most sufferers)
o hormones in women: PMS, use of BCP or HRT
o skipped meals, hypoglycemia
o loss of sleep, changes in normal sleeping patterns, sleeping in late
o changing weather conditions
o odors, lights, smoke
o exercise
o food intolerances/ allergies: studies range from 30-93%
o Tyramine-containing foods:
• What are some changing weather conditions that can trigger migraine?
o storm fronts, changes in barometric pressure, strong winds, changes in altitude or temperature (heat)
• What are some food intolerances/allergies that can trigger migraine?
o common: cow’s milk, eggs, chocolate, wheat, oranges, walnuts, tomato, alcohol, MSG
• What are some tyramine-containing foods that can cause migraine?
o Cheeses (blue cheeses, brie, cheddar, feta, gorgonzola, mozzarella, Muenster, parmesan, swiss, stilton); aged, canned, cured or processed meats, certain beans (fava, broad, garbanzo, lima, pinto), onions, olives, pickles, avocados, raisins, canned soups, and nuts.
• What is the screening test for a migraine?
o Self-administered 3 question test has >90% accuracy at detecting migraine.
o 1. Has a headache limited your activities for a day or more in the last 3 months?
o 2. Are you nauseated or sick to your stomach when you have a headache?
o 3. Does light bother you when you have a headache?
• What is some other possible work-up for migraine, only to exclude secondary causes?
o EEG; CT and/or MRI; EMG; TMJ radiography; Cervical spine films; CMP; Psychometric testing
• What are the 2 classifications for migraine?
o Migraine without aura (previously termed “common migraine”)
o Migraine with aura (previously termed “classic migraine”)
• What is the diagnostic criteria for a migraine without aura?
o at least 5 attacks with the following:
o HA lasting 4-72 hr. (untreated or unsuccessfully treated)
o At least 2 of the following characteristics: unilateral location; pulsating quality; moderate to severe pain; worse with routine activity
o During headache at least one of the following occurs: nausea and/or vomiting; photophobia and phonophobia
o History, physical exam, and neuro exam show no evidence of organic dz.
• What are the 4 phases/sequence of symptoms of a migraine w/o aura?
o Prodrome, headache, resolution, recovery
• What symptoms are seen in the prodrome phase of a migraine?
o Food craving, fatigue, heightened perception, fluid retention
• What symptoms are seen in the HA phase of a migraine?
o Gradual onset; dull then pulsatile; 1/3 have sharp pain; unilateral may change sides;
o Duration <1 day – 72 hrs
o Decreased motion; vomiting; coughing; pallor, fluid gain; photophobia
o Nausea leading to vomiting in 50%
o Withdrawn, irritable
• What symptoms are seen in the resolution phase of migraine?
o Sleep: long, deep
o Catharsis through vomiting, lacrimation, urination, diarrhea, menses
• What symptoms are seen in the recovery phase of migraine?
o Hours to days
o Limited food tolerance, Fatigue, feeling drained
o Depression, some report elation
• What are the diagnostic criteria for a migraine with aura?
o at least two attacks of:
o aura includes at least one visual, sensory, or dysphasic quality
o Aura develops over 5-20 min, usu lasting < 60 min
o HA follows during or after aura, lasts 4-72 hr, similar to non-aura migraine
o History, physical exam, and neuro exam show no evidence of organic dz
What are the visual, sensory, and dysphasic symptoms of an aura (reversible)
o Visual: scintillating scotoma (area of loss of vision, irregular luminous patch); photopsia (flashing lights)
o Sensory: paresthesia on face; numbness; unilateral weakness; olfactory hallucinations
o Dysphasic: speech disturbance (aphasia)
• What are the prodromal symptoms that may be seen with an aura migraine?
occurring hours/day before migraine: hyperactivity, lethargy, depression, cravings, frequent yawning
• When/how does the headache occur in an aura migraine?
o Similar to non-aura migraine, starting during the aura or w/in 60 min
• What are the 6 subtypes/variants of migraine with aura (previously “complicated migraine”)?
o Hemiplegic migraine: temporary paralysis (hemiplegia) or nerve or sensory changes on one side of the body (such as muscle weakness--reversible). o Retinal (ocular) migraine: temporary, monocular scotoma or blindness in one eye, along with a dull ache behind the eye lasting about an hour, followed by headache. o Basilar-type migraine: dizziness, confusion or loss of balance can precede the headache; pain may affect the back of the head; symptoms usually occur suddenly and can be associated with the inability to speak properly, tinnitus, vertigo, diplopia, dysarthria, ataxia, decreased level of consciousness and vomiting. o Migraine aura without headache: confused as TIAs in elderly o Status migrainosus (rare): HA pain and nausea are very intense o Ophthalmoplegic migraine (rare) emergency!- Affecting CN III, IV, VI; pain around the eye, including paralysis in muscles surrounding the eye; other symptoms: ptosis, diplopia, or other vision changes.
• What is the most common form of HA?
o Tension-type HA (TTH)
• What are the 3 classifications of TTH?
o Infrequent episodic TTH: headache episodes less than one day a month (30-80% of pop)
o Frequent episodic TTH: headache episodes 1-14 days a month
o Chronic TTH: headaches 15 or more days a month (3% of pop)
• What is the pathophysiology of TTH?
o multifactorial
o Heightened sensitivity of pain pathways in the CNS and peripheral nervous system.
o Sensitization of dorsal horn neurons due to increased nociceptive inputs from pericranial myofascial tissue. Innocuous stimuli misinterpreted as pain.
o Nitric oxide and genetics may play a role.
• What is the epidemiology of TTH *sex, age, triggers)
o Sex: F:M 2:1
o Age: all ages are susceptible, but most pts are young adults.
o Triggers: Stress and mental tension. (common sources of stress include family, social relationships, friends, work and school). Head or neck movement
• What is the diagnostic criteria for TTH (ICHD-2)?
o At least 2 of the following 4 features:
o Location of the pain is bilateral in head or neck
o Quality of the pain is steady (pressing/tightening), non-throbbing
o Intensity is mild to moderate
o HA pain not aggravated by normal physical activity
o Additionally: Duration of pain between 30 minutes to 7 days; No evidence of organic dz
o There may be associated pericranial (neck, shoulder) tenderness
• What is the work-up for TTH?
o Assess triggers/stressors
o Neurologic and Musculoskeletal PE- typically all findings will be normal
• What is a cluster HA?
o neurovascular headache with severe pain attacks which recur daily for prolonged periods
• What is the epidemiology of cluster HA?
o Frequency: Prevalence in males is 0.4-1%
o Mortality/Morbidity: suicides have been reported in cases where attacks are frequent and severe.
o Genetics: some studies show autosomal dominant gene may play a role in some families
o Sex: Male-to-female ratio is 4.3:1.
Age: usually begin in middle-age, mean age of onset is 30 yrs for men and later for women.
• What are the triggers for cluster HA?
o Season (spring or autumn), often mistakenly associated with allergies o Common in cigarette smokers. During a cluster period, the sufferer is more sensitive to the action of nicotine and alcohol
• What is the pathophysiology of cluster HA?
o not well understood, some proposed mechanisms include:
o Hemodynamic: Vascular dilatation may play a role
o 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.
o Autonomic nervous system: Sympathetic (e.g., Horner syndrome, forehead sweating) and parasympathetic (e.g., lacrimation, rhinorrhea, nasal congestion) effects occur.
o Circadian rhythm: often recur at the same time every day, suggesting that the hypothalamus, which controls circadian rhythms, may be the site of activation.
o Mast cells: Increased numbers of mast cells have been found (inconsistently) in the skin of painful areas of some patients
• What is the diagnostic criteria for the 2 types of cluster HA (ICHD-2)?
o Episodic cluster headache: at least 2 cluster periods lasting 7 days to 1 year, are separated by pain-free periods lasting ≥ 1 month
o Chronic cluster headache: attacks occur for >1yr without remission or with remission for <1mo
• What are the characteristics of cluster HA onset?
o 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.
• What is the pain quality of cluster HA?
o boring, constant, searing, “a knife cutting through my head”
• What is the location of cluster HA?
o Unilateral facial - remains on the same side during the cluster period, typically are located at the temple and periorbital region (trigeminal V1 or V2). Scalp may be tender, and pulsing in the arteries often can be felt
• What is the duration of cluster HA? Frequency?
o Duration: 10-30 minutes to 3 hours per episode
o Frequency: 1-3 (more common) but up to 8 episodes per day for up to 12 months (often nocturnal)
• What are some concomitant symptoms of cluster HA?
o nausea restlessness, agitation
• Cluster HA has at least 1 of the following on ipsilateral side:
o conjunctival injection; lacrimation (84-91%); miosis ; ptosis; eyelid edema; facial sweating (26%); nasal congestion (48-75%); rhinorrhea
• describe the course of a cluster HA (remission):
o Long symptom-free intervals occur in some patients. Avg 2 yrs, but can range from 2 mos to 20 yrs.
• What is the workup for cluster HA?
o for initial diagnosis, CT or MRI is warranted to rule out brain or pituitary pathology
• What is the differential diagnosis of cluster HA?
o paroxysmal hemicrania, trigeminal neuralgia, HA with intracranial lesion, SUNCT (Short-lasting unilateral neuralgiform headache with conjunctival injection and tearing) syndrome
• What are the common characteristics of migraine?
o Location: Unilateral in 70%, bifrontal in 30%
o Characteristics: Gradual onset, crescendo pattern, pulsating, mod or severe intensity; aggrav by routine activities
o Pt appearance: Pt prefers to rest in dark quiet room
o Duration: 4 to 72 hrs
o Associated symptoms: Nausea, vomiting, photophobia, may have aura (usu visual, may be other senses)
• What are the common characteristics of TTH?
o Locations: bilateral
o Characteristics: Pressure or tightness that waxes and wanes
o Pt appearance: Pt may remain active or may need to rest
o Duration: variable
o Assoc sxs: none
• What are the common characteristics of cluster HA?
o Locations: Always unilateral, eye or temple
o Characteristics: Pain begins quickly, reaching crescendo in minutes; deep pain, continuous, excruciating
o Pt appearance: Patient remains active
o Duration: 30 min to 3 hrs
o Assoc sxs: Ipsilateral lacrimation and redness of eye, stuffy nose, rhinorrhea, pallor, sweating; Horner’s syndrome, focal neurological sx are rare; sensitivity to alcohol
• What is trigeminal neuralgia (TN)? Aka?
o Aka Tic Douloureux
o Paroxysmal, severe attacks of lightning-like pain in the branches of the trigeminal nerve
• What is the pathogenesis of TN?
o Compression of trigeminal nerve root by aberrant loop of an artery or vein (80-90%), acoustic neuroma, meningioma, cyst, AV malformation.
o Compressed area demyelinates, setting up ectopic impulse generation
• What is the epidemiology of TN?
o Mortality/Morbidity: the severity of the pain may lead to suicide
o Sex: M:F 1:1.5
o Age: in 90%, begins >40yrs, but occasional reports of pediatric cases
• What are the diagnostic criteria for TN (HIS)?
o Paroxysmal attacks of facial or frontal pain occur, lasting a fraction of a second to 2 minutes.
o 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
o Attacks are stereotypical for each individual patient
o Not attributed to another disorder
• What is the location, duration, triggers for TN HA?
o Location: right side > left; 14% bilateral; most commonly V2 or V3 and rarely in V1
o Duration: paroxysms from few seconds to few minutes; bouts from few days - weeks or months with remissions from weeks- years
o Trigger examples: touching or applying heat or cold to the cheek or gum; chewing, yawning, grimacing or talking; shaving, washing, brushing teeth; wind blowing in the face
• What is the workup for TN?
o head CT or MRI is indicated in patients with trigeminal sensory loss (light touch); pts with bilateral symptoms; pts under the age of 40
o Electrophysiologic trigeminal reflex testing
• What is the ddx for TN?
o SUNCT syndrome, cluster-tic syndrome, jabs and jolts syndrome, post-herpetic neuralgia (varicella zoster virus) and other neuralgias
• What is hemicrania continua?
o a type of trigeminal autonomic cephalagia
o Headache of unknown origin. Different from cluster HA in higher frequency/shorter duration of attacks; higher incidence in women, 2:1
o indomethacin is effective treatment (COX 1&2 inhibitor)
• What are the 4 diagnostic criteria for hemicrania continua? Other SSX?
o headache for > 3 mos with 3 other criteria
o 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)
o At least one of the following occurring on ipsilateral side: conjunctival injection and/or lacrimation; nasal congestion and/or rhinorrhea; ptosis and/or miosis
o treatment with indomethacin is effective
o eyelid edema, forehead sweating, nausea, vomiting, photophobia
• What is the work-up for hemicrania continua?
o may include head CT to rule out other causes
• What is SUNCT syndrome?
o Short lasting, unilateral neuralgiform headache attacks with conjunctival injection and tearing)
o Rare. Unknown cause. A type of trigeminal autonomic cephalagia
o Sudden brief attacks of severe unilateral head pain in orbital, periorbital, or temporal areas, with concomitant ipsilateral cranial autonomic symptoms
o Attacks last 5-240 seconds, with 3-200 attacks a day; 1-2 bouts a year, with remissions lasting mos
• What are the triggers for SUNCT?
o touching the face, bathing, washing/brushing hair, shaving, chewing, coughing
• What is the workup for SUNCT?
o Workup may include head CT or MRI to rule out other causes
• What are the 2 substance related HAs?
o Medication overuse HA and dietary related HA
• What is medication overuse HA?
o “rebound HA”
o worsening of head pain in chronic HA sufferers due to frequent and excessive use of analgesics
• What is the epidemiology of medication overuse HA?
o ~20% of patients with chronic HAs and most with daily HAs have analgesic overuse headaches
o Low doses daily carry greater risk than larger doses taken weekly.
o 30-40 year age group: most have migraine or tension type headache.
o F:M 5:1
o compound analgesics are more likely to induce analgesic rebound headaches
• What is the diagnosis criteria for medication overuse HA?
o HA > 15 days/mo
o regular overuse of > 3 mos: ergotamine, triptans, opioids, combination analgesics > 10d a month for > 3 mos
o HA has developed or worsened during medication overuse
• What are some SSX of medication overuse HA?
o daily or almost daily headache, with daily use of analgesic medication (possible multiple drugs)
o Headache is often worst on waking and often increased after physical exertion.
o The history may begin with episodic headache months or years earlier.
o Sx often include N/V, abd. cramps, diarrhea, restlessness, anxiety, sleeplessness, sweating
o Depression and sleep disturbances frequently co-exist.
• What is the ddx for medication overuse HA?
o Migraine, tension-type headache, chronic rhinosinusitis, intracranial pathology and space occupying lesions.
• What are the 5 common causes of dietary related HA? Symptoms
o Nitrates/Nitrites: flushed face
o MSG: tightness of skin on head, GI problems
o NutraSweet
o Hangover: alcohol w/d with dehydration and general toxicity; fine tremor in extremities; mild nausea or stomach pain; mental dullness with mild in-coordination
o Hypoglycemia: variable HA, similar to tension-type HA, relieved by eating, worse fasting or after foods (i.e. 2 hours or less after sugar)
• What are some causes for HA from inflammation and infection in skull/brain?
o Meningitis
o Sinus HA, dental pain
• What is the etiology of meningitis HA?
o Microbial infection/inflammation of pain sensitive structures around brain; often in younger ppl
o Organisms: Streptococcus pneumoniae, Neisseria meningitides (Meningococcal meningitis), staphylococci, Haemophilus influenza type B (in those not vaccinated), Mycobacterium tuberculosis
o Viral, fungal, parasitic, and non-infectious cases
• Describe the onset of meningitis HA?
o Rapid and gradual
• What are the SSX of meningitis HA? Associated ssx?
o generalized HA (may be worse in occiput), throbbing, very severe
o Triad: nuchal rigidity; change in mental status, fever. (Not all have 3!) LOOK SICK
o Associated: seizure, collapse, loss of consciousness, vomiting, petechial rash
• What PE is done for a meningitis HA?
o Kernig’s sign: positive= guarding in hamstrings to prevent traction of spinal cord
o Brudzinski’s sign: positive = involuntary flexion of hip/ knee and neck pain
o fundoscopic exam to check for papilledema
o Mental status exam
o dermatologic exam to assess for rash (later sign)
o Associated sx and signs: seizure, collapse, loss of consciousness, vomiting, petechial rash
• How is meningitis HA diagnosed?
o by lumbar puncture, blood culture/gram stain
• What are 3 types of HA related to blood pressure?
o HrTN HA; intracranial HrTN; intracranial HoTN
• What is a HrTN HA?
o From severe, sudden increase in BP (malignant hypertension)
o Concomitant tinnitus, epistaxis, bruits in carotids arteries
• What is etiology of an intracranial HrTN HA?
o edema, tumor of brain or pseudo tumor (benign intracranial hypertension)
• What are the ssx of intracranial HrTN HA if a tumor?
o usu mild HA, lasting a few seconds to 3 hours, often worse laying, progressive increase in frequency & duration
o in later stages - continuous deep aching pain, worse from abrupt change in position
o slowly progressive signs of cerebral dysfunction, focal or generalized convulsions, papilledema, persistent vomiting
• How is intracranial HrTN HA diagnosed?
o neuro exam, visual acuity, visual fields, CT, chest x-ray for metastasis
• When would intracranial HrTN HA be ruled out?
o aura of migraine persists during and after HA
o change in a previous HA pattern
o epilepsy onset after age 20
• What is etiology and ssx of intracranial HoTN HA?
o Etiology: due to loss of CSF from a lumbar puncture or dural tear
Signs & Sxs: worse sitting upright, better lying (opposite of temporal arteritis)
• What can cause intracranial masses HA? Ssx? How is it diagnosed?
o Eg pituitary tumor (compressing on sella turcica)
o 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
o Associated signs of pituitary hormone deficits
o Dx by CT or MRI of cranium
• What is giant cell (temporal) arteritis HA (GCA)?
o Chronic inflammation of large and medium sized vessels; thrombosis may develop at sites of active inflammation– temporal, occipital or frontal-occipital head pain
• What is the etiology of GCA? Mean age of onset?
o Aging, familial, heavy smoking, Northern European ancestry, inc Il-6, HLA-DR4, viral?
o mean age at diagnosis is 72 (almost never in individuals <50)
• What are ssx of GCA?
o unilateral or bilateral
o usu superficial tenderness, not throbbing, variable intensity.
o Pain worse brushing hair, pressure, when lying, possibly on exposure to cold
• What are associated sx of GCA?
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
• What is found on PE for GCA? Lab? Diagnostic procedure?
o PE: palpable nodules over the artery, temporal artery tenderness, pulse often absent
o Lab: marked increase in ESR, Elevated CRP; CBC: May be leukocytosis and mild normochromic anemia; Elevated liver enzymes, decreased serum albumin
o Procedure: Arterial biopsy is diagnostic.
• What complications are seen with GCA?
o permanent blindness, stroke, aortic aneurism and dissection, MI, peripheral arterial insufficiency
• When is HA seen with subarachnoid hemorrhage? Onset? Ssx?
o Bleeding is due to head trauma or spontaneous rupture of a congenital intracranial aneurysm
o Onset: sudden, followed by chronic, persistent intense HA (worst and worsening)
o Signs & Sxs: see meningitis
• What is a subdural hematoma?
o Seen in subarachnoid hemorrhage HA
o onset gradual, steady aching, gradual personality changes, altered consciousness, hemiparesis
• What is TMJ syndrome HA? What sex?
o mal-position, inflammation or arthritis in TMJ, post-whiplash injury
o Sex: usu younger women, men mostly asymptomatic
• What are ssx for TMJ HA?
o usu unilateral (may be bilateral) head pain in TMJ or jaw, radiate to ear
o tenderness in masseter & temporalis mm. < during chewing or opening widely
o may complain of popping or clicking
o limited ROM
o bruxism - see hypertrophy of masseters, malocclusion, tooth enamel wear
• What tests are done for TMJ HA?
o 3 fingers vertical in mouth to check ROM
o slowly open & close jaw- watch for midline deviation
o palpate over TMJ for crepitus (pops, clicks)
• What is a depressive HA?
o vague, generalized, may have other somatic complaints
• What is an eye pain HA?
o Errors of refraction: near or far sighted which is not corrected, eyestrain
o Strabismus: mal-alignment of the eyes (look for corneal light reflex)
o Glaucoma (acute): increased intraocular pressure
o Conjunctivitis, iritis, uveitis
• How is PE done for nose and sinus?
o Nose: use nasal illuminator or otoscope to examine nasal vestibule and turbinates
o Sinus: palpate or percuss for tenderness. Transilluminate for patency
• What are 7 conditions of the nose/sinus?
o Anosmia: loss of sense of smell
o Epistaxis: nosebleed
o Rhinitis: infection of mucus membranes of nose with stuffy, obstructed, runny nose
o Polyps: Soft, pedunculated lesions that emanate from any portion of the nasal mucosa or paranasal sinuses
o Nasal septum problems
o Rhinophyma: Enlarged, bulbous, reddened nose; may obstruct breathing or vision
o Rhinosinusitis: paranasal sinuses; previous term: Sinusitis
• What may cause anosmia?
o Consider CN I abnormality if unilateral, with accompanying visual problems, behavior change
o Consider local problem if bilateral, with concomitant nasal symptoms.
o Also seen in neurological conditions (eg Alzheimer’s disease or Parkinson’s disease)
• What is etiology of anterior epistaxis? Risk factors?
o Kiesselbach plexus- most common in children and young adults
o Risk factors: winter weather: low temps and exposure to dry air, irritants; following URI (nose blowing), acute rhinitis, chronic sinusitis; allergies, trauma, nose-picking
What is etiology of posterior epistaxis?
o Woodruff’s plexus: more likely in older adults; More prolonged bleeding and difficult to control
o Risk factors: HTN; arteriosclerosis; cocaine use; liver disease; alcoholism; blood thinners (coumadin, ASA)
• What other conditions may be considered in case of epistaxis?
o bleeding disorders: hemophilia, cancer, anemia
What are the 2 major classes of rhinitis and their subtypes?
o Bilateral: acute, allergic, atrophic, vasomotor, cocaine use
o Unilateral: trauma, choanal atresia, foreign body, neoplasm
• What is acute rhinitis? Ssx? PE?
o Common cause is Rhinovirus; usually self-limiting in 7 days
o Ssx: watery, profuse discharge with sneezing, clear and later yellow or green, malaise, mouth breathing
o PE: erythematous, swelling of mucosa, low fever
• What is allergic rhinitis? Etiology?
o Chronic, recurrent, very common!
o antigen triggers IgE on mast cells which releases histamine cascade
o seasonal: usu pollens of trees, grass, weeds
o perennial (year-round): animal dander, dust, mold
• What are ssx of allergic rhinitis?
o itchy nose and eyes, watery lacrimation
o episodic nasal obstruction, sneezing, nasal voice
o allergic salute (crease above bridge of nose)
o allergic shiners - bluish discoloration under eyes 2° to obstruction of venous drainage of nasal and sinus congestion
o halitosis from mouth breathing
• What is PE for allergic rhinitis? Labs?
o PE: red mucosa (paler than bacteria; rhinitis), if chronic - pale, bluish mucosa; enlarged adenoids; may also have atopic dermatitis (eczema), asthma
o Lab: eosinophilia maybe present if stain the d/c, also on CBC
• What is atrophic rhinitis? Etiology?
o Nasal mucous membrane to stratified squamous epithelium
o Etiology: unknown, although bacterial infection frequently plays a role.
• What are ssx of atrophic rhinitis?
o anosmia or hyposmia and epistaxis may be recurrent and severe
o nasal congestion, unpleasant smell (ozoena) resulting from a progressive atrophy of the nasal mucosa and underlying bone
o Painful nasal passage, may be foul smelling d/c (discharge?)
• What is the PE for atrophic rhinitis?
o membranes dry & shiny, atrophy of tissues
o yellow and green crusts that bleed when removed
• What is vasomotor rhinitis? Ssx?
o Non-allergic, non-infectious syndrome caused by parasympathetic dominance, leading to vasodilation and edema of nasal vasculature
o Signs & Sxs: similar to allergic rhinitis with rhinorrhea: sneezing, pruritus, congestion. May alternate sides
• What are triggers for vasomotor rhinitis?
o 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
• What is PE for vasomotor rhinitis? Labs?
o PE: swollen inferior nasal turbinates; dark red to bluish mucosa
o Labs: all allergy tests negative, nasal smear negative for organisms
• What are ssx of cocaine use in rhinitis? PE?
o Signs & Sxs: constant runny nose; watery d/c when drug affected, congested when not chronic sore throats, hoarseness
o PE: may see chemical burns, septal perforation
• How can trauma cause unilateral rhinitis?
o 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)
• What is choanal atresia rhinitis? Test?
o congenital defect in septal development
o Test: infant will become distressed if block unaffected nares
• How does foreign body rhinitis present? Neoplasm?
o Foreign body- discharge, odor
o Neoplasm- bloody discharge
• What are nasal polyps linked to? Epidemiology?
o chronic inflammation, ANS dysfunction, genetic predisposition; chronic infection or allergy predispose
o M:F incidence 2 - 4:1 in adults; more common in pts > 40 years
• What are some conditions associated with multiple benign polyps?
o bronchial asthma; cystic fibrosis; allergic rhinitis; allergic fungal sinusitis; chronic rhino-sinusitis
• What are ssx of nasal polyps?
o (depends on the size of the polyp) no sx to nasal obstruction, postnasal drainage, Dull headaches, snoring, rhinorrhea, epistaxis, hyposmia or anosmia
o Often surgically removed and then return unless real cause is managed
• What are 3 examples of nasal septum problems?
o Deviation from trauma- eg. boxers
o Perforation from chronic infection, crusting, nasal surgery, TB, syphilis, cocaine use
o Abscess: rare, dangerous, may lead to cavernous sinus thrombosis
• What is pathophysiology of rhinophyma? Associated with? Sex and age? Psychological?
o Granulomatous infiltration/hypertrophy of sebaceous glands
o Associated with untreated acne rosacea, worsened by (but not caused by) alcoholism
o More common in men >50; significant psychological toll
• Epidemiology of rhinosinusitis? Etiology? Predisposing factors?
o > 30 million pts in the US have sinus disease
o Organisms: Viral (common, less severe); Bacterial (Staph, Strep, H. flu; more severe); Fungal (Mucor, Aspergillis)
o Predisposing factors: decongestants, fatigue, dental problems, food sensitivities, GI issues, septal deviation, large adenoids, foreign bodies
• What are 4 types of rhinosinusitis?
o Acute suppurative; chronic suppurative; serious complications; upper airway cough syndrome
• What are ssx of acute suppurative RS?
o >1 week, but < 3 weeks duration (most rhinoviral infections improve within 7-10 days so the complaint of persistent or worsening symptoms may indicate a developing bacterial sinusitis.)
o nasal congestion, purulent drainage, and facial pain with headache
o pain is often exacerbated by leaning forward or any head movement
o may have dental pain or altered smell
o Kids: may complain of a daytime cough and persistent nasal discharge
• What are sx of acute suppurative RS by the sinus involved?
o Maxillary: dull, throbbing pain in cheek, tender, painful max. teeth, tenderness over maxilla; DDX infected tooth
o Frontal: tenderness over forehead area, swelling of eyelids, frontal h/a
o Ethmoid: pain more medial to eye, feels deep in head or eye, splitting h/a on one side, swelling of eyelids
o Sphenoid: pain behind eye or in occiput or vertex, deeper pain, not local tenderness
• What is found in PE of acute suppurative RS?
o purulent secretions in the middle meatus (highly predictive of maxillary sinusitis)
o Fever is rare unless bacterial cause. (usu no fever if viral)
o facial tenderness to palpation or percussion
o complete opacification of sinus on transillumination—sinus not patent (partial opacification is a nonspecific finding, and it is not as reliable)
• What is epidemiology of chronic suppurative RS? Etiology?
o approximately 32 million cases/ year
o Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis > 70% of cases
o Osteo-meatal obstruction, allergies, polyps, immunodeficiency states, and dental problems
• What are ssx of chronic suppurative RS?
o Manifests more subtly than acute sinusitis; typical sx of acute sinusitis (facial pain and fever) are usually absent.
o 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
• What is found in PE for chronic suppurative RS (not endoscopic)?
o tenderness on palpation over frontal or maxillary sinuses
o transillumination of maxillary or frontal sinuses shows little opacity
o oropharyngeal erythema, purulent secretions
o check for dental caries
• What is found on endoscopic (rhinoscopic) PE for chronic suppurative RS? Eye?
o nasal mucosal erythema, edema, purulent secretions
o check for nasal obstruction from deviated nasal septum or hypertrophied turbinates
o check for nasal polyps
o Eye: conjunctival congestion, lacrimation; Check extraocular movements
• What are some serious complications of Rhinosinusitis?
o Orbital or periorbital cellulitis- edema, pain moving the eye, chemosis (conj. edema) - very sick pt.
o cavernous sinus thrombosis - very dangerous, mortality 50%; high fever, chills, prostrated, comatose, change in mental status; early signs - have deep eye pain, ocular palsy (III, IV, VI), diplopia; late sign- both eyes involved, edema, death within 2-3 days.
• What is upper airway cough syndrome? Ssx? PE?
o common sequellae to rhinosinusitis; “post-nasal drip”
o SSX: cough, rhinorrhea, frequent swallowing, halitosis, frequent spitting, tickling in throat, constant clearing of throat, chronic sore throat
o PE: may see tonsilloliths, cobblestoning of oropharyngeal mucosa, tenderness of sinuses
