10. altered somatic and special sensory function

what is pain?

• universal experience that’s unique to every individual

• multifactorial process

what are the two types of pain?

objective and subjective

what is subjective pain?

pain that relies on patient’s personal description and perception

what is objective pain?

pain that is measurable and can be observed and verified by medical professionals

what system transmits pain and sensations of touch, temperature, and body position?

somatosensory system

the diversity of the somatosensory system is the result of what?

receptors and pathways associated sensations of pain, itch, touch, temperature, and body position

nociceptive pain stimuli may cause?

tissue damage and include pressure, sharp objects, electric current, or heat/cold applied to the skin

nociceptive pathways are composed of what type of neurons?

first, second, and third order neurons

neuropathic pain arises from what?

direct injury or dysfunction of the sensory axons of peripheral or central nerves

what type of pain are nociceptors focused on?

pain and itch

what type of nerve endings are nociceptors?

free nerve endings

first-order neurons

• detect stimuli that threatens the integrity of innervated tissues

• carries sensory information from the periphery to the central nervous system (CNS) - dorsal to spinal cord

second-order neurons

• carry sensory impulse to brain

• relays information from the spinal cord and travels to the thalamus

third-order neurons

• communicates sensory information from the thalamus to the cerebral cortex

• processes pain information

discriminative pathway

used for the rapid transmission of sensory information such as discriminative touch (used for spatial orientation)

anterolateral pathway

involves both the anterior & lateral spinothalamic pathways that provides transmission of sensory information such as pain, thermal sensations, crude touch and pressure that does not require discrete localization of signal source (slow conduction)

what is the anterolateral pathway broken down into?

the paleospinothalamic tract (slower)

what is the paleospinothalamic tract?

• diffuse aching and unpleasant sensation

• seen with chronic and visceral pain

• associated with the mood-altering (emotions) and attention-narrowing effect of pain

• can influence hypothalamic functions and lower heart rate and blood pressure

• travels through small unmyelinated c fibers

• activates the reticular activating system (controls sleep/wake cycles)

specificity

pain is a separate sensory modality and specific receptors (nociceptors) that detect and then transmit info to the brain for interpretation

pattern theory

• group of theories that propose that pain receptors share pathways with other sensory receptors but different patterns of activity signal painful vs. non-painful stimuli

• light touch produces low intensity firing vs intense pressure causes high frequency firing

gate control theory

peripheral receptors generate impulses along the afferent neurons and enter the spinal cord serving as a gate regulating the transmission of impulses. pain is carried by distinct fibers in the spinal cord, small and large diameter fibers; local stimuli can block (close the gate) the pain experience

neuromatrix theory

the brain (thalamus, limbic, spinal) identifies pain and there are multiple dimensions and determinants of pain, including stress, attention, culture, expectation, personality and genetics

type a fibers

• myelinated, largest size fiber, and have the fastest rate of conduction

• conveys cutaneous pressure (touch, cold, mechanical, and heat pain)

• fast pain

type b fibers

myelinated and transmit from cutaneous and subcutaneous receptors

type c fibers

• unmyelinated, smallest diameter, and slowest rate of conduction

• warm-hot, mechanical, chemical, and heat/cold

• slow pain

dermatome

sensory region of the body that's innervated and supplied by a single pair of dorsal ganglia

how do dermatomes prevent a loss of sensory innervation?

neighboring dermatomes can overlap so if one dorsal root (ganglion) is lost, it can result in a decrease of sensory innervation but not total loss

classification of pain

location, quality, and duration

location of pain

cutaneous, deep, visceral, and referred

quality of pain

sharp, burning, diffuse, throbbing, stabbing

acute (duration)

• results from disease, inflammation, or injury to tissue

• sudden onset

• responsive to treatment

• self-limiting (lasting less than 3 months)

• associated with autonomic responses

• self-reported

chronic (duration)

• persistent (lasting longer than 3 months)

• resistant to treatment

• associated with anorexia, insomnia, and depression

referred pain

• perceived at a site different from its point of origin

• results from the network of interconnecting sensory nerves that supplies many different tissues

• can be derived from visceral or somatic structures

phantom limb pain

• ongoing painful sensations that seem to be coming from the part of the limb that is no longer there

• onset of this pain often occurs soon after surgery

• stems from multiple theories including the neuromatrix

• treatment includes TENS, hypnosis, relaxation training, sympathetic blocks

• associated with unmyelinated c fibers

COLDSPA

• c → characteristics

• o → onset

• l → location

• d → duration

• s → severity

• p → pattern

• a → assessment

general treatment of pain

• pain relief (analgesia) is the goal for pain

• careful assessment is key due to subjectivity

• anything that relieves or exacerbation the pain

pain onset

• description of pain, controlling pain to allow individuals to pain, personal reaction to pain

• non-pharmacologic interventions first before OTC and narcotics

pharmacologic treatment of pain

• use of drugs in the management of pain

• combination of narcotic and nonnarcotic analgesics as well as adjuvant medications

• analgesics help decrease eliminate pain without causing unconsciousness, but do not cure underlying cause

• analgesics help make pain tolerable

• ong term use may cause a need for increase in dosage (tolerance)

non-narcotic analgesics

aspirin, acetaminophen, and other NSAIDS some OTC medicines can provide safe and effective relief for mild to moderate pain

aspirin and other nsaids

• antipyretic and anti-inflammatory effect

• inhibition of COX-enzymes

• decrease sensitivity of blood vessels to bradykinin, histamine, decrease release of inflammatory mediators

acetaminophen

• equal to aspirin and other NSAIDS but not anti-inflammatory

• no more than 4,000 milligrams

• seen in other OTC such as Nyquil, and prescription drugs

refraction

bending of light

myopia

nearsightedness

hyperopia

farsightedness

astigmatism

irregular curvature of the cornea

presbyopia

farsightedness-inability of the ciliary muscles and lens to accommodate for near vision

strabismus

cross-eye

amblyopia

lazy eye

diplopia

double vision

nystagmus

involuntary eye movement

glaucoma

a group of conditions that damage the optic nerve is associated with increased intraocular pressure (IOP)

what is the leading cause of blindness in people over age 60?

glaucoma

most common form of glaucoma

primary open-angle glaucoma

pathophysiology of glaucoma

• typically associated with increased IOP due to increased aqueous humor production and decreased outflow of aqueous humor

• angle refers to the point where the iris and cornea

• hereditary

• trabecular network draining the aqueous humor becomes obstructed → increase of IOP

• IOP of 22 mm Hg or more is considered abnormal

pathophysiology of angle-closure glaucoma AKA acute or narrow angle

• Rapid rise in IOP caused by blockage of aqueous humor drainage due to narrowing or closure of the anterior chamber angle

• Buildup of fluid and pressure promotes further narrowing of the angle

• Complete closure is an acute crisis known as acute glaucoma

• More common in people with hyperopia. Angle-closure glaucoma is an inheritable trait

• Normal-tension or low-tension glaucoma is characterized by normal IOP and progressive optic nerve damage with loss of visual fields

clinical manifestations of glaucoma

• eye pain, headache, nausea, blurred vision, and "rainbows" around lights at night

• scarring of the trabecular network may result in chronic glaucoma and cataracts

• damage to optic nerve may result in permanent vision loss

• surgical management is often indicated

diagnostics of glaucoma

• Vision Screening to assess acuity levels

• Snellen Chart

• Jaeger eye Chart

treatment of glaucoma

Goal: lower IOP by decreasing aqueous humor production and increasing aqueous humor outflow

• May be pharmacologic or surgical

• Miotics → drugs that contract the pupil, thereby increasing the outflow of fluid

• Epinephrine-based → increase the outflow of fluid

• Beta blockers → decrease fluid levels

• Carbonic anhydrase inhibitors → decrease fluid levels

• Alpha-adrenergic agonists → decrease fluid levels

• Prostaglandin analogs → increase fluid flow through secondary drainage

• Trabeculoplasty → correction of the trabecular network to promote fluid outflow from the eye in open-angle glaucoma

• Iridotomy → incision into the iris to promote fluid outflow in angle-closure glaucoma

• Cyclophotocoagulation → correction of ciliary tissue to decrease the production of fluid

• Trabeculectomy → surgical removal of a small portion of the trabecular meshwork under the lid to create new drainage

pathophysiology of macular degeneration

• Eye condition affecting the macula, resulting in distortion or loss of central vision.

• Contributing factors-aging, inflammation, injury, and infection

• Gene–gene and gene–environment interactions influence susceptibility.

• Leading cause of blindness among older Americans in the United States.

what are the two forms of macular degeneration?

dry (atrophic) and wet (exudative)

• Dryness causes retinal deterioration resulting from deposition of drusen, small yellow deposits, under the macula next to the basement membrane of the retinal pigment epithelium

• Drusen thins and dries out the macula, promoting loss of function.

• Loss of vision is correlated with increases in drusen deposits.

risk factors of macular degeneration

• age older than 60 years

• smoking cigarettes

• hypertension

• being overweight or obese

• family history

clinical manifestations of macular degeneration

• atrophic macular degeneration → characterized by fluctuating vision, difficulty reading, and limited night vision

• dry form → progression of symptoms is usually slow

• wet form, exudative MD → vision loss may be rapid and severe

• early symptoms are not always apparent, although some affected individuals may report a dark central spot

• consequences of MD include distortion of central vision; decreased ability to read, recognize faces or colors, or drive cars; and blindness

diagnostics of macular degeneration

• regular eye examinations by an ophthalmologist or an optometrist are important

• identify early → thorough eye examination is necessary for at-risk individuals (older adults)

• dilation of the eyes and visualization of the retina allow detection of leakage bulging macula, and drusen deposition

• amsler chart evaluation - evaluates changes in vision consistent with progressive MD

• Fluorescein angiography → colored dye is injected into a peripheral vein and pictures of the retina are taken as dye passes through it to detect the presence of abnormal fluid or progressive changes

• Optical coherence tomography → imaging technique used to obtain detailed retinal images

treatment of macular degeneration

• currently no treatment options for dry MD

• dry MD is a slowly progressive condition

• treatment of wet MD is targeted toward limiting progression of retinal damage and loss of vision

• goal of therapy is to reduce choroidal neovascularization, reducing lesion size and leakage

• inoal of therapy is to reduce choroidal neovascularization, reducing lesion size and leakage

• intraocular use of drugs that block vascular endothelial growth factor (VEGF) is the primary pharmacologic treatment effective in blocking the formation of new blood vessels

• Laser or conventional photocoagulation can be used to target neovascularization, though reduction in vision is a potential risk

• Photodynamic therapy involves irradiation of retinal neovascularization through activation of an injected drug by laser.

disorders of the ear are frequently caused by

inflammation, drainage, or obstruction

alterations in the middle ear

• Inflammation, trauma, and obstruction are often related to middle ear hearing loss

• Auditory tube dysfunction may lead to loss of hearing due to altered patency or obstruction

• Abnormally patent auditory tubes promote fluid movement from the nasopharynx into the middle ear

• Common in infants and children because crying may precipitate the movement of secretions into the tube

otitis media

• most common infection of the middle ear

• Hearing loss may result from immobility of the tympanic membrane, fluid accumulation of the middle ear, and scarring from rupture of the tympanic membrane, altering function

• Can be acute or recurrent, and it is associated with effusion (fluid) in the middle ear and seen across all age groups but has greatest prevalence in infants and children

clinical manifestations of otitis media

• Pain

• Pressure

• Tinnitus

• Irritability

• Difficulty sleeping

• Fever

• Tugging at ears

• Fluid drainage

• Loss of balance

• Hearing difficulties

diagnostics of otitis media

• Hearing Evaluation should include a thorough examination of all structural and functional auditory components

• Audiometric testing can help determine the specific nature of hearing loss

• Auditory acuity is the basic assessment of hearing and provides a general sense of hearing sensation

• History & Physical should be completed to determine the duration, severity, and quality of the hearing loss

• Tympanometry measures the degree of movement of the tympanic membrane to identify middle ear fluid, perforation, or cerumen blockage of the ear canal

• Acoustic reflex measurement can be used to determine movement of the tympanic membrane in response to sound

• Bone conduction testing used to evaluate the internal ear, independent of middle and external ear function. A small vibrator is placed on either the forehead (frontal bone) or the mastoid bone, directly stimulating the cochlear nerve

evaluation of hearing

• The degree of hearing loss can be quantified using a unit of measure known as decibels (dB). The frequency or pitch of the sound, equal to one cycle per second, is referred to in hertz (Hz)

• Pure tone audiometry is used to identify hearing thresholds at different frequencies. Based on pure-tone average, hearing levels can be categorized based on frequencies from 500 to 4,000 Hz. Individuals who have normal hearing can detect sounds at a minimal frequency of −10 to +15 dB

• Individuals who have hearing impairment require sounds with increasing decibels for detection. Minimal decibels needed for sound recognition may help determine the degree of hearing loss

what decibels is profound hearing loss?

91 dB or more

treatment of hearing loss (?)

• Antibiotic therapy for two weeks, administration of pain meds and

observation in clients greater than 23 months of age.

• Corrected by using hearing aids or assistive listening devices to amplify sound

• Cochlear implants are artificial devices surgically placed behind the ear

• Electrical stimulation of nerve endings

• Early screening of hearing loss

pathophysiology of meniere disease

• Swelling of the membranous labyrinth in the cochlea and vestibular system of the internal ear

• Altering hearing and balance.

• A condition associated with severe vertigo (spinning sensation), sensorineural hearing loss, and tinnitus, is related to overproduction or decreased absorption of endolymph

• AKA Endolymphatic hydrops or endolymphatic hypertension, hearing loss is caused by the progressive degeneration of vestibular and cochlear hair cells, described in greater detail in the clinical models

clinical manifestations of meniere disease

• related to vestibular dysfunction, often unilateral

• symptoms can vary from mild to disabling. primary complaint of episodic dizziness

• vertigo → feeling of spinning and a hallmark of meniere disease and is often associated with nausea and vomiting

• nystagmus and tinnitus may also develop

• a feeling of fullness and pain in the ear and sensorineural hearing loss may also complicate the condition

diagnostics of meniere disease

• auditory examination can indicate sensorineural hearing loss

• auditory brainstem responses that measure electrical activity of the cochlear nerve and the brainstem help to identify the type of hearing loss

• electrocochleography (ECOG) is a test that records sound-induced electrical activity in the internal ear, assists with diagnosis

• videonystagmography (VNG) determines communication between balance-related sensors and head movement on eye control

• electronystagmography (ENG) is a group of tests that determine vestibular function based on eye movement

• caloric test uses warm and cool water or air irrigation to induce nystagmus for doctor

treatment of meniere disease

• treatment is symptomatic

• regulation of body fluid through reduced salt intake or diuretic therapy, smoking cessation, and stress reduction may decrease symptom occurrence

• antiemetics to prevent nausea and drugs to reduce vertigo are the main pharmacologic treatments

• treatment for acute symptoms include vestibular suppressants

• betahistine, a histamine analog, is the first-line treatment to reduce the frequency and severity

• direct administration of the antibiotic gentamicin into the middle ear promotes ototoxicity, reducing vertigo with potential of hearing loss

• vestibular neurectomy, severing of the vestibular nerve, also helps reduce vertigo with no direct effect on hearing

• labyrinthectomy, or surgical removal of the labyrinth, may help reduce vertigo with no direct effect on hearing

• nondestructive therapies include endolymphatic-sac decompression or shunting, designed to improve drainage of endolymph

pathophysiology of fibromyalgia

• A condition of the soft tissues and muscle

• Estimated to affect 2% of the population

• Occurs in women seven times more frequently than in men

• Women in the sixth or seventh decade of life have the highest prevalence of fibromyalgia

• Causes significant pain and fatigue but is not linked to a well-defined pathogenesis

• Serotonin levels are decreased in some individuals, consistent with symptoms of depression, pain, sleep alteration, anxiety, and altered muscle function

• Alterations in brain structure and function including changes in brain matter volume and cerebral blood flow have been associated

diagnostics of fibromyalgia

• Subjective findings of fatigue and chronic musculoskeletal pain of at least 3 months duration

• Pain must be present in 12 of the 18 tender point sites for diagnosis

• Some people with the disease develop trigger points or ropybands (tender, tight bands of muscle fibers) occurring throughout the body

treatment of fibromyalgia

• Focus on symptom management that includes both nonpharmacologic and pharmacologic options.

• No diagnostic tests exist to confirm fibromyalgia. It is a diagnosis of exclusion, meaning that tests to confirm other likely diagnoses (including hypothyroidism or hyperparathyroidism) rule out other possibilities

• Analgesics, antidepressants, anticonvulsants, muscle relaxants, tricyclic antidepressants, antiseizure medications, and nonsteroidal anti-inflammatory medications

pathology of migraine headaches

• recurrent, moderate to severe headaches that last 1-2 days

• often associated with nausea, vomiting, and sensitivity to noise and light

• Characterized by neurologic dysfunction involving impairment of cortical, subcortical, and brainstem areas leading to altered autonomic, affective, cognitive, and sensory functions

manifestations of migraines

• Severe, resulting in significant loss of productivity and quality of life

• Migraines are more common in women

• Have four phases, each with distinctive clinical manifestations 1- prodrome (few hours to days), 2-aura (5 to 60 minutes), 3-headache (4 to 72 hours) 4-postdrome (24 to 48 hours)

• Affective symptoms (e.g., mood changes), food cravings, constipation, neck stiffness, and yawning characterize the prodrome, occurring 24 to 48 hours before headache

• Increased energy, sweet cravings, fatigue, and irritability

• Classical or uncommon migraines affecting approximately 15% of individuals include Aura

• Migraine Aura- includes short-duration, focal neurologic events including visual, auditory, somatosensory, or motor symptoms

• Unilateral, pulsing, and throbbing, nausea, vomiting, and photosensitivity are often associated with increasing migraine headache severity

diagnostics of migraines

• Accurate assessment of history and physical examination. For acute headaches, a computed tomography (CT) or magnetic resonance imaging (MRI) scan, may be warranted done to rule out other pathologies such as meningitis, tumor, or increased intracranial pressure

• Need five episodes for diagnosis

• Headache of 4 to 72 hours duration (untreated or treatment resistant)

treatment for migraines (1)

• Nonpharmacologic & pharmacologic measures for prevention, alleviating existing pain.

• Uses pain-relieving medications more than two times a week

• Does not get relief from analgesic treatments

• Avoid triggers, regular exercise, smoking cessation, and stabilization of hormone levels with oral contraceptives or hormone replacement therapy

• Simple analgesics, triptans, and ergots. Acute treatment includes simple analgesics (e.g., acetaminophen, nonsteroidal anti-inflammatory drugs [NSAIDs], aspirin) as the first-line therapy for mild migraine headache

• Botox injections: OnabotulinumtoxinA injections every 12 weeks can help prevent chronic migraines .

• CGRP (Calcitonin gene-related peptide) monoclonal antibodies: Injectable protein medications like erenumab (Aimovig) and fremanezumab (Ajovy) that involves in the transmission of pain signals during a migraine.

treatments for migraines (2)

• If moderate to severe, triptans are recommended

Oral, nasal spray, and injectable triptans (serotonin receptor agonists) mimic the action of serotonin, promoting constriction of blood vessels and interrupting pain pathways.

• Antiemetic medications

• Ergots are a group of medicines called ergot alkaloids and include

dihydroergotamine (DHE-45) and ergotamine

• Calcitonin gene–related peptide (CGRP) inhibitors are also used to help

prevent migraine attacks or make them less severe

• Topiramate (Topamax) is an antiepileptic/antiseizure drug used to prevent

migraine headaches its mechanism of action is uncertain but does reduce

hyperexcitability in brain neural tissue.

• Chronic migraine headaches are also treated with Botox injections