Chapter 16 PDF

CHAPTER 16- Pain, Temperature Regulation, Sleep, and Sensory Function What is the gate control theory of pain? Gate control theory (GCT): o Integrates and builds upon features of other theories (specificity theory, pattern theory, etc.) to explain the complex multid...

CHAPTER 16- Pain, Temperature Regulation, Sleep, and Sensory Function What is the gate control theory of pain? Gate control theory (GCT): o Integrates and builds upon features of other theories (specificity theory, pattern theory, etc.) to explain the complex multidimensional aspects of pain perception and pain modulation Pain transmission is modulated by a balance of impulses conducted to the spinal cord where cells in the substantia gelatinosa function as a “gate” – spinal gate that regulates pain transmission to higher centers in the CNS Nociceptive transmission (mechanical, thermal, and chemical) → opening of the gate→ transmit the perception of pain o Large myelinated A-delta fibers and small, unmyelinated C fibers terminate on interneurons in the substantia gelatinosa (laminae in the dorsal horn of the spinal cord) Non-nociceptive stimulation (from touch sensors in the skin; rubbing a painful area) → closure or partial close of the spinal gates → decreased pain perception: o Larger A-beta fibers Know the type of nerve fibers that transmit pain impulses. Nociceptors (primary order neurons): o Free nerve endings in the afferent PNS that selectively respond to different chemical, mechanical and thermal stimuli o Lateral spinothalmic spinal tract carries the most nociceptive information o When stimulated they cause nociceptive pain. o Categorized according to the stimulus to which they respond and by the properties of the axons associated with them. o Nociception has four phases: 1. Transduction 2. Transmission 3. Perception 4. Modulation A-delta fibers are lightly myelinated, medium-sized fibers that are stimulated by severe mechanical deformation or by mechanical deformation and/or extremes of temperature. o Transmit sharp, well-localized “fast” pain sensations o Cause reflex withdraw of affected body part from the stimulus BEFORE a pain sensation is perceived (i.e. pulling a hand away from a hot stove) Unmyelinated C fibers are smaller, unmyelinated polymodal fibers; stimulated by mechanical, thermal, and chemical nociceptors o Slowly transmit dull, aching, or burning sensations that are poorly localized and longer lasting A-beta fibers are large myelinated fibers o Transmit touch and vibration sensations o DO NOT transmit pain but play a role in pain modulation What are the two types of fibers that transmit the nerve action potentials generated by excitation of any of the nociceptors. Nociceptors are free nerve endings in the afferent peripheral nervous system that selectively respond to different chemical, mechanical, and thermal stimuli. A-delta and C fibers o Comprise the primary, first-order sensory afferents coming into the gate at the dorsal horn of the spinal cord A-delta fibers: o lightly myelinated, medium-sized fibers that are stimulated by severe mechanical deformation (mechanonociceptors) or by mechanical deformation and/or extremes of temperature (mechanothermal nociceptors). o Rapidly transmit sharp, well-localized “fast” pain sensations. o Responsible for causing reflex withdrawal of the affected body part from the stimulus before a pain sensation is perceived. Unmyelinated C fibers: o polymodal; stimulated by mechanical, thermal, and chemical nociceptors. o Slowly transmit dull, aching, or burning sensations that are poorly localized and longer lasting. Pain transmission is the conduction of pain impulses along the A-delta and C fibers into the dorsal horn of the spinal cord and brainstem, thalamus, and cortex. Where in the CNS does pain perception occur? Definition Pain perception: Conscious awareness of pain that occurs primarily in the reticular and limbic systems and the cerebral cortex. Three systems interact to produce the perception of pain and individual responses to pain: 1. Sensory-discriminative system: o Mediated by the somatosensory cortex o Responsible for identifying the: ▪ Presence of pain ▪ Character of pain ▪ Location of pain ▪ Intensity of pain 2. Affective-motivational system: o Mediated through the ▪ Reticular formation ▪ Limbic system ▪ Brainstem with projections to the prefrontal cortex o Determines an individual’s conditioned avoidance behaviors and emotional responses to pain 3. Cognitive evaluative system: o Mediated through the cerebral cortex o Overlies the individual’s learned behavior concerning the experience of pain and can modulate perception of pain Know different clinical descriptions of pain (acute, chronic, neuropathic); pain threshold/tolerance Pain threshold: o point at which a stimulus is perceived as pain o does not vary significantly among people or in the same person over time o Intense pain at one location may increase threshold in another location – perceptual dominance – therefore, pain at one site may mask other painful areas o Generally DECREASED with repeated exposure to pain Pain tolerance: o duration of time or the intensity of pain that an individual will endure before initiating overt pain responses o Generally decreased by person’s ▪ cultural perceptions ▪ expectations ▪ role behaviors ▪ physical and mental health ▪ gender ▪ age ▪ fatigue ▪ anger ▪ boredom ▪ apprehension ▪ sleep deprivation o Tolerance may be INCREASED by alcohol consumption, persistent use of pain medication, hypnosis, warmth, distracting activities, and strong beliefs or faith ACUTE PAIN (nociceptive pain) o Definition: normal protective mechanism that alerts the individual to a condition or experience that is immediately harmful to the body and mobilizes the individual to take prompt action to relieve it o Duration: lasts seconds to days, and sometimes up to 3 months o Patho: relieved after chemical mediators that stimulate pain receptors are removed o S/S: stimulation of ANS → increased HR, HTN, diaphoresis, and dilated pupils o Etiology: arises from cutaneous & deep somatic tissue or visceral organs → classified as: ▪ Somatic: arises from muscle, bone, joints, and skin sharp and well localized (especially fast pain carried by a-fibers) dull, aching, throbbing, and poorly localized (polymodal C fiber transmissions) ▪ Visceral Pain: transmitted by C fibers and refers to pain in internal organs and the lining of body cavities aching, gnawing, throbbing, or intermittent cramping quality; poorly localized; associated with nausea, vomiting, hypotension, restlessness, shock (rare) radiates (spreads away from) the actual site or is referred ▪ Referred Pain:  pain felt in an area removed or distant from its point of origin The area of referred pain is supplied by spinal segment as the actual site of pain. Can be acute or chronic CHRONIC PAIN (Persistent pain) o Definition: pain lasting well beyond the expected normal healing time. o Function: serves no purpose; often accompanied by anxiety and depression and causes suffering. It often appears to be out of proportion to apparent tissue injury. o Duration: lasts for more than 3 to 6 months; may be ongoing (low back pain) or intermittent (migraine headaches) o *Changes in PNS and CNS that cause dysregulation of nociception and pain modulation processes (peripheral and central sensitization) are thought to lead to chronic pain o **Persistent pain allows for physiologic adaptation →normal heart rate and BP→ leads to mistakenly conclude that people with chronic pain are malingering because they don’t appear to be in pain NEUROPATHIC PAIN o Definition: chronic pain initiated or caused by primary lesion or dysfunction in the nervous system and leads to long-term changes in pain pathway structures and abnormal processing of sensory information. o Function: amplification of pain without stimulation by injury or inflammation o S/S: burning, shooting, shock-like, tingling; characterized by hyperalgesia (increased sensitivity to a normally painful stimulus – touch, pressure, pinprick, cold, and heat) and allodynia (induction of pain by normally nonpainful stimuli) o Types of Neuropathic pain: ▪ Chronic neuropathic pain: Leads to long-term plastic changes along somatosensory pathways from the periphery to the cortex and abnormal processing of sensory information by the PNS and CNS ▪ Peripheral neuropathic pain: caused by Peripheral nerve trauma Diabetic or alcohol abuse-induced neuropathy Carcinoma Nutritional deficiencies HIV ▪ Central neuropathic pain: caused by a lesion or dysfunction in the CNS, including: Brain or spinal cord trauma Tumors Vascular lesions MS Parkinson disease Postherpetic neuralgia (PHN) Phantom limb pain Sympathetic dystrophy ▪ Deafferentation pain syndromes:  Neuropathies that result from lesions in the PNS or CNS that interrupt the spinothalamic pathways at any level of the nervous system and are associated with hyperexcitability of the somatosensory thalamus and cortex ▪ Hemiagnosia pain: Form of central pain associated with stroke that produces paralysis and hypersensitivity/allodynia on one half of the body ▪ Phantom limb pain: Pain in an amputated limb after the stump has completely healed. ▪ Sympathetically mediated pain (SMP) or complex regional pain syndromes (CRPSs): Can occur after peripheral nerve or extremity injuries (usually develop 1-2 weeks after), and include two types: o Type I: associated with injury but no apparent nerve injury. o Type II: evidence of nerve injury. Know endogenous opioids. Definition: family of morphine-like neuropeptides that inhibit transmission of pain impulses in the spinal cord, brain, and periphery Their receptors play a role in various CNS, GI system, immune system, and other organ system disorders. There are 4 types of opioid neuropeptides (substances that act as neurotransmitters by binding to one or more G-protein-coupled opioid receptors): o Enkephalins: best known and most prevalent; 1st endogenous opioids extracted in research ▪ Location: found concentrated in the hypothalamus, the periaqueductal gray (PAG) matter, the nucleus raphe magnus of the medulla, and the dorsa; horns of the spinal cord ▪ Binds to the δ receptors Two types: o Methionine-enkephalin (ratio to leucine-enkephalin is 4:1) o Leucine-enkephalins o Endorphins (endogenous morphine): 1st discovered in the human PAG ▪ Location: produced in the hypothalamus and pituitary gland ▪ Binds to μ receptors in the hypothalamus and pituitary gland ▪ Function: produces the greatest sense of exhilaration or “high” than all other endorphin types; strong mu-receptor agonist and believed to provide substantial natural pain relief o Dynorphins: most potent endogenous neurohormone ▪ Location: found in the hypothalamus, brainstem, PAG-rostral ventromedial medulla (RVM) system, and spinal cord ▪ Binds strongly with the κ receptors ▪ Function: serves to impede pain signals in the brain but can, in certain circumstances, incite pain through mechanisms of up-regulation (paradoxically stimulating chronic pain); plays a role in mood disorders and drug addiction o Endomorphins: potent analgesic, GI, and anti-inflammatory effects ▪ Location: Endomorphins 1 and 2 are peptides isolated from the brain and spinal cord and show highest affinity and selectivity for the (μ) mu-opiate receptor ▪ Binds to almost all tissue in body; receptors throughout the brain, brainstem and GI tract  ▪ Function: can modulate stress and anxiety, feeding behavior, cough suppression, immune and inflammatory responses, and alcohol intake What is the relationship between epinephrine and body temperature? Heat production: hypothalamus + endocrine system → hypothalamic hormone called thyroid stimulating hormone release hormone TSH-RH → stimulates anterior pituitary to release TSH → acts on thyroid gland to stimulate release of thyroxine (T4) → acts on adrenal medulla, causing release of epinephrine into the bloodstream Epinephrine causes vasoconstriction (improves thermal regulation), stimulates glycolysis, and increases metabolic rate, thus increasing body heat. Heat is distributed by the circulatory system. Know mechanisms of heat production and heat loss. In human, body temperature is maintained around 37C (98.6F) and rarely exceeds 41C. Normal range is 36.2C to 37.7C. Temperature regulation (thermoregulation) is mediated by o Hypothalamus o Peripheral thermoreceptors in the skin and abdominal organs (unmyelinated C fibers and thinly myelinated A-delta fibers) o Central thermoreceptors in the spinal cord o Trigeminal ganglia provide the hypothalamus with information about skin and core temperatures HEAT PRODUCTION o Chemical reactions of metabolism: ▪ Chemical reactions that occur during ingestion and metabolism of food and those required to maintain the body at rest (basal metabolism) require energy and produce heat. ▪ These processes occur in the body core (primarily the liver) and are in part responsible for the maintenance of core temperature. o Skeletal muscle contraction: ▪ Produces heat through two mechanisms (both which are controlled by the posterior hypothalamus and occur in response to cold): Gradual increase in muscle tone. Production of muscle oscillations – shivering→ does not occur in neonates o Chemical thermogenesis: ▪ Also called nonshivering or adrenergic thermogenesis ▪ Results from release of epinephrine and norepinephrine → a rapid, transient increase in heat production by raising the body’s basal metabolic rate. ▪ Occurs in brown adipose tissue (rich with mitochondria and blood vessels) and is essential for nonshivering thermogenesis. HEAT LOSS: o Radiation: ▪ Heat loss through electromagnetic waves ▪ These waves emanate from surfaces with temperatures higher than the surrounding air temperature (temperature of the skin is higher than that of air, the skin and the body lose heat to the air) o Conduction:  ▪ Heat loss by direct molecule-to-molecule transfer from one surface to another, with warmer surfaces losing heat to cooler surfaces. (skin loses heat through direct contact with cooler air, water, or another surface) o Convection: ▪ The transfer of heat through currents of gases or liquids and occurs passively as warmer air at the surface of the body rises away from the body and is replaced by colder air ▪ Process may be aided by fans or wind → combined effect of conduction and convection by wind is conventionally measured as the wind-chill factor. o Vasodilation: ▪ Peripheral vasodilation increases heat loss by diverting core-warmed blood to the surface of the body. ▪ As the core-warmed blood passes through the periphery, heat is transferred by conduction to the skin surface and from the skin to the surrounding environment. ▪ Occurs in response to autonomic stimulation under the control of the hypothalamus. o Decreased muscle tone: ▪ To decrease heat production, muscle tone may be moderately reduced and voluntary muscle activity curtailed ▪ This may explain in part the “washed-out” feeling associated with high temperatures and warm weather. o Evaporation: ▪ Evaporation of body water from the surface of the skin and the linings of the mucous membranes is a major source of heat reduction. ▪ Insensible water loss accounts for about 600ml of water loss per day. ▪ Sweating may result in 2.2L of fluid lost per hour. ▪ Electrolytes are also lost. ▪ Large volume loss through sweating may result in decreased plasma volume, decreased BP, weakness, & fainting. Heat loss by sweating/evaporation is affected by: Sympathetic neural activity. Favorable temperature difference between the body and the environment. Humidity: when high, sweat does not evaporate and instead remains on the skin or drips, when low, evaporates quickly. o Increased pulmonary ventilation: ▪ Exchanging air with the environment through the normal pulmonary ventilation provides some heat loss, although it is minimal in humans. ▪ This normal process occurs faster at higher body temperatures through and increase in ventilator rates; thus, hyperventilation is associated with hyperthermia. o Voluntary mechanisms: ▪ In response to high body temperatures, people physically “stretch out,” thereby increasing the body surface area available for heat loss ▪ They also “take it easy,” thereby decreasing skeletal muscle work, and they “dress for warm weather” in garments that reflect heat and promote convection, conduction, and evaporation ▪ (light-colored, loose-fitting clothes). o Heat adaptation:  ▪ The body of an individual who goes from a cooler to a much warmer climate undergoes a period of adjustment, a process that takes several days to several weeks Heat exhaustion and heat stroke HEAT EXHAUSTION / COLLAPSE: Most common heat related injury; result of prolonged high core or environmental temperatures. o High temperatures cause the appropriate hypothalamic response of profound vasodilation and profuse sweating → (prolonged period) produce dehydration, decreased plasma volumes→ hypotension, decreased cardio output, and tachycardia S/S: Individual feels weak, dizzy, nauseated, and faint. o Ceasing activity = decreases muscle work → decreased heat production and lying down redistributes vascular volume. o Should be encouraged to drink warm fluids to replace fluid lost through sweating. HEAT STROKE Rectal temp > 41C or 106F Potentially lethal result of breakdown in control of an overstressed thermoregulatory center Causes/Patho: →overexposure to environmental heat or impaired physiologic mechanisms for heat loss → sweat cools the person starting with the face and forehead, and fanning the face enhances this mechanism → brain cannot tolerate temperatures greater than 40.5C (104.9F) → cardiovascular and thermoregulatory system stops functioning → body’s heat loss mechanisms fail → sweating ceases (skin becomes dry and flushed; irritability, confusion, stuporous, comatose with possible visual disturbances) Continued progression → high core temperatures and vascular collapse → cerebral edema, degeneration of the CNS, swollen dendrites, renal tubular necrosis, hepatic failure with delirium, multi-system organ failure Coma or death results unless immediate, effective treatment is initiated Treatment: o Remove from warm environment, use cooling blankets or cool water bath, or ice packs on head, neck, axillae, and groin area. o Care must be taken to prevent too rapid cooling of the surface, which causes peripheral vasoconstriction and prevents core cooling. Children more susceptible to heat stroke than adults because: o They produce more metabolic heat when exercising. o They have greater surface area to body mass ratio. o Their sweating capacity is less. Stages of sleep Sleep is an active, multiphase, complex brain process that provides restorative functions and promotes memory consolidation. Major sleep center is located in the Hypothalamus Normal sleep has two phases that can be documented by EEG:  o Rapid eye movement (REM) sleep o Non-REM (NREM) or slow-wave sleep Sleep cycle (NREM and REM sleep alternate – each cycle lasting for approximately 9-100 minutes) 1. Awake: wakefulness with eyes closed and predominated by alpha waves. 2. NREM sleep a. 75-80% of sleep time b. N1: light sleep with alpha waves interspersed with low-frequency theta waves; slow eye movements cycle lasts 10-12min (3-8% of sleep time) c. N2: further slowing of EEG with the presence of sleep spindles and slow eye movements; cycle lasts 30-60 min; 45-55% of sleep time; temperature drops d. N3: low-frequency high-amplitude delta waves with occasional sleep spindles (known as slow-wave sleep); no slow eye movements; 13-23% of sleep time 3. REM sleep: a. 20-25% of sleep time b. Time of most dreaming c. low-voltage fast activity that occurs for 5-60 min about every 90 minutes REM SLEEP NREM SLEEP Etiology: controlled by the pontine and reticular Etiology: initiated by the withdrawal of neurotransmitters formation; vivid dreaming from the reticular formation and by the inhibition of also known as paradoxic sleep because the EEG pattern arousal mechanisms in the cerebral cortex. is like the normal awake pattern. Patho: Patho: Respiration is DEPENDENT and controlled by Bursts of conjugate rapid eye movement in all metabolic processes. directions Basal metabolic rate is decrease by 10-15%. Atonia of antigravity muscles Temperature decreased 0.5C to 1C. Suppressed temperature regulation HR decreases by 10-30 beats per minute. Alteration in heart rate/blood pressure/respiration Respiration, BP, and muscle tone all decrease, pupils Penile erection in men/clitoral engorgement in women constrict, and knee jerk reflexes are absent. High rate of memorable dreams During N1 and N2 Steroids released in short bursts Cerebral blood flow to brainstem and cerebellum Respiratory control thought to be largely is decreased. INDEPENDENT of metabolic requirements and During N3 oxygen variation. Cerebral blood flow to cortex is decreased and Cerebral blood flow to both hemispheres is increased. growth hormone is released, with depressed levels *Respiratory obstruction common because of loss of of corticosteroids and catecholamines. tongue muscle control **Loss of REM sleep impairs memory and learning. Disorders of the conjunctiva of the eye. Conjunctivitis is an inflammation of the conjunctiva (mucous membrane covering the front part of eyeball). The inflammatory response produces photophobia, visual blurring, redness, edema, pain, and lacrimation (treatment related to cause) Acute bacterial conjunctivitis (“pinkeye”):  o Highly contagious o Often caused by gram-positive bacteria (staphylococcus, haemophilus, proteus) o Children ages 6 and under o Haemophilus may lead to otitis media o Onset is acute; disease is often self-limiting, resolving spontaneously in 10-14 day o S/S: mucopurulent drainage from one or both eyes o Tx: preventing spread of organism with handwashing and use of separate towels; Viral conjunctivitis: o Contagious o Caused by an adenovirus (some strains of virus cause conjunctivitis and pharyngitis, and others cause keratoconjunctivitis) o S/S: watering, redness, and photophobia o Tx: symptomatic Allergic conjunctivitis: o Associated with a variety of antigens (pollens) o S/S: Ocular itching, photophobia, burning/gritty feel in eye o Tx: antihistamines, low-dose corticosteroids, mast cell stabilizers, and vasoconstrictors. Chronic conjunctivitis: o Result of any persistent conjunctivitis o Requires identification for effective treatment Trachoma (chlamydial conjunctivitis): o Caused by Chlamydia trachomatis, often associated with poor hygiene and is the leading cause of preventable blindness in the world o S/S: inflammation with scarring of the conjunctiva and eyelids → distorted lashes to abrade the cornea → corneal scarring and blindness o Tx: surgery for in-turned lashes, systemic or local antibiotics, facial cleanliness, and environmental improvement (WHO “SAFE” strategy for treatment) Keratitis: o Inflammation of the cornea that can be noninfectious or caused by bacteria, viruses, or fungi o Bacterial infections→ corneal ulceration; require intensive antibiotic treatment (staphylococcus aureus is the most common bacterial infection) o Virus (type 1 herpes simplex) can involve the cornea and conjunctiva o Causes: contact use, trauma, and penetrating keratoplasty (corneal grafting) o S/S: photophobia, pain, and lacrimation; severe ulcerations with residual scarring require corneal transplantation.