Venous Structure	Location and Area Drained
Superior sagittal sinus	Courses along the midline at the superior border of the falx cerebri; superior cerebral veins empty into it
Straight sinus	Lies in the midline attachment of the falx cerebri and the tentorium; drains the system of internal cerebral veins (including the inferior sagittal sinus and great cerebral vein of Galen)
Transverse sinuses	Lie in the bony groove along the fixed edge of the tentorium cerebelli; drain the straight sinus and the superior sagittal sinus
Sigmoid sinuses	Lie on the mastoid process of the temporal bone and jugular process of the occipital bone; receive blood from the transverse sinuses and empty into the internal jugular veins
Inferior sagittal sinus	Lies along the free inferior border of the falx cerebri just above the corpus callosum; receives blood from the medial aspects of the hemispheres
Emissary veins	Connect the dural sinuses with veins outside the cranial cavity

(b) Internal jugular veins collect blood from the large dural venous sinuses and return blood to the heart

iv. Blood-brain barrier: Specialized permeability of the brain capillaries that limits transfer of certain substances from blood into brain tissue. Barrier formed by tight junctions between brain capillary endothelial cells, reduced transport mechanisms of these cells, and footlike projections from the astrocytes that encase the capillaries.

(a) Water, carbon dioxide, oxygen, glucose, and lipid-soluble substances cross the cerebral capillaries with ease. Uptake of other substances, such as dyes and ions (e.g., Na⁺, K⁺), is much slower.

(b) Regulates the entry or removal of various substances to maintain a homeostatic environment for the central nervous system (CNS)

(c) Clinically significant in treating and diagnosing CNS disease. Blood-brain barrier disruption and increased permeability occurs with brain injury, tumors, infections, and stroke.

d. Ventricular system and CSF (Figure 4-11)

FIGURE 4-11 Ventricular system. A, Circulation of cerebrospinal fluid. B, Ventricles of the brain. (From Applegate EJ: The anatomy and physiology learning systems textbook, ed 2, Philadelphia, 2000, Saunders, p 169.)

i. Ventricles: Four cavities containing CSF

(a) Lateral ventricles: Largest ventricles, one in each cerebral hemisphere. The anterior (frontal) horns lie in the frontal lobes; the bodies extend back through the parietal lobes to the posterior (occipital) horns, which project into the occipital lobes; the inferior (temporal) horns lie in the temporal lobes.

(b) Third ventricle: Midline between the two lateral ventricles, surrounded by the diencephalon

(c) Fourth ventricle: In the posterior fossa bordered by the pons, medulla, and superior cerebellar peduncles; continuous with the cerebral aqueduct (aqueduct of Sylvius) superiorly and the central spinal canal inferiorly

ii. CSF functions

(a) Cushions the brain and spinal cord from injury

(b) Provides support and buoyancy for the brain, decreasing its effective weight on the skull

(c) Its displacement out of the cranial cavity (and, to an extent, its increased reabsorption) compensates for increases in intracranial volume and pressure

(d) Regulates the nervous system chemical environment to preserve homeostasis

(e) Enables water-soluble metabolites to diffuse from the brain

(f) Serves as a channel for neurochemical communication within brain

iii. CSF properties: See Table 4-4

TABLE 4-4

Normal Properties of Cerebrospinal Fluid (CSF)

iv. CSF formation

(a) Rate of synthesis estimated as 500 ml/day or 22 to 25 ml/hr

(b) Choroid plexus: Tuft of capillaries covered by epithelial cells found in all ventricles; principal source of CSF; lateral ventricles produce most

v. Circulation and absorption of CSF (see Figure 4-11)

(a) CSF circulates from the lateral ventricles through the interventricular foramina (foramina of Monro) to the third ventricle and to the fourth ventricle via the aqueduct of Sylvius; CSF then circulates to the subarachnoid space via the foramina of Luschka and Magendie

(b) Most CSF is absorbed via the arachnoid villi into the dural sinuses

vi. Blood-CSF barrier: Choroid plexus epithelium imposes a barrier analogous to the blood-brain barrier; permits selective transport of substances from the blood into the CSF

e. Brain metabolism

i. Brain has high metabolic energy requirements; energy primarily used for neuronal conductive and metabolic activities

ii. At rest, the brain consumes 25% of body glucose and 20% of body oxygen; cerebral oxygen consumption averages 49 ml/min

iii. Brain utilizes glucose as its principal energy source

iv. Minimal storage of oxygen and glucose in the brain necessitates a constant supply for normal neuronal function

v. Anaerobic glucose metabolism (glycolysis) yields insufficient adenosine triphosphate (ATP) to meet cerebral energy demands. Rate of glycolysis increases markedly during hypoxia in an attempt to maintain functional neuronal activity.

vi. Within seconds to minutes of anoxia, the energy-dependent sodium-potassium pump fails; cytotoxic cerebral edema results

vii. Hypoglycemia causes neuronal dysfunction and may lead to convulsions, coma, and death

f. Cells of the nervous system

i. Neuron: Basic functional unit of the nervous system; transmits nerve impulses

(a) Components of each cell (Figure 4-12)

FIGURE 4-12 Structure of a typical neuron. (From Thibodeau GA, Patton K: Anatomy and physiology, ed 5, St Louis, 2003, Mosby, p 348.)

(1) Cell body: Carries out the metabolic functions of the cell; contains a nucleus, cytoplasm, and organelles surrounded by a lipoprotein cell membrane

(2) Dendrites: Short branching extensions of the cell body; conduct impulses toward the cell body

(3) Axon hillock: Thickened area of the cell body from which the axon originates

(4) Axon: Long extension of the cell body; conducts impulses away from the cell body; usually myelinated. Outside the brain, axons are also covered with neurilemma. Branch into several processes at the terminal end.

(5) Myelin sheath: White protein-lipid complex that surrounds some axons; laid down by oligodendrocytes in the CNS and by Schwann cells in the PNS

(6) Nodes of Ranvier: Periodic interruptions in the myelin covering along the axon. Impulses are conducted from node to node (saltatory conduction), which makes conduction more rapid and efficient.

(7) Synaptic knobs: At the terminal ends of the axon; contain vesicles that store neurotransmitter substances

(b) Functions

(1) Receive input from other neurons, primarily via the dendrites and cell body

(2) Conduct action potentials or impulses along the axon

(3) Transfer information by synaptic transmission to other neurons, muscle cells, or gland cells

ii. Neuroglial cells: Support, nourish, and protect the neurons; about 5 to 10 times as numerous as neurons. Four types:

(a) Microglia: Phagocytize tissue debris when nervous tissue is damaged

(b) Oligodendroglia: Responsible for myelin formation on axons in the CNS

(c) Astrocytes: Contribute to the structure of the blood-brain barrier. Provide nutrients for neurons. Constitute the structural and supporting framework for nerve cells and capillaries. Remove excess potassium and neurotransmitters. Contribute to scar formation in response to neuronal cell injury or death.

(d) Ependyma: Line the ventricles of the brain and the central canal of the spinal cord. Regulate the flow of substances from these cavities into the brain. Aid in CSF production.

g. Synaptic transmission of impulses: Unidirectional conduction of an impulse from a presynaptic neuron across a junction or synapse to a postsynaptic neuron

i. Resting membrane potential (RMP): Voltage difference across the cell membrane when the neuron is resting. Determined by the difference in ion concentrations on either side of the membrane. At rest, cells are positively charged outside and negatively charged inside.

ii. Depolarization: Stimulus causes sodium channels to open, which results in an intracellular influx of sodium ions (Na⁺)

(a) These ionic fluxes decrease RMP

(b) This depolarization is called the excitatory postsynaptic potential (EPSP)

iii. Action potential: If a transient voltage change that occurs with depolarization is of sufficient magnitude (threshold level), an action potential is produced and transmitted (conducted as an impulse) along the nerve fibers in an active, self-propagating process

iv. Summation: Simultaneous excitation of numerous excitatory presynaptic terminals (or rapidly successive discharges from the same presynaptic terminal) can add together to cause a progressive increase in the postsynaptic potential that may eventually reach threshold to generate an action potential

v. Neurotransmitters (Table 4-5): Chemicals secreted by presynaptic knobs or vesicles (usually located at the axon terminal) that excite, inhibit, or modify the response of a postsynaptic neuron. When an action potential reaches the synaptic knob, calcium channels are opened, allowing Ca⁺⁺ influx into the knob, which triggers neurotransmitter release.

TABLE 4-5

Major Neurotransmitters: Type, Location, and Action

^*Action is determined by the postsynaptic receptor rather than the neurotransmitter.

(a) Transmitter diffuses across the synapse and binds with postsynaptic membrane receptors, which causes certain ion channels to open

(b) Excitatory neurotransmitters: Open sodium and potassium channels, which results in postsynaptic membrane depolarization

vi. Refractory period

(a) Absolute refractory period: Membrane is unresponsive to any stimulus, so that the neuron is incapable of producing an action potential. Occurs for a fraction of a second after the membrane surpasses the threshold potential. Limits the frequency of the impulses that a cell can generate.

(b) Relative refractory period: Neuron can be excited again but only by a very strong stimulus (i.e., summation above threshold); occurs during membrane repolarization

vii. Repolarization

(a) At the peak of an action potential, the cell membrane again becomes impermeable to Na⁺; potassium channels open and allow rapid efflux of K⁺ from the cell, which thereby reestablishes the RMP

(b) RMP returns with the aid of the sodium–potassium–adenosine triphosphatase (ATPase) pump, which pumps Na⁺ out of the cell and K⁺ into the cell

viii. Inhibition

(a) Inhibitory postsynaptic potential (IPSP)

(1) Inhibitory neurotransmitters open potassium and/or chloride channels; this causes increased negativity of the membrane potential, which results in hyperpolarization of the cell membrane

(2) Decreases excitability and inhibits impulse transmission

(b) Presynaptic inhibition: Reduced amount of neurotransmitter is released; this reduces the magnitude of the EPSP to subthreshold levels

2. Spine and spinal cord

a. Vertebral column (Figure 4-13)

FIGURE 4-13 Spinal nerves. Each of the 31 pairs of spinal nerves exits the spinal cavity from the intervertebral foramina. The names of the vertebrae are given on the left and the names of the corresponding spinal nerves on the right. Note that after leaving the spinal cavity, many of the spinal nerves interconnect to form plexuses. I, Inferior; L, left; R, right; S, superior. (From Thibodeau GA, Patton K: Anatomy and physiology, ed 5, St Louis, 2003, Mosby, p 414.)

i. Composed of 33 vertebrae

(a) Cervical: Seven vertebrae

(1) Support the head and neck; smallest vertebrae

(2) Atlas (first cervical vertebra): Supports the head; articulates with the occipital bone superiorly and the axis inferiorly

(3) Axis (second cervical vertebra)

a) Odontoid process (dens): Projection of the axis that protrudes upward through the anterior arch of atlas

b) Allows for rotation of the head

(b) Thoracic: Twelve vertebrae; articulate with the ribs; support the chest muscles

(d) Sacral: Five fused vertebrae; form a large triangular bone, the sacrum

(e) Coccygeal: Four fused rudimentary vertebrae

ii. Anatomic features of a typical vertebra

(a) Body: Flat round, solid portion; lies anteriorly

(b) Arch: Posterior part of the vertebra. Consists of:

(1) Pedicles: Two short bony projections that extend posterior from the body

(2) Lamina: Join each pedicle and fuse posteriorly at the midline to complete the arch; processes project from the laminae

(3) Spinous process: Midline projection protruding posteriorly from the laminae

(4) Transverse processes: Projections from the laminae on each side of the vertebrae

(5) Articular processes (facets): Projections from the laminae that protrude upward or downward (superior or inferior articulating processes); inferior processes articulate with the superior processes of the vertebra directly below

(d) Spinal foramina: Opening between the arch and the body through which the spinal cord passes

iii. Intervertebral discs

(a) Fibrocartilage layer between the bodies of adjoining vertebrae

(b) Act as shock absorbers

iv. Spinal ligaments: Hold the vertebrae and discs in alignment; prevent excessive spinal flexion or extension

b. Spinal cord

i. Location: Extends from the superior border of the atlas to the first or second lumbar vertebra

(a) Continuous with the medulla oblongata

(b) Conus medullaris: Caudal end of the spinal cord

(d) Filum terminale: Nonneural filament that extends downward from the conus medullaris and attaches to the coccyx; helps maintain the position of spinal cord during trunk movement

ii. Meninges: Continuous with the layers covering the brain

iii. Gray matter (Figure 4-14)

FIGURE 4-14 Transverse section of the spinal cord. A, Anterior; L, left, R, right, P, posterior. (From Ozuna JM: Nursing assessment neurologic system. In Lewis SM, Heitkemper MM, Dirksen SR: Medical surgical nursing assessment and management of clinical problems, ed 5, St Louis, 2000, Mosby, p 1584.)

(a) An H-shaped, internal mass of gray substance surrounded by white matter; consists of cell bodies and their dendrites and axons

(b) Anterior gray column (anterior horn): Contains cell bodies of efferent motor fibers

(d) Posterior gray column (posterior horn): Contains cell bodies of afferent sensory fibers

iv. White matter (see Figure 4-14)

(a) Composed of three longitudinal columns (funiculi): Anterior, lateral, and posterior

(b) Contains mostly myelinated axons

(c) Funiculi contain tracts (fasciculi): Composed of axons with similar origin, course, and termination that perform specific functions; clinically significant tracts are summarized in Table 4-6; classified as follows (Figure 4-15):

TABLE 4-6

Major Spinal Cord Tracts

FIGURE 4-15 Major ascending (sensory) and descending (motor) tracts of the spinal cord. A, Anterior; L, left; R, right; P, posterior. (From Thibodeau GA, Patton K: Anatomy and physiology, ed 5, St Louis, 2003, Mosby, p 382.)

(1) Ascending or sensory tracts: Pathways to the brain for impulses that enter the cord via the dorsal roots of the spinal nerves

(2) Descending or motor tracts: Transmit impulses from the brain to the motor neurons of the spinal cord that exit via the ventral root of the spinal nerves

(d) Most tracts are named to indicate the column in which the tract travels, the location of its cells of origin, and the location of axon termination

v. Upper and lower motor neurons

(a) Lower motor neurons (LMNs): Spinal and cranial motor neurons that directly innervate muscles. LMN lesions cause flaccid paralysis, muscular atrophy, absent reflexes.

(b) Upper motor neurons (UMNs): Located completely in the CNS; regulate LMN activity. UMN lesions are associated with spastic paralysis, clonus, increased tone, hyperactive reflexes, Babinski’s sign.

c. Reflexes

i. Reflex arc: Requires a receptor, sensory neuron, motor neuron, and effector (e.g., muscle or gland) (Figure 4-16)

FIGURE 4-16 The two-neuron patellar reflex or “knee jerk.” (From Phipps WJ, Marek JF, Monahan FD, et al: Medical-surgical nursing health and illness perspectives, ed 7, St Louis, 2003, Mosby, p 1311.)

ii. Monosynaptic reflex arc: Direct synapse between the afferent and efferent neurons

(a) Stimulation of afferent nerve fibers sends impulses to the spinal cord through the dorsal roots of spinal nerves

(b) Impulse synapses with anterior motor neurons, sending out an efferent discharge confined to the axons supplying the muscle from which the afferent impulse originated

iii. Polysynaptic reflex arc

(a) More than one synapse required to complete the reflex arc

(b) Most reflexes are polysynaptic; may involve interneurons (neurons in the CNS that transmit impulses from a sensory neuron to or toward a motor neuron) and multiple spinal segments and/or areas of brain

iv. Reciprocal innervation: Impulses that excite motor neurons supplying a particular muscle also inhibit motor neurons of antagonistic muscles

3. Peripheral nervous system (PNS)

a. Spinal nerves

i. Thirty-one symmetrically arranged pairs of nerves, each possessing a sensory (dorsal) root and a motor (ventral) root: 8 cervical pairs, 12 thoracic pairs, 5 lumbar pairs, 5 sacral pairs, 1 coccygeal pair (see Figure 4-13)

ii. Fibers of the spinal nerves

(a) Motor fibers: Originate in the anterior gray column of the spinal cord, form the ventral root of the spinal nerve, and pass to skeletal muscles

(b) Sensory fibers: Originate in the spinal ganglia of the dorsal roots; peripheral branches distribute to visceral and somatic structures as mediators of sensory impulses to the CNS

(1) Sympathetic

a) Originate from cells between the posterior and anterior gray columns from the first thoracic to second lumbar cord segment

a) Innervate the viscera, blood vessels, glands, and smooth muscle

(2) Parasympathetic

a) Arise from sacral cord segments S2 to S4

b) Pass to the pelvic and abdominal viscera

(d) Cauda equina: Spinal nerves that arise from the lumbosacral portion of the spinal cord contained within the lumbar cistern

iii. Dermatomes (Figure 4-17): Skin areas supplied by the dorsal root (sensory fibers) of a given spinal nerve; adjacent dermatomes overlap

FIGURE 4-17 Dermatomes. (From Russo-McCourt TA: Spinal cord injuries. In McQuillan KA, Von Rueden KT, Hartsock RL, et al, editors: Trauma nursing from resuscitation through rehabilitation, ed 3, St Louis, 2002, Saunders, p 522.)

iv. Plexuses: Network of spinal nerve roots (Table 4-7)

TABLE 4-7

Plexuses and Their Locations and Areas of Innervation

b. Neuromuscular transmission (Figure 4-18)

FIGURE 4-18 Neuromuscular junction. This figure shows how the distal end of a motor neuron fiber forms a synapse, or “chemical junction,” with an adjacent muscle fiber. Neurotransmitters (specifically, acetylcholine) are released from the neuron’s synaptic vesicles and diffuse across the synaptic cleft. There they stimulate receptors in the motor endplate region of the sarcolemma. (From Thibodeau GA, Patton K: Anatomy and physiology, ed 5, St Louis, 2003, Mosby, p 316.)

i. Physiologic anatomy at the neuromuscular junction

(a) Motor end plate: Distal end of motor axon loses its myelin sheath and flattens out at the end lying close to the muscle fiber membrane (sarcolemma)

(b) Synaptic cleft: Space between the motor endplate and the muscle fiber membrane

(c) Synaptic gutter: Invagination of the muscle fiber membrane where numerous folds increase the surface area available for neurotransmitter to act

(d) Vesicles: Nerve terminal structures that store and release the neurotransmitter acetylcholine (ACh)

ii. When an action potential reaches the neuromuscular junction, vesicles release ACh into the synaptic cleft. Amount released depends on the magnitude of the action potential and the presence of calcium. ACh attaches to receptor sites on the postjunctional muscle membrane and increases its permeability to Na⁺, K⁺, and other ions.

iii. End-plate potential: Motor nerve action potential that is local (e.g., nonpropagated) and graded, rather than all or nothing

iv. Muscle contraction: Action potentials subsequently form on either side of the endplate and conduct in both directions along the muscle fiber, initiating a series of events that result in muscle contraction

v. Acetylcholinesterase: Catalyzes the hydrolysis of ACh to choline and acetic acid and thus limits the duration of ACh action on the endplate, which ensures production of only one action potential

c. Cranial nerves: 12 pairs of nerves considered part of the PNS (Figure 4-19 and Table 4-8)

TABLE 4-8

Cranial Nerves: Origin, Course, and Function

FIGURE 4-19 Cranial nerves. Ventral surface of the brain showing the attachment of the cranial nerves. (From Thibodeau GA, Patton K: Anatomy and physiology, ed 5, St Louis, 2003, Mosby, p 421.)

d. ANS (Figure 4-20)

FIGURE 4-20 Diagram of the autonomic nervous system. The parasympathetic nervous system division (left) arises from cranial nerves III, VII, IX, and X and from spinal cord segments S2 to S4. The sympathetic division (right) arises from spinal cord segments T1 to T12. (From DeMyer W: Neuroanatomy, ed 2, Baltimore, 1998, Williams & Wilkins, p 99.) Williams & Wilkins

i. Structure

(a) Composed of two neuron chains

(b) Preganglionic cell bodies are located within the lateral gray column of the spinal cord or brainstem nuclei

(d) Axons of postganglionic neurons terminate on visceral effectors (i.e., smooth and cardiac muscle, glandular epithelium)

ii. Divisions

(a) Sympathetic (thoracolumbar)

(1) Preganglionic axons emerge from cell bodies within the lateral horn of the spinal cord gray matter at the thoracic and upper two lumbar levels. Axons leave the spinal cord via the ventral roots and pass to

a) Paravertebral sympathetic ganglion chain via white rami communicantes, ending on cell bodies of postganglionic neurons

b) Collateral ganglia, ending on postganglionic neurons closer to the viscera

c) Adrenal medulla, ending on modified postganglionic neurons that are secretory endocrine cells

(2) Postganglionic axons pass to

a) Viscera via the sympathetic nerves

b) Gray rami communicantes, which return to the spinal nerve and are distributed to autonomic effectors in areas supplied by these nerves

(3) Functions (Table 4-9)

TABLE 4-9

Autonomic Nervous System Effects on Various Effector Sites

From Russo-McCourt T: Spinal cord injuries. In McQuillan KA, Von Rueden KT, Hartsock RL, et al, editors: Trauma nursing: from resuscitation through rehabilitation, ed 3, Philadelphia, 2002, Saunders, p 512.

a) Come into widespread activity under emergency conditions (“fight or flight”)

b) Generally antagonistic to parasympathetic activity

c) Synapse with many postganglionic fibers

(b) Parasympathetic (craniosacral) (see Table 4-9)

(1) Preganglionic cell bodies are located in brainstem nuclei and the lateral gray columns of the middle three sacral spinal cord segments (S2 to S4)

(2) Preganglionic fibers end on short postganglionic neurons located on or near visceral structures

(3) Supplies visceral structures in the head via the oculomotor (III), facial (VII), and glossopharyngeal (IX) cranial nerves and those in the thorax and upper abdomen via the vagus (X) nerve

(4) Sacral outflow supplies the pelvic viscera via the pelvic branches of S2 to S4

(5) Produces localized reactions rather than the mass action of sympathetic stimulation

iii. Chemical mediation: ANS is divided into cholinergic and adrenergic divisions based on the neurotransmitter released

(a) Cholinergic neurons release ACh and include

(1) All preganglionic neurons

(2) Parasympathetic postganglionic neurons

(3) Sympathetic postganglionic neurons to the sweat glands and skeletal muscle blood vessels (vasodilation)

(b) Adrenergic neurons release norepinephrine and include

(1) Sympathetic postganglionic endings, except as noted earlier

(2) Constrictor fibers of the skeletal muscle blood vessels

4. Physiology of pain

a. Core Curriculum focuses primarily on acute (nociceptive or physiologic) pain. Chronic pain is discussed briefly because unrelieved acute pain can result in the development of chronic (pathologic) pain.

b. Acute pain results when mechanisms such as surgery, trauma, or disease cause inflammation and cellular damage

i. Warns of potential for, or extent of, tissue damage; initiates protective behaviors to minimize damage and promote tissue repair

ii. Usual characteristics include the following:

(a) Activates sympathetic nervous system (autonomic, involuntary) responses, such as increased heart rate, blood pressure (BP), respiratory rate

(b) Proportional to intensity and extent of stimuli; however, wide variations exist among patients

(1) Long-term alterations in neural tissue are initiated within the first few hours after injury (Blakely and Page, 2001)

(2) Inadequately managed acute pain can persist after injured tissue is repaired (McCaffery and Pasero, 1999)

iii. Classifications of acute pain

(a) Somatic: Arising from tissues (e.g., skin, muscle, bone). Descriptors include sharp, dull, aching, cramping. Is localized or diffuse; may radiate.

(b) Visceral: Arising from organs (e.g., liver, pancreas, bowel). Descriptors include sharp, stabbing, deep ache. Is well or poorly localized; may be referred.

iv. Key physiologic concepts

(a) Nociception: Neurochemical process of transmitting the pain response to a peripheral noxious (thermal, mechanical, or chemical) stimulus to an intact spinal cord and brain

(1) Pain perception requires cortical integration of many factors (e.g., physiologic factors, psychosocial factors, past experiences); often results in emotional responses (e.g., anger, anxiety)

(2) Nociception does not always result in pain (e.g., pain perception can be blunted by endogenous endorphin release); pain can occur without nociception (e.g., phantom limb pain)

(b) Nociceptors: Peripheral neurons (primary afferent peripheral fibers) that sense unpleasant or potentially damaging noxious stimuli. Examples are

(1) A delta: Large, thinly myelinated fibers that rapidly conduct impulses generated in response to mechanical or thermal stimuli; usually results in sharp, well-localized pain

(2) C: Smaller, unmyelinated fibers that slowly conduct impulses generated in response to all noxious stimuli; usually poorly localized, dull, aching pain; 75% of nociceptors are C fibers (Munden, Eggenberger, Goldberg, et al, 2003)

(c) Peripheral sensitization: Lowering of nociceptor activation threshold following exposure to chemical mediators or repeated noxious stimuli

(d) Four basic stages of nociception are described in Table 4-10 and illustrated in Figure 4-21

TABLE 4-10

Basic Stages of Nociception

Compiled from Ballantyne J, Fishman SM, Abdi S, editors: The Massachusetts General Hospital handbook of pain management, Philadelphia, 2002, Lippincott Williams & Wilkins; Blakely WP, Page GG: Pathophysiology of pain in critically ill patients, Crit Care Nurs Clin North Am 12(2):167–179, 2001; McCaffery M, Pasero C: Pain: clinical manual, ed 2, St Louis, 1999, Mosby; Melzack R, Wall PD, editors: Handbook of pain management, Edinburgh, 2003, Churchill Livingstone; and National Pharmaceutical Council: Pain: current understanding of assessment, management, and treatment, Reston, Va, 2001, Author. Churchill Livingstone

FIGURE 4-21 Four basic processes involved in nociception. BK, Bradykinin; 5HT, 5-hydroxytryptamine (serotonin); H, histamine; NE, norepinephrine; PG, prostaglandin; SP, substance P. (From McCaffery M, Pasero C: Pain: clinical manual, St Louis, 1999, Mosby, p 21.)

c. Chronic pain: Pain state persisting beyond the period of healing

i. Serves no useful purpose (St. Marie, 2002)

ii. Usual characteristics (McCaffery and Pasero, 1999)

(a) Neither tissue pathology nor sympathetic nervous system activation is identifiable

(b) Represents a disproportionate response to the stimulus and/or physical findings

iii. Often involves neuropathic pain: Abnormal processing of sensory input in PNS or CNS due to injury or impairment

(a) Described as either continuous or intermittent sensations (e.g., burning, shooting, shocklike, tingling, jabbing)

(b) Examples include pain caused by nerve root compression, diabetic neuropathy, Guillain-Barré syndrome; phantom limb pain, complex regional pain syndrome

iv. Key physiologic concepts

(a) Neuroplasticity: Ability of neurons to change their subsequent response to stimuli following long-term or sustained exposure to noxious stimuli

(b) Central sensitization: State of heightened excitability resulting in an exaggerated response to stimuli and an expanded distribution of pain

(1) Hyperalgesia: Lowered threshold for noxious stimuli

(2) Allodynia: Perception of normally benign stimuli as painful

Patient Assessment

1. Nursing history

a. Current health issues

i. Current symptoms, including chronologic sequence of onset, duration, location, and frequency

ii. Factors that relieve or exacerbate symptoms

iii. Difficulties performing activities of daily living (ADLs)

b. Patient health history: Significant medical and surgical history, including traumatic injury and childhood diseases

c. Medication history: Use of over-the-counter and prescription drugs, nutritional and herbal supplements, including amount, frequency, duration, last dose, effectiveness, adverse response. Especially note use of analgesics, anticonvulsants, tranquilizers, sedatives, anticoagulants, platelet aggregation inhibitors, stimulants, antihypertensives, cardiac medications.

d. Allergies

e. Family history: Note history of disease that may impact current illness (e.g., cardiac disease, stroke [especially early onset], aneurysms, arteriovenous malformations, seizures, migraines, dementia, autoimmune disorders)

f. Social history and habits

i. Significant others affected by the patient’s illness

ii. Support systems available to assist the patient and family

iii. Alcohol and tobacco use: Past and present, amount, duration

iv. Illicit drug use or abuse: Particularly cocaine, amphetamines

v. Type of work; impact of symptoms on work

vi. Hobbies, recreational activities

vii. Current dwelling, including layout and number of stairs

2. Nursing examination of patient

a. Physical examination data

i. First ABC: Evaluate airway patency, sufficiency of breathing and circulation

ii. Inspection then palpation of the head, face, and spine: Shape, symmetry, bony contour, coloration and skin integrity; irregularities may indicate injury, ventricular shunt, previous surgery, or congenital abnormality. Note nares or ear drainage.

iii. Auscultation: Heart for murmurs and clicks; carotid arteries and over eyes for bruits

iv. Assessment of neurologic function

(a) Level of consciousness (LOC) (Box 4-1)

BOX 4-1 ASSESSMENT OF LEVEL OF CONSCIOUSNESS

Consciousness is an awareness of self and the environment. A disturbance in consciousness is a sensitive indicator of neurologic dysfunction. Unconsciousness (coma) can result from extensive bilateral cerebral lesions, injury to the diencephalon or pontomesencephalic (pons-midbrain) reticular formation, or metabolic abnormalities. Unilateral lesions of the cerebrum (without prior contralateral injury) and lesions of the medulla or spinal cord do not cause coma.

Arousal: Evaluate what stimulus is necessary to elicit a response. Determine if the patient responds spontaneously; if not, apply the following stimuli in progressive order until a response is obtained: Address the patient by name, shake the patient, apply a peripheral pain stimulus (i.e., nail bed pressure), apply a deep central pain stimulus (i.e., sternal rub, supraorbital pressure).

Awareness or the content of consciousness reflects higher cortical functions; can be assessed via the following:

• General behavior and appearance; appropriateness to the situation

• Attention span, long- and short-term memory, insight, orientation, and calculation

• Intellectual capacity appropriate for educational level, judgment

• Emotional state, affect

• Thought content: Illusions, hallucinations, delusions

• Execution of intentional motor activity: Apraxia is the inability to perform these movements

• Recognition and interpretation of sensations

• Language: Fluency, clarity, content, comprehension of written and spoken word, ability to name objects and repeat phrases, patient’s awareness of a language disorder

Aphasia: Difficulty in the expression of language (expressive aphasia) or understanding of language (receptive aphasia) indicates dominant hemisphere dysfunction

Motor speech apraxia: Inability to perform the mouth movements to produce the sounds for the intended words; a motor speech programming disorder indicates a lesion in Broca’s speech area

Dysarthria: Difficulty with articulation due to impaired movement of the speech musculature may result from dysfunction of cranial nerves V, VII, IX, X, or XII or cerebellar dysfunction that interferes with the coordination of the muscles innervated by these nerves; represents speech impairment without a language deficit

(b) Glasgow Coma Scale (GCS) (Table 4-11): Used to assess LOC; total score also used to classify severity of brain injury. Limitations include inability to assess eye opening in patients with periorbital swelling or verbal response in intubated patients. Hypoxia, hypotension, hypothermia, drug intoxication, postictal state, and administration of sedatives, analgesics, or paralytic agents can interfere with GCS responses. Presence of any confounding variable should be noted when reporting score. Neurologic deterioration that affects only one side of the body is not reflected in GCS score.

TABLE 4-11

Glasgow Coma Scale

^*Rigid flexion, internal rotation, and adduction of the upper extremity; extension, internal rotation, and plantar flexion of the lower extremity.

^†Rigid extension, adduction, and internal rotation of the upper extremity; extension, internal rotation, and plantar flexion of the lower extremity.

(1) Assess size and contour of muscles: Note atrophy, hypertrophy, asymmetry, and joint malalignments

(2) Observe for involuntary movements, such as fasciculations, tics, tremors, abnormal positioning

(3) Determine motor response to stimuli

a) Ability to follow simple commands such as “Hold up two fingers.” Do not ask the patient to squeeze your hand because this may be a reflex response to palmar stimulation.

b) Localization: Able to locate a noxious stimulus (e.g., deep pain stimulus) and attempt to remove it; indicates cortical dysfunction

c) Withdraws: Pulls limb(s) away from painful stimuli with normal flexor movement; indicates extensive cortical damage

d) Abnormal flexion (decorticate posturing; see Table 4-11): Associated with lesions to the corticospinal tract just above the brainstem near or in the cerebral hemispheres, in the area of the diencephalon

e) Extensor (decerebrate) posturing (see Table 4-11): Indicates damage to the midbrain or upper pons

f) No response: Associated with lower brainstem or high spinal cord dysfunction

(4) Strength testing (if the patient is able to follow commands)

a) Evaluate the integrity and function of UMNs and LMNs that innervate a specific muscle or muscle group (Table 4-12)

TABLE 4-12

Muscle Groups, Associated Level of Spinal Cord Innervation, and Method of Testing

Muscle(s) Tested	Primary Level(s) of Spinal Nerve Innervation	Method of Testing
Deltoids	C5	Raising of arms
Biceps	C5	Flexion of elbow
Wrist extensors	C6	Extension of wrist
Triceps	C7	Extension of elbow
Hand intrinsics	C8-T1	Hand squeezing, finger flexion, finger abduction
Iliopsoas	L1, L2	Hip flexion
Hip adductors	L2-L4	Adduction of hips (squeezing legs together)
Hip abductors	L4, L5, S1	Abduction of hips (separating hips)
Quadriceps	L3, L4	Knee extension
Hamstrings	L5, S1, S2	Knee flexion
Tibialis anterior	L4, L5	Dorsiflexion of foot
Extensor hallucis longus	L5	Extension of great toe
Gastrocnemius	S1	Plantar flexion of foot

Adapted from McIlvoy L, Meyer K, McQuillan KA: Traumatic spine injuries. In Bader MK, Littlejohns LR, editors: AANN core curriculum for neuroscience nursing, ed 4, St Louis, 2004, Saunders, p 345.

b) Grade strength on a 0 to 5 scale (Table 4-13)

TABLE 4-13

Muscle Strength Grading Scale

Score	Muscle Function
0	Absent, no muscle contraction
1	Contraction of muscle felt or seen
2	Movement through full range of motion with gravity removed
3	Movement through full range of motion against gravity
4	Movement against resistance but can be overcome
5	Full strength against resistance

c) Note whether weakness follows a distributional pattern (proximal-distal, right-left, or upper-lower extremity)

(5) Strength testing for a patient unable to follow commands:

a) Observe which extremities move spontaneously or to noxious stimuli

b) Hemiparesis or hemiplegia may be detected by lifting both arms off the bed and releasing them simultaneously. The limb on the hemiparetic side will fall more quickly and more limply than that on the normal side.

(6) Muscle tone: State of muscle tension assessed by palpating muscles at rest and during passive range-of-motion (ROM) movement; possible abnormalities include:

a) Rigidity: Increased muscular resistance throughout passive ROM movement; seen with a basal ganglia lesion

b) Spasticity: Increased muscular resistance to joint movement, often followed by release of resistance; increased tone indicates corticospinal tract lesion

c) Hypotonia (flaccidity): Decreased muscle tone associated with LMN lesions, cerebellar dysfunction, or spinal shock related to acute spinal cord injury

(7) Deep tendon or muscle stretch reflexes: Elicited by percussing the tendon with a reflex hammer, which causes stretching of the muscle spindles and subsequent contraction of muscle fibers when the monosynaptic reflex arc is intact. Compare responses side to side.

a) Hyperreflexia usually indicates UMN lesion

b) May be diminished initially after an acute intracranial injury due to cerebral shock or at and below the level of spinal cord injury due to spinal shock

c) Areflexia most often due to LMN lesions

d) Deep tendon reflexes commonly tested: See Table 4-14

TABLE 4-14

Deep Tendon or Muscle Stretch Reflexes and Level of Spinal Cord Innervation

Reflex	Level of Spinal Cord Innervation
Biceps	C5, C6
Brachioradialis	C5, C6
Triceps	C7, C8
Quadriceps (patellar)	L2-L4
Achilles (ankle jerk)	S1, S2

e) Grade deep tendon reflexes on a 0 to 4 scale: See Table 4-15

TABLE 4-15

Grading Scale for Strength of Deep Tendon Reflexes

Score	Reflex Response
4+	Hyperreactive, clonus
3+	Very brisk
2+	Normal, average
1+	Diminished
0	No response, flaccid

From McIlvoy L, Meyer K, McQuillan KA: Traumatic spine injuries. In Bader MK, Littlejohns LR, editors: AANN core curriculum for neuroscience nursing, ed 4, St Louis, 2004, Saunders, p 346.

(8) Superficial reflexes: Tested by stroking the skin with a moderately sharp object (Table 4-16). These reflexes are lost or abnormal with UMN or LMN lesions.

TABLE 4-16

Superficial Reflexes, Level of Spinal Nerve Innervation, and Method for Assessment

Adapted from McIlvoy L, Meyer K, McQuillan KA: Traumatic spine injuries. In Bader MK, Littlejohns LR, editors: AANN core curriculum for neuroscience nursing, ed 4, St Louis, 2004, Saunders, p 347.

(9) Pathologic reflexes: See Box 4-2

BOX 4-2 ASSESSMENT OF PATHOLOGIC REFLEXES, ABNORMAL MOVEMENTS, BALANCE, AND COORDINATION

Pathologic reflexes

Primitive reflexes present in infants but normally absent in adults may reappear in association with frontal lobe impairment. Examples include the following:

• Grasp reflex: In response to palmar stimulation

• Sucking reflex: In response to lip stimulation

• Rooting reflex: Mouth opens, head deviates toward a stimulus applied to the lower lip or cheek

Babinski’s sign

• Stroking the lateral aspect of the sole of the foot from the heel upward and across the ball causes abnormal dorsiflexion of the great toe and extensor fanning of the other toes

• In an adult, indicates a lesion of the corticospinal tract anywhere from the motor cortex to the anterior horn of the spinal cord

Abnormal movements: Note the distribution, rate, duration, and relationship to activity of any involuntary movements, such as the following:

Seizures (refer to Seizures under Specific Patient Health Problems)

Tremors: Rhythmic trembling movement of muscles

Clonus: Abrupt onset of brief jerking movements of a muscle or muscle group (e.g., oscillation of the foot between flexion and extension with sudden passive extension of the foot)

Balance and coordination: Primarily evaluate cerebellar function; tested in patients able to perform voluntary movements

Romberg’s test: Patient stands erect with the feet together, first with the eyes open and then with the eyes closed. Positive test result indicating posterior column or cerebellar dysfunction occurs when the patient loses balance and sways or falls when the eyes are closed.

Observe the patient while sitting; swaying indicates cerebellar dysfunction

Evaluate for dystaxia or ataxia (muscle incoordination with volitional movements) and dysmetria (inability to halt a movement at a desired point), which indicate cerebellar dysfunction

• Have the patient first touch the examiner’s finger, positioned at the length of patient’s arm from the face, and then touch his or her nose

• Have the patient slap the thigh first with the palm and then with the back of the hand in quick, alternating movements

• Have the patient run the heel from the opposite knee down the shin

• Rebound test: Have the patient extend the arms forward while the examiner taps the patient’s wrist; in cerebellar disease, the arm moves markedly out of place and overshooting occurs as the patient attempts to move the arm back into position

Gait

• Observe the gait and have the patient perform tandem (heel-to-toe) walking

• A wide-based, staggering gait and the inability to perform tandem walking indicate cerebellar dysfunction

• Gait disturbances with different clinical characteristics can be correlated with other specific neurologic or muscular dysfunction (e.g., spastic hemiparesis following an upper motor neuron lesion causes the patient to walk with the arm flexed close to the body and the spastic leg to move outward and forward in a semicircle, often with the toe dragged)

(10) Abnormal movements: See Box 4-2

(11) Balance and coordination: See Box 4-2

(d) Sensory function

(1) In an unresponsive or uncooperative patient, a cursory sensory examination is performed by noting the patient’s response to painful stimuli applied while performing various interventions (e.g., venipuncture)

(2) In an awake, cooperative patient able to understand and follow commands, a complete sensory assessment can be performed. Test with the patient’s eyes closed and compare one side of the body with the other

(3) Sensory function is scored using a 0 to 2 scale: See Table 4-17

TABLE 4-17

Sensory Function Scoring

Score	Sensory Function
0	Absent
1	Impaired or hyperesthetic
2	Normal or intact

Adapted from McIlvoy L, Meyer K, McQuillan KA: Traumatic spine injuries. In Bader MK, Littlejohns LR, editors: AANN core curriculum for neuroscience nursing, ed 4, St Louis, 2004, Saunders, p 344.

(4) When possible, delineate sensory impairments based on dermatome distribution (see Figure 4-17)

(5) Spinothalamic tracts: See Box 4-3

BOX 4-3 ASSESSMENT OF SPINOTHALAMIC TRACTS, POSTERIOR COLUMNS, AND CORTICAL DISCRIMINATORY SENSATION

Lesions or dysfunction of the peripheral nerves, ascending nerve tracts, or sensory perceptive areas of the cerebral cortex (i.e., parietal lobe) may impair sensory function

SPINOTHALAMIC TRACTS (ANTERIOR AND LATERAL)

Test either pain or temperature sensation, because both functions are carried in the same lateral spinothalamic tracts

Pain: Have the patient distinguish sharp from dull stimuli randomly applied; gently touch the skin using a clean pin for sharp sensation and using a blunt edge (head of a pin) for dull sensation

Temperature: Ask the patient to distinguish between hot and cold stimuli when randomly touched with test tubes filled with hot or cold water

Light touch: Lightly touch the patient with a wisp of cotton

POSTERIOR COLUMNS (FASCICULUS GRACILIS AND FASCICULUS CUNEATUS)

Test either proprioception or vibration sense, because both are carried in the same tracts

Vibration: Apply a vibrating tuning fork to bony prominences; ask the patient to report when vibration is felt; apply first to the distal aspect of each extremity and move proximally

Proprioception (position sense): Ask the patient to close the eyes and report whether a finger or toe is being moved up or down; assess in all four extremities

CORTICAL DISCRIMINATORY SENSATION

In addition to the sensory pathways, assesses the association portions of the cortex (i.e., the parietal lobe). Deficits are called agnosias (not knowing). Examples include the following:

• Stereognosis: Ask the patient, without the aid of vision, to identify familiar objects placed in his or her hand. The inability to identify objects is astereognosia.

• Graphesthesia: Ask the patient to identify numbers or letters traced on the palm. Inability to discern what is written is agraphesthesia.

• Simultaneous double stimulation: With the patient’s eyes closed, touch the patient’s limb and then touch both sides of the body in corresponding locations. Determine if the patient can detect the number and location of stimuli. Inability to identify that he or she is being touched on both sides of body simultaneously is tactile inattention. Inability to locate a single touch sensation is atopognosia.

(6) Posterior columns: See Box 4-3

(7) Cortical discriminatory sensation: See Box 4-3

(e) Cranial nerves: See Table 4-18 and Figure 4-22

TABLE 4-18

Cranial Nerve Assessment and Anticipated Deficits

FIGURE 4-22 Visual pathways. Transection of the pathways at the locations indicated by the letters causes the visual field defects shown in the diagrams on the right. Occipital lesions may spare fibers from the macula (as in D) because of the separation in the brain of these fibers from the others subserving vision. (From Ganong WF: Review of medical physiology, ed 21, New York, 2003, Lange Medical Books/McGraw-Hill, p 153.) Lange Medical Books/McGraw-Hill

(f) Eye and pupil signs: In addition to cranial nerve assessment, other findings may include the following:

(1) Pupil abnormalities (Table 4-19)

TABLE 4-19

Pupil Abnormalities Associated with Specific Areas of Brain Dysfunction

Pupil Finding	Related Brain Dysfunction
Small, equal, reactive	Bilateral diencephalic damage that affects the sympathetic innervation originating from the hypothalamus; metabolic dysfunction
Nonreactive, midpositioned	Midbrain damage
Fixed and dilated	Ipsilateral oculomotor (cranial nerve III) compression or injury
Bilateral fixed and dilated	Brain anoxia and ischemia; bilateral cranial nerve III compression
Pinpoint, nonreactive	Pons damage, often from hemorrhage or ischemia that interrupts the sympathetic nervous system pathways
One pupil is smaller that the other, but both reactive to light; associated with ptosis and an inability to sweat on the same side as the smaller pupil (Horner’s syndrome)	Interruption of ipsilateral sympathetic innervation that can be caused by a lesion of the anterolateral cervical spinal cord or lateral medulla, damage to the hypothalamus, or occlusion or dissection of the internal carotid artery

(2) Gaze deviation or gaze preference: Horizontal or vertical gaze deviations indicate a cortical or brainstem lesion

a) Eyes deviate toward the side of a destructive hemispheric lesion affecting the frontal gaze centers

b) Gaze deviates away from irritative foci (seizures) affecting the frontal gaze centers

c) Inability to gaze upward is associated with dorsal midbrain lesions

d) Eyes deviate away from the side of a unilateral pons lesion

(3) Nystagmus (rhythmic, oscillatory eye movements)

a) Detected by having the patient follow your finger through the fields of gaze

b) Due to lesions of the cerebellum, vestibular system, or brainstem pathways, or toxic-metabolic disorders; clinical features vary with the part of the pathway affected

(g) Vital signs

(1) Temperature

a) Hyperthermia increases cerebral oxygen consumption by 10% for every 1.8° F (1° C) elevation. Higher metabolic demand increases the risk for CNS ischemia. Neurogenic fever can be caused by damage to the hypothalamus, where the thermoregulation center is located.

b) Hypothermia, if extreme, can lead to cardiac dysrhythmias, coagulopathies, other complications. Seen with hypothalamic lesions, spinal cord injury with autonomic dysfunction, and metabolic or toxic encephalopathy.

(2) Respirations: Respiratory dysrhythmias often correlate with lesions at specific locations in the brain, although effects may vary and may be influenced by other factors (Table 4-20)

TABLE 4-20

Respiratory Patterns Associated with Specific Areas of Brain Dysfunction

Breathing Pattern	Description	Location of Brain Lesion or Type of Dysfunction
Cheyne-Stokes	Regular cycles of respirations that gradually increase in depth to hyperpnea and then decrease in depth to periods of apnea	Usually bilateral lesions deep within the cerebral hemispheres, basal ganglia, or diencephalon; metabolic disorders
Central neurogenic hyperventilation	Deep, rapid respirations	Midbrain, upper pons
Apneustic	Prolonged inspiration followed by a 2- to 3-sec pause; occasionally may alternate with an expiratory pause	Pons
Cluster	Cluster of irregular breaths followed by an apneic period lasting a variable amount of time	Lower pons or upper medulla
Ataxic or irregular	Irregular, unpredictable pattern of shallow and deep respirations and pauses	Medulla

Adapted from McQuillan KA, Mitchell PH: Traumatic brain injuries. In McQuillan KA, Von Rueden KT, Hartsock RL, et al, editors: Trauma nursing from resuscitation through rehabilitation, ed 3, St Louis, 2002, Saunders, p 420.

(3) Pulse and BP

a) Both are notoriously unreliable parameters in detecting CNS disease or neurologic deterioration. May change late in the course of increased ICP and thus are of limited clinical use.

b) Cardiac dysrhythmias may be seen with neurologic disorders, particularly with blood in the CSF, after posterior fossa surgery, with increased ICP, or with stroke in certain locations

c) Tachycardia and hypertension may be seen with injury or compression of the hypothalamus that results in sympathetic nervous system stimulation

d) Cushing’s response occurs when intracranial hypertension causes compression of the medullary vasomotor center. Systolic pressure rises, widens pulse pressure, and may slow pulse.

(4) Pain—the fifth vital sign

a) Pain that is assessed at regular intervals and treated with the same zeal as abnormalities in other vital signs has a much better chance of being treated effectively (Campbell, 1995)

b) Key concepts in pain assessment: See Box 4-4

BOX 4-4 BASIC PAIN ASSESSMENT “PEARLS”

All patients have the right to appropriate assessment and management of pain and should be educated and encouraged to report unrelieved pain.

Pain is an individual, subjective sensation. It cannot be proved or disproved.

Your attitudes and beliefs about pain can affect the way you treat pain.

Pain assessment is conducted and documented as appropriate to the patient’s condition.

1. Include pain intensity, quality, location, pain-related complications, and adverse effects of treatment whenever possible.

2. Increase assessment frequency during times of inadequately controlled pain.

3. Obtain a detailed pain assessment, history, and focused physical examination as the patient improves to ensure an accurate diagnosis of pain.

Make every effort to obtain the patient’s self-report of pain, because this is the most reliable indicator of pain. (Do not assume that a patient cannot provide a self-report without asking.)

1. Ask simple questions, allow time for response, and repeat or rephrase as needed.

2. Documenting a simple “yes” or “no” (or nod or shake of head) is acceptable.

Assess pain in a patient unable to provide a self-report of pain.

1. Never assume that a sedated and/or chemically paralyzed patient does not feel pain—medications such as propofol and midazolam do not provide analgesia.

2. The absence of observable signs does not mean that pain does not exist.

3. When conditions exist that are known to be painful, assume that pain is present.

Reassessment after intervention has taken effect is essential and should include these questions:

1. How much relief was obtained and how long did it last?

2. Were there any adverse effects?

c) Components of pain assessment: See Table 4-21

TABLE 4-21

Components of Pain Assessment

d) Adequate pain assessment poses a special challenge in the critically ill patient

e) Acute pain assessment tools

1) Pain tools should estimate the severity of pain and accurately reflect changes in pain intensity following interventions

2) General guidelines for successful use:

a) Tool should be valid, reliable, and appropriate for the patient’s age and cognitive, cultural, developmental, and physical status

b) Patient and caregivers should be educated on tool use and purpose

c) Whenever possible, the same tool should be used consistently with a given patient

d) Whenever possible, a pain tool in the patient’s language should be used

3) Unidimensional tools measure a single element of pain (e.g., intensity). Figure 4-23 shows examples of reliable and valid self-reporting tools for measuring intensity.

FIGURE 4-23 Pain assessment tools. (Numeric rating scale, Wong-Baker faces scale, and Visual Analog Scale from McCaffery M, Pasero C: Pain: clinical manual, ed 2, St Louis, 1999, Mosby, pp 62, 67; faces pain scale modified by McCaffery and Pasero from Whaley LF, Wong DL: Essentials of pediatric nursing, St Louis, 1997, Mosby, pp 1215-1216; Verbal Descriptor Scale from Acute Pain Management Guideline Panel: Acute pain management in adults: operative procedures, Quick reference guide for clinicians No 1, AHCPR Pub No 92-0019, Rockville, Md, February 1992, Agency for Health Care Policy and Research, Public Health Service, US Department of Health and Human Services, p 116.) Agency for Health Care Policy and Research, Public Health Service, US Department of Health and Human Services

a) Numeric rating scale (NRS)

i) Either 0 to 5 or 0 to 10 range

ii) Use horizontally or vertically

iii) Present verbally or visually

b) Faces rating scales

i) Patient selects face

ii) Often used with other scales

c) Verbal descriptor scales

i) Present verbally or visually

ii) Use words the patient understands

d) Visual analogue scale (0 to 100): May be difficult for critically ill patients to use

4) Multidimensional tools measure characteristics and effects of pain on the patient’s life. More appropriate with complex pain situations than for critically ill patients. Examples include the following:

a) Initial Pain Assessment Inventory: Includes a diagram to identify pain location(s)

b) Brief Pain Inventory: Addresses pain experienced over the preceding 24 hours

c) McGill Pain Questionnaire: Looks at sensory, affective, and evaluative dimensions

f) Pain assessment when the patient cannot communicate

1) Lack of self-report can lead to undertreatment

2) When self-report is not possible, assume pain is present based on the presence of a painful condition or procedure (American Pain Society, 2003)

3) Behavioral and physiologic signs are not always reliable indicators of pain but may be useful to confirm suspicion of pain or evaluate the response to intervention when no alternative exists

a) Behaviors are often more reliable indicators than physiologic signs

b) Physiologic signs are temporary, may resolve before pain resolves, and may reflect other phenomena (e.g., anxiety)

4) Hierarchy of importance of basic measures of pain intensity (criteria are listed in order of reliability) (McCaffery and Pasero, 1999):

a) Patient’s self-report of pain

b) Pathology (e.g., fractures, incisions)

c) Behaviors (e.g., grimacing, frowning, wincing) (Table 4-22)

TABLE 4-22

Behaviors Often Associated with Pain in Nonverbal Patients (Pasero, 2004b)

See chapter text for references.

d) Report of a parent, family member, or other person close to the patient (“proxy pain rating”)

e) Physiologic indices (e.g., increased heart rate, BP) (Table 4-23)

TABLE 4-23

Harmful Effects and Clinical Manifestations of Acute Pain

Compiled from Graf C, Puntillo K: Pain in the older adult in the intensive care unit, Crit Care Clin 19(4):749–770, 2003; Hamill-Ruth RJ, Marohn ML: Evaluation of pain in the critically ill patient, Crit Care Clin 15(1):35–54, 1999; McCaffery M, Pasero C: Pain: clinical manual, ed 2, St Louis, 1999, Mosby; Melzack R, Wall PD, editors: Handbook of pain management, Edinburgh, 2003, Churchill Livingstone; Pasero C: Pain in the critically ill patient, J Perianesth Nurs 18(6):422–425, 2003; and Payen, Olivier, Bosson, et al, 2001.

5) Behavioral pain tools designed for use in critically ill patients require further testing before general use can be recommended (Pasero, 2004a)

a) If used, evaluate each time a low score is obtained with potentially painful conditions as patients may not be able to demonstrate specific behaviors required for scoring (Pasero, 2004a)

b) Examples include Behavioral Pain Scale (Payen et al, 2001), Nonverbal Pain Scale (Odhner et al, 2003), Checklist of Nonverbal Pain Indicators (Feldt, 2000)

b. Monitoring data

i. ICP monitoring: See specific patient health problems

ii. Jugular venous oxygen saturation (Sjo₂)

(a) Principle: Assesses the coupling or uncoupling of cerebral oxygen delivery (CBF) and cerebral oxygen consumption (metabolism). Placement of a fiberoptic catheter into the jugular bulb allows for continuous measurement of Sjo₂ and intermittent venous blood gas sampling. Reflects a global view of oxygenation in the cerebral hemisphere on the side of catheter placement.

(b) Clinical uses: May detect episodes of uncoupling between CBF and metabolism indicating cerebral ischemia (CBF is less than the metabolic demand) or hyperemia (CBF exceeds the metabolic demand). Factors that decrease cerebral oxygen supply (i.e., hypoxemia, anemia, insufficient cerebral perfusion) or increase cerebral metabolic demand (e.g., seizures, hyperthermia) lower Sjo₂ and can cause ischemia. Factors that increase oxygen supply (i.e., increased CBF, hyperoxia) or reduce cerebral oxygen demand (e.g., large area of cerebral infarction, hypothermia) raise Sjo₂ and can cause hyperemia.

(1) Normal Sjo₂ is 55% to 75%; Sjo₂ below 55% is indicative of global ischemia and warrants treatment; Sjo₂ above 80% indicates hyperemia

(2) Cerebral extraction of oxygen (CEo₂): Calculated by subtracting Sjo₂ from arterial oxygen saturation (Sao₂). Normal = 24% to 40%; lower than 24% indicates hyperemia; higher than 40% indicates cerebral oxygen supply insufficient for demand.

(3) When venous and arterial blood gas levels are analyzed simultaneously, arteriovenous oxygen difference (AVDo₂) can be calculated. Abbreviated formula: AVDo₂ = 1.34 (Sao₂ − Sjo₂) hemoglobin/100. Normal AVDo₂ is 4.5 to 8.5ml/dl; less than 4.5 ml/dl indicates hyperemia and more than 8.5 ml/dl indicates cerebral oxygen supply insufficient for demand.

(4) Knowledge of uncoupling between cerebral oxygen delivery and demand can prompt implementation of interventions to improve the balance and prevent ischemia or hyperemia (Box 4-5)