The head and face are made up of the cranial vault and facial bones. The cranial vault, or skull, is composed of several bones: one frontal, two sphenoid, two parietal, two temporal, and one occipital (Figure 2-1). Of these, the strongest is the occipital bone, and the weakest are the temporal bones. The frontal bone forms the forehead, and the temporal and sphenoid bones form the anterolateral walls of the skull, or the temples of the head. The parietal bones form the top and posterolateral portions of the skull, and the occipital bones form the posterior portion of the skull. The cranial vault reaches 90% of its ultimate size by age 5.

In addition to the cranial vault bones, there are 14 facial bones. These bones develop more slowly than the cranial bones, reaching only 60% of their ultimate size by age 6. The facial skeleton is composed of the mandible, which forms the lower jaw; the maxilla, which forms the upper jaw on each side; the nasal bones, which form the bridge of the nose; and the palatine, lacrimal, zygomatic, and ethmoid bones, which form the remainder of the face. It is the zygomatic bone that gives the cheek its prominence. The sphenoid bones also form part of the orbital cavity. The facial skull has several cavities for the eyes (orbital), nose (nasal), and mouth (oral), as well as spaces for nerves and blood vessels to penetrate the bony structure. Weight is saved in the skull area by the addition of sinus cavities (Figure 2-2).

The muscles of the head and face are controlled primarily by the 12 cranial nerves. The cranial nerves and their chief functions are shown in Table 2-1. The cranial nerves generally contain both sensory and motor fibers. However, some cranial nerves are strictly sensory (olfactory and optic), whereas others are strictly motor (oculomotor, trochlear, and hypoglossal).

The external eye is composed of the eyelids (upper and lower), conjunctiva (a transparent membrane covering the cornea, iris, pupil, lens, and sclera), lacrimal gland, eye muscles, and bony skull orbit (Figure 2-3). Muscles of the eye, their actions, and their nerve supply are shown in Table 2-2. The muscles and movements of the eye are shown in Figure 2-4. To produce some of the actions, the various muscles of the eye must work in concert. The eyelids protect the eye from foreign bodies, distribute tears over the surface of the eye, and limit the amount of light entering the eye. The conjunctiva is a thin membrane covering the majority of the anterior surface of the eye. It helps to protect the eye from foreign bodies and desiccation (drying up). The lacrimal gland provides tears, which keep the eye moist (Figure 2-5). The eye itself is made up of the sclera, cornea, and iris as well as the lens and retina (Figure 2-6). The sclera is the dense white portion of the eye that physically supports the internal structures. The cornea is very sensitive to pain (e.g., the extreme pain that accompanies corneal abrasion) and separates the watery fluid of the anterior chamber of the eye from the external environment. It permits transmission of light through the lens to the retina. The iris is a circular, contractile muscular disc that controls the amount of light entering the eye and contains pigmented cells that give color to the eye. The lens is a crystalline structure located immediately behind the iris that permits images from varied distances to be focused on the retina. It is primarily the lens and its supporting ligaments that separate the eye into chambers: the anterior chamber (aqueous humor) and the posterior chamber (vitreous humor). Finally, the retina is the primary sensory structure of the eye that transforms light impulses into electrical impulses that are then transmitted by the optic nerve to the brain, which interprets the impulses as the objects seen.

The external ear consists of cartilage covered with skin. Its primary purpose is to direct sound and to protect the external auditory meatus, through which sound is transmitted to the eardrum. The external ear, which is sometimes called the pinna, auricle, or trumpet, consists of the helix and lobule around the outside and the triangular fossa, antihelix, concha, tragus (a cartilaginous projection anterior to external auditory meatus), and antitragus on the inside (Figure 2-7). The middle ear structures consist of the tympanic membrane, or eardrum, which vibrates when sound hits it and sends vibrations through the ossicles—called the malleus (hammer), incus (anvil), and stapes (stirrup)—to the cochlea. The cochlea, which is part of the inner ear, transmits the sound waves to the vestibulocochlear nerve (cranial nerve VIII), which transmits electrical impulses to the brain for interpretation. The semicircular canals, the other part of the inner ear, play a significant role in maintaining balance.

The external nose, like the external ear, consists primarily of cartilage covered with skin. However, its proximal portion contains bone covered with skin. Figure 2-8 shows the bone and cartilage makeup of the nose. The floor of the nose consists of the hard and soft palates and forms the roof of the mouth (Figure 2-9). Cartilage and the nasal, frontal, ethmoid, and sphenoid bones form the roof of the nose. The frontal and maxillary bones form the nasal bridge. Three bony structures called turbinates (superior, middle, and inferior) form the lateral aspects of the nose, which increase the surface area of the nose and thereby warm, humidify, and filter more of the inspired air. The nose is divided into two chambers (vestibules) by a septum. These chambers are lined with a mucous membrane containing hairs that collect debris and other foreign substances from the inspired air. The cribriform plate of the ethmoid bone contains the sensory fibers of the olfactory nerve (cranial nerve I) for smell.

In addition to the questions listed under Patient History in Chapter 1, the examiner should obtain the following information from the patient who has sustained an injury to the head or the face:

1. What happened? This question determines the mechanism of injury and, potentially, the area of the brain or face injured (Table 2-3). A pathological classification for acute traumatic brain injuries is shown in the box on p. 89.¹ A forceful blow to a resting, movable head usually produces maximum brain injury beneath the point of impact (Figure 2-10). This type of injury, called a coup injury, is usually caused by linear or translational acceleration.² It often causes focal ischemic lesions, especially in the cerebellum, leading to alterations in smooth, coordinated movements, equilibrium, and posture. If the head is moving and strikes an unyielding object, such as the ground, maximum brain injury is usually sustained in an area opposite the site of impact.

Pathological Classification of Acute Traumatic Brain Injury

• Diffuse brain injury

 Cerebral concussion

 Diffuse axonal injury

• Focal brain injury

 Epidural hematoma

 Subdural hematoma

 Cerebral contusion

 Intracerebral hemorrhage

 Subarachnoid hemorrhage

 Intraventricular hemorrhage

• Skull fracture

• Penetrating brain injury

Modified from Jordan BD: Brain injury in boxing. Clin Sports Med 28:561–578, 2009.

This contrecoup injury is the result of impact deceleration. The injury occurs on the side of the head opposite to that receiving the blow, because the head is accelerating before impact, which squeezes the cerebrospinal fluid away from the trailing edge (the side away from the impact). The fluid moves toward the impact side, thereby thickening the cerebrospinal fluid and offering a cushioning effect at the point of impact. Because of the lack of cushioning on the trailing edge, greater injury is likely to occur to the brain on the side opposite the impact. The brain may also experience a “shaking” caused by repeated reverberation within the brain after the head has been struck. This type of injury often results in the signs and symptoms of a concussion with the degree of the concussion depending on the severity of the injury (Table 2-4). Concussion severity is only determined after signs and symptoms have disappeared and any neurological and cognitive testing is normal.³ If the cervical spine is taken beyond its normal range of motion, especially into rotation or side flexion, there may be a twisting of the cerebral hemisphere, brain stem, carotid artery, or carotid sinus that can result in injury to these structures or ischemia to the brain. Those areas of the brain that are most susceptible to damage include the temporal lobes, anterior frontal lobe, posterior occipital lobe, and upper portion of the midbrain.⁴

2. Did the patient lose consciousness? If so, how long was the patient unconscious? Has the patient suffered a concussion before? These questions are often difficult for the patient to answer or the examiner to know, because the patient may have been momentarily stunned and the time may have been so short that the patient believed there was no loss of consciousness. In other words, loss of consciousness may have been only momentary or, more traditionally, it may have lasted seconds to minutes. If the examiner is working with a sports team, accurate records are essential to record the severity (see later discussion) and the number of concussions suffered by the athlete and to ensure that proper care is instituted so that the athlete is not allowed to return to competition too soon. A concussion (a subset of mild traumatic brain injury) is a pathophysiological process that affects the brain and is caused by direct or indirect biomechanical forces. At present, there is no known threshold for a consussion.5–8 Risk factors are shown in Table 2-5,⁹ and stages of concussion are shown in Table 2-6.¹⁰ Signs and symptoms of concussions are shown in Table 2-7.^11–13 Women appear to be more susceptible to concussions than men,¹⁴ and traumatic brain injury is different in children than adults.^9,15,16 Concussions can result from a blow to the head or jaw or a fall on the buttocks from a height and can result in an inability to process information. Their effect is cumulative, and the risk of having another concussion following an initial concussion is four to six times greater than someone who has not had a concussion.^12,17 Concussions can lead to continued and severe problems (e.g., post-concussion syndrome, second-impact syndrome).^{10,12,17–20} To be maximally effective, athletes should have done baseline tests in their pre-participation evaluation and have an extensive concussion history taken covering somatic, neurobehavioral, and cognitive symptoms (Table 2-8).^3,12,21–26 In 2012, the International Conference on Concussion in Sport updated a Sideline Concussion Assessment Tool—3rd edition (SCAT3) (Figure 2-11) and added the Sport Concussion Assessment Tool for children ages 5 to 12 years (Child-SCAT3)⁸ (Figure 2-12). Kelly and Rosenberg^12,13 have developed a Standardized Assessment of Concussion (SAC) (Figure 2-13),^27,28 which provides a concise evaluation method for concussion by including measures of orientation, immediate memory, concentration, delayed recall, and other parameters. Lovell and Burke have developed a similar form for ice hockey.²⁹
These tests are often combined with computerized neurocognitive testing to try to predict how long recovery will take.30,31 Ideally, this neurocognitive testing should be done individually at preseason evaluations to establish a baseline and should be updated every 2 years.^32,33 If pre-injury values are not available, normative data may be used.³⁴ An example of such a computerized post-concussion assessment is the ImPACT test; ImPACT stands for Immediate Post-Concussion Assessment and Cognitive Testing.^{31,32,35–37}
There are several different grading systems for concussions (Table 2-9). It should be pointed out, however, that the International Conference on Concussion in Sport³ recommended that grade scales be abandoned, because concussion severity can only be determined retrospectively after all signs and symptoms have cleared, the neurological examination is normal, and cognitive function has returned to normal.³⁸ The conference group felt concussions should be grouped as simple or complex. Simple concussion implies that the injury resolves over 7 to 10 days without complications. Neurophysiological screening does not play a role, but mental status screening is part of the assessment. Complex concussions are those in which persistent symptoms and specific sequelae (i.e., convulsions, loss of consciousness for longer than 1 minute, prolonged cognitive impairment) occur.³ This includes people with more than one concussion. In this case, neurophysiological testing does play a role.^13,39–42 Table 2-10 shows some neurophysiological tests that could be used for post-concussion assessment.
Grades of concussion, such as those advocated by Torg (see later discussion and Table 2-4), can play a role in the acute phase but should be used with caution if making return to activity decisions.⁴³ With each grade, the signs and symptoms worsen, and the sequelae are more evident. No signs and symptoms under exertion (i.e., simulating the activity the person will return to) should be evident, even with simple concussions.
With a grade I concussion, the patient is slightly confused and may have a dazed look. The patient is completely lucid within 5 to 15 minutes; has no amnesia, sequelae, or residual symptoms; and has had no loss of consciousness. Some people refer to the grade I concussion as the patient’s having his or her “bell rung.”
With a grade II concussion, there is slight confusion, and posttraumatic amnesia becomes evident. Posttraumatic (anterograde) amnesia is the loss of memory for events occurring immediately after wakening or from the moment of injury. Posttraumatic amnesia is considered to be the length of time from injury until conscious memory returns. In the acute state, it may take time for posttraumatic amnesia to become obvious. Sometimes, the patient will remember what happened immediately after the injury, but as time goes on (up to 1 to 2 hours after the injury), posttraumatic amnesia becomes evident. This is one of the reasons it is advisable to reassess acute head injuries every 15 to 30 minutes. Manzi and Weaver reported that a patient who had sustained a period of posttraumatic amnesia of less than 60 minutes was considered to have sustained a mild head injury.44 If the period of posttraumatic amnesia lasted from 1 to 24 hours, moderate head injury was considered to have occurred. If the posttraumatic amnesia lasted for more than 1 week, the patient was considered to have sustained a serious head injury. If the duration of the posttraumatic amnesia was more than 7 days, full return to neurological function was highly unlikely.⁴⁴ With a grade II concussion, the patient may experience mild tinnitus (ringing in the ears), mild dizziness, and a dull headache with some disorientation. Dizziness at the time of injury has been reported to be a sign of risk for protracted recovery.⁴⁵ The patient who experienced a grade II concussion may also develop a post-concussion syndrome (i.e., have continual neurological problems after the concussion), which is observed in about 10% of concussion cases. The signs and symptoms of this syndrome include persistent headaches, especially with exertion; inability to concentrate; and irritability. The symptoms may last from several weeks to several years.

 Head Injury Severity Based on Length of Posttraumatic Amnesia

Less than 60 minutes:	Mild
1 to 24 hours:	Moderate
More than 1 week:	Serious (full return of neurological function unlikely)

A patient with a grade III concussion has the same symptoms as someone with a grade II concussion and also experiences retrograde amnesia. Retrograde amnesia is loss of memory of events that occurred before the injury. It may take 5 to 10 minutes for retrograde amnesia to develop after the concussion, and amnesia may involve only a few minutes before the injury. For this reason, the patient should be questioned frequently about what happened before the injury occurred and how it occurred, to see if there is any change in the patient’s memory pattern. There is always some degree of permanent retrograde amnesia with these patients.
With a grade IV concussion, the patient loses consciousness for 5 minutes or less. The level of consciousness may vary; the patient may be comatose, stuporous, obtunded, lethargic, confused, or fully alert. The patient goes through the following stages of recovery: unconsciousness (also called paralytic coma), stupor, obtundity, lethargy, confusion (with or without delirium), near lucidity with automatism, and finally full alertness. Stupor implies that the patient is only partially conscious and has reduced responsiveness. Obtundity implies the patient has reduced sensitivity to painful or unpleasant stimuli. Lethargy implies a state of sluggishness, dullness, or serious drowsiness. Confusion implies that the patient is disoriented in terms of time, place, or person. Delirium means that the patient may experience illusions, hallucinations, restlessness, or incoherence. Lucidity with automatism implies that the patient appears to be alert and fully recovered but acts only mechanically and is not really aware of what he or she is doing. With a grade IV concussion, there may be subtle changes in the patient’s personality and memory function. Both retrograde and posttraumatic amnesia are evident, and the patient demonstrates mental confusion and complains of tinnitus and dizziness to a greater degree than is seen with a grade III concussion. The patient also has residual headaches and is unsteady for 5 to 10 minutes after regaining consciousness. The literature has reported that loss of consciousness, by itself, is not a good predictor of the degree of neurophysiological loss or damage with a head injury.46 The severity of the head injury is best determined by the administration of different neurophysiological tests (e.g., GOAT test,⁴⁷ Hopkins Verbal Learning Test,⁴⁸ Trail Making Test, Wisconsin Card Sorting Test, Digit Symbol Substitution Test [DSST],⁴⁹ and measures of decision time⁴⁹) as well as considering all signs and symptoms the patient demonstrates.^{6,8,15,50–53} To ensure adequate data, however, these tests must also have been administered before the injury (e.g., in a pre-participation evaluation in sports).^6,35

Levels of Consciousness

• Alertness	Is readily aroused, oriented, and fully aware of surroundings
• Confusion	Memory is impaired Is confused and disoriented
• Lethargy	Sleeps when not stimulated Is drowsy and inattentive Responds to name Loses train of thought Shows decreased spontaneous movement Has slow and fuzzy thinking
• Obtundity	Responds to loud voice or shaking Responds to painful stimulus (withdrawal) Is confused when aroused Talks in monosyllables Mumbles and is incoherent Needs constant stimulation to cooperate
• Stupor (semicoma)	Responds to painful stimuli (withdrawal), shaking Groans, mumbles Exhibits reflex activity
• Coma	Does not respond to painful or any other stimuli

With a grade V concussion, the patient has experienced a paralytic coma or unconsciousness for 5 minutes or longer. This grade of concussion involves bruising of the brain, and there is prolonged retrograde amnesia as well as posttraumatic amnesia. The patient complains of severe tinnitus, unsteadiness for longer than 10 minutes, blurred vision, poor light accommodation, and a headache that feels “different” from most headaches. Both the autonomic and the peripheral nervous systems can be affected through their control by the brain. These patients may also experience nausea, vomiting, and sometimes convulsions. The recovery after a grade V concussion may be one of two types. In type A, the patient goes from a paralytic coma through stupor, confusion, lucidity, and full alertness, which is similar to a grade IV concussion but more severe. The individual with a type B grade V concussion experiences a paralytic coma that is associated with secondary cardiorespiratory collapse and is of much greater concern to the examiner, especially during the initial assessment, when the body’s essential functions must be maintained.
More severe diffuse brain injuries are associated with more severe neurological dysfunction. With these injuries, loss of consciousness lasts for more than 24 hours, and recovery is never complete, leading to deficits in intelligence, reasoning, and memory and to changes in personality. Shearing brain injuries tend to be more severe than diffuse brain injuries and lead to abnormal brain stem signs, such as decerebrate rigidity.43

3. If the patient has had an injury to the head, are there any associated symptoms in the neck or problems with breathing, altered vision, discharge from the nose or ears, or urinary or fecal incontinence? These symptoms indicate severe brain or spinal cord injury, and the patient must be handled with extreme care.

4. What are the sites and boundaries of pain? This question helps the examiner determine what structures have been injured. It is important to keep in mind that the patient may be experiencing a referral of pain.

5. What type of pain is the patient experiencing? The type of pain indicates the type of structure injured (see Table 1-3).

6. Is there any paresthesia, abnormal sensation, or lack of sensation? Are smell (cranial nerve I), vision (cranial nerve II), taste (cranial nerve VII), and hearing (cranial nerve VIII) normal? These questions give the examiner some idea of whether neurological structures (especially the cranial nerves) have been injured and, if so, which ones.

 Head Signs and Symptoms Requiring Specialist Care

• Presence of amnesia

• Prolonged residual symptoms

• Loss of consciousness

• Prolonged headache

• Post-concussion syndrome

• Personality changes

• More than one first- or second-degree concussion

• Prolonged disorientation, unsteadiness, or confusion (more than 2 to 3 minutes)

• Blurred vision

• Dizziness (more than 5 minutes)

• Tinnitus (more than 5 minutes)

7. What activities aggravate the particular problem?

8. What activities ease the particular problem?

9. Does the patient have a headache, and, if so, where (Tables 2-11 and 2-12)? Is the headache tolerable? What type of headache is it? Is it a throbbing, pounding, boring, shocklike, dull, nagging, or constant-pressure type of headache? Is the pain of the headache aggravated by movement or by rest? What is the exact location of the headache? Is the headache affected by position or time of day (Table 2-13)? Does it cover the entire head, the sinus region, or behind the eyes? Does it present a “hat band” distribution, or does it affect the neck or the occiput area? It is important for the examiner to record the location, character, duration, and frequency of the headache, as well as any factors that appear to either aggravate or relieve the pain so that a diagnosis can be made and any changes can be noted (Table 2-14). Figure 2-14 shows a headache disability questionnaire that may be used to determine the severity of headache and its effect on everyday activity.⁵⁴

10. Is the patient dizzy, unsteady, or having problems with balance? The examiner should also note whether the dizziness occurs when the patient suddenly stands up, turns, or bends, or whether it occurs without movement. Remember that “dizziness” is a word that patients sometimes use to indicate unsteadiness in walking. Dizziness is usually associated with problems of the middle ear, vertebrobasilar insufficiency, or problems in the upper cervical spine. Vertigo implies a rotary component; the patient’s environment seems to whirl around the patient, or the patient’s body seems to rotate in relation to the environment. If the patient complains of dizziness or vertigo, the time of onset and duration of these attacks should be noted. A description of the type of motion that occurs and any other associated symptoms should be included. Balance may be affected by problems within the brain or the semicircular canals in the inner ear. The examiner should also note whether the patient is talking about unsteadiness, loss of balance, or actual falling.

11. Is the patient unduly irritated or having trouble concentrating? The patient’s state indicates the severity of the injury.

12. Does the patient know where he or she is, who he or she is, the day, and the time of day? Does the patient have some idea of what was happening when the injury occurred? These types of questions reveal the severity of the injury.

13. Does the patient have any memory of past events or what occurred before or after the injury? This type of question tests for retrograde amnesia, posttraumatic amnesia, and injury severity, which can be determined by asking the patient straightforward questions about events in the patient’s own past, such as birth date or year of graduation from high school or university. The examiner may also ask questions about the injury, preceding events, and posttraumatic events. Questions such as “What day is it?” “Who is the opposition?” “Who is winning?” and “What is your telephone number and address?” test the patient’s static memory ability. The examiner must ensure that he or she or someone present at the time of the examination knows the answer to these questions. Although it is common to ask these orientation questions (e.g., time, place), it has been shown that these questions can be unreliable in sporting situations when compared with memory assessment.55,56 The examiner can assess recent memory by asking the patient to remember the names for two to five persons or common objects, such as the color “red,” the number “five,” the name “Mr. Smith,” and the word “pride,” and then asking the patient to name them 5 or 10 minutes later. The patient may be asked to repeat the words two or three times when the examiner initially says them to test immediate recall or to ensure that the patient can say and recall the words. Immediate recall, another form of memory, is best tested by asking the patient to repeat a series of single digits. Normally, a person can repeat at least six digits, and many people can repeat eight or nine. The examiner may also ask the patient to repeat the months of the year backward in a similar type of test. Memory is generally thought to be formed and stored in certain regions of the temporal lobes. The parietal lobe of the brain is thought to enable one to appreciate the environment, to interpret visual stimuli, and to communicate.

Common Head Injury Tests

• Static memory (What day is it? Who’s winning?)

• Immediate recall (repeat series of single digits)

• Recent memory (recall three common objects or names after 15 minutes)

• Short term memory (What is the game plan?)

• Processing and concentration ability (minus-7 test, multiplying)

• Abstract relationships

• Coordination (eye-hand tests)

• Balance (Romberg test)

• Myotomes

• Eye coordination

• Visual disturbance tests

14. Can the patient solve simple problems? Because concussions reduce one’s ability to process information, it is important to determine the patient’s reasoning and processing ability. For example, does the patient know his or her home telephone number? Is the patient able to do the “minus 7” or “serial 7” test (i.e., count backward from 100 by sevens)? This test gives the examiner some idea of the patient’s calculating ability and concentration skills. Mathematic ability (the ability to add, subtract, multiply, and divide) can also be evaluated to test processing ability. In addition, the examiner can ask the patient to name several important people from the present in reverse chronological order (e.g., the last three presidents of the United States) or to give the names of some familiar capital cities. Finally, the patient should be tested on his or her ability to comprehend abstract relations. For example, the examiner may quote a common proverb, such as “A bird in the hand is worth two in the bush,” and then ask the patient to explain what the expression means. Patients with organic mental impairment and certain patients with schizophrenia may give a concrete answer, failing to recognize the abstract principle involved.44 The ability to conceptualize, abstract, plan ahead, and formulate rational judgments of problems or events is largely a function of the frontal lobes.

15. Can the patient talk normally? Patients with lesions of the parietal lobe have difficulty communicating and understanding what is occurring around them. Dysarthria indicates defects in articulation, enunciation, or rhythm of speech. It usually results from extraneural problems, such as poor-fitting dentures, malformation of the oral structures, or impairment of the musculature of the tongue, palate, pharynx, or lips because of incoordination, weakness, or abnormal innervation. It is characterized by slurring, slowness of speech, indistinct speech, and breaks in normal speech rhythm. Dysphonia is a disorder of vocalization characterized by the abnormal production of sounds from the larynx. Dysphonia is usually caused by various abnormalities of the larynx itself or of its innervation. The principal complaint of dysphonia is hoarseness, ranging from mild roughness of the voice to an inability to produce sound. Dysphasia denotes the inability to use and understand written and spoken words as a result of disorders involving cortical centers of speech or their interconnections in the dominant cerebral hemisphere. With all of these conditions, the peripheral mechanisms for speech remain intact.

16. Does the patient have any allergies, or is the patient receiving any medication? Allergies may affect the eyes and nose, as may medications. Medications themselves may mask some symptoms.

17. Is the patient having any problems with the eyes? Monocular diplopia (blurred vision when looking with one eye) may result from hyphema, a detached lens, or other trauma to the globe of the eye.57 Binocular diplopia (blurred vision when looking through both eyes) occurs in 10% to 40% of patients with a zygoma fracture. It may be caused by soft-tissue entrapment, neuromuscular injury (intraorbital or intramuscular), hemorrhage, or edema. It disappears when one eye is closed. Double vision, which occurs when the good eye is closed, indicates that some structure of the eye is injured. If it occurs with both eyes open, something is affecting the free movement of the eyes (Tables 2-15 and 2-16).

18. Does the patient wear glasses or contact lenses? If the patient wears glasses, are the lenses treated (hardened) or made of polycarbonate? If they are hardened, how long ago were they treated? If the patient wears contact lenses, are they hard, soft, or extended-wear lenses? Did the patient wear eye protectors? If so, what type were they? Are the patient’s eyes watering? Is there any pain in the eyes? Small perforating injuries may be painless. If the patient complains of flashes of bright light, “a curtain falling in front of the eye,” or floating black specks, these findings may indicate retinal detachment. These questions tell the examiner whether the eyewear or eyes need to be examined in greater detail.

19. Is the patient having any problem with hearing? Does the patient complain of an earache? If so, when was the onset, and what is the duration of the earache? Does the patient complain of pain or a discharge from the ear? Is the earache associated with an upper respiratory tract infection, swimming, or trauma? The patient should also be questioned on his or her method of cleaning the ear. If there appears to be a hearing loss, the patient should be asked whether the hearing loss came on quickly or slowly, whether the patient hears best on the telephone (amplified sound) or in a quiet or noisy environment, and whether speech is heard soft or loud. Does the patient use a hearing aid?

20. Is the patient having any problems with the nose? Has the patient used nose drops or spray? If so, how much, how often, and for how long? Does the patient have any nasal discharge, and if so, is its character watery, mucoid, purulent, crusty, or bloody? Does the discharge have any odor (indicative of infection), and is it unilateral or bilateral? Does the patient exhibit any associated nasal symptoms, such as sneezing, nasal congestion, itching, or mouth breathing? Does the patient complain of a nosebleed, and has the patient had many nosebleeds? If so, how frequent are the nosebleeds, what is the amount of the bleeding, and what appears to be causing the bleeding? Positive responses to any of these questions indicate that the nose must be examined in greater detail.

21. If the examiner is concerned about the mouth and teeth or the temporomandibular joints, questions related to these areas can be found in Chapter 4. It is important, however, to ensure that the patient’s dental occlusion and biting alignment have not been altered. Are all the teeth present, and are they symmetrical? Is there any swelling or bleeding around the teeth? Are the teeth mobile, or is part of a tooth missing? Is the pulp exposed? Each of these questions helps determine whether the teeth have been injured. Teeth that have been avulsed, if intact, should be reimplanted as quickly as possible. If reimplanted after cleansing (rinsed in saline solution or water) within less than 30 minutes, the tooth has a 90% chance of being retained. If it is not possible to reimplant the tooth, it should be kept moist in saline, or the patient should keep it between the gum and cheek while dental care is sought.

22. Questions concerning the neck and cervical spine can be found in Chapter 3.

TABLE 2-3

Areas of the Brain and Their Function

Area of the Brain	Function
Cerebrum	Cognitive aspects of motor control Memory Sensory awareness (e.g., pain, touch) Speech Special senses (e.g., taste, vision)
Cerebellum	Coordinate and integrate motor behavior Balance Motor learning Motor control (muscle contraction and force production)
Diencephalon (thalamus)	Regulation of body temperature and water balance Control of emotions Information processing to cerebrum
Brain stem	Control of respiratory and heart rates Peripheral blood flow control

TABLE 2-4

Signs and Symptoms* of Concussion (Torg Classification)

	Grade 1	Grade 2	Grade 3	Grade 4	Grade 5
Confusion	None or momentary	Slight	Moderate	Severe	Severe
Amnesia	No	Posttraumatic amnesia <30 min	Posttraumatic amnesia <30 min Retrograde amnesia	Posttraumatic amnesia >30 min Retrograde amnesia	Posttraumatic amnesia >24 hours Retrograde anmesia
Residual symptoms	No	Perhaps	Sometimes	Yes	Yes
Loss of consciousness	No	No	No	Yes (<5 min)	Yes (>5 min)
Tinnitus	No	Mild	Moderate	Severe	Often severe
Dizziness	No	Mild	Moderate	Severe	Usually severe
Headache	No	May be present (dull)	Often	Often	Often
Disorientation and unsteadiness	None or minimal	Some	Moderate	Severe (5 to 10 min)	Often severe (>10 min)
Blurred vision	No	No	No	Not usually	Possible
Post-concussion syndrome	No	Possible	Possible	Possible	Possible
Personality changes	No	No	No	Possible	Possible

*These signs and symptoms should only be used as a guide in acute situations.

Data from Vegso JJ, Torg JS: Field evaluation and management of intracranial injuries. In Torg JS, editor: Athletic injuries to the head, neck and face, St Louis, 1991, Mosby, pp. 226–227.

TABLE 2-5

Risk Factors That May Prolong or Complicate Recovery from Concussion

Factors	Modifier
Symptoms	Number of concussions Duration of symptoms (>10 days) Severity (intensity and duration)
Signs	Prolonged loss of consciousness (>1 min), amnesia (anterograde and/or retrograde)
Sequelae	Concussive convulsions
Temporal	Frequency—repeated concussions over time Timing—injuries close together in time “Recency”—recent concussion or traumatic brain injury
Threshold	Repeated concussions occurring with progressively less impact force or slower recovery after each successive concussion
Age	Child and adolescent (<18-years-old) may recover slower
Co- and pre-morbidities	Migraine Depression or other mental health disorders Attention deficit hyperactivity disorder Learning disabilities Sleep disorders
Medication	Psychoactive drugs Anticoagulants
Behavior	Dangerous style of play
Sport	High risk activity Contact and collision sport High sporting level

Modified from McCrory P, Meeuwisse W, Johnston K, et al: Consensus statement on concussion in sport—The 3rd International Conference on Concussion in Sport held in Zurich, November 2008. Clin J Sport Med 19(3):189, 2009.

TABLE 2-6

Severity Stages of Concussive Injury

Acute Concussion	Post-Concussion Syndrome	Prolonged Post-Concussion Syndrome	Chronic Traumatic Encephalopathy
• Physical (somatic) symptoms: Headache, dizziness, hearing loss, balance difficulty, sleep disturbances, nausea/vomiting, sensitivity to light or noise, diminished athletic performance • Cognitive deficits: Loss of short-term memory (anterograde and/or retrograde), difficulty with focus or concentration, confusion, loss of consciousness, disorientation, inability to focus, delayed verbal and/or motor responses, excessive drowsiness, decreased attention, diminished work or school performance • Emotional (affective) disturbances: Irritability, anger, fear, mood swings, decreased libido	• Persistent concussion symptoms • Usually lasting 1 to 6 weeks after MTBI • Self-limiting	• Symptoms lasting over 6 months • Lowered concussion threshold • Diminished athletic performance • Diminished work or school performance	• Latency period (usually 6 to 10 years) • Personality disturbances • Emotional lability • Marriage/personal relationship failures • Depression • Alcohol/substance abuse • Suicide attempt/completion

MTBI, Mild traumatic brain injury.

Modified from Sedney CL, Orphanos J, Bailes JE: When to consider retiring an athlete after sports-related concussion. Clin Sports Med 30(1):189–200, 2011.

TABLE 2-7

Signs and Symptoms of Concussions

Acute	Late (Delayed)
• Lightheadedness • Delayed motor and/or verbal responses • Memory or cognitive dysfunction • Disorientation • Amnesia • Headache • Balance problems/incoordination • Vertigo/dizziness • Concentration difficulties • Loss of consciousness • Blurred vision • Vacant stare (befuddled facial expression) • Photophobia • Tinnitus • Nausea • Vomiting • Increased emotionality • Slurred or incoherent speech	• Persistent low grade headache • Easy fatiguability • Sleep irregularities • Inability to perform daily activities • Depression/anxiety • Lethargy • Memory dysfunction • Lightheadedness • Personality changes • Low frustration tolerance/irritability • Intolerance to bright lights, loud sounds

TABLE 2-8

Concussion Symptoms

Somatic	Neurobehavioral	Cognitive
• Headache • Nausea • Vomiting • Balance problems • Light/sound sensitivity • Numbness/tingling • Dizziness	• Sleeping more or less than usual • Drowsiness • Fatigue • Sadness • Nervousness • Trouble falling asleep	• Feeling “slowed down” • Feeling “in a fog” • Concentration difficulty • Remembering difficulty • Confusion • Amnesia (anterograde and/or retrograde) • Loss of consciousness • Inability to focus • Delayed motor and verbal responses • Excessive drowsiness

Data from Piland SG, Motl RW, Guskiewicz KM, et al: Structural validity of a self-report concussion-related symptoms scale, Med Sci Sports Exerc 38(1):27–32, 2006; Herring SA, Cantu RC, Guskiewicz KM, et al: Concussion (mild traumatic brain injury) and the team physician: a consensus statement—2011 update. Med Sci Sports Exerc 43(12):2414, 2011.

TABLE 2-9

Classification Systems for Concussions

System	Grade I (Mild)	Grade Ia	Grade II (Moderate)	Grade III (Severe)	Grade IV
Cantu	No LOC or PTA < 30 min	N/A	LOC < 5 min, PTA 30 min to 24 hrs	LOC > 5 min, PTA > 24 hrs	N/A
Torg	(Grade I to II) No LOC or amnesia (except PTA)			(Grade III–IV) LOC < few minutes, PTA or retrograde amnesia	(Grade V–VI) LOC/coma, confusion, amnesia
Colorado Consortium	Confusion without amnesia, no LOC	N/A	Confusion and amnesia, no LOC	LOC	N/A
Virginia Neurological Institute	Short LOC, PTA < 1 hr, GCS score = 15	Short LOC, PTA 1 to 24 hrs, GCS score = 15	LOC < 5 min, PTA ≥ 24 h, GCS score > 15 for < 5 min	LOC < 5 min, PTA N/A, GCS score < 15 for < 1 hr	LOC 5 to 60 min, PTA N/A, GCS score < 12 for > 5 min or < 15 for > 1 hr
American Academy of Neurology	No LOC, Symptoms < 15 min	N/A	No LOC, Symptoms > 15 min	Any LOC	N/A

GCS, Glasgow Coma Scale; LOC, loss of consciousness; PTA, posttraumatic amnesia.

From Durand P, Adamson GJ: On-the-field management of athletic head injuries, J Am Acad Orthop Surg 12:194, 2004. Adapted with permission from Macciocchi SN, Barth JT, Littlefield LM: Outcome after mild head injury. Clin Sports Med 17:27–36, 1998.

TABLE 2-10

Examples of Neurophysiological Tests

Test	Ability Evaluated
Continuous Performance Test	Sustained attention, reaction time
Controlled Oral Word Association Test	Word fluency, word retrieval
Delayed Recall (from Hopkins Verbal Learning Test)	Delayed learning from previously learned word list
Digit Span (from Wechsler Memory Scale—revised)	Attention span
Grooved-Pegboard Test	Motor speed and coordination
Hopkins Verbal Learning Test	Verbal memory (memory for words)
Immediate Measurement of Performance and Cognitive Testing (IMPACT)	Attention span, sustained and selective attention, reaction time, memory
Number/Symbol Matching	Processing speed, visual motor speed
Orientation Questionnaire	Orientation, post traumatic amnesia
Sequential Digit Tracking	Sustained attention, reaction time
Stroop Test	Mental flexibility, attention
Symbol Digit Modalities	Visual scanning, attention
Symbol Memory	Immediate visual memory
Trail-Making Test	Visual scanning, mental flexibility
Verbal Working Memory	Word memory, working memory
Visual Span	Visual attention, immediate memory
Visual Symbol Search	Visual scanning, reaction time
Word/Colour Tracking	Focused attention, response inhibition

Data from Maroon JC, Lovell MR, Norwig J, et al: Cerebral concussion in athletes: evaluation and neurophysiological testing. Neurosurg 47:659–672, 2000.

TABLE 2-11

Type of Headache Pain and Usual Causes

Type of Pain	Usual Causes
Acute	Trauma, acute infection, impending cerebrovascular accident, subarachnoid hemorrhage
Chronic, recurrent	Migraine (definite pattern of irregular interval); eyestrain; noise; excessive eating, drinking, or smoking; inadequate ventilation
Continuous, recurrent	Trauma
Severe, intense	Meningitis, aneurysm (ruptured), migraine, brain tumor
Intense, transient, shocklike	Neuralgia
Throbbing, pulsating (vascular)	Migraine, fever, hypertension, aortic insufficiency, neuralgia
Constant, tight (bandlike), bilateral	Muscle contraction

TABLE 2-12

Location of Headache and Usual Causes

Location	Usual Causes
Forehead	Sinusitis, eye or nose disorder, muscle spasm of occipital or suboccipital region
Side of head	Migraine, eye or ear disorder, auriculotemporal neuralgia
Occipital	Myofascial problems, herniated disc, eyestrain, hypertension, occipital neuralgia
Parietal	Hysteria (viselike), meningitis, constipation, tumor
Face	Maxillary sinusitis, trigeminal neuralgia, dental problems, tumor

TABLE 2-13

Effect of Position or Time of Day on Headache

Position or Time of Day When Headache Is Worst	Usual Causes
Morning	Sinusitis, migraine, hypertension, alcoholism, sleeping position
Afternoon	Eyestrain, muscle tension
Night	Intracranial disease, osteomyelitis, nephritis
Bending	Sinusitis
Lying horizontal	Migraine

TABLE 2-14

Headaches: A Differential Diagnosis

Disorder	Sex/Age Predominance	Nature of Pain	Frequency	Location	Duration	Prodromal Events	Precipitating Factors	Cause	Familial Predisposition	Other Possible Symptoms
Migraine	Female/20 to 40 years	Builds to throbbing and intense	Usually not more than twice a week; may be noctural	Usually unilateral	Several hours to days	Visual disturbances can occur contralateral to pain site	Unknown, may be physical, emotional, hormonal, dietary	Vasomotor	Yes	Nausea, vomiting, pallor, photophobia, mood disturbances, fluid retention
Cluster (histamine) headache	Male/40 to 60 years	Excruciating, stabbing, burning, pulsating	1 to 4 episodes per 24 hours; nocturnal manifestation	Unilateral, eye, temple, forehead	Minutes to hours	Sleep disturbances or personality changes can occur	Unknown, may be serotonin, histamine, hormonal blood flow	Vasomotor	Minor	Ipsilateral sweating of face, lacrimation, nasal congestion or discharge
Hypertension headache	None	Dull, throbbing, nonlocalized	Variable	Entire cranium, especially occipital region	Variable	None	Activity that increases blood pressure	High blood pressure; diastolic >120 mm Hg	Only as related to hypertension
Trigeminal neuralgia (tic douloureux)	Female/40 to 60 years	Excruciating, spontaneous, lancinating, lightning	Can occur many (12 or more) times per day	Unilateral along trigeminal nerve area	30 seconds to 1 minute	Disagreeable tingling	Touch (cold) to affected area	Neurological	None	Reddened conjunctiva, lacrimation
Glossopharyngeal neuralgia	Male/40 to 60 years	Excruciating, spontaneous, lancinating, lightning	Can occur many (12 or more) times per day	Unilateral retrolingual area to ear	30 seconds to 1 minute	None	Movement or contact of the pharynx	Neurological	None
Cervical neuralgia	None	Dull pain or pressure in head		Bilateral, occipital, frontal, or facial	Variable	None	Posture or head movement	Neurological, pressure on roots of spinal nerves	None	Dizziness, auditory disturbances
Eye disorders	None	Generalized discomfort in or around the eyes	Intensify with sustained visual effort	Entire cranium	During and after visual effort	None	Impairment of eye function	Cornea, iris, or intraocular pain	Possible	Diminished vision, sensitivity to light
Sinus, ear, and nasal disorders	None	Dull, persistent	Variable	Frontal, temporal, ear, nose, occipital	Variable	None	Infection, allergy, chemical, bending, straining	Blockage, inflammation, infection	None

Modified from Esposito CJ, Grim GA, Binkley TK: Headaches: a differential diagnosis. J Craniomand Pract 4:320–321, 1986.

TABLE 2-15

Common Visual Eye Symptoms and Disease States

Visual Symptom	Associated Causes
Loss of vision	Optic neuritis Detached retina Retinal hemorrhage Central retinal vascular occlusion
Spots	No pathological significance*
Flashes	Migraine Retinal detachment Posterior vitreous detachment
Loss of visual field or presence of shadows or curtains	Retinal detachment Retinal hemorrhage
Glare, photophobia	Iritis (inflammation of the iris) Meningitis (inflammation of the meninges)
Distortion of vision	Retinal detachment Macular edema
Difficulty seeing in dim light	Myopia Vitamin A deficiency Retinal degeneration
Colored haloes around lights	Acute narrow angle glaucoma Opacities in lens or cornea
Colored vision changes	Cataracts Drugs (digitalis increases yellow vision)
Double vision	Extraocular muscle paresis or paralysis

*May precede a retinal detachment or be associated with fertility drugs.

From Swartz MH: Textbook of physical diagnosis, Philadelphia, 1989, WB Saunders, p. 132.

TABLE 2-16

Common Nonvisual Eye Symptoms and Disease States

Nonvisual Symptom	Associated Causes
Itching	Dry eyes Eye fatigue Allergies
Tearing	Emotional states Hypersecretion of tears Blockage of drainage
Dryness	Sjögren syndrome Decreased secretion as a result of aging
Sandiness, grittiness	Conjunctivitis
Fullness of eyes	Proptosis (bulging of the eyeball) Aging changes in the lids
Twitching	Fibrillation of orbicularis oculi
Eyelid heaviness	Fatigue Lid edema
Dizziness	Refractive error Cerebellar disease
Blinking	Local irritation Facial tic
Lids sticking together	Inflammatory disease of lids or conjunctivae
Foreign body sensation	Foreign body Corneal abrasion
Burning	Uncorrected refractive error Conjunctivitis Sjögren syndrome
Throbbing, aching	Acute iritis (inflammation of the iris) Sinusitis (inflammation of the sinuses)
Tenderness	Lid inflammations Conjunctivitis Iritis
Headache	Refractive errors Migraine Sinusitis
Drawing sensation	Uncorrected refractive errors