The first thing typically noticed is the patient’s appearance. Aspects of appearance that warrant observation and characterization include the apparent degree of development (i.e., the patient is well developed or, if not, describes what aspects of development deviate from normal), the nutritional status (i.e., well nourished, overweight, cachectic, emaciated, etc.), and the degree of grooming/dress/hygiene (i.e., well groomed, appropriately dressed, disheveled, poor hygiene, etc.). Because various drugs encountered in pain care can directly or indirectly cause either weight gain (increased body mass from antidepressants or fluid retention from corticosteroid injections) or weight loss (stimulant use/abuse, cocaine abuse, opioid abuse), note should be made of changes in appearance over time.

Eye contact can be revealing, but like many signs, whether a patient makes good eye contact with the examiner can have different meanings. For example, it is common, in Western cultures, to infer that someone not making good eye contact is being evasive. However, this behavior must be interpreted carefully because in certain cultures, looking at an authority figure, such as a physician, directly in the eye is considered disrespectful or sexually provocative [2, 3].

Overall comments about the nature of the interaction deserve documentation, such as the patient’s demeanor, courtesy, and cooperativeness. The term guarded is used to describe a person who appears to be inappropriately cautious or reserved about the interaction or reluctant to provide information.

This aspect of a patient’s presentation is virtually always perceived by the clinician, but is often not reported. The normal level of consciousness in a clinical situation is, of course, is alert (which implies that the person being evaluated is also awake). Other descriptors commonly employed included somnolent (i.e., drowsy, or sleepy), lethargic (i.e., very sleepy, in which the person can be verbally or physically aroused to a level of communication, but when unprovoked, will drift back to sleep), obtunded (i.e., more sleepy than lethargic), stuporous (i.e., repeated, vigorous stimuli can arouse the person, but ceasing the stimuli results in immediate return to sleep), and comatose (i.e., unresponsive to any stimulus mode – auditory, tactile, etc.) [4]. Degree of attention or engagement is important to observe and report. For example, an alert patient can be disengaged from the interaction (e.g., a person with drug-induced hallucinations may be alert, but completely or intermittently disengaged with the clinician because they are attending to the hallucinations).

Orientation is typically assessed and described in four domains: orientation to person, place, time, and situation. A patient who is oriented to person knows who they are and who others they should know are. Orientation to place is the ability to indicate where they are. With organic brain syndromes, whether degenerative, metabolic, traumatic, infectious, or drug-induced, orientation to time can be an especially sensitive indicator. In a rapidly changing organic brain syndrome (e.g., a person who is admitted to hospital for an overdose of a tricyclic antidepressant), incremental improvement in orientation to time can be a useful adjunct to monitoring progress, as the toxicity resolves, in that the person may initially be disoriented with respect to time, then may know what year it is, but still be disoriented to season or month and will gradually regain orientation to month and date. Orientation to situation is sometimes referred to as situational insight and is used to describe the person who demonstrates an understanding of the context of what is happening at that time.

The quantity, quality, fluidity, spontaneity, and speed of motor activity should be described, as should the presence of any abnormal motor signs. The terms used to quantify activity include normoactive, hypoactive (less spontaneous or responsive activity than normally observed, as might be seen in a patient with drug-induced Parkinsonian syndrome or a person with chronic benzodiazepine toxicity), and hyperactive. Hyperactivity specifically describes an excess amount of goal–directed activity, such as might be seen in a child with attention deficit hyperactivity disorder, in which the clinical presentation may include the child hopping out of their chair, opening and closing the examining room door or drawers in the cabinetry, taking off their shoes, etc.

Excess, purposeless, voluntary motor activity is referred to as agitation. Agitation is often associated with alteration in affect or mood. Pacing, frequently switching positions, hand wringing, finger drumming, or pulling on one’s hair are all examples of agitation. Purposeless, involuntary motor activity, such as tremors, should be described. Tremors can be characterized with regard to their location (e.g., finger, arm), amplitude (small or large), frequency (low or high), whether they are resting or intention (intention tremors appear when an action is attempted, such as reaching for a pencil), and whether they diminish or disappear with distraction. A well-described tremor of note is the pill–rolling tremor, which describes a low-amplitude, high-frequency resting tremor involving the thumb and index finger (with possible involvement of other digits, as well), that is named because it is reminiscent of the rolling of medicinal compounds into round pills by early apothecaries (the dominant technique of creating oral formulations before tableting presses were invented). Another tremor equivalent is that of constant or nearly constant head bobbing or low-amplitude shaking (as if one was repeatedly signaling “no”) that is referred to as titubation. This is seen in a variety of neurodegenerative diseases and drug-induced neurological syndromes.

Drugs may induce several disorders of motor activity, including agitation (e.g., cocaine, stimulants), cogwheel rigidity, tics, and stereotypies. Cogwheel rigidity is the term used to describe a ratchet-like quality of the muscles when flexing and extending a joint. This can be visually observed in some cases, with the hand moving through the flexion-extension arc in a jerky or “start-and-stop” fashion, but often is detectable only by placing the examiner’s thumb over, for example, the biceps tendon and asking the patient to allow the examiner to smoothly, but relatively quickly, flex and extend the elbow (passive flexion and extension). It results in a subtle “bumping” or “ratcheting” feeling of the tendon under the thumb, likened by some to feeling as though a string of pearls is being pulled subcutaneously under the examiner’s thumb. Cogwheel rigidity is an extrapyramidal phenomenon (i.e., it is mediated via neural pathways that are outside of the corticospinal tracts – most of which cross the midline in the medulla oblongata at the pyramidal decussation). Drug–induced extrapyramidal side effects (EPSE) result from dopamine antagonism. Extrapyramidal findings can also occur with disease processes that cause the loss of dopaminergic neurons in the basal ganglia, such as Parkinson’s disease. In general, the corticospinal tracts mediate coarse motor activity and the extrapyramidal paths mediate fluidity and “fine-tuning” of movement. A person with basal ganglia dysfunction may be able to reach for a glass of water, but the movement will be so coarse that they will overshoot the target or knock the glass over. Other features of the Parkinsonian syndrome, whether drug-induced or naturally occurring, include gait abnormalities (see below), masklike facies (i.e., far less activity in the muscles of facial expression than is normal – which can also be seen in chronic depression resulting in so-called pseudodementia and myotonic dystrophy), general hypoactivity, and difficulty initiating an activity or initiating a change in activity. For example, a person with Parkinsonian syndrome may appear to sit comfortably in an examination room chair, but at the conclusion of the visit demonstrate significant difficulty rising from the chair. This difficulty initiating or changing movement is often reported to the physician as difficulty rising from the toilet, or going up stairs (which requires initiation of change of activity with every step). Another characteristic presentation that can be induced by administration of dopamine antagonists is tardive dyskinesia (Fr, tardif, late, as in tardy, + Gk, dys + kinesia, movement). Tardive dyskinesia usually affects the muscles of the head, causing involuntary lip pursing or tongue protrusion, but can affect other muscle groups, as well, even creating restrictive pulmonary compromise.

Drug-induced EPSE can also occur acutely, following the administration of dopamine antagonists used as antiemetics (e.g., droperidol, promethazine), and can manifest as an overwhelming urge to move, or restlessness, called akathisia (Gk, a + kathízein, to sit). This phenomenon can typically be treated with the administration of a drug with antimuscarinic properties, such as diphenhydramine or benztropine. It is important to remember that akathisia refers to the urge to move, not to the movement itself, which may take the form of agitation or hyperactivity. Administration of dopamine antagonists (e.g., some antiemetics or antipsychotics) rarely results in acute dystonias, or sudden increased tone of certain muscles, but not their antagonist muscles, such that the person presents, for example, with their head painfully rotated to one side, and is unable to voluntarily rotate it to a neutral, forward-looking position. The most dramatic of the drug-induced acute dystonias is opisthotonos (Gk, opistho, behind + tonos, tension) in which the extensor muscles of the axial spine and extremities are acutely contracted such that the only contact with the floor is the occiput and the heels – a bridging or arching posture.

Tic (Fr, from It, ticchio) is the term used to describe a rapid, involuntary, repetitive movement of small muscles, such as it can involve the muscles of facial expression. Common tics are throat clearing, blinking, and nose twitching. Tics often disappear during sleep, and can be exacerbated in frequency with anxiety. It is common for persons with tics to describe increasing emotional discomfort the longer they consciously suppress a tic, which discomfort is relieved when they allow the tic to reemerge.

Complex, repetitive, voluntary movements of larger muscle groups are referred to as stereotypies (pronounced “stereo-TIP-eez”) (Gk, stereos, hard or fixed + type). Stereotypies can involve many muscle groups, including muscles involved in speech. They can appear almost mechanical in their repetition and can be difficult for a patient to consciously suppress. A stereotypy can take the form of assuming a particular posture, movements that appear almost purposeful (crossing and uncrossing legs, periodic rubbing a body part not due to pain, rocking, arm flapping), or utterances as one might observe in Tourette’s syndrome. Abusers of methamphetamine or amphetamines may engage in sterotypies that involve picking at their skin, excessive grooming, and disassembling and reassembling or plucking at things. These stereotypies are sometimes referred to in the addiction community as tweaking or punding. Tweaking may also occur in patients treated for Parkinson’s disease with _L-DOPA.

Chorea, or choreia, (Gk, choreia, a circle dance) is used to describe brief, irregular contractions that are not repetitive or rhythmic, but appear to flow from one muscle to the next [5]. Chorea is common in Huntington’s disease, but can also occur following infection with group A beta-hemolytic streptococci (GABHS) which cause rheumatic fever; some cases of which can present with Sydenham chorea, which is characterized by rapid, irregular, and aimless involuntary movements of the arms and legs, trunk, and facial muscles, affecting females more often and typically occurring between the ages of 5 and 15 years. The etiology is likely via an autoimmune reaction from infection-induced antibodies that attack neurons [6]. Chorea can also present in Wilson’s disease, can be drug-induced (dopamine agonists and antagonists, and anticonvulsants), or can be due to cerebrovascular accidents.

Not infrequently, chorea is accompanied by athetosis (Gk, a + thetos, not placed), which is the term used to describe writhing, twisting movements involving multiple muscle groups. When chorea is accompanied by athetosis, the term choreoathetosis is used.

One aspect of a patient’s motor behavior typically observed by pain physicians is gait. A normal gait includes a reasonable stride length, a fluid shift from leg to leg, a moderate arm swing, and an upright or nearly upright posture.A common gait abnormality encountered in care of persons with pain is referred to as antalgic (literally, “against pain,” in clinical use, “pain avoiding”) gait which is characterized by limping, guarding, one lower extremity consistently moving more rapidly than the contralateral extremity to reduce the amount of time weight is borne on the painful side, or significant flexion of the lumbar spine or hips, any of which is done to avoid or minimize pain on ambulation. Ankylosing spondylitis resulting in a fused vertebral column presents with the so-called simian (“apelike”) gait in which there is prominent, fixed flexion of the spine, which pitches the upper body well forward of the feet. A simian gait, because of the forward position of the torso, is also characterized by arms dangling in front of the feet. A person with a simian gait who is wearing a coat or jacket may not be able to see their feet because the forward position of the torso causes the jacket to drape in front of the person and obscures their view of their feet. This can, of course, make the person prone to trips and falls, especially when descending stairs.

An ataxic gait is an unsteady or uncoordinated manner of walking that often includes a broad–based gait (i.e., the lateral distance between the feet is greater than normal and often exceeds the shoulder-to-shoulder width). Ataxic gaits can result from inherited or acquired neurodegenerative conditions (e.g., Friedreich’s ataxia, cerebellar ataxia from inhalant toxicity), acute or chronic drug exposure (e.g., ethanol, benzodiazepines), may be due to conditions affecting the vestibular system (e.g., Meniere’s disease, drug-induced vertigo from calcium antagonists, orthostatic hypotension), or may be due to cerebrovascular disease.

A festinating gait is characterized by short, staccato, accelerating steps in an effort to move forward, almost as if the person is falling forward in order to move and they are having trouble making their feet keep pace with their body. It is often seen in Parkinsonian conditions, as well as other neurological syndromes.

Fortunately, neurologic complications from syphilis infection are currently rare in the USA, but its prevalence is rising. Persons who have tabes dorsalis (peripheral neuropathy, ataxia, autonomic dysfunction) have a characteristic gait due to dorsal column disease causing them to lose proprioception. The tabetic gait is characterized by several distinct components – an inordinate degree of hip flexion, resulting in a high lift of the knee (to ensure that the foot clears the floor, since the lack of proprioception prevents the person from sensing if their ankle is flexed or extended), followed by a forceful “slapping” of the foot on the floor wherein the entire plantar surface contacts the floor at or nearly at once (instead of a normal gait, wherein the heel strikes the floor and the rest of the sole “rolls” down to the floor as weight is shifted). The forceful slapping, in addition to accommodating for a partial or complete foot drop, also provides a supranormal amount of proprioception, so that the person perceives some feedback with regard to position in space, even though dorsal columnar function is impaired. Dorsal spinal space tumors, hematomas, and infection can cause a tabetic-like presentation. Persons with unilateral foot drop, due to tibial nerve injury or early amyotrophic lateral sclerosis, may exhibit features of a tabetic-like gait only in the affected extremity.