The challenges inherent in sensibility assessment of the upper extremity have increased in recent years. In the past, it seemed the majority of patients referred for evaluation had diagnoses of median nerve compression at the wrist or nerve lacerations at the wrist. The latter 1980s and 1990s saw a shift in referral population toward nerve lesions in continuity at all segments of upper extremity nerves. Schwartzman states that brachial plexus traction injuries are “common, overlooked, and often misdiagnosed.” Whitenack et al. and Hunter et al. attribute the increasing incidence of high-level traction neuropathies to several factors, including high-speed vehicular trauma, falls on the outstretched arm, extensive computer use, repetitive assembly work (especially lateral abduction or overhead lifting), women in the workplace performing heavy work that exceeds their physical capacity, and poor posture.
With these trends in referral population in mind, the therapist must have a working knowledge of the sensory patterns of the upper extremity nerves at all levels, from roots to distal cutaneous branches. In addition, the evaluating therapist must approach sensibility assessment of nerve lesions in continuity differently than for nerve lacerations. The purpose of this chapter is to discuss prerequisites for sensibility assessment and current clinical techniques for assessment of nerve lesions in continuity and nerve lacerations.
Prerequisites for Assessment
Meaningful sensibility assessment requires adequate history, good clinical skills in assessment of sympathetic function, and appropriate test selection and administration. However, before the therapist ever meets the patient, certain prerequisites of knowledge are essential to clinical competence in sensibility assessment. These knowledge domains are nerve pathways and areas of cutaneous supply, knowledge of the effects of nerve injury, and control of test variables. These prerequisites are discussed before proceeding to the actual components of clinical assessment ( Table 14-1 ).
|Prerequisites of Sensibility Assessment||Components of Sensibility Assessment|
Prerequisite: Knowledge of Nerve Pathways and Cutaneous Supply
The region of skin that the therapist assesses for sensibility will depend on the cutaneous distribution of the affected nerve segment. Therefore the therapist must be familiar with upper extremity nerve pathways from spinal roots to distal cutaneous branches. In addition, the therapist must be aware of the location of sensory signs and symptoms resulting from lesions at different sites along the nerve pathways ( Table 14-2 ). In some cases, clinicians may use certain provocative positions or maneuvers to duplicate the patient’s symptoms; some examples are listed in Table 14-2 .
|Nerve Segment||Location of Sensory Signs and Symptoms||Provocative Tests and Maneuvers|
|Roots||Segmental distribution; focal signs in part of the nerve root distribution||Spurling’s maneuvers|
|Upper trunk||Pain in C2 distribution of cranium; pain across trapezial ridge; pain radiating down the medial scapular border to its tip|
|Lower trunk||Dull ache and paresthesias in IV and V and medial forearm|
|Cords||Cutaneous nerve distribution|
|Lateral cord||Paresthesias of I, II, and radial half of III. (If there is concomitant median nerve injury, the tip of II will be subjectively more insensitive to pinprick than either I or tip of III.)|
|Medial cord||Medial aspect of upper arm and forearm; ulnar half of III, IV, and V have decreased sensitivity to pinprick||Deep pressure to supraclavicular fossa|
|Posterior cord||Paresthesias with minimal sensory loss from dorsal area of the forearm, I and II|
|Superficial radial nerve||Dorsal web space between I and II (autonomous supply)||Hyperpronation of forearm|
|Ulnar nerve palmar digital branches||Distal ulnar pulp V (autonomous supply)|
|Median nerve terminal branches||Distal radial pulp II (autonomous supply)|
* Also listed is a sampling of provocative tests and maneuvers. Note: Contrary points of view exist regarding the specificity of certain of these maneuvers. †
Roots of the Brachial Plexus
Operative words in anatomic descriptions of the brachial plexus are “usually, generally, mainly, and most often”; variations are common. The roots of the brachial plexus, C5, C6, C7, C8, and T1 anterior primary rami exit the spinal cord at the intervertebral foramina. (Branches from C4 and T2 ventral rami also may contribute.) C5, C6, and C7 nerve roots give rise to the long thoracic nerve close to the intervertebral foramina; it innervates serratus anterior. The dorsal scapular nerve arises mainly from the C5 nerve root and provides variable innervation to levator scapulae and full innervation to the rhomboids ( Fig. 14-1 ).
There is considerable innervation overlap between the sensory fibers of adjacent spinal nerves at the periphery. Sunderland has represented the sensory dermatomes “without reference to variations or the zones of overlap of adjacent spinal nerves” ( Fig. 14-2 ). Despite variations in dermatome charts, one can confidently use these reference points when assessing segmental innervation: C5 supplies the outer aspect of the shoulder tip, C6 supplies the thumb, C7 (longest cervical spinous process) supplies the middle finger (the longest finger), C8 the little finger, and the T3 dermatome lies in the axilla. Division of a single nerve root generally does not result in anesthesia in its dermatomal area because of the innervation overlap between cutaneous branches at the periphery. However, irritation of a nerve root does result in focal pain, paresthesia, dysesthesia, and altered sensation, often in only a part of the nerve root distribution (see Table 14-2 ).
According to Schwartzman, Spurling’s (foraminal compression) test (see Chapter 7 ) may help differentiate nerve root from plexus injury; it also may be positive with brachial plexus injury but usually not to the same degree.
The roots combine to form the upper, middle, and lower trunks at the level of the scalene muscles. Fibers from C5 and C6 combine to form the upper trunk. The middle trunk is a continuation of C7 fibers. C8 and T1 fibers combine to form the lower trunk. These trunks are located mainly in the supraclavicular fossa. Two nerves come off the upper trunk: the subclavian nerve to the subclavian muscle and the suprascapular nerve. The latter nerve passes through the suprascapular foramen to the supraspinatus and infraspinatus muscles ( Fig. 14-3 ). According to Backhouse, the upper portion of the plexus is much more vulnerable to traction, compression, and direct trauma than the lower portion. The lower roots and trunk are more susceptible to trauma related to adjacent anatomic structures.
Schwartzman has described the sensory and motor effects of traction injuries to the upper and lower trunks of the brachial plexus. He states that no single test is diagnostic of brachial plexus traction injury or thoracic outlet syndrome at this time, but some maneuvers are helpful in localizing the site of injury (see Table 14-2 ).
Each of the three trunks divides into an anterior and posterior division. The divisions lie deep to the middle third of the clavicle and extend distally to the lateral border of the first rib ( Fig. 14-4 ). Fibers in the anterior divisions innervate the anterior aspect of the upper extremity; fibers in the posterior divisions innervate the posterior aspect.
The divisions unite to form the lateral, posterior, and medial cords, named for their position relative to the axillary artery. The cords lie below the clavicle behind the pectoralis minor tendon in the axilla. The posterior divisions from all three trunks combine to form the posterior cord. The anterior divisions from the upper and middle trunks form the lateral cord; the anterior division of the lower trunk forms the medial cord (frequently with a contribution from the middle trunk) ( Fig. 14-5 ).
Similar to the upper and lower trunks, the lateral and medial cords are vulnerable to compromise by traction and epineural fixation to surrounding tissues (see Table 14-2 ).
The lateral cord gives rise to three nerves ( Fig. 14-6 ):
The lateral pectoral nerve, which branches off from the proximal portion of the cord and provides partial innervation to pectoralis major
The musculocutaneous nerve (motor to coracobrachialis, biceps, and brachialis; sensory via the lateral cutaneous nerve of the forearm, to the lateral forearm on both its dorsal and volar surfaces)
The lateral head of the median nerve (motor to all median innervated muscles except the intrinsics)
The posterior cord gives rise to five nerves ( Fig. 14-7 ):
Upper subscapular nerve innervates subscapularis.
Lower subscapular nerve innervates teres major and provides a branch to subscapularis.
Thoracodorsal nerve (also called the middle subscapular nerve ) motors latissimus dorsi.
Axillary nerve innervates the deltoid and teres minor muscles and a small area of skin overlying the lower part of the deltoid muscle.
Radial nerve motors the extensors of the elbow, wrist, and digits.
The cutaneous branches of the radial nerve are as follows:
Lower lateral cutaneous nerve of the arm supplies lower lateral aspect of the arm.
Posterior cutaneous nerve of the arm supplies central posterior aspect of the arm.
Posterior cutaneous nerve of the forearm supplies the central posterior aspect of the forearm.
Terminal sensory branches supply the dorsal aspect of I, II, and (radial half of) III to the level of the proximal interphalangeal joints.
There is considerable overlap with other cutaneous nerves in each of these areas.
The medial cord gives rise to five nerves ( Fig. 14-8 ):
Medial pectoral nerve branches off proximally and provides partial innervation to pectoralis major and full innervation to pectoralis minor.
Medial brachial cutaneous nerve supplies the medial aspect of the arm on its dorsal and volar surfaces.
Medial antebrachial cutaneous nerve of the forearm supplies the medial aspect of the forearm on its dorsal and volar surfaces.
Ulnar nerve motors the ulnar wrist flexors, ulnar digital flexors, and ulnar intrinsics in the hand. It provides cutaneous innervation to the skin overlying the ulnar half of IV and all of V.
Medial head of the median nerve innervates the median intrinsic muscles in the hand and the skin overlying I, II, III, and radial half of IV on the volar surface and distal to the proximal interphalangeal joints on the dorsal surface.
Box 14-1 lists common sites for nerve lesions in continuity caused by compression, entrapment, or traction.
Within the Scalene Triangle
The roots or trunks of the brachial plexus and the subclavian artery are vulnerable to potential mechanical pressure from the borders of the triangle or from other structures. The lower trunk and the subclavian artery are the most susceptible. Their locations adjacent to the first rib or perhaps their arching courses across the first rib make them susceptible to tension exerted by the dependent limb.
Potential hazards are as follows:
Hypertrophied scalene muscles
Sharp fibrous bands associated with the scalene attachments to the first rib
Presence of a cervical rib (the most clearly documented cause and effect)
Presence of a scalene minimus muscle
Lateral to the Scalene Triangle
As it exits the posterior triangle of the neck, the brachial plexus passes between the clavicle and first rib. Clavicle depression or rib cage elevation reduces the bony interval, especially medially, and can compress the nerve trunks or axillary vessels.
More laterally, the neurovascular bundle passes inferior to the coracoid process and posterior to the pectoralis minor. During extreme excursions of the upper limb, especially abduction and external rotation, the brachial plexus is stretched around the coracoid process where it is thought to be vulnerable to stretching.
This nerve is vulnerable where its terminal branch, the lateral antebrachial cutaneous nerve, pierces investing fascia in the distal arm lateral to biceps and becomes superficial. Here, external compression, such as the strap of a heavy handbag, can injure the nerve.
In the arm:
In the axilla, it is vulnerable to the fibrous tendinous edges of latissimus dorsi and the long head of triceps as it passes through the angle between them. It also is vulnerable to an external compressive force such as an axillary crutch.
In the spiral groove, it is vulnerable to lacerations by sharp bony edges of midshaft humeral fractures.
Posterior and then inferior to the deltoid tuberosity, it is vulnerable because it is superficial.
It also is vulnerable where it pierces the lateral intermuscular septum to enter the anterior compartment in the distal lateral arm.
In the forearm and hand:
The radial nerve crosses the anterolateral aspect of the elbow to enter the forearm. At or about the level of the elbow, the nerve splits into its superficial (cutaneous) and deep (posterior interosseous) branches.
The superficial radial nerve is vulnerable to laceration throughout its course in the hand because it is superficial. It also is vulnerable to compression by external weight.
In the arm:
The median nerve descends in the neurovascular bundle (median nerve, ulnar nerve, and brachial artery) that passes through the arm at the junction of the investing fascia and the medial intermuscular septum. It is vulnerable to compression by aneurysm within this bundle.
In the forearm, the median nerve is vulnerable:
At the sharp proximal edge of the bicipital aponeurosis
By supracondylar fracture or elbow dislocation
Where it passes between the two heads of pronator teres
At the proximal border of flexor digitorum superficialis (the “sublimus bridge”). The anterior interosseous nerve branches off distal to the sublimus bridge. The median nerve is vulnerable to compression at pronator or the sublimus bridge. There is no sensory defect.
In the hand:
The most ventral structure passing through the carpal tunnel, the median nerve is subject to compression within the tunnel.
The palmar cutaneous branch of the median nerve arises proximal to the wrist and passes superficially to the carpal tunnel; it is spared in carpal tunnel syndrome.
In the arm:
Within the neurovascular bundle the nerve is vulnerable to compression by aneurysm.
At the midarm level, it enters the posterior compartment by passing through a fibrous opening where it is subject to entrapment.
In the posterior compartment, it occupies a groove in the medial head of the triceps brachii muscle (the arcade of Struthers), where it is firmly anchored and has little padding between it and the bone. Here, it is vulnerable to external compression such as from a tourniquet or the hard edge of an operating table.
In the forearm:
The ulnar nerve enters the forearm by passing posterior to the medial epicondyle in the cubital tunnel. Here it is vulnerable to major and mild trauma.
In the hand:
The nerve passes through Guyon’s canal. It gives off its superficial and deep branches, which are vulnerable to compression.
The dorsal cutaneous branch of the ulnar nerve arises deep to flexor carpi ulnaris, approximately 5 to 7 cm proximal to the wrist and passes to the dorsum of the hand, sparing the dorsal ulnar innervated skin when the ulnar nerve proper is injured at the wrist.
Prerequisite: Knowledge of the Effects of Nerve Injury
Pathomechanics and Degrees of Injury
Agents of nerve injury are mechanical, thermal, chemical, or ischemic. Trauma results in a nerve lesion in continuity (i.e., compression, constriction, entrapment, or traction) or a divided nerve in which continuity is disrupted and the ends retract (i.e., laceration). Gilliat has noted distinctions between compression, constriction, and entrapment, and defined them as indicated in Table 14-3 .
|Compression||Sustained pressure is applied to a localized region of nerve, either through the skin or internally (e.g., from a hematoma adjacent to the nerve). There is a pressure differential between one part of the nerve and another.|
|Constriction||A reduction in nerve diameter caused by adjacent tissues.|
|Entrapment||Constriction or mechanical distortion by a fibrous band or within a fibrous or fibroosseous tunnel.|
|Traction||Stretching of neural tissue. This condition may coexist with compression, constriction, or entrapment.|
The prognosis for recovery of nerve function depends on which nerve structures are damaged (i.e., axons, endoneurium, perineurium, or epineurium) and the degree of severity. Sunderland describes five degrees of severity of nerve injury, ranging from axonal conduction block in a first-degree injury to transection of the nerve in a fifth-degree injury. His classification is described in detail in Chapter 32 .
Sunderland’s first-degree injury corresponds to Seddon’s “neuropraxia.” Sunderland observed that third-degree injury often occurs in entrapment lesions; in these cases, recovery is spontaneous but incomplete because regenerating axons may be prevented by scar from reentering their original endoneurial tubes . Fourth-degree injury results in much more scarring and internal disorganization than lower levels of injury because the strong perineurial sheath that surrounds fiber bundles is disrupted. There may be some hardly useful spontaneous recovery; therefore surgical intervention is essential if functional recovery is to occur. Even so, residual deficits are to be expected because of internal scarring and faulty regeneration and reinnervation. In fifth-degree injury, the entire nerve trunk is transected. As in level four injury, surgical repair is necessary; residual sensory and motor deficits are to be expected. Third-, fourth-, and fifth-degree injuries are the most commonly referred for sensibility assessment.
Patterns of Sensibility Loss and Recovery
When the injury is above the clavicle, affecting the roots and/or trunks, the motor and sensory deficits are segmental in nature. If the injury is below the clavicle, the cords and/or the nerves to which they give rise are affected. The motor and sensory deficits then follow the distribution of the affected peripheral nerves. Because of the overlap between adjacent cutaneous nerves, the area of sensory deficit in a peripheral nerve lesion may be limited to a small region of autonomous supply (see Table 14-2 ).
Nerve Lesions in Continuity
Pattern of Loss as Detected by Conventional Test Instruments *
* In this chapter, tests or instruments referred to as “conventional” denote handheld instruments as opposed to computer-assisted test instruments.Sensory fibers are more susceptible to early compression than motor fibers, and the large myelinated (touch) fibers are more susceptible than the small thinly myelinated (pain) or unmyelinated (burning pain, hot, cold) fibers. A specific pattern of sensory loss in nerve compression, specifically carpal tunnel syndrome (CTS), has been demonstrated by the work of Dellon, Lundborg et al., Gelberman et al., and Szabo et al.
Dellon studied a group of 45 patients with 61 compressed nerves, using vibration (256- and 30-cps tuning forks), static and moving two-point discrimination, electrodiagnostic studies, Tinel’s sign, and Phalen’s sign. Among these seven tests, he found that diminished vibratory perception was the earliest detectable clinical abnormality in compression syndromes of insidious onset.
Lundborg et al. studied the effects of controlled acute external compression to the median nerves of 16 volunteer subjects. They compared motor nerve conduction, sensory nerve conduction, and two-point discrimination findings at three different levels of compression. Among these three tests, the researchers found a decrease in sensory potential amplitude to be the first detectable abnormality. In several cases, even when sensory potential amplitude was severely reduced, two-point discrimination tested within normal limits.
In another study using the same model of controlled compression on 12 volunteer subjects, Gelberman et al. compared findings from the following tests: vibration (256 cps), Semmes-Weinstein Pressure Aesthesiometer (monofilament test), static two-point discrimination, and moving two-point discrimination. They also monitored sensory and motor nerve conduction, subjective findings, and muscle strength. Their results follow:
A decrease in sensory amplitude was the earliest electrodiagnostic indication of impaired nerve function.
A high correlation was present between the Semmes- Weinstein monofilament test, vibratory testing, and sensory amplitude.
Changes in static and moving two-point discrimination consistently occurred together and occurred significantly later than abnormalities on the threshold test (i.e., Semmes-Weinstein and vibration tests).
Regarding the two threshold tests, they noted a problem with the quantitation of vibratory stimulus and response using the tuning fork, and they described the Semmes-Weinstein monofilament test as the most accurate quantitative test in their model of acute compression.
In the next study in the series, Szabo, Gelberman, and Dimick evaluated 20 patients with idiopathic CTS. All patients had objective abnormalities in median nerve conduction at the wrist level. Sensibility tests were administered before and after surgery. The researchers used a fixed-frequency (120 Hz), variable-amplitude vibrometer (Bio-Thesiometer), and a 256-cps tuning fork to test vibration. The other tests were Semmes-Weinstein Pressure Aesthesiometer, two-point discrimination, Phalen’s test, Tinel’s test, and the tourniquet test. Their study confirmed that the threshold tests (i.e., vibrometry and Semmes- Weinstein monofilaments) are more sensitive than two-point discrimination in assessing sensibility in chronic compression neuropathies.
In the next study, Szabo et al. returned to the model of controlled acute compression in 12 volunteer subjects. Because of the previously noted problem with quantitation of the tuning fork, they sought to compare findings from the vibrometer with findings from the 256-cps tuning fork, Semmes-Weinstein Pressure Aesthesiometer, static and moving two-point discrimination, and electrodiagnostic tests. They used the same vibrometer (Bio-Thesiometer) as in the previously cited study. They found that vibrometer abnormalities were the earliest clinical findings and had a high correlation with the less quantifiable tuning fork and slightly less sensitive Semmes-Weinstein Pressure Aesthesiometer. All three threshold tests were significantly more sensitive than two-point discrimination ( p = .01). They concluded that the vibrometer has significant potential as a clinical and research instrument in nerve compression syndromes.
To summarize, the conclusions to be drawn from these studies of acute and chronic compression neuropathies using conventional test instruments, are the following:
The earliest objective finding is decreased sensory amplitude in electrodiagnostic testing.
The threshold tests, vibration and Semmes-Weinstein pressure test, are the most sensitive indicators of clinical abnormality in compression neuropathies.
A vibrometer offers the advantage of quantification over a tuning fork.
Abnormalities in moving and static two-point discrimination are late findings in compression neuropathy.
Pattern of Loss as Detected by the Pressure-Specified- Sensory-Device
In his recent text, Dellon describes a test instrument that he helped develop, the Pressure-Specified-Sensory-Device, which became available in 1989. Dellon reports that it detects a different sequence of sensory loss in chronic nerve compression than the previously cited studies. The instrument is designed to measure four submodalities of touch threshold: cutaneous pressure threshold for one-point static and for one-point moving touch, the pressure threshold for distinguishing one from two static points, and the distance threshold for distinguishing one from two points. In a study of 125 CTS and 71 cubital tunnel syndrome patients, Dellon and Keller found the following:
The first parameter to become abnormal with chronic nerve compression was the pressure threshold for static two-point discrimination. (This result occurred while the distance for discriminating one from two points remained normal, that is, 3 to 4 mm.)
Often, when the pressure threshold for distinguishing one from two static points was already abnormal, the pressure threshold for one-point testing (static or moving) tested normal.
These clinical findings are specific to this instrument. The same order of abnormal thresholds was found in a separate study of patients with tarsal tunnel syndrome and compression of the peroneal nerve at the fibular head. Dellon’s conclusion is that given a sensitive enough test instrument, the earliest change that can be detected in chronic nerve compression is the pressure required to distinguish one from two static points touching the skin. He states that for evaluation or screening of chronic nerve compression, just the static touch thresholds (one point and two point) need to be measured.
Some patients with nerve lesions in continuity complain of sensory symptoms brought on or intensified by certain positions or activities. At rest, they may test normal on both electromyography and clinical sensibility tests. These patients are candidates for “stress testing” in which the affected extremity is subjected to positions or activities selected to provoke sensory symptoms. The patients are tested at rest and after stress. Results of prestress and poststress testing are compared for indications of transient stress neuropathy.
Bell noted the use of sensory stress testing at the Philadelphia Hand Center in 1978. Stress electromyography has been a formal part of the testing protocol there since 1982. Recent reports have confirmed the clinical usefulness of stress testing in patients with transient symptoms of neuropathy.
Pattern of Recovery
The degree of recovery depends on the severity of compression. Mild compression can undergo spontaneous recovery if the initiating cause is removed. Moderate to severe cases that require surgical intervention might respond in one of several ways, including immediate full recovery; gradual full recovery; a period of postoperative hypersensitivity and nerve irritability followed by gradual full recovery; and partial recovery, with or without accompanying hypersensitivity and nerve irritability. Gelberman et al. have classified CTS into four stages (early, intermediate, advanced, and acute) and have described the response to treatment of patients in each category.
Pattern of Loss
Immediately after denervation, the autonomous area of nerve supply is anesthetic. Overlapping areas of supply with neighboring cutaneous nerves are hypesthetic. Therefore careful testing should elicit a borderline transition area between the zones of normal and absent sensibility. The transition area is smaller for touch sensibility than for pain sensibility.
During the early weeks after denervation, some ingrowth of nerve supply from normal nerves occurs along the borders of the anesthetic area, thereby causing apparent shrinkage of the anesthetic zone. The exact mechanism for initiation of this phenomenon is not known.
Pattern of Recovery
The rate of regeneration of sensory fibers in humans generally falls within an average range of 1 to 2 mm per day, with wider ranges reported by some investigators An initial recovery rate of 3 mm per day is not unusual, with slowing of the rate over time. Factors affecting the rate of regeneration within an individual include the nature and level of the lesion and the age of the patient.
Pain elicited by pinch is a very early sign of sensory recovery and may precede a positive Tinel’s sign. Tenderness to pressure and to pinprick precede sensitivity to moving touch, which precedes light touch and discriminative touch. At first, perceptions are poorly localized and may radiate proximally or distally. Accurate localization is among the last sensory functions to recover.
Prerequisite: Control of Test Variables
Many variables contribute to the subjective nature of sensibility testing. Ideally, sensory instruments should meet stringent tests of reliability and validity. Although efforts are being made to achieve that goal, * none of our conventional instruments yet meets all seven requirements of standardized tests noted by Fess. These requirements are (1) reliability, (2) validity, (3) administrative instructions, (4) equipment criteria, (5) norms, (6) instructions for interpretation, and often, (7) a bibliography. Note that Dellon states that the Pressure-Specified-Sensory-Device meets all of the criteria of the consensus reports of the American Diabetes Association and the American Peripheral Neuropathy Association for quantitative sensory testing. In a clinical setting, skilled evaluators attempt to control as much as possible for the variables discussed in the following sections.
* References .
Background noise is distracting to the patient and the tester. A test administered in a noisy environment is not the same as one administered in a quiet environment. All testing should be done in a quiet room. The examiner must be alert for sound made by a testing instrument before or during the application of a stimulus, which will cue the patient to a change in stimulus. Similarly, the sound of a starched lab coat sleeve as the examiner moves about will cue the patient to the arrival of a stimulus. These extraneous noises must be eliminated from the sensibility examination.
Patient-related variables haveto do with patient attitude, level of concentration, and possibly anxiety level (see Chapter 122 for helpful guidelines on evaluating elderly patients in whom inattention might be a problem). Each patient brings his or her own agenda to a sensibility test. Some will want to test well; others will not. Some are suggestible and may imagine a stimulus when there is none; others admit a sensation only if they are absolutely positive they felt it.
Normal callused skin has a higher sensory threshold than normal uncallused skin in the hand because a given stimulus will deform callused skin less than soft, supple skin. Therefore areas of callosity should be noted so that test results can be more validly assessed. Because sensitivity varies within the normal population, the uninvolved hand is usually the best control in the determination of sensibility dysfunction.
Instrument-related variables include quality control in the manufacturing of instruments and variations in the same instrument over time. Instruments that can be calibrated should be calibrated regularly. Dellon notes that the National Institute of Standards and Technology (NIST) defines measurements, for example, for grams. If a testing device can be calibrated to meet NIST’s standards, the device is said to be traceable; the Pressure-Specified-Sensory-Device is a traceable instrument.
The examiner should be aware of the idiosyncrasies of each instrument that he or she uses. For example, some two-point discrimination instruments are heavier than others; the examiner must be careful not to exert a heavier pressure when testing with a heavier instrument.
Greenspan and LaMotte note that in laboratory studies of sensitivity, the experimenter controls either the amount of force that is applied to the skin or the amount of skin indentation (displacement) induced by the instrument. The clinical evaluator should be able to do the same with his instruments. Regardless of which of the two variables are controlled, the evaluator also must be able to control or at least measure various temporal factors, such as the rate and duration of the stimulus. Each of these variables can influence the measurement of threshold sensitivity.
The same test instrument in two different examiners’ hands can produce different results because of differences in the methods of administration. For example, one examiner may use more pressure than the other or may stimulate with a moving instead of a constant touch. Control of method-related variables can be assisted by the following:
Provide standard instructions to the patient before each test.
Use a standard method of supporting the hand during threshold testing and certain functional tests. Brand has recommended that the hand be fully supported in the examiner’s hand so that inadvertent stretch of tissues and movement of joints can be avoided ( Fig. 14-9, A ). He has further suggested that a better method of support would be to rest the hand in putty or a similar medium that would provide full support ( Fig. 14-9, B ). Use of such a medium would have the advantage of eliminating transmission of random vibration in the supporting hand to the hand being tested.
Parameters of stimulus application must remain the same within a test and between tests. Important parameters include speed of stimulus application, which is known to affect perception, the amount of pressure exerted on the skin, and whether the stimulus is moving or constant.
Vary the time interval between applications of the stimulus and the spacing of stimuli so that the patient cannot anticipate the timing or location of the next stimulus.
Carefully document the results for better comparison between successive tests. Bell and Buford demonstrated that when a stimulus is applied with a handheld instrument, the examiner is unable to control for force of application. In part, this is caused by vibration of the hand holding the instrument. An exception is the Semmes-Weinstein Pressure Aesthesiometer. Bell and Tomancik showed that if the lengths and diameters of the filaments are correct, the application forces they produce are repeatable within a predictable range.