Which response to the Brachioradialis reflex test is documented as normal?

Reflex enhancement

When reflexes are difficult to elicit, they may be enhanced by asking the patient to clench the teeth or to try to pull clasped hands apart (Jendrassik's manoeuvre).

Plantar response

Check that the big toe is relaxed. Stroke the lateral aspect of the sole and across the ball of the foot. Note the first movement of the big toe. Flexion should occur. Extension due to contraction of extensor hallucis longus (a ‘Babinski’ reflex) indicates an upper motor neuron lesion. This is usually accompanied by synchronous contraction of the knee flexors and tensor fasciae latae.

Elicit Chaddock's sign by stimulating the lateral border of the foot. The big toe extends with upper motor neuron lesions.

To avoid ambiguity do not touch the innermost aspect of the sole or the toes themselves.

A Amplitude of Reflex

The amplitude of muscle stretch reflexes depends on the integrity of the lower and upper motor neurons innervating the reflex (see Fig. 61.2 in Chapter 61 for definition of lower and upper motor neurons). (1) The lower motor neurons of a reflex are its peripheral nerve (second column in Table 63.1) and its spinal segment (third column in Table 63.1): disease at either of these locations reduces or abolishes the relevant reflex. (2) The upper motor neurons are the descending corticospinal pathways innervating the reflex: disease anywhere along this pathway (e.g., cerebral hemisphere, brain stem) exaggerates the reflex. (3) Disease of the spinal cord, where both upper and lower motor neurons reside, abolishes the reflex at the level of the lesion (lower motor neuron response) and exaggerates all reflexes from spinal levels below the level of the lesion (upper motor neuron response).

Nonetheless, absent or exaggerated reflexes, by themselves, do not signify neurologic disease.29-31 For example, 6% to 50% of elderly persons without neurologic disease lack the ankle jerk bilaterally, despite the Jendrassik maneuver,28,32 and a small percentage of normal individuals have generalized hyperreflexia.29-31,33 Instead, the absent or exaggerated reflex is significant only when it is associated with one of the following clinical settings:

The absent reflex is associated with other findings of lower motor neuron disease (weakness, atrophy, fasciculations).

The exaggerated reflex is associated with other findings of upper motor neuron disease (i.e., weakness, spasticity, Babinski sign).

The reflex amplitude is asymmetric, which suggests either lower motor neuron disease of the side with the diminished reflex or upper motor neuron disease of the side with exaggerated reflex.

The reflex is unusually brisk compared with reflexes from a higher spinal level, which raises the possibility of spinal cord disease at some level of the spinal cord between the segments with exaggerated reflexes and those with diminished ones.

C Reinforcement: The Jendrassik Maneuver

According to the NINDS scale (see Table 61-2), grade 1 reflexes describe reflexes made conspicuous by reinforcement maneuvers and grade 0 reflexes are those that are absent despite reinforcement. The most common method of reinforcing reflexes is the Jendrassik maneuver. In 1885, Erno Jendrassik reported that having the patient “hook together the flexed fingers of his right and left hands and pull them apart as strongly as possible” while the clinician taps on the tendon enhances the reflexes of normal patients.2 Reflex enhancement with this maneuver persists as long as the patient is pulling apart the arms, up to 10 seconds in some studies.13,14 In one study of normal elderly patients, the absent ankle jerk was made to appear 70% of the time using reinforcing maneuvers.15

F Response Procedure

To obtain an F response, the setup is essentially the same as that for a routine motor conduction study using distal stimulation. Several adjustments must be made to the EMG machine to record F responses, however. The gain should be increased to 200 µV (because the amplitude of the F response is quite low), and the sweep speed should be increased to 5 or 10 ms, depending on the length of the nerve being studied. Supramaximal stimulation must always be used, and the stimulator should be turned around so that the cathode is more proximal (Figure 4–5). Although F responses typically can be obtained with the stimulator in the standard position (cathode distal), there is the theoretical possibility of anodal block (wherein the nerve hyperpolarizes under the anode, blocking antidromic travel of the action potential from the depolarization site under the cathode). One should stimulate at a rate no faster than once every two seconds (0.5 Hz). This is done in order to avoid the effects of the previous stimulus on a subsequent response. In addition, stimulating at this rate is much more comfortable for the patient and avoids the “temporal summation of pain” that occurs when the stimulation frequency is too fast (i.e., the patient is stimulated again before recovering from the discomfort of the previous one).

Because each F response varies in latency and amplitude, it is important to obtain at least ten F responses, preferably on a rastered trace. Indeed, the normal values of F waves are based on doing at least ten stimulations. If one is unable to obtain an F response, first ensure that the nerve has been stimulated supramaximally. Second, the Jendrassik (reinforcement) maneuver can be of help in “priming” the anterior horn cells. The patient can be asked to make a fist with the contralateral hand or clench the teeth prior to each stimulation. This maneuver often will elicit an F response where one was not present at rest. It should be noted that one should not do the Jendrassik maneuver unless the F responses are difficult to elicit. Paradoxically, performing a Jendrassik maneuver when not necessary can actually decrease the likelihood of obtaining F responses.*

Of the various F response measurements (minimal latency, chronodispersion [maximal minus minimal F response latency], and F wave persistence [Figure 4–6]), the minimal F wave latency is the most reliable and useful measurement, although occasionally side-to-side differences in F wave persistence and chronodispersion help in identifying an abnormality. Unfortunately, because F responses are quite small, there is often some inherent error in placing the latency markers. It is best to place the latency marker on the F response at the point where it departs from the baseline, with either a positive or negative deflection. In addition, superimposing the rastered traces once all the responses are obtained is often helpful in determining the minimal latency.

It is important to emphasize that although F responses usually are thought of as assessing the proximal nerve segments, they actually check the entire nerve. For example, any nerve with a prolonged distal motor latency on routine nerve conduction studies will also have prolonged F responses, because the F response must travel through the distal segment of nerve as well as the proximal segment. This situation is commonly seen in patients with median neuropathy at the wrist, wherein the median minimal F latency is often prolonged; in this situation, the depolarization travels antidromically from the stimulation site at the wrist up the nerve to the anterior horn cell, and then back down the nerve to the point of stimulation. However, once the depolarization proceeds past the point of stimulation, through the area of slowing at the wrist, this results in prolongation of the F response. Likewise, if there is generalized conduction velocity slowing from a polyneuropathy, the F response will also be slowed, reflecting the slowed conduction velocity of the entire nerve. The F response latency is shorter in the arms than in the legs, reflecting the shorter length of nerve traveled. Therefore, it should be no surprise that taller patients have longer F responses than do shorter patients. Thus, the distal motor latency, the conduction velocity, and the height of the patient must all be taken into account before a prolonged F response is interpreted as indicating a proximal nerve lesion.

REFLEXES AND COORDINATION

In coordination with the sensory and motor examinations deep tendon reflexes (muscle stretch reflexes) serve as a valuable guide to the anatomical localization of a lesion. Similar to motor and sensory tests, reflexes are indicative of specific spinal levels. The most commonly tested reflexes are listed in Table 4-3. A standardized grading system for deep tendon reflexes from 0 to 4 is presented in Table 4-4. In cases of hypoactive reflexes, Jendrassik's maneuver, which is the facilitation of underactive reflexes by voluntary contraction of other muscles, can provide a more accurate assessment of the reflex. Clonus, a grade four reflex, is characterized by rhythmic, uniphasic muscle contractions in response to sudden sustained muscle stretch. Clonus is typical of upper motor neuron disease. A positive plantar or Babinski's reflex, wherein the great toe moves upward and the toes fan outward in response to a key scratch along the lateral aspect and metatarsal heads on the plantar surface of the foot, further indicates upper motor neuron disease. Ultimately the confidence level in the localization of a lesion is quite high when confirmed by sensory, motor, and a reflex derangement.1,5

Coordination and gait testing is a sensitive indicator of cerebellar function and equilibrium. Cerebellar function is tested by traditional finger-nose-finger and heel-knee-shin tests. Equilibrium is assessed by observation of normal gait, heel and toe walk, and tandem gait testing. Tandem gait instructs a patient to walk heel to toe along an imaginary line and observes the results. Equilibrium is further tested by Romberg's test.6

Doppler Ultrasonic Vascular Testing

Doppler vascular testing allows the assessment of pulses in noisy environments or when pulses are weak. This test is efficient when palpation of a pulse is questionable or not possible. The Doppler instrument aids in the assessment of circulation distal to fracture sites, burns, and other injuries that potentially compromise vascular tissue, quickly determining the extent of injury (Fig. 1-25).

Laser Doppler flowmetry is a valuable noninvasive method for investigation of the very early skin venoarteriolar dysfunctions, for evaluation of focal autonomic dysregulation and skin vasomotor abnormalities in patients with Raynaud phenomenon. Laser Doppler-recorded venoarteriolar reflex testing is a simple procedure and an adequate additional diagnostic tool, which contributes to diagnose Raynaud phenomenon and differentiate primary from secondary Raynaud phenomenon (Stoyneva, 2004).

CRITICAL THINKING

In the complaint history of a musculoskeletal condition, what essential points should be included for proper history taking by an experienced examiner?

Name the five essential steps in drawing a working diagnosis for your patient.

Name the Critical 5 questions in orthopedics.

Describe Jendrassik maneuver.

You have a patient who is complaining of unrelenting spinal pain who demonstrates full and pain-free range of motion. What two problems should you consider with this presentation?

Describe the difference and what information can be obtained from the five rung test and the maximal static grip when using a Jamar dynamometer.

What are the significances of the clinical findings of the static grip test and the REG test?

How are the two tests performed?

How would you describe the presentation of a patient with scleratogenous pain?

Why is serial radiography useful in a patient with rheumatoid arthritis?

What area or areas would you monitor?

How frequent should radiography be used?

You have just diagnosed a case of AS. How frequent should you perform serial studies of this patient?

What areas should be monitored?

A question of causation arises in a child with multiple complaints. What imaging procedure would you recommend for this child?

SSEPs are useful in the evaluation of various pathologic conditions. What part of the nervous system is evaluated with this process?

Reflex Testing

The deep tendon reflexes are mediated by a monosynaptic arc. The afferent limb is provided by sensory fibers, which innervate muscle spindles. These fibers project centrally toward the spinal cord and synapse with alpha motor neurons in the ventral horn. The alpha motor neurons comprise the efferent limb of the reflex arc. It is important to note that normal individuals can have diminished deep tendon reflexes. The Jendrassik maneuver can be used to elicit deep tendon reflexes in this situation. The patient is asked to interlock the fingers of both hands and pull them apart. Jaw clenching can also be used to achieve a similar effect. Lesions of the afferent or efferent limb of this arc can cause diminished or absent deep tendon reflexes. This includes conditions such as peripheral neuropathy and radiculopathy. However, patients with small-fiber neuropathy have preserved deep tendon reflexes because the neural deficit spares large myelinated Ia fibers.

Deep tendon reflexes are best examined with a Queen Square or Troemner hammer while the patient is seated comfortably in the upright position. Table 13.4 explains the grading of deep tendon reflexes. Table 13.5 reviews the important deep tendon reflexes and their corresponding nerve root level.

Upper motor neuron lesions cause hyperreflexia. The Babinski and Hoffman signs may be present in patients with upper motor neuron dysfunction. A subtly positive Hoffman response can be seen in young women, as well as in people taking selective serotonin reuptake inhibitor antidepressants, and in these scenarios may not represent pathology. The Babinski sign is elicited by stroking the lateral aspect of the sole of the foot with a blunt object (e.g., a disposable wooden spatula). A positive sign is indicated by extension of the great toe (Fig. 13.1). Care should be taken to not stimulate the more medial aspect of the sole, which will evoke a withdrawal response. Hoffman’s sign is elicited by briskly flicking the dorsal or volar aspect of the distal phalanx of the middle finger. Reflex flexion of the index finger and thumb constitutes a positive response.4

Reflexes

Reflex testing is an essential part of the examination and provides a means of differentiating between spinal cord and peripheral pathology.

A simple monosynaptic reflex consists of an afferent input that synapses in the spinal cord and returns to the extremity through an efferent output (Fig. 2-12). Upper motor neurons inhibit the output of the efferent signal; therefore, if reflexes are increased, the examiner should suspect a decrease in upper motor influence.

Decreased reflexes may imply the loss either of sensory input or of motor neuron or muscle integration.

Reflexes are graded from 0 to 4. Hyperactive reflexes are graded 3 or 4 and suggest the presence of spinal cord pathology or upper motor nerve dysfunction.

Reflex grading is as follows:

0—Absence

1—Diminished

2—Normal reflex

3—Hyperactive reflex

4—Clonus present

Distracting patients may help elicit reflexes through techniques such as the Jendrassik maneuver (having patients pull their hands apart while the stimulus is being applied).

The examination of the upper extremity deep tendon reflexes includes tests of the biceps tendon, the brachioradialis, and the triceps tendon reflexes. Reflexes in the lower extremities include the quadriceps reflex (knee jerk) and the gastrocnemius reflex (ankle jerk). In addition, reflexes of the hamstring muscles (biceps femoris) can be tested.

Reflexes and Coordination

Deep tendon reflexes (muscle stretch reflexes) can also help the clinician to localize a neurologic lesion. Similar to motor and sensory tests, specific reflexes are activated at specific spinal levels. The most commonly tested reflexes are listed in Table 4.9. A standardized grading system for deep tendon reflexes from 0 to 4+ is presented in Table 4.10. In cases of hypoactive reflexes, distraction techniques such as Jendrassik maneuver (hooking the digits of both hands together and attempting to forcibly separate both hands) can be used to better elucidate between true loss of reflex and examination artifact. The voluntary contraction of muscles not being tested results in facilitation of underactive reflexes and can provide a more accurate assessment of the reflex. Clonus, a grade-four reflex, is characterized by rhythmic, uniphasic muscle contractions in response to sudden sustained muscle stretch. Clonus is not always an abnormal finding but may be indicative of an upper motor neuron disease. Plantar reflex testing (elicited with a sharp stimulus on the lateral aspect of the sole of the foot) should be documented in terms of an upgoing (Babinski sign) or downgoing great toe. Babinski first noted the great toe moving upward and the toes fanning outward in response to a key scratch along the lateral plantar surface of the foot in patients with pyramidal lesions. It is now well established that Babinski sign can be seen with many upper motor neuron diseases and is also a normal variant in children up until 12 to 18 months of age. In the hand, one can elicit a Hoffmann sign, which is thumb and index finger flexion that is observed with flicking of the terminal phalanx of the third or fourth digit. This is indicative of an upper motor neuron disease. Ultimately, the confidence level in the localization of a lesion is quite high when confirmed by sensory, motor, and reflex derangements.4 Reflexes are valuable tools in distinguishing true neurologic weakness from poor effort or malingering.

Coordination and gait testing complement reflex assessment and are sensitive indicators of cerebellar function and equilibrium. Cerebellar function is tested by traditional finger-nose-finger and heel-knee-shin tests. Equilibrium is assessed by observation of normal gait, heel-and-toe walk, and tandem gait testing (heel-to-toe walking in a straight line). Equilibrium is further tested by Romberg test (having a patient stand with feet together and eyes closed). Romberg test is positive when the patient sways and loses balance with eyes closed and is suggestive of mild lesions of the sensory, vestibular, or proprioceptive systems.

ACKNOWLEDGMENTS

The authors wish to thank Kenneth Stone and Amy Long for their assistance with the footnotes, tables, and figures. Also thanks to Mary P. Schumer and to Drs. Michael Pfeifer and Douglas Green for their contributions to the sixth edition of this text.