10: Examination of the General Somatosensory System

A. Special and general senses

The special senses consist of sight, smell, taste, hearing, and equilibrium. The general senses tested in the Standard Neurological Examination (NE) consist of touch, pain, temperature, position, vibration, and stereognosis. Unique receptors and unique central pathways mediate each of the special senses. Some skin receptors and somatosensory pathways serve one general sensory modality, but other receptors in the skin are polymodal.

B. Negative and positive sensory phenomena after lesions of central and peripheral sensory pathways

1. Abnormal or noxious sensations like pain may arise in two ways: from stimulation of receptors or from intrinsic disease of the nerves or central pathways. Disease of afferent nerve fibers centrally or peripherally causes not only negative or deficit phenomena, with lack of sensation, as you would expect, but also, paradoxically, may cause positive phenomena, with excessive sensation, i.e., pain and tingling (Nashold and Ovelmen-Levitt, 1991).

2. Nomenclature for deficits in superficial sensation

   1. Esthesia = touch or feeling, so hypesthesia = partial loss of touch, and anesthesia = total loss. Anesthesia is also used to mean lack of pain.

   2. Therm = heat, so thermhypesthesia = partial loss of temperature sensation, and thermanesthesia = total loss.

   3. Algesia = pain, so hypalgesia = partial loss of pain sensation, and analgesia (or anesthesia) = total loss.

3. Nomenclature for pain and other noxious irritative phenomena after disease of peripheral or central sensory pathways

   1. Hyperesthesia, hyperalgesia, and hyperthermesthesia refer to an increased sensitivity to touch, pain, and temperature, respectively. For example, after a burn of an area of skin, even slight exposure to heat may cause intense pain, i.e., hyperthermesthesia.

   2. Paresthesias and dysesthesias are uncomfortable sensations of numbness, tingling, pins and needles, or burning pain short of neuralgia or causalgia. Paresthesias describes such sensations when they accompany a normal external stimulus to the skin. Dysesthesias describes their spontaneous occurrence without any obvious external stimulus (Wartenberg, 1953). (Unfortunately some writers reverse the definitions.) You will notice paresthesias and dysesthesias if you study your own sensations when recovering from a local anesthetic for a dental procedure or after having sat too hard on your own sciatic nerve, causing it to "go to sleep."

   3. Hyperpathia means an extreme overresponse to pain. Hyperpathia associated with a raised pain threshold is called anesthesia dolorosa.

   4. Neuralgia means multiple, very severe, electric shock-like pains that radiate into a specific root or nerve distribution. Examples include trigeminal neuralgia and post-herpetic neuralgia that commonly follow herpetic infection of a dorsal root ganglion (Gilden et al., 1991). The neuralgias may or may not alter the sensory threshold, but they complicate testing because of the intense pain and the presence of trigger points that, if touched, elicit a jolt of pain.

   5. Causalgia, named by S. Weir Mitchell (1829–1914) but now called reflex sympathetic dystrophy, designates an unbearable, burning, relentless hyperesthesia and hyperalgesia that ensue after injury to a peripheral nerve (Low, 1997; Sunderland, 1978). Merely a puff of air or slight movement triggers unbearable pain.

   6. Special irritative or positive sensory disorders of cranial nerves: See Section II C.

   7. Neurophysiologic mechanisms of such hyperesthesias might include:

      1. Excessive firing of diseased neurons because of destabilization of their membranes.

      2. Changes in the sensitivity of receptors or of central conducting mechanisms (Layzer, 2001).

      3. A discrepancy or imbalance of the sensory information conveyed when disease affects the ratio of impulses delivered by fibers of different diameters.

      4. Cross talk or short circuiting of impulses in demyelinated axons.

A. Principle 1: The signs and symptoms of peripheral nervous system (PNS) lesions will be expressed in the anatomic distribution of roots, nerve trunks, plexuses, or peripheral nerves

B. Principle 2: The signs and symptoms of PNS lesions depend on the functional types of axons in the nerve: motor (general somatic and visceral efferent, branchial efferent), sensory (general somatic and visceral afferent, special visceral and somatic afferent, or mixed sensorimotor, visceral, and somatic)

C. Principle 3: The signs and symptoms of PNS lesions depend on whether the lesions cause deficit phenomena, irritative phenomena, or both

1. Deficit phenomena after lesions of the somatomotor axons (general somatic efferent, branchial efferent):

   1. Paresis or paralysis of individual muscles.

   2. Decreased or absent muscle stretch reflexes (MSRs).

   3. Denervation atrophy (early and severe).

2. Release phenomena after lesions of somatomotor neurons:

   1. Fasciculations

   2. Fibrillations

3. Autonomic deficit phenomena after lesions of visceromotor neurons (general visceral efferent):

   1. Paralysis and atony of smooth muscle, impairing peristalsis, propulsion, and emptying

   2. Vasomotor paralysis with vasodilation, orthostatic hypotension, and impotence

   3. Anhidrosis

   4. Trophic changes consisting of hair loss, atrophy of skin, and dystrophy of nails

4. Autonomic release phenomena after lesions of the visceral motor neurons (general visceral efferent)

   1. Hyperhidrosis

   2. Vasomotor instability with vasoconstriction and hyperhidrosis, rather than anhidrosis and vasodilation. Often Raynaud's phenomenon

5. Deficit phenomena after lesions of the somatosensory axons (general somatic afferent)

   1. Anesthesia or hypesthesia

   2. Analgesia or hypalgesia

   3. Thermanesthesia or thermhypesthesia

   4. Loss of dorsal column modalities

6. Irritative phenomena after lesions of the somatosensory or special sensory axons or, in some cases, their central pathways

   1. Hyperesthesias: paresthesias and dysesthesias

   2. Hyperalgesia

   3. Hyperthermesthesia

   4. Hyperpathia (anesthesia dolorosa)

   5. Neuralgia

   6. Complex regional pain syndrome Type II (Causalgia)

   7. Symptoms specific to irritation of sensory cranial nerves

      1. Cranial nerve (CrN) I: hyperosmia (usually central in origin)

      2. CrN II: flashes of light, scintillating scotomas (phosphenes or "seeing stars")

      3. CrNs V and IX: trigeminal and glossopharyngeal neuralgia

      4. CrN VII: hypergeusia (increased sense of taste, usually central lesion)

      5. CrN VIII: tinnitus, hyperacusis, diplacusis (auditory division), and vertigo (vestibular division)

D. Principle 4: The sensory nerves function according to the doctrine of specific nerve energies of Johannes Muller (see page 349)

E. Principle 5: To localize lesions of the PNS to a root, plexus, peripheral nerve or branch, detect and list the weak muscles and outline with ink the area of sensory deficit on the patient's (Pt's) skin or on a diagram. Then compare the results with charts of dermatomal, myotomal, and peripheral nerve distributions

(Chapter 2)

F. Principle 6: For the localizing analysis, "think along" the course of the PNS nerve fibers, in the direction of the nerve impulse.

1. To analyze a sensory disorder in the PNS, commence with the skin and "think along" the PNS from the receptor through the nerve branch or trunk, plexus, and dorsal root into the spinal cord. Continue thinking along the pathway to the primary receptive cortex.

2. To analyze a motor disorder, start with the motor cortex and think through the pyramidal tract, ventral motoneuron, ventral root, plexus, nerve trunk, neuromyal junction, and the muscle fiber itself.

G. Principle 7: The size of the nerve fiber and its myelination determine its conduction velocity and relates to its function. Measurement of sensory or motor nerve conduction velocity is often an important adjunct to the clinical examination

1. Peripheral nerves contain unmyelinated and myelinated nerve fibers ranging in diameter from 0.2 to 20 micra (myelin sheath included).

   1. The unmyelinated axons are around 1 micra in diameter (a red blood cell is 7 micra) and conduct at about 1 m/s. They range in size from approximately 0.2 to 0.3 micra to approximately 3 micra.

   2. The myelinated fibers range from 1 to 2 micra to 20 micra in diameter and conduct at rates up to 120 m/s, with a mean near 60 m/s.

      60 m/s × 60 s/min × 60 min/h × 1/mile 1609.3 m = 216,000/1609.3, or 134 miles/h.

2. In general, the larger the fiber diameter, the longer the internodal distance and the faster the conduction. Those fibers conducting faster than 3 m/s are myelinated.

3. The largest nerve fibers innervate joint receptors and muscle fibers.

4. Purely cutaneous peripheral nerves, such as the sural nerve (often chosen for biopsy) or the superficial radial nerve, contain no afferents from joints or muscles and generally have fibers smaller than 12 micra in diameter.

5. In mixed nerves the smallest fibers, generally unmyelinated, are postganglionic sympathetic efferents, visceral afferents, or serve as pain and temperature afferents. The small fibers of purely cutaneous nerves contain only the latter.

6. To classify nerve fibers by size, physiologists use a confusing mixture of three systems: English alphabets (A, B, and C), Greek alphabets (α, β, γ, and δ), and Roman numerals (I to IV) (DeMyer, l998).

A. For the patient

1. To enliven the proceedings, make each test a game or a matter of curiosity: "Let's see how light a touch you can feel." "Let's see whether you can feel the buzz of the tuning fork."

2. Demonstrate and describe the tests. Ask for yes or no responses, or "Is [stimulus] one different from [stimulus] two?" a procedure called forced-choice testing.

3. Have the Pt close the eyes to avoid visual cues.

B. For the examiner

1. Compare homologous areas of the right and left sides and compare normal areas to any suspected abnormal areas.

2. The skin areas differ greatly in sensitivity. The highly sensitive skin of the face and armpits contrasts with the horny skin of palms and soles. Hairy skin perceives tickling and touch better than glabrous skin. The forehead is the most sensitive area for temperature discrimination. Because cold skin loses sensitivity, ensure a warm skin before testing the Pt.

3. Plan follow-up examinations to recheck any doubtful results.

4. Determine whether sensory deficits match a central pathway, segmental (dermatomal), plexus, or peripheral nerve pattern (Figs. 2-10 and 2-11) or match a nonorganic distribution (Chapter 14).

5. Recognize that the Pt's mental state, legal wrangling, or secondary gain from the illness may drastically alter sensory test results.

BIBLIOGRAPHY · Introduction to Testing General Somatic Sensations

A. Functions of the afferents of cranial nerve V

1. Sensory domain of the trigeminal nerve: With a single scimitar blow, let us slice the face off from the head, along the line shown in Fig. 10-1, creating the mask of Trigeminus.

2. The three dimensions of the mask of Trigeminus

   1. The mask sliced away by the scimitar is no ordinary Halloween mask. It has three dimensions. It contains all the territory that receives motor and sensory innervations from CrN V: chewing muscles and their proprioceptors, proprioceptors from the eye muscles and general sensation from the facial skin, eyeball and orbit, mucous membranes of the nose, mouth, tongue, and sinuses, the dura mater, and a tad of the external ear.

   2. Of the tissues in the slice, only the cerebrum has no nerve supply. CrN V conveys no special sensory fibers. Notice that the cut spares the angle of the mandible, leaving it behind with the head. See the mandibular angle in Fig. 10-2.

3. How to best appreciate (and remember) the amazing variety of functions of afferents from CrN V

   1. First, observe a newborn baby: It roots for a nipple, sucks, chews, swallows, searches with its tongue, blinks, cries, and sneezes. Stimuli acting through CrN V initiate all of these reflexes. Then, too, you will understand that the turning of the head toward the stimulus in the rooting reflex depends on the descending root of CrN V that connects with the head-turning muscles of the neck. In fact, the very first cutaneous reflex that the human fetus exhibits is turning of the head in response to stimulation of the upper lip (Hooker, 1969). This behavior appears when the fetus reaches week 8 of gestation, just after the axons of the root of CrN V have grown down into the cervical region to make this reflex possible. To further understand the descending connections of CrN V, consider the rat, a nocturnal animal with weak eyes, as it feels its way along a totally dark passage. By touching its whiskers against the wall, it gains afferent information to orient the head, neck, and body.

   2. Next consider the autonomic responses mediated by CrN V: lacrimation from corneal irritation, rhinorrhea, salivation from mechanical stimulation of the oral mucosa (as opposed to taste), and pupillodilation and bradycardia or tachycardia from facial pain.

   3. Then, think of the role of CrN V in sinus pain and toothache, not to mention headache in general. Sensory V is a busy nerve, and that's why it has the largest sensory ganglion in the body.

B. Distribution of the sensory divisions of cranial nerve V

1. From Fig. 10-2 learn the three divisions of the tri geminal nerve, their facial skin areas, and central connections.

2. CrN V receives its name trigeminal because of its three large sensory divisions, the __________________, ________________, and _________________.

   ophthalmic; maxillary; mandibular

3. The three sensory branches funnel into a single root that attaches to the □ mesencephalon/□ pons/□ medulla.

   ☑ pons

4. The sensory ganglion of CrN V, the trigeminal (semilunar, gasserian) ganglion, contains the □ primary/□ secondary/□ tertiary neuron of the sensory pathway from the face.

   ☑ primary

5. The trigeminal ganglion corresponds to the __________________ ganglia of the spinal nerves.

   dorsal root

6. The primary ganglia for the special senses that are very near their end organs belong to CrNs ____________________. If you don't recall the answer readily, how should you systematize your approach?

   __________________________________________________.

   I and VIII

   Start at CrN I and sort through them one by one.

7. The trigeminal nuclei (nuclei, not ganglia) contain the □ primary/□ secondary/□ tertiary neuron of the trigeminal pathway.

   ☑ secondary

8. Where is the tertiary neuron? __________________________.

   Thalamus (diencephalon). Review Fig. 10-2 if you missed this.

9. The mesencephalic nucleus of CrN V violates the rule that the primary neuron of a sensory pathway is outside the central nervous system. This nucleus consists of primary neurons within the neuraxis, a unique fact but of no clinical use. The mesencephalic portion of CrN V probably mediates proprioception; the pontine and rostral medullary portion mediates touch; and the spinal nucleus mediates pain and temperature (Humphrey, 1969). Thus, in rostrocaudal order, the functions mediated by the three portions of the sensory nucleus of CrN V are ______________, ________________, and _____________________.

   proprioception; touch; pain and temperature

10. Taken together, trigeminal sensory fibers and nuclei extend from the rostral part of the cervical region of the spinal cord to the mesencephalon (Fig. 10-2).

C. Technique for testing touch in the area of cranial nerve V

1. Instruction to the Pt. Ask the Pt to say touch in response to each touch by a wisp of cotton. After the Pt closes the eyes, lightly brush each area of the three sensory divisions of CrN V with a wisp of cotton. Touch alternate areas and sides of the face randomly. Also, change the time between touches to keep the Pt from getting into a rhythm of answering without actually attending to the stimulus.

2. If you used a rigid test object to test for light touch, which principle of sensory testing did you violate?

   __________________________________________________________________

   ____________________________________________________.

   A rigid object causes pressure and touch, violating the rule to test one sensory modality at a time.

3. After the Pt has responded several times, how would you test the Pt's reliability and attentiveness?

   ___________________________________________________________________

   ____________________________________________________

   Occasionally withhold the stimulus and ask whether the Pt felt something. Recall that in testing smell, the examiner (Ex) also withheld the stimulus at times.

4. As a rule, if the history indicates a specific area of sensory loss, start sensory testing in a normal area, to give the Pt the experience of the normal sensation. Then start in the middle of the abnormal area and work outward.

D. The corneal reflex

1. Anatomy of the corneal reflex arc

   1. The corneal reflex consists of closure of both eyelids in response to touching one cornea. It is entirely distinct from the corneal light reflection described earlier.

   2. The afferent arc of the corneal reflex travels through the ______________ division of CrN V.

      ophthalmic

   3. The muscle that closes the eyelid is the ______________ innervated by CrN ______________.

      orbicularis oculi; VII

   4. The corneal reflex thus tests the integrity of two cranial nerves, (afferent) ______________ and (efferent) ______________.

      V; VII

2. Technique for the corneal reflex

   1. Use a free piece of cotton, rolled to a fine point. Do not use cotton attached to a stick (Q tip). Avoid sticks around the eyes. A demented, retarded, or delirious Pt may flinch against the tip of the stick and injure an eye.

   2. Tell the Pt, "I am going to just touch your eyeball very lightly." Instruct the Pt to look to one side and a little up. Gently hold the lids apart to avoid stimulating the eyelashes.

   3. Bring in a wisp of cotton from the lateral side to touch the lateral side of the cornea of the adducted eye. Bring the cotton directly in from the side to avoid entering the field of vision. That would cause a visually mediated flinch, not a corneal blink reflex. In Fig. 10-3, make an X on the exact spot to stimulate the cornea without entering the Pt's field of vision.

3. Clinical interpretation of the corneal reflex: Most normal individuals display a corneal reflex. Exceptions include some elderly or postcataract surgery Pts. If no response occurs, do not conclude that the arc from CrN V to VII is interrupted until you have checked for a contact lens. Acute deep hemispheric parietal lesions may abolish the corneal reflex on the contralateral side for hours or days as a deficit or "shock" phenomenon (Ross, 1972). The corneal reflex behaves like other superficial reflexes, the abdominal and cremasteric reflexes, and they all temporarily disappear after an acute upper motoneuron (UMN) lesion. As with the gag reflex, in the absence of symptoms, the Ex may elect to eliminate the corneal reflex from the screening NE.

E. The corneomandibular reflex (von Sölder phenomenon)

Stimulation of one cornea causes contraction of the ipsilateral lateral pterygoid muscle and a twitch of the jaw to the opposite side (Lawton et al., 1963). The jaw twitches contralaterally after stimulation of the cornea ipsilateral to a hemispheric lesion. A bilateral reflex may occur in coma, multiple sclerosis, or bilateral hemispheric lesions (Guberman, 1982). It may indicate a UMN lesion more sensitively in amyotrophic lateral sclerosis than other UMN signs. It may also appear in parkinsonism (Okuda, 1999).

F. The glabellar blink reflex

This reflex consists of bilateral contraction of the orbicularis oculi muscles in response to percussion of the glabella with the fingertip or a percussion hammer or to electrical stimulation of the supraorbital branch of the trigeminal nerve. Electrical stimulation during electromyographic (EMG) recording provides an objective, quantitative method of measuring the afferent and efferent arcs of a CrN V to VII reflex. Various lesions of the afferent or efferent arc reduce the blink response. It disappears unilaterally in acute hemiplegia and bilaterally in deep coma (Fine et al., 1992). Usually it fatigues by about 10 taps, but in dementias and parkinsonism (Parkinson's disease, progressive supranuclear palsy, multiple system atrophy) it persists (disinhibited).

G. Technique for testing temperature discrimination

1. Instruction to the Pt: State, "I want to see how well you can tell warm from cool. Please close your eyes, and I will place something on your cheek. Tell me whether it is warm or cool."

2. Tuning fork or finger test: Apply the metal shaft of a tuning fork to the side of the Pt's cheek for a few seconds and then remove it and apply the side of your little finger to the same spot. Ask the Pt whether each is cool or warm (Fig. 10-4).

   1. Use the fork first to establish immediate communication because it will feel colder than the finger. The Pt will attend to the temperature and not to texture or size.

   2. Randomly alternate the finger and tuning fork as you proceed over the three trigeminal sensory areas and then over the dorsum of both hands and both feet. Try this test on yourself.

   3. To sharpen ambiguous results, say "Which is cooler, number 1 [the tuning fork] or number 2 [the finger]?"

3. Warm and cold tube test: Fill one tube with warm water and one with cold. Avoid extremes of temperature. You want to test temperature discrimination, not how much heat or cold the Pt can withstand.

4. Because pain and temperature receptors somewhat overlap and share a common pathway in the spinal tract of CrN V and in the trigeminothalamic tract, disease generally affects both modalities. For screening purposes, testing one tests both. Test temperature discrimination first. If the Pt discriminates temperature normally, and the history does not suggest neurologic disease, you do not need to prick every Pt with a pin to test pain. No one relishes a pinprick, especially about the face. If you approach (attack) a young child with a pin first, you will have ended the entire sensory examination. Yet even an intelligent 3- to 4-year-old child will play the temperature game with the tuning fork. By testing temperature sensation, you avoid leaving a trail of pinpricks across the skin, oozing blood, a matter of some importance in this era of acquired immunodeficiency syndrome.

H. Testing pain perception

If the history suggests a sensory disorder, test pain sensation over the face after testing temperature discrimination. See page 391.

I. Differentiation of hysterical from organic loss of facial sensation

1. Draw a line across the head in Fig. 10-5 to show the exact dividing line between the part of the head innervated by CrN V and the cervical dermatomes. Compare it with Fig. 10-2 to see how exact your line is.

2. Now shade and label the parts of the face supplied by each of the three major sensory branches of CrN V. Check with Fig. 10-2.

3. Does CrN V innervate the skin over the angle of the mandible? If you included it in your drawing above, check Fig. 10-2 again. You missed a point of importance. Organic sensory loss of facial sensation from trigeminal nerve lesions spares the angle of the mandible, whereas hysterical loss of facial sensation includes it. Review Figs. 2-10 and 10-2 to recall where CrN V abuts on spinal nerve root C2. Comparison of hysterical with organic sensory losses on the face leads to a useful general law: In psychogenic illness, Pts lose sensation according to their mental image of the body parts; organic Pts lose sensation according to the wiring diagram of the nervous system. As another example, in hysteria the loss of sensation in the upper extremity usually cuts off sharply at the wrist, elbow, or shoulder, because that agrees with one's mental image of an arm, but it does not agree with the actual anatomic distribution of peripheral nerves, nerve roots, or their central pathways. See Fig. 14-3.

4. Therefore, in hysterical sensory loss of facial sensation, the angle of the mandible is □ spared/□ affected, whereas in organic loss of affected facial sensation due to a CrN V lesion, the angle of the mandible is □ spared/□ affected.

   ☑ affected; ☑ spared

J. Analyze this patient

1. This 76-year-old woman complains of severe facial pain, starting 4 months ago and gradually worsening. She describes very brief, shock-like jolts of unbearable pain that runs from the side of her cheek down to the tip of her jaw, on the right side only. She has become irascible and impossible to live with according to her husband. Because eating triggers the pain, she has lost 18 lb. The NE discloses normal motor and sensory functions of the CrNs, except that she will not allow the Ex to test sensation over the right lower jaw because touching the right lower lip triggers excruciating shocks of pain (allodynia).

2. In analyzing a sensory complaint, the Ex must determine its nature and whether its distribution conforms to an anatomic pattern or to the person's mental image of the body and, hence, is psychogenic. The term that best matches the Pt's sensory disorder is (review the descriptors in Section I B 3a to e before answering): □ hyperesthesia/□ hyperalgesia/□ causalgia/□ neuralgia.

   ☑ neuralgia

   Although some other terms more or less apply, neuralgia is the most specific.

3. Does the location of the sensory disorder match:

   □a. The distribution of a central pathway?

   □b. The distribution of a dermatome?

   □c. The distribution of a peripheral nerve or nerve branch?

   □d. A nonanatomic distribution that, in combination with the Pt's obvious personality change, indicates a psychogenic disorder?

   ☑ C

4. Which peripheral nerve area does the Pt's pain correspond to?

   __________________________________________________

   Mandibular division of CrN V on the right.

5. This Pt had no other abnormalities on the general physical examination or the radiographic examination of the skull with a basilar view to show the foramina of exit of CrN V. She had trigeminal neuralgia (tic douloureux), a very typical neuralgia, characterized by repetitive excruciating shocks of pains in one or more of the branches of the trigeminal nerve (Fromm and Sessle, 1991; Rose, 1999). Typically the pain erupts spontaneously and also after touching a "trigger point" on the cheek or the inside of the mouth. It occurs idiopathically with multiple sclerosis (Ferroli and Farina, 2001) and apparently as a result of vascular compression of the root of CrN V by the superior cerebellar artery (Fromm and Sessle, l991). Medication or surgical treatment may alleviate it (Theodosopoulos et al., 2002). Victor and Ropper (2001) tabulated many other causes of facial pain.

K. Summary of the tests for the sensory functions of the cranial nerves

Get a partner and rehearse Section V, steps C and D, of the Standard NE.

BIBLIOGRAPHY · Examination of Sensory Functions of Cranial Nerve V

A. Testing light touch sensation

1. Test touch over the rest of the body exactly as described for the face. For screening purposes, test only the dorsum of the hands and feet, in addition to the face. The history determines how far to extend the sensory examination. Review Fig. 2-10 to understand why the Ex would move the touch stimulus up and down the trunk to discover a dermatomal loss or spinal cord sensory level but around the limbs.

2. Quantitative testing of touch and pressure can be done with graded monofilaments (Semmes-Weinstein Esthesiometer, Smith & Nephew Roylan, Inc., Germantown, WI) or hairs (von Frey hairs) of different strengths (Dyck and Thomas, 1993; Perkins et al., 2001; Spreen and Strauss, 1991).

3. Review the anatomy of touch in Fig. 2-28.

   1. Recall that touch impulses ascend to the somesthetic cortex by two spinal pathways: one in the ______________________________ column of the cord and the other in the ______________________________ of the cord.

      dorsal columns (fasciculi gracilis and cuneatus); ventrolateral column (spinothalamic tract or spinal lemniscus)

   2. The dorsal column pathway decussates at the ________________ junction, whereas the spinothalamic tract decussates at the _____________________.

      cervicomedullary; level of entry of the dorsal root

4. The pathway for touch in the ventrolateral columns most closely resembles the pathway for □ pain and temperature/□ vibration and position sense.

   ☑ pain and temperature

   1. These two tracts, the ventral and lateral spinothalamic tracts, run together as the ____________________ lemniscus.

      spinal

   2. All lemnisci unite in the brainstem to travel to the thalamus as one with the medial lemniscus (DeMyer, 1998). Complete Table 10-1.

   3. The one sensation that lacks a lemniscus and a specific thalamic relay nucleus is mediated by CrN ____________.

      I

B. Testing temperature sensation from the body and extremities

Proceed exactly as described for the face. Test temperature discrimination first. Use the tuning fork and finger or warm and cold tube tests (Fig. 10-4).

C. Physiology and anatomy of pain

1. Relation of pain and temperature sensation to types of peripheral axons

   1. Prick yourself with a pin. After a pinprick you will experience two types of pain: fast and slow. Small myelinated fibers of the A group mediate the first pain, a sharp, bright, localized "fast" pain. This pain is mediated mainly through the classic lateral spinothalamic pain and temperature pathway. Small myelinated axons (IA γ fibers) also mediate cold sensation (Wall and Melzack, 1999; Willis and Coggeshall, 1991; Yarnitsky and Ochoa, 1991).

   2. Unmyelinated C fibers mediate the second type of pain, an afterglow of dull, diffuse, stinging, and burning pain. Diffuse polysynaptic pathways rather than solely the classic spinothalamic pathway likely mediate this pain. This pain connects with the reticular formation and ultimately the limbic system (Casey, 1991; Weiner, 2002). The small, unmyelinated axons (C fibers) also convey warm sensations. In contrast, the largest fibers of the peripheral nerves mediate the so-called dorsal column modalities (Section V).

2. Clinical classification of pain

   1. Pain can be classified as nociceptive and neurogenic (neuropathic).

   2. Pain of nociceptive origin is divided into somatic and visceral and arises from some local lesion, such as an invasive carcinoma or trauma that stimulates local pain endings (Victor and Ropper, 2001).

   3. Pain of neurogenic origin arises from some form of heightened sensitivity or overactivity from a lesion that affects the peripheral or central nervous system, apart from stimulation of local pain endings. A wide variety of agents, such as a herniated disc, neuropathies, or central lesions, cause neuropathic pain (Bowsher et al., 1998; Casey, 1991). Neurogenic pain may be mediated through the sympathetic nervous system, nonsympathetically mediated or centrally.

   4. The debilitating types of neurogenic pain, i.e., neuralgias, such as trigeminal neuralgia and causalgia, were described in Section I. In these and similar neurogenic pain syndromes such as erythromelalgia, the sensory examination may be difficult or inconclusive (Layzer, 2001). For such Pts, a simple rating scale provides additional insight into the severity and nature of the pain (Galer and Jensen, 1997).

   5. Referred pain: The site at which the Pt feels the pain may not correspond to the site of the lesion (Casey, 1991; Hockaday and Whitty, 1967). Thus, cardiac pain is referred down the left arm. In carpal tunnel syndrome, with median nerve compression at the wrist, the Pt may feel pain proximally in the arm and distally in the distribution of the median nerve.

3. Anatomy of the pain and temperature pathways from the body and extremities

   1. Learn Fig. 10-6 and review Fig. 2-28.

   2. Draw and verbally trace a nerve impulse for pain and temperature sensation from the skin on the lateral side of the foot to the cerebral cortex. Start by enumerating the dermatome.

      _______________________________________________________________

      _______________________________________________________________

      ____________________________________.

      The S1 dermatome receptor relays to the peripheral branch of dorsal root axon to the central branch to the secondary neuron in the dorsal horn. The secondary axon crosses and ascends in the spinal lemniscus to the tertiary neuron in the nucleus ventralis posterior of the thalamus. The nucleus ventralis posterior relays to somesthetic cortex in the postcentral gyrus of parietal lobe.

4. The pain and temperature axons from the foot, trunk, and hand synapse on secondary neurons at, or within one or two segments of, their level of entry into the spinal cord, but the axons from the face descend through the brainstem to reach their secondary neuron. Review Figs. 10-2 and 10-6.

   1. The descent of the axons from the face permits the secondary nucleus that relays pain and temperature sensation to be continuous from the medulla to the last sacral segment. The somatotopic pattern in this continuous long columnar nucleus is face, neck, arm, trunk, lower extremity, and sacral region. This nucleus, called the substantia gelatinosa of Rolando, that relays pain and temperature sensations occupies the tip of the dorsal horn.

   2. A surgeon who wanted to abolish only pain and temperature sensation without abolishing touch would make a cut in the □ ventrolateral/□ dorsal column to interrupt the ________________________________ tract.

      ☑ ventrolateral; lateral spinothalamic

   3. Neurosurgeons sometimes make such a cut, called a cordotomy, in the ventrolateral column of the spinal cord to relieve Pts of intractable pain. Would this cut eliminate touch sensation? □ Yes/□ No. Explain.

      _______________________________________________________________

      ____________________________________.

      ☑ No

      Touch impulses reach the thalamus by two pathways, ventral and dorsal columns. Section of only one pathway does not eliminate touch sensation

   4. In addition to the foregoing classic spinothalamic pathway (Keele, 1957), a multisynaptic pain pathway ascends from the face, body, and extremities to reach the thalamus and conscious appreciation (Willis and Coggeshall, 1991)

   5. Positron emission tomography discloses several cerebral areas that mediate the various affective aspects of pain: the anterior and posterior cingulate and inferior frontal cortices, and periventricular gray matter (Tolle et al., 1999).

D. Testing for pain sensation

1. Instructions for the Pt: Show the Pt a straight pin with its sharp and dull ends. Ask the Pt to respond sharp or dull when you apply the pin. Then have the Pt shut the eyes to prevent visual cues.

2. Use of the pin: Alternate touching the Pt with the two ends of the pin randomly to monitor the Pt's attentiveness and reliability. Hold the shaft of the pin lightly between the thumb and the index finger, as if to allow it to slip a little, thus applying the stimulus with the same pressure. Make about three successive pricks for each stimulus because not all individual pricks will hit a pain-sensitive spot. Start with a normal area to establish communication, so that the Pt knows what to expect. Test the face and dorsum of the hands and feet. Avoid the horny skin of the palms and soles. Recall the different sensitivities of various skin areas. Always discard the pin after use. Never use it again. I don't know how many angels can dance on the point of a pin, but several diseases can: syphilis, infectious hepatitis, and acquired immunodeficiency syndrome, for starters.

3. Delayed pain and deep pain perception: If the history and examination suggest a sensory disturbance, proceed as follows to test the extremities, but do not use these tests on the face.

   1. Testing for delayed pain: Pinch the dorsum of the Pt's foot briskly between the fingernails of your thumb and index finger. The normal person feels pain almost immediately. A delayed response indicates an abnormality in sensory conduction.

   2. Testing for deep pain: Test by squeezing very hard on an Achilles tendon (called Abadie's sign when the Pt feels no pain) or a muscle or by compressing very hard over a bony surface. The Pt may feel a delayed pain some seconds after ending the compression. Classic causes of delayed pain or absent deep pain are tabes dorsalis and other diseases that interrupt dorsal roots and dorsal columns.

4. Location of tender points: When examining Pts with any acute or chronic pain syndrome, palpate along nerves, muscles, and bony prominences for pain and trigger points. Compress the sites with the ball of the thumb by using firm pressure but short of causing pain in normal persons. Counting the number of tender points assists in the diagnosis of the fibromyalgia syndromes (Goldenberg, 1999).

5. Pain in neonates and fetuses: By custom physicians have done procedures such as circumcision on newborn infants without the use of anesthetics, as if the infant felt no pain. Certainly newborns and fetuses show the behaviors associated with pain: crying, agitation, and autonomic responses (Anand et al., 2000). Because infants do react to pain or cold, the Ex can ascertain the sensory level in an infant with a spinal cord transection. Start with the infant quiet. Apply a pin or ice cube to the feet and work up slowly toward the neck. The infant will cry as soon as the stimulus reaches an intact dermatome.

6. Ancillary methods of investigating pain

   1. Although available, quantitative or automated methods for testing touch, pain, and temperature are not in routine use (Dyck and Thomas, 1993; Hansson et al., 1991; Meilgaard et al., 1999; Smith et al., 1991; Yarnitsky and Ochoa, 1991). For compression tests to elicit reactions in comatose Pts, see Chapter 12.

   2. Skin biopsies provide an additional method of investigating the integrity of small, unmyelinated nerve fibers (Herrmann et al., 1999; McArthur et al., 1998; Periquet et al., 1999). Sural nerve biopsy likewise aids in categorizing neuropathies (Dyck and Thomas, 1993).

7. Some have remarked that the function of the internist or the surgical consultant is to do the rectal examination (and discover a prostatic carcinoma that has caused the Pt's baffling weight loss and back pain). Physicians habitually neglect the same things, such as the rectal examination, and pain and temperature testing. As a neurologist, my function sometimes is to do the temperature and pain testing that no one else has done, and frequently it pays off.

BIBLIOGRAPHY · Examination of Somatosensory Functions of the Body and Extremities

A. Classification of neuropathies

1. Sensory or sensorimotor neuropathies fall into two main types: diffuse symmetrical polyneuropathies (Cros, 2001) and focal neuropathies or mononeuritides (Stewart, 1999). A second major classification consists of pure sensory, pure motor, and combined sensorimotor neuropathies. The disease may cause an autonomic neuropathy, somatic neuropathy, or combined autonomic-somatic neuropathy.

2. Diffuse symmetrical polyneuropathies generally cause sensory disturbances in the distal part of the upper and lower extremities. The Pt has a "stocking and glove" distribution of numbness, tingling, paresthesias, dysesthesias, and pain (Fig. 10-7).

   1. The sensory examination is straightforward. The Ex compares the results of testing pain, temperature, and light touch distally in the extremities with the results of testing proximally. Common causes of polyneuropathies are toxins, drugs, alcoholism, autoimmune disorders, and heredity (Dyck et al., 1996; Victor and Ropper, 2001).

   2. Some symmetrical polyneuropathies cause palpable enlargement of nerve trunks. Inspect and palpate the nerves that cross the posterior triangle of the neck, the ulnar, and the common peroneal nerves. Leprosy also may enlarge peripheral nerves.

   3. Mononeuritis multiplex, such as in diabetes mellitus, may imitate diffuse symmetric neuropathies.

3. Focal neuropathies or mononeuropathies generally result from entrapment or mechanical compression (Dawson et al., 1998), but metabolic disorders may predispose to them and may coexist (Stewart, 1999). The entrapment neuropathies often cause extreme pain. The investigation involves a search for trigger factors, often a posture or position, that will elicit or exacerbate the symptoms and for any postures or positions that relieve the discomfort. Compression or percussion over the site of entrapment often will trigger or reproduce the sensory symptoms distal to the entrapment site, a phenomenon called Tinel's sign (dysesthesias produce by tapping over the nerve). The phenomenon is equivalent to the pain that radiates down into your little finger when you bang your ulnar nerve at the elbow, called "hitting your crazy bone." Local anesthetic block at the entrapment site abolishes the sensory disturbance and Tinel's sign in the entrapment neuropathies. The text will describe special features of the NE for some of the more common entrapment neuropathies. Granted the importance of corroborative findings on the examination, the diagnosis depends very strongly on the history. Some Pts with entrapment neuropathies by history will not show changes by the clinical or electrophysiologic examination. Most of the entrapment neuropathies respond well to surgical decompression, if conservative therapy fails.

4. Ancillary tests include quantitative sensory testing, EMG and nerve conduction tests, metabolic screening tests, biopsy of sensory nerves or nerve endings in skin, cerebrospinal fluid examination, genetic testing, and sometimes magnetic resonance imaging (MRI) (Dyck et al., 1996; Mendell et al., 2001; Ouvrier et al., 1999; Rosenberg et al., 2001; Andreisek et al., 2006). The Ex can follow the course of neuropathies over long periods by combining clinical and laboratory results into a total neuropathy score (Cornblath et al., 1999).

B. Special features in the examination for entrapment neuropathies

1. Occipital neuralgia causes pain radiating from the base of the skull up the occiput. The Pt may notice positions of the head that elicit the pain. Palpate the occipital region for masses, such as lymph nodes. Tap (Tinel's sign) and use the ball of your thumb to compress over the site where the greater occipital nerve exits from the fascial ring, about 2 cm caudolateral to the inion. Local anesthetic block may be tried in doubtful cases.

2. Median nerve entrapment at the wrist (carpal tunnel syndrome)

   1. Carpal tunnel syndrome is the most common entrapment neuropathy of the upper extremity.

   2. Review the median nerve motor distribution by the LLOAF/2 mnemonic page 59, and the sensory distribution in Fig. 10-8.

   3. The Pt experiences pain, tingling, and numbness extending from the palmar aspect of the thumb to the radial half of the fourth digit (Rosenbaum and Ohoa, 2002). The symptoms may worsen with the use of the hands, as when driving a car, or may awaken the Pt at night, causing the Pt to pace the floor because of the intense discomfort. The Pt often flaps or flicks the hands to get relief. Women older than 55 years show the peak prevalence. Elevated pressure in the carpal tunnel and resultant ischemia of the median nerve cause the symptoms and signs (Katz and Simmons, 2002).

   4. Inspect the thenar eminence for atrophy. In children with longstanding median nerve lesions, the index finger on the affected side may be smaller (Spinner et al., 1989). Test for loss of strength specifically in the abductor pollicis brevis. The abductor pollicis brevis apparently receives its motor axons exclusively from T1 (Levin, 1999). Thus, testing its strength is one of the few opportunities to test a single motor nerve root. To test it specifically, the Pt must abduct the thumb at an absolute right angle to the plane of the palm. The Ex then matches the Pt's strength with the Ex's own abductor strength (Fig. 10-9).

   5. Test all median nerve sensory modalities in the hand, especially the pad of the index finger. Include two-point discrimination and check for anhidrosis by use of the ophthalmoscope. Provocative maneuvers: Try to elicit Tinel's sign by percussing over the median nerve at the wrist (sensitivity ~60%, specificity ~67%) and Phalen's sign by having the Pt flex the hands to a right angle and holding them there for 1 min (sensitivity ~75%, specificity ~47%) by pressing the backs of the hands together (Phalen, 1972).

   6. EMG and sensory and motor conduction studies (sensitivity ~85%, specificity ~98%) often prove helpful (Chang et al., 2002), but Pts may experience severe symptoms without diagnostic electrophysiologic changes. False negatives and false positives occur (Padua et al., 1999). MRI, although useful in some Pts, does not replace standard examination techniques (Fleckenstein and Wolfe, 2002; Jablecki et al., 2002; Jarvik et al., 2002).

3. Anterior interosseus neuropathy (Kiloh-Nevin syndrome): Anterior interosseus syndrome is caused by entrapment or compression of the anterior interosseus nerve in the proximal part of the forearm (Kiloh & Nevin, 1952). The anterior interosseus nerve, the largest branch of the median nerve, innervates the flexor pollicis longus (FPL), flexor digitorum profundus (FDP) of the index and middle fingers, and the pronator quadratus muscles. Typically patients with anterior interosseus nerve syndrome experience pain in the proximal part of the volar aspect of the forearm and are not able to form an "O" [OK sign] with the thumb and index finger due to involvement of the FPL and radial half of the FDP. A brachial neuritis (Parsonage-Turner syndrome) may mimic the clinical manifestations of an anterior interosseus neuropathy (Parsonage MG et al., 1972).

4. Ulnar nerve entrapment (the ulnar condyle and cubital tunnel syndromes): The compression site is at the medial epicondyle of the humerus or the cubital tunnel just distal to the medial epicondyle. The cubital tunnel syndrome is the second most common entrapment neuropathy of the upper extremity. Flexion of the arm may trigger sensation into the little finger (Fig. 10-8). The same diagnostic principles apply as for the median nerve, including matching your ad ductor pollicis and your ab ductor digiti quinti manus strength directly against the Pt's.

5. Radial neuropathy: Wrist drop, the most common presentation of the radial nerve palsy, results from weakness of the extensor carpi radialis longus and extensor carpi ulnaris. It most commonly results from compression of the radial nerve in the spiral groove (Saturday night palsy). Other causes include diabetes, fracture of the humerus, tourniquets, and misplaced injection injuries. Wrist extension weakness may also result from corticospinal lesions.

6. Lateral femoral cutaneous nerve (meralgia paresthetica): The Pt experiences sensory disturbances in the anterolateral aspect of the thigh (Fig. 10-10; Williams and Trzil, 1991).

   1. The compression site is where the nerve passes distally under the inguinal ligament. A particular position of the thigh may elicit symptoms. Obesity, pregnancy, diabetes, and a tight belt around the waist, predispose to meralgia paresthetica. Meralgia paresthetica may also develop following surgical procedures (Seror and Seror, 2006)

   2. The nerve is purely sensory. Check for Tinel's sign by percussing and compressing along the lateral third of the inguinal ligament and for symptoms from various positions of the thigh, as in Patrick's sign.

7. Common peroneal nerve palsy: The Pt experiences numbness and tingling down the anterolateral aspect of the foot into the dorsum of the foot and has a foot drop (Stewart, 1999). See Fig. 10-10.

   1. The compression site is where the nerve crosses the head of the fibula (Fig. 7-35). Predisposing factors are overt trauma, habitual crossed-kneed sitting posture, lithotomy position, diabetes, knee cast, trauma, and recent weight loss.

   2. Test for loss of skin sensation in a triangular area over the dorsum of the foot (Fig. 10-10) and for weakness of foot and toe dorsiflexion.

8. Posterior tibial nerve entrapment (tarsal tunnel syndrome): The Pt feels pain in the lateral aspect of the foot, toes, and sole, particularly when standing or walking, and pain may awaken the Pt at night. The compression site is where the nerve passes under the flexor retinaculum, which runs diagonally anteriorly and upward from the heel (Stewart, 1999).

9. Interdigital nerve entrapment (Morton's metatarsalgia): The Pt feels pain, numbness, and tingling in the ball of the foot and into toes 3 and 4 or 2 and 3 when walking or wearing shoes that are the least bit tight. The compression site is where the interdigital nerves run along the metatarsal heads, where a neuroma forms. Compression over the neuroma reproduces the sensory symptoms in the toes.

BIBLIOGRAPHY · Examination Techniques in Peripheral Neuropathies

A. The backache syndromes

1. Everyone at one time or another has low back pain, often initiated by a "pop," when lifting or exercising, often recurrent over years or decades. The pain mechanism often remains a mystery, whether muscular, ligamentous, or articular. Despite a thorough workup, the diagnosis often ends up nonspecifically as "lumbosacral strain," if the pain localizes to the back, or "sciatica" if the pain radiates down the leg (Frymoyer, 1988; Rothman and Simeone, 1992; Seimon, 1990).

2. This text focuses on the more specifically neurologic signs of sciatica caused by nerve root compression from a herniated intervertebral disc in the low back.

B. Patient analysis

Off and on for several years, this 34-year-old man has suffered from low back and leg pain. Twelve days ago, when straightening up, he felt a pop in his back. Since then, sharp pain has radiated intermittently into his right foot along its lateral side and into the little toe. Movement or coughing elicits a shock of pain into the leg. He sits rigidly in his chair, with his trunk slightly tilted. When arising, he pushes himself erect with his arms. He stands with most of his weight on his unaffected left leg, holding the knee of the right leg slightly bent. You can confirm the uneven weight distribution by placing your hand around his ankle with your thumb on his Achilles tendon. By squeezing firmly with your thumb, the tendon on the non-weight-bearing leg yields. He stands with his lumbar spine virtually straight, rather than with the normal concavity. Thus simple inspection of how the Pt sits, stands, and walks provides strong objective evidence of the acute back disorder. Palpation of the back discloses paravertebral muscle spasm and mild tenderness. Palpation along the course of the sciatic nerve discloses no tenderness. The triceps surae reflex on the right side is reduced. Plantar flexion is weak on the right, as shown when he tries to rise onto the ball of his right foot, but the action is still too strong for the Ex to overcome by manual opposition. His right calf measures 1.8 cm less than the left. Sensory examination produces uncertain differences between the right and left legs.

C. Localizing the origin of radiating pain

An accurate description of where the pain radiates often identifies the affected nerve or nerve root in a compression syndrome better than the formal examination. Because the Pt has motor and sensory findings, the lesion cannot be limited to one of the small superficial cutaneous nerves of the lateral aspect of the foot. Review Figs. 2-10 and 2-11.

1. If the Pt complains that the pain radiates along the lateral side of the foot and into the little toe, you would suspect the involvement of the root to the ____________ dermatome.

   S1. Review Figs. 2-10 and 7-29.

2. If the Pt complains of pain radiating toward the medial side of the foot or into the great toe, you would suspect the ___________ nerve root.

   L5. Review Fig. 2-10, if you erred.

3. What evidence does the history and physical provide that the weakness results from a UMN or lower motoneuron lesion?

   __________________________________________________________________

   __________________________________________________________________

   The evidence for a lower motoneuron lesion is weakness confined to one muscle group, atrophy, and a decreased MSR at the ankle (decreased triceps surae reflex). This evidence suggests a lesion confined to the S1 motor root.

4. What would an EMG of the muscles innervated by the S1 nerve root show?

   __________________________________________________________________

   Fibrillations, giant motor unit potentials, and possibly fasciculations (Fig. 7-21). In this Pt, the 12-day interval is short for denervation changes to appear, but he has had previous bouts.

5. Notice in Fig. 10-11A that the herniation of a disc at one level (L4 to L5) affects the root of the next level (L5).

D. Leg-raising tests for nerve root compression

Although the foregoing clinical data point to the diagnosis of a nerve root compression syndrome, the leg-raising tests help to confirm it. The tests consist of the straight-knee leg-raising test (Lasègue's sign) and the bent-knee leg-raising test (Kernig's sign).

1. Technique of the straight-knee leg-raising test for pain (Laseague's sign)

   1. The Pt lies supine with the legs relaxed. Grasp the calf or heel of the affected limb and elevate it gently as far as possible, flexing the hip while keeping the knee straight (Fig. 10-12).

   2. Normally the thigh permits elevation to about 90 degrees. The Pt with nerve root compression winces with pain and flexes the knee at some point less than 90 degrees. Then, if the Ex holds the leg just short of the position of pain, gentle dorsiflexion of the foot produces another twinge of pain, as before, radiating into the foot. The same maneuvers on the unaffected limb may show a nearly normal range of movement without pain or may cause Fajersztajn's crossed, straight leg-raising sign that is nearly pathognomonic of a herniated disc (Frymoyer, 1988; Hudgins, 1977).

2. Explanation of the pain and limitation of leg elevation

   1. Elevation of the lower extremity with the knee straight stretches the sciatic nerve. We might appropriately call it the sciatic nerve stretching test. As the nerve stretches, it pulls against any impediment to free movement. The resultant pain causes hamstring muscle spasm that arrests farther extension, stretch, and pain. The most common impediment by far is a ruptured intervertebral disc, which impinges on the nerve root (Figs. 10-11A and 10-11B).

   2. Explain what caused the Pt to splint his knee as you reached the end point of excursion in the straight-knee leg-raising test.

      ____________________________________________________________

      ___________________________________________________

      Continued stretch caused nerve root impingement and pain.

   3. When you held the limb just short of maximum permissible elevation, why did dorsiflexion of the foot elicit a twinge of pain?

      ___________________________________________________________

      ________________________________________

      Foot dorsiflexion stretched the sciatic nerve more.

   4. We can understand all the postural and movement limitations in this nerve root compression syndrome as protection against pain: the splinting of the back by paravertebral muscle spasm to prevent movement and the limitation of straight leg raising. To test this theory, start with the Pt supine and sit him up, leaving his legs flat against the bed. This action stretches the sciatic nerve. What do you predict that the Pt will do with the affected lower extremity to avoid pain? ______________________.

      Flex it

3. The bent-knee leg-raising test (Kernig's sign): With the Pt supine as for the straight-knee leg-raising test, keep the knee flexed and flex the limb at the hip. When the thigh reaches the vertical position, gently, gently straighten the knee. The Pt will wince with pain, and the reflex hamstring spasm will prevent further straightening of the knee.

4. Xavier et al. (1989) suggested that antidromic activation of peripheral pain receptors, rather than simple mechanical impingement, causes the pain of sciatica.

E. Variations in the sciatica syndrome

1. The typical findings differ in distribution depending on whether the lesion compresses the L5 or S1 root (or both; Table 10-2).

2. Within the syndrome of compression of one root, the clinical expression may vary. This Pt may have findings limited to weakness, with little or no pain. In another Pt, pain predominates, with little or no weakness. The next Pt may have well-outlined dermatomal loss on examination, but the next, with equal pain, has no convincing changes on the sensory examination. The findings depend on which motor or sensory axons happen to get compressed. Axons need not be affected equally.

3. In yet another Pt, the pain maximizes in the buttock or hip, imitating hip disease. Such localizations are explained by referral of the pain to sclerotomes and myotomes that come from the L5 and S1 somites. These somites contribute to the pelvic bones, femur, and the associated muscles, and all derivatives retain their innervation from the L5 and S1 roots (Fig. 10-13).

4. Cofactors and comorbidities may confound the diagnosis: anatomic variations in the relation of the nerve roots to the foramina and discs, arthritis, spondylosis, spondylolisthesis, tethered spinal cord or other congenital malformations, diabetes mellitus or other neuropathies, age, occupation, activity level, life style, and secondary gain.

F. Summary of the clinical findings in nerve root compression from herniation of an intervertebral disc

1. Symptoms and signs of disc disease: motor, sensory, and antalgic posture and gait.

   1. Motor: weakness and atrophy in a radicular (myotomal) distribution and reduced triceps surae MSR.

   2. Sensory: pain, paresthesias, dysesthesias, numbness in dermatomal distribution. Pain may be local in the back, radicular, referred, or muscle spasm pain.

      1. Pain may be referred to or from viscera. Local radicular and referred pain may coexist.

      2. Pain may be felt locally in the back, at the level of disc herniation.

      3. Pain in a radicular (dermatomal sclerotomal/myotomal) distribution (Fig. 10-13).

      4. Pain over the course of the sciatic nerve (points of Valleix): sciatic notch, retrotrochanteric gutter, posterior surface of thigh, and the head of the fibula.

   3. Antalgic posture and gait: pain protective splinting posture, spinal tilt, flattening of the lumbar curve, and a limping gait.

2. Special features and tests in Pts with suspected disc herniation or radicular compression

   1. Examine the Pt when sitting standing, reclining, and walking.

   2. Do the Achilles tendon compression test as an aid in demonstrating less weight-bearing in the affected leg when the Pt stands.

   3. Look for sagging gluteal fold in S1 lesions.

   4. Compare the circumferences of both legs.

   5. Percuss the spine.

   6. Palpate for tender points or masses from the costovertebral angle down over lower back, buttock, and along the course of the sciatic nerve.

   7. Do the straight-knee leg-raising test, ipsilaterally and contralaterally (Fajersztajn's sign)

   8. Test the strength of dorsiflexion and plantar flexion of the foot and the strength of the extensor hallucis longus (L5).

   9. Have the Pt bend forward (if possible) as if to touch the floor. The fingertip-to-floor distance should be shorter than 25 cm (Vroomen et al., 2002).

G. Differential diagnosis of low back pain and the sciatica syndrome

1. Disc herniation, lateral or medial: L5 and S1 most frequently.

2. Acute low back strain.

3. Sacroiliac strain: tenderness over the sacroiliac joint pain into the buttocks.

4. Degenerative low back syndrome.

5. Arthritis

6. Myofascial pain, fibromyalgia.

7. Vertebral fractures

8. Spinal Stenosis

9. Spondylolisthesis

10. Facet syndrome

11. Piriformis syndrome

12. Lumbosacral plexus neuritis

13. Coccydynia

14. Osteomyelitis

15. Sacroiliitis

16. Arachnoiditis

17. Carcinoma, pelvic or metastatic

18. Tethered cord or other malformation

19. And, as always, psychosocial factors, pending litigation, secondary gain, etc.

H. Ancillary studies in low back pain and sciatica

1. In view of the numerous causes of low back pain, the sciatic syndrome, and the multiplicity of pain patterns (Jinkins, 1989; Rothman and Simeone, 1992; Seimon, 1990), additional studies may be required to establish the correct diagnosis. These include EMG, somatosensory evoked potentials, plain radiographs, myelography, computed tomography, MRI, and sometimes nuclide scan. None of these is routine and must be judiciously selected, depending on the overall results of a complete history and physical examination (Deen, 1996; Deyo and Weinstein, 2001).

2. Treatment has shifted from bed rest to early mobilization. Manipulative methods of treatment appear to offer no benefit over nonmanipulative methods (Hsieh, 2002).

I. Radicular pain in the neck and arms

1. The causes of local or radiating pain in the neck and shoulders overlap with the causes of low back pain and require a similar workup (McNab and McCulloch, 1994; Nachemson and Jonsson, 2000; Victor and Ropper; 2001).

2. An additional sign to seek with cervical lesions, whether from midline disc herniation, intrinsic neoplasm, or multiple sclerosis, is Lhermitte's head flexion sign. Sharp flexion of the head by the Pt causes an electric shocklike sensation of pain or "pins and needles" in the body and extremities. Stretch of the neural tissue at the site of the lesion of the cord apparently causes the sensation. See Fig. 12-23.

BIBLIOGRAPHY · Examination Techniques in Low Back Pain and Pain Radiating Down the Leg: The Sciatica Syndrome

A. Definition of proprioception

Sherrington's term proprioception comes from proprius (one's own as in property, and capio = to take or capture; literally, to take or capture one's own). The term refers to the capturing, by receptors within the depth of one's own body, of the movements of one's own body parts. The body parts that move consist of one's own muscles and joints, i.e., the skeletomuscular apparatus, and one's vestibular fluid and otoliths. Formally defined, proprioception is the sense of movement, of position, and of skeletomuscular tension provided by deep mechanical receptors in muscles, joints, connective tissue, and the vestibular system. Along with vision and touch, it provides a sense of equilibrium or verticality.

B. Neuroanatomy of skeletomuscular proprioception

1. Review the pathway through the dorsal columns in Fig. 10-14.

   Compare your answers with Fig. 10-6.

2. A variety of receptors in the connective tissue of joints and tendons mediates proprioception. The muscle spindles would, a priori, seem ideal to mediate a sense of movement, yet no relevant pathway to the somesthetic cortex is known. The primary skeletomuscular proprioceptive neurons, like all primary somatic sensory neurons, occupy _____________________________.

   dorsal root ganglia

3. CrN VIII has two ganglia that are homologous to dorsal root ganglia, the ___________________ ganglion and the ___________________ ganglion.

   cochlear (spiral); vestibular

4. The axons ascending in the dorsal columns arise from □ primary/□ secondary/□ tertiary neurons.

   ☑ primary

5. Figure 10-13 shows that the processes of dorsal root ganglion cells extend from the toe to the dorsal column nuclei, the remarkable distance of 170 cm in man, the astonishing distance of 450 cm in a giraffe, and the incredible distance of 2000 cm in the blue whale.

6. The axons from the foot ascend □ lateral to/□ intermingled with/□ medial to those from the arm.

   ☑ medial to

7. Nomenclature note: Anatomists call the leg dorsal column the fasciculus gracilis or column of Goll and the arm dorsal column the fasciculus cuneatus or column of Burdach. I prefer the terms arm dorsal column and leg dorsal column rather than fasciculus gracilis and cuneatus, which you will forget 2 days after you lay aside the text. The sensory homunculus in the dorsal columns is a headless man sitting with his rump on the dorsal median septum. The head gets added to the homunculus as the trigeminal lemniscus joins the medial lemniscus (DeMyer 1998). Review Fig. 2-12D.

8. At what level of the neuraxis is the secondary neuron of the dorsal column pathway? ________________________________________.

   At the medullocervical junction.

9. The decussating axons are secondary axons conveying impulses to the thalamus, impulses destined to affect consciousness. In the brainstem they form a tract named the ______________________________________.

   medial lemniscus

10. The medial lemniscus terminates in a thalamic nucleus called the nucleus ____________________.

    ventralis posterior

11. From the nucleus ventralis posterior, the pathway for the dorsal column modalities goes to the somesthetic cortex in the ____________________ gyrus of the ____________________ lobe.

    postcentral; parietal

12. Try the whole thing at once. Wiggle your toe and think through the pathway to the cortex by which you know your toe has wiggled. Can you draw the pathway (Fig. 10-14)?

13. Chapter 9 describes the anatomy of the other component of the proprioceptive system, the vestibular system.

C. The general concept of the dorsal column, discriminative, or deep modalities

1. The dorsal columns mediate many sensations besides position and movement. In general, these sensations depend on receptors deeply placed in the dermis and the connective tissue of the joints, tendons, and muscles. These deep receptors are attuned, as Sherrington said, to mass, inertia, pressure, and movement. Because distance is inherent in the concept of movement, we have the ingredients of classic Newtonian mechanics. The proprioceptive or proprioceptive-related discriminatory sensations mediated by the dorsal columns are

   1. Sense of position or posture

   2. Sense of movement of joints and body (kinesthesia) and of something moving on the skin

   3. Vibration (pallesthesia)

   4. Two-point discrimination

   5. Sense of pressure

   6. Texture

   7. Touch localization (topognosia)

   8. Sense of weight (baresthesia)

   9. Sense of numbers or letters written on the skin (graphesthesia)

   10. Sense of form (stereognosis)

2. The following considerations rationalize the association of these sensations as basically mechanical stimuli:

   1. Vibration is easy to associate with proprioception as mediated by mechanical receptors. Recall that the cochlea, a receptor exquisitely specialized for detecting vibration, developed as the phylogenetic kin of the vestibular apparatus, a receptor exquisitely specialized for detecting the movement of fluids and otoliths. Vibration sense is merely the detection of fast changes in the pressure on and position of a minute portion of tissue, the eardrum being the most specialized example.

   2. The amount of pull on the joint and connective tissue proprioceptors leads to a sense of weight.

   3. To a large extent, discriminative touch, such as texture, depends on minute variations in the pressure on any area of skin. You feel texture best by moving an object across your skin or across your fingernail, causing almost a slow vibration sense. Discrimination of characters written on the skin demands first of all the perception of the path traced by an object pressing on the skin (a sense of movement), followed by comparison of the pattern with memory traces. Touch itself involves some mechanical displacement, i.e., some pressure. Two-point discrimination is the distance between two pressure points. Localization of a touch stimulus depends on comparing the location of a touch stimulus with the mental image of the body parts. It is essentially the problem of distance. In contrast with all these mechanical deformations of skin or joints that cause sensations conveyed by dorsal columns, an object that does not directly touch you, such as the sun 93,000,000 miles away, can burn you and cause pain. Ventrolateral, not dorsal, column pathways mediate these temperature and pain sensations.

D. Technique for testing digital position sense

1. Instruction to the Pt

   1. With one hand, support the Pt's hand or foot and ask the Pt to remain completely relaxed. With the other hand, grasp the digit by its side and wiggle it up and down, stopping randomly in one direction or the other. Separate the digit being tested so that you do not touch other digits (Fig. 10-15).

   2. While the Pt watches, stop the digit at one position or the other and instruct the Pt to report whether the finger is up or down. This step communicates what the Ex expects of the Pt. Then, for the actual testing, the Pt closes the eyes. In addition, instruct the Pt not to move the digits at all. The digits should remain totally passive. Tell the Pt, "Let me do all of the moving." Test the digits of all four extremities.

   3. Take care not to apply different pressures or use a different tone of voice on the up or down movement. The Pt may attend to the wrong stimulus.

2. Use of the fourth digit in testing position sense

   1. When testing position sense, the novice instinctively grasps the thumb, index finger, or large toe; but using digit 4 presents the greatest challenge to and therefore the best test of position sense. Not infrequently in early central nervous system disease, such as in degenerative diseases of the dorsal columns, you can demonstrate definite loss of position sense in the fourth digit when it is preserved in the other digits. Figure 10-16 shows why.

   2. The first, second, and fifth digits of the hands and feet have the richest innervation and the largest cortical representation. Therefore, interrupting position sense of these digits requires a relatively large lesion. Practice using digit 4 of the hand and foot (Fig. 10-15).

   3. When initial testing suggests loss of position sense, always test several digits several times. After understanding the test, the Pt should reply promptly and make no, no errors. Occasionally, the Pt will become bored or carelessly state one direction while meaning the other. A delay in responding means lack of attention or genuine loss of position sense. Immediate repetition and inquiry will disclose whether the error implies carelessness or disease.

3. If position sense is normal distally, it will be normal proximally. If abnormal at the digits, work proximally to test it at the wrist or ankle to establish the severity of the loss.

E. Position sense testing, probability theory, and yes or no forced-choice sensory tests

1. Patients with defective position sense often give an answer because they know a reply is expected, and they try to please the Ex. The Ex who does not understand probability theory may misinterpret the responses of the Pt with mild or even complete position sense loss or the malingering Pt who deliberately gives wrong answers.

2. Even with no position sense at all, what percentage of the time would the Pt guess the correct direction when a digit is randomly placed up or down? □ 0%/□ 25%/□ 50%/□ 75%.

   ☑ 50%

3. The situation exactly duplicates trying to call heads or tails in flipping a coin. The guesser wins 50% of the time on average.

4. Next consider impaired but not absent position sense. The Pt responds correctly, sometimes because of chance and sometimes because of correct perception of the position. The novice Ex may erroneously conclude that the Pt is unreliable, because he misses one time and then gives several correct responses. If you are satisfied that the Pt has not simply made a careless error, recall the rule that says the normal person makes ________________% errors.

   0

5. The next problem is how to reduce the probability of getting the correct answer by chance. How can you accomplish this?

   __________________________________________________________________

   _____________________________________.

   One method is to give three alternatives, up, down, and straight. Start by wiggling the finger up and down and then stop up, down, or in the neutral position; or you can move the digit medially or laterally.

6. By giving three alternatives instead of two, you reduce the chance of guessing the correct answer from one in two to one in ________________.

   three

7. Ordinarily, two-alternative testing is easier and faster than three-alternative testing and is as reliable. Probability theory sets the minimum number of trials that should be made in a two-alternative testing of position sense. As in flipping a coin, you will expect to call heads or tails correctly about one-half the time; the mathematical notation is (1/2)¹. When you try to call the coin twice in a row, the probability of being right is (1/2)², or one in four. The probability of calling three in a row would be (1/2)³, or one in ________________.

   0 (1/2)³ = one in eight

8. Each time you try to stretch your luck one more time, the denominator □ halves/□ doubles/□ triples/□ quadruples. Soon the odds against chance are very great.

   ☑ doubles

9. In testing position sense, the problem is where to cut off the trials to have confidence that the Pt has not succeeded by chance alone, when in fact the Pt has no position sense. Statisticians agree that when the probability of an event is 1 in 20 or less, chance is an unlikely explanation. Thus, in testing position sense, where chance has a 50% success rate, the smallest number of trials the Pt must get right to make chance success unlikely is ________________.

   five trials: (1/2)⁵ = 1/32, which is less than the needed 1/20 and therefore makes chance unlikely.

10. Some mental Pts reply exactly the opposite to each up or down position, ipso facto proving intact position sense. Even with no position sense, a Pt just guessing gets ________________% right by chance.

    50

11. Final admonition: In previous sensory tests, we implicitly relied on statistical concepts. If we offer coffee as a smell stimulus to anosmic Pts, some will reply because they expect to smell something. The question then becomes, How many Pts with anosmia will report coffee when they smell nothing? Because the probability of reporting coffee is less than 1 in 20, chance is an unlikely explanation for a correct answer. The same consideration holds for taste. In testing pain, we have to consider probability and the fact that some pinpricks do not stimulate pain endings. Hence, the Pt may report no pain on a particular prick, even though you stuck him. Moreover, pain thresholds differ considerably from Pt to Pt and from age to age. These facts lead to a general observation: as a teacher I find that medical students and residents often report that the history or the sensory examination "was unreliable." What that generally means is that the student failed to communicate adequately with the Pt to derive the historical information or produce the test results that the Pt was actually capable of. Usually such a Pt has a different culture, diction, syntax, and dialect than the student. Nothing tests the skill of the Ex more than the sensory examination. Make a successful sensory examination a matter of personal pride. By practicing sensory testing on yourself and many other subjects, you will appreciate the variables and avoid coming to erroneous conclusions about the Pt's reliability.

F. Clinical testing of position sense by the swaying (Romberg) test

1. Technique and instructions to the Pt: Ask the Pt to stand with the feet together. Note whether the Pt sways. Then ask the Pt to close the eyes, and note whether the swaying increases. Stand behind the Pt with arms held up ready to catch the Pt, but do not touch the Pt.

2. Results of Romberg swaying test

   1. Normal subjects will sway minimally with the eyes closed but not fall. Stand up and try this test yourself. Stand on both feet and then on one foot.

   2. Patients with acute unilateral vestibular disease tend to sway to the side of the lesion, but the nervous system compensates in chronic vestibulocerebellar disease, unilateral or bilateral (Lanska and Goetz, 2000). Many Pts with vestibular disease perform well on the Romberg test (Hotson and Baloh, 1998).

   3. Patients with dorsal column lesions, such as tabes dorsalis, sway much more with eyes closed and may fall unless supported. They do not compensate with time. Patients with severe sensory polyneuropathies also sway more with eyes closed. Swaying is never the sole sign of peripheral nerve or dorsal column lesions. It provides an auxiliary test for pathways tested more directly and specifically by digital position sense, vibration, directional scratch test, and stereognosis.

   4. Patients with hysteria cause the most difficulty in interpreting the swaying test. Hysterical Pts often gyrate wildly but usually do not fall, thus proving that they have intact balance.

      1. The Ex often can divert the hysterical Pt into performing well on the swaying test. At some time later in the examination, have the Pt stand with the feet together, arms straight out in front, and eyes open. Ask the Pt to continue alternately touching his nose with his right and left index fingers. While the Pt concentrates on repeating the finger-to-nose action, ask the Pt to close the eyes. Usually the Pt, now engrossed in the finger-to-nose task, will automatically maintain the posture without swaying.

      2. Hysteria never manifests solely by a positive swaying test. It is only one shadow in a pattern of psychiatric findings.

3. Interpreting the Romberg swaying test

   1. Students often mistakenly consider the swaying test as a test of cerebellar function, but the cerebellum does not depend on vision to do its job of coordinating. An analysis of the three operations of the test will explain how to interpret it.

      1. Operation 1 requires the Pt to stand with the feet together, thus narrowing the base and increasing the stress on balance.

      2. Operation 2 requires the Pt to close the eyes, thus removing visual clues for balance.

      3. Operation 3 requires the Ex to judge whether the Pt sways more with eyes open or eyes closed.

   2. Hence, we compare the degree of swaying when the Pt stands with heels together and eyes open with the degree of swaying with the eyes closed. This is an □ operational/□ interpretational definition.

      ☑ operational

   3. We interpret the test as showing that the removal of vision places the burden of afferent information for balance on the dorsal column proprioceptive system. We believe this because loss of dorsal column modalities, as in tabes dorsalis, causes the most severe swaying with eyes closed. Normally, a distributed sensorimotor complex, consisting of the proprioceptive system (including the vestibular apparatus, dorsal columns, and cerebellum), visual system, thalamus, basal ganglia, pyramidal tracts, and parietal lobes, maintains the standing posture and verticality.

   4. Why do you ask the Pt to close the eyes for the swaying test?

      _______________________________________________________________

      ___________________________________________________.

      To deprive the Pt of visual cues for balance and to place the afferent responsibility on the dorsal column proprioceptive system

   5. Which part of the gait examination uses the principle of narrowing the base, thus increasing the stress on balance? _________________________.

      tandem walking

G. Cerebellar versus sensory dystaxia

1. Earlier we stated that the cerebellum could coordinate muscular contractions only if it received the proper proprioceptive information. Loss of proprioceptive afferents via dorsal roots and dorsal columns results in sensory dystaxia that has to be distinguished from cerebellar dystaxia.

2. In theory, we might expect dystaxia from lesions of the corticopontine pathways. In practice, ataxia from corticopontine pathway lesions is unusual, although a controversial form of ataxic hemiplegia has been advocated and questioned (Landau, 1988).

3. Romberg's test shows that vision can substitute for proprioception. Hence, in distinguishing sensory from cerebellar dystaxia, have the Pt perform with eyes open and then closed. Which type of dystaxia, sensory or cerebellar, would distinctly worsen with the Pt's eyes closed? □ sensory/□ cerebellar. Explain.

   __________________________________________________________________

   ___________________________________________________.

   ☑ sensory

   Because visual guidance substitutes for proprioceptive guidance, eye closure increases sensory dystaxia much more than cerebellar.

4. The differentiation of cerebellar from sensory dystaxia comes from the pattern of cerebellar signs and the pattern of sensory and reflex findings. Complete Table 10-3.

H. Testing for loss of vibration sense (pallanesthesia)

1. Preparation of the Pt: As usual, start with the Pt's eyes open and show the Pt what you will do, but do the test with the Pt's eyes closed.

2. Test procedure: Hold a tuning fork (128 or 256 cps) by the round shaft and strike the tines a crisp blow against the ulnar side of your palm to set the fork vibrating. Apply the free end of the shaft to the Pt's fingernails and toenails or just proximal to the nail bed. If you press upward with the index finger pad of your free hand against the Pt's finger pad, you can feel the fork nearly as long as the Pt can.

3. Inquire: "Do you feel the buzz?" If the Pt fails to feel vibration at the nails for as long as you can, apply the fork to proximal bony prominences: ulnar styloid process or distal radius and internal malleolus or shin.

4. Reliability monitoring in testing for pallanesthesia

   1. How would you monitor the Pt's attentiveness and reliability in this test?

      ______________________________________________________________

      ___________________________________________________.

      Sometimes apply the tuning fork when it is not vibrating.

   2. To monitor reliability, strike the tines to set them vibrating. Although the Pt's eyes are closed, the Pt hears the strike and expects to feel vibration; instead, squeeze the vibrating tines immediately after striking the fork, stopping its vibration before applying the fork to the Pt. Strike your fork and squeeze its ends to familiarize yourself with the action. Thus, sometimes when you apply the fork, it is vibrating but not at other times.

5. Interpretation of vibration testing

   1. Aging increases the threshold to vibration and reduces the sensitivity. Normally the hands feel vibration better than the feet at all ages (Calne and Pallis, 1966; Martina et al., 1998).

   2. At spinal levels, dorsal column pathways mediate vibration, but some evidence suggests that the pathway may also travel in the dorsal part of the lateral columns (Willis and Coggeshall, 1991). Interruption of the pathway from the peripheral receptors up through the thalamus reduces vibratory perception. Suprathalamic lesions more or less spare vibration (Roland and Nielsen, 1980).

   3. Of the quantitative tests of vibration, the Reidel-Seiffer tuning fork is the most practical for routine use (Dimitrakoudis and Bril, 2002; Martina et al., 1998; Merkies et al., 2000).

I. Alternative efficient tests for dorsal column dysfunction

1. Directional scratch test

   1. Draw two transverse lines 2 cm apart across the distal shin and the dorsum of the hand.

   2. Using your finger tip, the tip of a tongue blade broken longitudinally, or the butt of the tuning fork, make a 2-cm-long stroke between the two lines, randomly alternating between a proximal (up) and distal (down) direction.

   3. Ask the Pt to state whether the object moved up or down. Start with two practice trials with the Pt's eyes open to establish communication. Then, with the Pt's eyes closed, make 10 trials in random up or down directions. The normal person gets all 10 correct. If the Pt errs, increase the distance to 5 cm and then to 10 cm to get a quantitative estimate of the deficit. Hankey and Edis (1989) claimed this test is superior to the standard tests of position and vibration, and that it correlates well with abnormal evoked responses (Motoi et al., 1992).

2. Two-point discrimination

   1. Test items: Use a calipers or a device called a Disccriminator. A paper clip bent to free the ends substitutes for a formal device.

   2. Technique: Start with the device wider than the expected distance to establish communication and gain the Pt's cooperation. Randomly alternate touching one or two points of the calipers. The Ex may use the static method in which the two points remain in place or the moving test in which the calipers are moved a slight distance.

   3. The Pt should discriminate two points at a distance: 2 to 4 mm on the fingertips, 4 to 6 mm on the dorsum of the fingers, 8 to 12 mm on the palm, and 20 to 30 mm on the dorsum of the hand (Meilgaard et al., 1999; Richards et al., 1998). Children older than 7 years can respond reliably (Cope and Anthony, 1992). Two-point discrimination decreases somewhat with aging, but is equal between the sexes.

   4. Peripheral nerve, central pathway, and parietal lobe lesions impair two-point discrimination. Although an excellent test (Krumlinde-Sundholm and Eliasson, 2002), it takes too much time for the screening NE.

3. Stereognosis: stereo = form, gnosis = knowing. Test form knowing by presenting objects of different shapes for recognition: a square or rectangular block, pyramid, cone, or marble. See the distinction between stereognosis and tactile agnosia in Section IX.

J. Review of somatosensory pathways

1. Practice testing yourself and a companion with a cotton wisp, a pin, and a tuning fork for temperature (Fig. 10-4) and vibration sense and then do the directional scratch test and test position sense. As you test each modality, "think through" the pathway to the cerebral cortex. You must, in particular, review the location of the secondary neuron and the level of the decussation. To prove that you can "think through" these pathways, draw them (Figs. 10-6 and 10-14).

2. Cortical lesions may somewhat impair the simple modalities of touch, pain, and temperature sensation but less than infracortical lesions of the pathways (Adams and Burke, 1989). Some appreciation of these modalities may occur at thalamic or infracortical levels. Unilateral suprathalamic lesions do not increase the vibration threshold (Roland and Nielsen, 1980).

BIBLIOGRAPHY · Examination of the Dorsal Column or Deep Modalities

A. The concept of agnosia

1. We can regard sensations as requiring two stages of cortical activity. The first stage occurs in the primary cortical receptive areas as they register the sensory impulses that shuttle in from the thalamic relay nuclei. For the next stage, the brain has to elaborate the meaning or significance of the cascade of sensory impulses. The brain matches these impulses with stored memories and integrates them into the value system of the individual to adjudicate their significance and to know whether to act on them or ignore them. For example, to recognize a dime placed in your hand in the dark, you have to recognize its distinct form, its weight, its size and texture, its metallic nature, and its symbolic significance as money.

2. The parietal lobe mediates these subsequent, discriminative aspects of somatic sensations, such functions as stereognosis, graphesthesia, two-point discrimination, and position sense (Bassetti et al., 1993): The part of the parietal lobe adjacent to the primary sensory cortex of the post-central gyrus acts as the association area for "knowing" the symbolic significance or meaning of sensations. The association areas for sight and sound occupy the zones adjacent to their primary sensory receptive areas in the occipital and temporal lobes. These zones meet and become confluent at the parieto-occipito-temporal junction, a region called the posterior parasylvian area. The anterior part of this area also integrates vestibular sensation with the other senses. See Fig. 10-17.

B. The gnosias, the nomenclature of knowing

1. Clinicians have devised a sensory nomenclature based on the theory that the ultimate meaning of afferent stimuli depends on an association cortex (Critchley, 1966). The sensations that require a high degree of cortical integration, i.e., that require a great deal of knowing, we call gnosias. The terms knowledge and gnosia are etymologically related: diagnosis literally means through or thorough knowing (dia = through as in dia r-rhea; gnosis = know). Prognosis means knowing beforehand (pro = before; gnosis = knowing).

2. The three-dimensional sense of form is called stereo ___________________.

   gnosis

3. Sense of localization of a skin stimulus is topo_____________________.

   gnosia (topo = place)

4. The graphic sense of numbers or letters written on the skin is ___________________________.

   graphognosia

5. Sense of awareness of a bodily defect is named by using the root nosos for disease. Hence, nosology is the science of disease classification, and the sense of awareness of disease is ___________________.

   nosognosia

6. Give the medical meanings of these roots:

   1. Stereo- means _______________________.

      form (three-dimensional)

   2. Topo- means ________________________.

      place

   3. Grapho- means ______________________.

      writing

   4. Noso- means ________________________.

      disease

C. The agnosias, the terms for not knowing

1. The negating prefix to designate lack of or absence of is ___________ before a vowel or ___________ before a consonant. Hence, agnosia literally means ________________________________.

   an; a; not knowing

2. To designate a gnostic defect secondary to a lesion in the association cortex or its circuitry, we negate the term for the normal sensation:

   1. Loss of form sense is called ____________________ognosis.

      astere

   2. Loss of cutaneous localization is called ____________________ognosia.

      atop

   3. Loss of graphic sense is called ____________________ognosia.

      agraph

   4. Loss of disease awareness is called ____________________ognosia.

      anos

D. Is the lesion in the sensory pathway or the association circuit

1. Lesions may interfere with the knowing of sensory stimuli in two ways: by interrupting the sensory pathways from receptor to primary sensory cortex or by interrupting the association cortex or its circuits with the thalamus and hippocampal formation.

   1. If the lesion destroys the receptor, the sensory pathway through nerve or neuraxis, or the primary receptive cortex, the impulses cannot reach the association cortex for interpretation. The Pt does not know because the association cortex does not receive sensory information. We return to one of Müller's laws: all we know of the external world is a change of state in the impulses in one of our afferent pathways (see page 349).

   2. If the lesion destroys the association cortex or its circuits with the thalamus or hippocampal formation, the Pt does not know because of inability to appreciate the significance or meaning of the impulses that reach the primary cortex.

2. After transection of a peripheral nerve or the spinal cord, the complete loss of sensation is called anesthesia. If sensation is merely reduced, it is called ___________esthesia.

   hypesthesia

3. Similarly, complete lack of pain sensation is called ___________algesia, reduced pain sensation is called ___________algesia, and excessive pain sensation is called ___________algesia.

   analgesia; hypalgesia; hyperalgesia

4. Loss of sense of form because of interruption of the pathway between the receptor and the primary sensory cortex is called stereoanesthesia. Loss of sense of form because of a lesion of the association cortex is called ___________.

   astereognosis

5. Loss of hearing because of interruption of CrN VIII is □ deafness/□ auditory agnosia.

   □ deafness

6. What would auditory agnosia mean?

   _________________________________________________________________

   ________________________________________________________________

   Inability to understand the meaning of words or sounds because of a defect in the auditory association cortex.

7. If a lesion in the optic pathways or calcarine cortex causes hemianopsia, the Pt has □ blindness/□ visual agnosia in that field of vision.

   ☑ blindness

8. Explain why we say the Pt in frame 7 is blind, rather than having visual agnosia.

   _________________________________________________________________

   _________________________________________________________________

   ___________________________________________________

   Because the lesion affects the optic pathway or calcarine cortex, not the association cortex, the primary impulses for vision cannot get to the visual association cortex for interpretation. It is improper to diagnose agnosia, if impulses fail to reach the association cortex.

E. Testing for astereognosis and tactile object agnosia

1. Definition

   1. Stereognosis as commonly used means object recognition through touch. Some tests also use vision.

   2. Distinction between stereognosis and tactile agnosia: Caselli (1991) separated tactile gnosia, or full recognition of objects placed in the hand, from simple form perception, such as distinguishing a cone from a pyramid, which he called stereognosis. Although lesions of the postcentral gyrus of the parietal lobe may cause astereognosis and tactile object agnosia (Takeda et al., 2000), functional MRI studies show that the cerebral circuitry for tactile object recognition involves not only the parietal lobe but also the visual association cortex and, surprisingly, the frontal polar cortex (Deibert et al., 1999).

2. Technique to test for astereognosis and tactile agnosia

   1. Test items: Use a series of common objects known to the Pt, such as keys, safety pins, paper clips, buttons, and coins, such as a penny, dime, nickel, and quarter. The penny and dime are especially hard to distinguish, and the normal person may miss occasionally.

   2. With the Pt's eyes closed, place various common objects that the Pt has not seen in the Pt's hand. Test each hand separately. Instruct the Pt to feel the object and identify it.

   3. Lack of dexterity, as with the spastic or paralyzed hand, reduces the Pt's ability to recognize objects (Krumlinde-Sundholm and Eliasson, 2002). If the Pt's hand is paralyzed, the Ex may move the item over the fingers to substitute for the Pt's active finger movement.

3. If you place the object in the Pt's right hand, you are testing the □ left/□ right parietal lobe.

   ☑ left

4. If the Pt has lost the sense of form because of a lesion in the periphery, spinal cord, brainstem, or thalamus, the term astereognosis is incorrect. The correct term is stereo____________.

   stereoanesthesia

5. The term agnosia correctly applies only if the lesion is in the □ nerve/□ spinal cord/□ brainstem/□ thalamus/□ association circuitry.

   ☑ association circuitry

BIBLIOGRAPHY · Examination for Astereognosis and Tactile Agnosia

A. Figure 10-18 summarizes distributions of sensory symptoms

B. Note: This section distinguishes tongue-tip neuroanatomy that you need to be able to recite as you analyze the patient and fingertip neuroanatomy that you look up as needed

1. Dermatomal distributions: Review Fig. 2-10 and recite the mnemonic for remembering dermatomal distributions. Start with the "hooded cape" and end with L5 and S1 and the coccygeal bull's eye.

2. Peripheral nerve distributions: Review Fig. 2-11.

   1. For focal or mononeuropathies, recall the trigeminal, ulnar/median (Fig. 10-9), lateral femoral cutaneous (Fig. 1-10), and common peroneal distributions and then use Fig. 2-11 to look up the other nerves. Distinguishing symptoms of some dermatomal and some peripheral nerve distributions is often difficult.

   2. For symmetrical polyneuropathies, recall the "stocking and glove" distribution (Fig. 10-7).

3. Plexus distributions: Use the motor, sensory, and segmental distribution tables and figures in Chapter 2 to look up the information as needed (fingertip neuroanatomy).

4. Spinal cord distributions

   1. Conus medullaris distribution (Fig. 10-19)

   2. Transverse section: distinct sensory level with loss of all somatosensory sensation caudal to the lesion or with sacral sparing (Fig. 10-20).

   3. Hemisection of the right or left half of the spinal cord (Brown-Sequard syndrome; Figs. 10-21A and 10-21B; Aminoff, 1993).

   4. Syringomyelia distribution (Figs. 10-22A and 10-22B).

5. Lateral medullary wedge syndrome of Wallenberg): Ipsilateral face/contralateral body and extremities. See Fig. 10-23A and 10-23B and Table 10-4.

6. Hemisensory distribution: Medial lemniscus/thalamic/internal capsule/cortical/distributions (Fig. 10-24).

BIBLIOGRAPHY · Review of Somatosensory Symptom Distributions

1. Inquire whether the symptom is intermittent or constant.

2. Ask the Pt to delineate the area of pain or sensory change. If intelligent, observant, and nonpsychiatric, the Pt will map it out as well or better than the Ex can with pin and cotton, and much more quickly.

3. Inquire about any factors or maneuvers that exacerbate or relieve the symptom. Have the Pt demonstrate any postures or maneuvers that alter the symptom. Ask the Pt's opinion as to the cause for the complaint. Frequently the answer discloses fears of cancer or some other dreaded malady. You can then plan how to discuss the differential diagnosis effectively, and Pts appreciate your interest in their observations and opinions.

4. Before each test, establish communication. State clearly what you expect. Don't equivocate but don't suggest responses. Ask for yes or no responses, or "Is [stimulus] 1 different from [stimulus] 2?"

5. Isolate the modality for testing from other sensory modalities. Do most sensory tests with the Pt's eyes closed.

6. Monitor the suggestibility and attentiveness of the Pt by sometimes withholding the stimulus and asking whether the Pt perceived something.

7. Draw the area of the deficit on the Pt or on a diagram. Delineate the borders only as sharply as the results warrant. Repeat the examination on another day to test the reproducibility of the deficit. When satisfied with the accuracy of the drawing, place it in the Pt's chart.

8. Think through the anatomic pathway for the modality. Know the location of the secondary sensory neuron and therefore the site of decussation of the pathway.

9. Try to match the distribution of the Pt's sensory findings with the neuroanatomic distribution of the sensory pathways. As always in diagnosis, the clinician has to decide whether the finding is organic, nonorganic, or mixed organic/nonorganic.

10. Make a decision on the probable diagnosis and cause for the symptom (Fig. 10-24).

11. Final warning: Although the classic findings of lesions at various sites enable localization of most organic diseases, variations within the compass of the classic syndromes is frequent. The Pt may feel the discomfort of the carpal tunnel syndrome in the forearm, not just the hand. The Pt with Brown-Sequard cord hemisection syndrome often has ipsilateral hyperesthesias. The Pt with Wallenberg's lateral medullary wedge syndrome may not show the classic cruciate sensory pattern. See Kim et al. (1997) and Aminoff (1993) in the previous bibliography. The Pt's mental state and motives may drastically change the result of sensory testing.

Rehearse Section VII, steps A and B, of the Standard NE.