Chapter 9 - Sensory system evaluation
The evaluation of somatic sensation, or any sensory modality for that mattter, is highly dependent on the ability and desire of the patient to cooperate. Sensation belongs to the patient (i.e., is subjective) and the examiner must therefore depend almost entirely on their reliability. For example, a patient with dementia or a psychotic patient is likely to give only the crudest, if any, picture of their perception of sensory stimuli. An intelligent, stable patient may refine asymmetries of stimulus intensity to such a degree that insignificant differences in sensation are reported, only confusing the picture. Suggestion can also modify a subject's response to a marked degree (e.g., to ask a patient where a stimulus changes suggests that it must change and may therefore create false lines of demarcation in an all too cooperative patient). Obviously the examiner must not waste time and efficiency on detailed sensory testing of the psychotic or demented patient, and must warn even the most cooperative patient that minute differences requiring more than a moment to decipher are probably of no significance. Additionally, the examiner must avoid any hint of predisposition or suggestion. Nonetheless, even after all precautions are taken, problems with the sensory exam still arise. Uniformity in testing is almost impossible and there is considerable variability of response in the same patient.
Fatigue can be an additional confounding variable and is particularly likely to be induced by a long, detailed and tedious sensory examination. A rapid, efficient exam is the most practical means of diminishing fatigue.
Use of a pressure transducer, such as VonFrey monofilaments, allows more consistent stimulus intensities and therefore more objectivity in the examination; however, this is impractical at the bedside and does not eliminate patient variability.
Sensory changes that are unassociated with any other abnormalities (i.e., motor, reflex, cranial, hemispheric dysfunctions) must be considered weak evidence of disease unless a pattern of loss in a classical sensory pattern is elicited (for example, in a typical pattern of peripheral nerve or nerve root distribution). Therefore, one of the principle goals of the sensory exam is to identify meaningful patterns of sensory loss (see below). Bizarre patterns of abnormality, loss, or irritation usually indicate hysteria or simulation of disease. However, the examiner must be aware of their own personal limitations. Peripheral nerve distributions vary considerably from individual to individual, and even the classic distributions are hard to keep in mind unless one deals with neurologic problems frequently. Therefore, it is advisable for the examiner to carry a booklet on peripheral nerve distribution, sensory and motor (such as: Aids to the Examination of the Peripheral Nervous System, published by the Medical Council of the U.K.).
As in all components of the examination, an efficient screening exam must be developed for sensory testing. This should be more detailed when abnormalities are suspected or detected or when sensory complaints predominate. Basic testing should sample the major functional subdivisions of the sensory systems. The patient's eyes should be closed throughout the sensory examination. The stimuli should routinely be applied lightly and as close to threshold as possible so that minor abnormalities can be detected. Spinothalamic (pain, temperature, and light touch), dorsal column (vibration, proprioception, and touch localization), and hemispheric (stereognosis, graphesthesia) sensory functions should be screened.
Pain (using a pin or toothpick), vibration (using a C128 tuning fork), and light touch should be compared at distal and proximal sites on the extremities, and the right side should be compared with the left. Proprioception should be tested in the fingers and toes and then at larger joints if losses are detected. Stereognosis, the ability to distinguish objects by feel alone, and graphesthesia, the ability to decipher letters and numbers written on skin by feel alone, should be tested in the hands if deficits in the simpler modalities are minor or absent.
Significant defects in graphesthesia and stereognosis occur with contralateral hemispheric disease, particularly in the parietal lobe (since this is the somatosensory association area that interprets sensation). However, any significant deficits in the basic sensory modalities cause dysgraphesthesia and stereognostic difficulties whether the lesion or lesions are peripheral or central. Therefore, it is difficult or impossible to test cortical sensory function when there are deficits of the primary sensory functions.
It may be surprising that the more basic modalities are usually not greatly affected by cortical lesions. With acute hemispheric insults (e.g., cerebral infarction or hemorrhage), an almost complete contralateral loss of sensation may occur. It is relatively short-lived, however; perception of pin-prick and light touch, as routinely tested, returns to almost normal levels, whereas proprioception and vibration may remain deficient (though considerably improved) in most cases. This lack of a significant long-term deficiency in basic sensation following hemispheric lesions has no completely satisfactory explanation, although some basic sensations probably have considerable bilateral projection to the hemispheres.
Double simultaneous stimulation (DSS) is the presentation of paired sensory stimuli to the two sides simultaneously. This can be visual, aural or tactile. Light touch stimuli presented rapidly, simultaneously, and at minimal intensity to homologous areas on the body (distal and proximal samplings on extremities) may pick up very minor threshold differences in sensation. Additionally, this testing can also detect neglect phenomena due to damage of the association cortex.
Neglect may be hard to distinguish from involvement of the primary sensory systems. However, neglect usually can be demonstrated in multiple sensory systems (i.e., visual, auditory, and somesthetic), confirming that this is not simply damage to one sensory system. Association cortex lesions, particularly involvement of the right posterior parietal cortex, may become apparent only on double simultaneous stimulation.
The face-hand test is a further modification of DSS. This test takes advantage of the fact that stimuli delivered to the face dominate over stimulation elsewhere in the body. This dominance is best illustrated in children and in demented and therefore regressed patients. Before the age of ten, most strikingly earlier than age five, stimuli presented simultaneously to the face and ipsilateral or contralateral hand are frequently (more than three in ten stimulations) perceived at the face alone. Perception of the hand, and, if tested, other parts of the body is extinguished. In an older child or adult, several initial extinctions of the hand may occur, but very quickly both stimuli are correctly perceived. In the patient with diffuse hemispheric dysfunction (dementia), a regression to consistent bilateral extinction of the hand stimuli is frequently seen.
This test therefore can be doubly useful, first as an indication of diffuse hemispheric function and second by stimulating the face and opposite hand, a means of detecting minor hemisensory defects (e.g., if the patient consistently extinguishes only the right hand and not the left, a sensory threshold elevation due to primary sensory system or association cortex involvement on the left is suspect).
Since the main goal of the sensory exam is to determine which, if any, components of the sensory system are damaged, it is important to consider the principle patterns of sensory loss resulting from disease of the various levels of the sensory system. These patterns of loss are based on the functional anatomy and we will also briefly review some of this anatomy.
Peripheral neuropathy, that is, symmetrical damage to peripheral nerves, is a relatively common disorder that has many causes. Most of these can broadly be classified as toxic, metabolic, inflammatory or infectious. In this country, the most common causes are diabetes mellitus and the malnutrition of alcoholism, although other nutritional deficiencies or toxic exposures (either environmental toxins or certain medicines) are occasionally seen. Infections, such as Lyme disease, syphilis, or HIV can cause this pattern and there are inflammatory and autoimmune conditions that can also produce this pattern of damage. A more complete discussion can be found in Chapter 21. Because this is a systemic attack on peripheral nerves, the condition produces symmetrical symptoms. The initial symptoms are most often sensory and the longest nerves are affected first (the ones that are most exposed to the toxic or metabolic insult). The receptors of the feet are considerably farther removed from their cell bodies in the dorsal root ganglia than are the receptors of the hands. The metabolic demands on these neurons is substantial which accounts for their being the first affected and for the early appearance of sensory loss in the feet in a "stocking" distribution. Later on, as the symptoms reach the mid-calf, the fingers are involved and a full "stocking-glove" loss of sensation develops. Even later, when the trunk begins to be involved, sensory loss is noted first along the anterior midline (Figure 9-1).
Vibration perception is often the earliest affected modality since these are the largest, most heavily myelinated and most metabolically demanding fibers. Usually the loss of pin-prick, temperature, and light-touch perception follow, with conscious proprioception (joint position sense) being variably affected. Despite the fact that proprioception follows many of the same pathways as vibration it is usually not as noticeably affected because the testing procedure (i.e., moving the toes or fingers up or down) is quite crude and is not likely to pick up early loss.
The peripheral deep-tendon reflexes are depressed early in most cases of peripheral neuropathy, particularly the Achilles reflex. This is because the sensory limb of this reflex depends on large myelinated fibers.
As a rule, symptomatic motor involvement is late and, when it occurs, it affects the intrinsic muscles of the feet first.
Radiculopathy (nerve root damage) is the relatively common result of intervertebral disc herniation or pressure from narrowing of the intervertebral foramina due to spondylosis (arthritis of the spine). The most common presentation of this is sharp, shooting pain along the course of the nerve root (Figure 9-2). Damage to a single nerve root, even when severe, usually does not have any sensory loss because of the striking overlap of dermatomal sensory distribution (Figure 9-3). There may be slight loss, often accompanied with paresthesias (tingling or pins and needles) in small areas of the distal limbs where the sensory overlap is not great. Table 21-3 lists some of the common areas of paresthesia or decreased sensation with common nerve root injuries. Herpes zoster, which affects individual dorsal roots, nicely demonstrates dermatomal distribution because, despite the lack of sensory loss (attributable to overlap), vesicles ("shingles") appear at the nerve endings in the skin (see Figure 9-3).
Nerve root damage in the cauda equina often produces a "saddle" distribution of sensory loss by affecting the lower sacral nerve roots. This saddle distribution of sensory loss can also be seen in anterior spinal cord damage (see the next section) and, in either case, must be taken quite seriously due to the potentially serious sequellae of spinal cord and cauda equina damage.
Nerve root pain is often quite characteristic. It is often quite sharp and well localized to the dermatomal distribution and may be brought on by stretching of the nerve root (Figure 1-5) or by maneuvers that load the intervertebral discs and compress the intervertebral foramina (Figure 1-4). However, pain can also "refer" (see Chapter 19). This referred pain is less localized and is often felt in the muscles (myotomal) or skeletal structures (sclerotomal) that are innervated by the nerve root. The person usually complains of a deep aching sensation. Myotomes should not be memorized but can be looked up easily by referring to the motor root innervations of muscles, which are essentially the same as their sensory innervations. Sclerotomal overlap is so great that localization on their basis is impractical.
Spinal cord damage is characterized by both sensory and motor symptoms, both at the level of involvement, as well as below, by affecting the tracts running through the cord. Symptoms referable to the level of injury appear in the pattern of dermatomes and myotomes and, when present, are very useful for localizing the level of spinal cord damage. The symptoms of damage to the long sensory tracts (the dorsal columns and the spinothalamic tract) are less helpful in localizing the lesion because it is often impossible to determine the precise level of the sensory loss and also because, particularly in the case of the spinothalamic tract, there is considerable dissemination of the signal in the spinal cord before it is relayed up the cord. Similar difficulties make it difficult to localize the level of spinal cord damage by examining for damage to the descending (corticospinal) motor tracts. Therefore, when long tract damage is identified, one can only be certain that the lesion is above the highest level that is demonstrably affected.
Compression of the spinal cord from the anterior side first involves the spinothalamic paths from the sacral region, and a "saddle" loss of pain and temperature perception is usually the first symptom even with lesions high in the spinal cord (Figure 9-4). In this case, as symptoms progress with greater degrees of compression, symptoms progressively ascend the body up toward the level of the actual cord damage (see Figure 9-4).
Intramedullary lesions of the spinal cord (such as syrinx, ependymoma, or central glioma) may present with a very unusual pattern of "suspended sensory loss". This consists of an isolated loss of pain and temperature perception in the region of the expanding lesion because of damage to the crossing spinothalamic tract fibers (Figure 9-5). In this pattern of sensory loss due to expanding intramedullary lesions, there is "sacral sparing" of pain and temperature because the more peripheral spinothalamic fibers (the ones from the sacrum) are the last to be involved (see Figure 9-4). With intramedullary lesions, the dorsal columns are also usually spared until extremely late in the course of expansion, leaving touch, vibration, and proprioception intact. The loss of one or two sensory modalities (such as pain and temperature sense, in this case) with preservation of others (such as touch, vibration and joint position sense) is termed a "dissociated sensory loss" and is in contrast to the loss of all sensory modalities associated with major nerve or nerve root lesions or with complete spinal cord damage.
Complete hemisection of the cord is seen occasionally in clinical practice and is quite illustrative of the course of spinal cord sensory pathways. This lesion results in a characteristic picture of sensorimotor loss (Brown-Sequard syndrome), which is easily recognized due to the loss of dorsal columns sensations (vibration, localized touch, joint position sense) on the ipsilateral side of the body and of spinothalamic sensations (pain and temperature) on the contralateral side (Figure 9-6).
Brain stem involvement, like involvement of the spinal cord, is characterized by long-tract and segmental (cranial nerve) motor and sensory abnormalities and is localized by the segmental signs. The picture of ipsilateral cranial nerve abnormality and contralateral long-tract dysfunction is quite consistent (Figure 9-7). Both the dorsal columns and pyramids decussate at the spinomedullary junction (the spinothalamic system has already decussated in the spinal cord). This accounts for the typical crossed presentation of symptoms in the body. Below the level of the midbrain, the spinothalamic and dorsal column (medial lemniscus) systems remain separate and therefore lesions may involve the pathways separately (i.e., there may be a dissociated sensory loss). For example, an infarction caused by occlusion of the posterior inferior cerebellar artery typically involves only the lateral portion of the medulla. The ipsilateral trigeminal tract and nucleus and the spinothalamic tract are frequently included in the lesion, leaving a loss of pain and temperature perception over the ipsilateral face (see Chapter 5) and the contralateral side of the body from the neck down. The medial lemniscus and its modalities (i.e., vibration, joint position, and well-localized touch) are spared.
Thalamic lesions are associated with contralateral hemihypesthesia. Initially, if the lesion is acute, there is considerable loss bordering on anesthesia, but some recovery is expected over time, especially of touch, temperature, and pain perception. Vibration and proprioception remain more severely affected. Unfortunately, episodic paroxysms of contralateral pain may be a striking and not infrequent residual of thalamic destruction (this is one of the "central pain syndromes"). The pain can be controlled occasionally with anticonvulsants. An additional residual that may develop over time is marked contralateral hyperpathia in spite of the presence of diminished overall sensitivity of the skin. Stimulation of a site with a pin causes a very unpleasant, poorly localized and spreading sensation, which is frequently described as burning. This is presumably an irritative phenomenon of the nervous system, although it may also result from loss of normal pain-suppression mechanisms. It is seen most often after thalamic lesions, although it can occur as a residual of lesions in any portion of the central sensory systems. A hypersensitivity to cold sensation frequently accompanies the hyperpathia.
As discussed earlier, cortical lesions tend to leave minimal deficits in basic sensation. However, especially if the parietal lobe is damaged, there may be striking contralateral deficits in the higher perceptual functions (see Chapter 2). Stereognosis and graphesthesia are abnormal in spite of minor difficulties with vibration and proprioception and even less, if any, difficulty with pain, temperature, and light-touch perception. Of course, if there is significant deficit of primary sensations, it may be impossible to test for deficits of higher perceptual functions.
- Brodal, A.: Neurological Anatomy in Relation to Clinical Medicine, ed.2, New York, Oxford University Press, 1969.
- Medical Council of the U.K.: Aids to the Examination of the Peripheral Nervous System. Palo Alto, Calif., Pendragon House, 1978.
- Monrad-Krohn, GH, Refsum, S.: The Clinical Examination of the Nervous System, ed. 12, London, H.K. Lewis & Co., 1964.
- Wolf, J.: Segmental Neurology, Baltimore, University Park Press, 1981.
Define the following terms:conscious proprioception, agnosia (stereoagnosia), graphesthesia, dermatome, sclerotome, myotome, radiculopathy, myelopathy, anesthesia/hypoesthesia, hyperpathia, allodynia, hyperesthesia, dysesthesia, paresthesia, polyneuropathy, subjective.
9-1. What are the steps involved in the sensory exam?
9-2. How is it possible to lose some types of sensations and not others?
9-3. What sensations are conveyed by the small-diameter sensory nerve fibers in a peripheral nerve?
9-4. What sensations are conveyed by large-diameter sensory nerve fibers in a peripheral nerve?
9-5. What sensations are conveyed by the dorsal columns?
9-6. What sensations are conveyed by the spinothalmic tract?
9-7. What is tested by double simultaneous stimulation?
9-8. Where would the lesion be if the patient was able to detect all modalities of sensation but could not recognize an object placed in the right hand?
9-9. What is the common sensory loss from damage to the spinal cord?
9-10. What would be the expected sensory loss from damage restricted to the left side of the spinal cord?
9-11. What is the characteristic of sensory loss due to damage of peripheral nerves in a limb?
9-12. What is the pattern of sensory loss seen in diffuse damage to peripheral nerves (polyneuropathy)?