Sensory Abnormalities of the Limbs, Trunk, and Face

Clinical evaluation of sensory deficits is inherently more difficult than evaluation of motor deficits because of the subjective nature of the examination. Nevertheless, it is important to identify sensory deficits in order to localize lesions.

Anatomy and Physiology

Peripheral Pathways

Activation of sensory end organs produces a generator potential in the afferent neurons. If the generator potential reaches threshold, an action potential is produced that is conducted by the sensory axons to the spinal cord.

Sensory transducers are seldom directly affected by neuropathic conditions, although peripheral vascular disease can produce dysfunction of the skin’s sensory axons, and systemic sclerosis can damage the skin sufficiently to produce a primary deficit of sensory transduction ( eTable 31.1 ).

eTABLE 31.1

Sensory Receptors

Receptor	Type	Afferent Axon	Modality
Pacinian corpuscle	Multilayered capsule around a nerve terminal producing a rapidly adapting mechanoreceptor	Large-diameter myelinated axons	Touch and vibration
Golgi tendon organ	Specialized organs in tendons near joints	Large-diameter myelinated axons	Joint position and rate of movement
Free nerve ending	Branched terminal endings of axons	Small myelinated and unmyelinated axons	Strong tactile and thermal stimuli, especially painful inputs
Merkel disk	Slowly adapting mechanoreceptor	Myelinated axons	Touch
Meissner corpuscle	Specialized quickly adapting mechanoreceptor	Myelinated axons	Touch
Krause end bulbs	Specialized terminal axon ending	Small myelinated axons	Thermal sensation
Muscle spindles	Specialized organ involving intrafusal muscle fibers and associated nerves	Large-diameter myelinated axons	Muscle length and contraction

The rate of action potential propagation differs according to the diameter of the axons and depending on whether the fibers are myelinated or unmyelinated. In general, nociceptive afferents are small myelinated and unmyelinated axons. Nonnociceptive afferents are large-diameter myelinated axons. The characteristics of afferent fibers are shown in eTable 31.2 .

eTABLE 31.2

Sensory Afferents

Class (Older Terminology)	Diameter (mm)	Conduction Velocity (m/sec)	Modalities
Ia (Aα)	12–20	70–100	Proprioception (muscle spindles)
Ib (Aα)	12–20	70–100	Proprioception (Golgi tendon organs)
II (Aβ)	5–12	30–70	Touch and pressure from skin, proprioception from muscle spindles
III (Aδ)	2–5	10–30	Pain and temperature, sharp sensation, joint and muscle pain sensation
IV (C, unmyelinated)	0.5–2.0	0.5–2.0	Pain, temperature

NOTE: The terminology of sensory afferents has changed over the years. The older terminology, indicated in parentheses, spans motor and sensory modalities; therefore the newer classification for sensory fibers, presented here, should be used. The corresponding terminology is presented only for reference.

Spinal Cord Pathways

Sensory afferent information passes through the dorsal root ganglia to the dorsal horn of the spinal cord. Some of the axons pass through the dorsal horn without synapsing and ascend in the ipsilateral dorsal columns; these serve mainly joint position and touch sensations. Other axons synapse in the dorsal horns, and the second-order sensory neurons cross in the anterior white commissure of the spinal cord to ascend in the contralateral spinothalamic tract. Although this tract is best known for the conduction of pain and temperature information, some nonnociceptive tactile sensation is conducted as well.

The dorsal column tracts ascend to the cervicomedullary junction, where axons from the leg synapse in the nucleus gracilis and axons from the arms synapse in the nucleus cuneatus. Fig. 31.1 shows the ascending pathways through the spinal cord to the brain.

Fig. 31.1, Axial Section of the Spinal Cord Showing Dorsal and Ventral Roots Forming a Spinal Nerve.

Brain Pathways

Brainstem

Axons from the nucleus gracilis and nucleus cuneatus cross in the medulla and ascend in the medial lemniscus. The spinothalamic tracts in the brainstem are continuations of the same tracts in the spinal cord and ascend lateral to the medial lemniscus in the brainstem. Lesions of the brainstem can produce sensory deficits congruent with the anatomical localization, but these symptoms are usually eclipsed by motor and cranial nerve deficits.

Thalamus

Lesions of the thalamus rarely affect only a single region, but the functional organization of this structure may affect clinical findings. The ventroposterior complex is the main somesthetic receiving area and includes the ventroposterior lateral nucleus, which receives information from the body, and the ventroposterior medial nucleus, which receives sensory input from the head and face. Projections are to the primary somatosensory cortex on the postcentral gyrus. The posterior nuclear group receives nociceptive input from the spinothalamic tract and projects mainly to the secondary somesthetic region on the inner aspect of the postcentral gyrus, adjacent to the insula.

Cerebral Cortex

Classic neuroanatomical teaching presents a picture of the central sulcus bounded by the motor strip anteriorly and the sensory strip posteriorly. This division was derived largely from studying lower animals, in which the separation between these functions is marked. On ascending the evolutionary ladder, however, this division becomes less prominent, and many neurologists refer to the entire region as the motor-sensory strip. In general, sensory function is served prominently on the postcentral gyrus. The mapping of the cortex follows the same homunculus presented in Chapter 26 (see Fig. 26.1 ), with the head and arm portions located laterally on the hemisphere and the leg region located superiorly near the midline and wrapping onto the parasagittal cortex.

Sensory Input Processing

Elementary sensory inputs of all modalities provide data to the brain; they are then processed at a higher cortical level. The locations of these areas for processing are not as discrete as the primary sensory cortical regions. However, disorders in higher-level function certainly exist. Just as presbyopia and presbycusis have central as well as peripheral components, there is evidence that higher-level cerebral processing of other sensory data can deteriorate with age as well as disease ( ). Abnormalities in central sensory processing have been described in Alzheimer disease, autism, and stroke ( ).

Approach to Localization and Diagnosis

Sensory Abnormalities

Abnormalities of sensory perception are varied, and the pattern of symptoms is often a clue to diagnosis:

Loss of sensation (numbness)
Dysesthesia and paresthesia
Neuropathic pain
Sensory ataxia

Patients often use the term numbness to mean any of a variety of symptoms. Strictly speaking, numbness is the loss of sensation and usually manifests as decreased sensory discrimination and elevated sensory threshold; these are negative symptoms. Some patients use the term numbness to mean weakness; others are referring to positive sensory symptoms such as dysesthesia and paresthesia.

Dysesthesia is an abnormal perception of a sensory stimulus, as when pressure produces a feeling of tingling or pain. If large-diameter axons are mainly involved, the perception is typically tingling; if small-diameter axons are involved, the perception is commonly pain. Paresthesia is an abnormal spontaneous sensation similar in quality to dysesthesia. Dysesthesias and paresthesias are usually seen in localized regions of the skin affected by peripheral neuropathic processes such as polyneuropathy or mononeuropathy. These perceptual abnormalities can also be seen in patients with central conditions such as myelopathy or cerebral sensory tract dysfunction.

Neuropathic pain can result from damage to the sensory nerves from any cause. Peripheral neuropathic conditions result in failure of conduction of the sensory fibers, giving decreased sensory function plus pain from electrical discharge of damaged nociceptive axons ( ). The pathophysiology of neuropathic pain partly involves lowering of the membrane potential of the axons so that minor deformation of the nerve can produce repetitive action potentials ( ). An additional feature with neuropathic conditions appears to be unstable membrane potential, so that the crests of fluctuations of membrane potential can produce action potentials. Finally, crosstalk between damaged axons allows an action potential in one nerve fiber to be abnormally transmitted to an adjacent nerve fiber. These pathophysiological changes also produce exaggerated sensory symptoms, including hyperesthesia and hyperpathia. Hyperesthesia is increased sensory experience with a stimulus. Hyperpathia is augmented painful sensation.

Sensory ataxia is the difficulty in coordination of a limb that results from loss of sensory input, particularly proprioceptive input. The resulting deficit may resemble cerebellar ataxia, but other signs of cerebellar dysfunction are not seen on neurological examination.

Localization of Sensory Abnormalities

A general guide to sensory localization is presented in Table 31.1 . Guidelines for the diagnosis of sensory abnormalities are summarized in Table 31.2 . Details of specific sensory levels of dysfunction are discussed next.

TABLE 31.1

Sensory Localization

Level of Lesion	Features and Location of Sensory Loss
Cortical	Sensory loss in the contralateral body is restricted to the portion of the homunculus affected by the lesion. If the entire side is affected (with large lesions), either the face and arm or the leg will tend to be affected to a greater extent
Internal capsule	Sensory symptoms in the contralateral body that usually involve head, arm, and leg to an equal extent. Motor findings are common although not always present
Thalamus	Sensory symptoms in the contralateral body including the head. These may split at the midline. Sensory dysfunction without weakness is highly suggestive of a lesion of the thalamus
Spinal transection	Sensory loss at or below a segmental level, which may be slightly different for each side. Motor examination is also key to localization
Spinal hemisection	Sensory loss is ipsilateral for vibration and proprioception (dorsal columns) and contralateral for pain and temperature (spinothalamic tract)
Nerve root	Sensory symptoms follow a dermatomal distribution
Plexus	Sensory symptoms span two or more adjacent root distributions, corresponding to the anatomy of plexus divisions
Peripheral nerve	Distribution follows peripheral nerve anatomy or involves nerves symmetrically

TABLE 31.2

Diagnosis of Sensory Abnormalities

Abnormality	Features	Lesion	Cause
Distal sensory deficit	Sensory loss with or without pain distal on the legs. Arms may also be affected	Peripheral nerve	Peripheral neuropathy
Proximal sensory deficit	Sensory loss on the trunk without limb symptoms	Neuropathy with predominantly proximal involvement	Porphyria, diabetes, other plexopathies
Dermatomal distribution of pain and/or sensory loss	Pain and/or sensory loss in the distribution of a single nerve root	Nerve root	Radiculopathy due to disk, osteophyte, tumor, herpes zoster
Single-limb sensory deficit	Loss of sensation on one entire limb that spans neural and dermatomal distributions	Plexus or multiple single nerves	Autoimmune plexitis, hematoma, tumor
Hemisensory deficit	Loss of sensation on one side of body. May be associated with pain. Face involved with brain lesions but not spinal lesions	Thalamus, cerebral cortex, or projections. Brainstem lesion, spinal cord lesion, and lower lesions do not involve the face	Infarction, hemorrhage, demyelinating disease, tumor, infection
Crossed sensory deficit: unilateral facial and contralateral body	Unilateral loss of pain and temperature sensation on contralateral body	Lesions of uncrossed trigeminal fibers and crossed spinothalamic fibers	Lateral medullary syndrome
Pain/temperature and vibration/proprioception deficits on opposite sides	Unilateral loss of sensation on face, unilateral loss of vibration and proprioception on the other side	Spinal cord lesion ipsilateral to vibration and proprioception deficit and contralateral to pain and temperature deficit	Disk protrusion, spinal stenosis, intraspinal tumor, transverse myelitis. Intraparenchymal lesions are more likely to produce dissociated sensory loss
Dissociated suspended sensory deficit	Loss of pain and temperature sensation on one or both sides with normal sensation above and below	Syringomyelia in the cervical or thoracic spinal cord	Chiari malformation, hydromyelia, central spinal cord tumor, or hemorrhage
Sacral sparing	Preservation of perianal sensation with impaired sensation in the legs and trunk	Lesion of the cord with mainly central involvement, sparing peripherally located sacral ascending fibers	Cord trauma, intrinsic tumors of the cord

Peripheral Sensory Lesions

Lesions of the peripheral nerves and the plexuses produce sensory loss that follows their peripheral anatomical distribution. Peripheral sensory loss produces a multitude of potential complaints. Clues to localization are as follows:

Distal sensory loss and/or pain in more than one limb suggests peripheral neuropathy.
Sensory loss in a restricted portion of one limb suggests a peripheral nerve or plexus lesion; mapping of the deficit should make the diagnosis.
Sensory loss affecting an entire limb is seldom due to a peripheral lesion. A central lesion should be sought.

Unfortunately, especially with peripheral lesions, a discrepancy between the complaint and the examination findings is common. The patient may complain of sensory loss affecting an entire limb when the examination shows a median or ulnar distribution of sensory loss. Alternatively, the patient may complain of sensory loss but examination fails to reveal a sensory deficit. This discrepancy is more likely to be due to limitations of the examination than to malingering. Also, patients may have significant sensory complaints as a result of pathophysiological dysfunction of the afferent axons while the integrity and conducting function of the axons are still intact, so that the examination will show no loss of sensory function.

Fig. 31.2 summarizes the peripheral nerve anatomy of the body and Fig. 31.3 shows the dermatomal distribution.

Fig. 31.2, Cutaneous Fields of Peripheral Nerves (n.) .

Fig. 31.3, Dermatomes: Cervical (C) , Thoracic (T) , Lumbar (L) , and Sacral (S) .

Spinal Sensory Lesions

Certain sensory syndromes suggest a spinal lesion:

Sensory level on the trunk
Dissociated sensory loss on the trunk or limbs, sparing the face
Suspended sensory loss
Sacral sparing

Sensory level is a deficit below a certain level of the spinal cord segments. Dissociated sensory loss is disturbance of pain and temperature on one side of the body and of vibration and proprioception on the other. The term can also be used to describe loss of one sensory modality (e.g., pain and temperature) with normality of another—in this instance, vibration and proprioception. Suspended sensory loss describes the clinical situation in which sensory loss involves a number of dermatomes while those above and below are spared. Sacral sparing is a disturbance of sensory function in the legs with preservation of perianal sensation.

Sensory level

With a sensory level, loss of sensation in a myelopathic distribution without weakness and reflex abnormalities would be very unusual. Sensory symptoms with incipient myelopathy are more often positive than negative; the Lhermitte sign (electric shock–like paresthesias radiating down the spine and often into the arms and legs produced by flexion of the cervical spine) is a common presentation of cervical myelopathy. Although the Lhermitte sign is commonly thought of as being associated with inflammatory conditions such as multiple sclerosis, it is more often seen with cervical spondylotic myelopathy and has been reported after radiation therapy affecting the cervical spinal cord as well as even after cervical injections.

Although a spinal cord localization is suspected with a sensory level, the level of the sensory loss may be slightly different between the two sides; this finding does not indicate a second lesion. Also, a basic tenet of neurology for the evaluation of spinal sensory levels is to look for a lesion not only at the upper level of the deficit but also higher. Magnetic resonance imaging (MRI) is the best noninvasive test for assessing sensory loss of spinal origin. Of note, demyelinating disease and other inflammatory conditions of the spinal cord may not be visualized on MRI; if an inflammatory lesion is suspected, however, a contrasted study on a high-field scanner will have greater diagnostic sensitivity ( ).

Dissociated sensory loss

Pain and temperature fibers cross shortly after entering the spinal cord and ascend contralaterally in the spinothalamic tract, whereas vibration and proprioception fibers ascend uncrossed in the dorsal columns. Therefore unilateral lesions of the spinal cord can produce loss of vibration and proprioception ipsilateral to the lesion and loss of pain and temperature sensation contralateral to it. This dissociation of sensory loss is most prominent in patients with intrinsic spinal cord lesions such as tumors, but it can also be seen with focal extrinsic compression. MRI usually shows the spinal lesion. The level of the deficits is often not congruent because of intersegmental projection of the pain and temperature axons in the posterolateral tract before synapsing on second-order neurons.

A second form of dissociated sensory loss can arise from selective lesions of the dorsal or ventral aspects of the cord. Anterior spinal artery syndrome produces infarction of the ventral aspect of the cord, sparing the dorsal columns; therefore a deficit of pain and temperature sensation is found below the level of the lesion but vibration and proprioception are spared. A selective lesion of the dorsal columns is less likely, but predominant dorsal column deficits can occur in patients with tabes dorsalis, multiple sclerosis, subacute combined degeneration, or Friedreich ataxia as well as occasionally in focal spinal cord mass lesions.

Suspended sensory loss

A third form of dissociated sensory loss is seen in syringomyelia, with loss of pain and temperature sensation, sparing of touch and joint-position sensation (usually affecting the upper limbs), and normal sensation above and below the lesion (see “Syringomyelia,” later).

Sacral sparing

Ascending spinal afferents are topographically organized, with caudal fibers peripheral to more rostral fibers. Therefore central cord lesions can affect the higher fibers before the lower fibers, so that sensory loss throughout the legs with sparing of perianal sensation may be found. In some patients with severe cord lesions, this preserved sensation may be the only neurological function below the level of the lesion. The cause is usually trauma, but intrinsic mass lesions can also produce this clinical picture.

Brainstem Sensory Lesions

Brainstem lesions uncommonly affect sensory function without affecting motor function. The notable exception is trigeminal neuralgia, characterized by lancinating pain without sensory loss in the distribution of a portion of the trigeminal nerve.

Lateral medullary syndrome typically results from occlusion of the posteroinferior cerebellar artery and produces sensory loss on the ipsilateral face (from trigeminal involvement) plus loss of pain and temperature sensation on the contralateral body (from damage to the ascending spinothalamic tract). With this syndrome, however, the motor findings eclipse the sensory findings, which include ipsilateral cerebellar ataxia, bulbar weakness resulting in dysarthria and dysphagia, and Horner syndrome.

Medial medullary syndrome typically results from occlusion of a branch of the vertebral artery and is less common than lateral medullary syndrome. Patients have loss of contralateral position and vibration sensation, but again, the motor findings predominate, including contralateral hemiparesis and ipsilateral paresis of the tongue.

Ascending damage in the brainstem from vascular and other causes can also produce contralateral sensory loss. But as with the aforementioned syndromes, the sensory findings are trivial compared with the motor findings.

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