17 - 27 Numbness, Tingling, and Sensory Loss

27 Numbness, Tingling, and Sensory Loss

weakness usually is due to lower motor neuron or peripheral nerve dis­ ease, such as in a facial palsy. Weakness of part of a limb is commonly due to a peripheral nerve lesion such as an entrapment neuropathy. Relatively symmetric weakness of extraocular or bulbar muscles fre­ quently is due to a myopathy (Chap. 460) or neuromuscular junction disorder (Chap. 459). Bilateral facial palsy with areflexia suggests Guillain-Barré syndrome (Chap. 458). Worsening of relatively sym­ metric weakness with fatigue is characteristic of neuromuscular junc­ tion disorders. Asymmetric bulbar weakness usually is due to motor neuron disease. Weakness limited to respiratory muscles is uncommon and usually is due to motor neuron disease, myasthenia gravis, or polymyositis/dermatomyositis (Chap. 377).

PART 2 Cardinal Manifestations and Presentation of Diseases ■ ■FURTHER READING Brazis P et al: Localization in Clinical Neurology, 8th ed. Philadelphia, Lippincott William & Wilkins, 2021. Campbell WW, Barohn RJ: DeJong’s The Neurological Examination, 8th ed. Philadelphia, Lippincott William & Wilkins, 2019. O’Brien M on behalf of the Guarantors of Brain: Aids to the Examination of the Peripheral Nervous System, 6th ed. Amsterdam, Elsevier, 2023. Stephen L. Hauser

Numbness, Tingling,

and Sensory Loss Normal somatic sensation reflects a continuous monitoring process, little of which reaches consciousness under ordinary conditions. By contrast, disordered sensation, particularly when experienced as painful, is alarming and dominates the patient’s attention. Physicians should be able to recognize abnormal sensations by how they are described, know their type and likely site of origin, and understand their implications. Pain is considered separately in Chap. 14. ■ ■POSITIVE AND NEGATIVE SYMPTOMS Abnormal sensory symptoms can be divided into two categories: positive and negative. The prototypical positive symptom is tingling (pins and needles); other positive sensory phenomena include itch and altered sensations that are described as pricking, bandlike, lightninglike shooting feelings (lancinations), aching, knifelike, twisting, draw­ ing, pulling, tightening, burning, searing, electrical, or raw feelings. Such symptoms are often painful. Positive phenomena usually result from trains of impulses gener­ ated at sites of lowered threshold or heightened excitability along a peripheral or central sensory pathway. The nature and severity of the abnormal sensation depend on the number, rate, timing, and distribu­ tion of ectopic impulses and the type and function of nervous tissue in which they arise. Because positive phenomena represent excessive activity in sensory pathways, they are not necessarily associated with a sensory deficit (loss) on examination. Negative phenomena represent loss of sensory function and are characterized by diminished or absent feeling that often is experienced as numbness and by abnormal findings on sensory examination. In disorders affecting peripheral sensation, at least one-half of the affer­ ent axons innervating a particular site are probably lost or functionless before a sensory deficit can be demonstrated by clinical examination. If the rate of loss is slow, however, lack of cutaneous feeling may be unno­ ticed by the patient and difficult to demonstrate on examination, even though few sensory fibers are functioning; if it is rapid, both positive and negative phenomena are usually conspicuous. Subclinical degrees

of sensory dysfunction may be revealed by sensory nerve conduction studies or somatosensory-evoked potentials. Whereas sensory symptoms may be either positive or negative, sensory signs on examination are always a measure of negative phenomena. ■ ■TERMINOLOGY Paresthesias and dysesthesias are general terms used to denote positive sensory symptoms. The term paresthesias typically refers to tingling or pins-and-needles sensations but may include a wide variety of other abnormal sensations, except pain; it sometimes implies that the abnor­ mal sensations are perceived spontaneously. The more general term dysesthesias denotes all types of abnormal sensations, including painful ones, regardless of whether a stimulus is evident. Another set of terms refers to sensory abnormalities found on exam­ ination. Hypesthesia or hypoesthesia refers to a reduction of cutaneous sensation to a specific type of testing such as pressure, light touch, and warm or cold stimuli; anesthesia, to a complete absence of skin sensa­ tion to the same stimuli plus pinprick; and hypalgesia or analgesia, to reduced or absent pain perception (nociception). Hyperesthesia means pain or increased sensitivity in response to touch. Similarly, allodynia describes the situation in which a nonpainful stimulus, once perceived, is experienced as painful, even excruciating. An example is elicitation of a painful sensation by application of a vibrating tuning fork. Hyperal­ gesia denotes severe pain in response to a mildly noxious stimulus, and hyperpathia, a broad term, encompasses all the phenomena described by hyperesthesia, allodynia, and hyperalgesia. With hyperpathia, the threshold for a sensory stimulus is increased and perception is delayed, but once felt, it is unduly painful. Disorders of deep sensation arising from muscle spindles, tendons, and joints affect proprioception (position sense). Manifestations include imbalance (particularly with eyes closed or in the dark), clum­ siness of precision movements, and unsteadiness of gait, which are referred to collectively as sensory ataxia. Other findings on examina­ tion usually, but not invariably, include reduced or absent joint posi­ tion and vibratory sensation and absent deep tendon reflexes in the affected limbs. The Romberg sign is positive, which means that the patient sways markedly or topples when asked to stand with feet close together and eyes closed. In severe states of deafferentation involving deep sensation, the patient cannot walk or stand unaided or even sit unsupported. Continuous involuntary movements (pseudoathetosis) of the outstretched hands and fingers occur, particularly with eyes closed. ■ ■ANATOMY OF SENSATION Cutaneous receptors are classified by the type of stimulus that opti­ mally excites them. They consist of naked nerve endings (nociceptors, which respond to tissue-damaging stimuli, and thermoreceptors, which respond to noninjurious thermal stimuli) and encapsulated terminals (several types of mechanoreceptor, activated by physical deformation of the skin or stretch of muscles). Each type of receptor has its own set of sensitivities to specific stimuli, size and distinctness of receptive fields, and adaptational qualities. Afferent peripheral nerve fibers conveying somatosensory informa­ tion from the limbs and trunk traverse the dorsal roots and enter the dorsal horn of the spinal cord (Fig. 27-1); the cell bodies of first-order neurons are located in the dorsal root ganglia (DRG). In an analogous fashion, sensations from the face and head are conveyed through the trigeminal system (Fig. 452-2). Once fiber tracts enter the spinal cord, the polysynaptic projections of the smaller fibers (unmyelinated and small myelinated), which subserve mainly nociception, itch, tempera­ ture sensibility, and touch, cross and ascend in the opposite anterior and lateral columns of the spinal cord, through the brainstem, to the ventral posterolateral (VPL) nucleus of the thalamus and ultimately project to the postcentral gyrus of the parietal cortex and other cortical areas (Chap. 14). This is the spinothalamic pathway or anterolateral system. The larger fibers, which subserve tactile and position sense and kinesthesia, project rostrally in the posterior and posterolateral columns on the same side of the spinal cord and make their first syn­ apse in the gracile or cuneate nucleus of the lower medulla. Axons of

Leg Trunk Post-central cortex Arm Thalamus Face Internal capsule Ventral posterolateral nucleus of thalamus MIDBRAIN Principal sensory nucleus of V PONS Medial lemniscus Nucleus of funiculus gracilis Nucleus of funiculus cuneatus MEDULLA Spinothalamic tract Nucleus of spinal tract V Posterior column fibers SPINAL CORD Spinothalamic tract FIGURE 27-1  The main somatosensory pathways. The spinothalamic tract (pain, thermal sense) and the posterior column–lemniscal system (touch, pressure, joint position) are shown. Offshoots from the ascending anterolateral fasciculus (spinothalamic tract) to nuclei in the medulla, pons, and mesencephalon and nuclear terminations of the tract are indicated. (Reproduced with permission from AH Ropper, MA Samuels: Adams and Victor’s Principles of Neurology, 9th ed. New York, McGraw-Hill, 2009.) second-order neurons decussate and ascend in the medial lemniscus located medially in the medulla and in the tegmentum of the pons and midbrain and synapse in the VPL nucleus; third-order neurons project to parietal cortex as well as to other cortical areas. This large-fiber system is referred to as the posterior column–medial lemniscal pathway (lemniscal, for short). Although the fiber types and functions that make up the spinothalamic and lemniscal systems are relatively well known, many other fibers, particularly those associated with touch, pressure, and position sense, ascend in a diffusely distributed pattern both ipsilaterally and contralaterally in the anterolateral quadrants of the spinal cord. This explains why a complete lesion of the posterior columns of the spinal cord may be associated with little sensory deficit on examination. APPROACH TO THE PATIENT Clinical Examination of Sensation The main components of the sensory examination are tests of pri­ mary sensation (pain, touch, vibration, joint position, and thermal sensation) (Table 27-1). The examiner must depend on patient responses, and this complicates interpretation. Further, examina­ tion may be limited in some patients. In a stuporous patient, for

example, sensory examination is reduced to observing the briskness of withdrawal in response to a pinch or another noxious stimulus. Comparison of responses on the two sides of the body is essential. In an alert but uncooperative patient, it may not be possible to examine cutaneous sensation, but some idea of proprioceptive function may be gained by noting the patient’s best performance of movements requiring balance and precision. In patients with sensory complaints, testing should begin in the center of the affected region and proceed radially until sensa­ tion is perceived as normal. The distribution of any abnormality is defined and compared to root and peripheral nerve territories (Figs. 27-2 and 27-3). Some patients present with sensory symp­ toms that do not fit an anatomic localization and are accompanied by either no abnormalities or gross inconsistencies on examination. The examiner should consider in such cases the possibility of a psychological cause (see “Psychogenic Symptoms,” below). Sensory examination of a patient who has no neurologic complaints can be brief and consist of pinprick, touch, and vibration testing in the hands and feet plus evaluation of stance and gait, including the Romberg maneuver (Chap. V6). Evaluation of stance and gait also tests the integrity of motor and cerebellar systems. Numbness, Tingling, and Sensory Loss CHAPTER 27 PRIMARY SENSATION The sense of pain usually is tested with a clean pin, which is then discarded. The patient is asked to close the eyes and focus on the pricking or unpleasant quality of the stimulus, not just the pressure or touch sensation elicited. Areas of hypalgesia should be mapped by proceeding radially from the most hypalgesic site. Temperature sensation to both hot and cold is best tested with small containers filled with water of the desired temperature. An alternative way to test cold sensation is to touch a metal object, such as a tuning fork at room temperature, to the skin. For testing warm temperatures, the tuning fork or another metal object may be held under warm water of the desired temperature and then used. The appreciation of both cold and warmth should be tested because different receptors respond to each. Touch usually is tested with a wisp of cotton, mini­ mizing pressure on the skin. In general, it is better to avoid testing touch on hairy skin because of the profusion of the sensory endings that surround each hair follicle. The patient is tested with the eyes closed and should respond as soon as the stimulus is perceived, indicating its location. Joint position testing is a measure of proprioception. With the patient’s eyes closed, joint position is tested in the distal inter­ phalangeal joint of the great toe and fingers. The digit is held by its sides, distal to the joint being tested, and moved passively while more proximal joints are stabilized—the patient indicates the change in position or direction of movement. If errors are made, more proximal joints are tested. A test of proximal joint position sense, primarily at the shoulder, is performed by asking the patient to bring the two index fingers together with arms extended and eyes closed. Normal individuals can do this accurately, with errors of 1 cm or less. The sense of vibration is tested with an oscillating tuning fork that vibrates at 128 Hz. Vibration is tested over bony points, begin­ ning distally; in the feet, it is tested over the dorsal surface of the distal phalanx of the big toes and at the malleoli of the ankles, and in the hands, it is tested dorsally at the distal phalanx of the fingers. If abnormalities are found, more proximal sites should be examined. Vibratory thresholds at the same site in the patient and the exam­ iner may be compared for control purposes. CORTICAL SENSATION The most commonly used tests of cortical function are two-point discrimination, touch localization, and bilateral simultaneous stim­ ulation, and tests for graphesthesia and stereognosis. Abnormalities of these sensory tests, in the presence of normal primary sensation in an alert cooperative patient, signify a lesion of the parietal cortex or thalamocortical projections. If primary sensation is altered, these

TABLE 27-1  Testing Primary Sensation SENSE TEST DEVICE ENDINGS ACTIVATED FIBER SIZE MEDIATING CENTRAL PATHWAY Pain Pinprick Cutaneous nociceptors Small SpTh, also D Temperature, heat Warm metal object Cutaneous thermoreceptors for hot Small SpTh Temperature, cold Cold metal object Cutaneous thermoreceptors for cold Small SpTh Touch Cotton wisp, fine brush Cutaneous mechanoreceptors, also naked endings Vibration Tuning fork, 128 Hz Mechanoreceptors, especially pacinian corpuscles Joint position Passive movement of specific joints Joint capsule and tendon endings, muscle spindles PART 2 Cardinal Manifestations and Presentation of Diseases Abbreviations: D, diffuse ascending projections in ipsilateral and contralateral anterolateral columns; Lem, posterior column and lemniscal projection, ipsilateral; SpTh, spinothalamic projection, contralateral. cortical discriminative functions usually will be abnormal also. Comparisons should always be made between analogous sites on the two sides of the body because the deficit with a specific parietal lesion is likely to be unilateral. Two-point discrimination can be tested with calipers, the points of which may be set from 2 mm to several centimeters apart and then applied simultaneously to the test site. On the fingertips, a nor­ mal individual can distinguish about a 3-mm separation of points. Touch localization is performed by light pressure for an instant with the examiner’s fingertip or a wisp of cotton wool; the patient, whose eyes are closed, is asked to identify the site of touch. Bilateral simultaneous stimulation at analogous sites (e.g., the dorsum of I II Great auricular n. III Ant. cut. n. of neck Supraclavicular n’s. Axillary n. (circumflex) T2

Ant. Med. cut. n. of arm & intercostobrachial n. cut. Lower lat. cut. n. of arm (from radial n.) Lat. rami of cut. thor. Med. cut. n. of forearm Lat. cut. of forearm (from musculocut. n.) n’s. rami Iliohypogastric n. Iliohypogastric n. Radial n. Ilioinguinal n. Ilioinguinal n. Median n. Genital branch of genitofem. n. Femoral branch of genito- femoral n. (lumbo-inguinal n.)
Ulnar n. Dorsal n. of penis Lat. cut. n. of thigh Intermed. & med. cut. n’s. of thigh (from femoral n.) Scrotal branch of perineal n. Obturator n. Saphenous n. (from femoral n.) Lat. cut. n. of calf (from common peroneal n.) Superficial peroneal n. (from common peroneal n.) Deep peroneal n. (from common peroneal n.) Med. & lat. plantar n’s. (from posttibial n.) Sural n. (from tibial n.) FIGURE 27-2  The cutaneous fields of peripheral nerves. (Reproduced with permission from W Haymaker, B Woodhall: Peripheral Nerve Injuries, 2nd ed. Philadelphia, Saunders, 1953.)

Large and small Lem, also D and SpTh Large Lem, also D Large Lem, also D both hands) can be carried out to determine whether the percep­ tion of touch is extinguished consistently on one side (extinction or neglect). Graphesthesia refers to the capacity to recognize, with eyes closed, letters or numbers drawn by the examiner’s fingertip on the palm of the hand. Once again, side-to-side comparison is of prime importance. Inability to recognize numbers or letters is termed agraphesthesia. Stereognosis refers to the ability to identify common objects by palpation, recognizing their shape, texture, and size. Common standard objects such as keys, paper clips, and coins are best used. Patients with normal stereognosis should be able to distinguish a dime from a penny and a nickel from a quarter without looking. Greater Lesser n. occipital nerves Great auricular n. Ant. cut. n. of neck C5 C6 Supraclavicular n’s. T1 T2

5 6 7 8 9 10 11 12 Post. cut. rami of thor. n’s. Axillary n. (circumflex) Lat. cut.
rami
Med. cut. n. of arm & intercostobrachial n. Post cut. n. of arm (from radial n.) Post. cut. n. of forearm (from radial n.) Lower Lat. cut. of arm (from radial n.) L1 Lat. cut. n. of forearm (from musculocut n.) Med. cut. n. of forearm S1 Post. rami of lumbar sacral & coccygeal n’s. Radial n. Iliohypogastric n. Ulnar n. Inf. med. cluneal n. Inf. lat. cluneal n’s. Median n. Inf. med. n. of thigh Obturator n. Post cut. n. of thigh Med. cut. n. of thigh (from femoral n.) Lat. cut. n.of calf (from common femoral n.) Lat. plantar n. Med. plantar n. Lat. plantar n. Saphenous n. (from femoral n.) Superficial peroneal n. Superficial peroneal n. (from common peroneal n.) Saphenous n. Sural n. (from tibial n.) Sural n. Calcanean branches of tibial & sural n’s. Calcanean branches of sural & tibial n’s.

FIGURE 27-3  Distribution of the sensory spinal roots on the surface of the body (dermatomes). (Reproduced with permission from Receptors of the somatosensory system. In ER Kandel, JD Koester, SH Mack, SA Siegelbaum. Principles of Neural science, 6th ed. New York: McGraw Hill; 2021.) Patients should feel the object with only one hand at a time. If they are unable to identify it in one hand, it should be placed in the other for comparison. Individuals who are unable to identify common objects and coins in one hand but can do so in the other are said to have astereognosis of the abnormal hand. QUANTITATIVE SENSORY TESTING Effective sensory testing devices are commercially available. Quan­ titative sensory testing is particularly useful for serial evaluation of cutaneous sensation in clinical trials. Threshold testing for touch and vibratory and thermal sensation is the most widely used application. ELECTRODIAGNOSTIC STUDIES AND NERVE BIOPSY Nerve conduction studies and nerve biopsy are important means of investigating the peripheral nervous system, but they do not evalu­ ate the function or structure of cutaneous receptors and free nerve endings or of unmyelinated or thinly myelinated nerve fibers in the nerve trunks. Skin biopsy can be used to evaluate these structures in the dermis and epidermis. ■ ■LOCALIZATION OF SENSORY ABNORMALITIES Sensory symptoms and signs can result from lesions at many different levels of the nervous system from the parietal cortex to the peripheral sensory receptor. Noting their distribution and nature is the most important way to localize their source. Their extent, configuration, symmetry, quality, and severity are the key observations.

Numbness, Tingling, and Sensory Loss CHAPTER 27 Dysesthesias without sensory findings by examination may be difficult to interpret. To illustrate, tingling dysesthesias in an acral distribution (hands and feet) can be systemic in origin, for example, secondary to hyperventilation, or induced by a medication such as acetazolamide. Distal dysesthesias can also be an early event in an evolving polyneuropathy or may herald a myelopathy, such as from vitamin B12 deficiency. Sometimes, distal dysesthesias have no defin­ able basis. In contrast, dysesthesias that correspond in distribution to that of a particular peripheral nerve structure denote a lesion at that site. For instance, dysesthesias restricted to the fifth digit and the adja­ cent one-half of the fourth finger on one hand reliably point to disorder of the ulnar nerve, most commonly at the elbow. Nerve and Root  In focal nerve trunk lesions, sensory abnormalities are readily mapped and generally have discrete boundaries (Figs. 27-2 and 27-3). Root (“radicular”) lesions frequently are accompanied by deep, aching pain along the course of the related nerve trunk. With compression of a fifth lumbar (L5) or first sacral (S1) root, as from a ruptured intervertebral disk, sciatica (radicular pain relating to the sciatic nerve trunk) is a common manifestation (Chap. 18). With a lesion affecting a single root, sensory deficits may be minimal or absent because adjacent root territories overlap extensively. Isolated mononeuropathies may cause symptoms beyond the terri­ tory supplied by the affected nerve, but abnormalities on examination typically are confined to expected anatomic boundaries. In multiple mononeuropathies, symptoms and signs occur in discrete territories supplied by different individual nerves and—as more nerves are

affected—may simulate a polyneuropathy if deficits become confluent. With polyneuropathies, sensory deficits are generally graded, distal, and symmetric in distribution (Chap. 457). Dysesthesias, followed by numbness, begin in the toes and ascend symmetrically. When dysesthesias reach the knees, they usually also have appeared in the fingertips. The process is nerve length–dependent, and the deficit is often described as “stocking glove” in type. Involvement of both hands and feet also occurs with lesions of the upper cervical cord or the brainstem, but an upper level of the sensory disturbance may then be found on the trunk and other evidence of a central lesion may be pres­ ent, such as sphincter involvement or signs of an upper motor neuron lesion (Chap. 26). Although most polyneuropathies are pansensory and affect all modalities of sensation, selective sensory dysfunction according to nerve fiber size may occur. Small-fiber polyneuropathies are characterized by burning, painful dysesthesias with reduced pin­ prick and thermal sensation but with sparing of proprioception, motor function, and deep tendon reflexes. Touch is involved variably; when it is spared, the pattern is referred to as a dissociated sensory loss. Impor­ tantly, sensory dissociation may occur also with spinal cord lesions (Chap. 453, and below). Large-fiber polyneuropathies are character­ ized by vibration and position sense deficits, imbalance, absent tendon reflexes, and variable motor dysfunction but preservation of most cutaneous sensation. Dysesthesias, if present at all, tend to be tingling or bandlike in quality.

PART 2 Cardinal Manifestations and Presentation of Diseases Sensory neuronopathy (or ganglionopathy) is characterized by widespread but asymmetric sensory loss occurring in a non-length-

dependent manner so that it may occur proximally or distally, and in the arms, legs, or both. Pain and numbness progress to sensory ataxia and impairment of all sensory modalities over time. This condition is usually paraneoplastic or idiopathic in origin (Chaps. 99 and 457) or related to an autoimmune disease, particularly Sjögren’s syndrome (Chap. 373). Spinal Cord  (See also Chap. 453) If the spinal cord is transected, all sensation is lost below the level of transection. Bladder and bowel function also are lost, as is motor function. Lateral hemisection of the spinal cord produces the Brown-Séquard syndrome, with absent pain and temperature sensation contralaterally and loss of proprioceptive sensation and power ipsilaterally below the lesion (see Figs. 27-1 and 453-1); ipsilateral pain or hyperesthesia may also occur. Numbness or paresthesias in both feet may arise from a spinal cord lesion; this is especially likely when the upper level of the sensory loss extends to the trunk. When all extremities are affected, the lesion is probably in the cervical region or brainstem unless a peripheral neuropathy is responsible. The presence of upper motor neuron signs (Chap. 26) supports a central lesion; a hyperesthetic band on the trunk may suggest the level of involvement. A dissociated sensory loss can reflect spinothalamic tract involve­ ment in the spinal cord, especially if the deficit is unilateral and has an upper level on the torso. Bilateral spinothalamic tract involvement occurs with lesions affecting the center of the spinal cord, such as in syringomyelia. There is a dissociated sensory loss with impairment of pinprick and temperature appreciation but relative preservation of light touch, position sense, and vibration appreciation. Dysfunction of the posterior columns in the spinal cord or of the posterior root entry zone may lead to a bandlike sensation around the trunk or a feeling of tight pressure in one or more limbs. Flexion of the neck sometimes leads to an electric shock–like sensation that radiates down the back and into the legs (Lhermitte’s sign) in patients with a cervical lesion affecting the posterior columns, such as from multiple sclerosis, cervical spondylosis, or following irradiation to the cervical region. Brainstem  Crossed patterns of sensory disturbance, in which one side of the face and the opposite side of the body are affected, local­ ize to the lateral medulla. Here a small lesion may damage both the ipsilateral descending trigeminal tract and trigeminal nucleus, plus the ascending spinothalamic fibers subserving the opposite arm, leg, and

hemitorso (see “Lateral medullary syndrome” in Fig. 437-7). A lesion in the tegmentum of the pons and midbrain, where the lemniscal and spinothalamic tracts merge, causes pansensory loss contralaterally. Thalamus  Hemisensory disturbance with tingling numbness from head to foot is often thalamic in origin but also can arise from the ante­ rior parietal region. If abrupt in onset, the lesion is likely to be due to a small stroke (lacunar infarction), particularly if localized to the thala­ mus. Occasionally, with lesions affecting the VPL nucleus or adjacent white matter, a syndrome of thalamic pain, also called Déjerine-Roussy syndrome, may ensue. The severe, persistent, unrelenting unilateral pain often is described in dramatic terms. Cortex  With lesions of the parietal lobe involving either the cortex or subjacent white matter, the most prominent symptoms are contra­ lateral hemineglect, hemi-inattention, and a tendency not to use the affected hand and arm. On cortical sensory testing (e.g., two-point discrimination, graphesthesia), abnormalities are often found, but pri­ mary sensation is usually intact. Anterior parietal infarction may pres­ ent as a pseudothalamic syndrome with contralateral loss of primary sensation from head to toe. Dysesthesias or a sense of numbness and, rarely, a painful state may also occur. Focal Sensory Seizures  These seizures generally are due to lesions in the area of the postcentral or precentral gyrus. The principal symptom of focal sensory seizures is tingling, but additional, more complex sensations may occur, such as a rushing feeling, a sense of warmth, or a sense of movement without detectable motion. Symptoms typically are unilateral; commonly begin in the arm or hand, face, or foot; and often spread in a manner that reflects the cortical represen­ tation of different bodily parts, a pattern referred to as a Jacksonian march. Their duration is variable; seizures may be transient, lasting only for seconds, or persist for an hour or more. Focal motor features may supervene, often becoming generalized with loss of consciousness and tonic-clonic jerking. Psychogenic Symptoms  Sensory symptoms can have a psycho­ genic basis. Such symptoms may be generalized or have an anatomic boundary that is difficult to explain neurologically, for example, cir­ cumferentially at the groin or shoulder or around a specific joint. Pain is common, but the nature and intensity of any sensory disturbances are variable. The diagnosis should not be one of exclusion but based on suggestive findings that are otherwise difficult to explain, such as mid­ line splitting of impaired vibration, pinprick, or light touch apprecia­ tion; variability or poor reproducibility of sensory deficits; or normal performance of tasks requiring sensory input that is seemingly abnor­ mal on formal testing, such as good performance with eyes closed of the finger-to-nose test despite an apparent loss of position sense in the upper limb. The side with abnormal sensation may be confused when the limbs are placed in an unusual position, such as crossed behind the back. Sensory complaints should not be regarded as psychogenic simply because they are unusual. ■ ■TREATMENT Management is based on treatment of the underlying condition. Symp­ tomatic treatment of acute and chronic pain is discussed in Chap. 14. Dysesthesias, when severe and persistent, may respond to anticonvul­ sants (carbamazepine, 100–1000 mg/d; gabapentin, 300–3600 mg/d; or pregabalin, 50–300 mg/d), antidepressants (amitriptyline, 25–150 mg/d; nortriptyline, 25–150 mg/d; desipramine, 100–300 mg/d; or venlafax­ ine, 75–225 mg/d). ■ ■FURTHER READING Brazis P et al: Localization in Clinical Neurology, 8th ed. Philadelphia, Lippincott William & Wilkins, 2021. Campbell WW, Barohn RJ: DeJong’s The Neurological Examination, 8th ed. Philadelphia, Lippincott William & Wilkins, 2019. Waxman S: Clinical Neuroanatomy, 30th ed. New York, McGraw Hill Education, 2024.