Sensory Abnormalities of the Limbs, Trunk, and Face

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Chapter 28 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. Despite the best efforts of the clinician to make the sensory examination as precise as possible, inconsistency in the patient’s responses is common, and the types of sensory abnormalities may differ greatly among patients. Nevertheless, identifying sensory deficits is important in localizing lesions.

Accurate localization begins with a foundation of detailed anatomy. Presence or absence of motor deficits are also aids to differentiating anatomical localization, so sensory data are always considered together with evidence of other neurological dysfunction.

Anatomy and Physiology

Sensory Transduction

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 to the spinal cord by the sensory axons.

Sensory transducers are seldom directly affected by neuropathic conditions, although peripheral vascular disease can produce dysfunction of the skin sensory axons, and systemic sclerosis can damage skin sufficiently to produce a primary deficit of sensory transduction (Table 28.1).

Table 28.1 Sensory Receptors

Sensory Afferents

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. Non-nociceptive afferents are large-diameter myelinated axons. Afferent fiber characteristics are shown in Table 28.2.

Table 28.2 Sensory Afferents

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 conduction of pain and temperature information, some non-nociceptive 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. 28.1 shows the ascending pathways through the spinal cord to the brain.

Fig. 28.1 Axial section of the spinal cord, showing dorsal and ventral roots forming a spinal nerve. Sensory afferents give rise to two major ascending pathways: the anterolateral system (nociceptive, serving thermal sensation primarily) and posterior columns (serving large-fiber modalities primarily including touch, vibration, and proprioception). Inhibitory input derives from descending fibers as well as collaterals, via interneurons, from mechanoreceptive fibers. Dashed circle indicates the anterior white commissure. DRG, Dorsal root ganglion.

(Modified with permission from Rizzo, M.A., Kocsis, J.D., Waxman, S.G., 1996. Mechanisms of paresthesiae, dysesthesiae, and hyperesthesiae: role of Na⁺ channel heterogeneity. Eur Neurol 36, 3-12.)

Brain Pathways

Sensory Abnormalities

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

Neuropathic pain can result from damage of any cause to the sensory nerves. Peripheral neuropathic conditions result in failure of conduction of the sensory fibers, giving decreased sensory function plus pain from discharge of damaged nociceptive axons. The pathophysiology of neuropathic pain is interesting. Part of its basis is lowering of the membrane potential of the axons so that minor deformation of the nerve can produce repetitive action-potential discharges (Zimmermann, 2001). An additional feature with neuropathic conditions appears to be membrane potential instability, so that the crests of fluctuations of membrane potential can produce action potentials. Finally, cross-talk (ephaptic transmission) 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 seen on neurological examination.

Localization of Sensory Abnormalities

A general guide to sensory localization is presented in Table 28.3. Guidelines for diagnosis of these sensory abnormalities are summarized in Table 28.4. Details of specific sensory levels of dysfunction are discussed next.

Table 28.3 Sensory Localization

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

Table 28.4 Diagnosis of Sensory Abnormalities

Peripheral Sensory Lesions

Lesions of peripheral nerves and the plexuses produce sensory loss that follows their peripheral anatomical distribution. Exact mapping of sensory deficit is commonly difficult because sensory testing is subjective. Also recognized are interindividual differences in sensory peripheral anatomy including distribution and overlap of sensory fields. 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, and mapping of the deficit should make the diagnosis.

Sensory loss affecting an entire limb seldom is due to a peripheral lesion, because even proximal plexus lesions rarely affect the entire limb. 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 the examination will show no loss of sensory function.

Fig. 28.2 summarizes the peripheral nerve anatomy of the body, and Fig. 28.3 shows the dermatomal distribution.

Fig. 28.2 Cutaneous (cut.) fields of peripheral nerves (n.). Note that thoracic dermatomes are innervated by primary anterior and posterior rami of spinal nerves from the respective level. Spinous processes of T1, L1, and S1 are indicated. inf., Inferior; lat., lateral; med., median.

(Reprinted with permission from Haymaker, W., Woodall, B., 1953. Peripheral Nerve Injuries: Principles of Diagnosis. W.B. Saunders, Philadelphia.)

Fig. 28.3 Dermatomes: cervical (C), thoracic (T), lumbar (L), and sacral (S). Boundaries are not quite as distinct as shown here because of overlapping innervation and variability among individuals.

(Reprinted with permission from Martin, J.H., Jessell, T.M., 1991. Anatomy of the somatic sensory system. In: Kandel, E.R. (Ed.), Principles of Neural Science. Appleton & Lange, Norwalk, Conn.)

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 side. The term also can be used to describe loss of one sensory modality (e.g., pain and temperature) with normality of the other sensory modality—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 disturbance of sensory function in the legs, with preservation of perianal sensation.

Sensory Level

A spinal localization is suggested by loss of sensation below a certain spinal level (i.e., 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 commonly is thought of as being associated with inflammatory conditions such as multiple sclerosis, it more commonly is seen with cervical spondylotic myelopathy and has been reported after radiation therapy affecting the cervical spinal cord and also 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 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, although if an inflammatory lesion is suspected, a contrasted study on a high-field scanner has greater diagnostic sensitivity (Runge, Muroff, and Jinkins, 2001).

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 the lesion. This dissociation of sensory loss is most prominent in patients with intrinsic spinal cord lesions such as tumors but 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, so deficit of pain and temperature 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, and occasionally in focal spinal cord mass lesions.

Suspended Sensory Loss

A third form of dissociated sensory loss 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 is seen in syringomyelia (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 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 usually is trauma, but intrinsic mass lesions also can 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. The diagnosis is clinical, and MRI can serve to eliminate other possibilities.

Lateral medullary syndrome typically results from occlusion of the posterior inferior 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; these 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 also can produce contralateral sensory loss, but as with the aforementioned syndromes, the sensory findings are trivial compared with the motor findings.

Cerebral Sensory Lesions

Thalamic Lesions

Pure sensory deficit of cerebral origin usually arises from damage to the thalamus. The thalamus receives vascular supply from the thalamoperforate arteries, which are branches of the posterior cerebral arteries, often with some contribution from the posterior communicating arteries. In some patients, both thalami are supplied by one posterior cerebral artery, so bilateral thalamic infarction can develop from unilateral arterial occlusion. Thalamic pain syndrome is an occasional sequela of a thalamic sensory stroke and is characterized by spontaneous pain localized to the distal arm and leg, exacerbated by contact and stress.

Cortical Lesions

Lesions of the postcentral gyrus produce more sensory symptoms than motor symptoms. Infarction of this region involving a branch of the middle cerebral artery can produce sensory loss with little or no motor loss. More posterior lesions may spare the primary modalities of sensation (pain, temperature, touch, joint position) but instead impair higher sensory function, with manifestations such as graphesthesia, two-point discrimination, and the perception of double simultaneous stimuli.

Common Sensory Syndromes

Some common sensory syndromes are outlined in Table 28.5. Many of these are associated with motor deficits as well.

Table 28.5 Common Sensory Syndromes

Peripheral Syndromes

Sensory Polyneuropathy

The most common presenting complaint among patients with distal symmetrical peripheral polyneuropathy is sensory disturbance. The disturbance can be negative (decreased discrimination and increased threshold) or positive (neuropathic pain, paresthesias, dysesthesias), or both. Most neuropathies involve motor and sensory fibers, although the initial symptoms usually are sensory.

Nerve conduction studies can evaluate the status of the myelin sheath, thereby identifying patients with predominantly demyelinating polyneuropathies, including acute inflammatory demyelinating polyneuropathy (AIDP) and chronic inflammatory demyelinating polyneuropathy (CIDP). Electromyography (EMG) can demonstrate denervation and hence axonal damage, thereby identifying the motor involvement of many neuropathies with predominantly axonal features (Misulis and Head, 2002).

Cerebrospinal fluid (CSF) study is rarely performed for isolated neuropathy, but in patients with autoimmune demyelinating neuropathies, it will show increased protein levels. Increased cellularity suggests an inflammatory cause.

Muscle biopsy usually is performed for evaluation of myopathy but in neuropathy may show denervation and reinnervation. Nerve biopsy can show several of the important causes of neuropathy including inflammatory infiltrates, segmental demyelination, amyloid deposition, and axonal dropout. Nerve and muscle biopsy should be left to those who have expertise in performing the procedure and interpreting the data.

Diabetic Neuropathies

Diabetic sensory neuropathy affects mainly small myelinated and unmyelinated axons, thereby producing disordered pain and temperature sensation. The findings often appear to be a paradox to the affected patient: loss of sensation yet with burning pain. Pathophysiologically, this makes perfect sense. The damaged axons cannot carry the patterns of action potentials, which accounts for the loss of sensation, yet spontaneous action potentials from damaged nerve endings, plus increased susceptibility to discharge from mechanical stimuli, cause the perceived neuropathic pain.

Acquired Immunodeficiency Syndrome–Associated Neuropathies

Human immunodeficiency virus type 1 (HIV-1) infection can produce a variety of neuropathic presentations. One of the most common is a painful, predominantly sensory polyneuropathy (Robinson-Papp and Simpson, 2009). The diagnosis can be confirmed by nerve conduction studies, EMG, and the appropriate clinical findings. CSF analysis and biopsy usually are not necessary unless an HIV-1–associated vasculitis or infection (such as cytomegalovirus) is present.

Some toxic neuropathies can be predominantly sensory. Such presentations most commonly are seen in patients with chemotherapy-induced peripheral neuropathy (Gutiérrez-Gutiérrez et al., 2010). Although motor abnormalities do occur, the sensory symptoms eclipse the motor symptoms for most patients. Development of dysesthesias, burning, and loss of sensation is the characteristic presentation. The neuropathy can be severe enough to be dose limiting for some patients and may continue to progress for months after cessation of chemotherapy administration, after which time some recovery is expected.

Patients with neuropathy that develops during chemotherapy can be presumed to have toxic neuropathy. If the association is not clear, however, other possibilities should be considered, including paraneoplastic and nutritional causes. Atypical features of chemotherapy-induced neuropathy include appearance of symptoms after completion of the chemotherapy regimen and development of prominent neuropathy with administration of agents that are seldom neurotoxic.

Amyloid Neuropathy

Primary amyloidosis can produce a predominantly sensory neuropathy in approximately one third of affected patients (Simmons and Specht, 2010). Familial amyloid polyneuropathy is a dominantly inherited condition. Patients present with painful dysesthesias plus loss of pain and temperature sensation. Weakness develops later. Autonomic dysfunction is typical. Eventually the sensory loss can be severe enough to make the affected extremities virtually anesthetic. The diagnosis can be suspected on clinical grounds, and confirmation requires positive results on either DNA genetic testing or nerve biopsy. Findings on nerve conduction studies and the EMG are not specific.

Proximal Sensory Loss

Proximal sensory loss involving the trunk and upper aspects of the arms and legs is uncommon but can be seen in patients with porphyria or diabetes and in some patients with proximal plexopathies with a restricted distribution. Other rare causes of proximal sensory loss include Tangier disease, Sjögren syndrome, and paraneoplastic syndrome (Rudnicki and Dalmau, 2005). These neuropathic processes can be associated with pain in addition to the sensory loss. Motor deficit also is common, with weakness in a proximal distribution.

Patients with thoracic sensory loss also should be evaluated for thoracic spinal cord lesion, which may not always be associated with corticospinal tract signs.

Temperature-Dependent Sensory Loss

Leprosy can produce sensory deficits that predominantly affect cooler regions of the skin including the fingers, toes, nose, and ears (Wilder-Smith and Van Brakel, 2008). Temperature sensation initially is impaired, with subsequent involvement of pain and touch sensation in the cooler skin regions. The deficit gradually ascends to warmer areas, typically in a stocking-glove distribution, with frequent trigeminal and ulnar nerve involvement. The diagnosis of leprosy is suggested by these findings and can be confirmed by additional testing including assay for antibodies to phenolic glycolipid-I (PGL-I) and nerve biopsy.

Acute Inflammatory Demyelinating Polyradiculoneuropathy

Acute inflammatory demyelinating polyradiculoneuropathy (AIDP), or Guillain-Barré syndrome, is an autoimmune process characterized by rapid progression of inflammatory demyelination of the nerve roots and peripheral nerves. Patients present with generalized weakness that may spread from the legs upwards or occasionally from cranial motor nerves downwards. Sensory symptoms generally are overshadowed by the motor loss. Tendon reflexes are lost as the weakness progresses (Hughes and Cornblath, 2005).

The diagnosis of AIDP is suspected in a patient who presents with progressive weakness with areflexia. Nerve conduction studies can confirm slowing, especially proximally (F-waves are particularly affected). CSF analysis shows increased protein level without a prominent cellular response (albuminocytological dissociation).

Mononeuropathy

Of the many recognized mononeuropathies, the most common is carpal tunnel syndrome, with ulnar neuropathy a close second. Although not classically considered a mononeuropathy, radiculopathy can be considered to fall into this category because one peripheral nerve unit is affected.

Carpal Tunnel Syndrome

Compression of the median nerve at the wrist produces sensory loss on the palmar aspects of the first through the third digits. Motor symptoms and signs can develop with increasing severity of the mononeuropathy, but the sensory symptoms predominate, especially early in the course. Weakness and wasting of the abductor pollicis brevis can develop (Bland, 2005).

Nerve conduction studies usually show slowing of sensory and motor conduction of the median nerve through the carpal tunnel at the wrist. The slowing is present when conduction elsewhere is normal or at least when the distal slowing is far out of proportion to the slowing from neuropathy elsewhere. The EMG findings usually are normal, but denervation in the abductor pollicis brevis may develop with severe disease. MRI or ultrasound examination of the distal median nerve sometimes is used, though neither of these studies is part of routine evaluation.

Ulnar Neuropathy

Ulnar neuropathy is commonly due to compression in the region of the ulnar groove. Patients present with numbness in the ulnar two fingers (fourth and fifth digits). Weakness of the interossei develops with advanced ulnar neuropathy in any location, but sensory symptoms predominate, especially early in the course (Cut, 2007).

Motor nerve conduction studies show slowing of conduction across the elbow or wrist—the two common sites for ulnar nerve entrapment. Findings on sensory nerve conduction studies also will be abnormal if the lesion is at the wrist. EMG can show denervation in the ulnar-innervated intrinsic muscles of the hand; the muscle easiest to examine and study is the first dorsal interosseous muscle.

Radial Neuropathy

Radial neuropathy is often due to compression of the nerve in the spiral groove. Prototypically, this is seen in patients with alcohol intoxication, although cases are not confined to this association. Damage to the radial nerve in the spiral groove results in damage to muscles innervated distally to the triceps. Patients typically present with wrist drop, and sensory symptoms are minimal. Compression of the radial nerve distally in the forearm near the wrist can produce sensory loss and dysesthesias on the radial side of the dorsum of the hand, and in this case there is no motor loss.

Diagnosis is suspected clinically from the wrist drop in the absence of weakness of muscles of the arm innervated by other nerves; note that examination of median and ulnar-innervated muscles can be difficult if the radial deficit is severe. Sensory findings, when present, are typical. Sensory findings in a radial nerve distribution without motor involvement suggests distal radial sensory nerve damage (e.g., from pressure, handcuffs, intravenous catheter insertion, or other local trauma).

Radiculopathy

Radiculopathy commonly produces pain or sensory loss, or both, in the distribution of one or more nerve roots. Motor symptoms and signs develop with increasing severity, but sensory symptoms (usually pain) may be present for years without motor symptoms. Reflex abnormalities are common in radiculopathy, but such changes should be considered a sensory finding rather than a motor finding. Prominent weakness would have to be present to suppress a reflex, whereas mild sensory dysfunction may suppress or abolish the reflex.

Table 28.6 presents clinical features of common radiculopathies. Although cervical and lumbar radiculopathies are discussed here, any level can be affected. Diabetic radiculopathy and herpes zoster commonly affect thoracic dermatomes, as well as cervical and thoracic dermatomes usually unaffected by spondylosis or disk disease.

Table 28.6 Radiculopathies

Radiculopathy is best investigated using MRI. In patients younger than 45 years of age, the most common etiological disorder is disk disease. In older patients, spondylosis and osteophyte formation predominate. The latter is slower to progress and less likely to be associated with spontaneous remissions and exacerbations. EMG can be helpful to identify any axonal damage from radiculopathy, which may help determine the need, location, and timing of decompressive surgery.

Spinal Syndromes

Myelopathy

Myelopathy typically produces sensory loss, although the motor and reflex findings eclipse the sensory findings in most patients. Nevertheless, when a patient presents with back pain with or without leg weakness, a sensory level should be sought.

Some basic “pearls” regarding sensory testing in patients with suspected myelopathy follow:

A defined line-like level is not expected.

The sensory mapping is not as precise as that shown on dermatome charts.

The sensory loss is seldom complete, which makes precise localization even more difficult.

The sensory level may not be at the same level on the two sides of the body—a discrepancy of up to several levels can be seen.

Look for dissociated sensory loss due to crossed projections of pain/temperature versus uncrossed touch/proprioception projections.

Discrepancy in sensory level between posterior column and spinothalamic levels can occur because of intersegmental projections of the axons of the posterolateral (Lissauer) tract.

The sensory level may be much higher than might be expected from motor examination or pain. This is because the lesion may be much higher than indicated by the levels of clinical findings, reinforcing the basic precept that the examiner must start from the level of the symptoms and look up!

Syringomyelia

Syringomyelia is the presence of a syrinx, or fluid-filled space, in the spinal cord that extends over several to many segments. This is most commonly associated with a Chiari malformation (Koyanagi and Houkin, 2010). The pathogenic theory is that partial obstruction to CSF flow plus pressure waves in the CSF result in rupture of the central canal into the parenchyma of the spinal cord, which then produces symptoms by mechanical effects. The mass effect of the syrinx produces damage to the fibers crossing in the anterior commissure that are destined for the spinothalamic tract, which conveys pain and temperature sensation. With more severe enlargement of the syrinx, damage to the surrounding ascending tracts may occur, affecting sensation below the level of the lesion. By the time this develops, segmental motoneuron damage and descending corticospinal tract damage are almost always present, and clinical signs of these changes can be seen.