Evaluation of acute sensory loss involves clinical assessment of the nature of the sensory loss (Section I), localization of the pathologic process (Section II), association of other neurologic signs (Section III), evaluation of possible etiologies (Section IV), and diagnostic testing (Section V).
I. CLINICAL MANIFESTATIONS
The location, extent, and quality of the sensory deficit can help to localize the lesion and narrow the differential diagnosis, keeping in mind that often no sensory impairment can be found in persons reporting acute sensory disturbances. Conversely, the neurologic examination may show sensory deficits of which the patient is unaware.
A. Examination of sensory modalities in acute sensory loss.
1. Touch sensation is tested with a wisp of cotton or the light touch of a finger. The stimulus should be compared with that applied to the contralateral corresponding area with expected normal sensation.
2. Pain sensation is tested by indicating the intensity of the pinprick sensation in comparison with that in a corresponding area with normal pain sensation.
3. It must be determined if an area of decreased sensation suggests nerve root or peripheral nerve involvement. Dermatomal charts showing typical peripheral nerve or nerve root distributions vary somewhat from one book or study to another, and there can be variability among patients. Should the pinprick sensation indicate a decrease or loss of pain sensation at a certain level of the chest or abdomen, the level is determined more reliably by proceeding from the area of decreased or absent sensation to the area of normal sensation.
4. Position sense in fingers or toes is examined by holding the digit at the side opposite to the direction of movement. The patient is asked to identify the directions of passive flexion and extension.
5. Vibration sense is a composite sensation requiring preserved touch and deep pressure sensation. A 128-dv tuning fork should be used and placed over a boney prominence.
B. Positive sensory symptoms.
1. Paresthesia means spontaneous abnormal sensation frequently described as tingling, prickling, or “pins and needles.”
2. Dysesthesia is discomfort or pain triggered by normally painless stimuli.
3. Hyperesthesia indicates abnormally increased sensitivity to light touch, pinprick, or thermal sensation.
C. Negative sensory symptoms.
1. Numbness indicates decreased or absent sensation.
2. Anesthesia is complete loss of sensation.
3. Hypesthesia is decreased sensation.
4. Pallesthesia indicates loss of vibratory sensation.
D. Functional sensory loss. It often is difficult to establish with certainty that sensory impairment is functional, meaning inorganic or nonphysiologic. Functional sensory loss frequently occurs in a nonanatomic distribution, but so can CNS inflammatory demyelinating sensory loss. Losses of touch, pinprick, and vibration sensation exactly at the midline over the chest or abdomen, or in the entire limb with sharp delineation of the sensory loss, or poor reproducibility of the demarcation of the sensory deficits with repeated exams, all suggest functional sensory loss.
II. LOCALIZATION OF THE PATHOLOGIC PROCESSES
Localization of the pathologic processes resulting in acute sensory loss can be helpful in differential diagnostic considerations and in the selection of proper paraclinical investigations.
A. Sensory receptors.
1. Exteroceptors are localized in the skin and subserve superficial sensation to pain, touch, and temperature. The cutaneous sensory fibers run in sensory or mixed sensory and motor nerves. Sensory neurons have their cell bodies in the dorsal ganglia with their central projections to the posterior roots.
2. Proprioceptors are localized in deeper somatic structures, including tendons, muscles, and joints, dorsal columns of the spinal cord, and terminate in the gracile and cuneate nuclei of the medulla. The secondary afferent fibers from these nuclei cross the midline in the medulla and ascend in the brainstem as the medial lemniscus to the posterior thalamic complex. Proprioceptive information is carried through the spinocerebellar tracts in the lateral columns and in the cuneocerebellar and rostrocerebellar tracts in the dorsal columns of the cord.
B. Nerve roots. Individual nerve roots mediate sensation in segments oriented longitudinally in the extremities and horizontally over the trunk. Dermatomal charts depict typical nerve root distributions, but distributions vary from one study or book to another, and there can also be variability among patients.
C. Peripheral nerves. Dermatomal charts depict typical peripheral nerve and nerve bracnh distributions, but distributions vary from one study of book to another, and there can also be variability among patients.
D. Brachial and lumbosacral plexus. Acute sensorimotor deficits indicating multiple nerve or nerve root involvement in an arm or leg suggest plexopathy.
E. Spinal cord. Most fibers conducting pain and temperature sensation decussate over several segments by way of the ventral white commissure and ascend in the lateral columns of the cord as the lateral spinothalamic tract. Fibers conducting light touch and two-point discrimination ascend in the ipsilateral posterior column of the spinal cord and decussate in the medial lemniscus of the medulla.
F. Cranial nerve and brainstem. Cutaneous sensation from the face is carried to the brainstem by the trigeminal nerve. After entering the pons, part of the sensory fibers descend as a bundle to form the spinal tract of the trigeminal nerve, which reaches the upper cervical segment of the spinal cord. The spinal tract of the trigeminal nerve gives off fibers to the medially located nucleus of the spinal tract of the trigeminal nerve, which also descends into the upper cervical cord. The nucleus of the spinal tract of the trigeminal nerve receives fibers conducting sensations of pain, temperature, and light touch from the face and mucous membranes. Ascending fibers from the spinal nucleus travel mainly ipsilaterally in the trigeminothalamic tract and terminate in the ventral thalamus. The spinothalamic tract has connections with the brainstem reticular formation. It joins the medial lemniscus at the midbrain level and terminates in the posterior ventral complex of the thalamic nuclei.
G. Cortex. The cortical projections of the posterior ventral thalamic complex ascend through the medial portion of the internal capsule to reach the post-central cortex in a somatotopic arrangement with the face in the lowest area and the leg in the parasagittal region. In addition to the post-central cortex, the cortical thalamic projections include the superior parietal lobule, which is considered to represent sensations of numbness and tingling over the contralateral or bilateral aspects of the body. The fine sensory discrimination and fine location of pain, temperature, touch, and pressure (so-called primary modalities) require normal functioning of the sensory cortex. The cerebral cortex of the post-central gyrus also subserves cortical sensory processes, including perception of sizes and shapes of objects (stereognosis), ability to recognize numbers or letters drawn on the patient’s skin (graphesthesia), and two-point discrimination.
III. CLINICAL ASPECTS OF ACUTE SENSORY LOSS BY SOMATOTOPIC LOCALIZATION
Pure sensory loss is unusual. Accompanying signs referable to brainstem, motor loss, associated cortical signs, and reflex abnormalities can help localize a lesion and narrow the diagnostic considerations and evaluation.
A. Acute sensory disturbance in the face usually indicates a lesion in a branch or branches of the trigeminal nerve, the trigeminal nucleus in the brainstem, or in the lemniscal pathways of the brainstem. It would be less typical to have pure facial sensory disturbance from a lesion in the thalamus, cortical projections, or somatosensory cortex (see III.B). Involvement of the ophthalmic branch of the trigeminal nerve can also cause a decreased blink reflex.
1. Acute onset of facial paresthesia manifesting as numbness, tingling, or ill-defined discomfort, if lasting only several seconds or minutes in a person who is exposed to stressful circumstances, is often idiopathic and self-limited. Paresthesia in the perioral area can be caused by and reproduced by hyperventilation. A severe form of lancinating facial pain can be very focal and feel like an abscessed tooth if in the mandibular branch of the trigeminal nerve, also known as tic douloureux, can also be idiopathic. Recurrent or chronic frontal or maxillary sinusitis can cause numbness referable to the ophthalmic or maxillary branches of the trigeminal nerve. Sensory disturbance in the maxillary division of the trigeminal nerve, which then spreads to the entire half of the face, suggests inflammatory demyelination. Sensory disturbance in the area of the mandibular division of the trigeminal nerve can reflect inflammatory or traumatic events involving the mandible or fracture of the base of the skull in the area of the foramen ovale. Relatively abrupt onset of sensory disturbance in the area of the chin suggests neuritis affecting the mental nerve and can be caused by osteomyelitis or the numb chin syndrome as a paraneoplastic manifestation of lymphoma, breast or prostate cancer, or melanoma.
2. Numbness or abnormal sensation can occur over the paretic facial muscles of idiopathic peripheral facial nerve (Bell’s) palsy.
3. Alteration in sensation in the ophthalmic division of the trigeminal nerve and accompanying abrupt onset of fever, proptosis, chemosis, diplopia, and papilledema suggests cavernous sinus thrombosis,which can be caused by suppurative processes involving the upper half of the face, orbits, or nasal sinuses. Septic cavernous sinus thrombosis represents a life-threatening process necessitating immediate hospitalization. Sensory deficit in the ophthalmic division of the trigeminal nerve can also accompany acute onset of meningitis.
4. A relatively sudden onset of numbness over the first two divisions of the trigeminal nerve can result from a low-grade inflammatory process involving the cavernous sinus (Tolosa–Hunt’s syndrome),which also causes lateralized retroocular or periorbital pain and diplopia secondary to involvement of the abducens nerve in the lateral wall of the cavernous sinus.
B. Facial sensory disturbance in association with hemibody sensory disturbance, either ipsilateral or contralateral.
1. Abrupt onset of hypalgesia and thermoanesthesia over the entire half of the face accompanied by hypalgesia and thermoanesthesia over the contralateral half of the trunk and extremities indicates involvement of the lateral medulla. The acute sensory loss often is associated with dysphagia, dysarthria, vertigo, vomiting, ipsilateral cerebellar signs, and ipsilateral Horner’s syndrome. The most frequent cause of the lateral medullary (Wallenberg’s) syndrome is occlusion of the intracranial vertebral artery. Less common causes include vertebral artery dissection, hematoma, demyelination, metastatic disease, and abscess.
2. Acute onset of bilateral or unilateral facial numbness rapidly extending into the contralateral half of the face and associated with or followed by progressive weakness of facial muscles can be the earliest manifestation of acute demyelinating polyneuropathy or Guillain–Barré’s syndrome (GBS). Cases that begin in the face and descend are called the Fisher’s variant of GBS. Typical GBS starts with numbness, paresthesia, and weakness in the distal portion of the legs and ascends to eventually involve the face. Fisher’s variant GBS tends to involve the respiratory centers of the brainstem more quickly than typical GBS, making surveillance of respiratory status particularly important in Miller Fisher’s variant GBS. The diagnosis of GBS should be especially considered in persons with histories of respiratory or gastrointestinal viral infection, immunization, or surgical procedures preceding the onset of neurologic symptoms.
3. Recurrent hemifacial sensory disturbances, particularly among older patients with a clinical history of arterial hypertension, cardiovascular disease, diabetes, and cigarette smoking, may represent a carotid artery territory transient ischemic attack (TIA). The TIA episodes are of variable duration, usually lasting <20 to 30 minutes.
4. Loss of pain sensation and thermodysesthesia with preserved light touch sensation suggest syringobulbia, with an expanding syrinx involving the spinal nucleus of the trigeminal nerve.
5. The rostral part of the nucleus of the spinal tract of the trigeminal nerve represents the midline facial areas, whereas the sensation fibers from the lateral facial areas terminate in the more caudal part of the nucleus at the level of the medulla and spinal cord. In acute intraparenchymal processes involving the brainstem, facial sensory loss can occur in an “onionskin” distribution with decreased sensation in the central facial areas, indicating a pontine or pontomedullary lesion. Acute presentation of “onionskin-like” sensation deficits in the face can accompany acute brainstem encephalitis.
C. Acute sensory loss over the scalp and neck, that is, the “top of the head.” Some patients, after exposure to cold or for no obvious reason, may experience the sudden onset of lateralized discomfort or pain associated with decreased sensation in the occipital area, in the distribution of the greater or lesser occipital nerves. Acute sensory impairment in the area over the angle of the mandible, the lower part of the external ear, and the upper neck below the ear suggests neuropathy involving the great auricular nerve.
D. Acute sensory loss over half of the face, trunk, and corresponding extremities. Acute primary modality sensory loss over the entire half of the body often is a manifestation of a stroke or a traumatic CNS lesion.
1. Sensory loss in half of the body can indicate damage rostral to the upper brainstem up to the post-central gyrus and parietal area of the cerebral hemisphere contralateral to the side of the sensory deficit.
2. Acute onset of numbness, tingling, prickling, or a crawling sensation starting in the lips, fingers, or toes and spreading in seconds over half of the body may represent a partial seizure. The abnormal sensation may follow a rather stereotypical pattern, usually lasting <1 minute. The onset of focal seizures frequently reflects a focal pathologic condition such as a tumor or vascular malformation involving the contralateral hemisphere.
3. Transient hemisensory impairment can be caused by TIAs. The diagnosis of TIA is more probable if the hemisensory impairment is accompanied by motor deficits.
4. A patient with an acute vascular event in the area of the nondominant, right parietal lobe may be unable to give a reliable history because of decreased ability to appreciate motor or sensory deficits in the contralateral extremities (anosognosia).
5. Hemisensory impairment manifesting as a tingling sensation, numbness, or ill-defined pain can accompany an acute vascular lesion involving the contralateral thalamus. Patients often have midline demarcation of the sensory disturbances and may be unaware of the profound sensory loss in the involved areas. Thalamic paresthesia and pain often are disabling and difficult to manage. Vascular lesions of the thalamus typically are lacunar infarcts of small thalamoperforate vessels coming off the vasculature of the circle of Willis.
E. Clinical aspects of acute sensory loss in the area of the trunk. Acute unilateral or bilateral sensory loss with a horizontal sensory level over the chest or abdomen localizes a lesion to the spinal cord and necessitates emergency evaluation to minimize residual neurologic impairment secondary to a possible spinal cord lesion.
1. Complete transection of the spinal cord results in bilateral weakness of legs or arms and loss of all forms of sensation one to two segments below the level of the lesion. Absence of vibration sense at the spinous process below the lesion can be helpful in localizing the spinal cord damage. A zone of increased pinprick or light touch sensation at the upper border of the anesthetic zone may be established. Urinary and fecal incontinence is typically present.
2. Muscle weakness in a leg, with contralateral loss of pain and thermal sensation, suggests a hemispinal cord lesion on the side of the weakness, one or two segments above the sensory loss, also known as a Brown–Séquard’s syndrome.
3. Acute loss of pain and temperature sensation can accompany occlusion of the anterior spinal artery. Light touch, position, and vibration senses remain intact. Anterior spinal artery syndrome can occur during aortic surgery or in advanced atherosclerotic disease of the aorta. It also can develop in the course of meningovascular syphilis or as a manifestation of collagen-vascular disease. Dissociated sensory deficits also can occur in association with acute spinal cord infarction in the “watershed” areas (T1–4 and T12–L1 levels).
4. Occasionally after falls that involve landing on the buttocks, patients may have loss of pain and temperature sensation with preserved tactile sensation one to two segments below the level of the expected spinal cord involvement. Expanding hematomas in the spinal cord gray matter compromise the ventral white commissure conducting fibers for pain and temperature sensation. Light touch and vibration senses remain intact. The dissociated sensory deficit can extend over several segments.
5. Acute ascending sensory loss for pain, soft touch, and temperature can be a manifestation of an acute spinal cord inflammatory process, that is, acute transverse myelitis. Decreased or absent vibration and position senses below the level of the spinal cord involvement and functional alteration in sphincters with urinary and fecal incontinence can be present. Symmetric, severe muscle weakness in the lower extremities can develop over hours. Viral diseases or vaccinations may precede the onset of neurologic symptoms by 1 to 3 weeks.
6. Acute “saddle” sensory loss localizes a lesion to the tip of the spinal cord at the conus medullaris. Sphincteric disturbance of bowel and bladder function often is associated.
7. Individual nerve roots typically are affected by trauma from spondylotic vertebral bone spurs or herniated disc protrusions.
8. The brachial plexus can be affected by local trauma, either during operations in the area or in accidents involving the shoulder, including birth injuries, and can become inflamed. Acute onset of tingling, numbness, and pain, usually followed in several hours or days by muscle weakness and patchy hypesthesia in the area of the shoulder girdle and proximal arm muscles, is typical of brachial plexus neuritis (neuralgic amyotrophy). Brachial plexus neuritis can occur in epidemic form. It can follow infection, vaccination, coronary bypass surgery, or parenteral administration of serum or can be idiopathic.
9. The lumbosacral plexus can be affected by operations in the area, including those that cause retroperitoneal hematoma. Lumbosacral plexopathy causes sensorimotor deficits and pain in the lower extremities and is commonly caused by trauma or retroperitoneal hemorrhage.
10. Peripheral nerves are susceptible to trauma or compression in certain classic areas.
a. Axillary nerve. Dislocation of the shoulder joint, injury to the humerus, or prolonged pressure, stretching, or traction involving the arm during anesthesia or sleep can result in lesions of the axillary nerve.
b. Median nerve. The median nerve can be damaged by injuries involving the arm, forearm, wrist, and hand, including stab and bullet wounds. Procedures involving needle insertion, particularly in the cubital fossa, can also result in median nerve damage manifested by sensory deficits and pain, frequently with a burning, causalgic component. In rare instances, prolonged compression during anesthesia or sleep can cause acute median nerve involvement that manifests as sensory and motor deficits. Numbness and tingling in the distribution of the median nerve that wakes a person from sleep and is relieved by shaking the hand and arm are classic signs of carpal tunnel syndrome, which typically results from repetitive motion injury around the wrist. Persons with diabetes, hypothyroidism, arthritis, or acromegaly or those who are pregnant are particularly predisposed to development of carpal tunnel syndrome.
c. Ulnar nerve. Fractures and dislocations of the humerus involving the elbow, lacerating wounds, and pressure on the nerve during anesthesia, or drunkenness (“Saturday night palsy”) are the most frequent causes of acute ulnar nerve damage.
d. Radial nerve. The radial nerve is probably the most commonly injured peripheral nerve. Injuries including dislocation and fracture of the shoulder, extended pressure on the nerve (particularly at the groove of the nerve), and fractures of the neck of the radius are the most frequent causes of radial nerve damage.
e. Femoral nerve. Acute femoral nerve injury may follow fractures of the pelvis and femur, dislocation of the hip, pressure or traction during hysterectomy, forceps delivery, or pressure in hematoma in the area of the iliopsoas muscle or groin. Paresthesia and sensory loss in the area of the saphenous nerve can occur as a result of injury in the area above the medial aspect of the knee in medial arthrotomy or as a complication of coronary artery bypass graft surgery.
f. Obturator nerve. The nerve can be damaged during surgical procedures involving the hip or pelvis, in cases of obturator hernia, or secondary to iliopsoas hematoma.
g. Lateral femoral cutaneous nerve. The lateral femoral cutaneous nerve can be damaged by compression by the inguinal ligament, in iliopsoas hemorrhage, or by tightly fitting garments on obese individuals, causing tingling, numbness, and pain, that is, meralgia paresthetica.
h. Sciatic nerve. Acute sciatic nerve damage can occur in association with fractures or dislocations of the hip, hip joint surgery, other pathologic conditions of the pelvis including gunshot wounds or injections in the vicinity of the sciatic nerve.
i. Peroneal nerve. Most peroneal nerve lesions are traumatic, including those caused by compression exerted at the upper and outer aspects of the leg, stretching of the hip and knee, or surgical procedures involving the knee joint.
j. Tibial nerve. The tibial nerve is injured mostly in the popliteal fossa at the level of the ankle or foot. Injury at the tarsal tunnel where the nerve crosses the medial malleolus causes sensory loss in the toes and dorsum of the foot.
IV. ETIOLOGY OF ACUTE SENSORY LOSS
A. Infectious–parainfectious neurologic diseases are preceded by or associated with acute febrile diseases involving the upper respiratory or gastrointestinal system or the lower urinary tract. Parainfectious involvement of the CNS or peripheral nervous system (PNS) typically follows the onset of clinical symptoms of the infectious process by 1 to 3 weeks.
B. Inflammatory-demyelinating disease can be parainfectious or postinfectious but can also be idiopathic or autoimmune.
C. Ischemic–hemorrhagic neurologic disorders manifesting as acute CNS or PNS involvement usually occur among older persons with vascular risk factors.
D. Traumatic–compressive lesions of the CNS and PNS can manifest as acute sensory loss. Complications of surgical procedures, venipuncture, or intravascular injection can cause acute sensory loss, usually secondary to peripheral nerve damage.
V. DIAGNOSTIC APPROACHES TO ACUTE SENSORY LOSS
Diagnostic approaches to acute sensory loss are focused by the localization of the lesion (Sections I, II and III) and by suspected etiologic factor (Section IV).
A. PNS evaluation. If a lesion localizes to a particular peripheral nerve, the extremity and nerve can be evaluated radiographically and electrophysiologically.
1. Radiographs of the involved limb can help identify fractures or bony deformities that can cause focal compression of damage to the nerve. CT or MRI of the brachial or lumbosacral plexus can be useful in identifying the nature of damage.
2. EMG with nerve conduction velocity studies (NCVs) can be helpful in documenting and localizing damage to a peripheral nerve, a plexus, or a nerve root and in providing prognostic information (see Chapter 33). In a traumatized nerve or root, abnormalities may not appear immediately on nerve conduction studies. It also takes approximately 2 weeks for denervative change to occur in muscles innervated by damaged nerves, so an initially unremarkable or borderline EMG must be repeated if there is continued suspicion of damage. In the acute period, a demyelinated nerve can show slowing of nerve conduction, conduction block across demyelinated nerve segments, and slowing of F waves that reflect proximal nerve root damage. The greater the denervation and axonal dropout found at subacute EMG/NCV studies, the worse the prognosis.
B. Spinal cord evaluation. Localization of a lesion to the spinal cord necessitates neuroimaging of the cord. Traumatic lesions necessitate immediate imaging of an immediately stabilized spine by means of traditional radiographs and subsequent imaging of the spinal cord parenchyma by means of MRI or CT myelography.
1. MRI is the preferred technique for imaging the spinal cord parenchyma, and use of gadolinium can be helpful in identifying acute inflammatory lesions or syringomyelic cavities.
2. CT myelography can be used to examine segments of the cord and is especially good at depicting bone, disc, and ligamentous structures that may impinge on the spinal cord.
3. Somatosensory-evoked responses can help determine whether there is slowed conduction of somatosensory stimuli from arms or legs in the somatosensory pathways from spinal cord to cortex and can crudely localize the lesion.
4. MR angiography can occasionally noninvasively help identify a suspected vascular lesion in the spinal cord, but traditional angiography of spinal vessels is the gold standard to identify lesions.
C. Brain evaluation. Acute sensory loss that localizes to the brain, including cerebral cortex or brainstem, can be evaluated by several techniques.
1. Traditional radiographs, including sinus radiographs, can be helpful.
2. MRI can most precisely localize a lesion and can include MR angiography and MR venography to examine blood vessels. Diffusion-weighted imaging has very high specificity in acute stroke (see Chapter 32). For suspected inflammatory-demyelinating or postinfectious processes, MRI is the procedure of choice. Gadolinium contrast material should be administered to assess whether there is acute enhancement, which suggests active inflammation and breakdown of the blood–brain barrier. The presence of subclinical white matter lesions on MRI brain during a clinically isolated bout of transverse myelitis indicates increased risk of development of multiple sclerosis.
3. Cerebral angiography may be necessary to diagnose vascular abnormalities such as ruptured aneurysm, atherosclerotic narrowing, vasculitis, and sinus thrombosis.
4. Electroencephalography can aid in the diagnosis of seizures (see Chapter 33).
D. Blood work can be used to diagnose infectious or inflammatory conditions that can cause acute sensory loss, including complete blood cell count, blood cultures when indicated, erythrocyte sedimentation rate, antinuclear antibodies, rheumatoid factor, angiotensin-converting enzyme level, rapid plasma reagent test, Lyme’s titer, antineutrophil cytoplasm autoantibodies, glucose level, and hemoglobin AIc. Suspected vascular–hemhorragic processes should be assessed for hypercholesterolemia and hypercoagulable or prothrombotic states.
E. Examination of CSF can show whether there is acute protein elevation, glucose depression, or WBC elevation suggestive of infectious or inflammatory causes of for acute sensory loss (see Chapter 33). Hypoglycorrhachia can indicate the need for further attempts to isolate certain infectious agents such as fungi or acid-fast bacilli. The nature of CSF pleocytosis can dictate further evaluation; the most typical inflammatory causes of postinfectious sensory loss cause lymphocytic pleocytosis. To further pursue postinfectious and demyelinating etiologic factors, spinal fluid should be examined for IgG level and IgG index, both of which are elevated in multiple sclerosis and often in transverse myelitis, and for the presence of oligoclonal IgG bands in CSF but not serum. These bands are present in most cases of multiple sclerosis and in many forms of parainfectious or postinfectious encephalomyelitis. Myelin basic protein levels in CSF can indicate ongoing demyelination. For suspected infectious causes, cultures and smears for bacteria, acid-fast bacilli, and fungus are important. Serologic and PCR tests also can be done for many viruses, including herpes simplex types 1 and 2, Epstein–Barr virus, cytomegalovirus, human herpesvirus type 6. A CSF VDRL test and angiotensin-converting enzyme level are useful.
VI. REFERRALS
Cases of acute sensory loss should be referred to a neurologist if:
A. Sudden onset or resolution suggests TIAs.
B. Radiculopathy is suspected and focal neurologic deficits are present (weakness and reflex loss).
C. Fever is present, and there is a suspicion of encephalitis or cortical sinus thrombosis.
D. Deficits worsen, ascend, or evolve to include motor signs and symptoms, suggesting GBS.
E. Acute deficit localizes to the spinal cord. A neurosurgeon also should be informed.
Recommended Readings
Biller J, Gruener G, Brazis PW. DeMyer’s The Neurologic Examination: A Programmed Text. 6th ed. New York, NY: McGraw-Hill; 2011.
Brazis PW, Masdeu JC, Biller J. Localization in Clinical Neurology. 6th ed. Philadelphia, PA: Lippincott Williams & Wilkins, Wolters Kluwer; 2011.
Fisher CM. Pure sensory stroke and allied conditions. Stroke. 1982;13:434–447.
Kimura J. Electrodiagnosis in Diseases of Nerve and Muscle. Philadelphia, PA: FA Davis Co; 1984.
Koski CL. Guillain Barré syndrome and chronic inflammatory demyelinating polyneuropathy: pathogenesis and treatment. Semin Neurol. 1994;14:123–130.
Patten J. Neurological Differential Diagnosis. New York, NY: Springer-Verlag; 1980.
Polman CH, Reingold SC, Banwell B, et al. Diagnostic criteria for multiple sclerosis: 2010 revisions to the McDonald criteria. Ann Neurol. 2011;69:292–302.
Scott TF, Bhagavatula K, Snyder PJ, et al. Transverse myelitis: comparison with spinal cord presentations of multiple sclerosis. Neurology. 1998;50:429–433.