(Video 27.1).

D.  Brachial and lumbosacral plexus. Acute sensorimotor deficits indicating multiple nerve or nerve-root distributions 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 spinothalamic tract to terminate eventually in the ventral posterior lateral nucleus of the thalamus. Fibers conducting light touch, vibration, joint position, 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 and mucous membranes is carried to the brainstem by the trigeminal nerve; cell bodies for pain, temperature, light touch, and pressure are located in the gasserian ganglion. 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 (therefore patients with upper cervical cord lesions may exhibit ipsilateral facial numbness). The spinal tract of the trigeminal nerve, located laterally in the brainstem/upper cervical cord, gives off pain and temperature fibers to the more medially located nucleus of the spinal tract of the trigeminal nerve. Touch, vibration, and pressure sensation terminate in the chief sensory nucleus within the pons. Proprioception fibers from the muscles of mastication bypass the gasserian ganglion and ascend terminating in the mesencephalic nucleus in the midbrain (the only sensory ganglion located within the central nervous system [CNS]), which is the afferent component of the jaw jerk. Fibers from the spinal nucleus and many fibers from the chief sensory nucleus cross the midline (some also ascend ipsilaterally to the thalamus) and ascend in the contralateral trigeminothalamic tract terminating in the ventral posterior medial nucleus of the thalamus.

G.  Cortex. The cortical projections of the posterior ventral thalamic complex ascend to reach the postcentral cortex in a somatotopic arrangement with the face in the lowest area and the leg in the parasagittal region. In addition to the postcentral cortex, the cortical thalamic projections include the superior parietal lobule (Video 27.2). 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 postcentral 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, all of which can be impaired with cortical lesions in this region. Sensory neglect often accompanies a lesion of the nondominant sensory cortex. Pain fibers also project to limbic regions, hypothalamus, and brainstem reticular formation by complex pathways and are involved in the autonomic, endocrine, arousal, and emotional response to pain.

ASSOCIATION OF OTHER NEUROLOGIC SIGNS

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. Involvement of the ophthalmic branch of the trigeminal nerve can also cause a decreased corneal 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. Trigeminal neuralgia (also known as tic douloureux) is a severe form of recurrent lancinating facial pain lasting seconds and frequently triggered by a breeze hitting the face or brushing ones teeth; similar recurrent lancinating pain in the back of the throat occurs with glossopharyngeal neuralgia. Sjögren’s syndrome is a well-recognized cause of trigeminal neuropathy. 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. Sensory disturbance in the area of the chin can be caused by numb chin syndrome because of neoplastic invasion of the inferior alveolar or mental nerve from mandibular metastases of lymphoma, breast or prostate cancer, or melanoma.

2.  Involvement of other cranial nerves may occur with idiopathic peripheral facial nerve (Bell’s) palsy; trigeminal nerve involvement on that side may result in ipsilateral numbness of the face.

3.  Alteration in sensation in the ophthalmic and/or maxillary division of the trigeminal nerve and accompanying abrupt onset of fever, proptosis, chemosis, diplopia, and papilledema suggest 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 is life-threatening, necessitating immediate hospitalization. Sensory deficit in the ophthalmic division can also accompany 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 syndrome), which also causes eye movement abnormalities from involvement of one or more of the third, fourth, and sixth cranial nerves. Orbital pseudotumor is another inflammatory process that can involve similar regions. IgG4-related disease can manifest with either of these syndromes and should be considered as a potential etiology.

B.  Facial sensory disturbance in association with hemibody sensory disturbance, either ipsilateral or contralateral.

1.  Abrupt onset of pain and temperature loss over the entire half of the face and contralateral half of the trunk and extremities indicates involvement of the lateral medulla. The acute sensory loss is often associated with dysphagia, dysarthria, vertigo, vomiting, ipsilateral cerebellar signs, and ipsilateral Horner’s syndrome. The most frequent cause of the lateral medullary (Wallenberg) syndrome is ipsilateral posterior inferior cerebellar artery infarction.

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 inflammatory-demyelinating polyneuropathy or Guillain–Barré syndrome (GBS). Cases that begin in the face may have a triad of sensory ataxia, areflexia, and ophthalmoplegia called the Miller–Fisher 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. The Miller-Fisher variant of GBS tends to involve the respiratory centers of the brainstem more quickly than typical GBS, making surveillance of respiratory status particularly important in this variant. 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 less than 30 minutes.

4.  Loss of pain and temperature sensation in the face with preserved light touch sensation suggests 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, which both arise from the C2 cervical nerve root; the C1 cervical nerve root is entirely motor. 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 is often a manifestation of a stroke or a traumatic CNS lesion.

1.  Hemisensory loss can indicate damage rostral to the upper brainstem up to the postcentral 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 and typically lasting less than 1 minute may represent a partial seizure. Etiologies include tumors or vascular malformations 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 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. Thalamic paresthesia and pain (Dejerine–Roussy syndrome) are disabling and difficult to manage. Vascular lesions of the thalamus are typically lacunar infarcts of small thalamoperforate vessels coming off the basilar artery and proximal posterior cerebral arteries.

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 urgent 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 immediately 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 or urinary retention is typically present.

2.  Muscle weakness in a leg, with ipsilateral loss of vibration and proprioception immediately below the lesion and contralateral loss of pain and temperature sensation one to two segments below, suggests a hemispinal cord lesion on the side of the weakness, also known as a Brown–Séquard syndrome.

3.  Acute loss of pain and temperature sensation can accompany occlusion of the anterior spinal artery although rapid-onset paraplegia/quadriplegia usually predominates. 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, as a manifestation of collagen-vascular disease, from a fibrocartilaginous embolism (which may be preceded by trauma and have an accompanying collapsed disc space) or from watershed infarction in the setting of vertebral artery occlusion and thus anterior spinal artery hypoperfusion. The midthoracic spinal cord is a “watershed” area at increased risk for infarction. However, the most common region affected by spinal cord infarction is the lower thoracic cord.

4.  Acute ascending numbness is a characteristic manifestation of acute transverse myelitis. Functional alteration in sphincters with urinary and fecal incontinence can be present. Symmetric, severe muscle weakness in the lower extremities can develop over hours to days, particularly when caused by neuromyelitis optica spectrum disorders; magnetic resonance imaging (MRI) in such cases characteristically reveals a longitudinally extensive lesion ≥3 vertebral segments and serum testing positive for aquaporin-4-IgG is often diagnostic. Viral diseases or vaccinations may precede the onset of neurologic symptoms in acute idiopathic transverse myelitis by 1 to 3 weeks. Demyelinating lesions in the cervical cord often result in Lhermitte’s phenomenon (shooting tingling sensation down the spine or into finger tips with neck flexion) or a sensory useless hand syndrome with proprioceptive deficits in the hand resulting from a focal lesion in the ipsilateral dorsal column.

5.  Posterior column dysfunction with sparing of temperature and pinprick occurs with vitamin B₁₂ deficiency and may be accompanied by spastic weakness when corticospinal tracts are involved (subacute combined degeneration). Acute sensory loss can occur with nitrous oxide use precipitating vitamin B₁₂ deficiency. Methylmalonic acid should be assessed in those with low normal vitamin B₁₂ levels as it is more sensitive for detecting cellular deficiency. Copper deficiency causes a similar syndrome and zinc-containing denture creams or malabsorption syndromes (e.g., celiac disease) should be considered as potential underlying causes. Human immunodeficiency virus, human T-lymphotrophic virus type 1, and syphilis are infectious etiologies that have a predilection for the dorsal columns.

6.  Pain and temperature first-order neurons typically ascend ipsilaterally for one or two segments within the spinal cord in the tract of Lissauer before synapsing on their second-order neurons. These second-order neurons then cross to the opposite side through the commissural fibers just anterior to the central canal. Lesions of the spinothalamic tracts thus cause contralateral loss of pain and temperature sensation one or two vertebral segments below the lesion and may have ipsilateral loss of pain and temperature at the level of the lesion.

7.  Dissociated sensory loss with loss of pain and temperature sensation but preservation of light touch, proprioception, and vibration occurs when the crossing pain and temperature fibers in the anterior commissure adjacent to the central canal are damaged in syringomyelia or from trauma (hematomyelia). The dissociated sensory deficit can extend over several segments and often occurs in a hallmark “cape like” distribution when cervical cord involvement occurs.

8.  The spinothalamic fibers are arranged in a laminar fashion with sacral fibers most lateral and hence a central cord lesion may result in loss of pain and temperature sensation below a lesion with “sacral sparing.”

9.  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 is often associated.

10.  Individual nerve roots are typically affected by trauma from spondylotic vertebral bone spurs or disc herniation. Increased intraspinal pressure during coughing, sneezing, or Valsalva can worsen the associated radicular pain. Acute cauda equina syndrome with bilateral lumbosacral radiculopathies resulting in rapidly progressive weakness, sensory loss (saddle anesthesia), and urinary retention is a neurologic emergency requiring emergent lumbosacral spine MRI and neurosurgical consultation.

11.  A sensory neuronopathy (or sensory ganglionopathy) with disease affecting the dorsal root ganglia presents with numbness, sensory ataxia (positive Romberg sign), areflexia, and pseudoathetosis, and is classically associated with Sjögren’s syndrome and paraneoplastic disease (most often anti-nuclear-neuronal-autoantibody-type-1 or anti-Hu antibodies in association with an underlying small-cell lung cancer). Cisplatin toxicity may also present in this manner.

12.  The brachial plexus can be affected by local trauma during surgery in this region or in accidents involving the shoulder or birth injuries. Prolonged positioning during surgery is another well-recognized cause of brachial plexopathy from compression or stretching and usually resolves over days to weeks. Acute onset of severe pain (often requiring opiates for relief) accompanied by numbness and tingling and usually followed in several hours or days by muscle weakness and patchy hypoesthesia in the area of the shoulder girdle and proximal arm muscles is typical of brachial plexus neuritis (also known as neuralgic amyotrophy or Parsonage–Turner syndrome). It can follow infection, vaccination, or recent surgery. Hereditary autosomal-dominant recurrent brachial plexitis is described with SEPT9 gene mutations. Neoplastic involvement of the brachial plexus is often very painful and infiltration may be evident on MRI of the plexus.

13.  The lumbosacral plexus can be affected by operations in the area, including those that cause retroperitoneal hematoma. Diabetic lumbosacral radiculoplexus neuropathy (diabetic amyotrophy) is a well-recognized cause of pain, lower extremity numbness, and weakness in type 2 diabetics; the diabetes is usually well controlled and severe weight loss is commonly associated.

14.  Mononeuritis multiplex causes sensory and motor deficits in multiple peripheral nerves, and underlying systemic diseases such as diabetes, vasculitic disorders, and paraneoplastic disorders are among the diagnostic possibilities.

15.  Small-fiber neuropathies typically cause positive sensory symptoms in the feet and they are associated with normal nerve conduction studies and electromyography (EMG) (which are much better at detecting large-fiber neuropathies). Autonomic testing is helpful in such cases. An accompanying autonomic neuropathy is common and may result in orthostatic hypotension, decreased sweating, visual difficulty during transition from dark to light (pupil dysfunction), early satiety and bowel and bladder dysfunction. Common causes of small-fiber neuropathy include type 1 diabetes (including diabetic treatment–induced neuropathy [previously termed insulin neuritis]), amyloidosis, autoimmune disorders associated with antibodies directed against the 3 subunit of the ganglionic acetylcholine receptor, Sjögren’s syndrome, and Fabry’s disease (in young males with associated angiokeratomas of the skin and caused by -galactosidase deficiency).

16.  Peripheral nerves are susceptible to trauma or compression in certain classic areas. Hereditary neuropathy with liability to pressure palsy (from peripheral myelin protein 22 gene deletion) can also result in a general susceptibility to recurrent compressive neuropathies.

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. 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.

c.  Ulnar nerve. This is most frequently injured in the cubital tunnel at the elbow (e.g., during olecranon fractures or from recurrent or prolonged compression) or in Guyon’s canal at the wrist (e.g., acutely during blunt injury or more chronically from a ganglion cyst).

d.  Radial nerve. The radial nerve is probably the most commonly injured peripheral nerve. Sensory loss over the first web space with an accompanying wrist drop is characteristic. Injuries including dislocation and fracture of the shoulder, extended pressure on the nerve such as when a person falls asleep with their arm over a chair compressing the radial nerve at the spiral groove (“Saturday night palsy”), and fractures of the neck of the radius are the most frequent causes of radial nerve damage.

e.  Femoral nerve. Acute femoral nerve injury with sensory loss in the anterior thigh and quadriceps weakness may follow fractures of the pelvis and femur, dislocation of the hip, pressure or traction during hysterectomy, forceps delivery, femoral artery catheterization for coronary angiographic procedures, 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 an iatrogenic complication during venous graft harvesting for coronary artery bypass graft surgery.

f.  Obturator nerve. The nerve can be damaged during surgical procedures involving the hip or pelvis, or secondary to iliopsoas hematoma, and sensory loss is in the medial thigh and accompanied by weakness of hip adduction.

g.  Lateral femoral cutaneous nerve. The lateral femoral cutaneous nerve can be damaged by compression from the inguinal ligament, tightly fitting garments in obese individuals, or during pregnancy, causing tingling, numbness, and pain and is termed meralgia paresthetica.

h.  Sciatic nerve. Acute sciatic nerve damage results in variable sensory and motor dysfunction depending on the site of injury and can occur in association with fractures or dislocations of the hip, hip joint surgery, and other pathologic conditions of the pelvis including gunshot wounds or injections in the vicinity of the sciatic nerve.

i.  Peroneal nerve. Peroneal nerve lesions are most often caused by compression (e.g., habitual leg crossing, leg casting, or positioning during surgery) and may be precipitated by recent weight loss. Fibular fracture is another cause and iatrogenic injury may occur during knee surgery. Sensory loss is on the dorsum of the foot and lateral calf region sparing the fifth toe is typical. It can be distinguished from an L5 radiculopathy by its sparing of inversion strength. Fascicular involvement of the peroneal division of the sciatic nerve (which seems to be more susceptible to injury than the tibial division) can occur, mimicking a common peroneal neuropathy. EMG abnormalities found in the short head of the biceps femoris suggests involvement of the peroneal division of the sciatic nerve.

j.  Tibial nerve. The tibial nerve is injured mostly in the popliteal fossa or at the level of the ankle or foot. Tarsal tunnel syndrome, most common in athletes, results from compression of the tibial nerve as it passes through the tarsal tunnel behind the medial malleolus. Numbness and pain in the first three toes, dorsum of foot, and heel are typical.

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 and prolonged positioning during surgery can cause acute sensory loss, usually secondary to peripheral nerve damage.

DIAGNOSTIC APPROACHES TO ACUTE SENSORY LOSS

Diagnostic approaches to acute sensory loss are focused by the localization of the lesion (sections Clinical Manifestations, Localization of the Pathologic Processes, and Association of Other Neurological Signs) and by suspected etiologic factor (section Etiology of Acute Sensory Loss).

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. MRI of the brachial or lumbosacral plexus can be useful in identifying the nature of damage.

2.  EMG with nerve conduction velocity (NCV) studies can be helpful in documenting and localizing damage to a peripheral nerve, a plexus, or a nerve root and in providing prognostic information (see Chapters 24 and 25). In a traumatized nerve or root, abnormalities may not appear immediately on nerve conduction studies. It also takes approximately 3 weeks for denervation 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. Sensory axon potentials are spared in radiculopathies as the cell body in the dorsal root ganglion is typically proximal to the lesion. 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. EMG/NCV is normal in small-fiber neuropathy and autonomic testing should be performed if this diagnosis is being considered.

3.  MRI neurography and ultrasound of the nerve are additional imaging modalities that may be useful in the evaluation of acute sensory loss.

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 computed tomography (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.

2.  CT myelography is typically used in patients with contraindications to MRI (e.g., pacemaker) 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 peripheral nerve to cortex and can crudely localize the lesion.

4.  Formal spinal angiography is the gold standard to identify dural-arterio venous fistula in those with a suspicious presentation and MRI (e.g., MRI showing a longitudinally extensive swollen thoracic cord lesion with flow voids dorsal to the cord).

C.  Brain evaluation. Acute sensory loss that localizes to the brain, including cerebral cortex, thalamus, or brainstem, can be evaluated by several techniques.

5.  Computed tomography of the head can be helpful, particularly acutely such as in a suspected acute stroke; CT is particularly effective at evaluating for acute hemorrhage.

6.  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 for acute stroke (see Chapter 35). 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 typical demyelinating white matter lesions on MRI brain during a clinically isolated syndrome of demyelination (e.g., transverse myelitis) indicates increased risk of development of multiple sclerosis.

7.  Cerebral angiography may be necessary to diagnose vascular abnormalities such as ruptured aneurysm, atherosclerotic narrowing, and vasculitis.

8.  Electroencephalography (EEG) can aid in the diagnosis of seizures (see Chapter 36). However, in patients with simple partial sensory seizures the discharges may not be detectable with scalp EEG.

D.  Blood work can be used to diagnose infectious, inflammatory, or metabolic conditions that can cause acute sensory loss, including complete blood cell count, blood cultures when indicated, erythrocyte sedimentation rate, vitamin B₁₂, and methylmalonic acid, copper, antinuclear antibodies, SSA and SSB antibodies, antineutrophil cytoplasm autoantibodies, rheumatoid factor, angiotensin-converting enzyme, rapid plasma reagin, Lyme disease serology, HIV, HTLV-1, lactate dehydrogenase, peripheral smear, glucose level, and hemoglobin A_1c, serum protein electrophoresis and immunofixation, and paraneoplastic autoantibody evaluation. Serum testing for aquaporin-4-IgG is useful in the diagnosis of neuromyelitis optica spectrum disorders.

E.  Nerve biopsy may be considered in PNS disorders suspected to be from neoplasia, inflammation (e.g., sarcoid), vasculitis, or amyloidosis (fat pad biopsy is also a useful test of amyloidosis).

F.  Examination of cerebrospinal fluid (CSF) for cell count, protein, glucose, and inflammatory markers helps in the evaluation of acute sensory loss (see Chapter 36). An elevated white blood cell count is seen with infectious and inflammatory etiologies and the differential of the white cells can help suggest the underlying cause (neutrophilic predominance favors bacterial infection; lymphocytic favors viral infections or inflammatory etiologies). A markedly elevated protein with normal cell count known as albuminocytologic dissociation is typical of GBS, but is also seen with spinal block such as may occur in severe cervical stenosis. Hypoglycorrhachia (low CSF glucose) can indicate infectious (bacterial, fungal, or mycobacterial) etiologies but is also seen with neurosarcoidosis and lymphoma. CSF cytology and flow cytometry should be performed in cases suspicious for lymphoma. A positive IgG index or elevated oligoclonal bands are seen in greater than 85% of multiple sclerosis patients, but may also occur in other inflammatory/autoimmune disorders. For suspected infectious causes, cultures and smears for bacteria, acid-fast bacilli, and fungus are important. Serologic and polymerase chain reaction tests also can be done for many viruses, including herpes simplex types 1 and 2, Epstein–Barr virus, cytomegalovirus (a common cause of polyradiculopathy in immunosuppressed patients [e.g., HIV]), and varicella zoster virus. A CSF venereal disease research laboratory test can be undertaken if syphilis is suspected.

REFERRALS

Cases of acute sensory loss should be referred to a neurologist if:

A.  Sudden onset or resolution suggests TIAs or seizures.

B.  Radiculopathy is suspected and focal neurologic deficits are present (weakness and reflex loss).

C.  Fever is present, and there is a suspicion of epidural abscess, encephalitis, or cortical sinus thrombosis.

D.  Deficits progress rapidly, ascend, or evolve to include motor signs and symptoms, suggesting GBS.

E.  Acute deficit localizes to the spinal cord. Emergency MRI is important in this situation and if a compressive lesion is found, an urgent neurosurgical referral is appropriate.

Related posts:

Approach to the Patient with Gait Disturbances and Recurrent Falls Approach to the Patient with Acute Sensory Loss Multiple Sclerosis Approach to the Patient with Sleep Disorders Approach to the Patient with Chronic and Recurrent Headache Neuroimaging of Common Neurologic Conditions

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