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Old 08-23-2010, 01:21 PM
arizona1 arizona1 is offline
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how would you code, Peripheral sensorimotor neuropathy

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Old 08-23-2010, 02:31 PM
marilyngarry marilyngarry is offline
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Wink Peripheral Sensorimotor Neuropathy

Under ICD-9 CM guidelines - look at 357.2

I found this information in an article published by Up To Date: This may be helpful in identifying the true definition of your patient. Query the physician for clarification if clarity is not documented.

Approach to the patient with sensory loss
Authors
Hannah R Briemberg, MD, FRCPC
Anthony A Amato, MD
Section Editor
Michael J Aminoff, MD, DSc
Deputy Editor
Janet L Wilterdink, MD
Last literature review version 18.2: May 2010 | This topic last updated: March 31, 2010 (More)
INTRODUCTION — Sensory loss may be due to disorders of the central or peripheral nervous system. As in most of neurology, the initial goal when confronted with a patient with sensory loss is localization of the lesion using information from the history and physical examination. This narrows the differential diagnosis and directs further investigations. Localization requires an understanding of the anatomy of the sensory system.

ANATOMY OF THE SENSORY SYSTEM — Perception of a somatic sensation depends on detection of a stimulus by specialized receptors in the skin, muscle, or joints. Information from these receptors is then transmitted via peripheral nerves to the central nervous system. With the exception of the mesencephalic nucleus, whose projections carry proprioceptive information from the muscles of mastication [1], the cell bodies of the primary sensory neurons that constitute the peripheral nerves reside in ganglia outside of the central nervous system. Projections from these ganglia then enter the central nervous system to synapse with second order neurons.

The peripheral nerves are made up of large myelinated fibers that transmit proprioceptive, vibratory, pressure, and touch stimuli, and small, relatively unmyelinated fibers that transmit pain, temperature, and touch stimuli. (Note that touch is transmitted by both large and small fibers.) Projections from the cell bodies receiving pain, temperature, and touch stimuli enter the spinal cord via the dorsal nerve root. These fibers terminate in the dorsal horns, fanning out over several segments [2]. They synapse with the second order neurons in the dorsal horns. These neurons then cross the midline of the cord in the anterior commissure in front of the central canal, and these second order neurons ascend (now on the opposite side of the spinal cord to the peripheral nerve) in either the anterior spinothalamic tract (touch) or the lateral spinothalamic tract (pain and temperature) to the ventral posterolateral nucleus of the thalamus. Here, they synapse with neurons which ascend to the primary sensory cortex in the parietal lobe (figure 1).

Projections from the dorsal root ganglia that carry proprioceptive, vibratory, pressure, and touch stimuli directly enter the dorsal columns from the dorsal roots [1]. The gracile column is medial and carries stimuli from the lumbar and thoracic region; the cuneate column begins laterally in the cervical region, which it subserves. Thus, the dorsal columns consist of first order neurons traveling ipsilateral to the peripheral nerve from which they originate. These neurons synapse with second order neurons in the cuneate and gracile nuclei of the medulla. These second order neurons cross in the dorsal midline of the medulla and ascend through the brainstem as the medial lemniscus to the ventral posterolateral nucleus of the thalamus where they synapse with third order neurons which project through the internal capsule and the centrum semiovale to the primary sensory cortex in the parietal lobe (figure 2).

As with the motor cortex, the primary sensory cortex is arranged somatotopically, with the face represented laterally, close to the Sylvian fissure. The hand and arm are represented just above the region for the face and the leg is represented medially, similar to the layout of the motor homunculus.

DEFINITIONS — Sensory loss is categorized as follows:

Hypesthesia is the diminished ability to perceive pain, temperature, touch, or vibration.
Anesthesia is the complete inability to perceive pain, temperature, touch, or vibration.
Hypalgesia is the decreased sensitivity to painful stimuli.
Analgesia is the complete insensitivity to painful stimuli.
Hyperpathia, hyperesthesia, and allodynia refer to an increased sensitivity to sensory stimuli.

SENSORY EXAMINATION — The goal of the sensory examination is to "localize the lesion." This portion of the examination tends to be subjective because it relies on the patient's responses to various stimuli; thus, it is usually done following the motor examination. With the more objective data obtained from the motor examination, the examiner is often able to narrow down a differential and proceed with a more focused sensory examination, resulting in less frustration for both the patient and examiner. (See "The detailed neurologic examination in adults", section on 'Sensory examination'.)

The primary sensory modalities usually are examined first. These include touch, proprioception, vibration, temperature, and pain. Abnormalities in these sensations may occur with any sensory syndrome (eg, peripheral nerve injury, radiculopathy, spinal cord syndromes, thalamic and cerebral hemispheric syndromes). A disproportionate loss of vibration sense and proprioception, compared with pain and temperature sensation, tends to occur with diseases of the dorsal columns of the spinal cord (eg, tabes dorsalis, vitamin B12 deficiency, multiple sclerosis) and also with demyelinating neuropathies and sensory neuronopathies. (See "Pathogenesis, clinical manifestations, and treatment of late syphilis" and "Etiology and clinical manifestations of vitamin B12 and folic acid deficiency".)

Higher cortical sensation can be examined if touch sensation remains relatively preserved and the patient is suspected of having a cortical lesion. Examination of cortical sensation includes two point discrimination, graphesthesia, stereognosis, and extinction:

Two point discrimination is the ability to recognize two points applied simultaneously to the skin as distinct from a single point. (See "The detailed neurologic examination in adults", section on 'Two-point discrimination'.)
Graphesthesia is the ability of the patient to identify numbers or letters drawn in the palm of the hand.
Stereognosis is the ability to recognize common objects such as keys, coins or paper clips by touching or handling them with one's eyes closed.
Extinction is evaluated by simultaneously touching two separate points on either side of the body. The test is abnormal if the patient consistently identifies the stimulus on only one side of the body. Extinction is seen in relatively large parietal lesions.
The Romberg is a test of proprioception. It is positive when the patient is able to stand with feet together and eyes open without losing his balance but is unable to remain steady with the eyes closed. This occurs because patients are using their eyes to compensate for the lack of sensory feedback they are receiving from their lower extremities. A functional correlate of this often comes out in the history when the patient notes that he loses his balance when he gets up at night in a darkened room.

PATTERNS OF SENSORY LOSS — The history and physical examination are key to determining the cause of sensory loss. Ancillary studies may be helpful in selected circumstances.

Sensory loss that is confined to a part of a limb suggests injury to a peripheral nerve, nerve plexus, or spinal root (eg, mononeuropathy or radiculopathy). In contrast, sensory loss involving most of an extremity or the trunk suggests the presence of other disorders, that may be distinguished as follows (figure 3):

Involvement of both sides of the body is consistent with a polyneuropathy or spinal cord disease, while involvement of one side is consistent with contralateral disease of the brainstem, thalamus, or cerebral cortex.
A sensory level is consistent with spinal cord disease or, more rarely, lateral medullary infarction.
Sensory loss of the face suggests disease above the spinal cord (eg, brainstem, thalamus, or cerebral hemispheres). With lower brainstem disease (eg, lateral medullary syndrome), the sensory loss on the face is typically opposite that of the body, although ipsilateral sensory loss has also been reported [3]; sensory loss is on the same side of the face and body with upper brainstem, thalamic, or hemispheric disease.
"Stocking-glove" sensory loss is most commonly seen with length dependent axonal neuropathies, although other disorders may also present with this pattern.
Disproportionate loss of vibration sense and proprioception, compared with pain and temperature sensation, tends to occur with diseases of the dorsal columns of the spinal cord (eg, tabes dorsalis, vitamin B12 deficiency, multiple sclerosis) and demyelinating polyneuropathy.
A number of these disorders are discussed in more detail below.

Neuropathy

Mononeuropathy and radiculopathy — Mononeuropathies refer to pathology affecting an individual peripheral nerve. One common example is carpal tunnel syndrome; patients with carpal tunnel syndrome frequently complain of numbness and tingling in the median nerve distribution that can be particularly bothersome at night, often awakening them from sleep. This may or may not be accompanied by wrist pain that can radiate up the arm or into the hand. (See "Clinical manifestations and diagnosis of carpal tunnel syndrome".) Mononeuropathies are diagnosed clinically based on signs and symptoms that correlate with an individual nerve distribution (figure 4).

Radiculopathies refer to pathology affecting the nerve root, resulting in signs and symptoms in the corresponding dermatome (figure 5 and figure 6) and myotome. Because of the overlap in nerve root innervation of both individual muscles and dermatomes, weakness and sensory loss can be mild and/or not involve the entire region described on the dermatome/myotome maps. Instead, smaller "signature zones" of sensory loss may define the level of nerve root involvement (table 1). Although radiculopathies may not cause significant sensory loss, they characteristically result in paroxysmal severe lancinating pain that may be exacerbated by coughing, sneezing, or straining.

Occasionally it is difficult to differentiate a mononeuropathy from a radiculopathy clinically. As an example, both a peroneal nerve palsy and an L5 root lesion can result in a drop foot and numbness over the lateral aspect of the leg and dorsum of the foot. (See "Overview of lower extremity peripheral nerve syndromes".) Electrodiagnostic testing (nerve conduction studies and electromyography) are useful in distinguishing between these conditions. In a peroneal palsy, nerve conduction studies may demonstrate focal slowing in the peroneal nerve at the fibular head, while in an L5 radiculopathy there may be evidence of denervation in L5 muscles outside of the peroneal territory (eg, tibialis posterior or flexor digitorum longus, both of which are innervated by the tibial portion of the sciatic nerve).

Stocking-glove sensory loss — Stocking-glove sensory loss is a term used to describe sensory loss affecting the distal lower and upper extremities that is most commonly seen in length dependent axonal neuropathies. Axonal neuropathies are most frequently due to:

Diabetes mellitus
Alcohol
Vitamin B12 deficiency
Syphilis
Human immunodeficiency virus
Lyme disease
Uremia
Chemotherapy
Vasculitis
Paraneoplastic neuropathy
Amyloidosis
With axonal neuropathies, the longest axons are affected first and the symptoms start distally in these axons and progress proximally. Thus, patients do not start to notice numbness in their hands until the sensory symptoms or signs have progressed to just above the knee.

The examination usually reveals a decrease in vibration threshold, pinprick, and temperature distally. Diminished proprioception at the great toe is typically also evident on careful examination, but can be difficult to detect. In combined large and small fiber neuropathies, the ankle jerk is frequently diminished or absent. Patients with pure small fiber neuropathies will primarily demonstrate loss of pinprick and temperature distally, although vibration perception can also be affected. Proprioception and deep tendon reflexes remain intact.

Length dependent axonal neuropathies are generally very slowly progressive. Other etiologies need to be considered if the patient presents with a stocking-glove pattern of sensory loss in which symptoms present in the hands and feet simultaneously, or if the symptoms evolve quickly over several days to weeks.

Occasionally patients with mononeuritis multiplex due to vasculitis do not seek medical attention unless their symptoms and signs progress to become confluent and resemble a stocking-glove pattern. (See "Clinical manifestations of vasculitic neuropathy".) The history and examination help to differentiate mononeuritis multiplex from a length dependent axonal neuropathy: the patient will give a history of stepwise sensory loss in discrete nerve distributions (eg, ulnar aspect of hand, then peroneal distribution in foot, etc). Furthermore, weakness, which is not usually a significant complaint in length dependent axonal neuropathies, typically accompanies the sensory loss in mononeuritis multiplex.

Patients with Guillain-Barré syndrome may present with numbness or paresthesias affecting their feet and hands [4,5]. In this situation, the symptoms will have been present only a short time before the patient presents to medical attention. There may or may not be a history of an antecedent infection. The patient develops progressive weakness soon after the onset of sensory loss or paresthesias. The examination should reveal areflexia or depressed reflexes. Sensory loss should be minimal in comparison to the weakness and predominantly affects the larger myelinated fibers carrying proprioception and vibration. (See "Treatment and prognosis of Guillain-Barré syndrome in adults".)

Occasionally, patients with a variant of CIDP (chronic inflammatory demyelinating polyneuropathy) present with a history and examination that are most suggestive of a length dependent axonal neuropathy [6,7]. In this situation, the symptoms and signs are predominantly distal and sensory as opposed to the more common form of CIDP where symmetric proximal and distal motor weakness is the predominant symptom. EMG and nerve conduction studies are helpful in differentiating this variant of CIDP from an axonal neuropathy.

Central lesions affecting the cervical spinal cord can also present with a stocking-glove pattern of sensory loss. In the younger population, this may be the presenting symptom of a demyelinating lesion in the cervical cord. In the older population, this is frequently caused by cervical spondylosis with cord impingement. Imaging studies (eg, magnetic resonance imaging) are required to positively identify the precise etiology. Hyperreflexia, spasticity (clonus, increased tone), and extensor plantar responses are helpful in pointing to a central cause.

Sensory neuronopathies — Sensory neuronopathies are very rare causes of sensory loss. They result from degeneration at the level of the dorsal root ganglion and manifest with sensory ataxia, absent reflexes, and dysesthesias, as well as sensory loss [8]. They are differentiated from length-dependent sensory neuropathies in several ways:

Sensory neuronopathies do not necessarily follow a length-dependent pattern. In addition, they are frequently asymmetric. As an example, patients may present with initial numbness in a dermatomal distribution in one hand or even in the face.
Sensory neuronopathies lack motor involvement. In contrast, patients with length dependent neuropathies may not complain of weakness, but mild motor abnormalities can often be found on detailed clinical examination and/or nerve conduction studies.
Sensory neuronopathies tend to be much more disabling than length-dependent axonal neuropathies. As they progress, patients develop profound sensory ataxia, and almost always decline to the point where mobility aids are required (eg, cane, walker and/or wheelchair).
Sensory neuronopathies are most often associated with paraneoplastic phenomenon [8]. The latter is most commonly associated with small cell lung cancer and the presence of anti-Hu antibodies. (See "Paraneoplastic syndromes affecting the spinal cord and dorsal root ganglia", section on 'Subacute sensory neuronopathy'.)

Other causes of sensory neuronopathy include:

Sjogren's syndrome (see "Clinical manifestations of Sjögren's syndrome: Extraglandular disease and prognosis")
Guillain-Barre syndrome variant (see "Clinical features and diagnosis of Guillain-Barré syndrome in adults", section on 'Other variants')
Chemotherapy-induced, especially the platinum drugs (see "Neurologic complications of platinum-based chemotherapy")
Vitamin B6 toxicity (see "Overview of acquired peripheral neuropathies in children" section on Vitamin B6 (pyridoxine toxicity).)

Friedreich ataxia (see "Friedreich ataxia")
Investigations — Nerve conduction studies and electromyography can be helpful in characterizing neuropathies (eg, axonal versus demyelinating, acquired versus hereditary, etc). These studies are also helpful for discriminating whether sensory pathology is proximal or distal to the dorsal root ganglion (DRG). As an example, radiculopathies that are caused by pathology proximal to the DRG result in sensory loss in the corresponding dermatome, but nerve conduction studies reveal normal sensory responses. In contrast, axonal lesions at or distal to the DRG result in low amplitude or absent sensory responses.

Laboratory investigations are worthwhile to rule out treatable causes (eg, diabetes mellitus, lymphoproliferative disorders, uremia, vitamin B12 deficiency, syphilis, human immunodeficiency virus, and Lyme disease) if the history, physical examination, and electrophysiologic workup reveal a generalized sensorimotor axonal neuropathy (table 2) and (see "Overview of polyneuropathy"). Causes of painful sensory neuropathy and expected laboratory results are shown in the table (table 3A-B).

Unfortunately, the etiology is not always identified. In two separate studies of patients referred to tertiary care neuromuscular clinics for evaluation of peripheral neuropathy, approximately one-quarter remained undiagnosed after extensive workup [9,10].

Spinal cord lesions

Cape distribution sensory loss — Cape distribution sensory loss is an uncommon but well described pattern of sensory loss resulting from lesions of the central cervical cord (figure 3). The classic presentation involves diminution or loss of sensation for pinprick and temperature across the upper back, shoulders, and upper arms resulting from lesions that involve spinothalamic neurons as they cross in the anterior commissure in the cervical cord. The differential diagnosis includes tumor, syrinx, and demyelination.

Brown-Sequard syndrome — The Brown-Sequard syndrome results from a lesion involving only one side of the spinal cord. In this situation, the patient presents with diminished proprioception, vibration, and weakness on the side ipsilateral to the lesion, and decreased pinprick and temperature sensation on the contralateral side (figure 3). Hyperesthesia or pain may also occur ipsilateral to the lesion. Small lesions, such as those caused by demyelination, can result in isolated involvement of dorsal columns or spinothalamic tracts resulting in ipsilateral abnormalities in proprioception and vibration or contralateral abnormalities in pinprick and temperature, respectively.

Imaging studies — Magnetic resonance imaging (MRI) is the imaging method of choice in suspected spinal cord lesions as it is far more sensitive than CT in this situation. When a spinal cord lesion is suspected it is important to remember that the sensory level found on examination indicates that the lesion itself is at or above that level. The spinal cord levels or dermatomes are presented for the upper and lower extremities (figure 5 and figure 6). It is not uncommon for patients to present with an ascending pattern of sensory loss from a cervical cord lesion. Depending on when the patient is examined, different sensory levels will be found for the same lesion. Thus, in working up suspected spinal cord lesions, the physician must image the cord from the neck (cervical region) to the sensory level found on examination.

Brainstem lesions — There are several classic patterns of sensory loss found with lesions at various levels of the brainstem. Most brainstem lesions involve cranial nerves and/or their nuclei. The resultant signs and symptoms tend to be more useful in localizing the lesion than are the sensory findings in isolation.

Wallenberg syndrome is probably the most well known brainstem abnormality leading to sensory loss. It results from a lesion of the lateral medulla and was originally described as involving pain and temperature loss on the ipsilateral face and contralateral limbs and trunk. However, several other patterns of pain and temperature loss have been described in association with this syndrome, including contralateral face and bilateral face involvement [3]. Accompanying signs and symptoms include loss of vibration and proprioception as well as ataxia in the ipsilateral limbs. An ipsilateral Horner's syndrome, vertigo, nystagmus, hoarseness, and dysphagia are often present. (See "Posterior circulation cerebrovascular syndromes", section on 'Lateral medullary infarction'.)

The optimal initial investigation when the history and examination suggest a brainstem lesion is a brain MRI. Head CT scans are rarely useful as the artifact resulting from the skull base obscures the brainstem images.

Thalamic lesions — Thalamic lesions may cause a contralateral sensory deficit that involves all sensory modalities to varying degrees. Although tumors and abscesses can involve the thalamus, typically the onset of sensory loss in thalamic lesions is acute or subacute and is the result of a lacunar infarct [11]. (See "Lacunar infarcts".)

Thalamic pain syndrome, a type of central post-stroke pain, has been well described and is not uncommon in the recovery phase of these infarcts [12]. Often the sensory examination is normal but the patient experiences severe pain that may be paroxysmal and exacerbated by touch over the contralateral hemibody.

Sensory cortex — Discrete lesions of the sensory cortex are unusual. When they occur only a small part of the body is affected (corresponding to the region of the homunculus where the lesion is found). Any lesion large enough to affect a significant area of the body will result in other associated symptoms.

Cortical signs and symptoms, including aphasia, neglect, and/or cortical sensory loss (eg, graphesthesia), are useful in placing a lesion in the cortex. However, cortical signs and symptoms can only be assessed in patients who have adequate sensation for primary modalities; profound alteration of the primary sensory modalities, particularly touch, prevents sensory information from reaching the cerebral hemisphere, thereby rendering cortical sensory tests inaccurate.

Either a head CT scan or MRI is a useful initial investigation in the workup of cortical or thalamic sensory loss, although MRI is more sensitive in the diagnosis of demyelinating lesions (eg, multiple sclerosis).

SUMMARY — The following is a simplified approach to the localization of the lesion responsible for sensory loss:

Is disease confined to part of a limb or most of an extremity or trunk? — Disease that is confined to part of a limb is consistent with mononeuropathy or radiculopathy.

Mononeuropathies may involve disorders of the upper extremity (eg, median [carpal tunnel syndrome], ulnar, radial nerves or brachial plexopathy) or lower extremity (eg, peroneal, posterior tibial [tarsal tunnel], femoral, or lateral femoral cutaneous nerves [meralgia paresthetica], (table 4). (See "Overview of upper extremity peripheral nerve syndromes" and "Overview of lower extremity peripheral nerve syndromes".)
Radiculopathies classically present with sensory loss in the distribution of a dermatome or myotome, and may be caused by structural spine disease (eg, neck or lower back), infection (ie, varicella zoster virus, Lyme disease, cytomegalovirus), leptomeningeal carcinomatosis, or focal extramedullary tumors. Sensory loss may be relatively mild with radiculopathies or may only involve small "signature zones" rather than entire dermatomes (table 1); paroxysmal severe lancinating pain is common.
Disease that involves most of an extremity or trunk is consistent with polyneuropathy, spinal cord disease, or central nervous system problems.

For sensory loss that involves most of a limb or trunk, is one or both sides of the body involved? — Polyneuropathy and spinal cord disease present with sensory loss on both sides of the body:

Polyneuropathy may be caused by a variety of systemic diseases, drugs, or toxins. Stocking-glove sensory loss is characteristic of a length dependent axonal polyneuropathy. The work-up of polyneuropathy is summarized in algorithm 1 and discussed in more detail separately (algorithm 1) and (see "Overview of polyneuropathy").
Spinal cord disease typically presents with a sensory level. A cape distribution of sensory loss is characteristic of disease of the central cervical spinal cord. The Brown-Sequard syndrome is characterized by diminished proprioception, vibration, and weakness on the side ipsilateral to the lesion, and decreased pinprick and temperature sensation on the contralateral side.
Sensory loss confined to one side of the body is characteristic of disorders of the brainstem, thalamus, or cortex.

Brainstem lesions are unique in that cranial nerves are usually also involved, and there may be sensory loss of the face that is opposite that of the body.
In contrast, disease of the thalamus or cortex may involve sensory loss of the face that is on the same side as sensory loss of the body.
Cortical signs and symptoms (eg, aphasia, neglect, abnormalities of graphesthesia, stereognosis, two point discrimination, extinction) are useful for placing a lesion in the cerebral cortex
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Old 08-23-2010, 02:32 PM
marilyngarry marilyngarry is offline
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Join Date: Apr 2007
Location: Nashville
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Wink Peripheral Sensorimotor Neuropathy

Under ICD-9 CM guidelines - look at 356.2

I found this information in an article published by Up To Date: This may be helpful in identifying the true definition of your patient. Query the physician for clarification if clarity is not documented.

Approach to the patient with sensory loss
Authors
Hannah R Briemberg, MD, FRCPC
Anthony A Amato, MD
Section Editor
Michael J Aminoff, MD, DSc
Deputy Editor
Janet L Wilterdink, MD
Last literature review version 18.2: May 2010 | This topic last updated: March 31, 2010 (More)
INTRODUCTION — Sensory loss may be due to disorders of the central or peripheral nervous system. As in most of neurology, the initial goal when confronted with a patient with sensory loss is localization of the lesion using information from the history and physical examination. This narrows the differential diagnosis and directs further investigations. Localization requires an understanding of the anatomy of the sensory system.

ANATOMY OF THE SENSORY SYSTEM — Perception of a somatic sensation depends on detection of a stimulus by specialized receptors in the skin, muscle, or joints. Information from these receptors is then transmitted via peripheral nerves to the central nervous system. With the exception of the mesencephalic nucleus, whose projections carry proprioceptive information from the muscles of mastication [1], the cell bodies of the primary sensory neurons that constitute the peripheral nerves reside in ganglia outside of the central nervous system. Projections from these ganglia then enter the central nervous system to synapse with second order neurons.

The peripheral nerves are made up of large myelinated fibers that transmit proprioceptive, vibratory, pressure, and touch stimuli, and small, relatively unmyelinated fibers that transmit pain, temperature, and touch stimuli. (Note that touch is transmitted by both large and small fibers.) Projections from the cell bodies receiving pain, temperature, and touch stimuli enter the spinal cord via the dorsal nerve root. These fibers terminate in the dorsal horns, fanning out over several segments [2]. They synapse with the second order neurons in the dorsal horns. These neurons then cross the midline of the cord in the anterior commissure in front of the central canal, and these second order neurons ascend (now on the opposite side of the spinal cord to the peripheral nerve) in either the anterior spinothalamic tract (touch) or the lateral spinothalamic tract (pain and temperature) to the ventral posterolateral nucleus of the thalamus. Here, they synapse with neurons which ascend to the primary sensory cortex in the parietal lobe (figure 1).

Projections from the dorsal root ganglia that carry proprioceptive, vibratory, pressure, and touch stimuli directly enter the dorsal columns from the dorsal roots [1]. The gracile column is medial and carries stimuli from the lumbar and thoracic region; the cuneate column begins laterally in the cervical region, which it subserves. Thus, the dorsal columns consist of first order neurons traveling ipsilateral to the peripheral nerve from which they originate. These neurons synapse with second order neurons in the cuneate and gracile nuclei of the medulla. These second order neurons cross in the dorsal midline of the medulla and ascend through the brainstem as the medial lemniscus to the ventral posterolateral nucleus of the thalamus where they synapse with third order neurons which project through the internal capsule and the centrum semiovale to the primary sensory cortex in the parietal lobe (figure 2).

As with the motor cortex, the primary sensory cortex is arranged somatotopically, with the face represented laterally, close to the Sylvian fissure. The hand and arm are represented just above the region for the face and the leg is represented medially, similar to the layout of the motor homunculus.

DEFINITIONS — Sensory loss is categorized as follows:

Hypesthesia is the diminished ability to perceive pain, temperature, touch, or vibration.
Anesthesia is the complete inability to perceive pain, temperature, touch, or vibration.
Hypalgesia is the decreased sensitivity to painful stimuli.
Analgesia is the complete insensitivity to painful stimuli.
Hyperpathia, hyperesthesia, and allodynia refer to an increased sensitivity to sensory stimuli.

SENSORY EXAMINATION — The goal of the sensory examination is to "localize the lesion." This portion of the examination tends to be subjective because it relies on the patient's responses to various stimuli; thus, it is usually done following the motor examination. With the more objective data obtained from the motor examination, the examiner is often able to narrow down a differential and proceed with a more focused sensory examination, resulting in less frustration for both the patient and examiner. (See "The detailed neurologic examination in adults", section on 'Sensory examination'.)

The primary sensory modalities usually are examined first. These include touch, proprioception, vibration, temperature, and pain. Abnormalities in these sensations may occur with any sensory syndrome (eg, peripheral nerve injury, radiculopathy, spinal cord syndromes, thalamic and cerebral hemispheric syndromes). A disproportionate loss of vibration sense and proprioception, compared with pain and temperature sensation, tends to occur with diseases of the dorsal columns of the spinal cord (eg, tabes dorsalis, vitamin B12 deficiency, multiple sclerosis) and also with demyelinating neuropathies and sensory neuronopathies. (See "Pathogenesis, clinical manifestations, and treatment of late syphilis" and "Etiology and clinical manifestations of vitamin B12 and folic acid deficiency".)

Higher cortical sensation can be examined if touch sensation remains relatively preserved and the patient is suspected of having a cortical lesion. Examination of cortical sensation includes two point discrimination, graphesthesia, stereognosis, and extinction:

Two point discrimination is the ability to recognize two points applied simultaneously to the skin as distinct from a single point. (See "The detailed neurologic examination in adults", section on 'Two-point discrimination'.)
Graphesthesia is the ability of the patient to identify numbers or letters drawn in the palm of the hand.
Stereognosis is the ability to recognize common objects such as keys, coins or paper clips by touching or handling them with one's eyes closed.
Extinction is evaluated by simultaneously touching two separate points on either side of the body. The test is abnormal if the patient consistently identifies the stimulus on only one side of the body. Extinction is seen in relatively large parietal lesions.
The Romberg is a test of proprioception. It is positive when the patient is able to stand with feet together and eyes open without losing his balance but is unable to remain steady with the eyes closed. This occurs because patients are using their eyes to compensate for the lack of sensory feedback they are receiving from their lower extremities. A functional correlate of this often comes out in the history when the patient notes that he loses his balance when he gets up at night in a darkened room.

PATTERNS OF SENSORY LOSS — The history and physical examination are key to determining the cause of sensory loss. Ancillary studies may be helpful in selected circumstances.

Sensory loss that is confined to a part of a limb suggests injury to a peripheral nerve, nerve plexus, or spinal root (eg, mononeuropathy or radiculopathy). In contrast, sensory loss involving most of an extremity or the trunk suggests the presence of other disorders, that may be distinguished as follows (figure 3):

Involvement of both sides of the body is consistent with a polyneuropathy or spinal cord disease, while involvement of one side is consistent with contralateral disease of the brainstem, thalamus, or cerebral cortex.
A sensory level is consistent with spinal cord disease or, more rarely, lateral medullary infarction.
Sensory loss of the face suggests disease above the spinal cord (eg, brainstem, thalamus, or cerebral hemispheres). With lower brainstem disease (eg, lateral medullary syndrome), the sensory loss on the face is typically opposite that of the body, although ipsilateral sensory loss has also been reported [3]; sensory loss is on the same side of the face and body with upper brainstem, thalamic, or hemispheric disease.
"Stocking-glove" sensory loss is most commonly seen with length dependent axonal neuropathies, although other disorders may also present with this pattern.
Disproportionate loss of vibration sense and proprioception, compared with pain and temperature sensation, tends to occur with diseases of the dorsal columns of the spinal cord (eg, tabes dorsalis, vitamin B12 deficiency, multiple sclerosis) and demyelinating polyneuropathy.
A number of these disorders are discussed in more detail below.

Neuropathy

Mononeuropathy and radiculopathy — Mononeuropathies refer to pathology affecting an individual peripheral nerve. One common example is carpal tunnel syndrome; patients with carpal tunnel syndrome frequently complain of numbness and tingling in the median nerve distribution that can be particularly bothersome at night, often awakening them from sleep. This may or may not be accompanied by wrist pain that can radiate up the arm or into the hand. (See "Clinical manifestations and diagnosis of carpal tunnel syndrome".) Mononeuropathies are diagnosed clinically based on signs and symptoms that correlate with an individual nerve distribution (figure 4).

Radiculopathies refer to pathology affecting the nerve root, resulting in signs and symptoms in the corresponding dermatome (figure 5 and figure 6) and myotome. Because of the overlap in nerve root innervation of both individual muscles and dermatomes, weakness and sensory loss can be mild and/or not involve the entire region described on the dermatome/myotome maps. Instead, smaller "signature zones" of sensory loss may define the level of nerve root involvement (table 1). Although radiculopathies may not cause significant sensory loss, they characteristically result in paroxysmal severe lancinating pain that may be exacerbated by coughing, sneezing, or straining.

Occasionally it is difficult to differentiate a mononeuropathy from a radiculopathy clinically. As an example, both a peroneal nerve palsy and an L5 root lesion can result in a drop foot and numbness over the lateral aspect of the leg and dorsum of the foot. (See "Overview of lower extremity peripheral nerve syndromes".) Electrodiagnostic testing (nerve conduction studies and electromyography) are useful in distinguishing between these conditions. In a peroneal palsy, nerve conduction studies may demonstrate focal slowing in the peroneal nerve at the fibular head, while in an L5 radiculopathy there may be evidence of denervation in L5 muscles outside of the peroneal territory (eg, tibialis posterior or flexor digitorum longus, both of which are innervated by the tibial portion of the sciatic nerve).

Stocking-glove sensory loss — Stocking-glove sensory loss is a term used to describe sensory loss affecting the distal lower and upper extremities that is most commonly seen in length dependent axonal neuropathies. Axonal neuropathies are most frequently due to:

Diabetes mellitus
Alcohol
Vitamin B12 deficiency
Syphilis
Human immunodeficiency virus
Lyme disease
Uremia
Chemotherapy
Vasculitis
Paraneoplastic neuropathy
Amyloidosis
With axonal neuropathies, the longest axons are affected first and the symptoms start distally in these axons and progress proximally. Thus, patients do not start to notice numbness in their hands until the sensory symptoms or signs have progressed to just above the knee.

The examination usually reveals a decrease in vibration threshold, pinprick, and temperature distally. Diminished proprioception at the great toe is typically also evident on careful examination, but can be difficult to detect. In combined large and small fiber neuropathies, the ankle jerk is frequently diminished or absent. Patients with pure small fiber neuropathies will primarily demonstrate loss of pinprick and temperature distally, although vibration perception can also be affected. Proprioception and deep tendon reflexes remain intact.

Length dependent axonal neuropathies are generally very slowly progressive. Other etiologies need to be considered if the patient presents with a stocking-glove pattern of sensory loss in which symptoms present in the hands and feet simultaneously, or if the symptoms evolve quickly over several days to weeks.

Occasionally patients with mononeuritis multiplex due to vasculitis do not seek medical attention unless their symptoms and signs progress to become confluent and resemble a stocking-glove pattern. (See "Clinical manifestations of vasculitic neuropathy".) The history and examination help to differentiate mononeuritis multiplex from a length dependent axonal neuropathy: the patient will give a history of stepwise sensory loss in discrete nerve distributions (eg, ulnar aspect of hand, then peroneal distribution in foot, etc). Furthermore, weakness, which is not usually a significant complaint in length dependent axonal neuropathies, typically accompanies the sensory loss in mononeuritis multiplex.

Patients with Guillain-Barré syndrome may present with numbness or paresthesias affecting their feet and hands [4,5]. In this situation, the symptoms will have been present only a short time before the patient presents to medical attention. There may or may not be a history of an antecedent infection. The patient develops progressive weakness soon after the onset of sensory loss or paresthesias. The examination should reveal areflexia or depressed reflexes. Sensory loss should be minimal in comparison to the weakness and predominantly affects the larger myelinated fibers carrying proprioception and vibration. (See "Treatment and prognosis of Guillain-Barré syndrome in adults".)

Occasionally, patients with a variant of CIDP (chronic inflammatory demyelinating polyneuropathy) present with a history and examination that are most suggestive of a length dependent axonal neuropathy [6,7]. In this situation, the symptoms and signs are predominantly distal and sensory as opposed to the more common form of CIDP where symmetric proximal and distal motor weakness is the predominant symptom. EMG and nerve conduction studies are helpful in differentiating this variant of CIDP from an axonal neuropathy.

Central lesions affecting the cervical spinal cord can also present with a stocking-glove pattern of sensory loss. In the younger population, this may be the presenting symptom of a demyelinating lesion in the cervical cord. In the older population, this is frequently caused by cervical spondylosis with cord impingement. Imaging studies (eg, magnetic resonance imaging) are required to positively identify the precise etiology. Hyperreflexia, spasticity (clonus, increased tone), and extensor plantar responses are helpful in pointing to a central cause.

Sensory neuronopathies — Sensory neuronopathies are very rare causes of sensory loss. They result from degeneration at the level of the dorsal root ganglion and manifest with sensory ataxia, absent reflexes, and dysesthesias, as well as sensory loss [8]. They are differentiated from length-dependent sensory neuropathies in several ways:

Sensory neuronopathies do not necessarily follow a length-dependent pattern. In addition, they are frequently asymmetric. As an example, patients may present with initial numbness in a dermatomal distribution in one hand or even in the face.
Sensory neuronopathies lack motor involvement. In contrast, patients with length dependent neuropathies may not complain of weakness, but mild motor abnormalities can often be found on detailed clinical examination and/or nerve conduction studies.
Sensory neuronopathies tend to be much more disabling than length-dependent axonal neuropathies. As they progress, patients develop profound sensory ataxia, and almost always decline to the point where mobility aids are required (eg, cane, walker and/or wheelchair).
Sensory neuronopathies are most often associated with paraneoplastic phenomenon [8]. The latter is most commonly associated with small cell lung cancer and the presence of anti-Hu antibodies. (See "Paraneoplastic syndromes affecting the spinal cord and dorsal root ganglia", section on 'Subacute sensory neuronopathy'.)

Other causes of sensory neuronopathy include:

Sjogren's syndrome (see "Clinical manifestations of Sjögren's syndrome: Extraglandular disease and prognosis")
Guillain-Barre syndrome variant (see "Clinical features and diagnosis of Guillain-Barré syndrome in adults", section on 'Other variants')
Chemotherapy-induced, especially the platinum drugs (see "Neurologic complications of platinum-based chemotherapy")
Vitamin B6 toxicity (see "Overview of acquired peripheral neuropathies in children" section on Vitamin B6 (pyridoxine toxicity).)

Friedreich ataxia (see "Friedreich ataxia")
Investigations — Nerve conduction studies and electromyography can be helpful in characterizing neuropathies (eg, axonal versus demyelinating, acquired versus hereditary, etc). These studies are also helpful for discriminating whether sensory pathology is proximal or distal to the dorsal root ganglion (DRG). As an example, radiculopathies that are caused by pathology proximal to the DRG result in sensory loss in the corresponding dermatome, but nerve conduction studies reveal normal sensory responses. In contrast, axonal lesions at or distal to the DRG result in low amplitude or absent sensory responses.

Laboratory investigations are worthwhile to rule out treatable causes (eg, diabetes mellitus, lymphoproliferative disorders, uremia, vitamin B12 deficiency, syphilis, human immunodeficiency virus, and Lyme disease) if the history, physical examination, and electrophysiologic workup reveal a generalized sensorimotor axonal neuropathy (table 2) and (see "Overview of polyneuropathy"). Causes of painful sensory neuropathy and expected laboratory results are shown in the table (table 3A-B).

Unfortunately, the etiology is not always identified. In two separate studies of patients referred to tertiary care neuromuscular clinics for evaluation of peripheral neuropathy, approximately one-quarter remained undiagnosed after extensive workup [9,10].

Spinal cord lesions

Cape distribution sensory loss — Cape distribution sensory loss is an uncommon but well described pattern of sensory loss resulting from lesions of the central cervical cord (figure 3). The classic presentation involves diminution or loss of sensation for pinprick and temperature across the upper back, shoulders, and upper arms resulting from lesions that involve spinothalamic neurons as they cross in the anterior commissure in the cervical cord. The differential diagnosis includes tumor, syrinx, and demyelination.

Brown-Sequard syndrome — The Brown-Sequard syndrome results from a lesion involving only one side of the spinal cord. In this situation, the patient presents with diminished proprioception, vibration, and weakness on the side ipsilateral to the lesion, and decreased pinprick and temperature sensation on the contralateral side (figure 3). Hyperesthesia or pain may also occur ipsilateral to the lesion. Small lesions, such as those caused by demyelination, can result in isolated involvement of dorsal columns or spinothalamic tracts resulting in ipsilateral abnormalities in proprioception and vibration or contralateral abnormalities in pinprick and temperature, respectively.

Imaging studies — Magnetic resonance imaging (MRI) is the imaging method of choice in suspected spinal cord lesions as it is far more sensitive than CT in this situation. When a spinal cord lesion is suspected it is important to remember that the sensory level found on examination indicates that the lesion itself is at or above that level. The spinal cord levels or dermatomes are presented for the upper and lower extremities (figure 5 and figure 6). It is not uncommon for patients to present with an ascending pattern of sensory loss from a cervical cord lesion. Depending on when the patient is examined, different sensory levels will be found for the same lesion. Thus, in working up suspected spinal cord lesions, the physician must image the cord from the neck (cervical region) to the sensory level found on examination.

Brainstem lesions — There are several classic patterns of sensory loss found with lesions at various levels of the brainstem. Most brainstem lesions involve cranial nerves and/or their nuclei. The resultant signs and symptoms tend to be more useful in localizing the lesion than are the sensory findings in isolation.

Wallenberg syndrome is probably the most well known brainstem abnormality leading to sensory loss. It results from a lesion of the lateral medulla and was originally described as involving pain and temperature loss on the ipsilateral face and contralateral limbs and trunk. However, several other patterns of pain and temperature loss have been described in association with this syndrome, including contralateral face and bilateral face involvement [3]. Accompanying signs and symptoms include loss of vibration and proprioception as well as ataxia in the ipsilateral limbs. An ipsilateral Horner's syndrome, vertigo, nystagmus, hoarseness, and dysphagia are often present. (See "Posterior circulation cerebrovascular syndromes", section on 'Lateral medullary infarction'.)

The optimal initial investigation when the history and examination suggest a brainstem lesion is a brain MRI. Head CT scans are rarely useful as the artifact resulting from the skull base obscures the brainstem images.

Thalamic lesions — Thalamic lesions may cause a contralateral sensory deficit that involves all sensory modalities to varying degrees. Although tumors and abscesses can involve the thalamus, typically the onset of sensory loss in thalamic lesions is acute or subacute and is the result of a lacunar infarct [11]. (See "Lacunar infarcts".)

Thalamic pain syndrome, a type of central post-stroke pain, has been well described and is not uncommon in the recovery phase of these infarcts [12]. Often the sensory examination is normal but the patient experiences severe pain that may be paroxysmal and exacerbated by touch over the contralateral hemibody.

Sensory cortex — Discrete lesions of the sensory cortex are unusual. When they occur only a small part of the body is affected (corresponding to the region of the homunculus where the lesion is found). Any lesion large enough to affect a significant area of the body will result in other associated symptoms.

Cortical signs and symptoms, including aphasia, neglect, and/or cortical sensory loss (eg, graphesthesia), are useful in placing a lesion in the cortex. However, cortical signs and symptoms can only be assessed in patients who have adequate sensation for primary modalities; profound alteration of the primary sensory modalities, particularly touch, prevents sensory information from reaching the cerebral hemisphere, thereby rendering cortical sensory tests inaccurate.

Either a head CT scan or MRI is a useful initial investigation in the workup of cortical or thalamic sensory loss, although MRI is more sensitive in the diagnosis of demyelinating lesions (eg, multiple sclerosis).

SUMMARY — The following is a simplified approach to the localization of the lesion responsible for sensory loss:

Is disease confined to part of a limb or most of an extremity or trunk? — Disease that is confined to part of a limb is consistent with mononeuropathy or radiculopathy.

Mononeuropathies may involve disorders of the upper extremity (eg, median [carpal tunnel syndrome], ulnar, radial nerves or brachial plexopathy) or lower extremity (eg, peroneal, posterior tibial [tarsal tunnel], femoral, or lateral femoral cutaneous nerves [meralgia paresthetica], (table 4). (See "Overview of upper extremity peripheral nerve syndromes" and "Overview of lower extremity peripheral nerve syndromes".)
Radiculopathies classically present with sensory loss in the distribution of a dermatome or myotome, and may be caused by structural spine disease (eg, neck or lower back), infection (ie, varicella zoster virus, Lyme disease, cytomegalovirus), leptomeningeal carcinomatosis, or focal extramedullary tumors. Sensory loss may be relatively mild with radiculopathies or may only involve small "signature zones" rather than entire dermatomes (table 1); paroxysmal severe lancinating pain is common.
Disease that involves most of an extremity or trunk is consistent with polyneuropathy, spinal cord disease, or central nervous system problems.

For sensory loss that involves most of a limb or trunk, is one or both sides of the body involved? — Polyneuropathy and spinal cord disease present with sensory loss on both sides of the body:

Polyneuropathy may be caused by a variety of systemic diseases, drugs, or toxins. Stocking-glove sensory loss is characteristic of a length dependent axonal polyneuropathy. The work-up of polyneuropathy is summarized in algorithm 1 and discussed in more detail separately (algorithm 1) and (see "Overview of polyneuropathy").
Spinal cord disease typically presents with a sensory level. A cape distribution of sensory loss is characteristic of disease of the central cervical spinal cord. The Brown-Sequard syndrome is characterized by diminished proprioception, vibration, and weakness on the side ipsilateral to the lesion, and decreased pinprick and temperature sensation on the contralateral side.
Sensory loss confined to one side of the body is characteristic of disorders of the brainstem, thalamus, or cortex.

Brainstem lesions are unique in that cranial nerves are usually also involved, and there may be sensory loss of the face that is opposite that of the body.
In contrast, disease of the thalamus or cortex may involve sensory loss of the face that is on the same side as sensory loss of the body.
Cortical signs and symptoms (eg, aphasia, neglect, abnormalities of graphesthesia, stereognosis, two point discrimination, extinction) are useful for placing a lesion in the cerebral cortex
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