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The sensory system is that part of the nervous system responsible for processing sensory information, including the somatosensory and special senses: smell, vision, taste, hearing, and vestibular sensation. Abnormalities of sensation can be characterized by an increase, decrease, impairment, or loss of feeling. The diagnosis of sensory problems requires an understanding of the anatomy and an analysis of the presentation, location, characteristics, and distribution of symptoms.
ANATOMY OF THE SENSORY PATHWAYS
The first step in any sensory pathway is activation of a sensory receptor by a specific stimulus. Information from the receptor is then carried to the central nervous system (CNS) by the afferent nerves (peripheral or cranial) known as first-order neurons. Pain and temperature sensation is carried by thinly myelinated (A-δ) and unmyelinated slowly conducting (C) fibers that synapse as they enter the dorsal horn of the spinal cord. From there, axons from the second-order neurons cross and travel contralaterally in the spinothalamic tract (STT), also called the anterolateral system (Fig. 6-1). Proprioception, vibration, and light touch run ipsilaterally in heavily myelinated (A-α and A-β) fibers in the dorsal column system, reaching the second-order neuron at the level of the medulla in the nuclei gracilis and cuneatus. Axons from these nuclei cross in the lower medulla to form the medial lemniscus (Fig. 6-2).
There is a somatotopic arrangement of fibers in these tracts.
•STT: At the level of the spinal cord, sacral segments are located laterally and cervical segments medially.
•The dorsal columns: The most medial fibers convey input from sacral areas, whereas lateral fibers convey information from the arms. At the level of the medial lemniscus, the upper body fibers become medial and those of the lower body lateral.
Facial sensation is carried to the brainstem by the trigeminal nerve. The STT and the trigeminal tract terminate in the thalamus, ventroposterolateral and ventroposteromedial, respectively, with further cortical projections through the third-order neurons to the postcentral cortex in a somatotopic arrangement similar to that seen in the motor cortex, with the face in the lowest area of the parietal lobe and the leg in the parasagittal parietal area. Fine sensory discrimination and localization of pain, temperature, touch, and pressure require normal functioning of the sensory cortex (Fig. 6-3).
EXAMINATION OF THE SENSORY SYSTEM
The sensory examination is the most subjective, and sometimes the most difficult, component of the neurologic examination; it requires the patient’s cooperation. Inattention or aphasia may complicate interpretation of the sensory examination. The evaluation of different primary sensory modalities, including temperature, pain (or pinprick), light touch, vibration, and proprioception, is necessary to characterize sensory loss and its extent. In some instances, it is difficult to demonstrate sensory abnormalities in a patient with sensory symptoms. In others, the examination may show sensory findings in an asymptomatic patient. Whatever the situation, the sensory examination must be organized and methodical.
Touch sensation is tested using a very soft stimulus, such as a wisp of cotton. Pain sensation is tested with a pin. Thermal modalities are tested using objects with a temperature range between 10°C and 50°C because beyond those limits the stimulus becomes painful. Moving the great toe (or a finger) up and down, by just a few millimeters, and asking the patient to indicate the direction of movement (with the eyes closed) tests proprioception or joint position sense. Vibration sense requires a tuning fork (128 Hz) to be applied to the toes and other bony prominences.
FIGURE 6-1. The anterolateral system. VPL, ventroposterolateral.
The next step is to record the sensory symptoms and findings using accepted definitions. It is best to record the patient’s own words when possible. Not only the presence or absence of sensation but also slight differences and gradations should be recorded. The following list defines some of the terminology used to describe sensory abnormalities:
FIGURE 6-2. The posterior column—medial lemniscal system. VPL, ventroposterolateral.
•Paresthesias are abnormal sensations described by the patient as tingling, prickling, pins, and needles, and so on.
•Dysesthesias are abnormal and often unpleasant sensations in response to touch.
•Hyperesthesia is increased sensitivity to sensory stimuli. The opposite is hypoesthesia.
•Allodynia is pain provoked by normally innocuous stimuli.
•Dissociated sensory loss is a pattern of neurologic dysfunction of a single sensory tract (either posterior columns or STTs) in which the loss of proprioception and fine touch is not associated with loss of pain and temperature, or vice versa. For example, in syringomyelia, a condition in which the central canal of the spinal cord expands, the STT is compromised early. This leads to loss of pain and temperature sensation in the dermatomes involved but preservation of posterior column function and, therefore, a normal response to light touch and normal proprioception. Such dissociated sensory loss occurs frequently with central cord syndromes (see Chapter 22).
FIGURE 6-3. Somatotopic map (“homunculus”) of the sensory cortex. Reprinted with permission from Jensen S. Nursing Health Assessment. 1st ed. Baltimore, MD: Lippincott Williams & Wilkins; 2010. Figure 24.3.
APPROACH TO THE PATIENT WITH SENSORY LOSS
As with any aspect of the neurologic examination, the approach to sensory symptoms begins with a careful history. Patients complaining of sensory dysfunction can report negative symptoms, positive symptoms, or both. Negative symptoms include numbness, loss of cold or warm sensation, blindness, and deafness. Positive symptoms include pain, paresthesias (tingling, pins, and needles), visual sparkles, and tinnitus. Listening to the patient’s experience will help guide the physical examination and may even provide insight into potential causes. For example, negative symptoms usually imply disruption of nerve excitation (such as in a stroke), whereas positive symptoms refer in general to excitation or disinhibition (as seen with seizures or migraine).
Once the history is obtained, the next task is to establish the presence or absence of a neurologic lesion or deficit. If a lesion is identified, the extent or location of the lesion and its effect on different sensory modalities should be mapped out by a careful and detailed sensory examination. This is important because different pathologic processes can affect different sensory symptoms and lead to specific patterns of sensory loss.
Although in theory it is easy to distinguish peripheral nerve injury from disease in other locations, this is often not possible or at best imprecise in practice. Nevertheless, the history and complete physical examination together may help the clinician more definitively determine the neuroanatomic level at which the symptoms are produced, that is, at nerve, plexus, root, cord, or other CNS locations. In general, compression of a peripheral nerve causes sensory loss in the territory of that specific nerve. Root problems produce a dermatomal pattern of sensory loss (Fig. 6-4). Spinal cord disease leads to a characteristic loss of sensation below a certain spinal level (sensory level). With brainstem lesions, the sensory abnormalities may occur on the ipsilateral side of the face and contralateral side of the body. Central sensory loss involving the thalamus or sensory cortex will generally affect the contralateral face, arm, and leg.
Because there are many primary neurologic diseases as well as systemic illnesses that can present with sensory symptoms, putting the sensory examination into the context of the remainder of the physical examination may make potential etiologies more obvious. Sometimes, the sensory problems are accompanied by other signs such as weakness, neglect, visual field cuts, cognitive or behavioral problems, or seizures that may help to determine the location of the lesion.
FIGURE 6-4. Sensory dermatomes. Reprinted with permission from Hoppenfeld JD. Fundamentals of Pain Medicine: How to Diagnose and Treat your Patients. 1st ed. Baltimore, MD: Lippincott Williams & Wilkins; 2014. Figure 2.12.
Examples of different patterns of sensory loss and the location of the respective neurologic problem are shown in Table 6-1. This table serves as a guide to the process of localization and diagnosis based on clinical symptoms and the neurologic examination, without the need for further technologic resources.
TABLE 6-1. Patterns of Sensory Loss According to Localization | |||
Site of the Lesion | Sensory Findings | Other Neurologic Abnormalities | Examples |
Peripheral nerve | Loss of LT, T, PP, and proprioception in the affected area; associated weakness in muscles innervated by that nerve | Distal muscle weakness, muscle atrophy, areflexia | Peroneal neuropathy; median neuropathy (carpal tunnel syndrome); ulnar neuropathy |
Root | Variable loss of all sensory modalities in a dermatomal distribution | Weakness in a myotomal distribution, atrophy, segmental hyporeflexia | L5 radiculopathy; C6 radiculopathy |
Plexus | Sensory loss in the distribution of two or more peripheral nerves | Weakness and atrophy that cannot be localized to a single nerve or root, areflexia | Brachial plexopathy due to trauma, inflammation, tumor infiltration |
Spinal cord | •Sensory level: bilateral loss of all sensory modalities •Sensory dissociation •Contralateral hypoesthesia and ipsilateral loss of proprioception (Brown-Sequard syndrome) •Proprioceptive loss and corticospinal tract involvement | Paraplegia, tetraplegia. Initially areflexia, then hyperreflexia below the lesion; Babinski sign | Myelopathy; central cord syndromes; Brown-Sequard syndrome; vitamin B12 deficiency (subacute combined degeneration) |
Brainstem | Ipsilateral facial numbness and contralateral body numbness | Alternating hemiplegia; cranial nerve findings; ataxia | Posterior circulation strokes; brainstem tumor |
Thalamus | Hemibody anesthesia | May have motor findings | Lacunar stroke; hemorrhage |
Posterior limb of internal capsule | Hemibody anesthesia | Hemiplegia | Lacunar stroke; hemorrhage; tumor |
Cortex | All modalities affected on the contralateral side | Sensory neglect; agraphesthesia | Parietal stroke; hemorrhage; AVM |
Psychogenic | Hyperesthesia for one modality in one area with anesthesia for another modality in the same area; changing sensory findings; nonphysiologic sensory level changes (abrupt midline changes, vibration asymmetry over the forehead, etc.) | Any | Psychogenic (this is a diagnosis of exclusion) |
AVM, arteriovenous malformation; LT, light touch; PP, pinprick; T, temperature. |
The last step in evaluating these sensory abnormalities is to determine the cause. There are many primary neurologic diseases as well as systemic diseases that can present with sensory symptoms; many are explored in more detail in Chapter 23 on peripheral neuropathies.
●STT is the pathway for pain, temperature, and light (poorly localized) touch. Mnemonic: STT (sting, temperature, touch).
●The dorsal columns carry well-localized touch, pressure, vibration, and conscious proprioception.
●Nonconscious proprioception is conveyed by the spinocerebellar tracts.
●Damage to a peripheral nerve produces a sensory deficit in the territory innervated by that nerve. Damage to a nerve root may produce a dermatomal loss of sensation. Damage to the brachial or lumbar plexus produces sensory loss in multiple nerve territories.
●Spinal cord lesions often produce an identifiable sensory level on examination. Brainstem lesions cause crossed sensory loss. Thalamic and cortical lesions produce contralateral hypoesthesia or anesthesia.
●Examples of sensory dissociation include syringomyelia (loss of pain and temperature sensation, with preserved proprioception); Brown-Sequard syndrome (loss of proprioception on the side ipsilateral to the lesion, and loss of pain and temperature sensation on the contralateral side); and subacute combined degeneration (loss of proprioception, but preserved pain and temperature sensation).