1. Chapter 7: Somatosensation: Clinical Application Copyright © 2013 by Saunders, an imprint of Elsevier Inc.

2. Somatosensory Information Protects Against Injury  Somatosensation is necessary for accurate control of movements and protects against injury. 2 Copyright © 2013 by Saunders, an imprint of Elsevier Inc.

3. Tests for Somatosensation  Sensory exams cover conscious relay pathways:  Discriminative touch  Conscious proprioception  Fast pain  Discriminative temperature  Purpose of the exam: to establish whether sensory impairment is present and, if so, the location, type of sensation affected, and severity of the deficit. 3 Copyright © 2013 by Saunders, an imprint of Elsevier Inc.

4. Tests for Somatosensation  Six guidelines improve the reliability of sensory testing:  Administer tests in a quiet, distraction-free setting.  Position the patient seated or lying supported by a firm, stable surface to avoid challenging balance.  Explain the purpose of the test.  Demonstrate each test before administering.  Block the patient’s vision during the tests.  Apply stimuli near the center of the dermatomes being tested. 4 Copyright © 2013 by Saunders, an imprint of Elsevier Inc.

5. Tests for Somatosensation  Quick screening includes:  Testing proprioception and vibration in the fingers and toes  Testing fast pain sensation in the limbs, trunk, and face with a pinprick Use caution during pinprick testing; ensure sterilization guidelines are followed. Use caution during pinprick testing; ensure sterilization guidelines are followed.  If loss or impairment of sensation is found, additional testing is performed to determine the precise pattern of sensory loss. 5 Copyright © 2013 by Saunders, an imprint of Elsevier Inc.

6. Interpreting Test Results  Patterns can be mapped by comparing test results with maps of peripheral nerve distribution.  Overlap of adjacent dermatomes ensures that if only one sensory root is severed, a complete loss of sensation does not occur in any area.  Caveat: testing requires that the patient has conscious awareness and cognition. Tests do not test the ability to use somatosensation to prepare for movement or during movement. 6 Copyright © 2013 by Saunders, an imprint of Elsevier Inc.

7. Electrodiagnostic Studies  Electrical activity from nerves reveals the location of the pathologic function.  Two methods of testing function:  Nerve conduction study (NCS) testing measures peripheral nerve function.  Somatosensory-evoked potentials test peripheral nerves and central nervous system (CNS) pathways.  Measurements can be compared with unaffected nerves in the same patient or with published normal values. 7 Copyright © 2013 by Saunders, an imprint of Elsevier Inc.

8. Sensory Nerve Conduction Studies  Nerve conduction test: surface recording electrodes are placed along the course of a peripheral nerve, and the nerve is electrically stimulated.  NCS testing only measures the performance of the large-diameter fibers.  Conduction velocity is slowed throughout a nerve that has been demyelinated. 8 Copyright © 2013 by Saunders, an imprint of Elsevier Inc.

9. Sensory Nerve Conduction Studies  To determine if an NCS is normal, three numerical values are compared:  Distal latency  Amplitude of the evoked potential  Conduction velocity 9 Copyright © 2013 by Saunders, an imprint of Elsevier Inc.

14. Somatosensory-Evoked Potentials  Evaluate the function of the pathway from the periphery to the upper spinal cord or to the cerebral cortex.  Potentials are used to verify subtle signs and locate lesions of the dorsal roots, posterior columns, and brainstem. 14 Copyright © 2013 by Saunders, an imprint of Elsevier Inc.

15. Proprioceptive Pathway Lesions: Sensory Ataxia  Ataxia is incoordination that is not the result of weakness.  Three types of ataxia are sensory, vestibular, and cerebellar.  Romberg test is used to distinguish between cerebellar ataxia and sensory ataxia. 15 Copyright © 2013 by Saunders, an imprint of Elsevier Inc.

16. Peripheral Nerve Lesions  Neuropathy: general term for dysfunction or the pathologic condition of one or more peripheral nerves.  Severance of a peripheral nerve results in lack of sensation in the distribution of the nerve; pain may occur; sensory changes are accompanied by motor and reflex loss. 16 Copyright © 2013 by Saunders, an imprint of Elsevier Inc.

17. Peripheral Nerve Lesions  Sensory loss proceeds in the following order with pressure, compression or injury:  Conscious proprioception and discriminative touch  Cold  Fast pain  Heat  Slow pain 17 Copyright © 2013 by Saunders, an imprint of Elsevier Inc.

18. Spinal Cord Lesions  Common causes of dysfunction of the spinal region include the following:  Trauma to the spinal cord and complete or partial severing of the cord  Disease that compromises the function of specific areas in the spinal cord  Virus that infects the dorsal root ganglion 18 Copyright © 2013 by Saunders, an imprint of Elsevier Inc.

19. Spinal Cord Lesions  Transection of the cord:  All sensation is prevented at one or two levels below the lesion.  Voluntary motor control below the lesion is also lost.  Hemisection of the cord (Brown-Sequard lesion):  Complete loss of pain sensation occurs two to three dermatomes below the level of the lesion contralateral to the lesion.  Discriminative touch and conscious proprioception are lost ipsilateral to the lesion. 19 Copyright © 2013 by Saunders, an imprint of Elsevier Inc.

20. Brown-Sequard Lesion

21. Posterior Column Lesions  Conscious proprioception, two-point discrimination, and vibration sense are lost below the level of the lesion.  Movements are ataxic immediately after the lesion.  Individual may be unable to recognize objects by palpation if the lesion is above C6.  Common causes  Untreated syphillis  Extension injury 21 Copyright © 2013 by Saunders, an imprint of Elsevier Inc.

22. Central Cord Syndrome   Disrupts spinothalamic fibers that are crossing the midline   Usually occurs in cervical spinal cord   With small lesion, only pain and temperature sensation are lost at level of injury   Cape pattern   Causes   Syringomyelia   Trauma

23. Central Cord Syndrome

24. Infection - Shingles 24 Copyright © 2013 by Saunders, an imprint of Elsevier Inc.

25. Brainstem Region Lesions  Usually cause a mix of ipsilateral and contralateral signs.  Sensory loss may be entirely contralateral only in the upper midbrain after all discriminative sensation tracts have crossed the midline.  Lesions of the trigeminal nerve proximal axons or of the trigeminal nerve nuclei cause an ipsilateral loss of sensation from the face. 25 Copyright © 2013 by Saunders, an imprint of Elsevier Inc.

26. Brainstem Region Lesions 26 Copyright © 2013 by Saunders, an imprint of Elsevier Inc.

27. Brainstem Region Lesions – Caudal Medulla

28. Thalamic Lesions  Lesions result in decreased or lost sensation from the contralateral body or face.  Individuals who have a stroke that affects the ventral posterolateral (VPL) nucleus or ventral posteromedial (VPM) nucleus rarely have severe pain in the contralateral body or face.  Thalamic pain - can be very difficult to treat 28 Copyright © 2013 by Saunders, an imprint of Elsevier Inc.

29. Somatosensory Cortex Lesions  Sensory effects of a cortical lesion are contralateral and include decreased or loss of discriminative sensations.  Conscious proprioception  Two-point discrimination  Stereognosis  Localization of touch and pinprick (nociceptive) stimuli 29 Copyright © 2013 by Saunders, an imprint of Elsevier Inc.

30. Somatosensory Cortex Lesions  In cases of sensory extinction, the loss of sensation is only evident when symmetrical body parts are tested bilaterally.  Sensory extinction is a form of unilateral neglect because the person neglects stimuli on one side of the body when the other side of the body is stimulated simultaneously. 30 Copyright © 2013 by Saunders, an imprint of Elsevier Inc.

31. Clinical Perspectives on Pain  Pain is often associated with tissue damage or potential tissue damage can be experienced independently of tissue damage.  Nociceptors signal injury; nociceptor activity is insufficient to cause pain.  Pain is a perception. 31 Copyright © 2013 by Saunders, an imprint of Elsevier Inc.

32. Pain From Muscles and Joints  Signals interpreted as both fast and slow pain can occur with musculoskeletal injuries.  When tissue is injured or ischemic, biochemicals that awaken nociceptors are released.  Nociceptors that are excessively reactive to stimuli are called peripheral sensitization.  Sensitized neurons can fire in response to normally innocuous stimuli, with slight movements, and spontaneously. 32 Copyright © 2013 by Saunders, an imprint of Elsevier Inc.

33. Pain From Muscles and Joints  Unlike superficial pain, deep pain usually occurs after tissue has been damaged.  Function of deep pain may be to encourage rest of the damaged tissue.  After a lower extremity (LE) injury, pain with weight bearing often produces a modified gait; a modified gait is characterized by a shortened stance phase on the affected side. 33 Copyright © 2013 by Saunders, an imprint of Elsevier Inc.

34. Referred Pain  Pain that is perceived as coming from a site distinct from the actual site of origin.  Referred pain is usually referred from visceral tissues to the skin.  Explanation comes from the convergence and facilitation of nociceptive information from different sources. 34 Copyright © 2013 by Saunders, an imprint of Elsevier Inc.

35. Referred Pain - mechanism

36. Referred Pain - Patterns

37. Pain Matrix  Consists of brain structures that process and regulate pain information and are capable of creating pain perception in the absence of nociceptive input.  Includes parts of the brainstem, amygdala, hypothalamus, thalamus, and areas of the cerebral cortex. 37 Copyright © 2013 by Saunders, an imprint of Elsevier Inc.

38. Pain Matrix 38 Copyright © 2013 by Saunders, an imprint of Elsevier Inc.

39. Pain Matrix  Experience of pain is strongly linked to emotional, behavioral, and cognitive phenomena.  Understanding requires the consideration of discriminative, motivational-affective, and cognitive-evaluative components.  Discriminative aspect refers to the ability to localize the site, timing, and intensity of tissue damage or potential tissue damage. 39 Copyright © 2013 by Saunders, an imprint of Elsevier Inc.

40. Pain Matrix  Motivational-affective aspect refers to the effects of the pain experience on emotions and behavior, including increased arousal and avoidance behavior.  Cognitive-evaluative aspect refers to the meaning that the person ascribes to the pain. 40 Copyright © 2013 by Saunders, an imprint of Elsevier Inc.

41. Pain Matrix 41 Copyright © 2013 by Saunders, an imprint of Elsevier Inc. Injury to anterior cingulate cortex can block emotional aspects of pain but leave discrimination intact

42. Gate Theory  Typical response to hitting one’s thumb with a hammer is to withdraw the thumb, yell, and apply pressure.  First scientific explanation of how pressure and other external stimuli inhibit pain transmission was the gate theory of pain, proposed by Melzack and Wall in 1965.  Some details are incorrect, but the original theory is important because it inspired inquiry into the mechanics and control of pain, such as TENS. 42 Copyright © 2013 by Saunders, an imprint of Elsevier Inc.

43. Counterirritant Theory  Incorporates findings from research stimulated by the gate theory.  Theory: explains the inhibition of nociceptive signals by stimulation of non-nociceptive receptors occurs in the dorsal horn of the spinal cord. 43 Copyright © 2013 by Saunders, an imprint of Elsevier Inc.

44. Dorsal Horn Processing of Nociceptive Information  Processing of somatosensory information in the dorsal horn can be altered by abnormal neural activity or by tissue injury.  Four states of dorsal horn processing are:  Normal  Suppressed  Sensitized  Reorganized 44 Copyright © 2013 by Saunders, an imprint of Elsevier Inc.

45. Antinociceptive Systems  Antinociception is the suppression of pain in response to stimulation that would normally be painful.  Endorphins are endogenous substances that activate antinociceptive mechanisms.  Opiate receptors are receptor sites that bind with both endorphins and opiates. 45 Copyright © 2013 by Saunders, an imprint of Elsevier Inc.

46. Sites of Antinociception 46 Copyright © 2013 by Saunders, an imprint of Elsevier Inc.

47. Pronociception: Biological Amplification of Nociception  Pain transmission can be intensified at several levels.  Edema and endogenous chemicals can sensitize free nerve endings in the periphery.  Pronociception may occur when a person is anxious or depressed. 47 Copyright © 2013 by Saunders, an imprint of Elsevier Inc.

48. Pronociception and Antinociception 48 Copyright © 2013 by Saunders, an imprint of Elsevier Inc.

49. Chronic Pain 49 Copyright © 2013 by Saunders, an imprint of Elsevier Inc.

50. Nociceptive Chronic Pain  Due to continuing stimulation of nociceptive receptors.  Example: Chronic pain that results from a vertebral tumor pressing on nociceptors in the meninges surrounding the spinal cord  Neurons are functioning normally; chemical changes in the damaged tissue awaken sleeping peripheral nociceptors. 50 Copyright © 2013 by Saunders, an imprint of Elsevier Inc.

51. Nociceptive Chronic Pain  Primary hyperalgesia refers to excessive sensitivity to stimuli in the injured tissue.  Example: Pain resulting from mild heat on burned skin; if a fingertip is burned, picking up a hot plate is more painful than if the skin were not injured.  Nociceptive chronic pain serves a useful biological function as a warning to protect the injured tissue. 51 Copyright © 2013 by Saunders, an imprint of Elsevier Inc.