Smarter Decisions,
Better Care

UpToDate synthesizes the most recent medical information into evidence-based practical recommendations clinicians trust to make the right point-of-care decisions.

  • Rigorous editorial process: Evidence-based treatment recommendations
  • World-Renowned physician authors: over 5,100 physician authors and editors around the globe
  • Innovative technology: integrates into the workflow; access from EMRs

Choose from the list below to learn more about subscriptions for a:


Subscribers log in here


Approach to the patient with sensory loss

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.

                  

Subscribers log in here

To continue reading this article, you must log in with your personal, hospital, or group practice subscription. For more information or to purchase a personal subscription, click below on the option that best describes you:
Literature review current through: Mar 2014. | This topic last updated: May 24, 2013.
The content on the UpToDate website is not intended nor recommended as a substitute for medical advice, diagnosis, or treatment. Always seek the advice of your own physician or other qualified health care professional regarding any medical questions or conditions. The use of this website is governed by the UpToDate Terms of Use ©2014 UpToDate, Inc.
References
Top
  1. Gilman, S, Newman, SW. Manter and Gatz's Essentials of Clinical Neuroanatomy and Neurophysiology, 8, FA Davis, Philadelphia 1992..
  2. Duus, P. Topical Diagnosis in Neurology, 2nd revised edition, Thieme Medical, New York 1989..
  3. Kim JS, Lee JH, Lee MC. Patterns of sensory dysfunction in lateral medullary infarction. Clinical-MRI correlation. Neurology 1997; 49:1557.
  4. Barohn RJ, Saperstein DS. Guillain-Barré syndrome and chronic inflammatory demyelinating polyneuropathy. Semin Neurol 1998; 18:49.
  5. Ropper AH. The Guillain-Barré syndrome. N Engl J Med 1992; 326:1130.
  6. Rotta FT, Sussman AT, Bradley WG, et al. The spectrum of chronic inflammatory demyelinating polyneuropathy. J Neurol Sci 2000; 173:129.
  7. Katz JS, Saperstein DS, Gronseth G, et al. Distal acquired demyelinating symmetric neuropathy. Neurology 2000; 54:615.
  8. Kuntzer T, Antoine JC, Steck AJ. Clinical features and pathophysiological basis of sensory neuronopathies (ganglionopathies). Muscle Nerve 2004; 30:255.
  9. England JD, Gronseth GS, Franklin G, et al. Evaluation of distal symmetric polyneuropathy: the role of laboratory and genetic testing (an evidence-based review). Muscle Nerve 2009; 39:116.
  10. England JD, Gronseth GS, Franklin G, et al. Evaluation of distal symmetric polyneuropathy: the role of autonomic testing, nerve biopsy, and skin biopsy (an evidence-based review). Muscle Nerve 2009; 39:106.
  11. Dyck PJ, Oviatt KF, Lambert EH. Intensive evaluation of referred unclassified neuropathies yields improved diagnosis. Ann Neurol 1981; 10:222.
  12. Barohn RJ. Approach to peripheral neuropathy and neuronopathy. Semin Neurol 1998; 18:7.
  13. Kim JS. Pure sensory stroke. Clinical-radiological correlates of 21 cases. Stroke 1992; 23:983.
  14. Nasreddine ZS, Saver JL. Pain after thalamic stroke: right diencephalic predominance and clinical features in 180 patients. Neurology 1997; 48:1196.