The somatosensory system encompasses the pathways carrying sensation from the body’s surface and deep tissues to the brain. Two separate ascending systems with different decussation points — the dorsal column-medial lemniscus system for fine touch and proprioception, the spinothalamic system for pain and temperature — together produce the patterns of dissociated sensory loss that are diagnostic of specific lesions throughout the neuraxis. This page integrates the cord, brainstem, thalamic, and cortical pieces of the somatosensory system into a coherent picture.

The Two Ascending Systems Revisited

Dorsal Column-Medial Lemniscus System

Carries fine touch, vibration, joint position sense, two-point discrimination.

1. Primary neuron in dorsal root ganglion; central process enters cord and ascends ipsilaterally in dorsal columns.
2. First synapse in nuclei gracilis and cuneatus of the lower medulla.
3. Second-order neurons cross as internal arcuate fibers to form the contralateral medial lemniscus.
4. Medial lemniscus ascends through brainstem to VPL of thalamus.
5. Third-order neurons project to primary somatosensory cortex (S1) in the postcentral gyrus.

Decussation site: lower medulla. Below this, ipsilateral; above this, contralateral.

Spinothalamic System

Carries pain, temperature, crude touch.

1. Primary neuron in dorsal root ganglion (small fibers Aδ and C); central process enters cord and ascends 1-3 segments in Lissauer’s tract.
2. First synapse in dorsal horn (substantia gelatinosa, lamina II, and adjacent laminae).
3. Second-order neurons cross at or near the segmental level of entry through the anterior white commissure.
4. Ascend in contralateral lateral spinothalamic tract.
5. Project through brainstem to VPL of thalamus.
6. Third-order neurons project to S1.

Decussation site: cord, 1-3 segments above the level of entry.

Trigeminal Sensory System

Face sensation has its own pathways:

• Pain and temperature from face: CN V → spinal trigeminal nucleus and tract (extends from pons through medulla into upper cervical cord) → cross → trigeminothalamic tract → VPM of thalamus → S1 (face area, inferior on the postcentral gyrus).
• Touch and proprioception from face: CN V → principal sensory nucleus in mid-pons → cross → ascend with medial lemniscus → VPM → S1.
• Jaw proprioception: CN V → mesencephalic nucleus (unique nucleus in midbrain containing cell bodies of primary sensory neurons) → motor nucleus of V for jaw jerk reflex.

Thalamic Processing

The thalamus is the relay for somatosensation:

• VPL: relays body sensation from both dorsal column and spinothalamic systems. Lesions produce contralateral hemibody sensory loss.
• VPM: relays face sensation. Lesions produce contralateral face sensory loss.
• Pulvinar: receives multimodal input including somatosensory; involved in spatial attention.
• Intralaminar nuclei: process pain components.

The thalamic pain syndrome (Dejerine-Roussy) follows VPL infarction. After initial hemisensory loss, the patient develops severe spontaneous burning pain with hyperalgesia and allodynia in the previously numb hemibody weeks to months later.

Cortical Processing

Primary Somatosensory Cortex (S1)

The postcentral gyrus (Brodmann areas 3, 1, 2). Receives projection from VPL/VPM. Topographically organized as the sensory homunculus, with face inferior and laterally, hand in the middle, leg extending onto the medial paracentral lobule. The proportions are similar to the motor homunculus, with face, hand, and lips disproportionately large.

• Area 3a: deep proprioception.
• Area 3b: rapidly adapting touch.
• Area 1: complex touch.
• Area 2: proprioception with touch.

Somatosensory Association Cortex

The superior parietal lobule (Brodmann areas 5, 7). Integrates somatosensory information for higher-order processing. Inferior parietal lobule (areas 39, 40) integrates somatosensation with vision, audition, and other modalities.

Cortical Sensory Functions

Several “cortical” sensory functions require intact primary modalities but probe parietal cortex processing:

• Two-point discrimination: minimum distance at which two points are perceived as separate. Varies by body region.
• Stereognosis: identification of objects by touch with eyes closed.
• Graphesthesia: identification of numbers traced on the skin.
• Tactile localization: ability to identify exactly where on the body a touch occurred.
• Extinction: with simultaneous bilateral stimulation, one side is “extinguished” — a sign of contralateral parietal disease, especially right parietal.

Loss of these with preserved primary sensation localizes to contralateral parietal cortex.

Patterns of Sensory Loss

Pain Processing

Beyond the spinothalamic relay, pain is modulated at multiple levels:

• Gate control: in the dorsal horn, Aβ touch afferents inhibit transmission of pain signals via interneurons (the basis of why rubbing a stubbed toe helps).
• Descending modulation: from periaqueductal gray and brainstem raphe nuclei to dorsal horn. Substrate of endogenous opioid analgesia and stress-induced analgesia.
• Cortical processing: somatosensory cortex (sensory discriminative aspects), anterior cingulate cortex (affective aspects), insular cortex (interoceptive aspects).

Chronic pain involves sensitization at multiple levels — peripheral sensitization (nociceptor hyperexcitability), central sensitization (dorsal horn and cortical changes), and altered descending modulation. These mechanisms underlie the persistence of pain after the original tissue injury has healed.

Sensory Loss vs Sensory Symptoms

• Negative symptoms: loss of sensation. Numbness, “deadness.”
• Positive symptoms: tingling, burning, electric shock sensations. Reflect abnormal firing of damaged sensory fibers.
• Allodynia: pain from normally non-painful stimuli (light touch).
• Hyperalgesia: increased pain to normally painful stimuli.
• Hyperpathia: increased threshold for pain perception, but pain that follows is exaggerated and prolonged.

Negative symptoms point to large fiber dysfunction or central pathway involvement. Positive symptoms (especially burning) point to small fiber involvement or central sensitization.

Special Topics

Small Fiber Neuropathy

Selective involvement of Aδ and C fibers without large fiber involvement. Pain and temperature loss with normal vibration and joint position sense. Often with autonomic features. Diagnosis can be supported by skin biopsy for intraepidermal nerve fiber density. Causes include diabetes, prediabetes, amyloid, Sjögren syndrome, sodium channel mutations.

Sensory Neuronopathy

Selective damage to dorsal root ganglion neurons. Non-length-dependent (upper extremities can be affected before lower), severe joint position loss, pseudoathetosis, areflexia. Causes include paraneoplastic (anti-Hu), Sjögren syndrome, platinum chemotherapy, vitamin B6 toxicity.

Central Pain Syndromes

Beyond thalamic pain, central pain can follow lesions anywhere in the spinothalamic pathway or its cortical projections. Cord injury patients can develop neuropathic pain at and below the level of injury. Multiple sclerosis can produce central pain.

🔍 Did You Know?

The pattern of sensory loss following spinal cord hemisection — ipsilateral dorsal column loss and contralateral pain/temperature loss — was first described by Charles-Édouard Brown-Séquard in 1849. Brown-Séquard reportedly conducted his initial experiments by hemisecting the cord in animals (an ethically untenable practice today) and observing the characteristic dissociated pattern. The clinical syndrome bears his name and remains one of the most pathognomonic findings in neurology. When a patient presents with motor weakness on one side, loss of vibration and joint position sense on the same side, and loss of pain and temperature on the opposite side — all below a defined level — the localization to a cord hemisection is essentially certain.

Pitfalls and Pearls

• The dorsal column system decussates in the medulla; the spinothalamic system at the cord level of entry. Every dissociated sensory pattern follows from this.
• Brown-Séquard: ipsilateral motor and dorsal column loss + contralateral pain/temperature loss starting 1-3 segments below the lesion. Pathognomonic for cord hemisection.
• Wallenberg (lateral medulla): ipsilateral facial pain/temp loss + contralateral body pain/temp loss + ataxia + Horner. The classical “crossed sensory” syndrome.
• Thalamic VPL infarct produces hemibody loss of all modalities, sometimes followed weeks later by thalamic pain syndrome.
• Cortical sensory loss with preserved primary modalities localizes to contralateral parietal cortex.
• Extinction on double simultaneous stimulation is a sensitive sign of right parietal disease (left neglect).
• Small fiber neuropathy produces pain and temperature loss with preserved vibration and joint position sense. Diabetes is the most common cause.
• Sensory neuronopathy involves upper extremities early and produces severe joint position loss out of proportion to other findings.
• Always test perianal sensation in cord and cauda equina syndromes. Saddle anesthesia is the cardinal sign.
• Central pain syndromes can follow stroke, spinal cord injury, or MS plaques and are often resistant to standard analgesics.

References

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6. Brown-Séquard CE. De la transmission croisée des impressions sensitives par la moelle épinière. Compt Rend Soc Biol. 1850;2:33-44.