124. Sensory Abnormalities – Quiz

📌 Professor’s Notes: Quick Revision

High-yield revision notes for rapid review before university examinations.

• Sensory abnormalities occur when any part of the sensory pathway—from peripheral nerves to the cerebral cortex—is damaged. The pattern of sensory loss helps localize the site of the lesion and is therefore of great clinical importance.
• Peripheral nerve lesions produce sensory loss in the distribution of the affected nerve. Because adjacent nerves overlap, complete sensory loss is uncommon. Touch, vibration, and proprioception are often affected before pain and temperature in compressive neuropathies due to early involvement of large myelinated fibers.
• Polyneuropathy is usually caused by diabetes mellitus, nutritional deficiencies, toxins, inflammatory disorders, or vasculitis.
  • Produces bilateral, symmetrical “glove-and-stocking” sensory loss.
  • Longest nerve fibers are affected first.
  • Severe proprioceptive loss causes sensory ataxia, increasing the risk of painless injuries and trophic ulcers.
• Radiculopathy (nerve root lesion) causes sensory loss in the corresponding dermatome. Common causes include intervertebral disc prolapse and degenerative spinal disease. Patients may also have radicular pain, reduced reflexes, and weakness.
• Spinal cord lesions produce characteristic sensory syndromes:
  • Tabetic syndrome: Degeneration of the posterior columns causes loss of vibration sense and proprioception, sensory ataxia, and a positive Romberg sign.
  • Posterior column syndrome: Bilateral posterior column lesions impair vibration, proprioception, fine touch, graphesthesia, and stereognosis, while pain and temperature remain intact.
  • Brown-Séquard syndrome: Hemisection of the spinal cord causes ipsilateral loss of vibration, proprioception, discriminative touch, and motor function, with contralateral loss of pain and temperature below the lesion.
  • Complete spinal cord syndrome: Complete transection causes loss of all sensory, motor, and autonomic functions below the lesion.
  • Syringomyelia: Damage to crossing spinothalamic fibers produces dissociated sensory loss—loss of pain and temperature with preserved touch, vibration, and proprioception. The sensory loss typically has a cape-like distribution.
  • Anterior spinal artery syndrome: Bilateral loss of pain and temperature with motor weakness, while posterior column sensations are preserved.
• Brainstem lesions produce characteristic crossed sensory loss:
  • Ipsilateral loss of pain and temperature from the face with contralateral loss from the body due to involvement of trigeminal and spinothalamic pathways.
  • Larger lesions may also involve the medial lemniscus, causing loss of deep sensations.
• Thalamic lesions produce contralateral sensory impairment. Damage to the ventral posterior nuclei causes thalamic syndrome, characterized by hyperalgesia, unpleasant abnormal sensations, and exaggerated responses to mild stimuli.
• Cortical lesions mainly affect higher sensory functions rather than primary sensation. Patients have impaired tactile localization, two-point discrimination, stereognosis, vibration sense, and proprioception. Lesions of the parietal association cortex may produce sensory neglect and hemispatial inattention.
• Assessment of sensory function includes:
  • Clinical examination of touch, pain, temperature, vibration, and proprioception.
  • Sensory nerve conduction studies to evaluate peripheral nerve function.