Sensory Abnormalities

Introduction

Sensory abnormalities arise when normal neural pathways are disrupted by disease or injury. The pattern and severity of sensory loss vary with the location of the lesion, the underlying pathological process, and the extent of nervous system involvement, providing valuable clues for clinical diagnosis.

Functional Aspects

• The study of sensory physiology explains how sensory stimuli are detected, transmitted, processed, and consciously perceived by the nervous system.
• It provides the physiological basis for understanding and evaluating sensory abnormalities.
• Clinical assessment requires identification of both the type of sensory deficit and its anatomical location within the sensory pathway.
• Accurate localization depends on the pattern and distribution of sensory loss.
• Sensory disorders may result from lesions involving peripheral nerves, nerve roots, the spinal cord, brainstem, thalamus, or cerebral cortex.
• Careful neurological examination helps distinguish the site of injury and guides appropriate diagnosis and management.

Lesions at Different Levels

Single Peripheral Nerve Lesion

• The pattern of sensory loss varies according to the anatomical level of the lesion within the sensory pathway.
• Careful assessment of sensory deficits helps localize the site of neurological damage.
• A single peripheral nerve lesion produces sensory impairment within the distribution of the affected nerve.
• The clinical sensory deficit is usually smaller than the anatomical distribution because adjacent peripheral nerves provide overlapping innervation.
• Deep pressure and joint position sensation are often preserved because they receive additional input from neighboring nerves and deep tissues.
• In compressive neuropathies, large myelinated fibers are affected earlier than small fibers.
• Consequently, touch, vibration, and proprioception may be impaired before pain and temperature sensations.

Multiple Nerve Lesions (Polyneuropathy)

• Polyneuropathy commonly results from diabetes mellitus, inflammatory disorders, nutritional deficiencies, toxins, or vasculitic diseases.
• Sensory deficits are typically bilateral, symmetrical, and more pronounced in the distal parts of the limbs.
• The longest nerve fibers are affected first, producing a characteristic glove-and-stocking pattern of sensory loss.
• Multiple sensory modalities, including touch, pain, temperature, vibration, and proprioception, may be involved.
• Demyelinating neuropathies often present with early paresthesia, whereas axonal neuropathies primarily cause progressive sensory loss.
• Marked impairment of proprioception may produce sensory ataxia, resulting in an unsteady gait.
• Chronic sensory loss increases the risk of painless injuries, pressure sores, and trophic ulcers because protective sensation is diminished.

Nerve Root Lesion (Radiculopathy)

• Nerve root lesions (radiculopathy) produce sensory loss in the corresponding dermatome.
• Common causes include compression from an intervertebral disc herniation, degenerative spinal disease, or other space-occupying lesions.
• Complete sensory loss is uncommon because adjacent dermatomes overlap extensively.
• Radiculopathy may also be associated with radicular pain, reduced reflexes, and weakness in muscles supplied by the affected spinal segment.

Lesion of Sensory Ganglia

• Sensory ganglion lesions involve the dorsal root ganglia and may occur in inflammatory, toxic, infectious, or neoplastic disorders.
• These lesions produce sensory deficits similar to those seen in radiculopathy.
• Proximal sensory impairment is often more prominent because the cell bodies of primary sensory neurons are directly affected.
• Recognition of these characteristic patterns is essential for accurate clinical localization and appropriate management of sensory disorders.

Spinal Cord Lesions

• The clinical features of spinal cord lesions depend on the specific tracts and spinal segments involved.
• Characteristic sensory syndromes help localize the level and extent of spinal cord damage.
• Important spinal cord sensory syndromes include posterior column syndrome, Brown-Séquard syndrome, complete spinal cord syndrome, syringomyelic syndrome, and anterior spinal artery syndrome.

Tabetic Syndrome

• Tabetic syndrome results from degeneration of posterior column fibers, classically due to neurosyphilis but also seen in some metabolic neuropathies.
• It primarily affects large myelinated sensory fibers responsible for vibration and joint position sensation.
• Patients develop loss of proprioception, impaired vibration sense, numbness, and paresthesia.
• Sensory ataxia develops because of impaired position sense.
• The Romberg test is often positive, indicating defective proprioceptive input.

Posterior Column Syndrome

• Posterior column syndrome involves bilateral damage to the dorsal columns.
• Vibration sense, conscious proprioception, and fine tactile discrimination are markedly impaired.
• Pain and temperature sensations remain largely intact because the anterolateral pathways are unaffected.
• Patients may develop impaired graphesthesia, astereognosis, and difficulty recognizing limb position.

Brown‑Sequard Syndrome

• Brown-Séquard syndrome results from hemisection of the spinal cord, commonly following trauma or unilateral spinal tumors.
• Damage to the dorsal column produces ipsilateral loss of vibration sense, proprioception, and discriminative touch below the lesion.
• Interruption of the corticospinal tract causes ipsilateral spastic weakness below the affected level.
• Damage to the crossed spinothalamic tract produces contralateral loss of pain and temperature sensation beginning one to two spinal segments below the lesion.
• This characteristic pattern reflects the different crossing points of ascending sensory pathways.

Complete Spinal Sensory Syndrome

• Complete spinal cord syndrome results from complete transection or severe destruction of the spinal cord.
• All sensory modalities are abolished below the level of the lesion.
• Motor function and autonomic pathways are also interrupted below the injured segment.
• A narrow band of hyperesthesia may occur immediately above the level of complete sensory loss.

Syringomyelic Syndrome

• Syringomyelic syndrome is caused by expansion of a cavity within the central spinal cord, usually around the central canal.
• The lesion interrupts decussating spinothalamic fibers in the anterior white commissure.
• Patients develop dissociated sensory loss, characterized by loss of pain and temperature sensation with preservation of fine touch, vibration, and proprioception.
• The sensory deficit typically has a bilateral “cape-like” distribution over the shoulders and upper limbs when the cervical cord is involved.
• Progressive enlargement of the cavity may later involve anterior horn cells and corticospinal tracts, producing muscle weakness and spasticity.

Anterior Spinal Artery Syndrome

• Anterior spinal artery syndrome results from infarction of the anterior two-thirds of the spinal cord following occlusion of the anterior spinal artery.
• The corticospinal tracts and anterolateral pathways are affected, producing bilateral weakness and loss of pain and temperature sensation below the lesion.
• The posterior columns remain intact because they receive blood supply from the posterior spinal arteries.
• Consequently, proprioception, vibration sense, and discriminative touch are preserved.
• Recognition of these distinct neurological patterns is essential for accurate clinical localization, diagnosis, and management of spinal cord disorders.

Brainstem Lesion

• Brainstem lesions produce sensory deficits that depend on the level and pathways involved.
• Lesions in the medulla may affect the spinal trigeminal tract and the crossed spinothalamic tract simultaneously.
• This produces crossed sensory loss, with impaired pain and temperature sensation on the ipsilateral face and contralateral body.
• Lesions involving the upper medulla, pons, or lower midbrain may damage both trigeminothalamic and spinothalamic pathways.
• These lesions produce contralateral loss of pain and temperature sensation from the face and body while preserving dorsal column-mediated sensations if the medial lemniscus is unaffected.
• In the upper brainstem, involvement of both the medial lemniscus and spinothalamic tract causes contralateral loss of superficial and deep sensations.

Thalamic Lesion

• Thalamic lesions produce marked sensory impairment on the contralateral side of the body.
• Damage to the ventral posterior thalamic nuclei may result in thalamic syndrome, characterized by altered sensory perception.
• Patients may develop hyperalgesia, abnormal unpleasant sensations, and exaggerated responses to normally mild stimuli.

Cortical Lesion

• Cortical lesions mainly impair higher-order sensory processing rather than basic sensation.
• Deficits include impaired tactile localization, reduced two-point discrimination, astereognosis, and impaired vibration and proprioception.
• Lesions of the parietal association cortex may produce sensory neglect, extinction, or inattention to the contralateral side of the body or surrounding space.
• Recognition of these characteristic sensory patterns is essential for accurate neurological localization.

Sensory Function Tests

Assessment of sensory function combines clinical examination with electrophysiological investigations to identify the type and location of neurological lesions.

Clinical Examination of Sensory System

• A detailed clinical sensory examination is the first step in evaluating sensory abnormalities.
• Each sensory modality, including touch, pain, temperature, vibration, and proprioception, should be tested systematically.
• Sensation should be examined over all relevant dermatomes and compared on both sides of the body.
• The pattern of sensory loss helps localize lesions to peripheral nerves, nerve roots, the spinal cord, brainstem, thalamus, or cerebral cortex.

Sensory Nerve Conduction

• Sensory nerve conduction studies assess the integrity of peripheral sensory nerves by measuring sensory nerve action potentials and conduction velocity.
• These studies are valuable for diagnosing and characterizing sensory neuropathies.
• Late responses, including H-reflex and F-wave studies, provide additional information about proximal nerve segments and may assist in evaluating radiculopathy.

Somatosensory Evoked Potentials

• Somatosensory evoked potentials assess conduction through large myelinated sensory pathways from peripheral nerves to the cerebral cortex.
• They help identify abnormalities involving the peripheral nervous system, brainstem, thalamus, or cerebral cortex.
• Somatosensory evoked potentials are particularly useful for distinguishing peripheral from central sensory pathway disorders.