It may be difficult to decide if an apparent sensory loss is significant. Some patients may be vague In their perception of the sensory stimulus, while others may be obsessive and comment on minor variations in the intensity of the stimulus applied. Organic alterations of sensation are usually consistent and reproducible in their nature, degree and extent.
In the normal person two separate stimuli can be discriminated when they are applied as close together as 3-5 mm on the pulps of the index linger. On the soles of the feet, the distinguishing distance may be anything up to 10 times greater. It is one of the few objective parameters of sensory function. Its documentation prior to surgery or any other therapy is a useful way of gauging clinical response to treatment. Patients who have considerable alteration of superficial sensation will volunteer sensory symptoms. The finding of extensive or apparently severe sensory loss in the absence of symptoms should be assessed with caution.
Peripheral nerve damage. Impaired vibration sense over bony prominences occurs with age and is often lost al [he ankles over the age of 70. However, loss of vibration sense is seen in patients at an earlier stage than impairment of JPS. For example, it is an early feature in diabetic peripheral neuropathy.
Joint position sense impairment is also first detected distally. Joint position is most commonly impaired in patients with large-fibre peripheral neuropathies and spinal cord disorders (myelopathies) affecting the dorsal columns. Disturbances of JPS may occur withoul paresis. In such patients the following findings may be noted:
• impaired line-linger function and alterations of gait as a result of loss of feedback concerning muscle activity and joint position
• sensory ataxia when the finger-nose test is carried out with the eyes closed
• positive Romberg's test
• walking in the dark their gait becomes unsteady or ihey may fall when performing movements that require complex postural adjustments
« with the hands outstretched and eyes closed, the lingers may make small slow movements (pscudoathctosis).
Two-point discrimination in the fingers is impaired in many peripheral neuropathies, particularly those involving large sensory fibres, and In cervical myeloradiculopathies. In these conditions its loss is associated with other abnormal clinical findings suggestive of dorsal column dysfunction (light touch, JPS, vibration).
Disorders of touch, pain and temperature perception (hypoaesthesia, dysaesthesia and hyperesthesia). JPS and two-point discrimination are common in peripheral neuropathies and nerve injuries, discogenic radiculopathies and spinal injuries.
Lesions of individual peripheral nerves or sensory nerve roots commonly give rise to subjective feeling of numbness and diminution of all sensory modalities in their areas of distribution (Figs 6.45 and 6.46). Less commonly, partial lesions of the peripheral nerve give rise to pain of a burning, unpleasant quality, as in eausalgia, a condition occurring infrequently after injury to either the median or sciatic nerve. In polyneuropathies the numbness or paresthesia and objective sensory features affect the distal parts of Ihe limbs and often involve the legs before the arms. Superficial sensory loss in a polyneuropathy is found over the distal parts of the extremities and extends up the limbs to a level which may be relatively uniform around their whole circumference as a 'stocking and glove'-type sensory disturbance.
Spinal cord lesions. There may be a disassociated sensory loss (i.e. not all modalities are affected equally). Most commonly pain and temperature sensations are lost while touch, vibration and JPS arc intact. This pattern results from lesions which damage the lateral spinothalamic pathways but not the dorsal columns. Disassociated sensory loss is classically found in patients with cervical syringomyelia but may arise from other intramedullary and brain stem pathology. Other characteristic patterns of sensory (and motor) loss occur in the anterior spinal artery syn drome (preservation of dorsal column function, with loss of motor function and spinothalamic modalities) and in the Rrown-Sequard syndrome (ipsilateral loss of motor function, vibration and IPS with contralateral loss of spinothalamic sensations). Lesions of the conns medullaris and cauda equina (central disc prolapse, neurofibroma, ependymoma, primary and metastatic neoplasia) cause sensory loss from the feet, up ihe back of the legs, to the buttocks, perineum and genitalia.
Intracranial lesions are frequently vascular in origin. Various patterns of sensory abnormalities may be found:
• Unilateral lesions of the lower brain stem may causc impairment of pain and temperature perception on the ipsilateral side of the face (as a result of V nerve nucleus involvement) and on the contralateral side of the body below the neck (sometimes called alternating analgesia). Spinothalamic tract lesions above the mid-pontine level may damage both the spinothalamic tract and the medial lemniscus, which lie closc together. This will cause sensory impairment of all modalities on the contralateral face and body.
• Lesions of the thalamus may give rise to spontaneous, intense, burning pain on the contralateral side associated with diminution of touch over the same area. The pain is poorly localised and has a particularly unpleasant quality.
• Damage to the sensory cortex may not impair perception of pain, temperature and touch but causes alterations in the qualitative, affective and discriminatory aspects of sensory appreciation and is usually accompanied by loss of two-point discrimination or astercognosis.
Parietal lobe lesions may cause marked loss of two-point discrimination in the absence of other modality changes.
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