With posterior column lesions, only a few of which have been verified by postmortem examinations, touch sensation is not lost, or it recovers after an acute lesion, but the patient is deprived of knowledge of movement and position of parts of the body below the lesion. Nathan and colleagues confirmed that lesions of the posterior columns cause only slight defects in touch and pressure sensation. However, a combined lesion in both posterior columns and spinothalamic tracts causes a total loss of tactile and pressure sensibility below the lesion. If the posterior column lesion is in the cervical region, there is clumsiness in the palpation of objects and an inability to recognize the qualities of objects by touch (agraphesthesia), even though touch-pressure sensation is relatively intact. There may be unusual disturbances of touch and pressure, manifesting as lability of threshold, persistence of sensation after removal of the stimulus, and sometimes tactile and postural hallucinations.
The loss of sensory functions that follows a posterior column lesion—such as impaired two-point discrimination; figure writing; detection of size, shape, weight, and texture of objects; and ability to detect the direction and speed of a moving stimulus on the skin—may simulate a parietal “cortical” lesion (see below under “Sensory Loss Caused by Lesions of the Parietal Lobe”), but differs in that vibratory sense is also lost in lesions limited to the posterior columns.
It should be realized therefore, that not all proprioceptive fibers ascend to the gracile and cuneate nuclei; some proprioceptive fibers leave the posterior columns in the lumbar region and synapse with secondary neurons in the spinal gray matter and ascend in the ipsilateral posterolateral funiculus. Only cutaneous fibers continue to the gracile and cuneate nuclei.
The usual causes of the posterior column syndrome are multiple sclerosis, vitamin B12 deficiency, copper deficiency, tabes dorsalis, and HIV and human T-lymphotropic virus (HTLV) type 1 infection.
With infarction of the spinal cord in the territory of supply of the anterior spinal artery or with other lesions that affect the ventral portion of the cord predominantly, as in some cases of myelitis, one finds a loss of pain and temperature sensation below the level of the lesion but with relative or absolute sparing of proprioceptive sensation. Because the corticospinal tracts and the ventral gray matter also lie within the area of distribution of the anterior spinal artery, paralysis is a prominent feature (see Fig. 8-7).
Disturbances of Sensation from Lesions of the Brainstem
A characteristic feature of medullary lesions is the occurrence, in many instances, of a crossed sensory disturbance, that is, a loss of pain and temperature sensation on one side of the face and on the opposite side of the body. This is accounted for by involvement of the descending spinal trigeminal tract or its nucleus and the crossed lateral spinothalamic tract on one side of the brainstem and is nearly always caused by a lateral medullary infarction (Wallenberg syndrome). In the upper medulla, pons, and midbrain, the crossed trigeminothalamic and lateral spinothalamic tracts run together; a lesion at these levels causes loss of pain and temperature sense on the opposite half of the face and body. Spontaneous and induced thermal or painful dysesthesias are often reported (“feeling as if sunburned”). In the upper brainstem, the spinothalamic tract and the medial lemniscus become confluent, so that an appropriately placed lesion causes a contralateral loss of all superficial and deep sensation. Cranial nerve palsies, cerebellar ataxia, and motor paralysis are almost invariably associated, as indicated in the discussion of strokes in this region (Chap. 33). In other words, a lesion in the brainstem at any level is unlikely to cause an isolated sensory disturbance.
of the Thalamus