1.Touch sensation is tested with a wisp of cotton or the light touch of a finger. The stimulus should be compared with that applied to the contralateral corresponding area with expected normal sensation.

2. Pain sensation is tested by indicating the intensity of the pinprick sensation in comparison with that in a corresponding area with normal pain sensation.

3. It must be determined if an area of decreased sensation suggests nerve root or peripheral nerve involvement. Dermatomal charts showing typical peripheral nerve or nerve root distributions vary somewhat from one book or study to another, and there can be variability among patients. Should the pinprick sensation indicate a decrease or loss of pain sensation at a certain level of the chest or abdomen, the level is determined more reliably by proceeding from the area of decreased or absent sensation to the area of normal sensation.

4. Position sense in fingers or toes is examined by holding the digit at the side opposite to the direction of movement. The patient is asked to identify the directions of passive flexion and extension.

5. Vibration sense is a composite sensation requiring preserved touch and deep pressure sensation. A 128-dv tuning fork should be used and placed over a boney prominence.

1. Paresthesia means spontaneous abnormal sensation frequently described as tingling, prickling, or “pins and needles.”

2. Dysesthesia is discomfort or pain triggered by normally painless stimuli.

3. Hyperesthesia indicates abnormally increased sensitivity to light touch, pinprick, or thermal sensation.

1. Numbness indicates decreased or absent sensation.

2. Anesthesia is complete loss of sensation.

3. Hypesthesia is decreased sensation.

4. Pallesthesia indicates loss of vibratory sensation.

It often is difficult to establish with certainty that sensory impairment is functional, meaning inorganic or nonphysiologic. Functional sensory loss frequently occurs in a nonanatomic distribution, but so can CNS inflammatory demyelinating sensory loss. Losses of touch, pinprick, and vibration sensation exactly at the midline over the chest or abdomen, or in the entire limb with sharp delineation of the sensory loss, or poor reproducibility of the demarcation of the sensory deficits with repeated exams, all suggest functional sensory loss.

1. Exteroceptors are localized in the skin and subserve superficial sensation to pain, touch, and temperature. The cutaneous sensory fibers run in sensory or mixed sensory and motor nerves. Sensory neurons have their cell bodies in the dorsal ganglia with their central projections to the posterior roots.

2. Proprioceptors are localized in deeper somatic structures, including tendons, muscles, and joints, dorsal columns of the spinal cord, and terminate in the gracile and cuneate nuclei of the medulla. The secondary afferent fibers from these nuclei cross the midline in the medulla and ascend in the brainstem as the medial lemniscus to the posterior thalamic complex. Proprioceptive information is carried through the spinocerebellar tracts in the lateral columns and in the cuneocerebellar and rostrocerebellar tracts in the dorsal columns of the cord.

Individual nerve roots mediate sensation in segments oriented longitudinally in the extremities and horizontally over the trunk. Dermatomal charts depict typical nerve root distributions, but distributions vary from one study or book to another, and there can also be variability among patients.

Dermatomal charts depict typical peripheral nerve and nerve bracnh distributions, but distributions vary from one study of book to another, and there can also be variability among patients.

Acute sensorimotor deficits indicating multiple nerve or nerve root involvement in an arm or leg suggest plexopathy.

Most fibers conducting pain and temperature sensation decussate over several segments by way of the ventral white commissure and ascend in the lateral columns of the cord as the lateral spinothalamic tract. Fibers conducting light touch and two-point discrimination ascend in the ipsilateral posterior column of the spinal cord and decussate in the medial lemniscus of the medulla.

Cutaneous sensation from the face is carried to the brainstem by the trigeminal nerve. After e ntering the pons, part of the sensory fibers descend as a bundle to form the spinal tract of the trigeminal nerve, which reaches the upper cervical segment of the spinal cord. The spinal tract of the trigeminal nerve gives off fibers to the medially located nucleus of the spinal tract of the trigeminal nerve, which also descends into the upper cervical cord. The nucleus of the spinal tract of the trigeminal nerve receives fibers conducting sensations of pain, temperature, and light touch from the face and mucous membranes. Ascending fibers from the spinal nucleus travel mainly ipsilaterally in the trigeminothalamic tract and terminate in the ventral thalamus. The spinothalamic tract has connections with the brainstem reticular formation. It joins the medial lemniscus at the midbrain level and terminates in the posterior ventral complex of the thalamic nuclei.

The cortical projections of the posterior ventral thalamic complex ascend through the medial portion of the internal capsule to reach the post-central cortex in a somatotopic arrangement with the face in the lowest area and the leg in the parasagittal region. In addition to the post-central cortex, the cortical thalamic projections include the superior parietal lobule, which is considered to represent sensations of numbness and tingling over the contralateral or bilateral aspects of the body. The fine sensory discrimination and fine location of pain, temperature, touch, and pressure (so-called primary modalities) require normal functioning of the sensory cortex. The cerebral cortex of the post-central gyrus also subserves cortical sensory processes, including perception of sizes and shapes of objects (stereognosis), ability to recognize numbers or letters drawn on the patient’s skin (graphesthesia), and two-point discrimination.

usually indicates a lesion in a branch or branches of the trigeminal nerve, the trigeminal nucleus in the brainstem, or in the lemniscal pathways of the brainstem. It would be less typical to have pure facial sensory disturbance from a lesion in the thalamus, cortical projections, or somatosensory cortex (see III.B). Involvement of the ophthalmic branch of the trigeminal nerve can also cause a decreased blink reflex.

1. Acute onset of facial paresthesia manifesting as numbness, tingling, or ill-defined discomfort, if lasting only several seconds or minutes in a person who is exposed to stressful circumstances, is often idiopathic and self-limited. Paresthesia in the perioral area can be caused by and reproduced by hyperventilation. A severe form of lancinating facial pain can be very focal and feel like an abscessed tooth if in the mandibular branch of the trigeminal nerve, also known as tic douloureux, can also be idiopathic. Recurrent or chronic frontal or maxillary sinusitis can cause numbness referable to the ophthalmic or maxillary branches of the trigeminal nerve. Sensory disturbance in the maxillary division of the trigeminal nerve, which then spreads to the entire half of the face, suggests inflammatory demyelination. Sensory disturbance in the area of the mandibular division of the trigeminal nerve can reflect inflammatory or traumatic events involving the mandible or fracture of the base of the skull in the area of the foramen ovale. Relatively abrupt onset of sensory disturbance in the area of the chin suggests neuritis affecting the mental nerve and can be caused by osteomyelitis or the numb chin syndrome as a paraneoplastic manifestation of lymphoma, breast or prostate cancer, or melanoma.

2. Numbness or abnormal sensation can occur over the paretic facial muscles of idiopathic peripheral facial nerve (Bell’s) palsy.

3.Alteration in sensation in the ophthalmic division of the trigeminal nerve and accompanying abrupt onset of fever, proptosis, chemosis, diplopia, and papilledema suggests cavernous sinus thrombosis, which can be caused by suppurative processes involving the upper half of the face, orbits, or nasal sinuses. Septic cavernous sinus thrombosis represents a life-threatening process necessitating immediate hospitalization. Sensory deficit in the ophthalmic division of the trigeminal nerve can also accompany acute onset of meningitis.