In addition to patterns of weakness and reflex changes, clinical findings in other neural systems will confirm or further help in localizing the source of the weakness.
Cerebral. A command center for conjugate gaze is located in each frontal lobe. When one is damaged, the unopposed action of the other causes deviation of the eyes to the side of the lesion and away from the hemiplegia. The motor cortex is very close to Broca's area, and a nonfluent or Broca's aphasia often accompanies a right hemiplegia of cortical origin. The sensory cortex is across the Rolandic fissure, and a cortical sensory loss often accompanies hemiplegia. Lesions in the hemispheral visual pathways will result in a contralateral homonomous hemianopia.
Cranial Nerves. Cranial nerve dysfunction and the pattern of involvement define the brain stem as the source of the lesion causing the weakness. Since the pyramidal tract is a midline structure in the brain stem, midline damage causes weakness and hyperreflexia, usually bilaterally, and affects cranial nerves III and IV (midbrain), VI and VII (pons), and XII (medulla).
Cerebellar/Gait. Brain stem lesions causing weakness also commonly affect connections with the cerebellum, producing ataxia and dyssynergia. These components of cerebellar motor dysfunction may be difficult to see depending on the severity of the weakness. Proximal weakness can produce wavering when the patient puts a finger to the nose, which is very reminiscent of a cerebellar intention tremor. In this situation one must examine the patient's coordination in finger and hand movements. One helpful test is repetitive tapping of the forefinger against the flexor crease of the thumb. Pyramidal and extrapyramidal lesions slow the rate of movement, but accuracy in hitting the target is unaffected, whereas in patients with cerebellar disease, the rate may be normal, but the accuracy is impaired and the rhythm of tapping is erratic. Rapid alternating movements of the hands are slow and regular in pyramidal and extrapyramidal disease; in cerebellar disease the rate and rhythm are irregular and clumsy.
Walking is one of the most important tests in differentiating upper from lower motor lesions causing weakness. The spasticity caused by an upper motor neuron lesion can be seen in the very stiff jerky movements of the legs. Spasticity of the adductor muscles produces scissoring (i.e., a tendency for the legs to cross over one another from one step to the next). If the upper motor lesion is unilateral, the spastic leg is often circumducted with the leg extended at the knee while the arm is held in a flexed posture, that is, the typical hemiplegic posture. Distal weakness due to a lower motor neuron lesion produces floppy feet that slap on the floor and must be lifted high to prevent the toe from dragging and tripping the patient. Weakness of the hip girdle, most often seen in patients with myopathies, results in weakness of fixation of the pelvis and a waddling ducklike walk. Often the gait is widened to increase stability because otherwise the gait is made more unstable by the hip girdle weakness.
Sensory. The presence or absence of sensory symptoms and signs and the pattern and type of sensory change are very helpful in confirming which level of the motor system is involved in producing weakness. A relatively mild hemisensory loss affecting touch and proprioception more than pain and accompanied by impairment of stereognosis, graphesthesia, and two-point discrimination is characteristic of a lesion in the contralateral sensory cortex. A change
in touch and pain sensation in the ipsilateral face and contralateral body is characteristic of a unilateral lateral medullary lesion (Wallenberg's syndrome). Spinal cord lesions often affect sensation on both sides of the body; the upper level of the sensory loss, especially in regard to pain and temperature, help to define the level of the lesion. When half the cord is damaged, a pattern of loss of proprioception and vibration ipsilateral to the lesion and contralateral loss of pain and temperature sensation is characteristic of the Brown-Sequard syndrome. Central cord lesions produce a suspended sensory loss affecting pain and temperature sensation with sparing of the sacral dermatomes, and vibration and proprioception (see Chapter.1,9 and Chapter.2.0 ). Lesions of the conus medullaris or cauda equina produce loss of sensation in the perineum. Careful mapping of a more localized area of sensory loss in a limb can differentiate a dermatomal pattern of loss consistent with a spinal root lesion from a peripheral nerve distribution. An absence of sensory symptoms or signs indicates that the weakness results from disease in the motor neurons, muscle, or neuromuscular junction.
Autonomic Nervous System. At the bedside, some aspects of the autonomic nervous system can be tested. The most easily appreciated lesion is an impairment of sympathetic innervation to the cranial structures producing ipsilateral ptosis, miosis, and anhidrosis of the face (Horner's syndrome). Horner's syndrome may result from lesions of the descending sympathetic fibers in the brain stem and spinal cord in which the pattern of weakness, the presence or absence of cranial nerve signs, and sensory changes are more important in localizing the lesion. The presence of a Horner's syndrome is more helpful in localization of a lesion when a spinal root or brachial plexus lesion is suspected. The preganglionic sympathetic fibers leave the spinal cord with the C8 and T1 spinal roots, which become the lower trunk of the brachial plexus. Therefore, lesions of the C8 or Tl nerve roots (e.g., herniated disc) or lower trunk of the brachial plexus (e.g., apical lung tumor) may be associated with a Horner's syndrome. The postganglionic sympathetic fibers course along the carotid arteries into the cranium. Occasionally an occlusion of the common carotid artery produces an ipsilateral Horner's syndrome along with a contralateral hemiparesis.
The parasympathetic pupillomotor fibers from the Edinger-Westphal nucleus in the third nerve nuclear complex of the midbrain is impaired with lesions of the third nerve nucleus or nerve, which result in a paralysis of the pupillary sphincter, producing pupillary dilatation. Attention to autonomic function, especially sweating, can be helpful in defining the level of acute transverse spinal cord lesions. A loss of sweating occurs below the level of the lesion. Sometimes this can be appreciated by lightly rubbing the dorsal surface of the forefinger along the skin, starting below the expected level of the lesion and stroking upward; the finger slides easily over the smooth dry skin below the lesion but sticks momentarily as it meets the normal moist skin at the upper border of the lesion.
Orthostatic hypotension is sometimes described by the patient as weakness rather than as a presyncopal lightheaded fainting sensation. Diffuse autonomic dysfunction with orthostatic hypotension is a feature of multiple system atrophy (olivopontocerebellar atrophy and Shy-Drager syndrome). Orthostatic blood pressures are checked after 3 minutes in a recumbent posture and again after 3 minutes of standing. The pulse rates are also taken in the supine and standing positions. In patients with autonomic dysfunction the pulse rate does not rise to compensate for the fall in blood pressure, whereas in those with hypovolemic orthostasis a significant compensatory increase in pulse rate is seen.
Neurovascular. The neck vessels should be examined in patients in whom strokes are suspected. Evidence of small vessel disease in the form of poor pulses or trophic skin changes may suggest diabetes or vasculopathic causes of weakness.
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