The motor exam has several steps including 1. Observation, 2. Inspection, 3. Palpation, 4. Muscle tone testing, 5. Functional testing, and 6. Strength testing of individual muscle groups. Each of these steps will now be discussed in turn.
First, carefully observe the patient to detect any twitches, tremors, or other involuntary movements, as well as any unusual paucity of movement suggestive of a movement disorder (see Neuroanatomy Through Clinical Cases, Key Clinical Concepts 15.2, and 16.1). Note also the patient's posture. Next inspect several individual muscles to see if muscle wasting, hypertrophy, or fasciculations (spontaneous quivering movements caused by firing of muscle motor units) are present. The best muscles to look at for fasciculations in generalized LMN disorders are the intrinsic hand muscles, shoulder girdle, and thigh. In cases of suspected myositis, palpate the muscles to see if there is tenderness.
Before formally testing strength in each muscle, it is useful to do a few general functional tests that help detect subtle abnormalities. Check for drift by having the patient hold up both arms or both legs and close their eyes. Check fine movements by testing rapid finger tapping, rapid hand pronation—supination (as in screwing in a light bulb), rapid hand tapping, and rapid foot tapping against the floor or other object. Tests for subtle weakness are discussed further in Neuroanatomy through Clinical Cases, Key Clinical Concept 6.4.
Finally, test the strength of each muscle group and record it in a systematic fashion (see next section).
Involuntary movements and tremors are commonly associated with lesions of the basal ganglia or cerebellum (see Neuroanatomy Through Clinical Cases, Key Clinical Concepts 15.2, and 16.1). Tremors can also occasionally be seen with peripheral nerve lesions.
Many parts of the motor exam can help distinguish between upper motor neuron and lower motor neuron lesions (see Neuroanatomy through Clinical Cases Chapters 2 and 6). Recall that upper motor neurons project via the corticospinal tract to lower motor neurons located in the anterior horn of the spinal cord. Signs of lower motor neuron lesions include weakness, atrophy, fasciculations, and hyporeflexia (reduced reflexes). Signs of upper motor neuron lesions include weakness, hyperreflexia (increased reflexes), and increased tone. The hyperreflexia and increased tone seen with corticospinal lesions is apparently caused by damage to pathways that travel in close association with the corticospinal tract rather than directly by damage to the corticospinal tract itself. Note that with acute upper motor neuron lesions there is often flaccid paralysis with decreased tone and decreased reflexes. With time (hours to weeks), increased tone and hyperreflexia usually develop.
|Signs of Upper Motor Neuron (UMN) and Lower Motor Neuron (LMN) Lesions|
|Sign||UMN Lesions||LMN Lesions|
|*Mild atrophy may develop due to disuse.|
Increased tone can occur in upper motor neuron lesions, but can also occur in basal ganglia dysfunction (see Neuroanatomy Through Clinical Cases, Key Clinical Concept 16.1). In addition, slow or awkward fine finger movements or toe tapping in the absence of weakness can signify a subtle abnormality of the corticospinal pathways, but can also occur in lesions of the cerebellum or basal ganglia.