Neurological examination of the motor system

Types and functions

The tracts of the spinal cord can be compared to the busy highways that link one city to another. They are designed to carry impulses in a particular direction; either to or away from the brain. Those traveling to the brain are afferent tracts that carry sensory stimuli to be processed. Those traveling away from the brain are known as efferent tracts and they carry motor stimuli to target organs. Since the sensory tracts travel up the spinal cord to the brain, they are referred to as the ascending spinal tracts. Similarly, the motor fibers travel from the brain toward the periphery and are therefore referred to as the descending tracts of the spinal cord.

The spinal cord tracts are commonly found in the white matter of the spinal cord. They are named according to their location within the cord (i.e. lateral, medial, ventral/anterior, or dorsal /posterior, the point of origin, and the point of termination (i.e. the spinothalamic tract starts in the spinal cord and ends in the thalamus). The sensory stimuli commonly transmitted by the ascending tracts include pain, temperature, crude touch, vibration sense, two-point discrimination, and proprioception. On the other hand, the descending tracts carry skilled, discrete, voluntary movements to the muscles of the periphery. The descending pathway also has a regulatory function that promotes or inhibits varying muscle groups during particular activities.

Descending spinal tracts

Different areas of the brain (i.e. cortex, reticular formation, vestibular areas, tectum, and the red nucleus) are responsible for generating voluntary and involuntary responses to sensory stimuli. There are roughly six named descending tracts passing from the brain to through the spinal cord. Voluntary motor activity is regulated at the level of the cortices, and is therefore transmitted via the corticospinal tracts.

The reticular formation provides both excitatory and inhibitory impulses via the reticulospinal pathways. Activation of the flexors and inhibition of the extensors is achieved by the rubrospinal tracts, while the opposite is mitigated by the vestibulospinal tract. Motor response in response to visual stimuli is transmitted by the tectospinal pathway.

These nerve fibers eventually leave the spinal cord in the ventral rami in order to terminate in their target organs. Below is a list of the descending tracts and the motor signals they transmit:

The descending tracts of the spinal cord can be quite tricky to learn. Tackle the following learning materials and master the knowledge as easily as possible:

Inspection of the limbs

The patient should be adequately exposed such that both limbs being examined (upper or lower) can be thoroughly examined. Of course, the patients' dignity should be maintained during the entire examination. With the patient in the anatomical position, inspect their limbs for any significant scars. Neuromuscular damage following traumatic injury can result in significant motor deficits. Evidence of muscle wasting is often suggestive of decreased muscle use (i.e. disuse atrophy). Wasting is less common with acute upper motor neuron lesions than it is with lower motor neuron and chronic upper motor neuron disease. Alternatively, some patients may present with limb-length discrepancies if muscle wasting occurs during early childhood. A variety of involuntary movements can occur with nerve injuries. Examples of these include:

• Myoclonic jerks are sudden, involuntary, spasmodic twitches.
• Chorea is purposeless, rhythmic movements more commonly occurring in the upper limbs, but can be seen in random body parts. It comes from the greek word “χορός” which means “dance”.
• Athetosis is a slow-paced, writhing activity that is more similar to dystonia than it is to chorea.
• Tics are compulsive, stereotyped activities that can be temporarily controlled by the patient. 
• Dystonia is a repetitive, twisting motion that can affect the entire body or just an isolated area. These include torticollis (twisting the head to one side) and its variants (anterocolis and retrocolis).

Individuals with neurological disorders may also experience irregular spasmodic bursts to an area of skin that rests on the involved muscle group. These fasciculations can sometimes occur in normal individuals but is more commonly encountered in patients with lower motor neuron disease. Please note that this phenomenon is something that is appreciated visually, and is associated with muscle wasting.

Another abnormality of movement that can be picked up from inspection are tremors. These are back and forth motions that occur around a particular joint. They are grouped according to the position in which they are initiated (i.e. at rest or with movements), the frequency at which they occur (i.e. fast or slow), and the associated amplitude (i.e. fine tremors occur at low amplitudes). Non-pathological variants that occur with caffeine intake, or in states of anxiety are known as physiological tremor. Pathological forms of tremors include:

• Intention tremors – is a sign of cerebellar damage and is most often elicited with the past-pointing (or finger to nose test). They are most severe with movement and resolves with rest.
• Postural tremors – can be felt while trying to maintain a particular position for a prolonged period; such as the planking exercise.
• Task specific tremors – are restricted to situations where tasks that require fine skills are being performed. These include speaking, writing, or trying to site an intravenous access for the first time. 
• Isometric tremors – tend to occur while sustaining muscle activity without any movement. This can be observed while trying to hold a heavy object for an extended period.  
• Kinetic tremors – unlike isometric tremors, are associated with movements.
• Parkinsonian tremors – occurs at rest and improves with voluntary movements. It is a high-amplitude (coarse), low-frequency (slow), asymmetrical tremor that affects mostly the upper limbs and spares the head. 
• Essential tremors – affects upper limbs and head, occurs with postural changes, and may improve with alcohol ingestion.

The acronym SWIFT (scars, wasting, involuntary movements, fasciculation, and tremors) can be used to remember the key features to assess during inspection.

Palpation

Although fasciculations may be absent on inspection, they can sometimes be induced. Gently flick the different muscle groups to see if there are any inducible fasciculations. Afterwards, palpate the different muscle groups to further assess the muscle bulk. There may be unilateral wasting if there is a neurological lesion affecting only one side of the body. Conversely, muscle groups may appear hypertrophied but are soft, fatty, and weak as seen in pseudohypertrophy of Duchenne’s muscular dystrophy.

Assessing muscle tone

The tone of the limb is the resistance felt by the practitioner while mobilizing the limb passively about the joint. To execute this examination, place the patient in a supine position and advise them to let their limbs hang loosely (or go floppy). The idea is to not have any muscular influence while moving the limbs. Make note of any areas where they may be having pain and take extra precaution while moving that limb to avoid causing the patient additional distress. All movements performed while assessing tone should be randomized with respect to the speed at which they are done and the direction in which the joint is moved. This helps to prevent the patient from actively moving the limb during the examination.

Reach out for the patient’s hand as if you’re about to shake hands and support the limb at the elbow with the free hand. Use the opportunity to assess the tone at the wrist, elbows, and shoulders. Assess only one joint at a time; the elbow can only be assessed in a single plane (along flexion and extension), while the shoulder and wrist can be assessed in a multidirectional (circular) plane. Repeat the technique on the opposite limb to assess the tone there as well.

With the lower limb in the anatomical position, roll the limb from side to side to assess tone at the hips. Follow up this maneuver by briskly lifting the limb at the knee. Simultaneously observe the foot to see if the heel is lifted off the bed (occurs with increased tone) or moves up along the bed (normal or reduced tone) as the knee goes into a flexed position. Using the left hand to stabilize the patient’s thigh and the right hand holding the leg, flex and extend the knee to assess the tone at that joint. Finally, hold the leg with the left hand and the foot with the right and proceed to perform circular motions at the ankle to determine the tone at that joint as well. 

Tone can be normal, reduced, or increased. Increased tone is referred to as hypertonia, while reduced tone is called hypotonia. Patients with lower motor neuron lesions often become hypotonic and hyporeflexic. Conversely, those with upper motor neuron lesions tend to be hypertonic and hyperreflexic. The principle behind the phenomenon is such that upper motor neuron lesions remove the regulatory impulses on the alpha motor neurons of the anterior grey horn of the spinal cord. As such, the impulses arising from the anterior motor horn cells remain unregulated, resulting in increased motor tone. Similarly, lower motor neuron lesions occurring at or below the level of the anterior motor horn prevents impulses from reaching the target muscles. As a result, the limb becomes weak and hypotonic. There are two main types of hypertonia:

• Rigidity – refers to prolonged resistance throughout the range of motion. It is detected throughout slow passive movement. Patients from parkinsonism also have a form of rigidity referred to as often described ‘lead-pipe rigidity’ or ‘cogwheel rigidity’ (when there are parkinsonian tremors associated).
• Spasticity – is usually associated with increased reflexes and decreased power. Brisk movements of the limb while assessing the tone of the limb will elicit spastic responses. At the lower extreme of this disorder the examiner may only discover a ‘catch’ at the start or end of passive movements. At the advanced end, spasticity will limit the range of motion of the limb.

Assessing reflexes

The force generated from striking a tendon results in stretching of the tendon and subsequent involuntary contraction of the muscle. The local reflex arcs in the anterior grey horn of the spinal cord are regulated by descending motor neuron fibers from the brain. The common reflexes that are most frequently tested are the biceps, triceps, brachioradialis (supinator), knee, and ankle jerk reflexes.  Therefore, the same principle that applies to the hypertonic and hypotonic responses also applies to increased and decreased reflexes. 

It is important to have the patient relaxed in a recumbent position for this examination. The idea is to position the limb in a neutral position with the non-dominant hand and allow the weight of the patellar hammer to flex the wrist. The hammer should strike the tendon, and not the bone or muscle. The scoring system outlined below describes the responses that can be elicited.

The plantar response is a polysynaptic superficial reflex elicited by stimulating the skin on the sole of the foot. The sole of the foot is stroked along the lateral border from the heel to the fifth metatarsophalangeal joint and then medially across all the metatarsophalangeal joints. Observe the first movement of the great toe, flexion of the leg muscles, and the position of the other toes. Under normal circumstances there is plantar flexion of the great toe and remaining toes. In an individual with an upper motor neuron lesion, there is dorsiflexion of the great toe and fanning of the remaining toes, associated with contraction of the leg muscles. This is known as a Babinski response and is reproducible. The response is normal in infants and normally goes away during early childhood. 

Assessing power

While there are physiological parameters that determine the degree of strength that a person has, overall muscle power is a good indication of motor nerve function. The pattern of weakness varies according to the location of the lesion. It is impractical to assess every muscle group in the body. The arm, forearm, and hand muscles, as well as the hip, thigh, and leg muscles are most commonly tested. 

While testing the upper limbs, ask the patient to sit up (if possible) at the edge of the bed. Start examining the muscle groups proximally and work towards the distal groups. Ask the patient to first raise the arms to determine if they can overcome the power of gravity (i.e. at least a 3/5 on the Medical Research Council Scale [MRCS]). With the shoulders abducted (i.e. shoulders and elbows are in the horizontal plane at 180o), apply downward force at the elbows and ask the patient to resist your efforts. Then instruct the patient to adduct the shoulders as the examiner applies opposing (upward) forces at the elbows.

Assess the strength of the biceps by using the non-dominant hand to palpate the muscle and the dominant hand to apply opposing force to the wrist as the patient pulls their hand to their face. Similarly, the non-dominant hand is used to palpate the triceps while testing that muscle while the opposing force is applied at the wrist with the dominant hand as the patient attempts to straighten their elbow. Extension at the wrist can be assessed by supporting the forearm in pronation with the non-dominant hand and asking the patient to bend the hand backwards (it is probably easier to demonstrate the motion to the patient than it is to explain it). Place the dominant hand on the dorsum of the hand being tested to oppose the activity of the extensors. 

Assessment of the lower limbs should be done while the patient is recumbent. Instruct the patient to move each lower limb in the vertical plane to determine their baseline power. If they are unable to move either limb against gravity, then instruct them to move the limb in the horizontal plane (where gravity is not acting on the limb). If they’re unable to move the limb then observe and palpate the limb to see if there is any effort (i.e. muscle contraction) while they attempt to move the limb. However, if they are able to move the limb in the vertical plane, then proceed to apply an opposing force to the limb. Assess abduction at the hips by asking the patient to move their thighs apart in the horizontal plane while applying opposing forces to the lateral aspect of the thighs. The opposite is done to assess adduction at the hips. To assess flexion at the hip, position the thigh at 90 degrees with respect to the torso and position the knee in a 90 degrees angle as well. Support the leg with the right and place left hand on the anterior thigh. Instruct the patient to move the knee towards their face and oppose the option with the left hand. Repeat the procedure on the left side. With the limb in the same position, place the left hand on the posterior thigh and ask the patient to push their leg down. 

To assess flexion at the knee, position the limb in flexion, place the left hand on the posterior thigh and the right hand at the ankle. Ask the patient to move the heel of their foot toward the ipsilateral buttock. Use the right hand to oppose the motion of the limb, and the left hand to palpate the muscle. Extension at the knee is done with the limb in the aforementioned position. The right hand remains at the ankle, but the left hand is positioned on the anterior thigh. Ask the patient to straighten out the limb while the examiner’s right hand opposes the motion. 

Dorsiflexion of the ankle is assessed by placing the non-dominant hand on the leg and the dominant hand on the dorsum of the foot. Ask the patient to point the toes toward their face while the dominant examining hand opposes this activity. Plantar-flexion is assessed in a similar manner, but with the dominant hand on the plantar surface of the foot and asking the patient to point their toes downward.

Patients may experience partial paralysis (paresis) or complete loss of function (plegia). The deficit may involve a single limb (e.g. monoparesis), half of the body (e.g. hemiplegia), both legs (e.g. paraparesis), or all four limbs (e.g. tetraplegia). Weakness affecting a single muscle group or single muscle is more likely due to a lower motor neuron injury. In contrast, upper motor neuron lesions result in deficits in large muscle groups or an entire limb.

Assessing motor coordination

Motor coordination depends on ones special awareness of each body part relative to the environment. This is a semi-conscious process that depends on an interplay between proprioception, equilibrium, vestibular function, and other sensory modalities with an appropriate motor response. These functions are mostly regulated by the cerebellum and its intricate connections with the forebrain and midbrain structures. There are certain non-specific symptoms that patients experience if there is damage to the cerebellum. These include nausea, vomiting, vertigo, and many others. However, the practitioner can detect cerebellar injury by assessing the patient’s ability to perform the following tests:

• Past pointing: also known as the finger to nose test, this procedure involves positioning the patient in front of the examiner. While in this position, the patient is instructed to touch the tip of their nose with the tip of the index finger then to touch the examiner’s fingertip (which should be held at an arm’s length from the patient). Let the patient repeat this process; all while changing the position of the target (the fingertip) each time. Dysmetria are all potential findings with cerebellar dysfunction (going beyond the target point), dyssynergia (slow, interrupted, clumsy motions), and intention tremors.
• Rapid alternating movements: involves the patient switching between tapping the palm of one hand with the dorsal and palmar surface of the other hand. They are asked to increase the speed during the test to gauge the accuracy with which the task is completed. Patients who are unable to complete this task demonstrate dysdiadochokinesis. 
• Heel to shin test: this is conducted while the patient in the supine position. Instruct them to position the heel on the contralateral knee and stroke it back and forth between the ankle and the knee. The test is repeated on the contralateral side as well. This test is the lower limb counterpart to the finger-to-nose test.

Finally, patients with cerebellar dysfunction may also demonstrate cerebellar ataxia or an ataxic gait. This gait disorder cannot be compensated for with visual input (as is the case with sensory ataxia). Consequently, the Romberg’s test (standing in place with a narrow stance) or attempting to walk with the eyes close will not alter the gait abnormality. The patient with a cerebellar ataxia often has a broad-based gait and stance. They often wobble as they attempt to walk and appear insecure. There are irregularities with their stride length and movements of the legs. The defect can be exaggerated by instructing the patient to make an abrupt turn during a tandem walk. In an attempt to make up for the deficit, patients appear extra cautious while walking and may stoop at the hip to steady their stance.