Motor Examination

Testing of motor function involves inspection of muscles followed by assessment of tone, power, coordination and reflexes. The initial findings from the assessment of these will determine if other clinical examination testing needs to be done- this might include assessment for bradykinesia or tremor. The gait assessment should follow the examination of motor function- see gait assessment.


Anatomical components of the motor system:

Upper Motor Neuron:

- Motor Cortex

- Brainstem

- Corticospinal tracts

Lower Motor Neuron:

- Anterior horn cells

- Peripheral motor nerves

- Neuromuscular junction  and muscle


- Basal ganglia




Important anatomical concepts:

Voluntary unilateral movement begins in the SMA (motor planning) then moves to the lateral premotor area and finally the primary motor cortex which sends impulses down the corticospinal tracts (corticobulbar for the cranial nerves) through the centrum semiovale  and then posterior limb of the internal capsule down to the brainstem and spinal cord and activates the anterior horn cells and out to the periphery- and this is how we move!


The corticospinal tracts are also called the pyramidal tracts. These are the primary tracts involved in voluntary movement. But voluntary movement also involves several other tracts-





And others- altogether they allow smooth voluntary movement. For example, if you want to pick something up beside you not only does your arm need to move but your eyes need to know that your arm wants to move and this is an example of how pathways other than motor pathways are necessary for movement. It is unnecessary to know these pathways in detail just know they exist.


Corticospinal tracts-

Decussate at the medullary pyramid (hence the name pyramidal tract)- lateral corticospinal tract (85% of fibres).

Ipsilateral anterior corticospinal tract (about 15% of fibres).

Run medially for the upper extremities

Run laterally for the lower extremities


Basal Ganglia- The basal ganglia is important for the production of smooth voluntary movement.


Cerebellum- regulation of activity of motor cortices. Dentato-thalamic-cortical tract. The cerebellar hemisphere is functionally connected to the contralateral cerebral cortex and so cerebellar lesions cause ipsilateral symptoms.

This regulates movement so allowing limb movement to be executed skilfully and its impairment will result in clumsy execution of voluntary movements (ataxia).



Components of the examination:


This begins when the patient walks in to the room- observe gait, use of a walking aid, slowness, tremor etc .


The next part of inspection is looking for atrophy and fasciculations. When looking for atrophy you are thinking of patterns- is it bilateral involving mainly proximal or distal muscles? (thinking myotonic dystrophy for distal, limb girdle muscular dystrophy for proximal, inclusion body myositis affects the forearm flexors and knee extensors as examples).


Hypertrophy of muscles can also occur. It can occur in hypothyroid myopathy. It can also appear in inherited muscular dystrophies such as Duchenne muscular dystrophy and Becker muscular dystrophy although this is referred to as pseudhypertrophy because it is not real hypertrophy of the muscle fibre.


Fasciculations commonly occur in the calf muscles and proximal arms muscles or hand muscles. Look closely- the fasciculation can be quite subtle.


When testing tone have the muscle in a relaxed position. Tone is judged by the degree of resistance against passive stretch. Test the tone quickly and then slowly to help distinguish between spasticity and rigidity.


Spasticity- sudden increase in the resistance during stretch, and if a flexor stretch is maintained, the resistance may suddenly disappear leading to an extension movement- this is referred to as clasp-knife phenomenon. This is because the initial presynaptic muscle spindle part of the stretch (through the stretch receptor) is hyperactive (because of the upper motor neuron lesion) and then the alpha-motor neurons are inhibited post-synaptically (which should happen) and this leads to the extension causing the clasp-knife phenomenon.


Clonus- When there is marked spasticity a single muscle stretch can induce repetitive brisk contractions in the same muscle and this is what clonus is. This is most easily demonstrated at the ankle.


Rigidity- Here the increased tone is throughout the movement and is independent of the speed of the stretch. It is in a cog-wheel fashion which is caused by action tremor superimposed on the increased tone. Sometimes there is rigidity without the cog-wheeling. Rigidity is characteristically seen in Parkinson disease.


Hypotonia- this is reduced tone and is usually seen in disorders of the peripheral nerves or muscle. Tabes dorsalis can cause marked hypotonia. Hypotonia can also be seen in the very acute stages of a spinal cord injury. Acute cerebellar lesions can also lead to hypotonia although the mechanism of this is not fully understood.



Manual muscle testing:

5: normal

4: good (weaker than normal but the patient can move against the examiners moderate resistance)

3: fair (can move well against gravity)

2: poor (can move well if gravity removed)

1: trace (can contract the muscle but no joint movement)

0: zero (complete paralysis).


Muscle pain or myalgia can sometimes cloud the strength examination and thus should always be asked about and taken in to consideration. If muscle pain is a prominent symptom assessing for tender spots or trigger points may be useful in trying to reach a diagnosis.


During the assessment of strength you should begin to formulate your differential diagnosis- is it one limb that is weak or one side? Had you noticed atrophy on inspection? If so pay particular attention to the strength of this muscle. So for example, if you had noticed FDI wasting (+/- fasciculations) on inspection then pay close attention to ulnar nerve innervated muscles, lower trunk of the brachial plexus and the C8/T1 root innervated muscles. Or if you had noticed forearm atrophy pay particular attention to the strength of all of the finger flexors. If there is no atrophy and the patient is complaining of weakness try to sense the pattern- is it symmetrical? Is it proximal or distal? Etc etc


There are countless different forms of peripheral neuropathies that can lead to focal or diffuse weakness. It is unnecessary to know these in detail but formulating a differential diagnosis is important- this cannot be done from the examination alone. By the time you are doing the examination you will have the history taken and the examination is really to confirm your “working hypothesis”. As an example, if the symptoms came on fairly acutely possibly following some sort of infection then consider an acquired inflammatory  demyelinating polyneuropathy and this will usually be symmetrical. Similarly, if the symptoms began with severe pain and it was following the pain that the weakness was noted consider an idiopathic brachial plexopathy also called neuralgic amyotrophy. This tends to just involve one limb clinically but often more subtle findings are found in the “normal” limb.



Coordination is tested with the finger nose (upper extremities) and heel shin (lower extremities) test and rapid alternating movements.


When abnormal this is referred to as dysdiadochokinesis. It usually points to an abnormality in the cerebellum.


Sometimes a sensory ataxia can manifest as poor coordination on the finger-nose test. It can be easily distinguished from a cerebellar abnormality from the sensory examination which will reveal abnormal proprioception.



When testing reflexes you are looking for symmetry and whether they are increased or decreased. The muscle to be tested needs to be in a relaxed position with an intermediate length.


The tendon reflex will be lost when there is a lesion of either the afferent or efferent arc of the reflex. To confirm loss of a reflex you will need to perform reinforcement- this is where you ask the patient to clasp their hands together in front of their chest and then pull their hands apart when you give the instruction- this is when you check the reflex.


Hyperreflexia occurs as a result of loss of inhibitory modulation from  descending pathways. If symmetric increase in reflexes is the only pyramidal sign it may not be all that significant. If there are other upper motor neuron signs present, especially a Babinski sign, then they are suggestive of an upper motor neuron or pyramidal tract lesion. If the hyperreflexia is asymmetric then it is more likely to be diagnostically significant.


Jaw jerk- the jaw should be tapped downwards. Ask the patient to slightly open their mouth, place your thumb under their chin and then tap the hammer off your thumb. It is useful when it is brisk but when it is absent it has less meaning as the jaw jerk may be absent in normal people.


Biceps reflex- C5,C6


Triceps reflex-C6,C7


Brachioradialis reflex- C5,C6


Finger flexors reflex- this reflex may not be present even in normal subjects so it is valuable when it is enhanced. This is called Wartenberg reflex and is an important clue for pyramidal signs. This is similar to the Hoffman reflex which is elicited by taking the middle finger between your thumb and middle fingers and flip a quick extension of the DIP joint. When this is enhanced it is referred to as Hoffmans reflex.


Quadriceps reflex- L3, L4


Gastrocnemius-soleus reflex or ankle jerk- This is often decreased in elderly subjects. Its presence does not exclude a polyneuropathy as the circuit generating the ankle jerk is actually midway up the calf even though it is tested at the Achilles tendon. L5, S1


Plantar reflex- This is elicited by stroking the sole of the foot with a blunt end of the handle of the tendon hammer and is manifested as toe flexion in healthy subjects. The extensor plantar reflex consists of extension of the big toe with fanning and/or extension of the other toes. This is Babinski sign. The Babinski sign is the most specific sign among all neurologic signs. Its presence always indicates a lesion of the pyramidal tract or upper motor neurons.

Crossed adductors and spreading of reflexes are also upper motor neuron signs. Crossed adduction is when there is adduction of the opposite leg when the medial aspect of the knee is tapped. Spreading of reflexes is, for example,  where the biceps reflex elicits the brachioradialis reflex.


Extra tests

Pronator drift- ask the patient to hold the arms outstretched with the palms upward. If there is a pronator drift there will be a subtle pronation of the forearm as the flexors are stronger than extensors.


Asking the patient to stand on the heels and toes is a way of looking for a subtle foot drop (heels) or subtle plantar flexion weakness (toes).


Patterns on the motor examination:

  1. Upper motor neuron signs
    1. Hyperreflexia
    2. Spasticity
    3. Clonus
    4. Babinski sign
  2. Lower motor neuron signs
    1. Hyporeflexia
    2. Muscle weakness
    3. Atrophy
    4. Fasciculations


In the following section I have described some patterns of weakness. This is to give a sense of how to try and localise the lesion when you are faced with performing the neurological examination. Obviously all findings on the examination are put together to try and localise the lesion.


Patterns of weakness:

Unilateral face, arm and leg weakness

  1. Other symptoms- sensory function
  2. Localisation- above the spinal cord and medulla because face involved
  3. Pure motor- corticospinal and corticobulbar fibres below the cortex and above the medulla. Lacunar infarct of internal capsule would be a cause here.
  4. Other focal neurological symptoms, such as sensory symptoms for example, may localise this to the cerebral cortex as well as the localisation mentioned above.



Unilateral arm and leg weakness

  1. Localisation- unlikely to be the corticospinal tract above the medulla and below the cerebral cortex as the corticobulbar fibres run close to these so face would be involved. Arm and leg area of cortex or below the medulla and above C5 are possible localisations.
  2. Associated symptoms are important in helping with localisation
    1. Aphasia- may suggest a cortical localisation
    2. Watershed territory infarct of cerebral cortex can produce this pattern- here proximal muscles are affected more than the distal giving a “man in barrel” appearance.
    3. Loss of vibration and position sense on same side as weakness and contralateral tongue weakness- medial medulla
    4. Decreased facial sensation- may suggest a high cervical lesion that is also involving the spinal trigeminal nucleus.
    5. Brown-Sequard pattern with a cervical lesion- sensory findings will be on the opposite side to the weakness


Unilateral face and arm weakness

  1. Localisation- Face and arm areas of the primary motor cortex over the lateral frontal convexity.
  2. Associated symptoms- Dysarthria, Brocas aphasia in dominant hemisphere, hemineglect in non-dominant hemisphere.
  3. If it extends in to the parietal cortex there may be more sensory findings
  4. Infarct in the superior division of the middle cerebral artery.



Unilateral arm weakness

  1. Localisation- arm area of the motor cortex or peripheral nerves supplying the arm.
  2. Motor cortex- upper motor neuron signs, cortical sensory loss, aphasia. Distribution of the weakness is helpful here- if it is primarily distal weakness in the hand, fingers, wrist without sensory loss this will localise to the motor cortex as this is not expected in a peripheral nerve lesion. Infarct of small cortical branch of MCA.
  3. Peripheral nerve- lower motor neuron signs. Weakness and sensory loss in a particular distribution (think divisions of brachial plexus). Brachial plexopathy or mononeuropathy.




Unilateral leg weakness

  1. Localisation- unlikely to be in the corticospinal tract above the upper thoracic region as arm and/or face would likely be involved. Leg area of the motor cortex, lateral corticospinal tract below T1 or peripheral nerve in the leg.
  2. Associated symptoms such as upper motor neuron signs, cortical sensory loss, subtle involvement of face and arm- suggests leg area of cortex. Anterior cerebral artery infarction causes contralateral leg weakness.
  3. Spinal cord lesions- there may be a Brown-Sequard pattern.
  4. Peripheral nerve- lower motor neuron signs. Diabetic neuropathy would be a common cause.



the Neurologic Examination. Scientific Basis for Clinical Diagnosis. Shibasaki H and Hallett M.

Neuroanatomy through clinical cases. Blumefeld H.

Motor Examination

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