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Individual Muscle Testing

A very common complaint encountered in general medical practice is that of weakness. As discussed in the section on the neurological history, this complaint needs further clarification since weakness may be used to denote fatigue, malaise or other non-specific symptoms to certain patients. If the patient does indeed complain of loss of strength in an extremity or elsewhere, then it is the task of the examiner to determine the distribution, degree and type of weakness. The distribution of weakness (eg, extensors in the arm, flexors in the leg); associated deep tendon reflex (DTR) changes (eg, increased); presence or absence of atrophy (eg, absent); and type of motor tone (eg, spasticity) are the characteristics use to define type of weakness. The previous example defines upper motor neuron weakness. The following is a summary of types of weakness commonly encountered in clinical practice.

Table 1: Patterns of muscle weakness

           Exceptions to the above may occur in certain specific disease states such as motor neuron disease (amyotrophic lateral sclerosis) where weakness patterns vary, but the above patterns serve in most clinical situations.

           How muscle strength is tested is an extremely important and often under emphasized clinical skill. Many extraneous factors may influence the examiner’s interpretation as to whether or not the patient has weak muscles. Patients may not exert full effort because of pain, their wish to emphasize their own impairment, or lack of understanding as to what is desired of them during the examination. Individual doctors, as well as patients, vary in their own physical strength. This often leads to inter-examiner variability. The best one can do is to strive for standardization of how he or she performs the test from one patient to the next. By doing this you eventually develop a feel for how strong various types of patients should be when compared to yourself.

           A cardinal practice should be that you are the one exerting the force against the muscle being tested. The force you exert becomes the gauge for normality or abnormality. It is also easier to detect break-away or give-away weakness. Here the patient suddenly gives up on the force they exert and the examiner feels a sudden decrease in resistance in the muscle being tested. This is in contradistinction to true weakness where there is a smooth decrease in resistance as the examiner exerts increasing force. Your ability to recognize this will increase with experience in testing muscle strength.  The key to achieving this experience is standardization of your performance of the examination. For each muscle tested, it should be placed in the position of maximal mechanical advantage (vide infra) and then you begin exerting force to try and overcome the muscle. With true weakness there is a smooth movement of the extremity in the direction in which you are exerting force; at the same time you feel a constant steady counter-resistance on the part of the patient.

           What follows are descriptions and illustrations of commonly tested muscles as well as their innervations. There will be additional demonstrations of how to test the muscles on the video portion of the module and by your clinical preceptor. Some examiners may vary in just how the test is performed, and you may be exposed to more than one technique. Select the one that works best for you keeping in mind that you are striving for reliability and reproducibility in assessing muscle weakness.

           The most common rating system for muscle strength gives a score of 5 for normal, (100%) strength, and 0 for total paralysis. 1, 2, 3, etc. note increasing strength in approximately 20% increments.

Muscles
            The underlined root carries the majority of innervation to the listed muscle.

Neck Flexors  (C 1-6)
      Test:  The head is flexed to the chest.  The examiner places his hand on the patient’s forehead and exerts backward pressure, trying to place the head in the normal upright position. The patient resists. (Figure 2-46)

Neck Extensors         (C1 - T1)
      Test:  The patient extends the head backward and resists the examiners attempt to push the        head forward (Figure 2-47).

      Neck flexors and extensors usually are affected by myopathies, and not by root lesions because of the number of different roots innervating these muscles. Before testing the neck flexors and extensors make sure there is no bony neck injury that might be worsened by these maneuvers. Patients with rheumatoid arthritis may have lax ligaments binding the C1 and C2 vertebrae and the above maneuvers may cause vertebral subluxations.

Upper Extremity

Shoulder Girdle
Infraspinatus (C 5,6: Surascapular nerve)
           Action: External rotation at the shoulder.
           Test: The patients flexes at the elbow, with his elbows at his side. The examiner exerts force            at the dorsal wrist or forearm, trying to push the forearm inwards towards the patient’s            abdomen (Figure 2-48).

Pectoralis major (C 5 - T 1)
           Action: Internal rotation at the shoulder.
           Test:  Same position as above, but the examiner pushes outward against resistance.(Figure            2-49).

Deltoid (C 5,6: Axillary nerve)
           Action: Shoulder abduction.
           Test:  The patient holds his proximal arm out laterally at 90 degrees of abduction, and the
           examiner exerts force in a downward direction. (Figure 2-50).

Arm
Biceps (C 5,6: (Musculocutaneous nerve)
           Action: Flexion of the forearm at the elbow.
           Test:  The patient flexes the arm to about 45 degrees, forearm supinated, and the
           examiner tries to extend it against resistance. (Figure 2-51).

Triceps (C6, 7, 8: Radial nerve)
           Action: Extension of the forearm at the elbow.
           Test:  The forearm is flexed to about 70 degrees with the forearm fully supinated. The
           examiner tries to push it in the direction of flexion against resistance by the patient
           (Figure 2-52).

Forearm
Brachioradialis (C 5,6: Radial nerve)
           Action: Flexion of the forearm at the elbow.
           Test:  The forearm is flexed to about 70 degrees with the forearm midway between
           pronation and supination. The examiner again pulls in the direction of forearm extension,            against patient resistance (Figure 2-53).

Extensor Carpi Radialis Longus and Brevis (C 6,7: Radial nerve)
           Action: Extension of the hand at the wrist.
           Test:  The patient extends the wrist and holds that position while the examiner pushes
           downward in the direction of flexion (Figure 2-54).

Extensor Digitorum Communis (C 7,8: Radial nerve)
           Action: Extension of the fingers.
           Test:  The patient keeps the fingers extended. While supporting the wrist with his left
           hand the examiner exert downward pressure on the extended fingers, pushing them in the            direction of flexion (Figure 2-55).

Pronator Teres (C 6,7: Median nerve)
           Action: Pronation of the forearm.
           Test:  The arm is flexed, with elbow at the side of the trunk. The forearm is pronated. The
           examiner grips the patient’s hand and tries to supinate the forearm against resistance (Figure            2-56).

Flexor Carpi Radialis (C 6, 7: Median nerve)
           Action: Flexion of the wrist at the hand.
           Test:  The patient flexes the hand at the wrist. The examiner pushes in the direction of
           extension against resistance by the patient (Figure 2-57).

Flexor Digitorum Sublimis and Profundus (C 7,8: Median nerve, [ulnar nerve supplies the profundus to the 4th and fifth fingers])
           Action: Flexion of the fingers.
           Test: Flexion of the fingers, Examiner tries to open them against resistance (Figure 2-58).

Hand
Abductor pollicis brevis (C 8, T 1: Median nerve)
           Action: Moves the thump perpendicular to the plane of the palm (palmar abduction).
           Test:  The thumb is placed in palmar abduction and the examiner pushes it towards the
           dorsum of the hand. (Figure 2-59).

Interrosei (C 8,T 1: Ulnar nerve)
           Action: Abduction of the fingers.
           Test:  It is easiest to test the index finger. The 2-5th fingers are held to support the hand and            the index finger is pushed inwards to overcome abduction (Figure 2-60).

Hypothenar (C 8, T1: Ulnar nerve)
           Action: Abductor digiti quinti (ADQ): 5th finger abduction. Flexor digiti quinti (FDQ): flexion            of the 5th finger.
           Test: (ADQ) Push the abducted 5th finger towards adduction. (FDQ) Extend 5th finger,            against attempt to keep it flexed (Figure 2-61).

LOWER EXTREMITY

Hip Girdle
           Muscles
           Iliopsoas (L 2,3,4: Femoral nerve)
           Action: Flexion of the thigh at the hip.
           Test:  In the lying or sitting position, the patient flexes the thigh at the hip. The examiner
           pushes downward at the knee, towards hip extension. (Figure 2-62).

Gluteus Maximus (L 5, S 1,2: Inferior gluteal nerve)
           Action: Extension of the thigh at the hip.
           Test:  With the patient sitting or standing the patient pushes, (extends), his thigh
           downward into the chair or bed, against the examiner’s attempt to elevate the thigh by lifting            upwards under the heel. (Figure 2-63).

Gluteus Medius (L 4,5, S 1: Superior gluteal nerve)
           Action: Abduction of the thigh.
           Test:  While sitting or lying the patient holds the thigh in the outward abducted position,            against the examiner’s attempt to push it inward towards adduction. (Figure 2-64).

Thigh
Quadriceps Femoris (L 2,3,4: Femoral nerve)
           Action: Extension of the leg at the knee.
           Test:  The patient extends his leg, at the knee, to about 170 degrees. The examiner tries to
           flex the leg at the knee while the patient resists. (Figure 2-65).

Hamstrings
           External = Biceps Femoris (L 5, S 1,2: Sciatic nerve)
           Internal = Semitendinosis; Semimembranosus (L 4,5, S 1,2: Sciatic nerve)
                      Action: Flexion of the leg at the knee.
                      Test:  The leg is flexed at the knee. The examiner tries to extend the leg against                       resistance by the patient (Figure 2-66).

Adductors (Adductor Magnus, Longus, Brevis) (L 2,3,4: Obturator nerve)
           Action: Adduction of the thigh.
           Test:  The patient holds the knees in fairly close proximity. The examiner tries to
           individually force them apart against resistance by the patient (Figure 2-67).

Distal Leg
           Anterior Tibial (L 4,5: Deep peroneal nerve)
                      Action: Dorsiflexion of the foot at the ankle.
                      Test: The patient dorsiflexes the foot and the examiner pushes downward towards
                      plantar extension. Alternatively, to detect mild weakness, the patient is asked to walk                       on his heels. With normal strength each foot should stay equally dorsiflexed and the                       toes not touch the ground while walking. (Figure 2-68).

Peroneus Longus, Brevis (L 5, S 1: Superficial peroneal nerve)
           Action: Eversion of the foot at the ankle.
           Test:  The patient holds his foot in the everted position and the examiner pushes inward
           towards inversion (Figure 2-69).

Toe Extensors (Extensor Hallucis and Digitorum) (L 4,5, S 1: Deep peroneal nerve)
           Action: Extension of the toes.
           Test:  The patient extends the toes upward and holds them there against the examiner’s
           attempt to push them downwards towards flexion. (Figure 2-70).

Posterior Tibial ( L 5, S 1: Posterior tibial nerve)
           Action: Inversion of the foot at the ankle.
           Test:  The patient holds his foot in the inverted position while the examiner pushes
           outward towards eversion. (Figure 2-71).

Gastrocnemius (L 5, S 1,2: Tibial nerve)
           Action: Plantar flexion of the foot at the ankle.
           Test:  The patient holds his foot plantar flexed while the examiner tries to dorsiflex it
           against resistance. Subtle weakness may be detected by having the patient walk on his toes            and observing if the heel comes closer to the ground when stepping off the affected side            (Figure 2-72).

Toe Flexors (Flexor Hallucis and Digitorum) (L 5, S 1: Posterior tibial nerve)
           Action: Flexion of the toes.
           Test:  The patient flexes his toes and the examiner tries to extend them against resistance
           by the patient. (Figure 2-73).

Other muscles that are less frequently tested but are important to test in certain clinical situations are the following:

Abdominal Muscles (T6 - L1)
            Action: Flexion of the trunk.
           Test:  The patient lies supine and flexes his neck. The abdominal muscles are observed to            tighten. The mid abdomen (umbilical level) is innervated by T-10, a frequent site of spine            metastatic lesions. Spinal lesions at this level often cause weakness below T-10. This can be            detected in the abdominal muscles by Beevor’s sign. The patient lies supine and flexes his            neck while the examiner holds a pen over the umbilicus. When the abdominal muscles tense            the stronger upper abdominal muscles pull the umbilicus upward which is made easier            to observe by holding a pen over the original umbilical location.

Rectal Sphincter  (S 3,4: Pudendal nerve)
           Action: Constriction of the anus.
            Test:  The examiner performs a rectal examination and notes rectal tone and contractile            ability on command. Decreased tone and contractile ability denotes a lower motor neuron            lesion. When associated with an atonic bladder (overflow incontinence), it is almost always            due to a lesion of the conus medullaris, (distal end of the spinal cord) or the cauda equina            (distal lumbar and sacral nerve roots before they exit the spinal canal).

Summary

• Weakness is loss of strength in individual muscles or groups of muscles, not fatigue.
• Weakness should be defined in terms of its pattern. (Table 1)
• When testing muscle strength the examiner should exert the force and note the degree of resistance of individual muscles to determine degree of weakness.

Evaluation of Speech and Language

           Disorders of speech and communication are numerous and some of the neuroanatomical pathways are complex. For purposes of this examination we will be dealing with broad concepts and will limit our discussion to clinically relevant and common disturbances.

            If a patient is having a speech or language problem, it becomes evident early in the examination, since it interferes with proper communication of the problem by the patient. There are several types of speech difficulties, which may be encountered, and we will define the most common.

            Aphasia (dysphasia).  A disorder of speech where the patient has trouble understanding speech, (in the absence of hearing problems), or in the thought and word finding processes of speech.  There is a defect in comprehension and/or expression of language. Aphasia refers to the absence of speech and dysphasia to a less complete disorder of speech.   There are different types of aphasia depending on where the lesion is located (Figure 2-74).

      Wernicke’s aphasia (sensory aphasia, receptive aphasia, fluent aphasia.).  This is caused by lesions of the posterior portion of the superior temporal gyrus (Wernicke’s area). The disorder is characterized by copious speech that is not intelligible because of incorrect word and syllable choice. The patient does not understand what he is saying or what is said to him. If a patient is hungry he will speak volumes but not be able to convey the simple message that he wants to eat. If the lesion involves the surrounding cortex there may be contralateral sensory loss or a homonymous visual field defect.

            Broca’s aphasia (motor aphasia, expressive aphasia, nonfluent aphasia). It is caused by lesions of the inferior portion of the left frontal gyrus and its underlying white matter. The patient understands speech but speech production is distorted. There is difficulty with speech fluency and organization and sentences have few words (telegraphic speech). Unlike the patient with a fluent dysphasia, patients can understand what they themselves and others are saying and can convey ideas. In the example of the starving patient he might communicate his plight by saying “hungry...eat”. If the lesion involves the surrounding cortex the patient will also have upper motor neuron right facial and hand weakness.

            Conduction aphasia. In this aphasia a lesion interrupts the connection between Wernicke’s and Broca’s area (Arcuate fasciculus) The clinical manifestation of this lesion is an inability to repeat what is said. This fasciculus is often involved with lesions in Broca’s or Wernicke’s area so patients with this type of aphasia may also not be able to repeat. The disorder can occur in isolation as well.

            Global aphasia. A large lesion affecting both speech areas and their connections leaves the patient mute and unable to comprehend speech. There is also an associated dense contralateral hemiplegia. This can be seen with acute infarcts in the dominant hemisphere, usually left middle cerebral or carotid artery distribution.

            Transcortical aphasia.  This type of aphasia occurs with lesions that separate the speech areas from the motor and sensory areas of the cortex. It usually occurs with arterial border zone lesions (infarcts secondary to vasospasm or hypotension). The arcuate fasciculus is spared so the patient can repeat what is said to him. If the sensory area (transcortical sensory aphasia) is isolated, patients appear to have a Wernicke’s aphasia with spared repetition. If the motor area is isolated (transcortical motor aphasia) they appear to have a Broca’s aphasia with spared repetition. In rare cases where all speech areas are isolated the patient's only speech ability is to simply repeat what is said to him. The unusual nature of this symptom may lead the clinician to falsely assume that the symptom is functional.

            Dysarthria.  Speech comprehension and expression are intact but an articulation problem exists which affects word pronunciation. There are different types of dysarthria, which reflect the level of the neuraxis affected.

            Spastic dysarthria. This is caused by bilateral upper motor neuron lesions and produces speech, which is harsh and strained in character.

            Extrapyramidal dysarthria. This is secondary to lesions of the basal ganglia and can be seen in Parkinson’s syndrome. The speech has low volume, no change in pitch, and may be distorted by tremor.

            Ataxic dysarthria. The speech has an irregular rate, range and volume. It may be explosive in character. Ataxic speech can be seen with cerebellar lesions.

            Hyperkinetic dysarthrias. There are unpredictable contractions of the muscles of articulation producing speech that is distorted in terms of pronunciation, articulation and volume. This can be seen with diseases producing excessive movement such as chorea and dystonia.

            Dysphonia.  A mechanical or psychological disturbance of voice production. This can beseen in patients with laryngectomies, vocal cord paralysis, or laryngitis. It is recognized by the quality of speech and the diagnosis confirmed by demonstration of the suspected underlying cause.

            Speech abnormalities are most often recognized when they are obvious, such as the dysarthrias. Fluent or Wernicke’s dysphasia, on the other hand, can easily be attributed to patient “confusion.” Once this assumption is made valuable time can be wasted looking for conditions, which have no bearing on the patient’s problem. Often the true nature of the disorder is only recognized after a hemiparesis develops. If you think a patient is confused, test him for aphasia by giving him verbal commands to follow. This will test for Wernicke’s aphasia. Be sure not to give the patient visual cues. Families will often insist that an aphasic patient understands them. They demonstrate by asking the patient to wiggle his fingers but at the same time wiggle their fingers in front of him. The patient then responds to the visual cue. If one asks him to wiggle his fingers without simultaneously showing him what is wanted, he will not comply.

            Patients can be asked to respond to informational questions such as name and address. This will simultaneously test for comprehension and speech generation. By asking the patient to repeat simple phrases one can test for speech repetition.

            Dysarthrias are recognized by listening to the patient’s response to questions or his spontaneous speech. With proper demonstrations and experience, most patterns are easy to discern.

Finally, the location of the lesion responsible for the speech problem can be further corroborated by the sometimes accompanying neurological deficits as previously described.

Neuroanatomy Websites

Neuroanatomy Interactive Syllabus

Nueroanatomy Pathology on the Internet

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