Chapter 10 - Motor system examination

Sistem motorik terdiri dari sistem yang terlibat dalam pembentukan dan pengontrolan gerakan
volunteer dan reflex. Sistem motorik dibagi menjadi 1. apparatus perifer, yang terdiri dari
anterior horn cell dan axon perifer, neuromuscular junction, dan otot, dan 2. Apparatue sentral
yang lebih kompleks, yang terdiri dari traktus descending yang berperan dalam mengontrol
(mis sistem pyramidal) dan sistem yang terlibat dalam menginisiasi dan mengatur gerakan
(basal ganglia & cerebellum).
Disfungsi dalam komponen sistem motorik menyebabkan kelainan yang tampak pada
pemeriksaan fisik. Walaupun banyak komponen yang dapat terlibat (terutama dengan penyakit
SSP) keterlibatan khusus dari berbagai komponen sering terjadi
Pemeriksaan disfungsi motorik terdiri dari penilaian kekuatan, tonus otot, masa otot,
koordinasi, gerakan abnormal dan berbagai reflex. Beberapa dari pemeriksaan tersebut dapat
terdeteksi melalui pengamatan sederhana. Tetapi, beberapa pemeriksaan memerlukan alat
bantu pemeriksaan untuk mendeteksi abnormalitas.

Elemen pemeriksaan
Kekuatan otot
Kekuatan otot dengan mudah diuji dengan cara menginstruksikan penderita menahan kekuatan
pemeriksa pada saat penderita berusaha memindahkan bagian tubuhnya melawan tarikan otot
yang hendak dievaluasi. Penilaian terdiri dari tingkatan pada skala 0-5, 0 mencerminkan tidak
ada kontraksi otot yang tampak secara absolute; 1 menandakan bahwa tampak kontraksi otot
tetapi tidak ada gerakan; 2 terdapat gerakan tetapi tidak cukup untuk melawan gravitasi
(dengan ketidakmampuan menahan setiap kekuatan tambahan); 3 hampir mampu melawan
gravitasi ( dengan ketidakmampuan menahan setian kekuatan tambahan); 4 lebih lemah dari
normal (tetapi lebih dapat menahan gravitasi); 5 kekuatan otot normal.
Dalam upaya mengevaluasi kekuatandi berbagai tingkatan pada sistem saraf, beberapa
otot harus dievaluasi. Otot yang umum dievaluasi sehubungan dengan saraf perifer dan tingkat
serabut saraf ditemukan pada table 10-5.

TABLE 10-5. INNERVATION OF CLINICALLY IMPORTANT MUSCLES.

Movement tested

Main muscles

Nerve roots

Peripheral nerve

Shoulder
Shrug (elevation)

Trapezius

C2-5

Spinal accessory

Abduction

Deltoid/supraspinatus C5(6)

Axillary/suprascapular

External rotation

Infraspinatus/teres

C5(6)

Suprascapular

Internal rotation

Pectoralis major

C5-7

Lateral pectoral

Adduction

Latissimus/pectoralis

C6-8

Suprascapular/pectoral

Flexion

Deltoid/coracobr.

C5-6

Axillary/musculocut.

Flexion

Biceps/brachialis
Brachioradialis

C5-6
C5-6

Musculocutaneous
Radial

Extension

Triceps

C6-7

Radial

Flexion

Flexor carpi radialis

Flexor carpi ulnaris

C6-7
C7-8

Median
Ulnar

Extension

Extensor carpi radialis C6-7

Ext. carpi ulnaris
C7-8

Radial
Deep radial

Pronation

Pronator teres

C6-7

Median

Supinator

C5-6

Radial

Biceps

C5-6

Musculocutaneous

Flexion

Flexor digitorum mm.

C7-8

Median (ulnar)

Extension

Extensor digitorum

C7-8

Deep Radial

Ab- & Adduction

Interosseous muscles

C8-T1

Ulnar

Thumb abduction

Abductor pollicis br.

C8-T1

Median

Flexion

Iliopsoas

L2-3 (L4)

Lumbar plexus

Extension

Gluteus max

L5-S2

Inferior gluteal

Abduction

Gluteus medius

L5-S1

Superior gluteal

Adduction

Adductor mm.

L2-4

Obturator

Hamstring

L5-S1

Sciatic

Elbow

Wrist

Supination

Finger

Hip

Knee
Flexion

Extension

Quadriceps

L2-4

Femoral

Dorsiflexion

Tibialis anterior

L4-5 (S1)

Fibular (peroneal)

Plantar flexion

Gastroc/soleus

S1 (S2)

Tibial

Inversion

Posterior tibial

L5 (S1)

Tibial

Eversion

Fibular (peroneal)

L5 (S1)

Fibular (peroneal)

Dorsiflexion

Extensor hallucis

L5 (S1)

Fibular (peroneal)

Plantar flexion

Flexor hallucis

(S1) S2

Tibial

Ankle

Great toe

Lebih efisien menguji penderita dengan menggunakan tugas fungsional daripada menguji
setiap otot. Misalnya, menginstruksikan penderita untuk menahan lengan pada posisi
horizontal dengan telapak tangan terbuka dan mata tertutup. Kelemahan luas dari lengan atas
sering menyebabkan otot pronator menurun dengan tangan pronasi. Jika lengan menurun
tanpa pronasi, hal ini tidak mengesankan kelemahan fisiologis dan penderita menunjukkan
penyakit konversi atau malingering. Lengan diangkat tidak menentu dapat mencerminkan
hilangnya sensoris proprioseptik. When testing strength in the legs it is helpful to have the
patient attempt to walk on the toes and then heels. Other tests of the legs would include hopping
on each foot, standing from a chair (without use of the hands) or climbing a stair. These latter
tests examine more proximal muscles.
When confronting the patient with weakness, some assessment of effort should be made.
Poor effort is usually reflected as good initial contraction, followed by a collapse (often termed
"breakaway" or collapsing weakness). This is not a pattern seen in true neurologic injury
where strength is typically inadequate but relatively constant. It is usually easy to detect the
patient with "collapsing" weakness if you apply varying force during the muscle test. With true
neurologic weakness, the maximum force that the patient applies does not vary appreciably.
"Collapsing weakness" should not be graded. There are several potential causes of collapsing
weakness, ranging from pain to the conscious embellishment of symptoms. When this pattern is
seen, other more objective elements of the examination (such as reflex testing) become more
important.
The ultimate goal of strength testing is to decide whether there is true "neurogenic"
weakness and to determine which muscles/movements are affected. In correlation with the
remainder of the motor exam, it should be possible to determine the particular part of the

nervous system that is at fault to produce this weakness. Probably the most important decision
is whether the weakness is due to damage to upper or lower motor neurons (UMN or LMN). As
you may recall from chapter 8, upper motor neuron weakness is due to damage to the
descending motor tracts (especially corticospinal) anywhere in its course from the cerebral
cortex through the brain stem and spinal cord. UMN weakness is typically associated with
increased reflexes and a spastic type of increased tone. On the other hand, LMN weakness is due
to damage of the anterior horn cells or their axons (found in the peripheral nerves and nerve
roots). This results in decreased stretch reflexes in the affected muscles and decreased muscle
tone. Additionally, atrophy usually becomes prominent after the first week or two, and this
atrophy is out of proportion to the amount of disuse produced by the weakness.

"Deep tendon" (muscle stretch; myotatic) reflexes

The "deep tendon" (myotatic) reflexes are a critical part of the neurologic examination that is
discussed in Chapt. 8. Testing reflexes is the most important element of determining whether
weakness is of an upper or lower motor neuron type (limited only by the fact that only certain
muscles actually have reliably tested stretch reflexes (include the biceps, triceps, brachioradialis
(radial periosteal), quadriceps, hamstring and calf muscles). Since the reflex arc includes stretch
receptors and sensory fibers, it is not necessary to damage motor axons to abolish reflexes.
However, in the setting of the patient with known weakness, reflex testing is a powerful tool to
investigate the cause.
As you may recall from chapter 8, symmetry of reflexes is the most important consideration
in determining normality. Pathological "spread of reflexes" (i.e., contraction of muscles that
produce motions other than the one associated with the test muscle) is another objective sign of
hyperactivity. You may recall that sustained clonus (repeated muscle contraction when a muscle
is passively stretched) is an indicator of hyperactive reflexes.
Conditions that damage lower motor neurons decrease muscle stretch reflexes by
interrupting the reflex arc (Fig. 8-1).

Therefore, a diminished reflex in a weak muscle suggests damage to the lower motor
neurons somewhere along the course to the muscle (i.e., anterior horn cells, motor nerve root, or
peripheral nerve). Hyperactive reflexes are seen after damage to upper motor neurons (i.e.,
descending motor tracts). There are other confirmatory findings that may suggest upper or
lower motor neuron disease. These signs include atrophy (LMN), fasciculations (LMN),
spasticity (UMN), Babinski sign (UMN) or loss of superficial reflexes (UMN).

Superficial and "pathologic" reflexes

Superficial reflexes (abdominal, cremaster and plantar) are discussed in chapter 8. These
reflexes are mediated above the spinal cord. Therefore, disruption of the spinal cord or brain
stem can abolish these reflexes. Of course, the superficial reflexes can also be abolished if there
is extensive damage to sensory nerves or lower motor neurons in the region.
The "Babinski response" (up-going toe) is the classic pathological reflex seen with upper
motor neuron damage. This reflex replaces the normal plantar response. The findings upon
testing of superficial reflexes should be placed in the context of the remainder of the motor exam
when evaluating upper and lower motor neurons.

Muscle Bulk
Muscle bulk is primarily assessed by inspection. Symmetry is important, with consideration
given to handedness and overall body habitus. Generalized wasting or cachexia should be noted
and may reflect systemic disease, including neoplasia. Some areas can be adequately evaluated
by inspection alone, such as the thenar and hypothenar regions or the shoulder contour. Some
areas, like the thigh, leg, arm and forearm, may be better evaluated by measurement. These
measurements can also permit assessment over time.
Severe atrophy strongly suggests denervation of a muscle (such as with LMN lesions). This
usually begins at least a week after acute injury and gets progressively worse with time (unless
reinnervation takes place). Atrophy due to LMN damage must be distinguished from that which
occurs secondary to disuse. However, there is usually a clear substrate for disuse (bed rest, cast,
etc.) and there is little overall change in strength. Unfortunately, patients who have limited
functional reserve (such a those with prior neural disease or the elderly) can be severely affected
by disuse and deconditioning.

Coordination
Coordination is tested as a part of a sequence of movements. Typically the patient is asked to
hold his/her hands in front with the palms up, first with the eyes open and then closed (as when
examining pronator drift, above). It is usually good form to instruct the patient to prevent
movement of his/her hands, and to exert some force either toward the floor or in attempting to
push the hands apart. This force can be used to assess the strength of the patient and then
should be released suddenly and without warning. After a short excursion, the patient should
check this movement, and this checking should be symmetrical. The patient may then be asked
to touch his/her nose, and subsequently the examiners finger. This can be repeated a few times
to assess the smoothness and accuracy of the movement. Further assessment can be obtained by
having the patient perform a rapidly repeated movement such as tapping the thumb and
forefinger together, or by having the patient clap his hands. This test can be made somewhat
more difficult by having the patient repeatedly strike first the palmar and then the dorsal aspect
of one hand against the palm of the other. This, of course, must be done with each hand, and you
are evaluating rhythmicity and speed in performance of the movement.
Lower extremity coordination can be tested in the supine position by having them attempt
to place the heel of one foot on the opposite knee and subsequently tap or slide the heel down
the shin to the ankle. This should be done with each leg. Other tests of lower limb coordination
include tapping of the foot on the examiners hand, or attempting to draw a number in the air
with his/her foot. If the patient can stand and walk, it is usually only necessary to evaluate gait

in order to assess lower limb coordination. The patient who can stand on either foot for ten
seconds without excessive sway does not need further testing of leg coordination.
These maneuvers test several neurologic systems. Strength is required for all of these tests.
Excessive rebound (or loss of checking) is suggestive of cerebellar injury on the side of the
abnormality. Similarly, difficulty with rapid alternating movements (dysdiadochokinesia) or
marked overshoot or undershoot when attempting to hit a target (intention tremor) suggests
cerebellar problems on that side. Repetitive over and undershoot during voluntary movement
may reflect as "intention tremor". Extreme slowness of movement can be produced by
extrapyramidal disease (such as Parkinsons). Of course, problems with any part of the motor
systems may affect coordination. For example, if there is a marked alteration in muscle strength,
muscle tone, or if the patient is having abnormal movements this can influence your perception
of coordination. Therefore, although tests of coordination are mainly directed toward assessing
cerebellar function, you must decide whether other problems in the motor system are affecting
these tests.

Muscle Tone
Muscle tone may be increased or decreased, with increased tone being much easier to detect.
Tone can be assessed by one of two means. The most common method is for the examiner to
passively move the patients limb (especially at the wrist). The second method involves
evaluating arm swing (with the patient standing). Tone is often easily checked by having the
patient stand with his/her arms hanging loosely at their side. When the patients shoulders are
moved back and forth or rotated the arms should dangle freely. Increased tone is usually
reflected as the arms being held stiffly both in the standing position and when walking. The
lower limbs can be evaluated with the patient seated with the legs dangling. Movement of the
feet should result in gentle swinging of the legs of a brief duration. Increased tone results in
abrupt restriction on the excursion of the feet.
There are two common patterns of pathologically increased tone, spasticity and rigidity.
Spasticity is found with upper motor neuron injuries and manifests as a marked resistance to
the initiation of rapid passive movement. This initial resistance gives way and then there is less
resistance over the remaining range of motion (clasp-knife phenomenon). Rigidity is an increase
in tone that persists throughout the passive range of motion. This has been termed "lead pipe"
rigidity and is common with extrapyramidal disease, especially Parkinsons disease.
Many older individuals have another motor finding, called "paratonia." Paratonia is a
phenomenon in which the patient is essentially unable to relax during passive movements. You
will note that the resistance is irregular and generally greatest when you change the pattern of

movement. Of note, most of these individuals have apparently normal tone when you test them
in a standing position and move their shoulders about (as described above). Extreme paratonia
is common in patients with dementia.
Some types of increased tone appear to be prolongations of voluntary muscle contraction.
Myotonia is a slowness of relaxation of muscles after a voluntary contraction or a contraction
provoked by muscle percussion. This is a disorder of striated muscle and not an abnormality of
innervation and may be seen in conditions such as myotonic dystrophy or congenital myotonia
(a disorder of ion channels). Occasionally, metabolic diseases of muscle (such as
hypothyroidism) can result in myotonic discharges. Myotonia can be easily observed by asking
the individual to reverse a muscle action quickly (i.e., trying to rapidly open a tightly clenched
fist) or by tapping on a muscle belly (such as the thenar muscles). Neuromyotonia is a rare
condition of irritability of the nerve (possibly autoimmune) where there is persistent
contraction. Muscle contractions are not terminated and the patient becomes "stiff" with
movement.

Abnormal movements
There are a number of types of abnormal movements including tremor, chorea, athetosis,
dystonia, hemiballism and fasciculations. Each of these has clinical implications that require
discussion.
Tremor is the most common abnormal movement seen in practice. Three characteristics
are of particular importance. These include the symmetry (or asymmetry) of the tremor, the rate
of the tremor (basically, whether it is fast or slow, i.e., greater or less than 7 cycles per second)
and the circumstances under which the tremor is present (i.e., whether it is worst at rest, during
sustained postures or when moving). Physiological tremor comes in two types. Rapid (>7cps)
tremor is characteristic of states with increased sympathetic function (think of the last time you
had too much coffee). This is most commonly secondary to anxiety, but may occur with
increased adrenaline (such a pheochromocytoma) or thyrotoxicosis. A slower tremor must be
classified with regard to the conditions in which it is most evident. If it is present predominantly
at rest, and decreases with movement, this suggests extrapyramidal disease such as Parkinsons
disease (PD). In PD, the tremor is frequently asymmetrical and is usually associated with other
signs (bradykinesia, rigidity or delayed postural corrections). Tremors which are severe on
sustained postures (such as with the hands outstretched), but which may worsen slightly with
action are characteristic of essential tremor (this is also seen in senile tremor or familial
tremor). These tremors are absent at rest and are often worsened by anxiety. They are often
asymmetrical and characteristically affect the use of writing and eating implements. Damage to

cerebellar systems (particularly the hemispheres or dentate connections) often produces a

tremor that is most pronounced during voluntary actions.
The second most common type of abnormal movement that is seen in practice is
fasciculation. These are twitches in muscle (actually, contraction of a single motor unit, i.e., all
of the muscle fibers attached to a single motor neuron). These can be felt and often seen. They
are random and involuntary occurrences and do not result in movement of a joint.
Fasciculations may reflect damage to lower motor neurons, either the cell body or the motor
axon located in the nerve root or peripheral nerve. Of course, if the fasciculations were due to
LMN lesions one would expect some weakness, decreased tone and (after a while) atrophy. Also,
one would expect that the fasciculations would be persistent in a single group of muscles.
Fasciculations may also be a temporary finding in overused muscles or as a sign of local muscle
irritation. Also, there are some individuals who have benign fasciculations, particularly in the
calf muscles. Of course, these are not associated with weakness or other motor system
abnormalities.
There are several other, less common abnormal movements. Chorea is a rapid, fleeting,
random and non-stereotyped movement which is worsened by anxiety and which can be
suppressed for short periods by conscious effort. They differ from tics since tics are stereotyped
and repeat within the same muscle groups. Tics may affect the voice, as well, and consist of
repeated throat clearing, sniffing or coughing. Multiple vocal and motor tics are seen in Tourette
syndrome. Athetosis is a slow, writhing, snakelike movement of a body part or parts. Dystonia is
a sustained twisting of the body, usually the trunk or neck (where it is called torticollis).
Hemiballism is a flinging motion of one side of the body, potentially resulting in falls.
Involuntary movements are seen in a number of clinical situations. Chorea, athetosis and
hemiballism are reflections of basal ganglia disease. This may be congenital (a type of cerebral
palsy), post infectious (Sydenham's chorea), hereditary (Huntington's chorea), metabolic
(Wilson's disease) or cerebrovascular.

Station
This is the ability to maintain an erect posture. One should be able to stand both with the eyes
open and closed with a relatively narrow base of support (the feet close together). You should
record excessive sway, falling to one side, or marked worsening in the ability to stand when the
eyes are closed.
Excessive sway with the eyes open is common with cerebellar or vestibular problems. This
may be to one side (and commonly is with vestibular disorders) or may be to both sides
(especially with conditions that affect the midline portion of the cerebellum, such as

intoxication). You must consider the possibility of other explanations such as the patient not
having enough strength to stay upright or severely delayed reactions to destabilization (such as
with Parkinsons disease). Some patients can stand well with the eyes open, but have marked
increase in instability with the eyes closed. This is suggestive of a disorder of conscious
proprioception (i.e., joint position sense, as may be seen with peripheral neuropathy or dorsal
column/medial lemniscus dysfunction). This is termed a Romberg sign. Proprioceptive
problems on one side can be brought out with standing on one foot. Of course, there are other
tests of conscious proprioception, including evaluation of joint position and vibration sense in
the feet. These data must be correlated with the findings on station.

Gait
This is an important part of any neurologic exam. It is particularly important to observe the
symmetry of the gait, the ability to walk with a narrow base, the length of the stride when
walking at a normal pace, and the ability to turn with a minimum of steps and without loss of
equilibrium. When observing a normal person from behind, the medial parts of the feet strike a
line and there is no space visible between the legs at the time of heel strike. This is a narrowbased gait and deviation from this can be measured in the amount of distance laterally each foot
strikes from the line that their body is following. Tandem walking (the ability to walk on a line)
may be used to evaluate for stability of gait, recognizing that many normal elderly patients have
trouble with this.
Damage to virtually any part of the nervous system may be reflected in gait. An antalgic
gait, or the limp caused by pain is familiar to any practitioner. Patients with unilateral weakness
may favor one side, and if the weakness is spastic (i.e., from upper motor neuron damage) the
patient may hold the lower limb stiffly. S/he will drag the weak limb around the body in a
"circumducting" pattern. A staggering or reeling gait (like that of the drunk) is suggestive of
cerebellar dysfunction. Generally, the patient with true vertigo will tend to fall to the one side
repeatedly (especially with the eyes closed). A patient with foot drop will tend to lift the foot high
(steppage gait). Hip girdle weakness often results in a "waddle," with the hips shifting toward
the side of weakness when the opposite foot is lifted from the floor (of course, if both sides are
weak the hips will shift back and forth as they take each step). Patients with Parkinson disease
often have difficulty initiating gait; the steps are usually short, although the gait is narrowbased. If severe, the patient may be propulsive (they may even fall). Patients who are "glue
footed" (sliding their feet along the ground rather than stepping normally) may be suffering
from damage or degeneration of both frontal lobes or the midline portion of the cerebellum.
When damage to these areas is severe the patient may be severely retropulsive (tending to fall

over backwards repeatedly). Dorsal column injury may result in a gait in which the patient
"stamps" his or her feet, and usually also needs to look at the feet in order walk. Patients with
painful neuropathy of the feet may walk as if they are "walking on eggs" and patients with spinal
stenosis may walk with a stooped posture (a "simian" posture).

Disorders of the Motor Systems

The reflection of motor system disease depends on the particular part of the motor system that
is involved. Here we will discuss the characteristic deficits produced by lesions at each level of
the motor system.

Muscle Disease (see Chapt. 12)

Typically, muscle disease (myopathy) has its earliest and greatest effects on proximal
musculature. There is little atrophy (until very late) and deep-tendon reflexes are decreased only
in proportion to the weakness. Certain metabolic myopathies may result in cramping due to the
fact that energy is required to relax muscles and myotonia may also produce difficulty in
relaxation. There are no sensory changes in myopathy.

Neuromuscular Disease (see Chapt. 12)

Myasthenia gravis is the prototypical neuromuscular disease. This condition results from
autoimmune damage to acetylcholine receptors, which results in inefficient neuromuscular
transmission. Initial contraction is strong but during sustained contraction, depletion of
neurotransmitter results in progressive weakness. This can be seen during tonic actions (like
simply holding up the eyelids or maintaining the arms out in front) or in actions that require
sustained activity (like talking or swallowing a meal). For further information see Chapt. 12.

Lower Motor Neuron (LMN) Damage (see Chapt. 12)

These conditions occur due to damage to the anterior horn cells, the ventral roots or the
peripheral nerves anywhere along their course to the muscles. In the majority of cases, the
weakness is distal. The best explanation for the predominantly distal weakness in neuronal
disease is that longer motor (also sensory) nerve fibers are more exposed and vulnerable to the
many processes that damage nerve. An exception to this rule is the diffuse polyneuropathy of
Guillain-Barre syndrome (presumed to be an autoimmune process). In this case weakness may
begin in the proximal muscles and this is presumably because the primary damage to nerves is
occurring quite proximally (near the nerve root level).

LMN disease results in weakness in the muscles connected with the affected nerve fibers.
Understanding of the distribution of nerves and nerve roots to the individual muscles is
essential to correct interpretation (Table 10-5). Additionally, there is atrophy (after the first
week or two following an acute injury) that is out of proportion to simple disuse. Furthermore,
reflexes are usually affected quite early and severely. This is because most conditions that
damage LMNs also damage sensory nerve fibers that represent the afferent limb of the muscle
stretch reflex. Finally, when there is damage to LMNs in peripheral nerves, there is often an
accompanying sensory loss that can aid in diagnosis of the nerve that is involved.

Upper Motor Neuron Damage (UMN)

Historically, this has been associated with the corticospinal (pyramidal) tract. However, this is
not quite accurate since voluntary motor pathways arising in the cerebral cortex can function by
activating more primitive descending tracts from the brain stem. It is clear that the direct
projections in the corticospinal tract are responsible for highly skilled movements, especially of
the hands. In this section we will refer to direct and indirect corticospinal projections to
distinguish the corticospinal tract itself from the indirect activation of other descending motor
tracts by cerebral cortical input. Additionally, it must be understood that the motor cortex does
not act independently, but rather under the influence of the premotor cortex (involved in
planning and initiating movement) as well as "extrapyramidal" systems such as the basal ganglia
and cerebellum (see below).
The classic picture of acute damage to UMNs includes contralateral paralysis of distal limb
movements, while proximal limb movements are severely weakened and trunk movement
minimally involved. Muscle tone (measured as passive resistance to manipulation) is depressed
in this initial phase. The deep-tendon reflexes are also likely to be absent, recovering over time
to normal or hyperactive levels. The superficial reflexes (abdominal and cremasteric) opposite
the lesion are depressed or absent. A Babinski response is often present on the weak side.
Over weeks to months proximal strength improves to a significant degree, whereas distal
movements make only a poor recovery. A rudimentary grasping capability is frequently all that
remains in the hand. Extension, opposition, and individual finger movements remain severely
affected or lost. Presumably, the recovery of proximal functions relates to some bilaterality of
distribution of corticospinal fibers that innervate proximal muscles. The modest recovery of
distal movements is suspected to relate to preserved motor pathways from the brain stem
(presumably under extrapyramidal control).
Damage to the precentral gyrus (primary motor cortex) or isolated damage to the
medullary pyramid produces a rather pure corticospinal tract lesion. In these cases, the

weakness of distal muscles is severe but there is little appearance of other findings, such as
spasticity and hyperreflexia that are hallmarks of most UMN lesions. Other UMN lesions also
damage indirect descending connections between the cerebral cortex and spinal cord. This
happens with lesions of the premotor cortex, corona radiata, internal capsule, cerebral peduncle,
basal pons, and lateral columns of the spinal cord. Invariably, lesions in these areas also involve
other pathways leaving the cerebral cortex that are intermixed with the direct corticospinal
(pyramidal) projection. In addition to the weakness found in all of these patients, there is a
decrease in tonic inhibition of reflexes and an increase in resting muscle tone. This is
accompanied by hyperactivity of the deep-tendon reflexes and development of what is
traditionally called spasticity.
Spasticity is an increased in muscle tone that is detected during passive movement of the
limbs. The muscles at rest do not have excessive tone but any brisk stretch of a muscle group
(particularly the flexors in the upper extremity and the extensors in the lower extremity) will
result in a "catch" at about midlength of the muscle followed by a sudden release of the catch
and relaxation of the muscle. The last two components, the catch and release, have been likened
to a closing pen knife, which is the origin of the term "clasp-knife" spasticity. The overactive
muscle stretch reflexes that are resonsible for spasticity are also the mechanism behind the
hyperactive deep-tendon reflexes. The giving away or release portion of the clasp-knife
phenomenon is presumed to be caused by increased firing of the inhibitory Golgi tendon organs,
which produce an overactive reflex that inhibits the muscle.
If the lesion extends beyond the confines of the traditional corticospinal path, more
descending pathways are involved and a greater degree of spasticity is noted; there also is a
poorer recovery from weakness. This is presumably because of loss of more inhibitory influences
on the segmental reflex arc and loss of more facilitatory influences on the motor neuron effector
systems.
After very acute lesions of the descending motor systems there is often initial flaccid
weakness that is sometimes followed by stereotyped movements and postures (decorticate
posture, decerebrate posture or generalized withdrawal reactions)(Fig. 10-1). Acute destructive
lesions of the descending motor pathways cause a transient shock state of flaccid paralysis with
loss of reflexes. When progressively greater amounts of the descending pathways are involved, a
longer period of shock ensues. Acute cortical destruction may result in only hours to days of
shock, whereas acute transection of the spinal cord can cause a shock state that persists for
many weeks to months before spastic hyperreflexia and rudimentary spinal reflex behavior
return. The precise pathophysiology of spinal shock is not clear, but it may complicate the
evaluation of the patient following acute injury. It is always difficult to predict the final extent of
the neurological injury in the setting of shock. Chronic or slowly progressive destruction of the

descending motor pathways is not associated with a shock state. Presumably, this is because
compensatory reorganization of the motor function occurs in equal pace with the losses.
Lesions that extensively destroy the cerebral cortex and basal ganglia, and preserve at least
some of the diencephalon (like those caused by severe hypoxia) may result in stereotyped motor
responses that involve flexion of the upper extremities and extension of the lower extremities.
Noxious stimulation is usually necessary to elicit this reflex activity, which has been called
decorticate posturing (Fig. 10-1). It has been thought, on the basis of experimental data, that
release of the rubrospinal motor system is, at least in part, responsible for decorticate posturing.
Transection of the brain stem, for example by stroke, at the level of the midbrain or pons is
followed after a period of neuraxis shock by severe spasticity and reflex extension and pronation
of the upper extremities with extension of the lower extremities and trunk on noxious
stimulation (see Fig. 10-1). This response is called decerebrate posturing and depends on
preservation of the vestibular nuclei in the caudal brain stem, with the extension being produced
by vestibulospinal pathways.
Lesions transecting the lowest portion of the brain stem or the upper spinal cord result in
quadriplegia and severe spasticity after a period of shock. Later in the clinical course, reflex
flexion movements of the limbs can be elicited by noxious stimulation (see Fig. 10-1). These
probably represent primitive spinal withdrawal responses.
As a rule, UMN lesions affect large areas of the body below the level of injury. It is often
difficult to localize the specific level of damage by the pattern of weakness. Associated
neurologic findings may clarify the level. For example, cranial nerve involvement or involvement
of nerves or nerve roots may indicate a brain stem or spinal cord level of involvement,
respectively, while cortical findings such as language difficulties, visual field abnormalities,
dyspraxias, or other disorders of higher integrative function suggest cortical damage. In most
UMN lesions, the whole side of the body below the lesion is affected (hemiparesis or
hemiplegia). However, in the cerebral cortex the motor representation for the arm, face, and
trunk lie within the supply of the middle cerebral artery, whereas the leg lies within the
distribution of the anterior cerebral artery (Fig. 10-2). Loss of middle cerebral cortical perfusion
therefore causes a greater degree of weakness of the upper extremity than of the lower
extremity. Occlusion of the anterior cerebral artery, an uncommon event, is associated with
greater weakness in the leg than in the arm.
Because sensory and motor systems are near one another through the spinal cord, most of
the brain stem and the cerebral hemispheres, it is common to have some sensory as well as
motor symptoms. The sensory abnormality (see Chapt. 9) may help localize the lesion. Pure
involvement of UMNs without any sensory damage is most often seen with small lesions
(usually vascular) in the posterior limb of the internal capsule or in the base of the pons.

Basal Ganglia Disease

The abnormalities associated with lesions and degenerative processes in the basal ganglia are
discussed in some detail in Chapter 26. The findings are generally categorized into
"hyperkinesias" and "hypokinesias." The classic picture of parkinsonism (the most common
cause being Parkinson disease) includes bradykinesia (slow movements), rigidity, difficulty
initiating movements and delayed postural corrections. These symptoms all fall into the
category of "hypokinesia." There may also be a tremor at rest (suppressed by movement), which
is a form of hyperkinesia. The rigidity of parkinsonism is present in all ranges of passive
manipulation and cannot be abolished by sectioning the dorsal roots. Therefore, it is not due to
reflex overactivity (deep tendon reflexes are normal in parkinsonism). It is probably due to tonic
overactivity of the descending motor pathways and it can be abolished by cutting descending
motor tracts (see Chap. 26 ). Other types of "hyperkinesia" include chorea, athetosis,
hemiballism, tic and dystonia. These are indicative of dysfunction of the basal ganglia
(extrapyramidal) system. However, they are not diagnostic of a particular cause (see Chap. 26 ).

Cerebellar Disease
Cerebellar disease produces predominantly motor symptoms. There are three main parts of the
cerebellum, which have slightly different functions. The lateral cerebellar hemispheres (the
neocerebellum) are involved in controlling distal limb movement of the ipsilateral limbs. The
vermis of the cerebellum (midline) is involved in control of axial functions as well as the voice
and eye movements. The posteroinferiorly-located vestibulocerebellum (floculonodular lobe;
archicerebellum) is involved in vestibular functions and regulation of the vestibulo-ocular reflex
(see Chapt. 6).
Damage to the neocerebellum produces predominant symptoms of tremor, ataxia, and
hypotonia. The tremor is of a particular type, consisting of rhythmic, variably 3-8 Hz oscillations
that occur predominantly on voluntary activity and the tremor reaches its peak of oscillation
toward the end of the movement. It disappears with posturing or at rest. It is noticed
dramatically when reaching for objects (such as when performing finger-to-nose testing). The
ataxia (incoordination) is manifest in several ways. There is dysmetria (past-pointing) with
overshoot and/or undershoot of the target. Also, there may be a lack of checking (excessive
rebound). For example, if the patient is asked to hold their hand extended out in front of them
while pressure is applied and then suddenly released, there will be excessive movement before
the patient "checks" the motion. Additionally, the patient will have difficulty performing rapidly
repeated motions (tapping fingers, patting hands or tapping feet) and this may be even more
obvious if there are rapid alternating movements involved in the motion (such as pronation and

supination of the hands). Ataxia of the legs is manifest in difficulty in walking, often
characterized by a broad-based and/or drunken gait.
Disorders affecting the midline cerebellum (vermis) affect axial motor activity. This is likely
to be manifest as head and trunk instability as well as speech and eye movement problems. The
problems with trunk stability are usually brought out during attempts to stand still or to walk.
When there is both instability of the trunk and ataxia of the legs, patients will have severe ataxia.
After vermal lesions, the speech may sound drunken or inappropriately staccato, and eye
movements may be erratic and uncoordinated.
Because it is an important symptom of cerebellar disease, it would be appropriate to say a
few more words here about ataxia. Cerebellar ataxia is fairly easy to observe in the office and it
has at least two origins: (1) intention tremor of the legs, giving a dysmetric gait, and (2) truncal
imbalance. If it is advanced, the patient has a wide-based compensatory gait, and if there is
lateralized limb involvement, they tend to lean and fall toward the affected side. A sensitive test
for ataxia is heel-to-toe tandem walking; this should be part of any neurologic screening
examination in a patient with gait or balance complaints because it detects early cerebellar
dysfunction. If the trunk alone is involved, as in early alcoholic degeneration or with a tumor of
the vermis, there is a tendency to fall to either side, forward or backward. Some persons with
midline cerebellar damage may have a stronger tendency to fall backward. This is called
retropulsion and can also be seen in basal ganglia dysfunction (particularly parkinsonism) and
in frontal lobe disorders. When retropulsion is due to cerebellar involvement, it frequently has
an involuntary tonic character, i.e., the patients actually appear to be actively pushing
themselves backward. Even at rest, sitting or standing, there is a tendency to lean or fall
backward. With frontal lobe dysfunction and parkinsonism, the retropulsion is usually passive
rather than active. This means that the patient has difficulty recovering from being pushed
backward or from a backward-leaning position even though they may have no active or forced
retropulsion at rest.
Damage to the vestibulocerebellum (flocculonodular lobe; archicerebellum) produces
vestibular findings, including nystagmus that may be quite severe and in different directions
depending on which way the patient is looking ("gaze-shifting nystagmus"). This is often more
severe than symptoms due to vestibular damage since vestibulocerebellar damage is more
difficult to compensate.
Finally, cerebellar damage can occasionally be reflected in hypotonia. The examiner should
check for abnormalities of tone by asking the patient to relax and not resist. The limbs are then
moved rapidly by the examiner in several ranges. A lack of resistance or a floppiness is noticed
with hypotonia. Having the patient sit with his legs swinging free may test the legs. The leg is
lifted by the examiner and released. Normally the leg swings back and forth several times and

then stops, arrested by inertia and the normal resting muscle tone, which is a manifestation of
the sensitivity of the normal muscle stretch reflex. With cerebellar hypotonia, the leg swings
freely, unchecked, like a pendulum, arrested mainly by passive limb inertia.

References

Brodal, A.: Neurological Anatomy in Relation to Clinical Medicine, ed. 2, New York, Oxford
University Press, 1969.

Medical Council of the U.K.: Aids to the Examination of the Peripheral Nervous System,
Palo Alto, Calif., Pendragon House, 1978.

Monrad-Krohn, G.H., Refsum, S.: The Clinical Examination of the Nervous System, ed. 12,
London, H.K. Lewis & Co., 1964.

Wolf, J.K.: Segmental Neurology, A Guide to the Examination and Interpretation of

Sensory and Motor Function, Baltimore, University Park Press, 1981.