258 SECTION III Central & Peripheral Neurophysiology
electrical events in the cerebellum to its function in motor
control is another interesting problem. The cerebellar cortex
has a basic, 150 to 300/s, 200-μV electrical rhythm and, super-
imposed on this, a 1000 to 2000/s component of smaller am-
plitude. The frequency of the basic rhythm is thus more than
10 times greater than that of the similarly recorded cerebral
cortical alpha rhythm. Incoming stimuli generally alter the
amplitude of the cerebellar rhythm like a broadcast signal
modulating a carrier frequency in radio transmission. Howev-
er, the significance of these electrical phenomena in terms of
cerebellar function is unknown.
CEREBELLAR DISEASE
Damage to the cerebellum leads to several characteristic abnor-
malities, including hypotonia, ataxia, and intention tremor.
Figure 16–17 illustrates some of these abnormalities. Most abnor-
malities are apparent during movement. The marked ataxia is
characterized as incoordination due to errors in the rate, range,
force, and direction of movement. Voluntary movements are also
highly abnormal. For example, attempting to touch an object
with a finger results in overshooting to one side or the other. This
dysmetria, which is also called past-pointing, promptly initiates
a gross corrective action, but the correction overshoots to the oth-
er side. Consequently, the finger oscillates back and forth. This
oscillation is the intention tremor of cerebellar disease. Another
characteristic of cerebellar disease is inability to “put on the
brakes,” that is, to stop movement promptly. Normally, for exam-
ple, flexion of the forearm against resistance is quickly checked
when the resistance force is suddenly broken off. The patient with
cerebellar disease cannot brake the movement of the limb, and
the forearm flies backward in a wide arc. This abnormal response
is known as the rebound phenomenon, and similar impairment
is detectable in other motor activities. This is one of the important
reasons these patients show dysdiadochokinesia, the inability to
perform rapidly alternating opposite movements such as repeat-
ed pronation and supination of the hands. Finally, patients with
cerebellar disease have difficulty performing actions that involve
simultaneous motion at more than one joint. They dissect such
movements and carry them out one joint at a time, a phenome-
non known as decomposition of movement.
Other signs of cerebellar deficit in humans provide addi-
tional illustrations of the importance of the cerebellum in the
control of movement. Ataxia is manifest not only in the wide-
based, unsteady, “drunken” gait of patients, but also in defects
of the skilled movements involved in the production of
speech, so that slurred, scanning speech results.
Motor abnormalities associated with cerebellar damage vary
depending on the region involved. The major dysfunction seen
after damage to the vestibulocerebellum is ataxia, dysequilib-
rium, and nystagmus. Damage to the vermis and fastigial
nucleus (part of the spinocerebellum) leads to disturbances in
control of axial and trunk muscles during attempted antigrav-
ity postures and scanning speech. Degeneration of this portion
of the cerebellum can result from thiamine deficiency in alco-
holics or malnourished individuals. The major dysfunction
seen after damage to the cerebrocerebellum is delays in initiat-
ing movements and decomposition of movement.THE CEREBELLUM & LEARNING
The cerebellum is concerned with learned adjustments that
make coordination easier when a given task is performed over
and over. As a motor task is learned, activity in the brain shifts
from the prefrontal areas to the parietal and motor cortex and
the cerebellum. The basis of the learning in the cerebellum is
probably the input via the olivary nuclei. It is worth noting thatFIGURE 16–17 Typical defects associated with cerebellar
disease. A) Lesion of the right cerebellar hemisphere delays initiation of
movement. The patient is told to clench both hands simultaneously; right
hand clenches later than left (shown by recordings from a pressure bulb
transducer squeezed by the patient). B) Dysmetria and decomposition of
movement shown by patient moving his arm from a raised position to his
nose. Tremor increases on approaching the nose. C) Dysdiadochokinesia
occurs in the abnormal position trace of hand and forearm as a cerebellar
subject tries alternately to pronate and supinate forearm while flexing and
extending elbow as rapidly as possible. (From Kandel ER, Schwartz JH, Jessell
TM [editors]: Principles of Neural Science, 4th ed. McGraw-Hill, 2000.)
ABCGoNormalAbnormalNormalNormalAbnormalAbnormalDelayStart Finish