Page 326 - Color Atlas Of Pathophysiology (S Silbernagl Et Al, Thieme 2000)

Lesions of the Cerebellum
Lesions of the cerebellum may be caused by receive direct afferent signals via spinocere-
poisoning (especially by alcohol, but also DDT, bellar fibers (→ A7) as well as information on
piperazine, 5-fluorouracil, lithium, or diphe- the movements of the eye muscles. The neu-
nylhydantoin), heat stroke, hypothyroidism, rons of this part of the cerebellum project di-
malabsorption as well as by genetic defects of rectly to the vestibular nucleus (→ A11) as
Systems enzymes or transport (hexosaminidase, gluta- well as via the nuclei fastigii (→ A12) to the
mate dehydrogenase, pyruvate dehydroge-
thalamus, to the reticular formation (→ A13),
nase, α-oxidation, DNA repair, transport of
and to the contralateral vestibular nucleus
(→ A14). Spinal motoneurons receive impulses
neutral amino acids), partially hereditary de-
Neuromuscular and Sensory tiple sclerosis [→ p. 302], viruses, prions), cere- tracts, via the thalamocortical and corticospi-
via the vestibulospinal and reticulospinal
generative processes, inflammation (e.g., mul-
nal tracts. Lesions in the flocculus, nodulus,
bellar and extracerebellar tumors (paraneo-
plasia; → p.16). In hereditary Friedreich’s
and vermis mainly affect balance and body
posture as well as the muscles of the trunk
ataxia, cerebellar function is indirectly affect-
and face.
ed, for example, by degeneration of the spino-
cerebellar tracts. The effects of cerebellar le-
Clinical manifestations of lesions in the cer-
ebellum are delayed onset and stoppage of
sions depend on their location.
The lateral cerebellar hemispheres (cerebro-
ments (dyssynergia) and often the required
voluntary movements (manual dexterity). In
force, acceleration, speed, and extent of move-
10 cerebellum; → A, yellow) store programs for movements. There are no coordinated move-
voluntary movements, associative cortical
ments is misjudged (dysmetria). The patient
areas (→ A1) activate, via pontine nuclei cannot immediately withdraw the muscle ac-
(→ A2), neurons in the hemispheres (→ A3) tion when a resistance is suddenly reduced
whose efferent impulses (orange) project, via (rebound phenomenon), nor able to perform
the dentate nucleus (→ A4) and thalamus rapid and consecutive antagonistic move-
(→ A5), to the motor cortex (→ A5). From here ments (dysdiadochokinesia). An intention trem-
spinal motoneurons are activated via the pyra- or (3–5 oscillations per second) develops on
midal tract (violet). Lesions in the hemispheres moving the hand toward an object, the oscilla-
or in structures connected with them thus im- tions becoming increasingly marked the near-
pair initiation and planning of movements. er the object gets. Movements are discontinu-
The intermediate part of the hemisphere ous and divided into separate components (de-
(spinocerebellum, light blue) is mainly re- composition of movement). Less active resis-
sponsible for the control of movement. Via spi- tance is exerted against passive movements
nocerebellar afferents (blue) it receives infor- (hypotonia). On holding an object the muscle
mation about the state of the motor apparatus. tone cannot be maintained, and patients can
Neurons of the spinocerebellum project to the only stretch out their arms for a relatively
red nucleus (→ A9) and thalamus via the nu- short time (positioning attempt). Muscle
clei emboliformis and globosus (→ A8). Spinal stretch reflexes are diminished (hyporeflexia).
motoneurons are influenced by the red nu- Speech is slow, explosive, staccato, and
cleus via the rubrospinal tract and by the thal- slurred. The control of balance is disturbed; pa-
amus via the motor cortex and the pyramidal tients stand with their legs apart and walk un-
tract. Disorders of the spinocerebellum impair certainly (ataxia). Sitting and standing are also
the execution and control of voluntary move- made more difficult by tremors of the trunk
ments. muscles (titubation, 2–3 oscillations per sec-
The vestibulocerebellum, comprising floc- ond). Abnormal control of the eye muscles
culus and nodulus and portions of the vermis causes dysmetria of the eye movements and
(bright green), is responsible for control of bal- coarse nystagmus (→ p. 330) in the direction
ance. Neurons in the flocculus receive direct of the lesion. It increases when patients direct
316 afferents from the vestibular organ (→ A10). their gaze toward the lesion and decreases
In addition, the flocculus, nodulus, and vermis when their eyes are closed.
Silbernagl/Lang, Color Atlas of Pathophysiology © 2000 Thieme
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