Cerebellum and Basal Ganglia
David Roman Renner, MD
Suzanne Stensaas, PhD
2009 Kenya Curriculum
BG
CBLM
Courtesy of Stephen C. Voron, MD
BG
CBLM
Courtesy of Stephen C. Voron, MD
pyramidal cell
in the motor
homunculus
of the frontal
lobe
BG
CBLM
Courtesy of Stephen C. Voron, MD
corticospinal
tract
BG
CBLM
Courtesy of Stephen C. Voron, MD
BG
CBLM
decusation at
the pyramids
(spinomedullary
junction
Courtesy of Stephen C. Voron, MD
BG
thalamus:
AKA the
“gate keeper”
prevents
unwanted
movements
T
CBLM
Courtesy of Stephen C. Voron, MD
BASAL
GANGLIA
BG
consultant on
automatic
movements
T
CBLM
Courtesy of Stephen C. Voron, MD
provides
input into the
thalamus
Cerebellum:
consultant on
rapid
movements
BG
CBLM
Courtesy of Stephen C. Voron, MD
provides
input into the
thalamus
Basal Ganglia
Cerebellum
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resting tremor
postural instability
festination
rigidity
masked facies
bradykinesia
dyskinesia
torticollis
chorea
athetosis
hemiballismus
akathisia
intention tremor
dysmetria
dysdiadochokinesia
hypotonia
heal to shin
finger to nose
rebound
ataxic gait
titubation
nystagmus
dysmetric saccades
Basal ganglia lesions produce
contralateral signs.
Cerebellar lesions produce
ipsilateral signs.
Most movement disorders produced by
cerebellar and basal ganglia pathology
disappear during sleep.
Cerebellar and basal ganglia signs are
usually not present if the corticospinal tract
is damaged.
The cerebellum is the great comparator:
1. It compares cortical willful command
with muscle tension, joint position, &
tone (via ipsilateral spinocerebellar tracts)
2. Advises the cortex on how much,
how many, how fast
3. The motor cortex sends the revised
command down the corticospinal tract
The BASAL GANGLIA are the autopilot
for procedural movements.
The CEREBELLUM is the refiner of
finely controlled movements
(particularly of fingers).
COMPARISON OF MOTOR SYSTEMS
http://library.med.utah.edu/neurologicexam/html/home_exam.html
Lower Motor Ne uron
S pi n al C ord
Upper Motor Ne uron
C orticospin la Tract
C ere bel lum
Basal Gan gli a
Efferent part of
mon osyn apticreflex
Volu n tary moveme n t
Muscle t one by
inhibiting antagonists
Maintains muscle
fibers (trophic fact ors)
Muscle t one
Rapid coordi n ate dalternating
skil le d moveme n ts that are
learned
Eye-head movements
Facilitate sinte n tion al
moveme n ts an d in h ibit
extran e ou smoveme n ts
Aut opilot for motor activities
Normal
Weakness or paralysis
Fine control, espec. finger
flexors
Inhibit ory to Lower motor
neurons
Weakness or paralysis
Posture and Gait
Balance, equilibrium,
orientation in space
timing, duration, and amplitude
Voluntary movements in an
aut omatic manor.
Hyperreflexi a
Hyperactive deep tendon
reflexes
Babin ski- extensor plantar
reflex
S pasticity
Tru n cal ataxi a, gait ataxi a
S h ufflin gor fe stin at
in g gait,
small steps, hard to turn
Nystagmu s, Diz zin e ss,
Maske d facie s, few blinks
Decomposition of movement
Difficulty t urning or starting,
h ypokin e tic= bradykin e sia
P aucity of associated
movements
Abn ormal
Areflexi a
Fasciculation
Muscle Atroph y
Flaccid paralysis
Dysme tri a- ataxia of arms
Dysynergia
Dysdi adoch koin e sia
- inability
t o do rapid alternating
movements
Hypotonia- pendular reflexes
In te n tiontremor
Scanning speech
C h ore a, ath e tosis
,
hyperkinetic
Rigidi ty( lead-pipe )
(cogwheel),
Re stin g remor
t
Soft speech
Courtesy of Stephen C. Voron, MD