data pendukung cerebellum
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DATA PENDUKUNGSirkuit Internal Cerebellum
Jaras Propriosepsi
Spinocerebella tract
Vestibulo-cerebellar connection
Sindrom cerebellum
Infark cerebellum
Sindrom kognitif afektif cerebellum
Cerebropontocerebellar tract
Sirkuit serebellum
Gerakan volunter
Fisiologi cerebellum
Tumor cerebellum
Malformasi cerebellum
isfungsi cerebellum dan alko!ol
Vacularisasi Cerebellum
Pemeriksaan Cerebellum
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Vascularisasi cerebellum
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Vascularisasi Cerebellum
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"rteri inferior posterior cerebelli #PIC"$
- cabang terbesar%
- men&uplai bagian basal !emisfer cerebelli'bagian ba(a! vermis' sebagian nukleicerebelli' ple)us c!oroideus ventrikelkeempat' dorsolateral medulla
"rteri inferior anterior cerebelli - *occulus serebelli' anterior !emisfer
cerebelli%
"rteri superior cerebelli
- rostral !emisfer cerebelli' bagian atas vermis
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Serebellum
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Jaras Propiosepsi
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Jaras Propriosepsi
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Spinocerebellar Tract
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CerebropontoCerebellar
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Spinocerebellar Tractorsal SpinocerebellarTract
Cuneocerebellar Tract
+ote from (!ere t!esetracts originate%
Travels in ipsilateral
lateral column%,ot! of t!ese tracts entercerebellum t!roug! t!eipsilateral ipsilateralinferior cerebellar
peduncle%Sensor& info comes
from perip!er&
S i b ll T
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Spinocerebellar TractDescending Pathways:
Ventral Spinocerebellar Tract travels
after a decussation in the ventral
portion of the lateral column and enter
cerebellum via the superior cerebellar
peduncle.
Once in cerebellum, fibres cross
again so, input is ipsilateral!
"ostral Spinocerebellar
#oth relay internal feedbac$ signals
reflecting amounts of neural activity in
descending pathways.
,order ofventral andintermediateone of sc
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Sirkuit cerebellum
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"scenden Pat!(a& Cerebellum
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"scenden Pat!(a& Cerebellum
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Voluntary movement re%uires comple& interaction of
the corticospinal (pyramidal) tracts, basal
ganglia, and cerebellum'the center for motor
coordination( to ensure smooth, purposeful
movement without e&traneous muscular
contractions. The pyramidal tracts pass through the
medullary pyramids to connect the cerebral corte& to
lower motor centers of the brain stem and spinal
cord.
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Fisiologi Cerebellum Menerima informasi dari eksteroreseptor dan
proprioreseptor' reseptor visual dan auditorik'
formasio retikularis batang otak dan korteks cerebri%
Setela! mengola! impuls-impuls tersebut di atas' ia
memancarkan aktivitasn&a pada pusat pengelolaan
motorik di korteks serebri dan batang otak' se!ingga
gerakan &ang timbul memperli!atkan kelancaran dan
ketangkasan &ang teratur dan efektif%
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Fisiologi CerebellumControl of eye movements
)natomically, the flocculonodular lobe and the paraflocculus are
strongly interconnected with the vestibular nuclei. The cerebellum
controls the vestibuloocular refle& 'VO"( and the opto$inetic
refle&es. The VO" stabili*es vision during head turning by counter+
rotating the eyes in the orbit.
The gain 'eye velocityhead velocity( can be adapted by visual+
vestibular mismatch. Visual suppression of the VO" by fi&ating a
target moving simultaneously is reduced in cerebellar patients. The
initiation of the opto$inetic nystagmus, evo$ed when watching a
target moving rapidly in one direction, is often characteri*ed by either
e&aggerated or decreased e&cursions. Smooth pursuit depends on
the integrity of the cerebellum.
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Fisiologi Cerebellum
Control of eye movements
Single+unit recordings show a ma-or role of the fastigial
nucleus related to eye movements, control of head
position, and regulation of muscle activities during stance
and gait. The rostral fastigial nucleus controls head
orientation and eyehead ga*e shifts 'Pelisson et al.,
/001(.
The caudal fastigial nucleus controls oculomotor aspects,
such as saccades or smooth pursuit '2uchs et al., /003(.
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Fisiologi Cerebellum
Control of speech
4esions of the superior paravermal region are commonly
associated with speech deficits '4echtenberg 5 6ilman,
/071(.
) preparative loop includes the supplementary motor area,
dorsolateral frontal corte& including #roca area, anterior
insula, and superior cerebellum. The e&ecutive loop
comprises the sensorimotor corte&, basal ganglia,
thalamus, and inferior cerebellum.
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Control of limb movements
Single-unit recordings in t!e intermediatecerebellar corte) and t!e interpositus nucleus
!ave demonstrated t!at t!e& control re*e)
movements (!en a !olding position is suddenl&perturbed #Fr&singer et al%' ./01$%
T!e interpositus nucleus is implicated in
somest!etic re*e)es t!at control antagonist
muscles to damp 2oint oscillations and to correct
movements via feedback initiated b& t!e
movement itself #Vilis 3 4ore' ./05$%
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The dentate nucleus regulates reaction time through
initiation of movements triggered by vision or mental
percepts and accuracy of single+-oint and multi+-oint
goal+directed movements, such as reaching.
4esions of the dentate nuclei are associated typically
with an overshoot of the target 'hypermetria( and a
decomposition of multi+-oint movements 'Thach et
al., /008 #astian et al., /009(.
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Posture and gait
Due to its anatomical connections, the medial cerebellar*one can integrate spinal and vestibular inputs to
influence vestibulospinal and reticulospinal tracts.
The intermediate *one can integrate spinal and cortical
inputs to influence wal$ing via pro-ections to motor
cortical areas.
"egarding the lateral cerebellum, it influences wal$ing via
cortical interactions and contributes to the voluntary
modifications of the locomotor cycle '#astian 5 orton,
8;;7(
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Sitting, stance, and gait are usually impaired in midline cerebellar
lesions. Lesions in the medial and intermediate zones of the
cerebellum, especially in the anterior lobe, disturb movements
lin$ed to an e%uilibrium function '
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V!"#$%L&' !!"& central role in the maintenance of
e*uilibrium and gaze stability."he vestibular system, by means of its
receptors for the perception of linear andangular acceleration, plays a central role inorientation.
+esigned to answer two basic *uestions
-hich way is up
-here am # going
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Very elusive to test
/ive peripheral 0receptors1 (three semicircularcanals, utricule, saccule)
2erve (sub3divisions)
Central connections
Cortical area
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"he otoliths register linear acceleration and
static tilt
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Vestibular system
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Vestibular 2uclei (V2)
Vestibular signals originating in the two labyrinthsfirst interact with signals from other sensory systemsin the V2.
4nly one fraction of the neurons in the V2 receive
direct vestibular input, and most neurons receiveafferent input from other sensory systems (visual orproprioceptive) or regions of the C2! (cerebellum,reticular formation, spinal cord and contralateral V2).
Conse*uently the output of neurons from the V2
reflect the interaction of many systems.
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III
oculomotor IV
abducens
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Vestibulo3ocular and vestibulo3spinal refle5es
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Vestibulocerebellar and vestibulospinal pathways and
connections between vestibular and ocular motor nuclei
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Vestibular3cerebellar connectionsSome fibers of the vestibular nerve transmit impulses
directly via the -u&tarestiform tract 'ne&t to the ?>P( andruns to the flocculonodular lobe of the cerebellum.
@fferents from the fastigial nucleus turn through the
uncinate fasciculus of "ussell bac$ to the vestibular nuclei
and via the vestibular nerve to the hair cells of thelabyrinth 'predominantly inhibitory(
The flocculonodular lobe of the cerebellum also receives
secondary fibers from the superior, medial and inferior
vestibular nuclei. ?t returns efferent stimuli directly to thevestibular nuclei and spinal motor neurons via
cerebelloreticular and reticulospinal connections.
ach side of the cerebellum e5erts an influence on the
vestibular nuclei of both sides
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Vestibulo-okular re*eks)natomically, the flocculonodular lobe and the
paraflocculus are strongly interconnected with
the vestibular nuclei. The cerebellum controls the
vestibuloocular refle& 'VO"( and the opto$inetic
refle&es. The VO" stabili*es vision during head
turning by counter+rotating the eyes in the orbit.
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Vestibular Palsy
rapid horizontal head rotation toward thelesioned
side elicits compensator re!"ation saccades#
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C & L 4 ' # C " ! " # 2 6
"hermal convectivetheory
7eating or cooling the
e5ternal ear canal
causes convection
current in the
endolymph and
subse*uent
movement of the
cupula.
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Vestibular nuclei
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$indrom Cerebellar1 ge2ala cardinal6
.% "ta)ia
7% 4&potonus
8% Tremor
1% "st!enia #kelema!an' fatigue' malasbergerak$
$i d C b ll
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$indrom Cerebellar"ta)ia6 ataksia trunkal' limb' gait' stance%
Tremor 6 - ekstremitas #intention tremor' end-point'
kinetic$
- kepala' dan trunkal #titubasi$&sart!ria
+&stagmus
4&potonia
Peruba!an kepribadian&sdiadokinesia
&smetri
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Dsarthria
>erebellar disorders are typically associated with
slow speech accompanied by slurring.
>omprehension is spared. Temporal dysregulation
may lead to unintelligible words 'Aent et al., /007(.
Speech may turn out to be e&plosive, ta$ing a
staccato rhythm and a nasal character
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akibat lesi paravermis%
Gangguan sinergi otot-otot bicara%
Pasien bicara pelan-pelan' terputus-putus'artikulasi buruk' penekanan abnormal dandatar di setiap suku kata%
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&smetria Aetida$mampuan menghenti$an gera$an terarah
tepat pada wa$tunya, bermanifestasi 'misalnya(
sebagai gera$an -ari melewati lo$asi target .
Aegagalan fungsi cerebellum mengu$ur -ara$ $e
target.
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Dysmetria represents an error in tra-ectory of movement.
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&sdiadokinesia
gangguan gera$an bergantian secara cepat a$ibat
$erusa$an $oordinasi $etepatan wa$tu beberapa
$elompo$ otot antagonisti$: gera$an seperti pronasi
dan supinasi tangan secara cepat men-adi lambat,
terputus+putus, dan tida$ berirama.
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Tremor
%ntention tremor bermanifestasi selama
gerakan volunter' meningkat ketika
mendekati target%
Tremor postural $eti$a pasien mempertahan$an
tangan yang sedang pronasi tepat di depan, dengan
lengan terang$at.
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4&potonia dan
!&pore*eksPada lesi akut !emisfer cerebelli' resistensiotot ter!adap gerakan pasif meng!ilang'
postur abnormal #misaln&a pada tangan$%
9e*eks otot intrinsik meng!ilang pada otot
!ipotonik%
9e*eks pendular
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&esi 'estib(locerebell(m
6angguan fungsional lobus flo$ulonodularis atau
nu$leus fastigii:
/. Pasien $urang dapat menempat$an dirinya pada
lapangan gravitasi bumi.
8. Pasien tida$ dapat memfi$sasi tatapan pada obye$
yang diam saat $epalanya bergera$.
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isekuilibrium"stasia 6 sulit berdiri tegak
"basia 6 sulit ber2alan
"taksia trunkal 6
Ga&a ber2alan pasien lebar-lebar dan tidak stabil'
men&erupai ga&a ber2alan orang &ang mabuk%
4eel-to-toe (alking tidak dapat dilakukan%
:etidakseimbangan bukan karena de;siensi impuls
proprioseptif mencapai kesadaran' tapi akibat
koordinasi respon otot-otot ter!adap gravitasi &ang
sala!
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Gangguan okulomotor' nistagmus6angguan $emampuan mempertahan$an tatapan
terhadap ob-e$ diam atau bergera$.
Bi$a pasien mencoba mengi$uti ob-e$ yang bergera$
dengan matanya, ter-adi s%uare+wave -er$s, yang
terlihat oleh pemeri$sa.
6a*e+evo$ed nystagmus $eti$a mata bergera$ $e
sisi lesi serebellum dan menghilang bila pandangan
dipertahan$an $e sisi tersebut. #ila mata diarah$an
$e tengah, rebound nystagmus.
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6angguan refle$s vestibulo+o$ular, yaitu berupa
senta$an sa$adi$ mata $eti$a menoleh$an $epala.
?ndividu yang sehat dapat mene$an refle$ ini dengan
mempertahan$an tatapannya pada sebuah ob-e$.
&esi $pinocerebell(m
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&esi $pinocerebell(mSpinocerebellum berfungsi mengontrol tonus otot
dan $oordinasi $er-a $elompo$ otot antagonisti$
yang berpartisipasi pada postur dan gaya ber-alan.
4esi lobus anterior dan superior vermis :
ata$sia stance dan ata$sia gait 'lebih berat(.
>ara ber-alan yang lebar dan tida$ stabil, berdeviasi
$e sisi lesi, $ecenderungan -atuh di sisi lesi.
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)ta$sia stance terlihat dengan tes "omberg:
Pasien berdiri dengan mata tertutup, dorongan ringan pada sternum
a$an menyebab$an pasien berayun $e depan dan $e bela$ang
dengan fre$uensi 8+=
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&esi $erebrocerebell(mTida$ menimbul$an paralisis.
Aerusa$an berat pada e$se$usi gera$an volunter.
anifestasi $linis selalu ipsilateral terhadap lesi
penyebabnya.
"ebound phenomenon
Pasien mene$an tangan pemeri$sa dengan $e$uatan
ma$simum, pemeri$sa tiba+tiba menari$ tangannya,
gera$an pasien tida$ dapat dihenti$an, lengan terayun
memu$ul pemeri$sa.
C b ll $ d
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Cerebellar $ndromes9ostral vermis s&ndrome result from
alco!olism and nutritional de;cienc&%Caudal vermis s&ndrome implies a midline
cerebellar neoplasm 6 medulloblastoma'epend&moma' astroc&toma%
Cerebellar !emisp!er s&ndrome comes fromacute destructive lesion6 infarct' !emorr!age'neoplasm' abcess' trauma%
Pancerebellar s&ndrome6 vitamine de;sienc&'#vitamin
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Dist(rbancesGenerall& s&mptoms of anot!er disease
"ta)iaFailure to produce smoot! intentional
movements
Gait isturbance
Inabilit& to perform smoot! coordinated gaitMa& be described b& patient as
-=eakness -iiness
-Stroke -Falling
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Pat!op!&siolog&9esult from an& condition t!at a>ects t!e
central and perip!eral nervous s&stems
"ta)ia6 T&pesMotor ata)ia Sensor& ata)ia
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Motor "ta)iaCaused b& cerebellar disorders Intact sensor& receptors and a>erent pat!(a&s
Integration of proprioception is fault&Midline cerebellar lesions cause truncal ata)ia ?ateral cerebellar lesions cause limb ata)iaT!alamic infarcts ma& cause contralateral ata)ia
(it! sensor& loss
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Sensor& "ta)iaFailure of proprioceptive information to t!e
central nervus s&stem
Ma& be due to disorders of spinal cord orperip!eral nerves
Can be compensated for b& visual inputs
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i>erential iagnosesInto)ication
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e;nitions,est to use descriptive terms for gait
disturbances
Motor ata)ia6 (ide-based (it! irregular'unstead& steps
Sensor& ata)ia6 abrupt leg movement andslapping impact of feet
Festinating gait6 narro(-based miniatures!uBing steps% Commonl& seen in P
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"pra)ic gait6 dicult initiating gait% Ma& beseen in +P4 and P
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4istor&Dnset
9apidit&
Previous s&mptomsPM4
Medications
Social
"lco!ol intake Illicit drug use
"ssociated S&mptoms
4eadac!e ro(siness iiness VertigoTinnitus Fever +auseaEvomiting =eakness Parest!esia
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P!&sical
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Speci;c PopulationsGeriatric PatientGait normall& c!anges (it! age
S!ortened stride =idened baseSlo( gait
Senile gait ma& represent neuronal loss' reducedproprioception' slo(ing of corrective responses and(eakness
Can also be present in ot!er neurodegenerativediseases
Dccurs in 7H of elderl& populationTreatmentS&mptomatic
suall& admitted to rule out ot!er life-t!reatening
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T!e "lco!olic Patient"n& gait abnormalit& in an alco!olic patient s!ould
raise concern about nutritional de;ciencies
If acute ata)ia is associated (it! confusion and e&emovement abnormalities Wernickeencephalopathyneeds to be considered
Still ot!er intracranial pat!olog& needs to be ruledout
Treatment IV !&dration' Vit ,. and de)trose
Most often need to be admitted
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C!ildrenMa& appear (ell' but
(obbl& (!en sitting
Into)ications are mostcommon' follo(ed b&infectionEin*ammation
"sk about famil&member !omemedications
PM4
PF4
i>erential diagnoses
rug Into)ication Infection or in*ammation+eoplasmTrauma Inborn errors of
metabolism4&drocep!alus Idiopat!ic
isposition9ule out life t!reatening
processesMost are admittedPediatric neurolog&
consult
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i i
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Tipe "ta)ia
!imtom
Vestibular&ta5ia
Cerebellar&ta5ia
!ensory&ta5ia
Vertigo Possible K
Cystagmus K
Disartria K Possible K
)ta&iae&tremitas
K #onl& in legs$
Tes "omberg K #bot! (it!open andclosed e&es$
#(it! closede&es$
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Dccupational t!erap& L to ma)imie use oft!e limbs and to ma)imie safet& (!en(alking and doing transfers
Safet& bars' gait assist aids or (!eelc!airs=eig!ted bracelets ma& improve !and controlSpeec! and s(allo(ing t!erap& L to improve
communication and s(allo(ing safet&
#especiall& to prevent c!oking andpneumonia$ communication assist devicesPneumova) and in*uena vaccinations
General ata)ia treatments
i i d i !
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"ta)ia Friedreic!Sebelum usia 75 ta!un
4ilangn&a sel-sel ganglion radi) dorsalisdegenerasi kolumna posterior%
:linis6
- gangguan sensasi posisi' diskriminasi 7 titik'stereognosis%
- ataksia progresif tanpa diketa!ui pen&ebabn&a%
- romberg tes #$
- re*eks tendon dalam di ekstremitas ba(a! #-$ - disartria dalam ta!un setela! onset%
- autosomal resesif
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Tabes Dorsalis
egenerasi kolumna dorsalis dan dorsal root%Sensor& ata)ia' lutut pasien diangkat tinggi
ketika ber2alan' kemudian diturunkan cepat%
Gangguan sense of position' kompensasi ole!
visual%9omberg tes #$
Gangguan vibrasi
Pupil arg&ll robertson' serologi sip!&lis #$
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Motion Sickness
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Motion Sicknessotion sic$ness is a very common disturbance of the
inner ear that is caused by repeated motion such as fromthe swell of the sea, the movement of a car, the motion of
a plane in turbulent air, etc.
?n the inner ear, motion sic$ness affects the sense of
balance and e%uilibrium and, hence, the sense of spatialorientation.
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otion is sensed by the brain through three different
pathways of the nervous system that send signalscoming from the inner ear 'sensing motion, acceleration,
and gravity(, the eyes 'vision(, and the deeper tissues of
the body surface 'proprioceptors(.
hen there is unintentional movement of the body, asoccurs, the brain is not coordinating the input, and there
is thought to be discoordination or conflict among the
input from the three pathways.
?t is hypothesi*ed that the conflict among the inputs isresponsible for motion sic$ness.
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Infark serebellar
"ppro)imatel& )*+ of patients (it!
cerebellar infarction present (it! verti,o and
no localizin, ne(rolo,ic de!cits% T!e
ma2orit& of t!ese ma& !ave ot!er signs of
central vertigo' speci;call& direction-c!anging
n&stagmus and severe ata)ia%
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Cerebellar infarction represents appro)imatel& -./ + of
ac(te stro0es overall%7/
T!ese can result from occl(sion of t!e superior
cerebellar arter& #SC"$' anterior inferior cerebellar
arter& #"IC"$' or t!e posterior inferior cerebellar arter&
#PIC"$%
?arger cerebellar infarcts produce s&mptoms and signs
localiing to t!e brainstem' suc! as diplopia1
dsarthria1 limb ata"ia1 dspha,ia1 and wea0ness
or n(mbness.
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"ppro)imatel& .5H of patients (it! cerebellar
infarction can present (it! isolated vertigo' t!at
is' vertigo (it! no localiing ;ndings on motor'
sensor&' re*e)' cranial nerve' or limb
coordination e)amination%
Most of t!ese are infarcts of t!e medial branc!
of t!e PIC" #/OH$%
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First' stroke in general tends to present (it!t!e s(dden and immediate onset ofsmptoms' usuall& reac!ing ma)imal
intensit& at once%Second1 vasc(lar ris0 factors raise the
prior probabilit of disease% 4&pertensionand cardioaortic diseases are found in t!e
ma2orit& of patients (it! cerebellar infarction'and an embolic source is found in 71L15H%78'7/
Finall&' t(o easil& overlooked p!&sical signs!ave been s!o(n to indicate cerebellar
infarction%
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Tumor Cerebellum/. >erebellar )strocytoma + ==E tumor fossa posterior pada ana$.
+ 8FE tumor pediatri$.
+ rata+rata pada umur 0 tahun.
+ benigna, $isti$.
+ hemisfer vermis.
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8. edulloblastoma
+ infratentorial
+ malignan
+ cerebellar hemisfer
+ mendesa$ ventri$el $e 3hydrocephalus
Tumor cerebellum
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Tumor cerebellum$enign cerebellar tumors
Pilocytic astrocytoma, may be problematic in that
they often grow %uite large before producing
symptoms, because of the plasticity of the
cerebellum. Papilledema, an indirect sign of an
intracranial mass, may be lac$ing for a long time,
particularly in adults it is present in about 7FE of
affected children
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%n most cases 23* +4' cerebellar tumors
manifest t!emselves initiall& (it!
occipitocervical headache and na(sea
and vomitin, on an empt& stomac! #dr&
!eaves$% " forced !ead tilt is a clinical sign of
impending !erniation of t!e cerebellar tonsils
t!roug! t!e foramen magnum
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edulloblastoma is a malignant tumor that
preferentially affects children and adolescents and
accounts for one+third of all brain tumors in this age
group '1E of all brain tumors regardless of age(.
?t often arises from the roof of the fourth ventricle
and then grows into the vermian portion of the
flocculonodular lobe.
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#ecause this type of tumor often begins in the
vestibulocerebellum, its typical initial sign is
dyse*uilibrium: the affected child has a broad+based,
swaying, and staggering gait.
2urther cerebellar manifestations including ata5ia,
dysmetria, asynergia, adiadocho8inesia, andintention tremorgradually arise as the tumor grows
further and begins to affect the lateral portions of the
cerebellum 'the hemispheres(.
?n advanced stages of tumor growth, bloc$age of thefourth ventricle or of the cerebral a%ueduct causes
occlusive hydrocephalus, with clinical signs of
intracranial hypertension%
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&coustic neuroma (i.e., vestibular schwannoma).
This tumor arises from the Schwann cells of the
eighth cranial nerve 'usually its vestibular portion(
and is thus found in the cerebellopontine angle.
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5alformasi Cerebell(m
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5alformasi Cerebell(m.% "rnold-C!iari
- !erniasi tonsil cerebellum ke foramenmagnum%
- kadang menimbulkan !&drocep!alus non-communicating akibat dari obstruksi aliran
?CS%
- ge2ala klinik6
n&eri kepala' fatigue' kelema!an otot
(a2a! dan kepala' sulit menelan' diiness'nausea' gangguan koordinasi' paralisis#berat$%
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"da 1 tipe6
.% Tipe I
asimtomatik selama masa kanak-kanak'
kadang bermanifestasi dengan n&erikepala dan ge2ala cerebellar%
4erniasi tonsil cerebellar' 8 mm di ba(a!foramen magnum%
S&ringom&elia cervicot!oracic spinal cord%
iagnosa dan terapi sulit
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$a,ittal 56% 2T)4
shows cerebellartonsils -7/ cm belowforamen ma,n(m1where the C$8 spaceis narrow. There is
no srin" in thecervical cord 9 the:thventricle is normalsize 9 con!,(ration
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7% Tipe II
tonsilar !erniation di ba(a! foramenmagnum
displacement luas dari vermis?umbar m&elomeningocele
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C!iari II #"rnold-C!iariCerebellar tonsillar !erniationSmall posterior fossa
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8% Tipe III
- occipital encep!alocele%
- 2aringan neuroectodermal abnormal%
1% Tipe IV
- gangguan perkembangan cerebellum%
- cerebellum dan batang otak di dalam fossa
posterior' tapi tidak ber!ubungan denganforamen magnum%
Dand7;al0er
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Dand ;al0er
5alformation+andy3-al8er syndrome)genesis of cerebellar vermis
cystic dilatation of 3th venticle
enlargement of posterior fossa
Variable clinical manifestations
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DAND< ;A&KE6
$
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C'$LL&' &L/4'&"#42!
V'#&2 (P&L4C'$LL%4
9oubert syndrome>linical manifestations include episodic hyperpnea, ata&ia,
eye movement abnormalities, hypotonus, and retardasi
mental.
2amilial
)genesis of vermis, cystic dilatation of 3th venticle 'but
less than DS(
icroscopically normal cerebellar corte& with numerous
subcortical heterotopias
Pemeriksaan Cerebellum
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Pemeriksaan Cerebellum
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Cara ber:alan (gait) dan berdiri (stance)
?nspe$si pasien saat berdiri. )da$ah goyangan $eti$a
berdiri, -uga cara ber-alan dysta&ia. Gntu$
meng$ompensasi $etida$stabilan dari cara berdiri
dan cara ber-alan, cerebellum memerintah$an berdiri
dan ber-alan dengan melebar$an $edua $a$i.
Pasien ber-alan melalui garis lurus. Dengan -alantandem. )mati ada$ah $ecenderungan ayunan $e
salah satu sisi.
Pemeriksaan Cerebellum
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Pemeriksaan Cerebellum+ysta5ia lengan
/. Pasien diperintah$an untu$ melurus$an $edua
lengan secara horisontal. )mati ada$ah postural
tremor.
8. Tes telun-u$+hidung
Pasien disuruh melurus$an salah satu lengan,
$emudian menggera$$an -ari telun-u$ $e u-ung
hidung.
?nterpretasi:
#ila muncul tremor $eti$a mende$ati hidung disebut
intension tremor. Dan bila pasien gagal menyentuh
hidung secara tepat, disebut dysmetria.
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Pemeriksaan Cerebellum 4a$u$an tes tumit+tulang $ering di e$stremitasbawah.
Glang pemeri$saan = $ali bila hasil meragu$an.
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Pemeriksaan Cerebellum+ysdiado8inesia)dalah gangguan $oordinasi otot selama gera$an
cepat.
Pasien disuruh mela$u$an gera$an yangberlawanan secara cepat. isalnya pronasi dan
supinasi.
Pemeriksaan cerebellum
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Pemeriksaan cerebellum
Pemeriksaan cerebellum
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Pemeriksaan cerebellum4vershooting test
/. Pasien diminta menutup mata. Aemudian
melurus$an lengan. Pemeri$sa ber$ata $epada
pasien bila pemeri$sa a$an mene$an salah satu
lengan. Pasien disuruh menahan.
?nterpretasi: normal bila lengan pasien $embali $e
posisi semula secara cepat.
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9ebound sign of 4olmes
- pemeriksa memegang pergelangan tanganpasien%
- pasien menggenggam erat tanganpemeriksa%
- kemudian tangan pemeriksa dilepaskan tiba-tiba@
- interpretasi6
normal6 lengan pasien bera&un dengan2arak minimal' dan kembali ke posisi
semula%
Pemeriksaan Cerebellum
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Pemeriksaan Cerebellum
Cerebellar Cognitive ">ective S&ndrome
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Cerebellar Cognitive ">ective S&ndrome
Simptom 6
Gangguan fungsi eksekutif' visuo-spasial'ba!asa' peruba!an emosi dan kepribadian%
Causa6
cerebellar agenesis' d&splasia dan !ipoplasia'stroke serebellar' tumor' serebellitis'trauma'dan pen&akit neurodegeneratif%
era2at kepara!an CC"S tergantung lokasi
dan perluasan lesi%
Cerebellar Cognitive ">ective
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S&ndrome
Fungsi cerebellum adala! bertanggung2a(abregulasi motorik' kognitif dan emosional be!aviour%
Cerebellum ber!ubungan dengan regulasi emosi%
"rea kognitif di corte) cerebri &ang berpro&eksi ke
cerebellum6.% Corte) parietal posterior #spatial a(areness$%
7% G&rus temporal superior #ba!asa$
8% "rea para!ipocampal superior #spatial memor&$
1% "sosiasi visual% Corte) prefrontal #atensi' (orking memor&'
2udgement$
>erebellar >ognitive )ffective Disorder
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>erebellar >ognitive )ffective Disorder
4esions of the posterior corte&and vermis?mpairment of e&ecutive functions
Planning, verbal fluency, abstract reasoningDifficulties with spatial cognition
Visuo+spatial organi*ation, visual memory
Personality changes#lunting of affect, inappropriate behaviors
4anguage disorders)grammatism, disprosodia
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The cerebellar circuits are involved in many aspects
of memory, in particular, in nondeclarative memory.
This latter includes procedural learning (s8ills and
habits), priming and perceptual learning, basic
associative learning'including simple classical
conditioning of emotional and s$eletal muscle
responses(, and non3associative learning
Pschiatric Aspects of Cerebellar
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Disorders
#.$ Cerebellar Cognitive ">ective S&ndrome
#7$ "natomicall& Speci;c Ps&c!iatric "spectsof Cerebellar isorders
#8$ Dt!er Ps&c!iatric "spects of Cerebellarisorders
;. Cerebellar Cognitive &ffective !yndrome
(S h h 5 Sh /001(
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(Schmahman 5 Shermen, /001(.
Cerebellar lesions in ,enerale%g% acAuired lesions'congenital cerebellar malformations' cerebellar tumourresection' etc can cause motor impairments pl(s thefollowin,#Sc!ma!man et al' 755R Tavano et al' 755R ?eviso!net al' 7555$
Co,nitive impairments6 E"ec(tive dsf(nctionse%g% in (orking memor& and
planning 'is(o7spatial abnormalitiese%g% in visual memor& and
visuo-spatial organisation
&in,(istic dsf(nctione%g% d&sprosodia' agrammatism andanomia
A>ective impairments6 an)iet&' let!arg&' depression' lack of empat!&'
ruminativeness' perseveration' an!edonia and aggression
'8( )natomically Specific Psychiatric )spects of
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>erebellar Disorders
'ermal A,enesis severe ?' "utism 3abnormal motor development #Tavano et al' 755R$%
'ermal lesions a>ective and relational
disorders #Sc!ma!man et al' 755R$%$pinocerebellar Ata"ia impairment in
attention' memor&' e)ecutive functions andt!eor& of mind #Garard et al' 7550$%
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(
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"ssessment6
#.$ Motor disorders in ps&c!iatric disordersas signs of cerebellar d&sfunctioning
#7$ +on-motor s&mptoms eAuivalent tomotor s&mptoms related to cerebellum
Treatments6
#8$ Cerebellar e)ercises
#1$ Transcranial Magnetic Stimulation #TMS$ #$ 9outine disorders
+&stagmus
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& gT!e localiing signi;cance of n&stagmus is often a
mere indication of d&sfunction some(!ere in t!e
posterior fossa #i%e%' vestibular end-organ' brain
stem' or cerebellum$% 4o(ever' certain n&stagmus
patterns are Auite speci;c and permit reasonabl&
accurate neuroanatomic diagnosis% =!en
possible' t!e speci;c and nonspeci;c forms are
separated on t!e basis of clinical appearance and
associated signs and s&mptoms%
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o(nbeato(nbeat n&stagmus is de;ned as n&stagmusgae position (it! t!e fast p!ase beating in ado(n(ard direction% Patients (it! brain stemdisease or drug into)ications usuall& lack gae-evoked do(n(ard n&stagmus despite n&stagmusin all ot!er ;elds of gae% T!us' n&stagmusbeating do(n(ard in t!e primar& position is astriking p!enomenon and is !ig!l& suggestive of a
disorder of t!e craniocervical 2unction' suc! as"rnold-C!iari malformations
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pbeatPrimar&-position n&stagmus (it! t!e fast p!asebeating up(ard rarel& re*ects drug into)ication%Most often' t!e n&stagmus is acAuired andindicates str(ct(ral disease1 (s(all of thebrain stem% T!e location of t!e lesions inpatients (it! upbeat n&stagmus after meningitis'=ernickes encep!alopat!&' or organop!osp!atepoisoning is uncertain% =it! convergence' upbeat
ma& en!ance or convert to do(nbeat%T!e slo(-p!ase (aveform is usuall& linear but ma& be anincreasing-velocit& e)ponential%
P
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V
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Gae evoked n&stagmus6
Dne of t!e most common forms of centraln&stagmus
Inabilit& to maintain eccentric gae Uleak& integrator -- miscalibration bet(een pulse
and step inputs
S&mmetric cerebellar *occulus implicated "ge' anti-convulsant t!erap&' alco!olic
degeneration' stroke' dem&elination ,aclofen e>ective
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o(nbeat n&stagmus6
efect in vertical gae !olding "s&mmetric inputs from vertical semi-circular canals
produce up(ard slo( drift of e&esefect in fastigial nuclei calibration Secondar& do(n(ard corrective fast p!aseDbe&s "le)ander@s la( ?ocalies to cervico-medullar& 2unction "rnold-C!iari malformationTreatment (it! baclofen' clonaepam' base-out
prisms
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pbeat n&stagmus6
Present in primar& position or upgae Classicall& localies to a lesion of anterior cerebellar vermis More generall& implicates posterior fossa disease
ective
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#runs nystagmus:
associated with >P) tumors
high fre%uency, low amplitude
nystagmus 'fast+phase away from lesion(
low fre%uency, large amplitude
nystagmus on ipsilateral ga*e 'fast phase
toward lesion(
shift from eye movement response to
vestibular imbalance to that of defective
ga*e holding
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See-sa( n&stagmus6
iscon2ugate vertical n&stagmus #pendular vs% 2erk$ p(ard moving e&e intorts (!ile do(nard e&e e)torts ?ocalies to lesions of diencep!alon Visual ;elds ma& be useful #disruption of a>erents to cerebellum$
Dcular *utterEopsoclonus6
,urst-like' incoordinated saccadic e)cursions (it! !ig! freAuenc&' lo(amplitude
+o intersaccadic latenc&
Purel& !oriontal6 ocular *utter Multiplanar6 opsoclonus 9e*ect pause cell d&sfunction #pons$ Must consider paraneoplastic etiolog&6 SCC of lung' ovarian' breast C" +euroblastoma in c!ildren
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=ernicke@s S&ndrome"kut
"bnormal e&e movements
"ta)ia
ConfusionCausa 6 de;siensi t!iamin e%c poor nutrition
#"IS'!&peremesis gravidarum't!&roto)icosis'C4F (it! longterm diuretict!erap&$
9educed cerebral metabolism a)onal