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Vacularisasi Cerebellum

Vestibulo-cerebellar connection

Sirkuit Internal Cerebellum

Sindrom cerebellum
Infark cerebellum

Jaras Propriosepsi
Sindrom kognitif afektif cerebellum
Spinocerebella tract
Tumor cerebellum
Cerebropontocerebellar tract
Malformasi cerebellum
Sirkuit serebellum
Disfungsi cerebellum dan alkohol
Gerakan volunter
Pemeriksaan Cerebellum
Fisiologi cerebellum

Vascularisasi cerebellum

Vascularisasi Cerebellum



flocculus serebelli. Arteri superior cerebelli . anterior hemisfer cerebelli. sebagian nuklei cerebelli.rostral hemisfer cerebelli.Arteri inferior posterior cerebelli (PICA) . .cabang terbesar. plexus choroideus ventrikel keempat. bagian bawah vermis. dorsolateral medulla  Arteri inferior anterior cerebelli . bagian atas vermis .menyuplai bagian basal hemisfer cerebelli.

Serebellum .

Jaras Propiosepsi .

Jaras Propriosepsi .

Spinocerebellar Tract .

Cerebropon toCerebellar .

Sensory info comes from periphery . Travels in ipsilateral lateral column. Both of these tracts enter cerebellum through the ipsilateral ipsilateral inferior cerebellar peduncle.Spinocerebellar Tract Dorsal Spinocerebellar Tract Cuneocerebellar Tract Note from where these tracts originate.

. fibres cross again. input is ipsilateral! Rostral Spinocerebellar  Both relay internal feedback signals Border of ventral and intermediate zone of sc reflecting amounts of neural activity in descending pathways. Once in cerebellum.Spinocerebellar Tract  Descending Pathways: Ventral Spinocerebellar Tract travels after a decussation in the ventral portion of the lateral column and enter cerebellum via the superior cerebellar peduncle. so.

Sirkuit cerebellum .

Ascenden Pathway Cerebellum .

Ascenden Pathway Cerebellum .

basal ganglia. purposeful movement without extraneous muscular contractions. The pyramidal tracts pass through the medullary pyramids to connect the cerebral cortex to lower motor centers of the brain stem and spinal cord. and cerebellum (the center for motor coordination) to ensure smooth. .Voluntary movement requires complex interaction of the corticospinal (pyramidal) tracts.


ia memancarkan aktivitasnya pada pusat pengelolaan motorik di korteks serebri dan batang otak. .Fisiologi Cerebellum  Menerima informasi proprioreseptor. Setelah mengolah impuls-impuls tersebut di atas. dari reseptor eksteroreseptor visual dan dan auditorik. formasio retikularis batang otak dan korteks cerebri. sehingga gerakan yang timbul memperlihatkan kelancaran dan ketangkasan yang teratur dan efektif.

the flocculonodular lobe and the paraflocculus are strongly interconnected with the vestibular nuclei. The initiation of the optokinetic nystagmus. The VOR stabilizes vision during head turning by counterrotating the eyes in the orbit. evoked when watching a target moving rapidly in one direction.  The gain (eye velocity/head velocity) can be adapted by visual- vestibular mismatch. . The cerebellum controls the vestibuloocular reflex (VOR) and the optokinetic reflexes. Smooth pursuit depends on the integrity of the cerebellum.Fisiologi Cerebellum Control of eye movements  Anatomically. is often characterized by either exaggerated or decreased excursions. Visual suppression of the VOR by fixating a target moving simultaneously is reduced in cerebellar patients.

1998). 1994).. The rostral fastigial nucleus controls head orientation and eye–head gaze shifts (Pelisson et al. and regulation of muscle activities during stance and gait. control of head position. .Fisiologi Cerebellum Control of eye movements Single-unit recordings show a major role of the fastigial nucleus related to eye movements. The caudal fastigial nucleus controls oculomotor aspects.. such as saccades or smooth pursuit (Fuchs et al.

Fisiologi Cerebellum Control of speech Lesions of the superior paravermal region are commonly associated with speech deficits (Lechtenberg & Gilman. and inferior cerebellum. and superior cerebellum. The executive loop comprises the sensorimotor cortex. 1978).  A preparative loop includes the supplementary motor area. thalamus. . dorsolateral frontal cortex including Broca area. basal ganglia. anterior insula.

Control of limb movements Single-unit recordings in the intermediate cerebellar cortex and the interpositus nucleus have demonstrated that they control reflex movements when a holding position is suddenly perturbed (Frysinger et al. 1980). The interpositus nucleus is implicated in somesthetic reflexes that control antagonist muscles to damp joint oscillations and to correct movements via feedback initiated by the movement itself (Vilis & Hore.. 1984). .

. . Bastian et al. 1996). such as reaching. 1992..The dentate nucleus regulates reaction time through initiation of movements triggered by vision or mental percepts and accuracy of single-joint and multi-joint goal-directed movements. Lesions of the dentate nuclei are associated typically with an overshoot of the target (hypermetria) and a decomposition of multi-joint movements (Thach et al.

the medial cerebellar zone can integrate spinal and vestibular inputs to influence vestibulospinal and reticulospinal tracts. it influences walking via cortical interactions and contributes to the voluntary modifications of the locomotor cycle (Bastian & Morton. Regarding the lateral cerebellum. 2007) . The intermediate zone can integrate spinal and cortical inputs to influence walking via projections to motor cortical areas.Posture and gait Due to its anatomical connections.

1993. disturb movements linked to an equilibrium function (Horak & Diener. especially in the anterior lobe. see also Chapter 3). . Bastian & Morton. stance. and gait are usually impaired in midline cerebellar lesions. 1994). 2007. Lower vermal lesions tend to be associated with pluridirectional increased body sway at low frequency and high amplitudes. Lack of coordination of trunk and legs leads to an irregular gait in cerebellar patients. and lesions in the upper vermal zone tend to increase anteriorposterior body oscillations at higher velocities and lower amplitudes (Dichgans & Fetter. Lesions in the medial and intermediate zones of the cerebellum.Sitting.

The vestibular system. by means of its receptors for the perception of linear and angular acceleration. Designed to answer two basic questions:  Which way is up?  Where am I going? .VESTIBULAR SYSTEM A central role in the maintenance of equilibrium and gaze stability. plays a central role in orientation.

 Very elusive to test  Five peripheral “receptors” (three semicircular canals. utricule. saccule)  Nerve (sub-divisions)  Central connections  Cortical area .


The otoliths register linear acceleration and static tilt .

Vestibular system .


 Consequently the output of neurons from the VN reflect the interaction of many systems.  Only one fraction of the neurons in the VN receive direct vestibular input. .Vestibular Nuclei (VN)  Vestibular signals originating in the two labyrinths first interact with signals from other sensory systems in the VN. spinal cord and contralateral VN). reticular formation. and most neurons receive afferent input from other sensory systems (visual or proprioceptive) or regions of the CNS (cerebellum.

III oculomotor IV abducens .

Vestibulo-ocular and vestibulo-spinal reflexes .

Vestibulocerebellar and vestibulospinal pathways and connections between vestibular and ocular motor nuclei .

medial and inferior vestibular nuclei. Efferents from the fastigial nucleus turn through the uncinate fasciculus of Russell back to the vestibular nuclei and via the vestibular nerve to the hair cells of the labyrinth (predominantly inhibitory) The flocculonodular lobe of the cerebellum also receives secondary fibers from the superior. Each side of the cerebellum exerts an influence on the vestibular nuclei of both sides .Vestibular-cerebellar connections Some fibers of the vestibular nerve transmit impulses directly via the juxtarestiform tract (next to the ICP) and runs to the flocculonodular lobe of the cerebellum. It returns efferent stimuli directly to the vestibular nuclei and spinal motor neurons via cerebelloreticular and reticulospinal connections.

The VOR stabilizes vision during head turning by counter-rotating the eyes in the orbit. .Vestibulo-okular refleks Anatomically. The cerebellum controls the vestibuloocular reflex (VOR) and the optokinetic reflexes. the flocculonodular lobe and the paraflocculus are strongly interconnected with the vestibular nuclei.

Vestibular Palsy “rapid horizontal head rotation toward the lesioned side elicits compensatory refixation saccades” .

.CALORIC TESTING Thermal convective theory: Heating or cooling the external ear canal causes convection current in the endolymph and subsequent movement of the cupula.

Vestibular nuclei .

Sindrom Cerebellar
4 gejala cardinal:
1. Ataxia
2. Hypotonus
3. Tremor
4. Asthenia (kelemahan, fatigue, malas


Tremor : . dan trunkal (titubasi) Dysarthria Nystagmus Hypotonia Perubahan kepribadian Dysdiadokinesia Dysmetri . end- point.Sindrom Cerebellar Ataxia: ataksia trunkal. stance. kinetic) . gait.ekstremitas (intention tremor. limb.kepala.

. Comprehension is spared.Dysarthria Cerebellar disorders are typically associated with slow speech accompanied by slurring. Temporal dysregulation may lead to unintelligible words (Kent et al. taking a staccato rhythm and a nasal character . 1997). Speech may turn out to be explosive.

terputus-putus. artikulasi buruk. Gangguan sinergi otot-otot bicara. .  Pasien bicara pelan-pelan. penekanan abnormal dan datar di setiap suku kata.akibat lesi paravermis.

 Kegagalan fungsi cerebellum mengukur jarak ke target. bermanifestasi (misalnya) sebagai gerakan jari melewati lokasi target . .Dysmetria  Ketidakmampuan menghentikan gerakan terarah tepat pada waktunya.

Both forms of dysmetria are usually followed by corrective movements.Dysmetria represents an error in trajectory of movement.  Hypometria is less common..  Dysmetria affects both proximal and distal joints. . Patients presenting with chronic cerebellar disease display a worsening of dysmetria when the inertia of the limb is increased mechanically (Manto et al. Hypermetria is usually more evident during fast movements. 1994).

. terputus-putus. dan tidak berirama.Dysdiadokinesia gangguan gerakan bergantian secara cepat akibat kerusakan koordinasi ketepatan waktu beberapa kelompok otot antagonistik: gerakan seperti pronasi dan supinasi tangan secara cepat menjadi lambat.

Tremor postural ketika pasien mempertahankan tangan yang sedang pronasi tepat di depan. dengan lengan terangkat. bermanifestasi meningkat selama ketika mendekati target. .Tremor Intention tremor gerakan volunter.

resistensi otot terhadap gerakan pasif menghilang. Refleks otot intrinsik menghilang pada otot hipotonik.Hypotonia dan hyporefleks Pada lesi akut hemisfer cerebelli. postur abnormal (misalnya pada tangan). Refleks pendular .

.Lesi Vestibulocerebellum Gangguan fungsional lobus flokulonodularis atau nukleus fastigii: 1. Pasien tidak dapat memfiksasi tatapan pada obyek yang diam saat kepalanya bergerak. Pasien kurang dapat menempatkan dirinya pada lapangan gravitasi bumi. 2.

Heel-to-toe walking tidak dapat dilakukan. tapi akibat koordinasi respon otot-otot terhadap gravitasi yang salah . Ketidakseimbangan proprioseptif bukan karena mencapai defisiensi impuls kesadaran. menyerupai gaya berjalan orang yang mabuk.Disekuilibrium Astasia : sulit berdiri tegak Abasia : sulit berjalan Ataksia trunkal : Gaya berjalan pasien lebar-lebar dan tidak stabil.

Gangguan okulomotor. Jika pasien mencoba mengikuti objek yang bergerak dengan matanya. terjadi square-wave jerks. . yang terlihat oleh pemeriksa. Bila mata diarahkan ke tengah. Gaze-evoked nystagmus ketika mata bergerak ke sisi lesi serebellum dan menghilang bila pandangan dipertahankan ke sisi tersebut. rebound nystagmus. nistagmus Gangguan kemampuan mempertahankan tatapan terhadap objek diam atau bergerak.

yaitu berupa sentakan sakadik mata ketika menolehkan kepala. Individu yang sehat dapat menekan reflek ini dengan mempertahankan tatapannya pada sebuah objek. .Gangguan refleks vestibulo-okular.

Cara berjalan yang lebar dan tidak stabil. kecenderungan jatuh di sisi lesi. berdeviasi ke sisi lesi. .Lesi Spinocerebellum Spinocerebellum berfungsi mengontrol tonus otot dan koordinasi kerja kelompok otot antagonistik yang berpartisipasi pada postur dan gaya berjalan. Lesi lobus anterior dan superior vermis : ataksia stance dan ataksia gait (lebih berat).

Jika lesi terbatas pada bagian superior vermis: tes telunjuk-hidung dan tes tumit-lutut –tulang kering masih dapat dilakukan. .Ataksia stance terlihat dengan tes Romberg: Pasien berdiri dengan mata tertutup. dorongan ringan pada sternum akan menyebabkan pasien berayun ke depan dan ke belakang dengan frekuensi 2-3 Hz.

pemeriksa tiba-tiba menarik tangannya. Kerusakan berat pada eksekusi gerakan volunter. . lengan terayun memukul pemeriksa. gerakan pasien tidak dapat dihentikan. Manifestasi klinis selalu ipsilateral terhadap lesi penyebabnya.Lesi Serebrocerebellum Tidak menimbulkan paralisis. Rebound phenomenon Pasien menekan tangan pemeriksa dengan kekuatan maksimum.

abcess. Cerebellar hemispher syndrome comes from acute destructive lesion: infarct. trauma. immune mediated.Cerebellar Syndromes Rostral vermis syndrome result from alcoholism and nutritional deficiency. demyelinating. paraneoplastik. Caudal vermis syndrome implies a midline cerebellar neoplasm : medulloblastoma. ependymoma. . (vitamin E). Pancerebellar syndrome: vitamine defisiency. hemorrhage. hereditary. toxic or metabolic. astrocytoma. neoplasm.

Disturbances Generally symptoms of another disease Ataxia Failure to produce smooth intentional movements Gait Disturbance Inability to perform smooth coordinated gait May be described by patient as -Weakness -Dizziness -Stroke -Falling .

Pathophysiology Result from any condition that affects the central and peripheral nervous systems Ataxia: Types  Motor ataxia  Sensory ataxia .

Motor Ataxia Caused by cerebellar disorders Intact sensory receptors and afferent pathways  Integration of proprioception is faulty  Midline cerebellar lesions cause truncal ataxia  Lateral cerebellar lesions cause limb ataxia  Thalamic infarcts may cause contralateral ataxia with sensory loss  .

Sensory Ataxia Failure of proprioceptive information to the central nervus system May be due to disorders of spinal cord or peripheral nerves Can be compensated for by visual inputs .

Differential Diagnoses  Intoxication Ethanol  Sedative-hypnotics  Anticonvulsants   Hyponatremia  Cerebellar disorders  Tumor  Hydrocephalus  Cerebral vascular accidents  Inborn errors of metabolism  Parkinson’s Disease  Cervical spondylosis  Posterior column disorders  Peripheral neuropathy  Vestibulopathy  Disequilibrium of aging  Multiple Sclerosis  Thalamic disorders .

Commonly seen in PD .Definitions Best to use descriptive terms for gait disturbances Motor ataxia: wide-based with irregular. unsteady steps Sensory ataxia: abrupt leg movement and slapping impact of feet Festinating gait: narrow-based miniature shuffling steps.

Often a conversion disorder called astasia-abasia . sensory and cerebellar function. May be seen in NPH and PD Equine gait: high stepping gait due to peroneal weakness Functional gait disorder: unable to walk normally despite intact motor.Apraxic gait: difficult initiating gait.

History  Onset  Rapidity  Previous symptoms  PMH  Medications  Social Alcohol intake  Illicit drug use   Associated Symptoms Headache  Drowsiness  Dizziness  Vertigo  Tinnitus  Fever  Nausea/vomiting  Weakness  Paresthesia  .

Physical Exam Gait testing Tandem gait Full neurologic exam  Cerebellar function  Dysmetira  Dysdiadochokinesia Orthostatic VS  Dyssynergia  Stewart-Holmes rebound sign  Rhomberg .

slowing of corrective responses and weakness  Can also be present in other neurodegenerative diseases  Occurs in ~25% of elderly population  Treatment  Symptomatic  Usually admitted to rule out other life-threatening . reduced proprioception.Specific Populations  Geriatric Patient  Gait normally changes with age Shortened stride Widened base Slow gait  Senile gait may represent neuronal loss.

Vit B1 and dextrose  Most often need to be admitted .The Alcoholic Patient  Any gait abnormality in an alcoholic patient should raise concern about nutritional deficiencies  If acute ataxia is associated with confusion and eye movement abnormalities Wernicke encephalopathy needs to be considered  Still other intracranial pathology needs to be ruled out  Treatment  IV hydration.

but wobbly when sitting  Intoxications are most common.Differential diagnoses Children  May appear well. followed by infection/inflammation  Ask about family member home medications  PMH  PFH  Drug Intoxication  Infection or inflammation  Neoplasm  Trauma  Inborn errors of metabolism  Hydrocephalus  Idiopathic Disposition  Rule out life threatening processes  Most are admitted  Pediatric neurology consult .


Tipe Ataxia Simtom Vertigo Vestibular Ataxia Cerebellar Ataxia Sensory Ataxia + Possible _ Nystagmus + + _ Disartria _ Possible _ Ataxia extremitas Tes Romberg _ + + (only in legs) _ + (both with open and closed eyes) + (with closed eyes) .

General ataxia treatments Occupational therapy – to maximize use of the limbs and to maximize safety when walking and doing transfers Safety bars. communication assist devices Pneumovax and influenza vaccinations . gait assist aids or wheelchairs Weighted bracelets may improve hand control Speech and swallowing therapy – to improve communication and swallowing safety (especially to prevent choking and pneumonia).

refleks tendon dalam di ekstremitas bawah (-) . stereognosis. . Klinis: . diskriminasi 2 titik.romberg tes (+) .ataksia progresif tanpa diketahui penyebabnya.disartria dalam 5 tahun setelah onset.autosomal resesif . .gangguan sensasi posisi.Ataxia Friedreich Sebelum usia 20 tahun Hilangnya sel-sel ganglion radix dorsalis degenerasi kolumna posterior. .


kemudian diturunkan cepat. Gangguan sense of position. Romberg tes (+) Gangguan vibrasi Pupil argyll robertson.Tabes Dorsalis Degenerasi kolumna dorsalis dan dorsal root. kompensasi oleh visual. Sensory ataxia. serologi siphylis (+) . lutut pasien diangkat tinggi ketika berjalan.



. etc. hence. the motion of a plane in turbulent air. In the inner ear. motion sickness affects the sense of balance and equilibrium and.Motion Sickness Motion sickness is a very common disturbance of the inner ear that is caused by repeated motion such as from the swell of the sea. the movement of a car. the sense of spatial orientation.

and gravity). . and there is thought to be discoordination or conflict among the input from the three pathways. When there is unintentional movement of the body. acceleration. It is hypothesized that the conflict among the inputs is responsible for motion sickness.Motion is sensed by the brain through three different pathways of the nervous system that send signals coming from the inner ear (sensing motion. the brain is not coordinating the input. the eyes (vision). and the deeper tissues of the body surface (proprioceptors). as occurs.

.Infark serebellar Approximately 10% of patients with cerebellar infarction present with vertigo and no localizing neurologic deficits. The majority of these may have other signs of central vertigo. specifically direction-changing nystagmus and severe ataxia.

such as diplopia. or the posterior inferior cerebellar artery (PICA).3 % of acute strokes overall. and weakness or numbness. dysarthria. anterior inferior cerebellar artery (AICA).29  These can result from occlusion of the superior cerebellar artery (SCA). limb ataxia. . dysphagia.Cerebellar infarction represents approximately 2.  Larger cerebellar infarcts produce symptoms and signs localizing to the brainstem.

or limb coordination examination.Approximately 10% of patients with cerebellar infarction can present with isolated vertigo.  Most of these are infarcts of the medial branch of the PICA (96%). sensory. reflex. cranial nerve. . that is. vertigo with no localizing findings on motor.

vascular risk factors raise the prior probability of disease. two easily overlooked physical signs have been shown to indicate cerebellar infarction.First. usually reaching maximal intensity at once. 23. and an embolic source is found in 24–40%. stroke in general tends to present with the sudden and immediate onset of symptoms. Second. . Hypertension and cardioaortic diseases are found in the majority of patients with cerebellar infarction.29  Finally.

benigna.Tumor Cerebellum 1.rata-rata pada umur 9 tahun. . . kistik.25% tumor pediatrik. . .33% tumor fossa posterior pada anak.hemisfer vermis. . Cerebellar Astrocytoma .

Medulloblastoma .malignan .mendesak ventrikel ke 4  hydrocephalus .2.infratentorial .cerebellar hemisfer .

may be problematic in that they often grow quite large before producing symptoms. particularly in adults. because of the plasticity of the cerebellum. it is present in about 75% of affected children .Tumor cerebellum Benign cerebellar tumors Pilocytic astrocytoma. Papilledema. an indirect sign of an intracranial mass. may be lacking for a long time.

cerebellar tumors manifest themselves occipitocervical initially headache and with nausea and vomiting on an empty stomach (dry heaves). A forced head tilt is a clinical sign of impending herniation of the cerebellar tonsils through the foramen magnum .In most cases (90 %).

 It often arises from the roof of the fourth ventricle and then grows into the vermian portion of the flocculonodular lobe. .Medulloblastoma is a malignant tumor that preferentially affects children and adolescents and accounts for one-third of all brain tumors in this age group (8% of all brain tumors regardless of age).


Because this type of tumor often begins in the vestibulocerebellum. and intention tremor gradually arise as the tumor grows further and begins to affect the lateral portions of the cerebellum (the hemispheres). and staggering gait. In advanced stages of tumor growth. Further cerebellar manifestations including ataxia. . dysmetria. adiadochokinesia. blockage of the fourth ventricle or of the cerebral aqueduct causes occlusive hydrocephalus. its typical initial sign is dysequilibrium: the affected child has a broad-based. with clinical signs of intracranial hypertension. asynergia. swaying.

e.Acoustic neuroma (i. This tumor arises from the Schwann cells of the eighth cranial nerve (usually its vestibular portion) and is thus found in the cerebellopontine angle. vestibular schwannoma). ..


paralisis (berat).herniasi tonsil cerebellum ke foramen magnum.gejala klinik: nyeri kepala. . .kadang menimbulkan hydrocephalus noncommunicating akibat dari obstruksi aliran LCS. nausea. dizziness. . fatigue. sulit menelan. Arnold-Chiari . gangguan koordinasi. kelemahan otot wajah dan kepala.Malformasi Cerebellum 1.

Ada 4 tipe: 1. Tipe I  asimtomatik selama masa kanak-kanak.  Diagnosa dan terapi sulit . > 3 mm di bawah foramen magnum.  Herniasi tonsil cerebellar. kadang bermanifestasi dengan nyeri kepala dan gejala cerebellar.  Syringomyelia cervicothoracic spinal cord.

There is no syrinx in the cervical cord & the 4th ventricle is normal size & configuration .Sagittal MRI (T1) shows cerebellar tonsils 2-3 cm below foramen magnum. where the CSF space is narrow.

Tipe II  tonsilar herniation di bawah foramen magnum  displacement luas dari vermis  Lumbar myelomeningocele .2.

Chiari II (Arnold-Chiari Cerebellar tonsillar herniation Small posterior fossa Extension of medulla below foramen magnum Kinking of medulla (Z-formation) Beaking of the quadrigeminal plate Hydrocephalus Myelomeningocele .

cerebellum dan batang otak di dalam fossa posterior.gangguan perkembangan cerebellum.jaringan neuroectodermal abnormal. Tipe III . . Tipe IV .3. .occipital encephalocele. 4. tapi tidak berhubungan dengan foramen magnum. .

Dandy-Walker Malformation Dandy-Walker syndrome Agenesis of cerebellar vermis cystic dilatation of 4th venticle enlargement of posterior fossa Variable clinical manifestations Hypothesized to result from arrest of cerebellar development prior to the 3rd month .


Joubert syndrome
Clinical manifestations include episodic hyperpnea, ataxia,

eye movement abnormalities, hypotonus, and retardasi
Agenesis of vermis, cystic dilatation of 4th venticle (but

less than DWS)
Microscopically normal cerebellar cortex with numerous

subcortical heterotopias

Pemeriksaan Cerebellum

Adakah goyangan ketika berdiri. . Pasien berjalan melalui garis lurus. Untuk mengkompensasi ketidakstabilan dari cara berdiri dan cara berjalan. Amati adakah kecenderungan ayunan ke salah satu sisi.Pemeriksaan Cerebellum Cara berjalan (gait) dan berdiri (stance) Inspeksi pasien saat berdiri. cerebellum memerintahkan berdiri dan berjalan dengan melebarkan kedua kaki. juga cara berjalan dystaxia. Dengan jalan tandem.

Amati adakah postural tremor. Interpretasi: Bila muncul tremor ketika mendekati hidung disebut intension tremor. Pasien diperintahkan untuk meluruskan kedua lengan secara horisontal. kemudian menggerakkan jari telunjuk ke ujung hidung. . Tes telunjuk-hidung Pasien disuruh meluruskan salah satu lengan. 2. Dan bila pasien gagal menyentuh hidung secara tepat.Pemeriksaan Cerebellum Dystaxia lengan 1. disebut dysmetria.

.  Ulang pemeriksaan 3 kali bila hasil meragukan.Pemeriksaan Cerebellum  Lakukan tes tumit-tulang kering di ekstremitas bawah.

Pasien disuruh melakukan gerakan yang berlawanan secara cepat.Pemeriksaan Cerebellum Dysdiadokinesia Adalah gangguan koordinasi otot selama gerakan cepat. . Misalnya pronasi dan supinasi.

Pemeriksaan cerebellum .

Kemudian meluruskan lengan. Interpretasi: normal bila lengan pasien kembali ke posisi semula secara cepat. Pemeriksa berkata kepada pasien bila pemeriksa akan menekan salah satu lengan. Pasien diminta menutup mata.Pemeriksaan cerebellum Overshooting test 1. Pasien disuruh menahan. .


Rebound sign of Holmes . .interpretasi: normal: lengan pasien berayun dengan jarak minimal. .kemudian tangan pemeriksa dilepaskan tibatiba’ . dan kembali ke posisi semula.pemeriksa memegang pergelangan tangan pasien.pasien menggenggam erat tangan pemeriksa. .

Pemeriksaan Cerebellum .

trauma. serebellitis. visuo-spasial. dysplasia dan hipoplasia. stroke serebellar.  Causa: cerebellar agenesis. dan penyakit neurodegeneratif. .Cerebellar Cognitive Affective Syndrome Simptom : Gangguan fungsi eksekutif. perubahan emosi dan kepribadian. tumor. bahasa.  Derajat keparahan CCAS tergantung lokasi dan perluasan lesi.

Cerebellum berhubungan dengan regulasi emosi.Cerebellar Cognitive Affective Syndrome Fungsi cerebellum adalah bertanggungjawab regulasi motorik. Area kognitif di cortex cerebri yang berproyeksi ke cerebellum: 1. working memory. Gyrus temporal superior (bahasa) 3. 2. Asosiasi visual 5. judgement) . Cortex parietal posterior (spatial awareness). Cortex prefrontal (atensi. Area parahipocampal superior (spatial memory) 4. kognitif dan emosional behaviour.

inappropriate behaviors Language disorders Agrammatism.Cerebellar Cognitive Affective Disorder Lesions of the posterior cortex and vermis Impairment of executive functions Planning. abstract reasoning Difficulties with spatial cognition Visuo-spatial organization. verbal fluency. disprosodia . visual memory Personality changes Blunting of affect.


and non-associative learning .The cerebellar circuits are involved in many aspects of memory. priming and perceptual learning. This latter includes procedural learning (skills and habits). basic associative learning (including simple classical conditioning of emotional and skeletal muscle responses). in particular. in nondeclarative memory.

Psychiatric Aspects of Cerebellar Disorders (1) Cerebellar Cognitive Affective Syndrome (2) Anatomically Specific Psychiatric Aspects of Cerebellar Disorders (3) Other Psychiatric Aspects of Cerebellar Disorders .

anhedonia and aggression . cerebellar tumour resection. etc can cause motor impairments plus the following (Schmahman et al. 2007. perseveration.1. 1998). congenital cerebellar malformations. 2007. acquired lesions. dysprosodia. in visual memory and visuo-spatial organisation Linguistic dysfunction e.g. lack of empathy.g.  Cerebellar lesions in general e.g. Tavano et al. in working memory and planning Visuo-spatial abnormalities e. ruminativeness. Cerebellar Cognitive Affective Syndrome (Schmahman & Shermen. agrammatism and anomia  Affective impairments:  anxiety.g. 2000)  Cognitive impairments:    Executive dysfunctions e. Levisohn et al. depression. lethargy.

2008). . Autism & abnormal motor development (Tavano et al.(2) Anatomically Specific Psychiatric Aspects of Cerebellar Disorders Vermal Agenesis > severe LD. executive functions and theory of mind (Garard et al. 2007). Vermal lesions > affective and relational disorders (Schmahman et al. 2007). Spinocerebellar Ataxia > impairment in attention. memory.

(3) Other Psychiatric Aspects of Cerebellar Disorders:(Wolf et al. 2007) .

 Assessment:
 (1) Motor disorders in psychiatric disorders

as signs of cerebellar dysfunctioning
 (2) Non-motor symptoms equivalent to
motor symptoms related to cerebellum
 Treatments:
 (3) Cerebellar exercises
 (4) Transcranial Magnetic Stimulation (TMS)
 (5) Routine disorders

The localizing significance of nystagmus is often a

mere indication of dysfunction somewhere in the
posterior fossa (i.e., vestibular end-organ, brain
stem, or cerebellum). However, certain nystagmus
patterns are quite specific and permit reasonably
accurate neuroanatomic diagnosis. When
possible, the specific and nonspecific forms are
separated on the basis of clinical appearance and
associated signs and symptoms.

Downbeat nystagmus is defined as nystagmus

gaze position with the fast phase beating in a
downward direction. Patients with brain stem
disease or drug intoxications usually lack gazeevoked downward nystagmus despite nystagmus
in all other fields of gaze. Thus, nystagmus
beating downward in the primary position is a
striking phenomenon and is highly suggestive of a
disorder of the craniocervical junction, such as
Arnold-Chiari malformations

usually of the brain stem. The location of the lesions in patients with upbeat nystagmus after meningitis. With convergence. or organophosphate poisoning is uncertain. .Upbeat Primary-position nystagmus with the fast phase beating upward rarely reflects drug intoxication. Most often. Wernicke's encephalopathy. the nystagmus is acquired and indicates structural disease. upbeat may enhance or convert to downbeat.The slowphase waveform is usually linear but may be an increasing-velocity exponential.

upbeat. pharmacologic. toxic  Downbeat. CENTRAL VESTIBULAR NYSTAGMUS PERIPHERAL Severe vertigo Days to weeks duration Hearing loss. tinnitus associated Usually horizontal with torsion Very rarely purely vertical or torsional Dampened with visual fixation Commonly peripheral vestibular organ dysfunction: labyrynthitis. torsional . demyelination. meniere’s CENTRAL  None or mild vertigo  Often chronic  May be purely vertical or torsional  visual fixation usually has no effect  Etiologies commonly vascular.PERIPHERAL VS.

stroke.miscalibration between pulse and step inputs  Symmetric  cerebellar flocculus implicated  Age.Gaze evoked nystagmus: One of the most common forms of central nystagmus  Inability to maintain eccentric gaze  “leaky integrator” -. anti-convulsant therapy. demyelination  Baclofen effective  . alcoholic degeneration.

clonazepam. base-out prisms  .Downbeat nystagmus: Defect in vertical gaze holding  Asymmetric inputs from vertical semi-circular canals produce upward slow drift of eyes  Defect in fastigial nuclei calibration  Secondary downward corrective fast phase  Obeys Alexander’s law  Localizes to cervico-medullary junction  Arnold-Chiari malformation  Treatment with baclofen.

toxic exposures  Periodic alternating nystagmus: Horizontal oscillation characterized by a periodic reversal in the direction of nystagmus due a shift in the null point  Duration of cycles from 30 seconds to 6 minutes  Classically a lesion of the cerebellar nodulus  MS. drugs. paraneoplastic syndromes  Baclofen effective  .Upbeat nystagmus: Present in primary position or upgaze  Classically localizes to a lesion of anterior cerebellar vermis  More generally implicates posterior fossa disease  Etiologies include stroke. cerebellar degeneration. demyelination. ethanol.

large amplitude  nystagmus on ipsilateral gaze (fast phase  toward lesion)  shift from eye movement response to  vestibular imbalance to that of defective  gaze holding . Bruns nystagmus:  associated with CPA tumors  high frequency. low amplitude  nystagmus (fast-phase away from lesion)  low frequency.

incoordinated saccadic excursions with high frequency. ovarian.See-saw nystagmus: Disconjugate vertical nystagmus (pendular vs. jerk)  Upward moving eye intorts while downard eye extorts  Localizes to lesions of diencephalon  Visual fields may be useful (disruption of afferents to cerebellum)  Ocular flutter/opsoclonus: Burst-like. breast CA  Neuroblastoma in children  . low amplitude  No intersaccadic latency  Purely horizontal: ocular flutter  Multiplanar: opsoclonus  Reflect pause cell dysfunction (pons)  Must consider paraneoplastic etiology: SCC of lung.

c poor nutrition (AIDS.hyperemesis gravidarum. axonal conduction. thyrotoxicosis. DNA synthesis .Wernicke’s Syndrome Akut Abnormal eye movements Ataxia Confusion Causa : defisiensi thiamin e. synaptic transmission.CHF with longterm diuretic therapy) Reduced cerebral metabolism.