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Cerebellum
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- 2. Gross appearance ofthe cerebellum Posterior view Inferior view 2
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- 4. Radiographic anatomy: MRI SAGITALSECTION AXIAL SECTION 4
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- 6. of Cerebellum inEmbryo 6
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- 8. Gross Anatomy ofCerebellum • Cerebellum consists of two cerebeller hemispheres joined by a narrow median vermis. • Three bundles of nerve fibers connect the cerebellum to the brain stem - - Superior (midbrain), - Middle(pons) & - Inferior cerebellar peduncle (medulla ) 8
- 9. Gross Anatomy: cerebellum Cerebellum Surface HemisphereVermis Grey Matter Cerebellar cortex Deep Neuclei WhiteMatter 1.Arbor vitae 2.Peduncle 9
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- 12. ARBOR VITAE –TREEOF LIFE 12
- 13. 1. Vestibulocerebellum orarchiecerebellum 2. Spinocerebellum or paleocerebellum 3. Cerebrocerebellum or pontocerebellum or neocerebellum. Phylogenetical Division:cerebellum
- 15. 1. Cortex ofvermis: influences movements of the long axis of the body – neck, shoulders, thorax, abdomen, hips. 2. Intermediate zone: (Just lateral to vermis) controls distal parts of the limbs hands and feet. 3. Lateral zone: planning of sequential movements of conscious assessment of movement errors. Functional Division: Cerebellum
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- 17. Structure of theGrey Matter: Cortex • Layers of cortex: 1.External molecular layer 2.Middle granular layer. 3.Internal Medullary layer 17
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- 21. Cerebellar Cortical Mechanism •Purkinje cells form the center of a functional unit of cerebellar cortex. • Climbing fibers-terminal fibers of olivo-cerebellar tract. Excitatory effect on Purkinje cells. • Mossy fibers-terminal fibers of all other cerebellar afferent tracts. Diffuse excitatory effect on Purkinje cells. • Stellate, basket and Golgi cells- inhibitory interneurons. Influence the degree of Purkinje cell excitation by climbing and mossy fibers. 21
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- 23. FROM SPINAL CORD: Afferenttracts 1. Anterior Spinocerebellar tract 2. Posterior Spinocerebellar tract 3.Cuneo-cerebellar tract. 23
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- 26. FROM VESTIBULAR NUCLEI: Afferent +Effrent tract 26
- 27. Cerebellar Efferent Fibers •Globose-Emboliform-Rubral pathway • Dentothalamic pathway • Fastigial Reticular pathway • Fastigial Vestibular pathway 27
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- 30. PHYLOGENETIC ANATOMICAL and FUNCTIONAL ROLE Archicerebellum/ Vestibulocerebellum FloculonodularLobe Adjacent Vermis Regulate Balance and Eye Movements Paleocerebellum/ Spinocerebellum Vermis Paravermal Zone Regulate Body and Limb Movement. Able to elaborate proprioceptive Input in order to anticipate future position of the body during course Neocerebellum/ Cerebrocerebellum Lateral Part of Cerebellar Hemisphere Planning and Initiation Movement. Functions of the Cerebellum 30
- 31. • Arterial supply: -Superiorcerebellar artery<Distal Bacillar Artery -Anterior inferior cerebellar artery<proximal Bacillar Artery -Posterior inferior cerebellar artery<Vetebral Artery • Venous drainage: -Supirior and Inferior Cerebellar vein -Adjacent venous sinuses. Blood Supply of Cerebellum 31
- 32. Blood Supply ofCerebellum 32
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- 35. APPLIED PART OFCEREBELLUM 35
- 36. Cerebellar diseases- • Vascular:ischemia or hemorrhage • Infective: pyogenic abscess,tubercular abscess etc • Traumatic: SDH, EDH,Contusion etc • Autoimmune: autoimmune cerebellar atrophy • Metabolic: Hypoxia • Inflammatory: MS • Neoplastic: primary: medulloblastoma Secondary: metastasis Congenital & others: DWM,Chiari malformations,SCA etc.
- 37. HYPOTONIA Floppy joint Loose Joint Lossof Resistance to Passive Movement Pendular Knee Jerk DIEQUILIBRIUM Loss of Balance Truncal Ataxia Ataxic Gait DYSYNERGIA Dysarthria: Scanning Dystaxia/Ataxia:Gait,Trunk, Leg,Arm Dysmetria:Past-Pointpointing Intention Tremor:During Voluntary Movement Dysdiadokinesia:faiure to Perform Rapid Alternate Movements Nystigmus Rebound Phenomenon Signs& symptoms of cerebellar disease 37
- 38. Cerebellar Lesion 38 Anterior Vermis Syndrome Atrophy ofRostral Vermis Lower limb Region of anterior Lobe Trunk Ataxia Ataxic Gate Cause: Alcohol Abuse Posterior Vermis Syndrome Floculonodula r Lobe Trunk Ataxia Cause: Meduloblastoma Ependymoma Hemispheric Syndrome Unilateral hemispheric Involbement Arm,Leg Ataxia Gate Ataxia Cause:Tumor, Abscess Cerebellar Atrophy Friedreich Ataxia OPCA(Olivopo ntocerebellar Atrophy Tumors Astrocytoma Medulloblastoma Ependymoma
- 39. APPROACH TO THEPATIENT WITH ATAXIA: 39
- 40. ATAXIA Symmetrical/Bilateral Gradually Progressive Genetic, metabolic,immune or toxic etiology. Focal/Unilateral Impaired Consciousness Ipsi:Cranial nerve Palsy Contra:Limb Weakness Vascular lesion ICSOL Duration Acute:Hours to days Subacute: Weeks to Months Chronic:Months to Years 40
- 41. ETIOLOGY:CEREBELLAR ATAXIA Symmetrical AndProgressive Signs ACUTE SUBACUTE CHRONIC Intoxication: Alcohol,Li, Barbiturates Intoxication: Mercury,Glue, Cytotoxics Paraneoplastic Hypothyroidism Acute Viral Cerebritis Post-Infectious Alcoholic Nutritional (B1,B12def) Lyme disease Tabes Dorsalis Phenytoin Amiodarone 41
- 42. ETIOLOGY:CEREBELLAR ATAXIA Focal andIpsilateral Signs ACUTE SUBACUTE CHRONIC Infraction Hemorrhage Subdural hemtoma Neoplastic: Glioma or Metastatic Demyelinating: MS Stable gliosis Secondary to vascular lesion Or demyelinating plaque Infection: Cerebellar abscess AIDS-related Multifocal Leukoencephalopathy Congenital: Dandy-Walker Malformation, Arnold Chairi Malformation 42
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- 48. Dandy Walker syndrome(DWS) D:DialatedLateral,third ventricle W:Water:Cystic dialation of 4th Ventricle S:Small: vermis, Cerebellum 48
- 49. • These are– Autosomal dominant - Autosomal recessive -Mitochondrial inheritence • Clinical manifestation dominated by cerebellar signs but there are changes in -basal ganglia –spinal cord – Optic nerve- Retina – Peripheral nerves • Rarely dementia is present. INHERITED ATAXIAS: 49
- 50. • Begins inadult life. • Occurs in each generation of pedigree. • SCA type 1 to SCA type 28, episodic ataxia type 1&2. • Clinical phenotypes overlaps. • Genetic analysis is the gold standard for diagnosis and classification. AUTOSOMAL DOMINANT ATAXIAS 50
- 51. • Begins inchildhood or early adulthood. • Parental consanguinity of marriage is more likely but not essential. • Examples: Friedreich’s ataxia. Ataxia with isolated Vit-E deficiency. AUTOSOMAL RECESSIVE ATAXIAS 51
- 52. • Mutation inmaternal mitochondrial DNA • E.g.- MERRF syndrome ( Myoclonic epilepsy with ragged red fibres ). MELAS ( Mitochondrial myopathy, encephalopathy, lactic acidosis & stroke like episodes ). Kearns-Sayre syndrome. MITOCHONDRIAL ATAXIAS 52
- 53. • Findings- reflexesnormal but knee and ankles are lost, planter bilateral extensor. • Mild dementia • Sphincter disturbance • Summary: Ataxia Ophthalmoparesis Pyramidal and extrapyramidal features. SCA 1 53
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- 55. SCA1 (OPCA) MRI findings: -Atrophyof cerebellum -Marked shrinkage of ventral pons -Disappearance of Olivary eminence of medulla. 55
- 56. • Most commonhereditary ataxia • Presents before the age of 25yrs • Primary sites of pathology – Spinal cord, dorsal root ganglia, peripheral nerve and cerebellum • Neurological- nystagmus, optic atrophy, deep tendon reflex absent, planter b/l extensor. • Skeletal deformity- scoliosis, pes cavus • Presentation: Progressive staggering gait, frequent fall and titubation. FRIEDRIECH’S ATAXIA: 56
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- 58. • METASTASIS: In adultsmetastasis is the most common tumor. • Primary sites: -Bronchus - Breast -Thyroid -Stomach -Kidney -Prostate -Testes -Melanoma CEREBELLAR TUMORS 58
- 59. A)Hemangioblastoma: -Commonest tumor inadult -More in male -Benign tumor of vascular origin -Association: Polycythemia PRIMARY CEREBELLAR TUMOR: 59
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- 61. B) Medulloblastoma: -Primitive neuroectodermaltumor -Occurs in childhood -Peak age of onset is 5yrs of age -Highly malignant tumor -Arise in vermis and extend into 4th ventricle -Presentation- truncal ataxia, raised ICP, visual loss. - Treatment: Surgery, radiotherapy. 61
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- 63. C)Cerebellar Astrocytoma: -It islow grade in nature in contrast to astrocytoma of cerebral hemisphere. D) Ependymoma: -Arises from ependymal cells E) CP angle tumor: - Acoustic neuroma - Meningioma 63
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- 65. C-P angle tumor: •Vestibular schwannoma • Meningioma • Metastasis • Neurofibroma • Epidermoid
- 66. • Rapidly progressivecerebellar syndrome. • Associated with- - Ca. breast -Ca. ovary -Small cell lung ca of lung -Lymphoma • MRI of brain shows cerebellar atrophy. • Tumor markers: -Anti yo Ab – ovarian ca -Anti Hu Ab – SCLC -Anti ri Ab – Ca. breast PARANEOPLASTIC SYNDROME 66
- 67. • Investigations: -Neuroimaging (MRIof brain) -Thyroid function test -VDRL -CSF study -Vit B12, Vit E level -Anti Gliadin Ab -Anti GAD Ab -Anti Yo Ab, Anti- Hu Ab, Anti-Ri Ab -Genetic analysis 67
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