Layers Of The Cerebellar

Layers of the cerebellar    Molecular layer: o Basket and stellate cells. o Parallel fibres running perpendicular to dendrites of Purkinje cells. Purkinje cell layer: o Single layer of Purkinje cell bodies. o Receive input from climbing fibres. o Have an extensive network of dendrites that fan up into the molecular layer. Granule cell layer: o Granule and Golgi cells. o Input from mossy fibres. Cellular interaction  The Purkinje cell is the main cell for output, and is tonically inhibited.  It receives extensive input from deeper nuclei; input coming from mossy fibres and climbing fibres.  Mossy fibres: o Indirect connection from precerebellar nuclei; first synapsing at granule cells. o The axons of granule cells run parallel to those of Purkinje cells before entering the molecular layer.    o However, once inside the layer, they bend and run perpendicular. o Weak excitation (~1 million G cells/P cell). Climbing fibres. o Direct connection from inferior olivary nucleus cells. o Powerful excitation (1 climbing fibre/1 – 10 P cells). Inhibitory cells: basket stellate, Golgi and Purkinje cells. Excitatory cells: granule cells. Functional divisions   Each region has a distinct function with distinct inputs/outputs. Vestibulocerebellum. o Located in the flocculonodular lobe. o Input: vestibular apparatus, vision. o Output: to vestibular nuclei; alters activity in vestibulospinal, rubrospinal and corticospinal tracts. o Role: body equilibrium/movement during stance and gait. Also, automatic eye movements (vestibular-ocular reflex). o Damage: disturbances of equilibrium (wide based stance and ataxic gait), nystagmus. Symptoms are absent when patient lying down.  Spinocerebellum. o Arranged somatotopically. o Input: peripheral sensory receptors (via spinocerebellar tracts) and cerebral cortex. o Output: fastigial and interposed nuclei; alters activity in rubrospinal and corticospinal tracts. o Role: controls proximal and distal musculature, respectively. o Damage: hypotonia, dysmetria (inaccurate reaching), ataxia (uncoordinated movement), terminal tremor (tremor near target, none when resting), hyperreflexia. o Terminal tremor can be explained because role of cerebellum is to modulate intention and execution of action. If cerebellum is affected, there will be overshooting and undershooting during motion.  Cerebrocerebellum. o Lateral hemispheres – newest cerebellar region. o Input: exclusively from cerebral cortex via pontine nuclei. o Output: dentate nucleus to cortical motor and premotor regions, and red nucleus. o Role: planning/initiating movements, rehearsal of movements, timing of movements, disruption of agonist-antagonist bursts in rapid movements, hypermetria, terminal tremor. o Damage: problems with timing and initiation movements. Cerebellar movement disorders  Impaired balance.  Impaired coordination.  Decreased muscle tone.  Does not result in impairment of sensation or muscle strength, however, affects motor output indirectly.  Typical signs of cerebellar damage: o Hypotonia – decreased resistance to passive movement, pendular reflexes. o Lack of check – slow corrective movements. o Ataxia – lack of muscle coordination, delay in initiating movements, errors in range and force of movement (dysmetria, dysdiadochokinesia), problems with multijoint movements. o Intention tremor – during movement, particularly at endpoint. o Dysarthria – slurring. o Gait impairment – wide-based stance, ataxic gait. Alcoholism can affect vermis. Summary of cerebellum      Five types of cells, three types of layers. Divided into three functional zones, each with specific inputs and outputs. Receives and compares information about intended movements and actual movements, using these to correct ongoing movements which result in long term changes as well (motor learning). Involved in a wide variety of motor tasks including: equilibrium, eye movements, muscle tone, coordination of multi-joint movements initiation of movements, timing of movements, learning of movements. Damage can be identified by specific clinical tests.