Twelve Flashcards
What is the primary function of the cerebellum? What does each part primarily control?
The primary function of the cerebellum is to synchronize the activity of neurons in the cortex and brainstem motor centers for commanding lower motor neurons that result in muscle contractions resulting in coordinated voluntary movements. The three major anatomical subdivisions of the cerebellar cortex closely correspond to functional
subdivisions each controlling different types of voluntary movements. The flocculonodular lobe or vestibulocerebellum largely regulates postural movements. The anterior lobe or spinocerebellum mainly controls stereotype/automatic movements such as locomotion. The posterior lobe lateral hemisphere chiefly controls multi-joint, highly skilled, rapid movements.
What are the two principal afferent paths to the cerebellar cortex? What kind of information do they transmit? What happens with simple and complex spikes as motor learning is achieved? What is Long term Depression?
The two principal afferent paths to the cerebellar cortex transmit disparate types of information. The mossy fiber system transmits information about commands for upcoming movements (cerebro-ponto-cerebellar) and ongoing movements (spinocerebellar, vestibulocerebellar) whereas the olivocerebellar climbing fiber systems transmits information largely about deviations from expected movements or movement errors. Learning a new motor task has been correlated with changes in simple spike (evoked by mossy fiber activation of granule cells and granule cell/parallel fiber activation of Purkinje cells) and complex spike (olivocerebellar/climbing fiber activation of Purkinje cells) activity.
Correlated behavioral and electrophysiological studies in sub-human primates have elucidated the functional significance of the mossy and climbing fiber afferent pathways (Fig. 1). Perturbation of a smoothly performed learned movement (arrow A, C and D) results in the loss of coordination in subsequent movements (A) and a change in recorded simple and complex spike activity (C, D). Simple spike activity is depressed and complex spike activity is increased (D). As the subject adapts to the perturbation and learns again how to move the handle in a smooth or coordinated manner; complex spike activity returns to normal but simple spike activity remains depressed. The reduction in simple spike activity is identified as long-term depression (LTD). Different studies examining long-term depression identified the physiological basis for LTD as resulting from a decrease in postsynaptic responsiveness of Purkinje cells to those parallel fiber inputs temporally coactive with climbing fiber evoked activity. Long-term depression is an example of the plasticity of parallel fiber – Purkinje cell synapses. A similar form of plasticity can be seen in humans while performing a skilled movement (Fig. 2).
What are the two types of axons synapsing on cerbellar nuclear neurons? What normally inhibited and what is normally excited?
The result of cortical processing of sensory afferent information is transmitted to the cerebellar nuclei by Purkinje cell axons in corticonuclear projections. Cerebellar nuclear neurons are excited by glutaminergic afferent collaterals and inhibited by gabaergic Purkinje axons (Fig. 3). Normally, activity in nuclear neurons inappropriate for a desired movement or posture is selectively inhibited whereas neurons needed for guiding a required movement are selectively excited.
What are 4 general principles of cerebellar pathophysiology?
Midline Cerebellar Lesions Result in Bilateral Axial
and Proximal Movement Ataxia
Lateral Cerebellar Lesions Result In Ipsilateral Distal
Movement Ataxia
Chronically Developing Cerebellar Pathology Delays
the Onset of Cerebellar Signs
Acute Cerebellar Trauma Results in Immediate Onset
of Cerebellar Signs that May Diminish In Severity
What is truncal ataxia? What can and cannot patients do? What causes it?
Damage to the vermis and or the flocculonodular lobe results in a patient’s inability to maintain a posture while standing or in response to sudden perturbations to the body’s center of gravity. When patients with trunkal ataxia are posturally supported they are capable of performing normal skilled movements of the limbs.
Describe gate ataxia? What causes it? What does normal gait require?
Gait Ataxia
Damage to the anterior lobe (spinocerebellum) results in gait ataxia. Normal gait requires balance (postural) and locomotor (rhythmic stepping) movements. Following
degeneration of Purkinje cells in the anterior lobe body sway is increased in the anterior – posterior direction (Fig. 4) and the trunk jerks side to side and as a result the stance is supported by an abnormally wide spread of the feet. Locomotion is similarly characterized by shortened stride length, exaggerated stride width, and irregularities in
progression.
What is limb ataxia? What causes it? What is cerebellar hypotonia like?
Injury to the lateral cerebellar hemisphere, the dentate nucleus or its efferent projections results in the loss of coordination of highly skilled movements.
Intention tremors occur during the performance of limb movements and are characterized by 4-7 Hz oscillations that are exaggerated in proximal limb musculature near or at the termination of a limb movement (Fig. 5). Tremor is most commonly observed with damage to the cerebellar nuclei or their efferent projections.
Hypotonia occurs acutely following cerebellar damage and is most evident in proximal limb musculature. Cerebellar hypotonia is transient with the rapid return to normal muscle tone. Muscle strength is unaffected.
What is dysmetria? What are the two different types? What are they caused by? What is the rebound phenomenon? What happens in
Dysmetria is characterized by errors in movement trajectory that may be either hypometric (premature ending of movement) or hypermetric (overshooting) (Fig. 5). Normal movements are characterized by an initial burst of activity in agonist muscles, a later overlapping burst in antagonist muscles and finally a second burst in the agonist muscles. Hypermetric movements are caused by the delay in the braking of the movement by agonist muscle activity resulting in past-pointing. This late activation of antagonist muscles is observed most dramatically in the rebound phenomenon. More infrequently seen hypometric movements result from insufficient initial activation of agonists.
What is asynergia and dyssynergia?
Asynergia (lack of synergy) or dyssynergia (diminished synergy) of movements is characterized by the decomposition of complex (multi-joint) movements into their elementary single joint components. Movements become slowed because, instead of a smooth and sequential sequencing of a series of single joint movements into a complex motor action, movements at different joints need to be consciously controlled and
executed separately.
What is dysdiadochokinesia?
Dysdiadochokinesia is characterized by the patient’s inability to perform rapid alternating movements such as pronation/supination of the forearm, or rapid pinching movements of a finger (Fig. 7). These movements are both dysmetric and dyssynergic in execution.
What is dysarthria?
Dysarthria is an alteration in speech production characterized by either slurred or explosive speech. Speech comprehension and formulation are not impaired. It is a decomposition of speech.
What will damage to the vestibulocerebellum result in? What 5 symptoms of cerebrocerebellar syndrome? What are 2 general symptoms and 2 subsymptoms of spinocerebellar syndrome? Where does damage occur to cause all these things?
Postural or Trunkal Ataxia (very bad)——–Intention Tremor :Dysmetria – Abnormal range of movement : Dysdiadochokinesia – rapid alternating movements : Force of Muscle Contraction – rebound phenomena : Decomposition of Complex Movements———————–Gait Ataxia – Lower Limb Areas of Anterior Lobe
• Wide-based gait
• Staggering/Swaying of Lower Body
Trunkal Ataxia – Vermis of Anterior Lobe
• Instability when standing on balls and toes of feet
• Instability when tandem walking
