Eleven Flashcards
How do the cerebellum and basal ganglia control voluntary movements (where do their efferent pathways go)? What happens to voluntary movements if they’re damaged. Where do more significant BG and cerebellar projections do? Less significant? What is one of the largest nuclei in the the thalamus that BG and cerebellar projections target? Which part do BG target? cerebellar?
The cerebellum and basal ganglia control voluntary movements indirectly through their actions on descending cortical and brain stem command motor pathways. Accordingly, when the cerebellum or basal ganglia are damaged, voluntary movements are not lost but become abnormal. Some efferent projections from the basal ganglia and cerebellum are directed to brainstem motor centers that control posture and stereotype movements.
More significant basal ganglia and cerebellar projections target thalamic nuclei constituting the “motor” thalamus.
One of the largest nuclei in the thalamus is the ventral nucleus. The ventral nucleus can be further subdivided functionally and anatomically based on the relative spatial location of the subdivisions. For example, pathways transmitting somatosensory information terminate posteriorly in the ventral nucleus (ventral posterior nucleus) and will be considered later. Cerebellar and basal ganglia projections terminate in ventral nuclei located lateral and anterior to the ventral posterior nucleus. The ventral lateral nucleus (VL) is the principal target for cerebellar projections whereas the ventral anterior nucleus (VA) receives projections chiefly from the basal ganglia.
Where do striatal neurons with D1 DA receptors project? For which pathway? D2 DA receptors? Do Indirect and Direct pathways work together?
Striatal neurons with D1 dopamine receptors project in the direct pathway to the medial pallidum whereas other striatal neurons have D2 receptors and project in the
indirect pathway to the lateral pallidum.
Normally parallel direct and indirect basal ganglia circuits work together to enable desired movements to occur (direct) and inhibit undesired competing movements
(indirect).
What are 2 types of disorders that can affect the BG pathways and how do they manifest?
Neurodegenerative
• Temporally Protracted
• Progressive in Severity of Deficits
• Bilateral Manifestation
Vascular
• Sudden Onset
• Gradual Diminution of Deficits
• Unilateral Manifestation
What are some clinical manifestations of BG damage? What are positive signs called? Which pathway is involved? What are 4 examples of positive signs? Which pathway is involved in Negative signs? What are 2 examples of Negative signs?
Positive Signs - Dyskinesia (Indirect Path )
Abnormal Involuntary Movements and Muscle Tone • Tremor • Chorea/Athetosis • Ballismus • Rigidity • Postural Instability
Negative Signs (Direct Path)
• Akinesia – Absence of Movements
• Bradykinesia – Slowness of Movements
What are the signs and symptoms of Parkinsons Disease? What is it caused by? Explain the signs and symptoms?
• Akinesia / Bradykinesia – Shuffling Gait, Stooped Posture • Rigidity All Muscles Hypertonic – Cog Wheeling • Tremor at Rest • Postural Instability
The temporally progressive degeneration of dopaminergic neurons in the substantia nigra pars compacta results in Parkinson disease and the following clinical signs: 1) tremor at rest, 2) bradykinesia/akinesia, 3) muscle rigidity and, 4) postural instability. There is considerable variability in presenting symptoms of Parkinson disease in patients due to the progressive course of the disorder and possible involvement of other neural systems.
At rest tremor is characterized by the 4-5 Hz oscillations generally of the extremities, but also the eyelids, mouth and/or tongue. The tremor disappears with onset of movement and return after the movement is completed (at rest tremor). The pathophysiological basis for at rest tremor is not known.
Bradykinesia or slow movements are characterized by diminished agonist muscle activity and excessive antagonist muscle activity during the movement. Akinesia is the absence of movements suggesting an inability to initiate or a delay in initiation of movements. Movement initiation in Parkinson disease is more likely the result of the loss of dopaminergic input to the prefrontal, premotor and motor areas of the cerebral cortex.
Muscle rigidity or lead pipe rigidity is characterized by increased resistance to muscle stretch in both agonist and antagonists muscles. Lead pipe rigidity is different from the
hypertonicity seen following damage to the pyramidal system. In spasticity the increased in muscle tone builds with the speed of passive movement and is localized to antigravitymuscles (flexors in the upper limb and extensors in the lower limb). Cogwheel rigidity is typical of Parkinson patients where ratchet-like interruptions of the rigidity are observed with movements at the wrist and elbow joints. The interruptions appear correlated with tremor.
Postural instability and falling while standing is due to the inability to rapidly activate postural reflexes.
What causes Huntingtons Chorea? What are the signs and symptoms?
Huntington chorea is an autosomal dominate neurodegenerative disease resulting from the death of medium spiny neurons in the striatum. Early stages of the disorder are characterized by brief, random and rapid jerky movements involving more distal muscles in the limb and face. Patients frequently attempt to incorporate these abnormal and involuntary movements into a normal movement. Choroids movements can also be combined with slower, writhing involuntary movements identified as choreoathetosis. In later stages of Huntington disease cerebral cortical neurons degenerate leading to
dementia. Choreiform movements also occur with high doses of levodopa and/or long-term levodopa therapy.
Gait Huntingtons also occurs (a dance-like shuffling gait).
What is hemiballismus? Where does the damage occur? What are the signs and symptoms? How does it different from the other movement disorders?
Occlusion or rupture of a penetrating artery supplying the subthalamic nucleus results in involuntary large amplitude, flinging movements of proximal joints in the contralateral extremities. Hemiballismus, like other movement disorders, is mediated by the pyramidal system. Unlike other movement disorders which are bilateral hemiballismus is generally present only on one side and contralateral to the lesion in the subthalamic nucleus. Over time there is a gradual diminution in signs.
What is dystonia? What is it caused by?
Dystonia is characterized by sustained involuntary muscle contractions (spasms) that result in abnormal and sustained postures frequently seen after strokes involving the pallidum. During voluntary movements abnormal involuntary co-contractions of antagonists occur. There is developing evidence that dopamine deficiency or abnormalities in the dopamine D2 receptor may lead to increased activity in the “direct” striatopallidal pathway resulting in excessive inhibition of the medial pallidum and excessive disinhibition of cortical motor areas.
