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The basal ganglia, a cerebral structure involved in controlling movement, is believed to be one of the sites vulnerable to dopamine abnormalities and is implicated in the pathogenesis of TS. It is thought that dopamine, norepinephrine, and serotonin neurotransmitters are not able to exchange messages properly between nerve cells in a person ...
Basal ganglia disease is a group of movement disorders that result from either excessive output from the basal ganglia to the thalamus – hypokinetic disorders, or from insufficient output – hyperkinetic disorders. Hypokinetic disorders arise from an excessive output from the basal ganglia, which inhibits the output from the thalamus to the ...
Additional MRI findings include high T 2 signal intensity with possible swelling in basal ganglia, and abnormal diffuse involvement of the subcortical white matter, cortical, and infratentorial brain. [5] [11] Involvement in the thalami, brain stem, and cerebellum may also be observed. [11]
The cortico-basal ganglia-thalamo-cortical loop (CBGTC loop) is a system of neural circuits in the brain. The loop involves connections between the cortex , the basal ganglia , the thalamus , and back to the cortex.
Neurodegeneration with brain iron accumulation is a heterogenous group of inherited neurodegenerative diseases, still under research, in which iron accumulates in the basal ganglia, either resulting in progressive dystonia, parkinsonism, spasticity, optic atrophy, retinal degeneration, neuropsychiatric, or diverse neurologic abnormalities. [1]
As in images gathered through MRI, SPECT images indicated asymmetry in the presentation of abnormalities throughout the brain. [4] Additional studies have revealed the presence of perfusion anomalies in the thalamus, temporal cortex, basal ganglia, and pontocerebellar (from the pons to the cerebellum) locations within subjects' brains. [24]
Symptoms categorized as medically tested and diagnosed include iron accumulation in the brain, basal ganglia cavitation, and neurodegeneration. [4] Patients who are diagnosed with neuroferritinopathy have abnormal iron accumulation in the brain within the neurons and glia of the striatum and cerebellar cortices. [3]
Without the normal restraining influence of the basal ganglia, upper motor neurons of the circuit tend to become more readily activated by inappropriate signals, resulting in the characteristic abnormal movements. [11] There are two pathways involving basal ganglia-thalamocortical circuitry, both of which originate in the neostriatum.