In Huntington’s disease, the hyperkinetic features are due to are due to the loss of
A. Nigrostriatal dopaminergic systemB. Intrastriatal cholinergic system
C. subthalamic neurons
D. Intrastriatal GABA-nergic and cholinergic system
The Answer is. D (Interstitial GABA-nergic and cholinergic system)
Corpus
striatum sends inhibitory input to globus pallidus (external); globus pallid us
is reciprocally connected with subthalamic nucleus. In Huntington’s disease
there is loss of (inhibitory) GABAnergic and cholinergic neurons of the
striatum. Loss of inhibition of the external globus pallidus diminishes the
activity of neurons in the subthalamic nucleus. Hence, the excitation of
neurons of the internal globus pallidus (by subthalamic nucleus) would be
reduced. This will inhibit the neurons in the VA and VL nuclei of thalamus. The
resulting enhancement of activity of neurons in the cerebral motor cortex may
lead to choreiform movements or hyperkinetic features of Huntington’s disease.
Loss of dopaminergic neurons in the nigrostriatal tract will lead to
Parkinson’s disease. The net effect of such loss/lesion causes an increased
activity of neurons in the internal globuspaiidus (a feature opposite to that
in Huntington’s disease). This results in greater inhibition of neurons in the
VA and VL nuclei of thalamus, and hence less pronounced activation of motor
cortex. The consequence is slowed movements (bradykinesia). A lesion of
subthalamic nucleus on one side leads to hemiballism: involuntary, violent
flailing movements of the limbs on the side opposite to the lesion.
