Parkinson Disease

Explanation

Parkinson disease results from progressive loss of dopaminergic neurons in the substantia nigra pars compacta of the midbrain, with intracytoplasmic alpha-synuclein aggregates known as Lewy bodies in the surviving cells. Loss of nigrostriatal dopamine reduces excitation of the direct pathway and disinhibits the indirect pathway, so thalamocortical output falls and movement is slowed. The cardinal features are bradykinesia, which is mandatory for diagnosis and is demonstrated here by decrementing amplitude on repetitive finger tapping, plus rest tremor, rigidity, and later postural instability, all characteristically asymmetric at onset. Motor symptoms appear only after roughly 60 to 80 percent of nigral neurons are lost, which is why non-motor prodromal features such as hyposmia, constipation, depression, and rapid eye movement sleep behaviour disorder can precede the diagnosis by years. Micrographia and hypomimia are typical supportive findings. Lesions of the subthalamic nucleus cause hemiballismus, a violent flinging movement of the contralateral limbs, and the subthalamic nucleus is instead the main target for deep brain stimulation in advanced Parkinson disease. Caudate degeneration is characteristic of Huntington disease, producing chorea, behavioural change, and dementia with caudate atrophy on imaging. Cerebellar dentate pathology causes intention tremor, dysmetria, and ataxia, a pattern quite unlike rest tremor with rigidity. Normal ocular movements help exclude progressive supranuclear palsy, in which vertical gaze palsy and early falls dominate. Treatment centres on levodopa combined with a peripheral decarboxylase inhibitor, with dopamine agonists and monoamine oxidase B inhibitors as alternatives.

Why each option

A.

Correct. Loss of dopaminergic neurons in the substantia nigra pars compacta produces bradykinesia, rest tremor, and rigidity.

B.

Subthalamic nucleus lesions cause contralateral hemiballismus; the nucleus is a deep brain stimulation target, not the site of degeneration.

C.

Caudate atrophy underlies Huntington disease with chorea, psychiatric change, and dementia.

D.

Dentate nucleus disease produces cerebellar intention tremor and ataxia rather than a rest tremor with rigidity.

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