A physician-validated, board-style question from the Active Transport QBank. Try it, then check the reasoning for every option.
A 66-year-old man is brought to the clinic with a history of recurrent falls. He has been slow in his movements and walks clumsily. He denies fever, vision problems, limb weakness, numbness, abnormal sensation in his limbs, trauma, or inability to pass urine. The past medical history is unremarkable, and he only takes calcium and vitamin D supplements. The vital signs include: blood pressure 128/72 mm Hg, heart rate 85/min, respiratory rate 16/min, and temperature 36.9°C (98.4°F). He is awake, alert, and oriented to time, place, and person. His eye movements are normal. There is a tremor in his hands bilaterally, more in the left-hand which decreases with voluntary movements. The muscle tone in all 4 limbs is increased with normal deep tendon reflexes. He walks with a stooped posture and takes small steps with decreased arm swinging movements. During walking, he has difficulty in taking the first few steps and also in changing directions. The speech is slow and monotonous. His mini-mental state examination (MMSE) score is 26/30. What is the most likely pathophysiology of the patient’s condition?
-
A
Cerebellar atrophyIncorrect. Cerebellar atrophy produces ataxia, intention tremor, dysmetria, and dysdiadochokinesia — not the resting tremor with bradykinesia and cogwheel rigidity of Parkinson disease.
-
B
Dilated ventricles with increased CSF volumeIncorrect. Dilated ventricles with increased CSF describes normal-pressure hydrocephalus (the classic 'wet, wacky, wobbly' triad of gait apraxia, dementia, urinary incontinence) — but NPH has a magnetic/apraxic gait without resting tremor or cogwheel rigidity.
-
C
Generalized brain atrophyIncorrect. Generalized brain atrophy describes Alzheimer disease or other cortical dementias; PD has selective nigral pathology, not diffuse atrophy.
-
D
Loss of dopaminergic neurons in the substantia nigraCorrect. Parkinson disease is caused by loss of dopaminergic neurons in the substantia nigra pars compacta, with Lewy body inclusions and depletion of striatal dopamine.
-
E
Demyelination of the cerebral white matterIncorrect. Diffuse cerebral white-matter demyelination characterizes multiple sclerosis, with optic neuritis and spasticity — not the bradykinesia, resting tremor, and cogwheel rigidity of nigrostriatal dopamine loss in Parkinson disease.
↑ Tap an answer to reveal the reasoning
Answer: D. An older man with insidious onset of asymmetric resting tremor (more in the left hand) that decreases with voluntary movement, cogwheel rigidity, bradykinesia, stooped/shuffling gait with decreased arm swing, freezing-of-gait, hypomimia, and hypophonic monotone speech has idiopathic Parkinson disease (PD). The mini-mental score of 26/30 suggests mild cognitive involvement but is preserved enough to favor PD rather than a synucleinopathy with prominent early dementia like dementia with Lewy bodies.
The core pathophysiology of PD is degeneration of dopaminergic neurons in the substantia nigra pars compacta, with loss of dopamine input to the striatum and the histologic hallmark of intraneuronal Lewy bodies (alpha-synuclein aggregates). The motor symptoms emerge after approximately 60–80% of nigrostriatal dopaminergic neurons are lost. The classic tetrad TRAP — Tremor (resting, 4–6 Hz), Rigidity (cogwheel), Akinesia/bradykinesia, and Postural instability — is present here.
Treatment: levodopa-carbidopa is the most effective symptomatic therapy; dopamine agonists (pramipexole, ropinirole) and MAO-B inhibitors (selegiline, rasagiline) are alternatives, particularly in younger patients to delay levodopa-related motor complications. Amantadine helps tremor and dyskinesia; deep brain stimulation of the subthalamic nucleus is highly effective for advanced motor fluctuations.
**Why each option:**
**A.** Cerebellar atrophy produces ataxia, intention tremor, dysmetria, and dysdiadochokinesia — not the resting tremor with bradykinesia and cogwheel rigidity of Parkinson disease.
**B.** Dilated ventricles with increased CSF describes normal-pressure hydrocephalus (the classic 'wet, wacky, wobbly' triad of gait apraxia, dementia, urinary incontinence) — but NPH has a magnetic/apraxic gait without resting tremor or cogwheel rigidity.
**C.** Generalized brain atrophy describes Alzheimer disease or other cortical dementias; PD has selective nigral pathology, not diffuse atrophy.
**D.** Correct — Parkinson disease is caused by loss of dopaminergic neurons in the substantia nigra pars compacta, with Lewy body inclusions and depletion of striatal dopamine.