Cognitive disorders (dementia) — MCQs

A 52-year-old man presents with cognitive decline, chorea, and psychiatric symptoms. Family history reveals his father died at age 55 with similar symptoms, and his paternal grandfather also had progressive dementia and movement disorder. Genetic testing shows 45 CAG repeats in the huntingtin gene. His 25-year-old daughter, currently asymptomatic, requests genetic counseling. Evaluate the most ethically and clinically appropriate approach to her request.

A 65-year-old woman with early Alzheimer's disease (MMSE 23/30) on donepezil presents with worsening behavioral symptoms. She has developed paranoid delusions that her husband is stealing from her and has become physically aggressive. Her husband requests antipsychotic medication. She has no other medical conditions. Labs including TSH, B12, and metabolic panel are normal. Evaluate the most appropriate management strategy considering risk-benefit analysis.

A 78-year-old man with moderate Alzheimer's disease (MMSE 16/30) on donepezil develops progressive gait instability and urinary incontinence over 3 months. His daughter reports his memory seems worse. CT head shows enlarged ventricles with periventricular lucency. You suspect normal pressure hydrocephalus superimposed on Alzheimer's disease. Evaluate the most appropriate next step to guide management decisions.

A 58-year-old woman presents with rapidly progressive dementia over 8 weeks, myoclonus, and ataxia. MRI shows cortical ribboning and hyperintensity in the caudate and putamen on DWI sequences. EEG shows periodic sharp wave complexes. CSF analysis shows normal cell count and glucose, elevated protein, and positive 14-3-3 protein. Analysis of her clinical presentation suggests which molecular mechanism is primarily responsible?

A 70-year-old man with diabetes and hypertension presents with stepwise decline in cognitive function over 3 years, with periods of stability followed by sudden worsening. He has emotional lability and urinary incontinence. MMSE is 21/30 with prominent executive dysfunction. MRI shows multiple lacunar infarcts in basal ganglia and periventricular white matter hyperintensities. Which pathophysiological mechanism best explains his white matter changes?