Though subcortical dementia was first described in 1912,' the term was not used until the early 1970s.'Subcortical structures include the basal ganglia, diencephalon (thalamus and hypothalamus), mesencephalon (midbrain), and cere- bellum.They have a role in arousal, attention, mood, motivation, memory, abstraction, and visuospatial skills.Subcortical nuclei are affected in Parkinson's disease, progressive supranuclear palsy, Huntingdon's chorea, hydrocephalus, and the AIDS dementia complex.Additionally, depression may cause subcortical dementia.3By contrast, Alzheimer's disease is held to be the classic example of a cortical dementia.Subcortical dementia is noted for a special type of cognitive impairment, characterised by marked psychosocial in- competence associated with minimal memory loss and, as a rule, absence of aphasia, apraxia, or agnosia.Characteristic symptoms include forgetfulness, slowing of thought pro- cesses, mild intellectual impairment, apathy, inertia, depression (sometimes with irritability), and the inability to manipulate knowledge.24Difficulties in problem solving and abnormalities of judgment and insight may occur.5 Conceptually, cortical abilities can be categorised as subserving instrumental functions (language, perception, memory, and calculation) and subcortical abilities as sub- serving fundamental functions (arousal, mood, and motiva- tion).Cortical dysfunction leads to aphasia, agnosia, amnesia, and acalculia; subcortical dysfunction slows information processing and adversely affects memory, cognition, mood, and motivation.6 Memory impairment is characterised by a greater deficit of spontaneous recall than of encoding and storage of new material, which is characteristic of the cortical dementias.'As a result, memory assessed by clues and recognition tests is usually superior to free recall.Articulation and verbal fluency may be impaired, but language is largely spared in the subcortical dementias.6About a tenth of patients with Parkinson's disease develop cortical dementia, and two thirds may be affected by frontal subcortical dysfunction.8Early in the course of the disease many patients show subtle deficits of the subcortical type, which are attributed to the loss of striatal and cortical
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F J Dunne (1993) studied this question.
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