Pick disease is sometimes used synonymously with frontotemporal lobar degeneration, although this is probably unwise, as not all cases which fit clinically into a frontotemporal dementia have the underlying pathological changes seen in Pick disease.
Pick disease typically manifests between the ages of 40 and 60 years, with a male predilection 1.
Clinical presentation depends on the particular pattern of cortical involvement, and is discussed in the frontotemporal lobar degeneration (FTLD) article.
The characteristic features of Pick disease include 1:
- Pick bodies
- swollen chromatolytic neurons
- loss of large pyramidal neurons
- astrocytic gliosis
The primary radiographic abnormality is that of cortical atrophy of the frontal and temporal lobes. These changes can be markedly asymmetric and affect one region much more than another. They are discussed further in the frontotemporal lobar degeneration (FTLD) article.
Caudate head volumes are also often reduced 3.
Imaging differential diagnosis
On imaging, Pick disease may mimic other causes of frontal and temporal atrophy, especially:
- other varieties of frontotemporal lobar degeneration (FTLD)
- Alzheimer disease: parietal lobe involvement is more pronounced
- corticobasal degeneration: parietal lobe involvement is usually dominant
Clinical differential diagnosis
Clinically Pick disease may overlap with other neurodegenerative diseases with prominent frontal involvement, including 1:
- 1. Esiri MM, Trojanowski JQ. The neuropathology of dementia. Cambridge Univ Pr. (2004) ISBN:0521819156. Read it at Google Books - Find it at Amazon
- 2. Levine R. Defying dementia, understanding and preventing Alzheimer's and related disorders. Praeger Pub Text. (2006) ISBN:0275989704. Read it at Google Books - Find it at Amazon
- 3. Looi JC, Lindberg O, Zandbelt BB et-al. Caudate nucleus volumes in frontotemporal lobar degeneration: differential atrophy in subtypes. AJNR Am J Neuroradiol. 2008;29 (8): 1537-43. doi:10.3174/ajnr.A1168 - Pubmed citation
Neurodegenerative diseases are legion and their classification just as protean. A useful approach is to divide them according to underlying pathological process, although even using this schema, there is much overlap and thus resulting confusion.
neurodegenerative MRI brain (an approach)
- measurements and ratios
- midbrain to pons area ratio (for PSP)
- Magnetic Resonance Parkinsonism Index (MRPI) (for PSP)
- frontal horn width to intercaudate distance ratio (FH/CC) (for Huntington disease)
- intercaudate distance to inner table width ratio (CC/IT) (for Huntington disease)
- scoring systems
- measurements and ratios
- typical/classical Alzheimer disease
- variant (e.g. posterior cortical atrophy)
- chronic traumatic encephalopathy (CTE)
- corticobasal degeneration
- frontotemporal lobar degeneration (FTLD) (not all are tau)
- Pick disease
- progressive supranuclear palsy (PSP)
- Alzheimer disease
- cerebral amyloid angiopathy (CAA)
- transthyretine-associated cerebral amyloidosis
- neuronal intranuclear hyaline inclusion disease (NIHID)
- spinocerebellar ataxias
- Huntington disease
- hereditary spastic paraplegia
- amyotrophic lateral sclerosis (ALS)
- clinically unclassifiable parkinsonism (CUP)
- Unverricht-Lundborg disease
- prion diseases (not always included as neurodegenerative)