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Frontotemporal Dementia (FTD) and dizziness

Timothy C. Hain, MD Most recent update: April 2, 2016

This is a focused review of FTD, concentrating on the aspects that are associated with dizziness.

FTD is a common type of dementia, claimed by some to be the 2nd most common dementia, after Alzheimer's disease (Wang et al, 2013). FTD, actually a heterogeneous collection of conditions that manifest similarly, is characterized by a combination of dementia impairing particularly behavior or language, and a CT or MRI scan that shows selective atrophy of the frontal and temporal lobes (Rohrer and Rosen, 2013). Most FTD's are associated with an accumulation of a protein called "Tau" in the brain.

FTD is caused by permanent damage to the brain, with greater damage being done in the front. Neuropathologists are constantly reclassifying patients with FTD into variants with different acronyms (e.g. Chare et al, 2014), but as there is no treatment for FTD, so far this beehive of activity has no practical implication.

More than 1500 articles were published as of 2014 with "frontotemporal dementia" in their title. In other words, there has been an immense amount published about this largely untreatable brain condition.Pick

A particularly famous variant of FTD is "Pick" disease, named after Dr. Arnold Pick (Irwin et al, 2015), a Czech psychiatrist, and the head of the Prague neuropathological school at one point. As of 2016, roughly 1500 articles were published in Pubmed with "Pick disease" in their title. Like most of the other FTD's, Pick disease is a tauopathy. Generally Pick disease is associated with a disinhibited mental status -- called "frontal lobeish" by neurologists. These are people who may seem crude, or laugh at jokes that nobody else thinks are funny -- they are socially uninhibited and generally inappropriate. Pick disease pathology is associated with some variants of primary progressive aphasia (PPA), and the "corticobasal syndrome". In essence, we have a "cloud" of neuropathological findings with a highly inconsistent nomenclature and another "cloud" of disease patterns again with a highly inconsistent nomenclature, including a multitude of thinking deficits, and the two clouds overlap in some places, with varying strengths of association. A big mess ! One can only hope that things will get simpler as we learn more about these conditions.

FTD, like almost all dementias, increases greatly with age (Nilsson et al, 2014)

Diagnosis of FTD.

Dementia is unfortunately a common human condition and there are large number of possibilities (see the Alzheimer's page for a long list). In general, FTD affects behavior and speech more than raw intelligence. Thus you may see individuals who are socially very inappropriate, nevertheless doing relatively well with their stock investment portfolio.

Disorders similar to FTD that also commonly cause dizziness include:

FTD does not cause vertigo, but rather causes unsteadiness of gait.

FTD patients often have problems with driving due to "antisocial behaviors common among people with FTD (e.g., hit and run crashes, failure to stop at red lights, speeding infractions, and failure to recognize pedestrians at intersections). " (Turk and Dugan, 2014)

Treatments for FTD

As is the case for nearly all disorders characterized by neuron death, there is yet no effective causal treatment. All treatments are symptomatic. (Boutoleau-Bretonniere, C., et al., 2014). Often the purpose of treating is mostly to be "doing something". If there is no need on the part of the caregivers to be "treating", one can certainly choose to leave it untreated.

That being said, there are many drugs marketed with the hope of improving cognition.

Cholinesterase inhibitors -- increase the amount of acetylcholine, and slightly improve memory and thinking.

Memantine (Namenda) -- reduces glutamate mediated excitotoxicity. This treatment has largely been abandoned for FTD (Hodges, 2013).

Antipsychotic agents -- reduces thought disorders



Copyright April 2, 2016 , Timothy C. Hain, M.D. All rights reserved. Last saved on April 2, 2016