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Dementia with Lewy bodies (DLB) and dizziness

Timothy C. Hain, MD Most recent update: June 11, 2017

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

DLB was first described in 1996. Lewy bodies are accumulations of alpha-synuclein. In this disease, accumulation of Lewy bodies is associated with a slowly progressive neurological deterioration. Lewy bodies are intracytoplasmic, spherical, eosinophilic neuronal inclusion bodies.

DLB was reported as accounting for about 15-25% of all dementia, only trailing Alzheimer's disease. However, the #2 spot has also been claimed for frontotemporal dementia, and both can't be right. The high prevalence figure for DLB was derived from neuropathological autopsy sudies reported that Lewy bodies (LB) are found in  the brainstem and cortex of 15-25% of elderly demented patients, making diffuse Lewy body disease the largest pathologic subgroup after Alheimer's disease.

There may be an incidence of DLB of about 0.1% in the general population. More recently, a study from the Mayo clinic suggested that the incidence was overestimated, and instead is about 3.5/100,000 person years. (Saica et al, 2014), similar to the incidence of Parkinson's disease dementia (2.5/100,000).

In spite of an immense investment of money and national resources into finding treatment for both Alzheimer's and DLB, so far, no solution has been found.

Entities that can be confused with DLB include several that cause dizziness.

While we say "confused", perhaps it would be more accurate to say that these disorders overlap, as their definition is somewhat fuzzy.

Pathophysiology of DLB

Damage is thought to occur due to accumulation of Lewy bodies in the nervous system.

A 6-stage system has been suggested beginning with lesions in the medulla and olfactory cortex, and with progression to the cortex. Lewy bodies may also be found in sympathetic and intramural ganglia (i.e. outside the CNS). Lewy bodies are composed of alpha-synuclein.

It is currently thought that alpha-synuclein exists both as unfolded monomers, but also as folded tetramers, and the folded-tetramer is believed to lead to pathology in DLB and Parkinsonism. (Bartels, 2011). On the other hand, there is considerable evidence that tetramers are found in healthy brains, and mutations that increase monomers are associated with more disease. So these two observations appear to be mutually contradictory.

Diagnosis of DLB

DLB is characterized by dementia associated with any two of the following three core features:

Key symptoms suggestive of DLB are fluctuating cognitive impairment with episodic delirium, with prominant psychiatric symptoms, especially visual hallucinations. Parkinsonism may occur spontaneously or part of an abnormal sensitivity to neuroleptic medications.

Progressive disabling mental impairment is a mandatory requirement for diagnosis of DLB. Early on, there may be prominent deficits of tests of executive function and problem solving such as the Wisconsin Card sorting test or the Trail Making test. Later on, global impairment of mental function may blur the distinction between Alzheimer's disease where the major deficit lies in memory acquisition and consolidation. Patients with DLB decline more quickly than those with Alzheimers disease in both mental function as well as in survical time (Olichney et al, 1998)

Further features supportive of the diagnosis are:

CT or MRI may show generalized cortical atrophy. Sleep disturbance begins with or precedes onset of dementia in most cases (Boeve et al, 1998). Nevertheless, current clinical criteria are said to fail to identify 25% or more of true cases.

Autonomic failure may also accompany DLB ( Akaogi et al, 2009). Olfactory disturbances and autonomic failure may precede the motor symptoms and onset of dementia. Sweating disturbances and orthostatic hypotension are common.

How does DLB cause dizziness ?

DLB does not cause vertigo, but it can cause unsteadiness.

Treatments for DLB

As is the case for nearly all disorders characterized by neuron death, there is yet no effective causal treatment. All treatments, aside from some investigational ones, are symptomatic.

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

Memantine (Namenda) -- reduces glutamate mediated excitotoxicity

Antipsychotic agents -- reduces thought disorders

Investigational agents

There are also treatments for parkinsonism (mainly dopamine agonists) and low blood pressure


Copyright August 3, 2016 , Timothy C. Hain, M.D. All rights reserved. Last saved on August 3, 2016