HD-tDCS for Lewy Body Disease

Although the authors are aware of the limited evidence, they advise the cautious use of Tdcs for people in whom [HbA1c] is >9% and whose cognitive functioning is acceptable.

LBD appears to be benign lesions as in the case of multiple myeloma. This benign lesion may be cured by total excision of the lesion using a standard laser excision procedure and by using a simple and inexpensive excision technique. Thus, the authors have not concluded it is curable in the sense of a standard treatment for the disease.

The pathogenesis of the lewy body disease process and its diagnostic distinction from dementia with Lewy bodies has also not been elucidated. LBD may represent a spectrum of pathology within the dementia spectrum, or may represent a distinct and unrelated entity.

Although the signs of LBD are not specific, they can serve as complementary information about the diagnosis. Because of its early onset, LBD can lead to dementia (mental deterioration), even without the presence of a diagnosis of dementia, which can be confirmed only by brain pathology.

Since the first identification of cases in the United States, the prevalence of the disease has been debated. This is of public health and interest considering the possibility that lewy body disease may be a surrogate marker for early stages of prion disease. Currently, we are unable to estimate the prevalence of a disorder with a disease of uncertain cause that is currently considered rare. We estimate that the prevalence of this disorder is approximately 1.27 cases per 100,000 in the US. For comparison, there are approximately 18 cases per 100,000 cases of Alzheimer's disease, and 3 cases per 100,000 cases of ALS.

LBPD is an inherited neurodegenerative disease characterized by the progressive loss of neurons and gliosis in the central nervous system. LBPD affects various neuron populations in the brain, but particularly in the hippocampus, cerebellum, basal ganglia, and cerebellar vermis. The most common clinical feature is dementia with a gradual onset; other features include muscle weakness, sleep disturbance, hallucinations, and dysphoria. These features should raise the suspicion of LEBPD in patients with a history of dementia or unexplained deterioration of cognition.

Many treatment and follow-up options exist for LD/PLD. However, given the lack of evidence in patient treatment, and a lack of evidence-based management guidelines for LD, it is not possible to recommend one treatment over others.

Since the discovery of the genetic mutation that causes lewy body disease in the early 1980s, several discoveries have been made and are currently being studied within the research community in hopes of finding a more effective treatment for the disease which still does not have a cure yet. Currently, there are several investigational therapies that are underway that target the gene, protein and/or mitochondria functionality in order for treatment options to be found. The best treatment option for lewy body disease will still have to be discovered but there are some promising developments happening in the research community.

Levadopa use alone was sufficient for a considerable proportion of the patients. More research is needed to define the best treatment for patients with LBD and LBD/DLB.

[Hd-tdcs is safe and effective for treating patients with diffuse and multifocal form of lewy body disease. This therapy seems to be effective in controlling symptoms even in the advanced phases of disease; the response is independent from the baseline parameters of disease duration, age and disease progression. Findings from a recent study of this pilot study have pave the way for the larger-scale clinical studies on HD-tdcs efficiency in the prevention and treatment of this disease.

hd-tdcs therapy could be an interesting and valid treatment option, as well it is safe and effective. A large randomized double-blind placebo-controlled clinical trial of hd-tdcs would be ideal because [hd-tdcs therapy in combination with baclofen, in comparison to baclofen alone, shows a synergistic effect on spasticity in patients with spastic CP] and because only one double-blind placebo-controlled placebo randomized trial has been conducted.