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Low uptake of MIBG as biomarker for DLB and PD
The Japanese have really taken the lead in cardiac studies in PD, PDD, and DLB. In this recently-published article, Japanese researchers analyze 34 patients with low cardiac uptake of a chemical MIBG, who presumably have PD or DLB.
I didn't get much out of the abstract (copied below) or the full article except for the second paragraph of the Introduction. I liked the second paragraph because it gave a list of three biomarkers under consideration for diagnosing DLB during life -- low uptake of MIBG, PET with 6-18F fluorodopa, and cerebrospinal fluid level of dihydroxyphenylacetic acid.
Here are the first and second paragraphs from the Introduction:
"Lewy body disease (LBD) is comprised of a spectrum of diseases that involves an array of dementia and motor symptoms. The term of LBD includes Parkinsonâs disease (PD), dementia with LBD (DLBD) and PD dementia (PDD). DLBD is the second most common cause of degenerative dementia after Alzheimerâs disease... DLBD is characterized by cognitive disturbance, atypical parkinsonian syndromes, frequent falls with postural instability, consciousness fluctuation, and visual hallucinations. Depression, anxiety, delusion, and hallucinations are included into symptoms of LBD. These psychiatric symptoms sometimes precede the motor symptoms, which results in psychiatric misdiagnosis and neuroleptic hypersensitive sequelae. Particularly LBD has a tendency to manifest an isolated late-onset psychotic illness, called a pure psychiatric presentation of LBD, and depression and anxiety symptoms are frequently observed prior to clinical symptoms of PD. Thus, late-onset psychiatric manifestations, when they lack apparent neurological symptoms or cognitive disturbance, may be diagnosed as primary psychiatric disorders such as major depression or late-onset schizophrenic disorder. Therefore, late-onset psychiatric manifestations of LBD have been suffering from warrant of diagnosis." [Robin's note: frustratingly, they initially define LBD to mean Lewy body disease but later, in the same paragraph, it seems to mean Lewy body dementia.]
"Myocardial meta-iodobenzylguanidine (MIBG) scintigraphy is a useful, noninvasive technique for estimating local myocardial sympathetic nerve damage and detects early disturbances of the sympathetic nervous system in LBD irrespective of the duration of disease and autonomic failure. Low uptake of MIBG has been established as a biomarker for PD and DLBD as well as positron emission tomography (PET) with 6-18F fluorodopa and cerebrospinal fluid level of dihydroxyphenylacetic acid and validates the diagnosis of LBD in the absence of underlying diseases such as diabetic neuropathy and cardiac diseases that were known to affect myocardial uptake of MIBG. The mechanism of low uptake of MIBG has pathologically been studied, in which alpha-synuclein aggregates affect early the cardiac sympathetic nerves and later spread to the paravertebral sympathetic ganglions. During this pathological process, cardiac sympathetic denervation develops and causes low uptake of MIBG, and this finding has been confirmed in an autopsied case of incidental LBD. These pathological studies indicate that involvement of the cardiac sympathetic nerves precede the striatonigral degeneration."
Here's the abstract:
International Journal of Geriatric Psychiatry. 2009 Jul 28. [Epub ahead of print]
Detection of Lewy body disease in patients with late-onset depression, anxiety and psychotic disorder with myocardial meta-iodobenzylguanidine scintigraphy.
Kobayashi K, Sumiya H, Nakano H, Akiyama N, Urata K, Koshino Y.
Department of Psychiatry, Awazu Neuropsychiatric Sanatorium, Komatsu-shi, Japan.
PURPOSE: Lewy body disease (LBD) is comprised of a spectrum of diseases that includes Parkinson's disease (PD), PD dementia (PDD) and dementia with LBD (DLBD), an array of dementia, and motor symptoms. Low uptake of myocardial meta-iodobenzylguanidine (MIBG) validates diagnosis of LBD. Psychiatric symptoms sometimes precede atypical Parkinsonian syndromes in LBD. Of 34 patients with low MIBG uptake, late-onset depressive, anxiety, or psychotic symptoms were analyzed in term of clinical profiles.
METHOD: Thirty-four patients were classed into three groups according to three main symptoms, 11 patients with visual hallucination (VH), 13 with depression-anxiety (DA), and 10 with psychosis with cognitive disturbance (PCD). Cutoff values of heart-to-mediastinum (HM) ratio of MIBG were set at 1.78 in early phase or 1.68 in late phase.
RESULTS: Group VH patients showed a trend toward higher age at onset and occipital lobe hypoperfusion. Group DA patients lacked central and core features of DLBD and five of them showed frontal lobe hypoperfusion. Group PCD patients had the highest frequencies of suggestive symptoms and UPDRS scores and showed temporal lobe hypoperfusion. HM ratio was not associated with clinical profiles of three groups. Cognitive function was more severely disturbed in atypical Parkinsonian syndrome cases at an initial visit.
CONCLUSION: Group VH was considered to DLBD, and Group PCD was regarded as PDD or DLBD with early psychotic presentation. Group DA has a possibility of early depression or anxiety disorder of LBD although it lacked DLBD criteria. Atypical Parkinsonian syndromes are associated with cognitive disturbance irrespective of psychiatric profiles.
PubMed ID #19637401 (see pubmed.gov for abstract only)