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International

International
consultations

with Dr. Jacques Duff are welcomed via SKYPE or Telephone.
Please call the clinic on
+613 9848 9100
for an appointment.

Please note that international appointments need to be pre-paid at time of booking.

Autism ADHD Foundation

We recommend visiting the website of the Australian Autism ADHD Foundation. There's great information on the most common causes of ADHD and Autism. Joining as a member will support the research, advocacy and educational program of the foundation. Donations are tax deductible.

Alzheimer's dementia

Alzheimer's symptoms

Dementia is characterised by a loss of cognitive function. This can include disrupted thinking, memory, reasoning, communication, personality and cognitive speed. It is degenerative in nature, with cognitive abilities decreasing over time either slowly or more quickly depending on the cause of the dementia and the individual. Dementia is due to disease or injury in the brain, and is traditionally believed to be irreversible in the latter stages. Recent nutritional research suggests that it may be able to be stopped in very early stages (when it is known as Primary Degenerative Dementia).

The symptoms of dementia depend on the areas of the brain that are affected by disease, and therefore vary depending on the type of dementia that is present. However, memory problems are often the first indication of disease. Mild Cognitive Impairment refers to a condition that presents with disrupted memory without impairment in other areas of function. This particular symptomatology might indicate the initial stages of Alzheimer’s disease.

The more common types of dementia include Alzheimer’s Disease, vascular or multi-infarct dementia, Lewy Body Dementia and Parkinson’s disease. Dementia can also be caused by infectious diseases such as AIDS, or hereditary diseases such as Huntington's disease. Alcoholism and drug abuse may also result in some type of dementia.

Alzheimer’s Disease

Alzheimer's disease (AD) is the most common form of dementia. It is a progressive, degenerative disease of the brain, affecting up to 5% of people aged 65-74, increasing to up to 50% of people aged over 85 years. **check these stats – seems pretty high.

The main features of AD are the amyloid plaques and tangled neuronal fibres that disrupt the normal organization and function of the brain. These initially appear in the temporal lobe of the brain, the area that is responsible for memory and language. Thus, memory problems are often the first indicator of AD.

Because the presence of plaques and tangles cannot be determined until autopsy, diagnosis is made based on behavioural changes, memory tests and questionnaires and elimination of other possible causes. Therefore, diagnosis is generally given as ‘dementia of the Alzheimer’s type’ or ‘probable Alzheimer’s Disease’. However, QEEG technology may be able to provide a more conclusive diagnosis, particularly in the early stages which can start some 12 years before full blown dementia. In those early stages the symptoms are referred to as Primary Degenerative Dementia.

Depression and Primary Degenerative Dementia have very similar overlapping symptoms making it difficult to differentiate between them on the basis of memory tests and depression questionnaires. However, QEEG is able to differentiate with a high degree of specificity between depression and Primary Degenerative Dementia. This enables more effective treatment addressing the root causes of either disorders . QEEG differential diagnosis was developed by Dr Leslie Prichep and Dr E. Roy John from the Brain research Laboratory of New York University Medical Centre and is available at the Behavioural Neurotherapy Clinic. Treatment of Primary Degenerative Dementia is possible using specific nutrients and Neurotherapy.

Although some cognitive decline is expected with normal aging, AD should not be considered a normal part of aging, since it represents a pathological state. In AD, dementia progresses at a rate of around 10–15% per year compared with healthy people whose decline progresses at around 1–2% / year [9]

Causes<

There is no single known cause of AD, however there are a number of factors that may contribute to an increased likelihood of developing this disease. The presence of the apolipoprotein E variation is a genetic factor associated with greater incidence of the disease. History of head injury or depression and lower levels of education may contribute to higher incidence. Scientific studies have also associated a number of nutritional factors with AD. For example, people suffering from AD are more likely to have a poor nutritional status and be deficient in vitamin B12 and folate. This might be due to the increased levels of homocysteine that results from deficiency in these B-group vitamins. Homocysteine causes damage to the blood vessels in the brain and may damage the hippocampus, a region of the brain used for memory [20]. Another nutritional factor relates to antioxidants. Oxidative stress (damage from free radicals) may significantly contribute to the pathology of AD. Patients with AD are more likely to be deficient in the antioxidant vitamins C and E, or to have a lower dietary intake of these vitamins.

Treatment

At present there is no cure for AD. Slowing cognitive decline and postponing functional and behavioural impairment is important [Gauthier]. Currently the main drug treatment is Donepezil, which may be able to slow the progression of dementia. THowever, this delay may be only for as long as 6 months to one year. Evidence suggests that early treatment with this drug provides greater benefits over the long term [Winblad, 2003].

Treating dietary and nutritional deficiencies many years before dementia provide the opportunity for greater results. Reducing the impact of causative factors such as increased homocysteine and oxidative stress, particularly in groups that are at risk, may delay onset or decrease the likelihood of developing AD. Scientific studies have demonstrated that improving nutritional status via supplementation can improve cognition in older adults [Harris, 2005].

References

Gauthier S.G, 2005. Alzheimer's disease: the benefits of early treatment. European Journal of Neurology, 12(s3), 11 -16.

Winblad B, Engedal K, Soininen H et al. (2003). Long-term efficacy of donepezil in patients with mild to moderate Alzheimer's disease: results from a one-year placebo-controlled study and two-year follow-up study. Int Psychogeriatr 15: 293–294.

[1] Qiu C, Winblad B, Fratiglioni L. The age-dependent relation of blood pressure to cognitive function and dementia. Lancet Neurol 2005;4(8):487-99.

[2] Nilsson LG. Memory function in normal aging. Acta Neurol Scand Suppl 2003;179:7-13.

[3] Korten AE, Henderson AS, Christensen H, Jorm AF, Rodgers B, Jacomb P, et al. A prospective study of cognitive function in the elderly. Psychol Med 1997;27(4):919-30.

[4] Ronnlund M, Nyberg L, Backman L, Nilsson LG. Stability, growth, and decline in adult life span development of declarative memory: cross-sectional and longitudinal data from a population-based study. Psychol Aging 2005;20(1):3-18.

[5] Christensen H. What cognitive changes can be expected with normal ageing? Aust N Z J Psychiatry 2001;35(6):768-75.

[6] Petersen RC, Stevens JC, Ganguli M, Tangalos EG, Cummings JL, DeKosky ST. Practice parameter: early detection of dementia: mild cognitive impairment (an evidence-based review). Report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology 2001;56(9):1133-42.

[7] Collie A, Maruff P. The neuropsychology of preclinical Alzheimer's disease and mild cognitive impairment. Neurosci Biobehav Rev 2000;24(3):365-74.

[8] Collie A, Maruff P, Currie J. Behavioral characterization of mild cognitive impairment. J Clin Exp Neuropsychol 2002;24(6):720-33.

[9] Shah Y, Tangalos EG, Petersen RC. Mild cognitive impairment. When is it a precursor to Alzheimer's disease? Geriatrics 2000;55(9):62, 65-8.

[10] Petersen RC, Smith GE, Waring SC, Ivnik RJ, Tangalos EG, Kokmen E. Mild cognitive impairment: clinical characterization and outcome. Arch Neurol 1999;56(3):303-8.

[11] Jorm AF, Masaki KH, Petrovitch H, Ross GW, White LR. Cognitive deficits 3 to 6 years before dementia onset in a population sample: the Honolulu-Asia aging study. J Am Geriatr Soc 2005;53(3):452-5.

[12] MacDonald SW, Dixon RA, Cohen AL, Hazlitt JE. Biological age and 12-year cognitive change in older adults: findings from the Victoria Longitudinal Study. Gerontology 2004;50(2):64-81.

[13] Jagust W, Harvey D, Mungas D, Haan M. Central obesity and the aging brain. Arch Neurol 2005;62(10):1545-8.

[14] Correa Leite ML, Nicolosi A, Cristina S, Hauser WA, Nappi G. Nutrition and cognitive deficit in the elderly: a population study. Eur J Clin Nutr 2001;55(12):1053-8.

[15] La Rue A, Koehler KM, Wayne SJ, Chiulli SJ, Haaland KY, Garry PJ. Nutritional status and cognitive functioning in a normally aging sample: a 6-y reassessment. Am J Clin Nutr 1997;65(1):20-9.

[16] Selhub J, Bagley LC, Miller J, Rosenberg IH. B vitamins, homocysteine, and neurocognitive function in the elderly. Am J Clin Nutr 2000;71(2):614S-620S.

[17] Youdim KA, Shukitt-Hale B, Joseph JA. Flavonoids and the brain: interactions at the blood-brain barrier and their physiological effects on the central nervous system. Free Radic Biol Med 2004;37(11):1683-93.

[18] McCaddon A, Hudson P, Davies G, Hughes A, Williams JH, Wilkinson C. Homocysteine and cognitive decline in healthy elderly. Dement Geriatr Cogn Disord 2001;12(5):309-13.

[19] McCaddon A, Davies G, Hudson P, Tandy S, Cattell H. Total serum homocysteine in senile dementia of Alzheimer type. Int J Geriatr Psychiatry 1998;13(4):235-9.

[20] Clarke R, Smith AD, Jobst KA, Refsum H, Sutton L, Ueland PM. Folate, vitamin B12, and serum total homocysteine levels in confirmed Alzheimer disease. Arch Neurol 1998;55(11):1449-55.

[21] Racek J, Rusnakova H, Trefil L, Siala KK. The influence of folate and antioxidants on homocysteine levels and oxidative stress in patients with hyperlipidemia and hyperhomocysteinemia. Physiol Res 2005;54(1):87-95.

[22] Garcia A, Pulman K, Zanibbi K, Day A, Galaraneau L, Freedman M. Cobalamin reduces homocysteine in older adults on folic acid-fortified diet: a pilot, double-blind, randomized, placebo-controlled trial. J Am Geriatr Soc 2004;52(8):1410-2.

[23] Lewerin C, Nilsson-Ehle H, Matousek M, Lindstedt G, Steen B. Reduction of plasma homocysteine and serum methylmalonate concentrations in apparently healthy elderly subjects after treatment with folic acid, vitamin B12 and vitamin B6: a randomised trial. Eur J Clin Nutr 2003;57(11):1426-36.

ABA COURSE

 Intensive ABA Course based on Pivotal Response Treatment to train parents and caregivers are available.

Pre-booking is essential.

Cost $590

DSS (previously FaHCSIA) will pay for parents to do the course.