Debbie Anderson in Brisbane, Queensland, Australia | Medical and health

Debbie Anderson

Locality: Brisbane, Queensland, Australia

Phone: +61 7 3832 3591

Address: Suite 63, 6th Floor, Silverton Place, 101 Wickham Tce 4000 Brisbane, QLD, Australia

Website: http://www.debbieanderson.com.au

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25.01.2022 Tonight I went to a talk at the Brisbane Library- by Bri Lee, author of Eggshell Skull. She patiently signed all our books. Whilst some of the content is upsetting Im enjoying reading her book - about her experiences with the Qld Judicial System & sexual offenders. A thought provoking presentation, which I enjoyed.

22.01.2022 Learn the phases of sports concussion recovery. https://bit.ly/2MJMEJ5

21.01.2022 I was honoured to be invited to speak at the Qld Law Society Personal Injuries Conference today - on the topic of Neuropsychology. It went well and I received lots of interesting questions.

20.01.2022 Im pleased to be attending the MLSQ Annual Conference- titled High Society- the misuse of opioids at the lovely Marriott. Lots of interesting speakers on this challenging topic!

20.01.2022 It’s quite challenging to see that psychologists are involved in the American celebrity Learning Disability diagnosis scam. However, here’s a great response from AACN showing how the thorough work done by neuropsychologists can overcome this problem. Neuropsychologists are very attuned to combining the lifetime history with the test data, and make sense of it all. May not be popular, but it’s accurate and backed up by rigorous data!

20.01.2022 Unfortunately this illustrates the vulnerability of people with traumatic brain injury the being taken advantage of, including a neuropsychologists explanation and intervention.

19.01.2022 we've moved to our lovely new offices:

19.01.2022 weve moved to our lovely new offices:

15.01.2022 Im here at the lovely Marriott Gold Coast the attend the Medico-Legal Society of Qld Conference- to examine issues of consent.

12.01.2022 Ill be out of the office for the next couple of days, I have the honor of chairing the 2018 APS College of Clinical Neuropsychologists Conference. Im excited about the fantastic program that we have put together, exploring many current issues in neuropsychology, with an incredible range of international speakers and wonderful local talent. We will be reminded that both the neuro and the psychology matter in what we do, and that it matters that we always aim to operate at a level consistent with international standards

12.01.2022 A beautiful view today as I am attending a two day workshop on Structured Interviewing and Risk Assessment for the Family and Childrens Court. Looking forward to applying new skills and knowledge.

12.01.2022 This book arrived today - Id almost forgotten that it was coming! Karen was invited to contribute- and we wrote up one of my cases. I hope it helps the provisional psychologists with writing up their case studies.

10.01.2022 This is the way to do Professional Development- presenting in Bali on the use of psychometricians in neuropsychological assessment. Lots of very interesting discussion with colleagued

10.01.2022 AACN's Ask the Experts Series Do We Only Use 10% of Our Brains? Response by Jordan Robinson, PhD, ABPP... Do we only use 10% of our brains? If we could unlock that extra 90%, could we all become geniuses or develop extra powers such as telekinesis? The clear, uncontroversial answer within the scientific community is a resounding no. By now, most of us have seen this myth in some capacity, whether it be in a TV show or movie (e.g., Limitless, Lucy) or an ad for some kind of wonder drug supplement or cognitive training program trying to sell you something. The origin of this myth is still somewhat a mystery, with some claiming it dates back to a misrepresentation of a statement by William James, which was later used in the 1936 book How to Win Friends and Influence People. Despite where this myths origin lies, its effects still persist as some studies estimate that up to 65% of those surveyed believe the myth. Dr. Barry Gordon has responded to the myth through the magazine Scientific American with several clear rebuttals to tenets of the 10% myth. Several of these are 1) the notion that if we only use 10% of our brains, brain damage would not cause deficits in most areas of the brain, which is demonstrably false in countless studies and clinical cases, 2) brain activation mapping techniques (PET, fMRI, etc) show that almost all brain areas are active, even at rest, with some areas more active than others depending on what the person is doing, 3) in decades of research on finding localization and connectivity of cognitive/emotional/motor functioning, there has never been a region found that is not responsible for or intimately connected to some function. These are just a few facts used to dispel this myth. For more information feel free to explore the following links. https://www.wired.com//everything-you-need-to-know-about-/ https://www.scientificamerican.com//do-we-really-use-only/ https://faculty.washington.edu/chudler/tenper.html

09.01.2022 AACNs Ask the Experts Series Do We Only Use 10% of Our Brains? Response by Jordan Robinson, PhD, ABPP... Do we only use 10% of our brains? If we could unlock that extra 90%, could we all become geniuses or develop extra powers such as telekinesis? The clear, uncontroversial answer within the scientific community is a resounding no. By now, most of us have seen this myth in some capacity, whether it be in a TV show or movie (e.g., Limitless, Lucy) or an ad for some kind of wonder drug supplement or cognitive training program trying to sell you something. The origin of this myth is still somewhat a mystery, with some claiming it dates back to a misrepresentation of a statement by William James, which was later used in the 1936 book How to Win Friends and Influence People. Despite where this myths origin lies, its effects still persist as some studies estimate that up to 65% of those surveyed believe the myth. Dr. Barry Gordon has responded to the myth through the magazine Scientific American with several clear rebuttals to tenets of the 10% myth. Several of these are 1) the notion that if we only use 10% of our brains, brain damage would not cause deficits in most areas of the brain, which is demonstrably false in countless studies and clinical cases, 2) brain activation mapping techniques (PET, fMRI, etc) show that almost all brain areas are active, even at rest, with some areas more active than others depending on what the person is doing, 3) in decades of research on finding localization and connectivity of cognitive/emotional/motor functioning, there has never been a region found that is not responsible for or intimately connected to some function. These are just a few facts used to dispel this myth. For more information feel free to explore the following links. https://www.wired.com//everything-you-need-to-know-about-/ https://www.scientificamerican.com//do-we-really-use-only/ https://faculty.washington.edu/chudler/tenper.html

09.01.2022 Its quite challenging to see that psychologists are involved in the American celebrity Learning Disability diagnosis scam. However, heres a great response from AACN showing how the thorough work done by neuropsychologists can overcome this problem. Neuropsychologists are very attuned to combining the lifetime history with the test data, and make sense of it all. May not be popular, but its accurate and backed up by rigorous data!

09.01.2022 The conference is starting now - its hard to believe that there are over one thousand neuropsychologists (I think its 1800) in one place, getting up to date with the latest research from the experts. Im looking forward to bringing home lots of new information and ideas!

08.01.2022 Now we take memory problems very seriously- but its Sunday - Fun day

07.01.2022 Just preparing to return home after an assessment today in Cairns! Next time I will make sure I schedule it so I can make a long weekend of it - its nice to get away, and fabulous to meet our referrers in person.

07.01.2022 AACN's Ask the Experts Series: What is the difference between cortical and subcortical dementia? Response by Rus Bauer, PhD, ABPP... Dementia is an umbrella term that denotes a loss of cognitive and adaptive ability which impairs the persons ability to perform everyday life functions. Dementia is not a disease itself; it is a syndrome caused by a variety of diseases including degenerative conditions (e.g., Alzheimers disease, Parkinsons disease), infections (e.g., Creutzfeldt-Jacob disease), metabolic (e.g., hepatic, renal) disease, repetitive trauma (e.g., chronic traumatic encephalopathy), and other causes. The diseases that result in dementia can affect both the cortex (the brain matter responsible for higher cognitive function), as well as subcortical regions (where complex brain cells and their interconnections regulate motor, intentional, and emotional systems of the brain). The distinction between cortical and subcortical dementia evolved in the 1980s to provide a means for classifying the primary regions affected by dementia-producing illnesses, and to highlight behavioral features that may distinguish patients with cortical and subcortical disease. Cortical dementia refers to a syndrome in which the patient presents with symptoms attributable to dysfunction of major domains of cognition. In these patients, memory impairment, language disturbances, disorders of visual recognition, or problems with complex skilled movement are prominent. Patients with Alzheimers disease, frontotemporal dementia, Creutzfeldt-Jacob disease, and Lewy-Body Dementia tend to present in this way. As such diseases progress, what may have begun as relatively mild problems in brain function can progress to severely impaired memory, inability to speak or conduct purposeful movement. In subcortical dementias, cognitive problems are present but may not be as obvious or severe. Instead, the patient with subcortical dementia may more prominently display psychomotor slowing, problems initiating and maintaining activity, reduced motivation, and emotional symptoms such as apathy, indifference, or anhedonia. Word-finding problems or memory difficulties may be present, not from impairment in the cognitive domain itself, but from the patients inability to execute appropriate retrieval strategies needed to efficiently access information stored in the brain. Patients with subcortical dementia may have prominent impairment in skills like planning and organization owing to the dense interconnections between subcortical structures and the frontal lobe, which is responsible for these functions. Diseases such as Parkinsons disease and Huntingtons disease typically produce a subcortical picture. The cortical vs. subcortical dementia distinction remains heuristic but is not without its detractors. Several well-controlled studies have failed to find quantitative neuropsychological differences between cortical and subcortical groups, while others have been more successful. More important is the fact that many patients present with symptoms suggesting both cortical and subcortical damage. It is quite common, for example, for patients with behavioral and biomarker evidence of Alzheimers disease to also have extensive subcortical vascular disease, leading to a mixed AD-vascular picture. In these patients, the cortical-subcortical distinction may lose its utility, though it may still serve to remind the clinician to evaluate the full range of symptoms to determine whether the patients cognitive loss results from damage to cortical processors, impairment of subcortical systems regulating activation, motivation, and emotion, or both. Source of graphic: Huntingtons Outreach Project for Education, at Stanford (HOPES) Image Source: https://hopes.stanford.edu/dementia-in-huntingtons-disease/

05.01.2022 I'm here at the lovely Marriott Gold Coast the attend the Medico-Legal Society of Qld Conference- to examine issues of consent.

02.01.2022 Today is world MS (Multiple Sclerosis) Day. Here is a video of the very important research being undertaken towards slowing (or halting) the progress of MS. The team is led by the wonderful Prof Pender, who I was lucky enough to work with at the RBH many years ago. His interest in understanding the effects of MS in his patients helped encourage me to better understand the condition. Neuropsychological assessment can explore whether cognitive function is impacted by the disease, which can influence decisions (such as continuing work, accessing insurances). Careful evaluation and empathy is always important, the patients are a young group, facing a progressive neurological condition.

02.01.2022 I'll be out of the office for the next couple of days, I have the honor of chairing the 2018 APS College of Clinical Neuropsychologists Conference. I'm excited about the fantastic program that we have put together, exploring many current issues in neuropsychology, with an incredible range of international speakers and wonderful local talent. We will be reminded that both the 'neuro' and the 'psychology' matter in what we do, and that it matters that we always aim to operate at a level consistent with international standards

01.01.2022 AACNs Ask the Experts Series: What is the difference between cortical and subcortical dementia? Response by Rus Bauer, PhD, ABPP... Dementia is an umbrella term that denotes a loss of cognitive and adaptive ability which impairs the persons ability to perform everyday life functions. Dementia is not a disease itself; it is a syndrome caused by a variety of diseases including degenerative conditions (e.g., Alzheimers disease, Parkinsons disease), infections (e.g., Creutzfeldt-Jacob disease), metabolic (e.g., hepatic, renal) disease, repetitive trauma (e.g., chronic traumatic encephalopathy), and other causes. The diseases that result in dementia can affect both the cortex (the brain matter responsible for higher cognitive function), as well as subcortical regions (where complex brain cells and their interconnections regulate motor, intentional, and emotional systems of the brain). The distinction between cortical and subcortical dementia evolved in the 1980s to provide a means for classifying the primary regions affected by dementia-producing illnesses, and to highlight behavioral features that may distinguish patients with cortical and subcortical disease. Cortical dementia refers to a syndrome in which the patient presents with symptoms attributable to dysfunction of major domains of cognition. In these patients, memory impairment, language disturbances, disorders of visual recognition, or problems with complex skilled movement are prominent. Patients with Alzheimers disease, frontotemporal dementia, Creutzfeldt-Jacob disease, and Lewy-Body Dementia tend to present in this way. As such diseases progress, what may have begun as relatively mild problems in brain function can progress to severely impaired memory, inability to speak or conduct purposeful movement. In subcortical dementias, cognitive problems are present but may not be as obvious or severe. Instead, the patient with subcortical dementia may more prominently display psychomotor slowing, problems initiating and maintaining activity, reduced motivation, and emotional symptoms such as apathy, indifference, or anhedonia. Word-finding problems or memory difficulties may be present, not from impairment in the cognitive domain itself, but from the patients inability to execute appropriate retrieval strategies needed to efficiently access information stored in the brain. Patients with subcortical dementia may have prominent impairment in skills like planning and organization owing to the dense interconnections between subcortical structures and the frontal lobe, which is responsible for these functions. Diseases such as Parkinsons disease and Huntingtons disease typically produce a subcortical picture. The cortical vs. subcortical dementia distinction remains heuristic but is not without its detractors. Several well-controlled studies have failed to find quantitative neuropsychological differences between cortical and subcortical groups, while others have been more successful. More important is the fact that many patients present with symptoms suggesting both cortical and subcortical damage. It is quite common, for example, for patients with behavioral and biomarker evidence of Alzheimers disease to also have extensive subcortical vascular disease, leading to a mixed AD-vascular picture. In these patients, the cortical-subcortical distinction may lose its utility, though it may still serve to remind the clinician to evaluate the full range of symptoms to determine whether the patients cognitive loss results from damage to cortical processors, impairment of subcortical systems regulating activation, motivation, and emotion, or both. Source of graphic: Huntingtons Outreach Project for Education, at Stanford (HOPES) Image Source: https://hopes.stanford.edu/dementia-in-huntingtons-disease/