Orange County Neuropsychology

Dementia with Lewy Bodies and Parkinson’s Disease with Dementia: How are they different?

2010-04-07T21:35:00.000-07:00

Joanne M. Hamilton, PhD

Lewy Bodies, abnormal aggregates of several proteins including alpha-synuclein, develop in neurons of people with Parkinson’s disease (PD) and Dementia with Lewy bodies (DLB). Considerable confusion exists regarding the distinction between PD and DLB especially in light of estimates that upwards of 35% of people diagnosed with PD will develop cognitive problems of sufficient severity to meet criteria for dementia. Many scientists question the distinction between DLB and PD with dementia (PDD) because the disorders share so many clinical and neuropathological features. Both are associated with movement problems caused by damage to the extrapyramidal motor system and progressive cognitive decline. Currently, the Consortium on DLB (McKeith et al., 2005) recommends that a diagnosis of PDD be given if motor symptoms precede cognitive decline by more than a year and DLB be given if cognitive decline precedes or emerges in concert with motor symptoms. Clearly, these criteria contribute to the confusion since it is often difficult to judge which symptom came first.

In practice, both DLB and PDD are associated with prominent difficulties with attention and concentration, cognitive flexibility, problem-solving, and visuospatial processing. Visuospatial deficits can be particularly obvious even before changes in memory and language occur. Functionally, people whose visuospatial processing is impaired may tend to sit down on the edges of their chairs, bump into walls, trip on stairs, or misjudge distances while driving. Visual misperceptions and hallucinations are also associated with changes in visuospatial processing in patients with DLB and PD. These visual phenomena can be disturbing to people with the disorders and their caregivers and can be difficult to manage clinically because of drug sensitivities associated with the Lewy body disorders. A recent study has suggested a possible mechanism for the association between visuospatial problems and visual hallucinations in PD. Stebbins and colleagues (NEUROLOGY 2004;63:1409-1416) reported that visual information is abnormally processed in the frontal region rather than the posterior region of the brain in PD patients who have hallucinations. This transfer of functioning may occur because of damage to posterior regions where visual processing typically takes place. Thus, deficits in visuospatial functioning may serve as a proxy for the amount of posterior brain damage and signal an increased risk of developing hallucinations.

This hypothesis is being examined at the Dementia with Lewy Bodies Program at the University of California, San Diego. We are conducting studies to identify the mechanism associated with changes in visuospatial processing and the emergence of visual hallucinations. Individuals who are interested in participating are encouraged to call Kelly Landy at (858) 622-5839 or visit our website at dlb.ucsd.edu. We are currently enrolling individuals diagnosed with DLB and PD. To this end, we hope to enhance our understanding of the relationship between the cognitive deficits associated with DLB and PD and the course of these devastating illnesses with hopes of improving the treatments that are currently available.

Upcoming Neuropsychology Workshops & Seminars for Patients and Families

2009-10-05T09:55:00.000-07:00

Please follow this link to preview upcoming seminars and presentations in the southern California area

http://www.anhsocal.com/neuropsychology-seminars-workshops.html

Effects of Substance Use on Adolescent Brain Development

2009-10-05T09:27:00.000-07:00

By Sunita Bava PhD

Substance use during adolescence continues to be a prevalent concern. Marijuana and alcohol are consistently the most frequently used substances among teens [1], with 16% of 12-17 year-olds reporting lifetime marijuana use, and 15% of 12th graders endorsing past month intake [2]. Rates of past month alcohol use among 12-17 year-olds are similar (16%), with increasing prevalence at ages 16 and 17 (35%). For the estimated 9% of adolescents who meet criteria for substance abuse or dependence [2], harmful effects of marijuana and alcohol span physiological, social, and psychological functioning [3-5]. Because extensive brain maturation occurs during this time, adolescents who use substances are vulnerable to alterations in brain functioning, cognition and behavior.

Recent studies have shown alterations in brain functioning in adolescent substance users even after 28 days of sustained abstinence. These studies indicate weaknesses in neuropsychological functioning in the areas of attention, speeded information processing, spatial skills, learning and memory, and complex behaviors such as planning and problem solving [6-10]. There are also associated changes in brain structure and function that include altered prefrontal brain volumes, reduced white matter microstructural integrity, and atypical brain activation patterns [11-17]. There may be potential reversibility of brain structural changes with long-term abstinence [18], though additional studies are needed to understand the extent to which abnormalities persist or remit with time.

Adolescence is a time of extensive social, psychological, and biological change. There are also considerable academic demands and educational considerations that take place during this time. For youth that engage in heavy substance use, the potential impact of these substances on development warrants concern. Assessment of the adolescent’s neuropsychological functioning can provide valuable insight with regard to potential cognitive weaknesses that may affect academic performance, identify mood and behavioral changes that would benefit from treatment, and provide appropriate recommendations for substance use intervention.

References

1. Schweinsburg, A.D., S.A. Brown, and S.F. Tapert, The influence of marijuana use on neurocognitive functioning in adolescents. Current Drug Abuse Reviews, 2008. 1: p. 99-111.
2. SAMSHA, Results from the 2006 National Survey on Drug Use and Health: National Findings. 2007: Rockville, MD: Office of Applied Studies, DHHS.
3. Macleod, J., et al., Psychological and social sequelae of cannabis and other illicit drug use by young people: a systematic review of longitudinal, general population studies. Lancet, 2004. 363(9421): p. 1579-88.
4. Tucker, J.S., et al., Does solitary substance use increase adolescents' risk for poor psychosocial and behavioral outcomes? A 9-year longitudinal study comparing solitary and social users. Psychology of Addictive Behaviors, 2006. 20(4): p. 363-72.
5. Tucker, J.S., et al., Are drug experimenters better adjusted than abstainers and users?: a longitudinal study of adolescent marijuana use. Journal of Adolescent Health, 2006. 39(4): p. 488-94.
6. Brown, S.A., et al., Neurocognitive functioning of adolescents: effects of protracted alcohol use. Alcoholism: Clinical and Experimental Research, 2000. 24(2): p. 164-71.
7. Medina, K.L., et al., Neuropsychological functioning in adolescent marijuana users: subtle deficits detectable after a month of abstinence. Journal of the International Neuropsychological Society, 2007. 13(5): p. 807-20.
8. Tapert, S.F. and S.A. Brown, Neuropsychological correlates of adolescent substance abuse: four-year outcomes. Journal of the International Neuropsychological Society, 1999. 5(6): p. 481-93.
9. Tapert, S.F. and S.A. Brown, Substance dependence, family history of alcohol dependence and neuropsychological functioning in adolescence. Addiction, 2000. 95(7): p. 1043-53.
10. Tapert, S.F., et al., Substance use and withdrawal: neuropsychological functioning over 8 years in youth. Journal of the International Neuropsychological Society, 2002. 8(7): p. 873-83.
11. Jacobsen, L.K., et al., Functional correlates of verbal memory deficits emerging during nicotine withdrawal in abstinent adolescent cannabis users. Biological Psychiatry, 2007. 61(1): p. 31-40.
12. Schweinsburg, A.D., et al., Abstinent adolescent marijuana users show altered fMRI response during spatial working memory. Psychiatry Research: Neuroimaging, 2008.
13. Schweinsburg, A.D., et al., fMRI response to spatial working memory in adolescents with comorbid marijuana and alcohol use disorders. Drug and Alcohol Dependence, 2005. 79(2): p. 201-10.
14. Tapert, S.F., et al., fMRI measurement of brain dysfunction in alcohol-dependent young women. Alcoholism: Clinical and Experimental Research, 2001. 25(2): p. 236-45.
15. Tapert, S.F., et al., Blood oxygen level dependent response and spatial working memory in adolescents with alcohol use disorders. Alcoholism: Clinical and Experimental Research, 2004. 28(10): p. 1577-86.
16. Tapert, S.F., et al., Functional MRI of inhibitory processing in abstinent adolescent marijuana users. Psychopharmacology (Berl), 2007. 194(2): p. 173-83.
17. Bava, S., et al., Altered white matter microstructure in adolescent substance users. Psychiatry Res, 2009. 173(3): p. 228-37.
18. Delisi, L.E., et al., A preliminary DTI study showing no brain structural change associated with adolescent cannabis use. Harm Reduct Journal, 2006. 3: p. 17.

What is neuropsychology & how do I find a neuropsychologist?

2009-01-24T09:10:00.000-08:00

What is neuropsychology?

Neuropsychology is a subspecialty field of psychology. A psychologist is one who studies human behavior, and a neuropsychologist is one who specializes in the relationship between behavior and brain function.

See http://www.div40.org/def.html for a professional definition of a neuropsychologist.

Does a neuropsychological evaluation differ from those of a school psychologist or a clinical psychologist?

Yes, in both cases. School psychologists, clinical psychologists, and clinical neuropsychologists all have similar goals in wanting to provide the best interventions for their clients.

A clinical neuropsychologist, however, provides specialized services because he or she understands a person's behavior from multiple perspectives: medical, emotional, behavioral, cognitive, educational, and rehabilitative. Our evaluations are not limited by the objectives of a psychological treatment plan or a school setting. Instead, we incorporate extensive detail about one's medical history, developmental background, cognitive ability, academic achievement, and day-to-day functioning because we intend to make recommendations that are applicable in all major areas of a client's life.

How do I choose a neuropsychologist?

An appropriately trained clinical neuropsychologist has earned a doctorate degree in psychology from an APA-accredited university. These degree programs include a 12-month clinical psychology internship, ideally including neuropsychology training. Postdoctoral training in neuropsychology is also necessary, according to standards set within the field (referred to as "The Houston Conference"; see http://www.div40.org/pub/Houston_conference.pdf).

A list of board certified clinical neuropsychologists can be accessed via the American Academy of Clinical Neuropsychology website; http://www.theaacn.org/diplomates/database/view.php