Tanya P Lin
- Associate Professor, Neurology - (Clinical Scholar Track)
Contact
- (520) 626-2006
- AHSC, Rm. 6205
- TUCSON, AZ 85724-5023
- tlin@arizona.edu
Degrees
- M.D. Distinction in Research in Neurology
- Albert Einstein College of Medicine, Bronx, New York, United States
- M.S. Chemical Engineering Practice
- Massachusetts Institute of Technology, Cambridge, Massachusetts, United States
- B.S. Chemical Engineering
- Massachusetts Institute of Technology, Cambridge, Massachusetts, United States
Work Experience
- Southern Arizona Health Care System (2014 - Ongoing)
- University of Arizona: Department of Neurology (2013 - Ongoing)
- Locum Tenens Neurohospitalist (2013 - 2014)
- Genentech, Inc. (1999 - 2003)
Awards
- Educator of the Year
- University of Arizona, Department of Neurology, Spring 2020
Licensure & Certification
- Neurology, American Board of Psychiatry and Neurology (2012)
- California Medical License (2015)
- Arizona Medical License (2012)
Interests
Research
Clinical research projects in non-motor symptoms of Parkinson's disease.
Courses
2024-25 Courses
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Neuro+Rehab Med Clerkshp
NEUR 813C (Fall 2024)
2023-24 Courses
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Neuro+Rehab Med Clerkshp
NEUR 813C (Fall 2023)
2022-23 Courses
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Neuro+Rehab Med Clerkshp
NEUR 813C (Fall 2022)
2021-22 Courses
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Neuro+Rehab Med Clerkshp
NEUR 813C (Fall 2021)
2020-21 Courses
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Neuro+Rehab Med Clerkshp
NEUR 813C (Spring 2021) -
Neurology Clerkship Clinical
NEUR 813C2 (Spring 2021) -
Neuro+Rehab Med Clerkshp
NEUR 813C (Fall 2020)
2019-20 Courses
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Neuro+Rehab Med Clerkshp
NEUR 813C (Fall 2019)
2018-19 Courses
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Neuro+Rehab Med Clerkshp
NEUR 813C (Fall 2018)
2017-18 Courses
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Neuro+Rehab Med Clerkshp
NEUR 813C (Fall 2017)
2016-17 Courses
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Neuro+Rehab Med Clerkshp
NEUR 813C (Spring 2017) -
Neurology Gen. Inpatient Svc.
NEUR 850A (Spring 2017) -
Neuro+Rehab Med Clerkshp
NEUR 813C (Fall 2016)
2015-16 Courses
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Neuro+Rehab Med Clerkshp
NEUR 813C (Spring 2016)
Scholarly Contributions
Chapters
- Hishaw, G. A., Lin, T. P., & Rapcsak, S. Z. (2016). Visual Hallucination. In Encyclopedia of Clinical Neuropsychology.
- Lin, T. (2016). REM Sleep Behavioral Disorder. In SAGE Encyclopedia.
- Rapcsak, S. Z., Hishaw, G. A., & Lin, T. P. (2016). Cortical Blindness. In Encyclopedia of Clinical Neuropsychology.
Journals/Publications
- Chen, N. K., Chou, Y. H., Sundman, M., Hickey, P., Kasoff, W. S., Bernstein, A., Trouard, T. P., Lin, T., Rapcsak, S. Z., Sherman, S. J., & Weingarten, C. P. (2018). Alteration of Diffusion-Tensor Magnetic Resonance Imaging Measures in Brain Regions Involved in Early Stages of Parkinson's Disease. Brain connectivity, 8(6), 343-349.More infoMany nonmotor symptoms (e.g., hyposmia) appear years before the cardinal motor features of Parkinson's disease (PD). It is thus desirable to be able to use noninvasive brain imaging methods, such as magnetic resonance imaging (MRI), to detect brain abnormalities in early PD stages. Among the MRI modalities, diffusion-tensor imaging (DTI) is suitable for detecting changes in brain tissue structure due to neurological diseases. The main purpose of this study was to investigate whether DTI signals measured from brain regions involved in early stages of PD differ from those of healthy controls. To answer this question, we analyzed whole-brain DTI data of 30 early-stage PD patients and 30 controls using improved region of interest-based analysis methods. Results showed that (i) the fractional anisotropy (FA) values in the olfactory tract (connected with the olfactory bulb: one of the first structures affected by PD) are lower in PD patients than healthy controls; (ii) FA values are higher in PD patients than healthy controls in the following brain regions: corticospinal tract, cingulum (near hippocampus), and superior longitudinal fasciculus (temporal part). Experimental results suggest that the tissue property, measured by FA, in olfactory regions is structurally modulated by PD with a mechanism that is different from other brain regions.
- DiBaise, J. K., Crowell, M. D., Driver-Dunckley, E., Mehta, S. H., Hoffman-Snyder, C., Lin, T., & Adler, C. H. (2018). Weight Loss in Parkinson's Disease: No Evidence for Role of Small Intestinal Bacterial Overgrowth. Journal of Parkinson's disease, 8(4), 571-581.More infoWeight loss and small intestinal bacterial overgrowth (SIBO) are common in Parkinson's disease (PD). We aimed to study the relationship between weight loss and SIBO in PD.
- Lin, T. P., Rigby, H., Adler, J. S., Hentz, J. G., Balcer, L. J., Galetta, S. L., Devick, S., Cronin, R., & Adler, C. H. (2015). Abnormal Variable Contrast Acuity in Parkinson's Disease. Journal of Parkinson's disease, 5(1), 125-30.More infoLow-contrast vision is thought to be reduced in Parkinson's disease (PD). This may have a direct impact on quality of life such as driving, using tools, finding objects, and mobility in low-light condition. Low-contrast letter acuity testing has been successful in assessing low-contrast vision in multiple sclerosis. We report the use of a new iPad application to measure low-contrast acuity in patients with PD.
- Lin, T. P., Adler, C. H., Hentz, J. G., Balcer, L. J., Galetta, S. L., & Devick, S. (2014). Slowing of number naming speed by King-Devick test in Parkinson's disease. Parkinsonism & related disorders, 20(2), 226-9.More infoThe King-Devick (KD) test measures the speed of rapid number naming, and is postulated to require fast eye movements, attention, language, and possibly other aspects of cognitive functions. While used in multiple sports concussion studies, it has not been applied to the field of movement disorders.
- Lin, T. P., Thompson, R., & Coull, B. (2013). A 28-year-old i.v. drug user with bilateral basal ganglia and brainstem lesions. Neurology, 80(7), e73-6.
- Lin, T., Adler, C. H., Hentz, J. G., Adler, J., Balcer, L. J., Galetta, S., Devick, S., & Cronin, R. (2013). Abnormal Variable Contrast Acuity in Parkinson's Disease (P04.143). Neurology, 80.More infoOBJECTIVE: To establish the utility of the Variable Contrast Acuity Chart in Parkinson9s disease (PD). BACKGROUND: Visual contrast acuity is reduced in PD due to loss of dopamine in amacrine-containing retina cells. An iPad version of the Variable Contrast Acuity Chart recently became available and has not been tested in PD patients. DESIGN/METHODS: Twelve PD and 46 controls were enrolled in the study. All were participants in the Arizona PD Consortium/Banner Sun Health Research Institute Brain and Body Donation Program. Participants viewed the Variable Contrast Acuity Chart on an iPad at distances of 40cm and 2m, with 100% and 2.5% contrast at each distance. Visual acuity at each condition was converted into a numeric contrast acuity (CA) score using a predetermined scale. Mean scores of the PD and control groups adjusted for age and sex were compared using a general linear model. RESULTS: The mean age was younger in PD (74.3±8.1 years) vs. Control (82.8±7.2 years). More men were in the PD group (75% PD; 24% Control). The mean PD duration was 10.1+5.2 years (range 1.9-17 years). Adjusting for age and sex, PD patients had statistically lower scores (worse vision) than controls in two test conditions: 100% contrast at 40cm (CA mean score = 78 for PD vs. 84 for controls, p=0.02) and 2.5% contrast at 2m (16 vs. 28, p=0.001), with a trend in the other two conditions: 100% contrast at 2m (53 vs. 58, p=0.14) and 2.5% contrast at 40cm (42 vs. 52, p=0.06). CONCLUSIONS: In this preliminary study, Parkinson9s disease patients were found to have more difficulty in reading the Variable Contrast Acuity Chart compared to controls. The iPad version of this eye chart is adjustable for distances and contrast levels, and may be a rapid tool for quantifying visual changes in Parkinson9s disease. Disclosure: Dr. Lin has nothing to disclose. Dr. Adler has received personal compensation for activities with Ipsen, Merz Pharma, and Impax. Dr. Adler has received research support from Avid Radiopharmaceuticals and Phytopharm. ......Forest Laboratories, Inc: Nebivolol and inappropriate left ventricular mass. Eisai Inc.: Lusedra for sedation during regional anesthesia block. Caridian: Maintenance plasma exchange for neuromyelitis optica spectrum disorders. Millennium: CyBorD in multiple myeloma. Dr. Adler has nothing to disclose. Dr. Balcer has received personal compensation for activities with Biogen Idec, Questcor, Novartis, and Vaccinex. Dr. Galetta has received personal compensation for activities with Biogen Idec and Teva Neuroscience as a speaker. Dr. Galetta has received research support from Biogen Idec. Dr. Devik has received personal compensation for activities with King-Devick Test, LLC. Dr. Devik has received compensation for serving on the board of King-Devick Test, LLC. Dr. Devik holds stock and/or stock options in King-Devick Test, LLC. Dr. Cronin has received personal compensation for activities with King-Devick Test, LLC. Dr. Arizona Parkinson9s Disease Consortium has nothing to disclose.
- Lin, T., Adler, C. H., Hentz, J. G., Balcer, L. J., Galetta, S. L., & Devick, S. (2013). Slowing of Rapid Number Naming by King-Devick Test in Parkinson's Disease (P04.173). Neurology, 80.More infoOBJECTIVE: To establish the utility of King-Devick Test in Parkinson9s disease (PD). BACKGROUND: The King-Devick (K-D) test measures the speed of rapid number naming, and is postulated to be sensitive in capturing impairment of eye movements, attention, language, and possibly other aspects of cognitive function. While used in multiple sports concussion studies, it has not been applied to the field of movement disorders. DESIGN/METHODS: A total of 25 PD and 71 controls were enrolled in the study. All were participants in the Arizona PD Consortium/Banner Sun Health Research Institute Brain and Body Donation Program. Participants read aloud a series of single-digit numbers from left to right on 3 different test cards in two consecutive trials. The sum time of all 3 cards from the faster trial was designated the final test score. The mean K-D scores from the PD and control groups were compared by the two-sample t-test. Adjusted means were compared by using a general linear model with terms for PD, age, and sex. RESULTS: The mean age was younger in PD (73.8 ± 7.4 years) vs. controls (80.9 ± 6.2 years). More men were in the PD group (68% PD vs. 34% Control). The mean PD duration was 9.3 + 5.9 years (range 1.5-25 years). The mean K-D score for the PD group (60.9 ± 19.8 seconds) was statistically higher compared to the control group (50.4 ± 9.8 seconds), p = 0.001. After adjusting for age and sex, the mean K-D score remained higher in the PD group (63.7 seconds) vs. controls (49.0 seconds), p CONCLUSIONS: This is the first study of the King-Devick Test in Parkinson9s disease. PD patients were found to have a slower rapid number naming speed compared to controls. Therefore, the King-Devick test may be a rapid tool for quantifying visual and cognitive function in Parkinson9s disease. Disclosure: Dr. Lin has nothing to disclose. Dr. Adler has received personal compensation for activities with Ipsen, Merz Pharma, and Impax. Dr. Adler has received research support from Avid Radiopharmaceuticals and Phytopharm. ......Forest Laboratories, Inc: Nebivolol and inappropriate left ventricular mass. Eisai Inc.: Lusedra for sedation during regional anesthesia block. Caridian: Maintenance plasma exchange for neuromyelitis optica spectrum disorders. Millennium: CyBorD in multiple myeloma. Dr. Balcer has received personal compensation for activities with Biogen Idec, Questcor, Novartis, and Vaccinex. Dr. Galetta has received personal compensation for activities with Biogen Idec and Teva Neuroscience as a speaker. Dr. Galetta has received research support from Biogen Idec. Dr. Devik has received personal compensation for activities with King-Devick Test, LLC. Dr. Devik has received compensation for serving on the board of King-Devick Test, LLC. Dr. Devik holds stock and/or stock options in King-Devick Test, LLC. Dr. Arizona Parkinson9s Disease Consortium has nothing to disclose.
- Pourfar, M., Tang, C., Lin, T., Dhawan, V., Kaplitt, M. G., & Eidelberg, D. (2009). Assessing the microlesion effect of subthalamic deep brain stimulation surgery with FDG PET. Journal of neurosurgery, 110(6), 1278-82.More infoThe authors investigated whether the insertion of deep brain stimulation electrodes into the subthalamic nucleus can alter regional brain metabolism in the absence of stimulation.
- Eckert, T., Tang, C., Ma, Y., Brown, N., Lin, T., Frucht, S., Feigin, A., & Eidelberg, D. (2008). Abnormal metabolic networks in atypical parkinsonism. Movement disorders : official journal of the Movement Disorder Society, 23(5), 727-33.More infoSpatial covariance analysis has been used with (18)F-fluorodeoxyglucose (FDG) PET to detect and quantify specific metabolic patterns associated with Parkinson's disease (PD). However, PD-related patterns cannot necessarily serve as biomarkers of the processes that underlie the atypical parkinsonian syndromes. In this FDG PET study, we used strictly defined statistical criteria to identify disease-related metabolic patterns in the imaging data from patients with multiple system atrophy (MSA) and progressive supranuclear palsy (PSP), the two most common of these atypical conditions. We found that MSA and PSP were each associated with a specific, highly stable metabolic brain network (P < 0.0001, bootstrap estimation). The MSA-related pattern was characterized by decreased metabolism in the putamen and cerebellum. The PSP-related pattern was characterized by metabolic decreases in the brainstem and medial frontal cortex. For both conditions, pattern expression was significantly elevated in patients relative to age-matched healthy control subjects (P < 0.001). For each condition, we validated the associated disease-related metabolic pattern by computing its expression on an individual scan basis in two independent patient cohorts, and in one subsequent healthy volunteer cohort. We found that for both MSA and PSP, prospective assessments of pattern expression accurately discriminated patients from controls (P < 0.001). These findings suggest that the major atypical parkinsonian syndromes are associated with distinct patterns of abnormal regional metabolic activity. These disease-related networks can potentially be used in conjunction with functional brain imaging as quantifiable biomarkers for the assessment of these pathological conditions.
- Hsu, L. N., Lin, T. R., & Sane, S. U. (2008). Near infrared spectroscopic characterisation of secondary structure content of proteins. JOURNAL OF NEAR INFRARED SPECTROSCOPY, 16(5), 437-444.
- Lin, T. P., Carbon, M., Tang, C., Mogilner, A. Y., Sterio, D., Beric, A., Dhawan, V., & Eidelberg, D. (2008). Metabolic correlates of subthalamic nucleus activity in Parkinson's disease. Brain : a journal of neurology, 131(Pt 5), 1373-80.More infoOveractivity of subthalamic nucleus (STN) neurons is a consistent feature of Parkinson's disease (PD) and is a target of therapy for this disorder. However, the relationship of STN firing rate to regional brain function is not known. We scanned 17 PD patients with (18)F-fluorodeoxyglucose (FDG) PET to measure resting glucose metabolism before the implantation of STN deep brain stimulation electrodes. Spontaneous STN firing rates were recorded during surgery and correlated with preoperative regional glucose metabolism on a voxel-by-voxel basis. We also examined the relationship between firing rate and the activity of metabolic brain networks associated with the motor and cognitive manifestations of the disease. Mean firing rates were 47.2 +/- 6.1 and 48.7 +/- 8.5 Hz for the left and right hemispheres, respectively. These measures correlated (P < 0.007) with glucose metabolism in the putamen and globus pallidus, which receive projections from this structure. Significant correlations (P < 0.0005) were also evident in the primary motor (BA4) and dorsolateral prefrontal (BA46/10) cortical areas. The activity of both the motor (P < 0.0001) and the cognitive (P < 0.006) PD-related metabolic networks was elevated in these patients. STN firing rates correlated with the activity of the former (P < 0.007) but not the latter network (P = 0.39). The findings suggest that the functional pathways associated with motor disability in PD are linked to the STN firing rate. These pathways are likely to mediate the clinical benefit that is seen following targeted STN interventions for this disease.
- Feigin, A., Kaplitt, M. G., Tang, C., Lin, T., Mattis, P., Dhawan, V., During, M. J., & Eidelberg, D. (2007). Modulation of metabolic brain networks after subthalamic gene therapy for Parkinson's disease. Proceedings of the National Academy of Sciences of the United States of America, 104(49), 19559-64.More infoParkinson's disease (PD) is characterized by elevated expression of an abnormal metabolic brain network that is reduced by clinically effective treatment. We used fluorodeoxyglucose (FDG) positron emission tomography (PET) to determine the basis for motor improvement in 12 PD patients receiving unilateral subthalamic nucleus (STN) infusion of an adenoassociated virus vector expressing glutamic acid decarboxylase (AAV-GAD). After gene therapy, we observed significant reductions in thalamic metabolism on the operated side as well as concurrent metabolic increases in ipsilateral motor and premotor cortical regions. Abnormal elevations in the activity of metabolic networks associated with motor and cognitive functioning in PD patients were evident at baseline. The activity of the motor-related network declined after surgery and persisted at 1 year. These network changes correlated with improved clinical disability ratings. By contrast, the activity of the cognition-related network did not change after gene transfer. This suggests that modulation of abnormal network activity underlies the clinical outcome observed after unilateral STN AAV-GAD gene therapy. Network biomarkers may be used as physiological assays in early-phase trials of experimental therapies for PD and other neurodegenerative disease.