Browse Health
Neurologist (brain, nervous system)
22 years of experience
Accepting new patients

Education ?

Medical School Score Rankings
Columbia University (1988)
  • Currently 4 of 4 apples
Top 25%

Awards & Distinctions ?

Appointments
Weill Medical College Of Cornell University Formerly Cornell Univ Med Coll, Ny (1995 - Present)
New York University School Of Medicine, Ny, Ny (1995 - Present)
Associations
American Board of Psychiatry and Neurology

Affiliations ?

Dr. Feigin is affiliated with 7 hospitals.

Hospital Affilations

Score

Rankings

  • North Shore University Hospital
    300 Community Dr, Manhasset, NY 11030
    • Currently 3 of 4 crosses
    Top 50%
    • Currently 3 of 4 crosses
    Top 50%
  • North Shore University Hospital At Syosset
    221 Jericho Tpke, Syosset, NY 11791
    • Currently 2 of 4 crosses
  • North Shore Univ Hosp At Glen Cove
    101 Saint Andrews Ln, Glen Cove, NY 11542
    • Currently 2 of 4 crosses
  • North Shore Univ Hosp At Plainview
    888 Old Country Rd, Plainview, NY 11803
    • Currently 2 of 4 crosses
  • North Shore Univ Hosp At Forest Hills
    10201 66th Rd, Forest Hills, NY 11375
    • Currently 2 of 4 crosses
  • North Shore Univ at Manhasset
  • Publications & Research

    Dr. Feigin has contributed to 7 publications.
    Title Relationship Between Self-reported Apathy and Executive Dysfunction in Nondemented Patients with Parkinson Disease.
    Date November 2007
    Journal Cognitive and Behavioral Neurology : Official Journal of the Society for Behavioral and Cognitive Neurology
    Excerpt

    OBJECTIVE: The prevalence of apathy was assessed across select cognitive and psychiatric variables in 32 nondemented patients with Parkinson disease (PD) and 29 demographically matched healthy control participants. BACKGROUND: Apathy is common in PD, although differentiating apathy from motor, cognitive, and/or other neuropsychiatric symptoms can be challenging. Previous studies have reported a positive relationship between apathy and cognitive impairment, particularly executive dysfunction. METHOD: Patients were categorized according to apathy symptom severity. Stringent criteria were used to exclude patients with dementia. RESULTS: Approximately 44% of patients endorsed significant levels of apathy. Those patients performed worse than patients with nonsignificant levels of apathy on select measures of verbal fluency and on a measure of verbal and nonverbal conceptualization. Further, they reported a greater number of symptoms related to depression and behavioral disturbance than did those patients with nonsignificant levels of apathy. Apathy was significantly related to self-report of depression and executive dysfunction. Performance on cognitive tasks assessing verbal fluency, working memory, and verbal abstraction and also on a self-report measure of executive dysfunction was shown to significantly predict increasing levels of apathy. CONCLUSIONS: Our findings suggest that apathy in nondemented patients with PD seems to be strongly associated with executive dysfunction.

    Title L-dopa Infusion Does Not Improve Explicit Sequence Learning in Parkinson's Disease.
    Date June 2007
    Journal Parkinsonism & Related Disorders
    Excerpt

    We have recently introduced a set of sequence learning tasks that emphasize explicit learning and target anticipation and involve the activation of frontal lobes. This type of learning is impaired even in the early stages of Parkinson's disease (PD). Studies on the effects of L-Dopa on cognitive symptoms of PD have yielded controversial results. To verify whether L-Dopa acutely improves explicit sequence learning, we tested six normal subjects and seven PD patients both off-drug and during L-Dopa infusion with two tasks: SEQ, a motor task with multiple demands, where a sequence had to be learned while reaching for a targets; VSEQ, a visual task where a sequence had to be learned by attending to a visual display without moving. Motor performance was assessed with simple motor tasks. L-Dopa improved motor scores and movement speed, but had no beneficial effect on either type of sequence learning.

    Title Using Advances in Neuroimaging to Detect, Understand, and Monitor Disease Progression in Huntington's Disease.
    Date August 2005
    Journal Neurorx : the Journal of the American Society for Experimental Neurotherapeutics
    Excerpt

    Transgenic mouse models and other screens are being used to identify potential therapeutic agents for use in clinical trials in Huntington's disease (HD). The development of surrogate markers that can be used in clinical therapeutics is an active area of research. Because HD is relatively uncommon and only a portion of available subjects meet inclusion and exclusion criteria, therapeutic trials are limited by the availability of potential subjects as well as the relative insensitivity of the clinical measures used. Neuroimaging methods offer the potential to provide noninvasive, reproducible, and objective methods not only to better understand the disease process but also to follow in clinical studies to determine if a drug is effective in slowing down disease progression or perhaps even in delaying onset. Following is a review of the literature, which highlights the studies that have been published to date.

    Title Fdg Pet in the Differential Diagnosis of Parkinsonian Disorders.
    Date August 2005
    Journal Neuroimage
    Excerpt

    The differential diagnosis of parkinsonian disorders can be challenging, especially early in the disease course. PET imaging with [(18)F]-fluorodeoxyglucose (FDG) has been used to identify characteristic patterns of regional glucose metabolism in patient cohorts with idiopathic Parkinson's disease (PD), as well as variant forms of parkinsonism such as multiple system atrophy (MSA), progressive supranuclear palsy (PSP), and corticobasal degeneration (CBGD). In this study, we assessed the utility of FDG PET in the differential diagnosis of individual patients with clinical parkinsonism. 135 parkinsonian patients were referred for FDG PET to determine whether their diagnosis could be made accurately based upon their scans. Imaging-based diagnosis was obtained by visual assessment of the individual scans and also by computer-assisted interpretation. The results were compared with 2-year follow-up clinical assessments made by independent movement disorders specialists who were blinded to the original PET findings. We found that blinded computer assessment agreed with clinical diagnosis in 92.4% of all subjects (97.7% early PD, 91.6% late PD, 96% MSA, 85% PSP, 90.1% CBGD, 86.5% healthy control subjects). Concordance of visual inspection with clinical diagnosis was achieved in 85.4% of the patients scanned (88.4% early PD, 97.2% late PD, 76% MSA, 60% PSP, 90.9% CBGD, 90.9% healthy control subjects). This study demonstrates that FDG PET performed at the time of initial referral for parkinsonism accurately predicted the clinical diagnosis of individual patients made at subsequent follow-up. Computer-assisted methodologies may be particularly helpful in situations where experienced readers of FDG PET images are not readily available.

    Title Cytosol Activator Protein from Rat Reticulocytes Requires the Stimulatory Guanine Nucleotide-binding Protein for Its Actions on Adenylate Cyclase.
    Date August 1985
    Journal Endocrinology
    Excerpt

    Rat reticulocytes contain a cytosol activator protein (RCAP) that augments catecholamine-sensitive adenylate cyclase activity in reticulocyte membranes. A highly purified preparation of RCAP, obtained by Sephacryl S-200 chromatography, was used to elucidate further its mechanism of action. The specific activity of the S-200 fraction to augment isoproterenol responsiveness was increased approximately 1,100-fold over the starting material, from 1.2 to 1,300 nmol cAMP formed per mg RCAP. The mol wt of RCAP is approximately 20,000. The effect of RCAP to enhance isoproterenol responsiveness was apparent within 20 sec, virtually abolishing the normal lag time of hormone-activated adenylate cyclase. In addition to its effects on catecholamine-responsive adenylate cyclase, RCAP significantly increased basal [21 +/- 3 (+/- SEM) to 41 +/- 4 pmol/mg protein X 30 min; P less than 0.02], guanyl-5'-yl-imidodiphosphate-associated (3173 +/- 213 to 4339 +/- 365 pmol/mg X 30 min; P less than 0.03), and fluoride-associated (5152 +/- 64 to 5807 +/- 58 pmol/mg X 30 min; P less than 0.05) adenylate cyclase activities. RCAP also altered the characteristics of agonist binding to the beta-adrenergic receptor of reticulocyte membranes, causing an increase in the apparent IC50 for isoproterenol from 0.7 +/- 0.2 to 7.9 +/- 1.6 microM (P less than 0.001). Similar to its effects on reticulocytes, RCAP enhanced isoproterenol- and prostaglandin E2-sensitive adenylate cyclase activity in the wild-type S49 lymphoma cell and shifted the binding isotherm for isoproterenol rightward. In cyc-, the mutant that lacks the stimulatory guanine nucleotide-binding protein (Ns) and in UNC, the mutant in which receptors are uncoupled from N, RCAP was ineffective. Moreover, RCAP decreased agonist affinity for the beta-adrenergic receptor in wild-type S49 cells, but not in cyc- or UNC cells. These observations suggest that RCAP requires a functional Ns unit for its effects on hormone-sensitive adenylate cyclase activity.

    Title Reticulocyte Cytosol Activator Protein: Effects on the Stimulatory and Inhibitory Regulatory Proteins of Adenylate Cyclase.
    Date August 1985
    Journal Endocrinology
    Excerpt

    Rat reticulocytes contain a cytosol activator protein (RCAP) that augments hormone-sensitive adenylate cyclase activity in the rat reticulocyte and other systems. In a previous publication, using a highly purified preparation of RCAP, we reported that the stimulatory guanine nucleotide-binding protein (Ns) was required for the actions of RCAP. We investigated this possibility by studying the actions of RCAP on cholera toxin-dependent ADP ribosylation of Ns. RCAP decreased cholera toxin-dependent ADP ribosylation of the 42,000-dalton subunit of Ns of reticulocyte [40.2 +/- 3.7 (+/-SEM) to 26.5 +/- 3.8 fmol/mg; n = 10; P less than 0.001], S49 wild-type (33.9 +/- 2.4 to 24.9 +/- 2.8 fmol/mg; n = 9; P less than 0.01), and UNC (25.3 +/- 3.5 vs. 17.6 +/- 3.1; n = 5; P less than 0.02) membranes. In contrast, pertussis toxin-dependent ADP-ribosylation of the inhibitory guanine nucleotide binding protein, Ni in reticulocyte, S49 wild-type lymphoma, and its UNC and cyc- variant membranes were all significantly augmented by RCAP. Moreover, when reticulocyte Ni was functionally ablated by exposure to pertussis toxin, RCAP no longer enhanced isoproterenol-responsive adenylate cyclase activity in reticulocyte membranes. These results suggest that RCAP stimulates adenylate cyclase activity by inhibiting Ni function, thus permitting enhanced Ns coupling to the adenylate cyclase enzyme (C).

    Title Reticulocyte Cytosol Activator Protein: Its Actions Upon the Beta Adrenergic Receptor and the N-proteins of Adenylate Cyclase.
    Date April 1985
    Journal Journal of Receptor Research
    Excerpt

    Rat reticulocytes contain a cytosol activator protein (RCAP) that augments catecholamine-sensitive adenylate cyclase activity in reticulocyte membranes. A partially purified preparation of RCAP was obtained by Sephacryl S-200 chromatography and used to elucidate further its mechanism of action. The specific activity of the S-200 fraction to augment isoproterenol responsiveness is increased approximately 1100-fold over the starting material from 1.2 nmoles to 1300 nmoles cyclic AMP formed per milligram of RCAP. The molecular weight is approximately 20,000. In addition to its effects on catecholamine-responsive adenylate cyclase, RCAP is associated with significant increases in basal (0.9 +/- 0.2 to 1.5 +/- 0.4 nmol/mg; p less than 0.02), guanyl-5'-yl imidodiphosphate [Gpp(NH)p]; (3.9 +/- 0.9 to 4.4. +/- 1.1 nmol/mg; p less than 0.005) and fluoride (4.1 +/- 0.6 to 4.8 +/- 0.6 nmol/mg; p less than 0.005) associated activities. RCAP stimulates isoproterenol responsiveness in wild type S49 cell membranes but is inactive in the mutant line, cyc-. RCAP alters the characteristics of agonist binding to the beta-adrenergic receptor of reticulocyte and wild S49 cell membranes, causing a significant increase in the IC50 for isoproterenol. Direct assessment of Ns and Ni components of the adenylate cyclase complex demonstrates that RCAP inhibits cholera toxin-specific ADP-ribosylation of the 42K subunit of Ns and stimulates pertussis toxin-specific ADP ribosylation of the 39K subunit of Ni.

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