Not an actual patient

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2 TD CAN BE A BURDEN ON PATIENTS AND AFFECT THEIR LIVES 1 TD can be disruptive, whether they have mild, moderate, or severe TD. 2 Patients with TD may deal with many issues Abnormal and involuntary movements may cause embarrassment in public 1 Loss of physical control may make those around them feel uncomfortable 1 Psychiatric patients may already have difficulty gaining stability and social acceptance 1,3 I have isolated myself from a lot of people, because it s really hard to pay attention to a conversation when people are just paying attention to your lip movement or your eye movement. Patient Caregivers can also feel burdened by TD Caregivers may be the first to notice signs of TD. 4 * It s difficult to take care of somebody with those movements. You never know from one day to the next how bad it s going to be. It could change hour to hour, so it s really hard. Caregiver *Based on interviews with neurologists (n=88), psychiatrists (n=78), and primary care physicians (n=53) on the perceived burden of TD on patients and caregivers, and the question of who first noticed TD signs. 4

3 THE PREVALENCE OF TD MAY BE GREATER THAN YOU THINK TD is estimated to affect at least 500,000 people in the United States. 5,6 Up to 50% of TD patients may be uncoded. 7 * THE RATES OF NEW TD CASES ARE MORE SIMILAR BETWEEN ATYPICAL AND TYPICAL ANTIPSYCHOTICS THAN PREVIOUSLY REPORTED 8 3.9% ATYPICAL ANTIPSYCHOTICS 5.5% TYPICAL ANTIPSYCHOTICS THE RISK OF TD INCREASES AS THE EXPOSURE TO TYPICAL ANTIPSYCHOTICS INCREASES 9 5 YEARS 32 % 15 YEARS 57 % 25 YEARS 68 % *Based on online surveys with psychiatrists (n=101) and neurologists (n=100) who were familiar with coding processes. Physicians represented solo, group, and hospital/mental health center practice settings across each specialty. Physicians were asked how often TD is not coded. 7 Annualized incidence rates of TD. Based on a meta-analysis of 12 studies published since 2004: 28,051 patients, mean age 39.7 years, 59.7% male, 70.9% white. 8 Estimated risk of TD is based on a long-term study of 362 outpatients who were free of TD at enrollment between July 1, 1985, and June 30, 1987, and reexamined at least once during follow-up. The mean baseline age was 42 years (range years), 53% were women, and 25% were nonwhite. Net years of previous neuroleptic use without TD and additional years of neuroleptic use were used to determine the estimated risk for TD. 9

4 MANY PATIENTS OFTEN DO NOT BRING UP OR DISCUSS THE SIGNS OF TD10 American Psychiatric Association (APA) Guideline recommendations1 Screen for TD before starting or re-starting patients on dopamine receptor blocking agent (DRBA) treatment Monitor for signs of TD every few months Consider a diagnostic evaluation Signs of TD can develop in as early as a few months after starting DRBA treatment11 TD movements are often seen in the face, trunk, and extremities.1,11,12 LIP SMACKING, PUCKERING, OR PURSING12 TONGUE MOVEMENT OR PROTRUSION12 TRUNK AND LIMB MOVEMENTS12 JAW DISTENSION, CHEWING, OR GRIMACING12 BLINKING12 For some patients, signs of TD continue indefinitely, even after stopping or switching DRBA treatment.11

5 PROPOSED MECHANISM OF TD AND DOPAMINE RECEPTOR HYPERSENSITIVITY The hypersensitivity of postsynaptic dopamine D2 receptors in TD may occur after exposure to DRBAs. 13 It is hypothesized that this hypersensitivity in the nigrostriatal pathway manifests in the signs of TD. 14 NORMAL UPREGULATED Visit TakeOnTD.com for more information about tardive dyskinesia References: 1. Task Force on Tardive Dyskinesia. Tardive Dyskinesia: A Task Force Report of the American Psychiatric Association. American Psychiatric Association; Washington, DC; Othman Z, Ghazali M, Razak AA, et al. Severity of tardive dyskinesia and negative symptoms are associated with poor quality of life in schizophrenia patients. Int Med J. 2013;20(6): Boumans CE, de Mooij KJ, Koch PA, et al. Is the social acceptability of psychiatric patients decreased by orofacial dyskinesia? Schizophr Bull. 1994;20(2): Data on file. Neurocrine Biosciences. 5. Cloud LJ, Zutshi D, Factor SA. Tardive dyskinesia: therapeutic options for an increasingly common disorder. Neurotherapeutics. 2014;11(1): Data on file. Neurocrine Biosciences. 7. Data on file. Neurocrine Biosciences. 8. Correll CU, Schenk EM. Tardive dyskinesia and new antipsychotics. Curr Opin Psychiatry. 2008;21(2): Glazer WM, Morgenstern H, Doucette JT. Predicting the long-term risk of tardive dyskinesia in outpatients maintained on neuroleptic medications. J Clin Psychiatry. 1993;54(4): Macpherson R, Collis R. Tardive dyskinesia: patients lack of awareness of movement disorder. Br J Psychiatry. 1992;160: American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 5th ed. Arlington, VA: American Psychiatric Association; 2013: Guy W. ECDEU Assessment Manual for Psychopharmacology: Revised Rockville, MD: National Institute of Mental Health; Sayers AC, Bürki HR, Ruch W, et al. Neuroleptic-induced hypersensitivity of striatal dopamine receptors in the rat as a model of tardive dyskinesias: effects of clozapine, haloperidol, loxapine and chlorpromazine. Psychopharmacologia. 1975;41(2): Stahl SM. Essential Psychopharmacology Online. Based on: Stahl SM. Stahl s Essential Psychopharmacology. 4th ed. Cambridge, UK: Cambridge University Press; &title=Conventional%20antipsychotics#c Accessed March 14, Advancing the science of hyperkinetic movement disorders 2017 Neurocrine Biosciences, Inc. All Rights Reserved. CP-TD-US /17