JAMDA 16 (2015) 433e437
JAMDA journal homepage: www.jamda.com
Letters to the Editor
Elderly Nursing Home Resident With Head Drop To the Editor: The onset of pain, functional decline, and musculoskeletal problems can present a diagnostic challenge in demented nursing home residents who are unable to communicate history and symptoms. We present a case of an 87-year-old African American woman with painful spasm of the neck muscles for the past 3 weeks. She could not provide any further history but was constantly moaning in pain. Unable to feed herself, she required assistance and had lost 6 lbs during this period. Prior to the onset of her head drop, she was able to answer simple questions and follow commands. Her past medical history included Alzheimer dementia with psychosis, hypertension, atrial fibrillation, and rheumatoid arthritis. Her medications were valsartan, risperidone, diltiazem, and oxycodone. On review of her medications, it was noted that 9 months prior to developing neck pain her risperidone dose was increased from 0.5 mg to 1 mg daily to treat her worsening psychotic behavior. On examination, she had normal vital signs and was alert and oriented to her name only. She was grimacing and appeared to be in pain. There was obvious anterocollis of the neck with sustained muscle contractions and gross restriction of active and passive range of motion. There were no focal neurologic deficits, other abnormal movements, or extra pyramidal signs. Laboratory results showed a normal complete blood count and electrolytes. Cervical spine computed tomography scan showed mild multilevel cervical spondylosis. Computed tomography scan of the brain showed moderate diffuse cerebral atrophy and no intracranial hemorrhage or acute territorial infarct. Based on the results of the work-up, a diagnosis of acquired dystonia was made. Risperidone was stopped, and she was put on benztropine and a soft neck collar for support. There was gradual improvement in her anterocollis, and the pain subsided within 2 weeks. She was partially able to hold her head up, feed herself, and able to communicate more clearly. Her symptoms continued to improve but did not completely resolve, and a diagnosis of tardive dystonia was made after the patient met the criteria laid down by Burke et al.1 No further antipsychotic medications were prescribed, and the psychosis was managed with behavioral therapy. “Dystonia is defined as a movement disorder characterized by sustained or intermittent muscle contractions causing abnormal, often repetitive, movements, postures, or both.”2 Burke et al1 recognized tardive dystonia as a separate entity from tardive dyskinesia in 1982. The term tardive was originally intended to emphasize late appearance of these disorders during neuroleptic treatment. It is now evident that, these disorders can even occur early in course of therapy and tardive refers more to persistence of the disorder in spite of treatment than late appearance.3
Tardive dystonia is of rare occurrence compared with acute dystonia and a less understood variety.4 Estimates of tardive dystonia among patients taking antipsychotic medications range from 1% to 2%.5,6 The mean age of onset is 34e39 years, but this condition can still occur in elderly as in our case.7 The disorder seems to present differently between genders. Males develop the disorder early and more rapidly, and women were twice as likely as men to develop tardive dystonia.8,9 Second generation antipsychotics have generally shown less extra pyramidal symptoms (EPS) than first generation antipsychotics.10 EPS can be categorized as acute (dystonia, akathisia, and Parkinsonism) and tardive (tardive dyskinesia, tardive dystonia, and tardive akathisia). Risperidone is a second generation antipsychotic with affinity for both dopamine D2 receptors and 5-HT2A receptors. Blockade of D2 receptors in the brain plays a major role in the mechanism of antipsychotic action; however, it is also associated with occurrence of EPS.11 To date, there have been only 5 case reports of risperidone induced tardive dystonia.4,12e15 The current recommendations to treat dystonia are to taper or stop the causal drug. Antidopaminergic therapy is the basis for treatment. Dopamine-depleting agents like reserpine and tetrabenzine have been used with about 50% success rate. Dopamine receptor-blocking agents like clozapine are more effective with improvement in 77% of patients.16 Tardive dystonia unlike tardive dyskinesia has shown response to anticholinergic agents such as trihexyphenidyl and benztropine.7,16 Alternative treatments include local injection of botulinum toxin and deep brain stimulation.17,18 This case illustrates an uncommon side effectdtardive dystonia from risperidone. Health care providers need to be aware of both acute and late onset side effects of atypical antipsychotics. Antipsychotic medications must be prescribed at the lowest possible dosage for the shortest period of time, with gradual dose reduction, frequent review of efficacy, side effects, and discontinue antipsychotic drugs if there are side effects or no improvement in symptoms while on the medication. References 1. Burke BE, Fahn S, Jankovic J, et al. Tardive dystonia: Late onset and persistent dystonia caused by antipsychotic drugs. Neurology 1982;32: 1335e1346. 2. Albanese A, Bhatia K, Bressman SB, et al. Phenomenology and classification of dystonia: A consensus update. Mov Disord 2013;28:863e873. 3. Skidmore F, Weiner WJ, Burke R. Neuroleptic-induced tardive dyskinesia variants. In: Lang AE, Weiner WJ, editors. Drug-Induced Movement Disorders. New York: Futura Publishing Company; 2005. p. 257e285. 4. Magnuson TM, Roccaforte WH, Wengel SP, et al. Medication-Induced dystonia’s in nine patients with dementia. J Neuropsychiatry Clin Neurosci 2000;12: 219e225. 5. Yassa R, Nair V, Dimitry R. Prevalence of tardive dystonia. Acta Psychiatr Scand 1986;73:629e633. 6. Sachdev P. The prevalence of tardive dystonia in patients with chronic schizophrenia. Aust NZ J Psychiatry 1991;25:446e448. 7. Kang UJ, Burke RE, Fahn S. Natural history and treatment of tardive dystonia. Mov Disord 1986;1:193e208. 8. Kiriakakis V, Bhatia KP, Quinn NP, et al. The natural history of tardive dystonia. A long-term follow-up of 107 cases. Brain 1998;121:2053e2066.
434
Letters to the Editor / JAMDA 16 (2015) 433e437
9. van Harten PN, Matroos GE, Hoek HW, et al. The prevalence of tardive dystonia, tardive dyskinesia, Parkinsonism and akathisia. The Curacao Extra pyramidal syndromes Study. Schizophr Res 1996;19:195e203. 10. Nobutomo Y, Toshiya I. Dystonia secondary to use of antipsychotics agents. In: DystoniaeThe Many Facets. Croatia: InTech; 2012. p. 55e62. 11. Vasilyeva I, Biscontri RG, Enns MW, et al. Movement disorders in elderly users of risperidone and first generation antipsychotic agents: A Canadian population-based study. PLoS One 2013;8:e64217. 12. Tachikawa H, Suzuki T, Kawanishi Y, et al. Tardive dystonia provoked by concomitantly administered risperidone. Psychiatry Clin Neurosci 2000;54: 503e505. 13. Duggal HS, Mendhekar DN. Risperidone-induced tardive pharyngeal dystonia presenting with persistent dysphagia: A case report. Prim Care Companion J Clin Psychiatry 2008;10:161e162. 14. Vercueil L, Foucher J. Risperidone-induced tardive dystonia and psychosis. Lancet 1999;353:981. 15. Fdhil H, Krebs MO, Bayle F, et al. Risperidone-induced tardive dystonia: A case of torticollis. Encephale 1998;24:581e583. 16. Fahn S, The Tardive syndromes. Phenomenology, concepts on pathophysiology and treatment. A comprehensive review of movement disorders for the clinical practitioner. Clin Neuropharmacol 2003;20:181e265. 17. Tarsy D, Kaufman D, Sethi KD, et al. An open label study of botulinum toxin A for treatment of tardive dystonia. Clin Neuropharmacol 1997;20:90e93. 18. Trottenburg L, Paul G. Pallidal and thalamic neurostimulation in severe tardive dystonia. J Neurol Neurosurg Psychiatry 2001;70:557e559.
Rebakah Sumalini Abel Boenerjous, MD William Zirker, MD, MPH Temple University Hospital Philadelphia, PA Crozer Chester Medical Center Upland, PA Suhas Masilamani, AB, MS, DNB Srikara Hospital Hyderabad, India http://dx.doi.org/10.1016/j.jamda.2015.01.090
Hospice in the Nursing Homes: Perspectives of a Medical Director To the Editor: For more than 3 decades I have practiced and taught geriatric medicine, mostly in the nursing home setting. For those not familiar with nursing home care in the early 1980s, it was almost entirely long-term palliative care, as rehab was carried out in the hospital setting. There were no do-not-resuscitate regulations, as it seemed clearly futile to try to resuscitate nursing home patients. When a patient appeared to failing, usually from multiple comorbid cognitive and physical issues, measures were put in place to ensure a comfortable and dignified death. Experienced physicians were a key factor in recognizing when patients would obtain little benefit from hospitalization and artfully communicated this to patients and their families. Hospice was in its infancy in the United States, having started in Great Britain a few decades earlier. Congress enacted legislation in 1982 for hospice benefits under Medicare A. Hospice care started for the terminal cancer patient in the United States, with the bulk of patients being treated in the home care setting. Hospice services, originally entirely from nonprofit entities, was invaluable in helping the dying patient remain at home, with inpatient units used for a small percentage who could not be cared for by family members. In the 1990s, some hospice patients started to enter nursing homes, being discharged from inpatient hospice
units, unable to return to their home environment. A higher percentage of patients also carried noncancer terminal diagnoses. The entry of hospice into the nursing home seemed to be extraneous to me at the outset. Although the concept of knowledgeable and compassionate care at the end of life was laudable, it wasn’t clear exactly what the role of the hospice staff was. After all, an RN is on duty 24 hours per day with support from LPNs and nurses’ aides. Unroe et al1 and her associates found approximately one-third of nursing home staff noted coordination problems with hospice. My personal experience would suggest that percentage is much higher among nurses. I found it interesting that both Unroe et al1 and Swagerty2 concluded that these data represented an opportunity for better coordination between hospice and nursing home staff. I would argue for the opposite view, that hospice, through a formal arrangement with an outside vendor, and the nursing home is inherently a poor match. Although there are several factors in play creating this mismatch, 3 are most important: (1) Basic philosophy and skill set of long-term care facilities, (2) evolution of the role of the hospice nurse over time, and (3) cost. The long-term care section of the nursing home, despite limitations, has been the model for palliative care. Physicians, nurses, nurses’ aides, and social workers have been practicing expert and compassionate care for many decades without using the word “hospice.” I would take issue with Dr Swagerty2 that this is difficult and expensive, as it is neither of those. What is simply needed is the proper attentiveness by all staff members. Typically, nurses and nurses’ aides notify the physician of a resident in declining status. After assessment and in consultation with the patient and family, the physician will put in place a variety of palliative orders. Discussions often take place among staff so comfort is maximized. Many dozens of times I have instructed nurses to stop worrying about hypotension and poor intake and be concerned only with the comfort of the patient. After seeing more than 200 state and federal nursing home surveys, I have never noted a nursing home cited for weight loss or other “declining status” issues when clear documentation was in place. On those occasions in which hospice was formally consulted, I have not noticed any improvement in the comfort in which a patient passed away; having now signed more than 1000 death certificates of former nursing home residents. Over the years, the role of the hospice nurse has morphed from being a nurse to being a prescriber. Thirty years ago, a hospice nurse would often say that a given patient seems to have more pain or more anxiety. Nowadays, I receive written medication “recommendations” for a variety of symptoms having nothing to do with pain. It is very unclear to me just when hospice nurses became unofficial nurse practitioners. Although hospice nurses have excellent training and expertise in recognizing pain, they have little formal training in the medication management of the patient with dementia. When hospice is formally consulted for a patient with a primary diagnosis of dementia, all rational pharmacologic management is thrown out. Geriatric physicians are at their best when each medication is carefully thought out as to the benefits and risks of its use. I rarely see hospice nurses concerned or knowledgeable about the side effects of medications they are “suggesting.” I also cannot honestly recall a single instance when a hospice nurse noted a toxic side effect and recommended the offensive medication be discontinued. Some recent cases I have had illustrate this: An elderly woman with dementia is put on sublingual lorazepam as-needed for new-onset seizures. She was getting toxic doses of a selective serotonin reuptake inhibitor, and the seizures stopped once the dose was lowered. A woman in her 90s was titrated up to 9 mg a day of Haldol over a 2-week period due to agitation. When I saw her, the hospice
JAMDA journal homepage: www.jamda.com
Letters to the Editor
Elderly Nursing Home Resident With Head Drop To the Editor: The onset of pain, functional decline, and musculoskeletal problems can present a diagnostic challenge in demented nursing home residents who are unable to communicate history and symptoms. We present a case of an 87-year-old African American woman with painful spasm of the neck muscles for the past 3 weeks. She could not provide any further history but was constantly moaning in pain. Unable to feed herself, she required assistance and had lost 6 lbs during this period. Prior to the onset of her head drop, she was able to answer simple questions and follow commands. Her past medical history included Alzheimer dementia with psychosis, hypertension, atrial fibrillation, and rheumatoid arthritis. Her medications were valsartan, risperidone, diltiazem, and oxycodone. On review of her medications, it was noted that 9 months prior to developing neck pain her risperidone dose was increased from 0.5 mg to 1 mg daily to treat her worsening psychotic behavior. On examination, she had normal vital signs and was alert and oriented to her name only. She was grimacing and appeared to be in pain. There was obvious anterocollis of the neck with sustained muscle contractions and gross restriction of active and passive range of motion. There were no focal neurologic deficits, other abnormal movements, or extra pyramidal signs. Laboratory results showed a normal complete blood count and electrolytes. Cervical spine computed tomography scan showed mild multilevel cervical spondylosis. Computed tomography scan of the brain showed moderate diffuse cerebral atrophy and no intracranial hemorrhage or acute territorial infarct. Based on the results of the work-up, a diagnosis of acquired dystonia was made. Risperidone was stopped, and she was put on benztropine and a soft neck collar for support. There was gradual improvement in her anterocollis, and the pain subsided within 2 weeks. She was partially able to hold her head up, feed herself, and able to communicate more clearly. Her symptoms continued to improve but did not completely resolve, and a diagnosis of tardive dystonia was made after the patient met the criteria laid down by Burke et al.1 No further antipsychotic medications were prescribed, and the psychosis was managed with behavioral therapy. “Dystonia is defined as a movement disorder characterized by sustained or intermittent muscle contractions causing abnormal, often repetitive, movements, postures, or both.”2 Burke et al1 recognized tardive dystonia as a separate entity from tardive dyskinesia in 1982. The term tardive was originally intended to emphasize late appearance of these disorders during neuroleptic treatment. It is now evident that, these disorders can even occur early in course of therapy and tardive refers more to persistence of the disorder in spite of treatment than late appearance.3
Tardive dystonia is of rare occurrence compared with acute dystonia and a less understood variety.4 Estimates of tardive dystonia among patients taking antipsychotic medications range from 1% to 2%.5,6 The mean age of onset is 34e39 years, but this condition can still occur in elderly as in our case.7 The disorder seems to present differently between genders. Males develop the disorder early and more rapidly, and women were twice as likely as men to develop tardive dystonia.8,9 Second generation antipsychotics have generally shown less extra pyramidal symptoms (EPS) than first generation antipsychotics.10 EPS can be categorized as acute (dystonia, akathisia, and Parkinsonism) and tardive (tardive dyskinesia, tardive dystonia, and tardive akathisia). Risperidone is a second generation antipsychotic with affinity for both dopamine D2 receptors and 5-HT2A receptors. Blockade of D2 receptors in the brain plays a major role in the mechanism of antipsychotic action; however, it is also associated with occurrence of EPS.11 To date, there have been only 5 case reports of risperidone induced tardive dystonia.4,12e15 The current recommendations to treat dystonia are to taper or stop the causal drug. Antidopaminergic therapy is the basis for treatment. Dopamine-depleting agents like reserpine and tetrabenzine have been used with about 50% success rate. Dopamine receptor-blocking agents like clozapine are more effective with improvement in 77% of patients.16 Tardive dystonia unlike tardive dyskinesia has shown response to anticholinergic agents such as trihexyphenidyl and benztropine.7,16 Alternative treatments include local injection of botulinum toxin and deep brain stimulation.17,18 This case illustrates an uncommon side effectdtardive dystonia from risperidone. Health care providers need to be aware of both acute and late onset side effects of atypical antipsychotics. Antipsychotic medications must be prescribed at the lowest possible dosage for the shortest period of time, with gradual dose reduction, frequent review of efficacy, side effects, and discontinue antipsychotic drugs if there are side effects or no improvement in symptoms while on the medication. References 1. Burke BE, Fahn S, Jankovic J, et al. Tardive dystonia: Late onset and persistent dystonia caused by antipsychotic drugs. Neurology 1982;32: 1335e1346. 2. Albanese A, Bhatia K, Bressman SB, et al. Phenomenology and classification of dystonia: A consensus update. Mov Disord 2013;28:863e873. 3. Skidmore F, Weiner WJ, Burke R. Neuroleptic-induced tardive dyskinesia variants. In: Lang AE, Weiner WJ, editors. Drug-Induced Movement Disorders. New York: Futura Publishing Company; 2005. p. 257e285. 4. Magnuson TM, Roccaforte WH, Wengel SP, et al. Medication-Induced dystonia’s in nine patients with dementia. J Neuropsychiatry Clin Neurosci 2000;12: 219e225. 5. Yassa R, Nair V, Dimitry R. Prevalence of tardive dystonia. Acta Psychiatr Scand 1986;73:629e633. 6. Sachdev P. The prevalence of tardive dystonia in patients with chronic schizophrenia. Aust NZ J Psychiatry 1991;25:446e448. 7. Kang UJ, Burke RE, Fahn S. Natural history and treatment of tardive dystonia. Mov Disord 1986;1:193e208. 8. Kiriakakis V, Bhatia KP, Quinn NP, et al. The natural history of tardive dystonia. A long-term follow-up of 107 cases. Brain 1998;121:2053e2066.
434
Letters to the Editor / JAMDA 16 (2015) 433e437
9. van Harten PN, Matroos GE, Hoek HW, et al. The prevalence of tardive dystonia, tardive dyskinesia, Parkinsonism and akathisia. The Curacao Extra pyramidal syndromes Study. Schizophr Res 1996;19:195e203. 10. Nobutomo Y, Toshiya I. Dystonia secondary to use of antipsychotics agents. In: DystoniaeThe Many Facets. Croatia: InTech; 2012. p. 55e62. 11. Vasilyeva I, Biscontri RG, Enns MW, et al. Movement disorders in elderly users of risperidone and first generation antipsychotic agents: A Canadian population-based study. PLoS One 2013;8:e64217. 12. Tachikawa H, Suzuki T, Kawanishi Y, et al. Tardive dystonia provoked by concomitantly administered risperidone. Psychiatry Clin Neurosci 2000;54: 503e505. 13. Duggal HS, Mendhekar DN. Risperidone-induced tardive pharyngeal dystonia presenting with persistent dysphagia: A case report. Prim Care Companion J Clin Psychiatry 2008;10:161e162. 14. Vercueil L, Foucher J. Risperidone-induced tardive dystonia and psychosis. Lancet 1999;353:981. 15. Fdhil H, Krebs MO, Bayle F, et al. Risperidone-induced tardive dystonia: A case of torticollis. Encephale 1998;24:581e583. 16. Fahn S, The Tardive syndromes. Phenomenology, concepts on pathophysiology and treatment. A comprehensive review of movement disorders for the clinical practitioner. Clin Neuropharmacol 2003;20:181e265. 17. Tarsy D, Kaufman D, Sethi KD, et al. An open label study of botulinum toxin A for treatment of tardive dystonia. Clin Neuropharmacol 1997;20:90e93. 18. Trottenburg L, Paul G. Pallidal and thalamic neurostimulation in severe tardive dystonia. J Neurol Neurosurg Psychiatry 2001;70:557e559.
Rebakah Sumalini Abel Boenerjous, MD William Zirker, MD, MPH Temple University Hospital Philadelphia, PA Crozer Chester Medical Center Upland, PA Suhas Masilamani, AB, MS, DNB Srikara Hospital Hyderabad, India http://dx.doi.org/10.1016/j.jamda.2015.01.090
Hospice in the Nursing Homes: Perspectives of a Medical Director To the Editor: For more than 3 decades I have practiced and taught geriatric medicine, mostly in the nursing home setting. For those not familiar with nursing home care in the early 1980s, it was almost entirely long-term palliative care, as rehab was carried out in the hospital setting. There were no do-not-resuscitate regulations, as it seemed clearly futile to try to resuscitate nursing home patients. When a patient appeared to failing, usually from multiple comorbid cognitive and physical issues, measures were put in place to ensure a comfortable and dignified death. Experienced physicians were a key factor in recognizing when patients would obtain little benefit from hospitalization and artfully communicated this to patients and their families. Hospice was in its infancy in the United States, having started in Great Britain a few decades earlier. Congress enacted legislation in 1982 for hospice benefits under Medicare A. Hospice care started for the terminal cancer patient in the United States, with the bulk of patients being treated in the home care setting. Hospice services, originally entirely from nonprofit entities, was invaluable in helping the dying patient remain at home, with inpatient units used for a small percentage who could not be cared for by family members. In the 1990s, some hospice patients started to enter nursing homes, being discharged from inpatient hospice
units, unable to return to their home environment. A higher percentage of patients also carried noncancer terminal diagnoses. The entry of hospice into the nursing home seemed to be extraneous to me at the outset. Although the concept of knowledgeable and compassionate care at the end of life was laudable, it wasn’t clear exactly what the role of the hospice staff was. After all, an RN is on duty 24 hours per day with support from LPNs and nurses’ aides. Unroe et al1 and her associates found approximately one-third of nursing home staff noted coordination problems with hospice. My personal experience would suggest that percentage is much higher among nurses. I found it interesting that both Unroe et al1 and Swagerty2 concluded that these data represented an opportunity for better coordination between hospice and nursing home staff. I would argue for the opposite view, that hospice, through a formal arrangement with an outside vendor, and the nursing home is inherently a poor match. Although there are several factors in play creating this mismatch, 3 are most important: (1) Basic philosophy and skill set of long-term care facilities, (2) evolution of the role of the hospice nurse over time, and (3) cost. The long-term care section of the nursing home, despite limitations, has been the model for palliative care. Physicians, nurses, nurses’ aides, and social workers have been practicing expert and compassionate care for many decades without using the word “hospice.” I would take issue with Dr Swagerty2 that this is difficult and expensive, as it is neither of those. What is simply needed is the proper attentiveness by all staff members. Typically, nurses and nurses’ aides notify the physician of a resident in declining status. After assessment and in consultation with the patient and family, the physician will put in place a variety of palliative orders. Discussions often take place among staff so comfort is maximized. Many dozens of times I have instructed nurses to stop worrying about hypotension and poor intake and be concerned only with the comfort of the patient. After seeing more than 200 state and federal nursing home surveys, I have never noted a nursing home cited for weight loss or other “declining status” issues when clear documentation was in place. On those occasions in which hospice was formally consulted, I have not noticed any improvement in the comfort in which a patient passed away; having now signed more than 1000 death certificates of former nursing home residents. Over the years, the role of the hospice nurse has morphed from being a nurse to being a prescriber. Thirty years ago, a hospice nurse would often say that a given patient seems to have more pain or more anxiety. Nowadays, I receive written medication “recommendations” for a variety of symptoms having nothing to do with pain. It is very unclear to me just when hospice nurses became unofficial nurse practitioners. Although hospice nurses have excellent training and expertise in recognizing pain, they have little formal training in the medication management of the patient with dementia. When hospice is formally consulted for a patient with a primary diagnosis of dementia, all rational pharmacologic management is thrown out. Geriatric physicians are at their best when each medication is carefully thought out as to the benefits and risks of its use. I rarely see hospice nurses concerned or knowledgeable about the side effects of medications they are “suggesting.” I also cannot honestly recall a single instance when a hospice nurse noted a toxic side effect and recommended the offensive medication be discontinued. Some recent cases I have had illustrate this: An elderly woman with dementia is put on sublingual lorazepam as-needed for new-onset seizures. She was getting toxic doses of a selective serotonin reuptake inhibitor, and the seizures stopped once the dose was lowered. A woman in her 90s was titrated up to 9 mg a day of Haldol over a 2-week period due to agitation. When I saw her, the hospice
