Tremor Is a Common, Abnormal, Involuntary Move

Home , Essential tremor, Intention tremor, Movement disorder, Tremor

TremorsTTremorsTTremorsemorss By Laura M. Struble, PhD, GNP-BC

tremor is a common, abnormal, involuntary move- sleep.4 Tremors can be transient and vanish over time or ment of muscles that may be noted during a rou- chronic and progressive. Patients with a tremor may have A tine physical exam. It is defi ned as an unintentional minor functional consequences or extreme functional dis- rhythmical oscillatory movement of a body part.1 Tremors abilities. Tremors can be embarrassing, and some patients may be a sign of an underlying disease or simply an exag- are afraid to be seen in public. It is important for the NP to gerated physiologic tremor observed in healthy people. assess tremor symptoms quickly and accurately to maximize Identifying the type of tremor is necessary to determine therapy and avoid unnecessary referrals. underlying neurologic disorders. The gold standard for diagnosing tremors is still history and physical exam.1 ■ Classifi cation of tremor Tremors are broadly categorized as hyperkinetic. They have ■ What is a tremor? different activation conditions, frequencies, and amplitudes. Tremors are commonly associated with movement disorders To be defi ned as a tremor, a movement must be rhythmic that have multiple etiologies and an extensive list of differen- and have a pattern. The widely accepted classifi cation divides tial diagnoses. Most tremors are associated with neurologic tremors into two types: rest and action.1 conditions related to certain parts of the brain (such as basal motor nuclei, inferior olivary nucleus, and cerebellum) that Rest tremor control muscles throughout the body or a specifi c body part Rest tremor occurs in a body part that is relaxed and fully such as the hands.2 Pathologic tremors include brain injury supported against gravity (for example, hands resting in essential tremor, multiple sclerosis, Parkinson disease (PD), the lap). The rate of this type of tremor is usually between stroke, and neurodegenerative diseases that damage the 3 and 6 Hz/cycle/second.5 If the rest tremor is mild or inter- brainstem or cerebellum. Metabolic disturbances that affect mittent, it can be brought out or intensifi ed by having the the brain and may produce tremors include drugs, alcohol, patient concentrate on a different task, such as opening and mercury poisoning, hyperthyroidism, hypoglycemia, or closing the contralateral hand or performing arithmetic.4 vitamin deficiencies (magnesium, thiamin). Insect bites Rest tremors are commonly observed in PD and account from a black widow spider or red back spider may produce for about 75% of all cases of rest tremors.5 Rest tremors are tremors. Finally, genetics may play a role in the development seldom seen in other conditions.6 of tremors.3 Action tremor ■ Characteristics of tremor An action tremor is produced by voluntary muscle contrac- Tremors can happen at any age, but their likelihood increases tion and is further classifi ed as: postural, kinetic, isometric, with age. They can occur in the hands, head, jaw, tongue, or task-specifi c. palate, vocal cords, trunk, or legs. Tremor may occur in one 1. Postural tremor is produced when the affected body part part of the body and progress to others, or may be seen in maintains its position against gravity (such as extending multiple extremities all at once. Diagnosis of the underlying arms in front of the body). cause becomes diffi cult when there is more than one type 2. Kinetic tremor is produced during a voluntary move- of tremor present. The majority of involuntary tremors ment and can be subdivided into simple kinetic tremor increase during emotional stress, strong emotions, and/or or intention tremor. physical fatigue. However, if a person is calm and relaxed, a. Simple kinetic tremor occurs with movement of ex-

most tremors are dampened and usually disappear during tremities (such as ﬂ exion-extension of the wrist). Karapelou © Illustration by John W.

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www.tnpj.com The Nurse Practitioner • June 2010 19

b. Intention tremor is produced with visually guided toms of ET are largely symmetrical, occurring primarily in movements directed toward a specifi c target with sig- the upper limbs (95%), and specifi cally in the hands. ET nifi cant amplitude fl uctuation when approaching the symptoms may also be noted in the head (35%), lower limbs target (when performing point-to-point movements, (20%), voice (12%), and trunk (5%).18 The frequency of the such as fi nger-nose-fi nger).7 Intention tremors are tremor ranges from 4 to 12 Hz and is usually symmetrical. commonly seen with cerebellar lesions.4 The amplitude of ET tremors increases with fatigue, anxiety, 3. Isometric tremor occurs when there are voluntary mus- stress, certain medications, and/or cold temperatures. cle contractions without movement (such as pushing Pharmacologic treatment options do not cure the trem- against a wall). or, but may improve function and reduce embarrassment. 4. Task-specifi c tremor is rare and only occurs when per- The fi rst-line therapies are propranolol and primidone. If forming a specifi c task such as writing, playing music, the tremor is not reduced or the adverse reaction profi le is or speaking.4,7,8 too high, second-line therapies include gabapentin, alpra- zolam, nimodipine, and theophylline.12,15 Propranolol is the ■ Common tremor syndromes only drug with labeled-use for symptomatic treatment of Tremors are classifi ed according to clinical features (see essential tremor; other drugs listed are off-label use. Moder- Classifi cation and description of tremor syndromes).6,8,9 ate alcohol consumption can cause a transient decrease or alleviation of an ET; however, there may be a rebound effect Physiologic tremor once the alcohol has worn off. The use of alcohol to manage Physiologic tremor is an action tremor present in everyone. ET is not recommended but if the patient indicates that it This benign tremor is usually postural and does not interfere helps this information supports the diagnosis of ET.9,18,19 with activities of daily living. It is diffi cult to see with the naked eye and described as a high-frequency, low-amplitude Tremor in children tremor. Increased or enhanced physiologic tremor is de- Tremor syndromes appear throughout childhood from neo- scribed as an easily visible, high-frequency tremor with no nate through adolescence. Movement disorders are some- evidence of an underlying neurologic disease.1,11 Emotional times missed in the very young if they are less apparent or stress, fear, or anxiety can exacerbate this tremor. Other pre- slow progressing. It may not be until children show signs of cipitating factors include muscle fatigue, lack of sleep, and impairment in school or recreational activities that parents consuming large amounts of caffeinated drinks. Medical consult the primary care provider. As with adults, ET is the conditions that, if corrected, would reverse exacerbated physi- most common form of tremor in children and usually seen ologic tremor include thyrotoxicosis, hypoglycemia, certain in the teenage years. Infantile tremors resulting from vitamin

drugs (such as some anticonvulsants, antidepressants, and B12 defi ciency and Wilson disease between the ages of 6 and 20 neuroleptics),14 and withdrawal from benzodiazepines and years should always be ruled out. Other childhood tremors are alcohol.6,8,12 most likely due to underlying metabolic and endocrine disorders, heterodegenerative disorders, or are drug-induced.10,11 Essential tremor ET, formally known as benign ET, is the most common form Drug-induced tremors of action tremor. It is the most common movement disorder Tremor is a frequent adverse reaction of medications related in the world and is diagnosed primarily by clinical presenta- to drug toxicity and withdrawal from certain drugs.8 Rest tion.7,8,12,15 It is almost 20 times more prevalent than PD.16 tremor, action/postural tremor, and intention tremor can be Although ET is not life-threatening, the condition does drug-induced. (see Drugs that can cause rest, action/postural have devastating consequences. Typically, ET is a postural and intention tremors). Most drug-induced tremors are or kinetic action tremor mainly affecting the hands. Patients symmetrical except for parkinsonism tremor. To determine often complain of diffi culty writing, drawing, drinking from whether a tremor is drug-induced, NPs should rule out other a cup, or using a computer. Usually, no other neurologic medical etiologies. A temporal relationship to the start of symptoms are present.1 ET has an insidious onset and pro- a drug should be investigated to determine whether there gresses over time. The condition affects males and females is a dose-response relationship. Finally, the tremor course equally and occurs most often in adolescents and adults should not be progressive in drug-induced tremors.13 in their 50s or 60s. Almost half of ET cases are considered familial from an autosomal dominant gene.17 ET usually Parkinsonism tremor starts in the arms with the fl exion-extension of the wrists or Parkinsonism tremor is the most common form of rest trem- abduction-adduction movement of the fi ngers.4 The symp- or. Parkinsonism is a group of movement disorders that have

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Classiﬁ cation and description of tremor syndromes6,8,9

Type of tremor Tremor Amplitude Clinical features Syndromes frequency

Rest tremor Low to High Occurs when • PD Muscles are medium limb is supported • Neurodegenerative parkinsonism at rest against gravity, diseases (multiple systems atrophy, muscles are not progressive supranuclear palsy) activated • Drug-induced parkinsonism (neuroleptics, metoclopramide, phenothiazines) • Wilson disease

Action tremor produced by voluntary muscle contractions

Postural Medium Low but increases Occurs when the • Drug-induced (lithium, amiodarone, to high with voluntary limb maintains beta-adrenergic agonists) movement position against • ET gravity • Metabolic disorders (thyrotoxicosis, pheochromocytoma, hypoglycemia) • Neuropathic tremor (neuropathy) • Physiologic tremor • Toxins (alcohol withdrawal, heavy metals)

Kinetic Varies Does not change Occurs during any • Cerebellar lesions (stroke, multiple with movement voluntary move- sclerosis, tumor) ment • Drug-induced ET • Physiologic • Posttraumatic stress disorder • Psychogenic

Simple kinetic Varies Does not change Occurs during any tremor with movement voluntary movement

Intention Low Increases with Target directed guided movement toward a target

Task-speciﬁ c Varies Variable Occurs during spe- tremor ciﬁ c activities (for example, writing)

Isometric tremor Medium Variable Occurs during muscle contraction against a stationary object similar features and symptoms. Idiopathic PD is the most are diagnosed with PD under the age of 50.20 A rest tremor common form of parkinsonism and the cause is unknown.20 is commonly the ﬁ rst neurologic sign in PD. It is a progressive disease and primarily a consequence of Classically, the rest tremor has a low frequency of 2 to 5 degeneration of nuclei in a number of dopamine-producing Hz and large amplitude. The tremor manifests initially in one nerve cells in the basal ganglia and related structures. The other hand and/or foot and progresses to the ipsilateral limbs before forms of parkinsonism tremors have suspected causes such as spreading bilaterally. Active movement strongly inhibits the encephalitis, stroke, Lewy body disease, or are drug-induced. tremor. In the later stages of PD it is not unusual to see an There are approximately 1.5 million Americans who action or a postural tremor.4 A PD tremor rarely involves the currently have PD, and it affects both men and women voice or head tremor, starts in one hand or foot, and is unaf- equally.20 The age of onset is usually 65; only 15% of people fected by alcohol.16 www.tnpj.com The Nurse Practitioner • June 2010 21

Unlike people with ET who do not have any other neu- PD is idiopathic and neurodegenerative, so pharma- rologic abnormalities, the diagnosis of PD is made using cologic agents are used to alleviate the symptoms and slow other diagnostic criteria. The patient must have a positive the progression of the disease. A variety of agents may be sustained response to a dopaminergic agent and two to used for tremor, such as levodopa, dopamine agonists, three PD cardinal signs: anticholinergic agents (such as benztropine mesylate, bi- • Rest tremor that may involve the arms, legs, lips, jaw, chin, periden hydrochloride, and procyclidine hydrochloride), and tongue. The classic tremor is described as pill-rolling budipine (off-label), and second-line treatments such as tremor that looks like someone is rolling a coin or pill clozapine, propranolol, and clonazepam.12,21,22 The most between the thumb and index ﬁ nger important principle in management is to target the most • Rigidity or cogwheel rigidity (ratchet-like resistance) disabling symptoms and individualize the therapy. The during passive range of motion mainstay treatment is carbidopa/levodopa in older adults. • Bradykinesia such as decreased arm swing with walking Patients younger than 70 years with multiple features of PD and reduced facial animation should start with a dopamine agonist or monoamine oxi- • Postural instability.7 dase inhibitor. Younger patients will require dopaminergic

Drugs that can cause rest, action/postural, and intention tremors1,4,8,13,14

Drug classiﬁ cation Rest tremor Action/postural tremor Intention tremor

Antiarrhythmics Amiodarone (Cordarone), mexiletine (Mexitil), procainamide (Pronestyl)

Antibiotics and Co-trimoxazole (Septra, antifungals Bactrim), amphotericin B (Fungizone, Amphocin)

Antiepileptics Valproic acid (Depakene)

Beta-adrenergic Albuterol (Proventil), salmeterol agonists (Serevent)

Immunologic and Thalidomide (Thalomid) Tamoxifen (Nolvadex), cytarabine chemotherapeutics (Cytosar-U-), ifosfamide (Ifex)

Gastrointestinal Metoclopramide (Reglan) Metoclopramide (Reglan), cimetidine drugs (Tagamet)

Hormones Thyroid hormones, calcitonin (Miacalcin), medroxyprogesterone (Provera)

Methylxanthines Theophylline (Theo-24, Theochron), caffeine

Mood stabilizers Lithium (Eskalith, Lithobid) Lithium (Eskalith, Lithobid) Lithium toxicity (Eskalith, Lithobid)

Neuroleptics Haloperidol (Haldol)

Newer antidepres- SSRIs: Fluoxetine (Prozac), SSRIs: Fluoxetine (Prozac), sants Paroxetine (Paxil) Paroxetine (Paxil) SNRIs: Duloxetine (Cymbal- SNRIs: Duloxetine (Cymbalta), ta), Venlafaxine (Effexor) Venlafaxine (Effexor) Tetracyclic: Mirtazapine Tetracyclic: Mirtazapine (Remeron) (Remeron)

Tricyclic Amitriptyline, clomipramine (Anafranil), antidepressants nortriptyline (Pamelor)

Substance/drug Cocaine, alcohol withdrawal, 3,4-Methylene- Alcohol abuse dioxymethamphetamine (Ecstasy), nicotine (chronic use) (tobacco)

SSRI = selective serotonin reuptake inhibitor; SNRI = serotonin-norepinephrine reuptake inhibitor.

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therapy for a longer period and have an increased risk of trophysiologic studies may be useful. Successful treatment levodopa complications such as tremor fl uctuations and involves psychotherapy but may also require mild anxiolytics dyskinesias.4,23,24 Surgery may be an option in the later stages and antidepressants.12 of the disease. Thalamotomy, pallidotomy, and deep brain stimulation have shown some success in reducing tremors.25 ■ Key history questions NPs should ascertain the following information: age when the Cerebellar tremor tremor started, type of onset (sudden or gradual), duration, Cerebellar tremor is the most common form of kinetic progression, and any aggravating (such as tremor increases intention tremor. It is a slow, broad, low-frequency tremor when tired or when taking a certain medication) or alleviat- of the extremities that occurs at the end of a purposeful ing factors (such as tremor lessens with alcohol). Determine movement such as pressing an elevator button. This type where the tremor started and the rate of progression to other of tremor usually presents perpendicular to the direction of body parts. Ask the patient if the tremor occurs with action, movement and varies in amplitude. Classically, the tremor rest or when holding a body part in a particular position. In amplitude increases as the limb is visually guided to the addition, ask if the tremor interferes with the patient’s abil- target. The dominant feature is a unilateral or bilateral low- ity to use the hands or other body parts. Ask if there are any frequency tremor without the presence of a rest tremor. specifi c job-related disabilities and if the patient is socially Cerebellar tremor is caused by lesions or damage to the embarrassed by the tremor. Have the patient describe any cerebellum resulting from multiple sclerosis (most com- noticeable behavioral changes or memory losses (signifi cant mon), inherited degenerative disorders, stroke, or tumor. others may provide more accurate information about this). Rarely do these disorders present with just a tremor. Be- In addition, explore the patient’s family history of tremors sides an intention or sometimes postural tremor, other and medical history for neurologic (seizures, stroke, and head characteristics of cerebellar disorders include incoordina- injury), endocrine, and metabolic disorders. Obtain a com- tion, imbalance, dysarthria, and abnormal eye movements. plete drug history and alcohol use/abuse history.4,8,28 Be sure Toxic-related causes of intention tremor include chronic to assess for depression and anxiety because these psychologic alcohol abuse, lithium, heavy metals, antiepileptic drugs, sequelae are strongly associated neurologic conditions.29,30 antidepressants, and neuroleptic medications.4,15,26 To date, there are no established pharmacologic treatments avail- ■ Physical exam able for cerebellar tremors except treating the underlying The single most determining variable in diagnosing tremors causes. Surgical intervention such as thalamotomy or deep is rhythmicity and can be described as regular or irregular brain stimulation may benefi t some patients. Occupational oscillations. Other key tremor characteristics are body part therapists may be able to help by fi tting weight to the af- or parts, location (distal, proximal), activation condition fected limb or teaching patients to brace the proximal limb (when tremor is present), amplitude that is the degree of the during activity. limb displacement caused by the involuntary muscle contractions (fi ne/low, medium, coarse/large), and frequency Psychogenic tremor that is the number of oscillations per second (slower—2 Psychogenic tremor is complex and variable with unknown to 3 Hz, slow—less than 6 Hz, rapid—greater than 6 Hz).18 documented incidence or prevalence rates. The etiology may First, observe the patient sitting with hands resting in be different in each patient. The patient usually describes an the lap and document tremor characteristics. Be sure to rule abrupt onset associated with a stressful life event. There is a out other symptomatic movements such as chorea or dys- variable course of tremors and they spontaneously go into tonia (see Hyperkinetic-involuntary abnormal movements). remission. Patients are still able to carry out some activities Assess the face for oromotor dystonia (tardive dyskinesia) of daily living despite severe tremors.4 There are neurologic or masklike face. The patient should also be examined while signs in the majority of patients, so the diagnosis is not just assuming different positions (such as arms stretched out) based on exclusion. The tremor can be resting, postural, and when moving (such as fi nger-nose-fi nger). If an ET is intention, or a combination and can involve any body part. suspected, instruct the patient to stretch arms out in front, The tremor usually affects the extremities and does not palms down (full pronation), then turn hands sideways involve the fi ngers.27 It increases under direct observation (semipronation), then up into full supination. The semi- and decreases with distraction. When the patient is asked pronation may enhance ET oscillation, whereas tremor may to tap a beat with the limb contralateral to the tremulous be diminished in the supinate position.5 Proximal tremors limb, the tremor will decrease or shift to the frequency of (such as shoulder rotator tremor) are seen in multiple scle- the tapping. Referral to a neurologist and/or obtaining elec- rosis and other cerebellar dysfunctions. To elicit a proximal www.tnpj.com The Nurse Practitioner • June 2010 23

Hyperkinetic-involuntary abnormal movements18, 23, 31, 32 of tremor include bradykinesia or rigidity (PD), nystagmus or ataxia Type Description Comments (cerebellar lesion), and a wide dif- ference in tremor symptoms and Akathisia Patient feels restless and has Seen with use of antipsychotic 4 a desire to move to relieve medications. frequency (psychogenic). uncomfortable sensations of crawling, itching, stretching, ■ Lab workup or creeping feelings. This usu- To rule out some disorder s related to ally occurs in the legs physiologic causes NPs may want to Athetosis Slow, writhing, continuous, Seen with perinatal and adult obtain a complete blood cell count uncontrollable movement of hypoxic ischemic injury. with differential, thyroid-stimulating the arms and legs Movements are described as snakelike. hormone, plasma glucose, and B12 level. It is important to exclude Wil- Ballism Large, abrupt contractions of Seen with lesions of the sub- son disease in patients younger than the extremities that are ex- thalamus- (hemorrhage, tumor, plosive ﬂ ail-like movements or infarct). May only involve one 50. It is an autosomal recessive dis- side of the body. order that results in abnormal de- position of copper in the brain and Chorea Rapid, irregular, jerky, unco- Seen with Huntington disease, ordinated movements, and Wilson disease, and systematic other organs and is life-threatening. abnormal posture lupus erythematosus. Obtain a serum ceruloplasmin level, and a 24-hour urinary copper excre- Dystonia Sustained muscle contrac- Seen with: (1) primary dystonia 4,8 tions, often causing twisting (spasmodic torticollis, blepha- tion to rule out this disease. or repetitive movements and rospasm, or writer’s cramp), (2) abnormal postures secondary dystonia (Huntington ■ Differential diagnosis disease, PD), (3) syndromes or Tremors should be distinguished combinations of hereditary and degenerative causes. May be from other kinds of hyperkinetic painful as well as incapacitating. movements disorders or dyskinesias. Choric movements, tics, and other Myoclonus Random, sudden, shocklike, Seen with epilepsy and Creutzfeldt- brief jerking contraction of a Jakob disease. May occur once involuntary abnormal hyperkinetic muscle or repetitively and may persist in movements can quickly be distin- sleep. guished from tremor by observation

Tics Involuntary, rapid, nonrhyth- Seen with transient tics, chronic and physical exam. mic movement or sound, tics, and Tourette syndrome. usually involving the face Preceded by an urge to move and ■ Referral to a neurologist can be controlled briefl y. Any patient with a sudden onset of tremor, asymmetric exam, cerebellar tremor, have the patient form wings with their arms (shoul- dysfunction, or complicated presentation should be sent ders abducted, elbows fl exed, and palms facing down with for further evaluation. Failure to respond to appropriate index fi ngers pointing to each other in front of the chest).18 medication is another indication for referral. Electromy- Important maneuvers to document functional capabili- ography, accelerometry, and/or imaging studies may be ties and help determine the nature of the tremor include necessary.4,33 drinking from a cup (observe for swallowing diffi culties as REFERENCES well observe for intention tremor) and writing or drawing 1. Deuschl G, Bain P, Brin M. Consensus statement of the Movement Disorder a rhythmic pattern such as a spiral (small, cramped writ- Society on tremor. Ad hoc scientifi c committee. Mov Disord. 1998; 13(suppl 3):2-23. ing indicates PD and tremulous writing indicates ET).5 2. DeMyer W. Technique of Neurological Examination. 5th ed. New York: NY: Assess for other neurologic signs to help identify etiology. McGraw-Hill; 2004:343-344. Perform cranial nerve testing, muscle tone, strength, re- 3. Vaughan, JR, Davis MB, Wood, NW. Genetics of parkinsonism: a review. Ann Human Genet. 2001; 65(pt 2):111-126. fl exes, coordination, refl exes, and sensation. Test for rigid- 4. Jankovic J. Treatment of hyperkinetic movement disorders. Lancet Neurol. ity (passively fl ex and extend the wrists and elbows) and 2009; 8(9):844-856. cerebellar function (such as balance, gait, fi nger-nose-fi nger 5. Velickovic M, Gracies JM. Movement disorders. Keys to identifying and treating tremor. Geriatrics. 2002; 57(7):32-36. testing, heel-to-shin testing, rapidly alternate movements, 6. Chou KL. Diagnosis and management of the patient with tremor. Med and nystagmus). Exam fi ndings that give clues to etiology Health RI. 2004; 87(5):135-138.

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7. Colcher A, Simuni T. Clinical manifestations of Parkinson’s disease. Med Clin 22. Wasielewski PG, Burns JM, Koller WC. Pharmacologic treatment of tremor. North Am. 1999; 83(2):327-347. Mov Disord. 1998; 13(suppl 3):S90-S100. 8. Rehman H. Diagnosis and management of tremor. Arch Intern Med. 2000; 23. Sethi KD. Tremor. Curr Opin Neurol. 2003; 16(4):481-485. 160(16):2438-2444. 24. Jankovic J, Aguilar LG. Current approaches to the treatment of Parkinson’s 9. Zesiewicz TA, Hauser RA. Phenomenology and treatment of tremor disease. Neuropsychiatr Dis Treat. 2008; 4(4):743-757. disorders. Neurol Clin. 2001; 19(3):651-680. 25. Anderson VC, Burchiel KJ, Hogarth P, Favre J, Hammerstad JP. Pallidal vs 10. Smaga S. Tremor. Am Acad Fam Physicians. 2003; 68(8):1545-1552. subthalamic nucleus deep brain stimulation in Parkinson’s disease. Arch 11. Grimes DA. Tremor-easily seen but diffi cult to describe and treat. Can J Neurol Neurol. 2005; 62(4):554-560. Sci. 2003; 30(suppl 1):S59-S63. 26. Seeberger LC. Cerebellar tremor- defi nition and treatment. 2005 CNI Rev. 12. Uddin MK, Rodnitzky RL. Tremor in children. Semin Pediatr Neurol. 2003; http:www.thecni.org/review/17-fall05-all. 10(1):26-34. 27. Deuschl G, Köster B, Lücking CH, Scheidt C. Diagnostic and pathophysiological 13. Garewal G, Narang A, Das KC. Infantile tremor syndrome: a vitamin B12 aspects of psychogenic tremors. Mov Disord. 1998; 13(2):294-302. defi ciency syndrome in infants. J Trop Pediatr. 1998; 34(4):174-178. 28. Wyne KT. A comprehensive review of tremor. JAAPA. 2005; 18(12):43-50. 14. Watanabe N, Omori, IM, Nakagawa A, et al. Safety reporting and adverse- 29. Slaughter JR, Slaughter KA, Nichols D, Holmes SE, Martens MP. Prevalence, event profi le of mirtazapine described in randomized controlled trials in clinical manifestations, etiology, and treatment of depression in Parkinson’s comparison with other classes of antidepressants in the acute-phase treatment disease. J Neuropsychiatry Clin Neurosci. 2001; 13(2):187-196. of adults with depression. CNS Drugs. 2010; 24(1):35-53. 30. Miller KM, Okun MS, Fernandez HF, Jacobson CE, Rodriguez RL, 15. Bhidayasiri R. Differential diagnosis of common tremor syndromes. Postgrad Bowers D. Depression symptoms in movement disorders: comparing Med J. 2005; 81(962):756-762. Parkinson’s disease, dystonia, and essential tremor. Mov Disord. 2007; 16. Morgan JC, Sethi KD. Drug-induced tremors. Lancet Neurol. 2005; 4(12): 22(5):666-672. 866-876. 31. Leckman JF, Bloch MH, King RA, Scahill L. Phenomenology of tics and 17. Louis ED. Clinical practice: essential tremor. N Engl J Med. 2001; 345(12): natural history of tic disorders. Adv Neurol. 2006; 99:1-16. 887-891. 32. Stewart F, Winer W. Hyperkinetic movement disorders. In: Weiner WJ, 18. Uitti RJ. Tremor: how to determine if the patient has Parkinson’s disease. Goetz C, eds. Neurology for the Non-Neurologist. Philadelphia: PA, Lippincott Geriatrics. 1998; 53(5):30-36. Williams & Wilkins; 2004:155-204. 19. Elble RJ. Diagnostic criteria for essential tremor and differential diagnosis. 33. Popp AJ, ed. A Guide to the Primary Care of Neurological Disorders. New York, Neurology. 2000; 54(11 suppl 4): S2-S6. NY: Thieme; 1998:180-183. 20. Goetz CG, Horn SS. Treatment of tremor and dystonia. Neurol Clin. 2001; The author has disclosed that she has no fi nancial relationship related to this 19(1):129-144. article. 21. National Parkinson’s Foundation. 2008 about Parkinson’s disease. http://www. Dr. Laura M. Struble is a Clinical Assistant Professor at the University of Michigan, parkinson.org/NETCOMMUNITY/Page.aspx?pid=225&srcid=201. School of Nursing, Ann Arbor, Mich.

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