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How Best to Address These Common Movement Disorders Aylin Yaman, MD; Melahat Akdeniz, MD; How best to address these Hakan Yaman, MD, MS Antalya Training and Research Hospital, common movement disorders Neurology Clinic, Antalya, Turkey (Dr. A. Yaman); Akdeniz University, This review describes how to manage everything from Department of Family Medicine, Parkinson’s disease and tic disorders to restless legs Antalya, Turkey (Drs. syndrome and ataxia. Akdeniz and H. Yaman) hakanyaman@akdeniz. edu.tr The authors reported no potential conflict of interest ovement disorders often require consultation with a relevant to this article. This PrActice article was supported by the neurologist, and a working knowledge of established Akdeniz University Research recommendations and novel treatments can set the stage for optimal Management Unit. M 1 › Initiate neuroprotective long-term cooperative management. In this article, we review therapy with a monoamine therapeutic options for common movement disorders, including oxidase B inhibitor to slow the hypokinetic, hyperkinetic, and dyskinetic disturbances. progression of Parkinson’s dis- ease. With onset of functional impairment, give levodopa at Parkinson’s disease treatment: the lowest effective dose. A MAO-B inhibitor, levodopa are mainstays › Give propranolol for Parkinson’s disease, the most common hypokinetic move- essential tremor causing ment disorder, is a chronic, progressive, neurodegenerative a patient distress, starting disease. It affects 1% of individuals older than 65 years and 4% at 20 to 40 mg twice daily to 5% of individuals older than 85 years. Its cardinal symptoms and increasing the dose (to a maximum of 320 mg/d) are resting tremor, bradykinesia, rigidity, a flexed posture, and until relief is achieved. B loss of postural reflexes. Resting tremor, referred to as “pill roll- ing” tremor, is 4 to 6 Hz and usually begins unilaterally.2,3 Asso- › Consider giving a dopa- ciated symptoms can include dystonia, dementia, psychiatric mine receptor blocker for disorders, sleep disorders, and autonomic symptoms. Tourette syndrome or other tic z disorder; alternative agents Neuroprotective therapy is used to slow the pro- are clonidine or a newer gression of the disease, particularly in its early stage. The agent, tetrabenazine. B monoamine oxidase B (MAO-B) inhibitor selegiline has proven effective in this regard2 (strength of recommendation Strength of recommendation (SOr) [SOR]: A). In randomized controlled studies, selegiline has A Good-quality patient-oriented delayed the need for levodopa for 9 to 12 months4 (SOR: A). evidence B Inconsistent or limited-quality Another MAO-B inhibitor, rasagiline, has demonstrated neu- patient-oriented evidence roprotective effects as well5 (SOR: B). These medications may C Consensus, usual practice, opinion, disease-oriented also be used with levodopa for symptom control and as adju- evidence, case series vant therapy in patients with motor fluctuations.2 A conven- tional dose of selegiline is 10 mg/d (5 mg at breakfast; 5 mg at lunch). Rasagiline is given at 1 mg/d. Concomitant use of cip- rofloxacin or other CYP1A2 inhibitors limits its effectiveness.6,7 z Symptomatic therapy is indicated at the onset of func- tional impairment. The dopamine precursor levodopa is the most widely used and effective drug for Parkinson’s disease jfponline.com Vol 60, No 12 | DECEMBeR 2011 | The JouRnal of Family PracTice 721 symptoms, especially bradykinesia and rigid- Treating nonmotor symptoms of Parkin- ity. Use the lowest possible dose to control son’s disease can be challenging. For demen- symptoms (eg, 100 mg twice daily) and pro- tia in these patients, consider cholinesterase tect against motor complications of the drug7-9 inhibitors6,8 (SOR: C). For depression, selective (SOR: A). To prevent conversion of levodopa serotonin reuptake inhibitors are effective6,8,9 to dopamine outside the blood-brain barrier, (SOR: C). For psychosis, preferred agents combine it with the decarboxylase inhibitor are low-dose clozapine or quetiapine6,8-10 carbidopa. Dietary restriction of proteins may (SOR: C). Plan for supportive and symptom- be needed, because amino acids can interfere atic management of constipation, dysphagia, with the absorption of levodopa. sialorrhea, orthostatic hypotension, sleep dis- Especially with prolonged use, levodopa turbances, and urinary urgency.2,3 can cause disturbing adverse effects, such as nausea, vomiting, psychosis, cardiac ar- rhythmia, and orthostatic hypotension. tremor Dyskinesias and motor fluctuations are Tremor is a common form of hyperkinesia, complications of long-term treatment presenting either as a primary disorder or as and are irreversible. Adding a cathecol-O- a symptom of another condition.11 By defini- methyltransferase (COMT) inhibitor, such as tion, it is a rhythmical, involuntary, oscillatory entacapone, to increase levodopa’s effective- movement of 1 or more body parts. Tremors Propranolol ness has been shown to reduce motor fluctu- are classified as rest or action tremors, with is more ations2,3,10 (SOR: B). Dopamine agonists such the latter being further categorized as pos- effective for as bromocriptine, ropinirole, and pramipex- tural (occurring while the patient maintains a hand and ole used in early Parkinson’s disease can also position against gravity) or kinetic (occurring forearm tremor reduce dyskinesias and motor fluctuations. during voluntary movement).2,10 than for head Dopamine agonists may be preferred to le- and voice vodopa in early Parkinson’s disease because Physiologic tremor: tremor. they are better tolerated and cause fewer ad- Pharmacologic tx is usually not needed verse effects. Or they may be used as adjuncts Physiologic tremor is benign, high frequency for patients whose response to levodopa is (8-12 Hz), low amplitude, and postural. An ex- deteriorating or fluctuating3,7,8 (SOR: B). In aggerated form of this tremor may result from advanced disease, motor complications can anxiety, hyperthyroidism, pheochromocytoma, also be managed by augmenting levodopa hypoglycemia, excessive caffeine consumption, therapy with a dopamine agonist, MAO-B in- fever, withdrawal from opioids and sedatives, hibitor, or COMT inhibitor7,8 (SOR: A). and some medications. No drug treatment is Anticholinergics, mainly benztropine necessary unless symptoms become bother- and trihexyphenidyl, may be used as symp- some. Correct the underlying cause or have tomatic treatment, especially in young peo- the patient avoid the triggering factor, and ple with early Parkinson’s disease and severe offer reassurance that the condition is not tremor. However, they are not the first drugs pathological or progressive.2,12 For anxiety, con- of choice due to limited efficacy and the sider cognitive-behavioral/relaxation therapy potential for neuropsychiatric side effects8 or benzodiazepines (if tremor did not result (SOR: C). Amantadine can reduce dyskinesia from withdrawal of benzodiazepines) or beta- in people with advanced Parkinson’s disease8 adrenergic antagonists (eg, propranolol).12,13 (SOR: C). For patients who have Parkinson’s disease with severe motor complications, essential tremor: intermittent apomorphine injections can try propranolol or primidone first help reduce “off time” periods in the daily Essential tremor (ET) is the most common treatment cycle when the efficacy of drugs movement disorder. It often results in func- wanes9 (SOR: B). tional disability and leads to many physical Deep brain stimulation of the subtha- and emotional difficulties. ET is bilateral, lamic nucleus has only SOR C support for re- usually symmetric (although mild asymmetry ducing dyskinesias and off time.9 is possible), and postural or kinetic, typically 722 The JouRnal of Family PracTice | DecemBer 2011 | Vol 60, No 12 COMMON MOVEMENT DISORDERS affecting hands and forearms. The frequency term outcomes are lacking. Topiramate’s side of ET is 4 to 12 Hz. Cranial musculature may effects include weight loss and paresthesias. be involved in 30% of cases, affecting the Additionally, alprazolam, clonazepam, clozap- head and voice.3 Prevalence ranges from 4 to ine, olanzapine, atenolol, sotalol, nadolol, and 40 cases per 1000 people. The age-adjusted nimodipine may reduce limb tremor2 (SOR: C). incidence is 17.5/100,000 per year; it peaks Alcohol reduces tremor amplitude in 50% to during the teen years and the fifth decade.2,3 90% of patients, but tremor may worsen after Autosomal dominant type of inheritance the effect of alcohol has worn off.15 is common, and a family history of ET is often For patients with essential hand tremor present, particularly with younger patients. that fails to respond to oral agents, consider The differential diagnosis includes Parkinson’s botulinum toxin A16 (SOR: B). However, it is disease tremor; dystonic, cerebellar, rubral, also associated with dose-dependent hand and psychogenic tremors; and asterixis.3 Un- weakness16 (SOR: C). Botulinum toxin may like ET, many of these disorders have associ- reduce head and voice tremor16 (SOR: C), but ated neurologic, psychiatric, or systemic signs. hoarseness and swallowing difficulties may Treatment with propranolol or primi- occur after use for voice tremor.16 done is indicated if ET causes functional im- Invasive therapies may benefit patients pairment or social or emotional problems for with refractory tremor. Deep brain stimula- the patient.2,3,10,13 Both propranolol and prim- tion and thalamotomy are highly effective idone reduce limb tremor2,10,13 (SOR: B), but in reducing limb tremor13 (SOR: C). Each tic disorders,
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