Applied Evidence

Movement disorders often require consultation with a neurologist, and a working knowledge of established and novel treatments can set the stage for optimal long-term cooperative management.¹ In this article, we review therapeutic options for common movement disorders, including hypokinetic, hyperkinetic, and dyskinetic disturbances.

Parkinson’s disease treatment: MAO-B inhibitor, levodopa are mainstays

Parkinson’s disease, the most common hypokinetic movement disorder, is a chronic, progressive, neurodegenerative disease. It affects 1% of individuals older than 65 years and 4% to 5% of individuals older than 85 years. Its cardinal symptoms are resting tremor, bradykinesia, rigidity, a flexed posture, and loss of postural reflexes. Resting tremor, referred to as “pill rolling” tremor, is 4 to 6 Hz and usually begins unilaterally.^2,3 Associated symptoms can include dystonia, dementia, psychiatric disorders, sleep disorders, and autonomic symptoms.

Neuroprotective therapy is used to slow the progression of the disease, particularly in its early stage. The monoamine oxidase B (MAO-B) inhibitor selegiline has proven effective in this regard² (strength of recommendation [SOR]: A). In randomized controlled studies, selegiline has delayed the need for levodopa for 9 to 12 months⁴ (SOR: A). Another MAO-B inhibitor, rasagiline, has demonstrated neuroprotective effects as well⁵ (SOR: B). These medications may also be used with levodopa for symptom control and as adjuvant therapy in patients with motor fluctuations.² A conventional 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 ciprofloxacin or other CYP1A2 inhibitors limits its effectiveness.^6,7

Symptomatic therapy is indicated at the onset of functional impairment. The dopamine precursor levodopa is the most widely used and effective drug for Parkinson’s disease symptoms, especially bradykinesia and rigidity. Use the lowest possible dose to control symptoms (eg, 100 mg twice daily) and protect against motor complications of the drug^7-9 (SOR: A). To prevent conversion of levodopa to dopamine outside the blood-brain barrier, combine it with the decarboxylase inhibitor carbidopa. Dietary restriction of proteins may be needed, because amino acids can interfere with the absorption of levodopa.

Especially with prolonged use, levodopa can cause disturbing adverse effects, such as nausea, vomiting, psychosis, cardiac arrhythmia, and orthostatic hypotension. Dyskinesias and motor fluctuations are complications of long-term treatment and are irreversible. Adding a cathecol-O-methyltransferase (COMT) inhibitor, such as entacapone, to increase levodopa’s effectiveness has been shown to reduce motor fluctuations^2,3,10 (SOR: B). Dopamine agonists such as bromocriptine, ropinirole, and pramipexole used in early Parkinson’s disease can also reduce dyskinesias and motor fluctuations. Dopamine agonists may be preferred to levodopa in early Parkinson’s disease because they are better tolerated and cause fewer adverse effects. Or they may be used as adjuncts for patients whose response to levodopa is deteriorating or fluctuating^3,7,8 (SOR: B). In advanced disease, motor complications can also be managed by augmenting levodopa therapy with a dopamine agonist, MAO-B inhibitor, or COMT inhibitor^7,8 (SOR: A).

Anticholinergics, mainly benztropine and trihexyphenidyl, may be used as symptomatic treatment, especially in young people with early Parkinson’s disease and severe tremor. However, they are not the first drugs of choice due to limited efficacy and the potential for neuropsychiatric side effects⁸ (SOR: C). Amantadine can reduce dyskinesia in people with advanced Parkinson’s disease⁸ (SOR: C). For patients who have Parkinson’s disease with severe motor complications, intermittent apomorphine injections can help reduce “off time” periods in the daily treatment cycle when the efficacy of drugs wanes⁹ (SOR: B).

Deep brain stimulation of the subthalamic nucleus has only SOR C support for reducing dyskinesias and off time.⁹

Treating nonmotor symptoms of Parkinson’s disease can be challenging. For dementia in these patients, consider cholinesterase inhibitors^6,8 (SOR: C). For depression, selective serotonin reuptake inhibitors are effective^6,8,9 (SOR: C). For psychosis, preferred agents are low-dose clozapine or quetiapine^6,8-10 (SOR: C). Plan for supportive and symptomatic management of constipation, dysphagia, sialorrhea, orthostatic hypotension, sleep disturbances, and urinary urgency.^2,3

Tremor

Tremor is a common form of hyperkinesia, presenting either as a primary disorder or as a symptom of another condition.¹¹ By definition, it is a rhythmical, involuntary, oscillatory movement of 1 or more body parts. Tremors are classified as rest or action tremors, with the latter being further categorized as postural (occurring while the patient maintains a position against gravity) or kinetic (occurring during voluntary movement).^2,10

Physiologic tremor: Pharmacologic Tx is usually not needed
Physiologic tremor is benign, high frequency (8-12 Hz), low amplitude, and postural. An exaggerated form of this tremor may result from anxiety, hyperthyroidism, pheochromocytoma, hypoglycemia, excessive caffeine consumption, fever, withdrawal from opioids and sedatives, and some medications. No drug treatment is necessary unless symptoms become bothersome. Correct the underlying cause or have the patient avoid the triggering factor, and offer reassurance that the condition is not pathological or progressive.^2,12 For anxiety, consider cognitive-behavioral/relaxation therapy or benzodiazepines (if tremor did not result from withdrawal of benzodiazepines) or beta-adrenergic antagonists (eg, propranolol).^12,13

Essential tremor: Try propranolol or primidone first
Essential tremor (ET) is the most common movement disorder. It often results in functional disability and leads to many physical and emotional difficulties. ET is bilateral, usually symmetric (although mild asymmetry is possible), and postural or kinetic, typically affecting hands and forearms. The frequency of ET is 4 to 12 Hz. Cranial musculature may be involved in 30% of cases, affecting the head and voice.³ Prevalence ranges from 4 to 40 cases per 1000 people. The age-adjusted incidence is 17.5/100,000 per year; it peaks during the teen years and the fifth decade.^2,3

Autosomal dominant type of inheritance is common, and a family history of ET is often present, particularly with younger patients. The differential diagnosis includes Parkinson’s disease tremor; dystonic, cerebellar, rubral, and psychogenic tremors; and asterixis.³ Unlike ET, many of these disorders have associated neurologic, psychiatric, or systemic signs.

Treatment with propranolol or primidone is indicated if ET causes functional impairment or social or emotional problems for the patient.^2,3,10,13 Both propranolol and primidone reduce limb tremor^2,10,13 (SOR: B), but only propranolol is approved by the US Food and Drug Administration (FDA) for treatment of ET. Propranolol is more effective for hand and forearm tremor than for head and voice tremor. Start propranolol at 20 to 40 mg twice a day and increase the dose as needed to achieve symptom relief.¹⁴

A maintenance dose of 240 to 320 mg/d may be needed. Major adverse effects are fatigue, sedation, depression, and erectile dysfunction. Contraindications to propranolol include asthma, second-degree atrioventricular block, and insulin-dependent diabetes.

If starting with primidone alone, prescribe at a dose <25 mg at bedtime and increase the dose slowly over several weeks to prevent onset of nausea, vomiting, sedation, confusion, or ataxia. The maximum allowable dose is 750 mg/d in 3 divided doses.¹⁰ Primidone and propranolol may be used in combination to treat limb tremor when monotherapy is insufficient (SOR: B).¹³

Thirty percent of patients with ET will not respond to propranolol or primidone. An alternative choice is the anticonvulsant gabapentin^10,12-14 (SOR: C). However, clinical experience with it is limited. Lethargy, fatigue, decreased libido, dizziness, nervousness, and shortness of breath are adverse effects of gabapentin; they are usually mild and tolerable.¹³ Topiramate is another option that seems to be as effective as gabapentin^10,13 (SOR: C), but studies of long-term outcomes are lacking. Topiramate’s side effects include weight loss and paresthesias. Additionally, alprazolam, clonazepam, clozapine, olanzapine, atenolol, sotalol, nadolol, and nimodipine may reduce limb tremor² (SOR: C). Alcohol reduces tremor amplitude in 50% to 90% of patients, but tremor may worsen after the effect of alcohol has worn off.¹⁵

For patients with essential hand tremor that fails to respond to oral agents, consider botulinum toxin A¹⁶ (SOR: B). However, it is also associated with dose-dependent hand weakness¹⁶ (SOR: C). Botulinum toxin may reduce head and voice tremor¹⁶ (SOR: C), but hoarseness and swallowing difficulties may occur after use for voice tremor.¹⁶

Invasive therapies may benefit patients with refractory tremor. Deep brain stimulation and thalamotomy are highly effective in reducing limb tremor¹³ (SOR: C). Each carries a small risk of major complications. Some deep brain stimulation adverse events may resolve with time. Other adverse events may resolve with adjustment of stimulator settings. No evidence exists for surgical treatment for voice and head tremor or for gamma-knife thalamotomy.¹³

Drug-induced tremor
Drugs with the potential to cause postural tremor, intention tremor, or rest tremor include the following: ¹⁵

• alcohol (chronic)
• amiodarone
• amphetamines
• beta-adrenergic agonists
• caffeine
• calcitonin
• carbamazepine
• cocaine
• cyclosporine
• dopamine
• lithium
• metoclopramide
• neuroleptics
• procainamide
• steroids
• theophylline
• thyroid hormones
• tricyclic antidepressants
• trifluoperazine
• valproic acid

With drug-induced tremor, carefully evaluate a patient’s need for the drug. Discontinue the offending agent if possible, or try lowering the dose.

Psychogenic tremor: A history of somatization is a clue
Psychogenic tremor can occur at rest or during postural or kinetic movement. Clinical features include an abrupt onset, a static course, spontaneous remission, and unclassifiable tremors.¹⁷ Psychogenic tremor increases under direct observation and decreases with distraction. Patients with psychogenic tremor often have a history of somatization.¹⁸ Electrophysiologic testing can help confirm the diagnosis. If remission does not occur spontaneously, patients may find relief with psychotherapy or placebo.¹⁹

Tic disorders: Opt for dopamine receptor blockers

Tics are involuntary or semivoluntary movements or sounds that are sudden, brief, intermittent, repetitive, nonrhythmic, unpredictable, and purposeless. Tics can occur in any part of the body.²⁰

The most common tic disorder is Tourette syndrome—a combination of motor and phonic tics with onset before age 21. It affects approximately 5 to 10 children out of 10,000. Boys are more commonly affected than girls. Attention deficit hyperactivity disorder frequently accompanies this syndrome.²

The goal of treatment with any tic disorder is to improve social functioning, self-esteem, and quality of life. Education and support of patients is important. Tic disorders, including Tourette, rarely require drugs. But if tics become too distressing, first-line treatment would be a dopamine modulator, tetrabenazine, or clonidine. Randomized controlled trials with various neuroleptics have revealed dramatic reductions in tic severity. However, many patients do not tolerate the acute adverse effects (most commonly sedation, weight gain, depression, lethargy, and akathisia), and prolonged treatment confers a small risk of tardive dyskinesia. Behavioral therapy is an important part of management.²⁰

Dopamine-receptor blocking drugs such as haloperidol, pimozide, and fluphenazine are the most effective treatment for tics²⁰ (SOR: B). Tetrabenazine is a promising new dopamine-depleting drug; controlled trials are ongoing^2,20 (SOR: B). Clonidine, an alpha 2-adrenergic agonist, is useful in treating patients with Tourette syndrome, helping to improve sleep and attention^2,21 (SOR: C). Medically refractory motor and disabling phonic tics such as coprolalia can be ameliorated by botulinum toxin injections²¹ (SOR: B). Deep brain stimulation is being used at an increasing rate for medically refractory tics in Tourette syndrome²¹ (SOR: B).

Restless legs syndrome: Dopamine agonists are preferred

Restless legs syndrome (RLS) is a disorder characterized by sensory symptoms and motor disturbances of the legs, mainly during rest. Treatment may not be necessary for patients with mild or sporadic symptoms. For moderate to severe RLS with significant impairment, dopamine agonists are the preferred agents²² (SOR: A). RLS can also occur secondary to such conditions as iron deficiency and uremia, and correction of the underlying disorder is the goal. Prescribe iron replacement for patients with a ferritin level <50 ng/mL²² (SOR: C). Medications known to cause or exacerbate the symptoms of RLS are anti-dopaminergic agents (such as neuroleptics), diphenhydramine, tricyclic antidepressants, alcohol, caffeine, lithium, and beta-blockers. If a patient is taking medications that exacerbate symptoms of RLS, discontinue them and use appropriate substitutes²² (SOR: C).

Myoclonus: Clonazepam for essential disorder

Myoclonus is a brief, sudden, shock-like movement caused by involuntary muscle contractions or lapse of muscle contraction (asterixis). Given the complex origins of myoclonus, multiple drugs may be needed. Essential myoclonus is disabling and can be treated with clonazepam. Start with 0.25 mg orally twice daily, and increase the dosage over 3 days to 1 mg/d²³ (SOR: C). Most cases of myoclonus are secondary due to drugs such as lithium, toxins, advanced liver disease, infections including human immunodeficiency virus, dementia, and brain lesions. Treatment should also address the underlying disorder.^2,23

Chorea

Chorea is an abnormal involuntary movement disorder described as “a state of excessive, spontaneous movements, irregularly timed, nonrepetitive, randomly distributed, and abrupt in character.”²⁴

Treatment of chorea is symptomatic, aiming to reduce morbidity and prevent complications. Haloperidol and fluphenazine are effective but can impair voluntary movements^2,10,25 (SOR: C). The dopamine-depleting drugs reserpine and tetrabenazine are also effective^2,10,25 (SOR: C). GABAergic drugs, such as clonazepam, gabapentin, and valproate, can be used adjunctively.^10,25

Dystonia

Dystonia is a syndrome involving sustained contractions of opposing muscles that cause twisting, repetitive movements and abnormal postures. Primary dystonia can be treated successfully with high doses of trihexyphenidyl alone, starting with 1 mg orally per day and increasing gradually to 6 to 80 mg/d until symptoms are controlled; or in combination with baclofen, starting with 10 mg orally once daily and increasing to a maximum dose of 30 to 120 mg/d^1,2 (SOR: C).

Consider botulinum neurotoxin injection for focal upper extremity dystonia and adductor spasmodic dysphonia¹⁶ (SOR: B).

Ataxia

Ataxia is an unsteady gait associated with cerebellar dysfunction, proprioceptive defects, or both. Ataxia may be primary (Friedreich ataxia and spinocerebellar ataxia) or secondary to stroke, trauma, alcoholic degeneration, multiple sclerosis, vitamin B12 deficiency, and hydrocephalus. Treatment, when possible, should target the underlying cause.^1,2

CORRESPONDENCE Hakan Yaman, MD, Akdeniz University, Department of Family Medicine, Antalya, Turkey 07058; [email protected]

Movement disorders often require consultation with a neurologist, and a working knowledge of established and novel treatments can set the stage for optimal long-term cooperative management.¹ In this article, we review therapeutic options for common movement disorders, including hypokinetic, hyperkinetic, and dyskinetic disturbances.

Parkinson’s disease treatment: MAO-B inhibitor, levodopa are mainstays

Parkinson’s disease, the most common hypokinetic movement disorder, is a chronic, progressive, neurodegenerative disease. It affects 1% of individuals older than 65 years and 4% to 5% of individuals older than 85 years. Its cardinal symptoms are resting tremor, bradykinesia, rigidity, a flexed posture, and loss of postural reflexes. Resting tremor, referred to as “pill rolling” tremor, is 4 to 6 Hz and usually begins unilaterally.^2,3 Associated symptoms can include dystonia, dementia, psychiatric disorders, sleep disorders, and autonomic symptoms.

Neuroprotective therapy is used to slow the progression of the disease, particularly in its early stage. The monoamine oxidase B (MAO-B) inhibitor selegiline has proven effective in this regard² (strength of recommendation [SOR]: A). In randomized controlled studies, selegiline has delayed the need for levodopa for 9 to 12 months⁴ (SOR: A). Another MAO-B inhibitor, rasagiline, has demonstrated neuroprotective effects as well⁵ (SOR: B). These medications may also be used with levodopa for symptom control and as adjuvant therapy in patients with motor fluctuations.² A conventional 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 ciprofloxacin or other CYP1A2 inhibitors limits its effectiveness.^6,7

Symptomatic therapy is indicated at the onset of functional impairment. The dopamine precursor levodopa is the most widely used and effective drug for Parkinson’s disease symptoms, especially bradykinesia and rigidity. Use the lowest possible dose to control symptoms (eg, 100 mg twice daily) and protect against motor complications of the drug^7-9 (SOR: A). To prevent conversion of levodopa to dopamine outside the blood-brain barrier, combine it with the decarboxylase inhibitor carbidopa. Dietary restriction of proteins may be needed, because amino acids can interfere with the absorption of levodopa.

Especially with prolonged use, levodopa can cause disturbing adverse effects, such as nausea, vomiting, psychosis, cardiac arrhythmia, and orthostatic hypotension. Dyskinesias and motor fluctuations are complications of long-term treatment and are irreversible. Adding a cathecol-O-methyltransferase (COMT) inhibitor, such as entacapone, to increase levodopa’s effectiveness has been shown to reduce motor fluctuations^2,3,10 (SOR: B). Dopamine agonists such as bromocriptine, ropinirole, and pramipexole used in early Parkinson’s disease can also reduce dyskinesias and motor fluctuations. Dopamine agonists may be preferred to levodopa in early Parkinson’s disease because they are better tolerated and cause fewer adverse effects. Or they may be used as adjuncts for patients whose response to levodopa is deteriorating or fluctuating^3,7,8 (SOR: B). In advanced disease, motor complications can also be managed by augmenting levodopa therapy with a dopamine agonist, MAO-B inhibitor, or COMT inhibitor^7,8 (SOR: A).

Anticholinergics, mainly benztropine and trihexyphenidyl, may be used as symptomatic treatment, especially in young people with early Parkinson’s disease and severe tremor. However, they are not the first drugs of choice due to limited efficacy and the potential for neuropsychiatric side effects⁸ (SOR: C). Amantadine can reduce dyskinesia in people with advanced Parkinson’s disease⁸ (SOR: C). For patients who have Parkinson’s disease with severe motor complications, intermittent apomorphine injections can help reduce “off time” periods in the daily treatment cycle when the efficacy of drugs wanes⁹ (SOR: B).

Deep brain stimulation of the subthalamic nucleus has only SOR C support for reducing dyskinesias and off time.⁹

Treating nonmotor symptoms of Parkinson’s disease can be challenging. For dementia in these patients, consider cholinesterase inhibitors^6,8 (SOR: C). For depression, selective serotonin reuptake inhibitors are effective^6,8,9 (SOR: C). For psychosis, preferred agents are low-dose clozapine or quetiapine^6,8-10 (SOR: C). Plan for supportive and symptomatic management of constipation, dysphagia, sialorrhea, orthostatic hypotension, sleep disturbances, and urinary urgency.^2,3

Tremor

Tremor is a common form of hyperkinesia, presenting either as a primary disorder or as a symptom of another condition.¹¹ By definition, it is a rhythmical, involuntary, oscillatory movement of 1 or more body parts. Tremors are classified as rest or action tremors, with the latter being further categorized as postural (occurring while the patient maintains a position against gravity) or kinetic (occurring during voluntary movement).^2,10

Physiologic tremor: Pharmacologic Tx is usually not needed
Physiologic tremor is benign, high frequency (8-12 Hz), low amplitude, and postural. An exaggerated form of this tremor may result from anxiety, hyperthyroidism, pheochromocytoma, hypoglycemia, excessive caffeine consumption, fever, withdrawal from opioids and sedatives, and some medications. No drug treatment is necessary unless symptoms become bothersome. Correct the underlying cause or have the patient avoid the triggering factor, and offer reassurance that the condition is not pathological or progressive.^2,12 For anxiety, consider cognitive-behavioral/relaxation therapy or benzodiazepines (if tremor did not result from withdrawal of benzodiazepines) or beta-adrenergic antagonists (eg, propranolol).^12,13

Essential tremor: Try propranolol or primidone first
Essential tremor (ET) is the most common movement disorder. It often results in functional disability and leads to many physical and emotional difficulties. ET is bilateral, usually symmetric (although mild asymmetry is possible), and postural or kinetic, typically affecting hands and forearms. The frequency of ET is 4 to 12 Hz. Cranial musculature may be involved in 30% of cases, affecting the head and voice.³ Prevalence ranges from 4 to 40 cases per 1000 people. The age-adjusted incidence is 17.5/100,000 per year; it peaks during the teen years and the fifth decade.^2,3

Autosomal dominant type of inheritance is common, and a family history of ET is often present, particularly with younger patients. The differential diagnosis includes Parkinson’s disease tremor; dystonic, cerebellar, rubral, and psychogenic tremors; and asterixis.³ Unlike ET, many of these disorders have associated neurologic, psychiatric, or systemic signs.

Treatment with propranolol or primidone is indicated if ET causes functional impairment or social or emotional problems for the patient.^2,3,10,13 Both propranolol and primidone reduce limb tremor^2,10,13 (SOR: B), but only propranolol is approved by the US Food and Drug Administration (FDA) for treatment of ET. Propranolol is more effective for hand and forearm tremor than for head and voice tremor. Start propranolol at 20 to 40 mg twice a day and increase the dose as needed to achieve symptom relief.¹⁴

A maintenance dose of 240 to 320 mg/d may be needed. Major adverse effects are fatigue, sedation, depression, and erectile dysfunction. Contraindications to propranolol include asthma, second-degree atrioventricular block, and insulin-dependent diabetes.

If starting with primidone alone, prescribe at a dose <25 mg at bedtime and increase the dose slowly over several weeks to prevent onset of nausea, vomiting, sedation, confusion, or ataxia. The maximum allowable dose is 750 mg/d in 3 divided doses.¹⁰ Primidone and propranolol may be used in combination to treat limb tremor when monotherapy is insufficient (SOR: B).¹³

Thirty percent of patients with ET will not respond to propranolol or primidone. An alternative choice is the anticonvulsant gabapentin^10,12-14 (SOR: C). However, clinical experience with it is limited. Lethargy, fatigue, decreased libido, dizziness, nervousness, and shortness of breath are adverse effects of gabapentin; they are usually mild and tolerable.¹³ Topiramate is another option that seems to be as effective as gabapentin^10,13 (SOR: C), but studies of long-term outcomes are lacking. Topiramate’s side effects include weight loss and paresthesias. Additionally, alprazolam, clonazepam, clozapine, olanzapine, atenolol, sotalol, nadolol, and nimodipine may reduce limb tremor² (SOR: C). Alcohol reduces tremor amplitude in 50% to 90% of patients, but tremor may worsen after the effect of alcohol has worn off.¹⁵

For patients with essential hand tremor that fails to respond to oral agents, consider botulinum toxin A¹⁶ (SOR: B). However, it is also associated with dose-dependent hand weakness¹⁶ (SOR: C). Botulinum toxin may reduce head and voice tremor¹⁶ (SOR: C), but hoarseness and swallowing difficulties may occur after use for voice tremor.¹⁶

Invasive therapies may benefit patients with refractory tremor. Deep brain stimulation and thalamotomy are highly effective in reducing limb tremor¹³ (SOR: C). Each carries a small risk of major complications. Some deep brain stimulation adverse events may resolve with time. Other adverse events may resolve with adjustment of stimulator settings. No evidence exists for surgical treatment for voice and head tremor or for gamma-knife thalamotomy.¹³

Drug-induced tremor
Drugs with the potential to cause postural tremor, intention tremor, or rest tremor include the following: ¹⁵

• alcohol (chronic)
• amiodarone
• amphetamines
• beta-adrenergic agonists
• caffeine
• calcitonin
• carbamazepine
• cocaine
• cyclosporine
• dopamine
• lithium
• metoclopramide
• neuroleptics
• procainamide
• steroids
• theophylline
• thyroid hormones
• tricyclic antidepressants
• trifluoperazine
• valproic acid

With drug-induced tremor, carefully evaluate a patient’s need for the drug. Discontinue the offending agent if possible, or try lowering the dose.

Psychogenic tremor: A history of somatization is a clue
Psychogenic tremor can occur at rest or during postural or kinetic movement. Clinical features include an abrupt onset, a static course, spontaneous remission, and unclassifiable tremors.¹⁷ Psychogenic tremor increases under direct observation and decreases with distraction. Patients with psychogenic tremor often have a history of somatization.¹⁸ Electrophysiologic testing can help confirm the diagnosis. If remission does not occur spontaneously, patients may find relief with psychotherapy or placebo.¹⁹

Tic disorders: Opt for dopamine receptor blockers

Tics are involuntary or semivoluntary movements or sounds that are sudden, brief, intermittent, repetitive, nonrhythmic, unpredictable, and purposeless. Tics can occur in any part of the body.²⁰

The most common tic disorder is Tourette syndrome—a combination of motor and phonic tics with onset before age 21. It affects approximately 5 to 10 children out of 10,000. Boys are more commonly affected than girls. Attention deficit hyperactivity disorder frequently accompanies this syndrome.²

The goal of treatment with any tic disorder is to improve social functioning, self-esteem, and quality of life. Education and support of patients is important. Tic disorders, including Tourette, rarely require drugs. But if tics become too distressing, first-line treatment would be a dopamine modulator, tetrabenazine, or clonidine. Randomized controlled trials with various neuroleptics have revealed dramatic reductions in tic severity. However, many patients do not tolerate the acute adverse effects (most commonly sedation, weight gain, depression, lethargy, and akathisia), and prolonged treatment confers a small risk of tardive dyskinesia. Behavioral therapy is an important part of management.²⁰

Dopamine-receptor blocking drugs such as haloperidol, pimozide, and fluphenazine are the most effective treatment for tics²⁰ (SOR: B). Tetrabenazine is a promising new dopamine-depleting drug; controlled trials are ongoing^2,20 (SOR: B). Clonidine, an alpha 2-adrenergic agonist, is useful in treating patients with Tourette syndrome, helping to improve sleep and attention^2,21 (SOR: C). Medically refractory motor and disabling phonic tics such as coprolalia can be ameliorated by botulinum toxin injections²¹ (SOR: B). Deep brain stimulation is being used at an increasing rate for medically refractory tics in Tourette syndrome²¹ (SOR: B).

Restless legs syndrome: Dopamine agonists are preferred

Restless legs syndrome (RLS) is a disorder characterized by sensory symptoms and motor disturbances of the legs, mainly during rest. Treatment may not be necessary for patients with mild or sporadic symptoms. For moderate to severe RLS with significant impairment, dopamine agonists are the preferred agents²² (SOR: A). RLS can also occur secondary to such conditions as iron deficiency and uremia, and correction of the underlying disorder is the goal. Prescribe iron replacement for patients with a ferritin level <50 ng/mL²² (SOR: C). Medications known to cause or exacerbate the symptoms of RLS are anti-dopaminergic agents (such as neuroleptics), diphenhydramine, tricyclic antidepressants, alcohol, caffeine, lithium, and beta-blockers. If a patient is taking medications that exacerbate symptoms of RLS, discontinue them and use appropriate substitutes²² (SOR: C).

Myoclonus: Clonazepam for essential disorder

Myoclonus is a brief, sudden, shock-like movement caused by involuntary muscle contractions or lapse of muscle contraction (asterixis). Given the complex origins of myoclonus, multiple drugs may be needed. Essential myoclonus is disabling and can be treated with clonazepam. Start with 0.25 mg orally twice daily, and increase the dosage over 3 days to 1 mg/d²³ (SOR: C). Most cases of myoclonus are secondary due to drugs such as lithium, toxins, advanced liver disease, infections including human immunodeficiency virus, dementia, and brain lesions. Treatment should also address the underlying disorder.^2,23

Chorea

Chorea is an abnormal involuntary movement disorder described as “a state of excessive, spontaneous movements, irregularly timed, nonrepetitive, randomly distributed, and abrupt in character.”²⁴

Treatment of chorea is symptomatic, aiming to reduce morbidity and prevent complications. Haloperidol and fluphenazine are effective but can impair voluntary movements^2,10,25 (SOR: C). The dopamine-depleting drugs reserpine and tetrabenazine are also effective^2,10,25 (SOR: C). GABAergic drugs, such as clonazepam, gabapentin, and valproate, can be used adjunctively.^10,25

Dystonia

Dystonia is a syndrome involving sustained contractions of opposing muscles that cause twisting, repetitive movements and abnormal postures. Primary dystonia can be treated successfully with high doses of trihexyphenidyl alone, starting with 1 mg orally per day and increasing gradually to 6 to 80 mg/d until symptoms are controlled; or in combination with baclofen, starting with 10 mg orally once daily and increasing to a maximum dose of 30 to 120 mg/d^1,2 (SOR: C).

Consider botulinum neurotoxin injection for focal upper extremity dystonia and adductor spasmodic dysphonia¹⁶ (SOR: B).

Ataxia

Ataxia is an unsteady gait associated with cerebellar dysfunction, proprioceptive defects, or both. Ataxia may be primary (Friedreich ataxia and spinocerebellar ataxia) or secondary to stroke, trauma, alcoholic degeneration, multiple sclerosis, vitamin B12 deficiency, and hydrocephalus. Treatment, when possible, should target the underlying cause.^1,2

CORRESPONDENCE Hakan Yaman, MD, Akdeniz University, Department of Family Medicine, Antalya, Turkey 07058; [email protected]

Movement disorders often require consultation with a neurologist, and a working knowledge of established and novel treatments can set the stage for optimal long-term cooperative management.¹ In this article, we review therapeutic options for common movement disorders, including hypokinetic, hyperkinetic, and dyskinetic disturbances.

Parkinson’s disease treatment: MAO-B inhibitor, levodopa are mainstays

Parkinson’s disease, the most common hypokinetic movement disorder, is a chronic, progressive, neurodegenerative disease. It affects 1% of individuals older than 65 years and 4% to 5% of individuals older than 85 years. Its cardinal symptoms are resting tremor, bradykinesia, rigidity, a flexed posture, and loss of postural reflexes. Resting tremor, referred to as “pill rolling” tremor, is 4 to 6 Hz and usually begins unilaterally.^2,3 Associated symptoms can include dystonia, dementia, psychiatric disorders, sleep disorders, and autonomic symptoms.

Neuroprotective therapy is used to slow the progression of the disease, particularly in its early stage. The monoamine oxidase B (MAO-B) inhibitor selegiline has proven effective in this regard² (strength of recommendation [SOR]: A). In randomized controlled studies, selegiline has delayed the need for levodopa for 9 to 12 months⁴ (SOR: A). Another MAO-B inhibitor, rasagiline, has demonstrated neuroprotective effects as well⁵ (SOR: B). These medications may also be used with levodopa for symptom control and as adjuvant therapy in patients with motor fluctuations.² A conventional 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 ciprofloxacin or other CYP1A2 inhibitors limits its effectiveness.^6,7

Symptomatic therapy is indicated at the onset of functional impairment. The dopamine precursor levodopa is the most widely used and effective drug for Parkinson’s disease symptoms, especially bradykinesia and rigidity. Use the lowest possible dose to control symptoms (eg, 100 mg twice daily) and protect against motor complications of the drug^7-9 (SOR: A). To prevent conversion of levodopa to dopamine outside the blood-brain barrier, combine it with the decarboxylase inhibitor carbidopa. Dietary restriction of proteins may be needed, because amino acids can interfere with the absorption of levodopa.

Especially with prolonged use, levodopa can cause disturbing adverse effects, such as nausea, vomiting, psychosis, cardiac arrhythmia, and orthostatic hypotension. Dyskinesias and motor fluctuations are complications of long-term treatment and are irreversible. Adding a cathecol-O-methyltransferase (COMT) inhibitor, such as entacapone, to increase levodopa’s effectiveness has been shown to reduce motor fluctuations^2,3,10 (SOR: B). Dopamine agonists such as bromocriptine, ropinirole, and pramipexole used in early Parkinson’s disease can also reduce dyskinesias and motor fluctuations. Dopamine agonists may be preferred to levodopa in early Parkinson’s disease because they are better tolerated and cause fewer adverse effects. Or they may be used as adjuncts for patients whose response to levodopa is deteriorating or fluctuating^3,7,8 (SOR: B). In advanced disease, motor complications can also be managed by augmenting levodopa therapy with a dopamine agonist, MAO-B inhibitor, or COMT inhibitor^7,8 (SOR: A).

Anticholinergics, mainly benztropine and trihexyphenidyl, may be used as symptomatic treatment, especially in young people with early Parkinson’s disease and severe tremor. However, they are not the first drugs of choice due to limited efficacy and the potential for neuropsychiatric side effects⁸ (SOR: C). Amantadine can reduce dyskinesia in people with advanced Parkinson’s disease⁸ (SOR: C). For patients who have Parkinson’s disease with severe motor complications, intermittent apomorphine injections can help reduce “off time” periods in the daily treatment cycle when the efficacy of drugs wanes⁹ (SOR: B).

Deep brain stimulation of the subthalamic nucleus has only SOR C support for reducing dyskinesias and off time.⁹

Treating nonmotor symptoms of Parkinson’s disease can be challenging. For dementia in these patients, consider cholinesterase inhibitors^6,8 (SOR: C). For depression, selective serotonin reuptake inhibitors are effective^6,8,9 (SOR: C). For psychosis, preferred agents are low-dose clozapine or quetiapine^6,8-10 (SOR: C). Plan for supportive and symptomatic management of constipation, dysphagia, sialorrhea, orthostatic hypotension, sleep disturbances, and urinary urgency.^2,3

Tremor

Tremor is a common form of hyperkinesia, presenting either as a primary disorder or as a symptom of another condition.¹¹ By definition, it is a rhythmical, involuntary, oscillatory movement of 1 or more body parts. Tremors are classified as rest or action tremors, with the latter being further categorized as postural (occurring while the patient maintains a position against gravity) or kinetic (occurring during voluntary movement).^2,10

Physiologic tremor: Pharmacologic Tx is usually not needed
Physiologic tremor is benign, high frequency (8-12 Hz), low amplitude, and postural. An exaggerated form of this tremor may result from anxiety, hyperthyroidism, pheochromocytoma, hypoglycemia, excessive caffeine consumption, fever, withdrawal from opioids and sedatives, and some medications. No drug treatment is necessary unless symptoms become bothersome. Correct the underlying cause or have the patient avoid the triggering factor, and offer reassurance that the condition is not pathological or progressive.^2,12 For anxiety, consider cognitive-behavioral/relaxation therapy or benzodiazepines (if tremor did not result from withdrawal of benzodiazepines) or beta-adrenergic antagonists (eg, propranolol).^12,13

Essential tremor: Try propranolol or primidone first
Essential tremor (ET) is the most common movement disorder. It often results in functional disability and leads to many physical and emotional difficulties. ET is bilateral, usually symmetric (although mild asymmetry is possible), and postural or kinetic, typically affecting hands and forearms. The frequency of ET is 4 to 12 Hz. Cranial musculature may be involved in 30% of cases, affecting the head and voice.³ Prevalence ranges from 4 to 40 cases per 1000 people. The age-adjusted incidence is 17.5/100,000 per year; it peaks during the teen years and the fifth decade.^2,3

Autosomal dominant type of inheritance is common, and a family history of ET is often present, particularly with younger patients. The differential diagnosis includes Parkinson’s disease tremor; dystonic, cerebellar, rubral, and psychogenic tremors; and asterixis.³ Unlike ET, many of these disorders have associated neurologic, psychiatric, or systemic signs.

Treatment with propranolol or primidone is indicated if ET causes functional impairment or social or emotional problems for the patient.^2,3,10,13 Both propranolol and primidone reduce limb tremor^2,10,13 (SOR: B), but only propranolol is approved by the US Food and Drug Administration (FDA) for treatment of ET. Propranolol is more effective for hand and forearm tremor than for head and voice tremor. Start propranolol at 20 to 40 mg twice a day and increase the dose as needed to achieve symptom relief.¹⁴

A maintenance dose of 240 to 320 mg/d may be needed. Major adverse effects are fatigue, sedation, depression, and erectile dysfunction. Contraindications to propranolol include asthma, second-degree atrioventricular block, and insulin-dependent diabetes.

If starting with primidone alone, prescribe at a dose <25 mg at bedtime and increase the dose slowly over several weeks to prevent onset of nausea, vomiting, sedation, confusion, or ataxia. The maximum allowable dose is 750 mg/d in 3 divided doses.¹⁰ Primidone and propranolol may be used in combination to treat limb tremor when monotherapy is insufficient (SOR: B).¹³

Thirty percent of patients with ET will not respond to propranolol or primidone. An alternative choice is the anticonvulsant gabapentin^10,12-14 (SOR: C). However, clinical experience with it is limited. Lethargy, fatigue, decreased libido, dizziness, nervousness, and shortness of breath are adverse effects of gabapentin; they are usually mild and tolerable.¹³ Topiramate is another option that seems to be as effective as gabapentin^10,13 (SOR: C), but studies of long-term outcomes are lacking. Topiramate’s side effects include weight loss and paresthesias. Additionally, alprazolam, clonazepam, clozapine, olanzapine, atenolol, sotalol, nadolol, and nimodipine may reduce limb tremor² (SOR: C). Alcohol reduces tremor amplitude in 50% to 90% of patients, but tremor may worsen after the effect of alcohol has worn off.¹⁵

For patients with essential hand tremor that fails to respond to oral agents, consider botulinum toxin A¹⁶ (SOR: B). However, it is also associated with dose-dependent hand weakness¹⁶ (SOR: C). Botulinum toxin may reduce head and voice tremor¹⁶ (SOR: C), but hoarseness and swallowing difficulties may occur after use for voice tremor.¹⁶

Invasive therapies may benefit patients with refractory tremor. Deep brain stimulation and thalamotomy are highly effective in reducing limb tremor¹³ (SOR: C). Each carries a small risk of major complications. Some deep brain stimulation adverse events may resolve with time. Other adverse events may resolve with adjustment of stimulator settings. No evidence exists for surgical treatment for voice and head tremor or for gamma-knife thalamotomy.¹³

Drug-induced tremor
Drugs with the potential to cause postural tremor, intention tremor, or rest tremor include the following: ¹⁵

• alcohol (chronic)
• amiodarone
• amphetamines
• beta-adrenergic agonists
• caffeine
• calcitonin
• carbamazepine
• cocaine
• cyclosporine
• dopamine
• lithium
• metoclopramide
• neuroleptics
• procainamide
• steroids
• theophylline
• thyroid hormones
• tricyclic antidepressants
• trifluoperazine
• valproic acid

With drug-induced tremor, carefully evaluate a patient’s need for the drug. Discontinue the offending agent if possible, or try lowering the dose.

Psychogenic tremor: A history of somatization is a clue
Psychogenic tremor can occur at rest or during postural or kinetic movement. Clinical features include an abrupt onset, a static course, spontaneous remission, and unclassifiable tremors.¹⁷ Psychogenic tremor increases under direct observation and decreases with distraction. Patients with psychogenic tremor often have a history of somatization.¹⁸ Electrophysiologic testing can help confirm the diagnosis. If remission does not occur spontaneously, patients may find relief with psychotherapy or placebo.¹⁹

Tic disorders: Opt for dopamine receptor blockers

Tics are involuntary or semivoluntary movements or sounds that are sudden, brief, intermittent, repetitive, nonrhythmic, unpredictable, and purposeless. Tics can occur in any part of the body.²⁰

The most common tic disorder is Tourette syndrome—a combination of motor and phonic tics with onset before age 21. It affects approximately 5 to 10 children out of 10,000. Boys are more commonly affected than girls. Attention deficit hyperactivity disorder frequently accompanies this syndrome.²

The goal of treatment with any tic disorder is to improve social functioning, self-esteem, and quality of life. Education and support of patients is important. Tic disorders, including Tourette, rarely require drugs. But if tics become too distressing, first-line treatment would be a dopamine modulator, tetrabenazine, or clonidine. Randomized controlled trials with various neuroleptics have revealed dramatic reductions in tic severity. However, many patients do not tolerate the acute adverse effects (most commonly sedation, weight gain, depression, lethargy, and akathisia), and prolonged treatment confers a small risk of tardive dyskinesia. Behavioral therapy is an important part of management.²⁰

Dopamine-receptor blocking drugs such as haloperidol, pimozide, and fluphenazine are the most effective treatment for tics²⁰ (SOR: B). Tetrabenazine is a promising new dopamine-depleting drug; controlled trials are ongoing^2,20 (SOR: B). Clonidine, an alpha 2-adrenergic agonist, is useful in treating patients with Tourette syndrome, helping to improve sleep and attention^2,21 (SOR: C). Medically refractory motor and disabling phonic tics such as coprolalia can be ameliorated by botulinum toxin injections²¹ (SOR: B). Deep brain stimulation is being used at an increasing rate for medically refractory tics in Tourette syndrome²¹ (SOR: B).

Restless legs syndrome: Dopamine agonists are preferred

Restless legs syndrome (RLS) is a disorder characterized by sensory symptoms and motor disturbances of the legs, mainly during rest. Treatment may not be necessary for patients with mild or sporadic symptoms. For moderate to severe RLS with significant impairment, dopamine agonists are the preferred agents²² (SOR: A). RLS can also occur secondary to such conditions as iron deficiency and uremia, and correction of the underlying disorder is the goal. Prescribe iron replacement for patients with a ferritin level <50 ng/mL²² (SOR: C). Medications known to cause or exacerbate the symptoms of RLS are anti-dopaminergic agents (such as neuroleptics), diphenhydramine, tricyclic antidepressants, alcohol, caffeine, lithium, and beta-blockers. If a patient is taking medications that exacerbate symptoms of RLS, discontinue them and use appropriate substitutes²² (SOR: C).

Myoclonus: Clonazepam for essential disorder

Myoclonus is a brief, sudden, shock-like movement caused by involuntary muscle contractions or lapse of muscle contraction (asterixis). Given the complex origins of myoclonus, multiple drugs may be needed. Essential myoclonus is disabling and can be treated with clonazepam. Start with 0.25 mg orally twice daily, and increase the dosage over 3 days to 1 mg/d²³ (SOR: C). Most cases of myoclonus are secondary due to drugs such as lithium, toxins, advanced liver disease, infections including human immunodeficiency virus, dementia, and brain lesions. Treatment should also address the underlying disorder.^2,23

Chorea

Chorea is an abnormal involuntary movement disorder described as “a state of excessive, spontaneous movements, irregularly timed, nonrepetitive, randomly distributed, and abrupt in character.”²⁴

Treatment of chorea is symptomatic, aiming to reduce morbidity and prevent complications. Haloperidol and fluphenazine are effective but can impair voluntary movements^2,10,25 (SOR: C). The dopamine-depleting drugs reserpine and tetrabenazine are also effective^2,10,25 (SOR: C). GABAergic drugs, such as clonazepam, gabapentin, and valproate, can be used adjunctively.^10,25

Dystonia

Dystonia is a syndrome involving sustained contractions of opposing muscles that cause twisting, repetitive movements and abnormal postures. Primary dystonia can be treated successfully with high doses of trihexyphenidyl alone, starting with 1 mg orally per day and increasing gradually to 6 to 80 mg/d until symptoms are controlled; or in combination with baclofen, starting with 10 mg orally once daily and increasing to a maximum dose of 30 to 120 mg/d^1,2 (SOR: C).

Consider botulinum neurotoxin injection for focal upper extremity dystonia and adductor spasmodic dysphonia¹⁶ (SOR: B).

Ataxia

Ataxia is an unsteady gait associated with cerebellar dysfunction, proprioceptive defects, or both. Ataxia may be primary (Friedreich ataxia and spinocerebellar ataxia) or secondary to stroke, trauma, alcoholic degeneration, multiple sclerosis, vitamin B12 deficiency, and hydrocephalus. Treatment, when possible, should target the underlying cause.^1,2

CORRESPONDENCE Hakan Yaman, MD, Akdeniz University, Department of Family Medicine, Antalya, Turkey 07058; [email protected]

For patients with asthma or chronic obstructive pulmonary disease (COPD), inhalation therapy is the foundation of treatment. Yet all too often, patients don’t get the full value of their inhaled medications because they use their inhaler incorrectly. When technique is markedly flawed, suboptimal outcomes typically result.

Given the number of Americans with asthma (at least 22 million)¹ and COPD (more than 13 million adults),² faulty inhaler technique is a major public health problem. In fact, the number of people suffering from COPD may be even larger: Close to 24 million US adults are believed to have impaired lung function.^3,4 For patients with asthma or COPD—many of whom are treated by family physicians—comprehensive education with a focus on correct use of an inhaler is essential.

In this review, we present evidence of frequent inhaler errors (from clinical studies) and highlight some of the more common mistakes (based on our clinical experience [TABLE]⁵). Finally, we offer ‘‘time-efficient’’ solutions to inhaler problems—steps that physicians in busy primary care practices can take to ensure that patients with asthma or COPD get the maximum benefit from inhalation therapy.

TABLE
Caution patients about these device-specific mistakes*

Inhaler error is well documented

Since 1965, when it was first reported that many patients used metered dose inhalers (MDIs) incorrectly,⁶ evidence has accumulated supporting the magnitude of the problem.^7-12 (Studies conducted in family practice settings are described in “Researchers look at inhaler problems in primary care” and in TABLE W1.^13-20)

Error rates vary widely from one clinical trial to another, depending on study criteria, type of device, and extent of patient education, among other factors. Nonetheless, several studies (spanning 3 decades) found the error rate to be close to, or greater than, 90%.^7,10,21

The most recent of these, published in 2009,²¹ was based on observation of the inhaler technique used by patients with asthma or COPD directly following appointments in an outpatient clinic. The authors found that, although >98% of the study participants claimed to know how to use their inhalers, 94% committed at least one error. In this study and a number of others, user error was more likely in patients using MDIs.^13,18,21,22

Breath-activated dry powder inhalers (DPIs)—such as the Flexhaler, HandiHaler, Aerolizer, and Diskus—also reduce the likelihood of error. DPIs eliminate a step that MDI users often struggle with: the need to simultaneously press down on the canister and begin a slow, deep inhalation.

What’s more, DPIs do not have to be shaken before use. Nonetheless, using a DPI still involves a series of actions. For the HandiHaler and Aerolizer, patients must load the dose, and some patients fail to read the directions and swallow the capsule instead of loading it into the device. Patients must remember to exhale away from the device (ie, not into the dry powder) before inhaling, then hold their breath for approximately 10 seconds. There is potential for error at each step.

Stress the need to exhale before using the inhaler
Forgetting to exhale before inhaling is a common, and significant, mistake regardless of the type of device. It is paramount to stress the need to exhale gently for a few seconds before inhaling (slowly and deeply for patients using an MDI, rapidly and deeply with most DPIs). For MDI users, poor timing, described earlier, is another common and serious mistake. Patients using an MDI with a valved holding chamber sometimes inhale for too long before pressing down on the inhaler, then are unable to continue inhaling although the aerosol is still in the chamber. A common error made by patients using multidose DPIs is simply to forget to load the dose.

Physicians need to brush up on their skills, too

It’s not just patients who lack proficiency in inhaler technique. Numerous studies have demonstrated poor skill among physicians and other health care professionals.^27-34 Evidence also shows that targeted education results in substantial improvement.^32,35

In one study undertaken to evaluate family medicine residents’ proficiency in using asthma inhalers, participants (an intervention group at one clinic and a control group at another) all were given a pretest. The intervention group then received educational materials and a tutorial, as well as the opportunity for hands-on practice, after which both groups were given a post-test. The residents who received the training had a 170% jump, on average, in proficiency score, vs a 55% increase for the control group (P<.001).³⁵

WATCH THE VIDEOS

Inhaled Medication Instructional Videos
Courtesy of: National Jewish Health

Go to http://www.nationaljewish.org/healthinfo/medications/lung-diseases/devices/instructional-videos

Another study—this one involving first-year interns—looked at level of improvement based on the type of education provided. Initially, only 5% of the interns could use an MDI without error. After a lecture and demonstration, 13% had an error-free technique. But when each intern participated in an intensive one-on-one session, the error-free rate reached 73%. The researchers’ conclusion: Lectures are relatively ineffective in teaching interns inhaler technique compared with a one-on-one approach.³²

The Chicago Breathe Project,³⁶ a new program aimed at improving education in the use of asthma inhalers for physicians and minority patients, provides further evidence of the value of clinician education. After a series of workshops for residents at 5 academic institutions, the physicians’ knowledge of proper use of inhalers rose dramatically—from just 5% preprogram to 91% postprogram (P<.001). Six months after the educational activity, the residents (n=161) were more likely (44% vs 11% preprogram) to assess patients’ inhaler technique.³⁶

Teaching patients when time is tight

National and international guidelines stress the need to teach patients correct use of asthma and COPD inhalers.^1,37,38 Providing the requisite education includes observation of each patient’s inhaler technique with proper use demonstrated, as needed.

The problem, of course, is how to provide that level of patient education within the time constraints of a busy family practice. We recommend these time-efficient solutions:

Enlist the help of other clinicians. While it is important that someone in your office be well trained and able to instruct patients in the proper use of inhalers, that individual need not be you. The National Institutes of Health recommends that the “principal clinician” introduce key educational messages, which can be reinforced and expanded on by other members of the health care team.¹

After you advise patients that it is crucial for them to be trained in and adhere to proper inhaler technique, another health care professional—often a clinic nurse or pharmacist who has had special training—can provide the hands-on education. Studies have shown that when pharmacists who are competent in asthma management, including inhaler technique, work with physicians to optimize the education and overall management of patients with asthma, better outcomes often result, including a reduction in both emergency department visits and hospitalizations.^1,39,40

Use videos to demonstrate correct technique. Videos are an effective teaching tool,⁹ and many of them are device-specific. National Jewish Health, which is world renowned for its asthma care, has a set of instructional videos posted on You-Tube and accessible from its Web site (http://www.nationaljewish.org/healthinfo/medications/lung-diseases/devices/instructional-videos). In addition to videos that demonstrate the use of an MDI alone and an MDI plus a valved holding chamber, the site has links to 6 DPI videos, each covering a different device.

Use intermittent observation. After the patient views the appropriate video, you or a member of your staff will still need to observe the patient’s inhaler technique to ensure correct use. Ideally, this should occur at every visit.^1,37 When that’s not possible, use intermittent observation, starting with the first 2 or 3 visits after the introduction of inhalation therapy and then switching to periodic observation to ensure that the patient is maintaining good technique.

In determining how often observation is necessary, keep in mind that simply asking patients whether they are having inhaler problems is not sufficient.¹ Patients tend to say they have little or no trouble when, in fact, most struggle, at times, with the devices. What’s more, good technique tends to decrease over time, and repetitive education is important.

To motivate patients, try this communication technique
Motivational interviewing, a technique that has been used to help patients battle obesity, quit smoking, and control hypertension,^41-43 among other health problems, can help you identify inhaler problems that need to be addressed. It involves the use of open-ended questions (eg, “What worries you most about your asthma?”), affirmations (“You’ve done a great job testing your peak flow level every morning”), reflective listening (“You’re tired of taking medicine every day”), and summary statements (“You know you should take your medicine every day but you’re having trouble remembering it. Is that right?”).

A pilot study⁴⁴ showed that when this technique was incorporated into an asthma education session, patient motivation increased. The ratio of perceived advantages vs disadvantages of taking asthma medication correctly improved, as well. Another study⁴⁵ found that when motivational interviewing was used during home visits to inner-city African American adolescents for asthma care, the patients’ motivation, readiness to adhere to treatment, and asthma-related quality of life improved, although self-reported adherence to asthma medication did not. Further studies involving patients with asthma are under way (www.clinicaltrials.gov/ct2/results?term=asthma).

It is important to note that the use of motivational interviewing does not require a lengthy visit. One study found that on average, visits in which primary care physicians used this communication technique lasted less than 10 minutes.⁴⁶

CORRESPONDENCE Timothy H. Self, PharmD, University of Tennessee Health Science Center, 881 Madison Avenue, Room 235, Memphis, TN 38163; [email protected]

For patients with asthma or chronic obstructive pulmonary disease (COPD), inhalation therapy is the foundation of treatment. Yet all too often, patients don’t get the full value of their inhaled medications because they use their inhaler incorrectly. When technique is markedly flawed, suboptimal outcomes typically result.

Given the number of Americans with asthma (at least 22 million)¹ and COPD (more than 13 million adults),² faulty inhaler technique is a major public health problem. In fact, the number of people suffering from COPD may be even larger: Close to 24 million US adults are believed to have impaired lung function.^3,4 For patients with asthma or COPD—many of whom are treated by family physicians—comprehensive education with a focus on correct use of an inhaler is essential.

In this review, we present evidence of frequent inhaler errors (from clinical studies) and highlight some of the more common mistakes (based on our clinical experience [TABLE]⁵). Finally, we offer ‘‘time-efficient’’ solutions to inhaler problems—steps that physicians in busy primary care practices can take to ensure that patients with asthma or COPD get the maximum benefit from inhalation therapy.

TABLE
Caution patients about these device-specific mistakes*

Inhaler error is well documented

Since 1965, when it was first reported that many patients used metered dose inhalers (MDIs) incorrectly,⁶ evidence has accumulated supporting the magnitude of the problem.^7-12 (Studies conducted in family practice settings are described in “Researchers look at inhaler problems in primary care” and in TABLE W1.^13-20)

Error rates vary widely from one clinical trial to another, depending on study criteria, type of device, and extent of patient education, among other factors. Nonetheless, several studies (spanning 3 decades) found the error rate to be close to, or greater than, 90%.^7,10,21

The most recent of these, published in 2009,²¹ was based on observation of the inhaler technique used by patients with asthma or COPD directly following appointments in an outpatient clinic. The authors found that, although >98% of the study participants claimed to know how to use their inhalers, 94% committed at least one error. In this study and a number of others, user error was more likely in patients using MDIs.^13,18,21,22

Breath-activated dry powder inhalers (DPIs)—such as the Flexhaler, HandiHaler, Aerolizer, and Diskus—also reduce the likelihood of error. DPIs eliminate a step that MDI users often struggle with: the need to simultaneously press down on the canister and begin a slow, deep inhalation.

What’s more, DPIs do not have to be shaken before use. Nonetheless, using a DPI still involves a series of actions. For the HandiHaler and Aerolizer, patients must load the dose, and some patients fail to read the directions and swallow the capsule instead of loading it into the device. Patients must remember to exhale away from the device (ie, not into the dry powder) before inhaling, then hold their breath for approximately 10 seconds. There is potential for error at each step.

Stress the need to exhale before using the inhaler
Forgetting to exhale before inhaling is a common, and significant, mistake regardless of the type of device. It is paramount to stress the need to exhale gently for a few seconds before inhaling (slowly and deeply for patients using an MDI, rapidly and deeply with most DPIs). For MDI users, poor timing, described earlier, is another common and serious mistake. Patients using an MDI with a valved holding chamber sometimes inhale for too long before pressing down on the inhaler, then are unable to continue inhaling although the aerosol is still in the chamber. A common error made by patients using multidose DPIs is simply to forget to load the dose.

Physicians need to brush up on their skills, too

It’s not just patients who lack proficiency in inhaler technique. Numerous studies have demonstrated poor skill among physicians and other health care professionals.^27-34 Evidence also shows that targeted education results in substantial improvement.^32,35

In one study undertaken to evaluate family medicine residents’ proficiency in using asthma inhalers, participants (an intervention group at one clinic and a control group at another) all were given a pretest. The intervention group then received educational materials and a tutorial, as well as the opportunity for hands-on practice, after which both groups were given a post-test. The residents who received the training had a 170% jump, on average, in proficiency score, vs a 55% increase for the control group (P<.001).³⁵

WATCH THE VIDEOS

Inhaled Medication Instructional Videos
Courtesy of: National Jewish Health

Go to http://www.nationaljewish.org/healthinfo/medications/lung-diseases/devices/instructional-videos

Another study—this one involving first-year interns—looked at level of improvement based on the type of education provided. Initially, only 5% of the interns could use an MDI without error. After a lecture and demonstration, 13% had an error-free technique. But when each intern participated in an intensive one-on-one session, the error-free rate reached 73%. The researchers’ conclusion: Lectures are relatively ineffective in teaching interns inhaler technique compared with a one-on-one approach.³²

The Chicago Breathe Project,³⁶ a new program aimed at improving education in the use of asthma inhalers for physicians and minority patients, provides further evidence of the value of clinician education. After a series of workshops for residents at 5 academic institutions, the physicians’ knowledge of proper use of inhalers rose dramatically—from just 5% preprogram to 91% postprogram (P<.001). Six months after the educational activity, the residents (n=161) were more likely (44% vs 11% preprogram) to assess patients’ inhaler technique.³⁶

Teaching patients when time is tight

National and international guidelines stress the need to teach patients correct use of asthma and COPD inhalers.^1,37,38 Providing the requisite education includes observation of each patient’s inhaler technique with proper use demonstrated, as needed.

The problem, of course, is how to provide that level of patient education within the time constraints of a busy family practice. We recommend these time-efficient solutions:

Enlist the help of other clinicians. While it is important that someone in your office be well trained and able to instruct patients in the proper use of inhalers, that individual need not be you. The National Institutes of Health recommends that the “principal clinician” introduce key educational messages, which can be reinforced and expanded on by other members of the health care team.¹

After you advise patients that it is crucial for them to be trained in and adhere to proper inhaler technique, another health care professional—often a clinic nurse or pharmacist who has had special training—can provide the hands-on education. Studies have shown that when pharmacists who are competent in asthma management, including inhaler technique, work with physicians to optimize the education and overall management of patients with asthma, better outcomes often result, including a reduction in both emergency department visits and hospitalizations.^1,39,40

Use videos to demonstrate correct technique. Videos are an effective teaching tool,⁹ and many of them are device-specific. National Jewish Health, which is world renowned for its asthma care, has a set of instructional videos posted on You-Tube and accessible from its Web site (http://www.nationaljewish.org/healthinfo/medications/lung-diseases/devices/instructional-videos). In addition to videos that demonstrate the use of an MDI alone and an MDI plus a valved holding chamber, the site has links to 6 DPI videos, each covering a different device.

Use intermittent observation. After the patient views the appropriate video, you or a member of your staff will still need to observe the patient’s inhaler technique to ensure correct use. Ideally, this should occur at every visit.^1,37 When that’s not possible, use intermittent observation, starting with the first 2 or 3 visits after the introduction of inhalation therapy and then switching to periodic observation to ensure that the patient is maintaining good technique.

In determining how often observation is necessary, keep in mind that simply asking patients whether they are having inhaler problems is not sufficient.¹ Patients tend to say they have little or no trouble when, in fact, most struggle, at times, with the devices. What’s more, good technique tends to decrease over time, and repetitive education is important.

To motivate patients, try this communication technique
Motivational interviewing, a technique that has been used to help patients battle obesity, quit smoking, and control hypertension,^41-43 among other health problems, can help you identify inhaler problems that need to be addressed. It involves the use of open-ended questions (eg, “What worries you most about your asthma?”), affirmations (“You’ve done a great job testing your peak flow level every morning”), reflective listening (“You’re tired of taking medicine every day”), and summary statements (“You know you should take your medicine every day but you’re having trouble remembering it. Is that right?”).

A pilot study⁴⁴ showed that when this technique was incorporated into an asthma education session, patient motivation increased. The ratio of perceived advantages vs disadvantages of taking asthma medication correctly improved, as well. Another study⁴⁵ found that when motivational interviewing was used during home visits to inner-city African American adolescents for asthma care, the patients’ motivation, readiness to adhere to treatment, and asthma-related quality of life improved, although self-reported adherence to asthma medication did not. Further studies involving patients with asthma are under way (www.clinicaltrials.gov/ct2/results?term=asthma).

It is important to note that the use of motivational interviewing does not require a lengthy visit. One study found that on average, visits in which primary care physicians used this communication technique lasted less than 10 minutes.⁴⁶

CORRESPONDENCE Timothy H. Self, PharmD, University of Tennessee Health Science Center, 881 Madison Avenue, Room 235, Memphis, TN 38163; [email protected]

For patients with asthma or chronic obstructive pulmonary disease (COPD), inhalation therapy is the foundation of treatment. Yet all too often, patients don’t get the full value of their inhaled medications because they use their inhaler incorrectly. When technique is markedly flawed, suboptimal outcomes typically result.

Given the number of Americans with asthma (at least 22 million)¹ and COPD (more than 13 million adults),² faulty inhaler technique is a major public health problem. In fact, the number of people suffering from COPD may be even larger: Close to 24 million US adults are believed to have impaired lung function.^3,4 For patients with asthma or COPD—many of whom are treated by family physicians—comprehensive education with a focus on correct use of an inhaler is essential.

In this review, we present evidence of frequent inhaler errors (from clinical studies) and highlight some of the more common mistakes (based on our clinical experience [TABLE]⁵). Finally, we offer ‘‘time-efficient’’ solutions to inhaler problems—steps that physicians in busy primary care practices can take to ensure that patients with asthma or COPD get the maximum benefit from inhalation therapy.

TABLE
Caution patients about these device-specific mistakes*

Inhaler error is well documented

Since 1965, when it was first reported that many patients used metered dose inhalers (MDIs) incorrectly,⁶ evidence has accumulated supporting the magnitude of the problem.^7-12 (Studies conducted in family practice settings are described in “Researchers look at inhaler problems in primary care” and in TABLE W1.^13-20)

Error rates vary widely from one clinical trial to another, depending on study criteria, type of device, and extent of patient education, among other factors. Nonetheless, several studies (spanning 3 decades) found the error rate to be close to, or greater than, 90%.^7,10,21

The most recent of these, published in 2009,²¹ was based on observation of the inhaler technique used by patients with asthma or COPD directly following appointments in an outpatient clinic. The authors found that, although >98% of the study participants claimed to know how to use their inhalers, 94% committed at least one error. In this study and a number of others, user error was more likely in patients using MDIs.^13,18,21,22

Breath-activated dry powder inhalers (DPIs)—such as the Flexhaler, HandiHaler, Aerolizer, and Diskus—also reduce the likelihood of error. DPIs eliminate a step that MDI users often struggle with: the need to simultaneously press down on the canister and begin a slow, deep inhalation.

What’s more, DPIs do not have to be shaken before use. Nonetheless, using a DPI still involves a series of actions. For the HandiHaler and Aerolizer, patients must load the dose, and some patients fail to read the directions and swallow the capsule instead of loading it into the device. Patients must remember to exhale away from the device (ie, not into the dry powder) before inhaling, then hold their breath for approximately 10 seconds. There is potential for error at each step.

Stress the need to exhale before using the inhaler
Forgetting to exhale before inhaling is a common, and significant, mistake regardless of the type of device. It is paramount to stress the need to exhale gently for a few seconds before inhaling (slowly and deeply for patients using an MDI, rapidly and deeply with most DPIs). For MDI users, poor timing, described earlier, is another common and serious mistake. Patients using an MDI with a valved holding chamber sometimes inhale for too long before pressing down on the inhaler, then are unable to continue inhaling although the aerosol is still in the chamber. A common error made by patients using multidose DPIs is simply to forget to load the dose.

Physicians need to brush up on their skills, too

It’s not just patients who lack proficiency in inhaler technique. Numerous studies have demonstrated poor skill among physicians and other health care professionals.^27-34 Evidence also shows that targeted education results in substantial improvement.^32,35

In one study undertaken to evaluate family medicine residents’ proficiency in using asthma inhalers, participants (an intervention group at one clinic and a control group at another) all were given a pretest. The intervention group then received educational materials and a tutorial, as well as the opportunity for hands-on practice, after which both groups were given a post-test. The residents who received the training had a 170% jump, on average, in proficiency score, vs a 55% increase for the control group (P<.001).³⁵

WATCH THE VIDEOS

Inhaled Medication Instructional Videos
Courtesy of: National Jewish Health

Go to http://www.nationaljewish.org/healthinfo/medications/lung-diseases/devices/instructional-videos

Another study—this one involving first-year interns—looked at level of improvement based on the type of education provided. Initially, only 5% of the interns could use an MDI without error. After a lecture and demonstration, 13% had an error-free technique. But when each intern participated in an intensive one-on-one session, the error-free rate reached 73%. The researchers’ conclusion: Lectures are relatively ineffective in teaching interns inhaler technique compared with a one-on-one approach.³²

The Chicago Breathe Project,³⁶ a new program aimed at improving education in the use of asthma inhalers for physicians and minority patients, provides further evidence of the value of clinician education. After a series of workshops for residents at 5 academic institutions, the physicians’ knowledge of proper use of inhalers rose dramatically—from just 5% preprogram to 91% postprogram (P<.001). Six months after the educational activity, the residents (n=161) were more likely (44% vs 11% preprogram) to assess patients’ inhaler technique.³⁶

Teaching patients when time is tight

National and international guidelines stress the need to teach patients correct use of asthma and COPD inhalers.^1,37,38 Providing the requisite education includes observation of each patient’s inhaler technique with proper use demonstrated, as needed.

The problem, of course, is how to provide that level of patient education within the time constraints of a busy family practice. We recommend these time-efficient solutions:

Enlist the help of other clinicians. While it is important that someone in your office be well trained and able to instruct patients in the proper use of inhalers, that individual need not be you. The National Institutes of Health recommends that the “principal clinician” introduce key educational messages, which can be reinforced and expanded on by other members of the health care team.¹

After you advise patients that it is crucial for them to be trained in and adhere to proper inhaler technique, another health care professional—often a clinic nurse or pharmacist who has had special training—can provide the hands-on education. Studies have shown that when pharmacists who are competent in asthma management, including inhaler technique, work with physicians to optimize the education and overall management of patients with asthma, better outcomes often result, including a reduction in both emergency department visits and hospitalizations.^1,39,40

Use videos to demonstrate correct technique. Videos are an effective teaching tool,⁹ and many of them are device-specific. National Jewish Health, which is world renowned for its asthma care, has a set of instructional videos posted on You-Tube and accessible from its Web site (http://www.nationaljewish.org/healthinfo/medications/lung-diseases/devices/instructional-videos). In addition to videos that demonstrate the use of an MDI alone and an MDI plus a valved holding chamber, the site has links to 6 DPI videos, each covering a different device.

Use intermittent observation. After the patient views the appropriate video, you or a member of your staff will still need to observe the patient’s inhaler technique to ensure correct use. Ideally, this should occur at every visit.^1,37 When that’s not possible, use intermittent observation, starting with the first 2 or 3 visits after the introduction of inhalation therapy and then switching to periodic observation to ensure that the patient is maintaining good technique.

In determining how often observation is necessary, keep in mind that simply asking patients whether they are having inhaler problems is not sufficient.¹ Patients tend to say they have little or no trouble when, in fact, most struggle, at times, with the devices. What’s more, good technique tends to decrease over time, and repetitive education is important.

To motivate patients, try this communication technique
Motivational interviewing, a technique that has been used to help patients battle obesity, quit smoking, and control hypertension,^41-43 among other health problems, can help you identify inhaler problems that need to be addressed. It involves the use of open-ended questions (eg, “What worries you most about your asthma?”), affirmations (“You’ve done a great job testing your peak flow level every morning”), reflective listening (“You’re tired of taking medicine every day”), and summary statements (“You know you should take your medicine every day but you’re having trouble remembering it. Is that right?”).

A pilot study⁴⁴ showed that when this technique was incorporated into an asthma education session, patient motivation increased. The ratio of perceived advantages vs disadvantages of taking asthma medication correctly improved, as well. Another study⁴⁵ found that when motivational interviewing was used during home visits to inner-city African American adolescents for asthma care, the patients’ motivation, readiness to adhere to treatment, and asthma-related quality of life improved, although self-reported adherence to asthma medication did not. Further studies involving patients with asthma are under way (www.clinicaltrials.gov/ct2/results?term=asthma).

It is important to note that the use of motivational interviewing does not require a lengthy visit. One study found that on average, visits in which primary care physicians used this communication technique lasted less than 10 minutes.⁴⁶

CORRESPONDENCE Timothy H. Self, PharmD, University of Tennessee Health Science Center, 881 Madison Avenue, Room 235, Memphis, TN 38163; [email protected]

CASE Jim F, 40 years old and overweight (BMI=28 kg/m²), has come to see you because of foot pain that began shortly after he took up running. Jim tells you that turning 40 was “an eye opener” that prompted him to “get healthy.” He says that while he was a competitive athlete in high school, he never ran regularly—until he embarked on a running program 3 months ago.

Jim denies acute injury, bruising, swelling, redness, fever, or chills, but states that the pain, which he describes as dull and achy, is gradually getting worse. It hurts the most when he stands for long periods of time. He says that he occasionally takes ibuprofen for the foot pain, but has not tried icing or stretching. When you ask him what kind of sneakers he wears during his runs, Jim reports that his running shoes—purchased at a discount store—are about 5 years old.

Participation in running has grown by more than 40% in the United States in the past decade.¹ As a result, patients like Jim are bound to have their share of aches, pains, and injuries that prompt them to visit their family physician. And that’s where this review can help. This rundown of the most common foot pain diagnoses, as well as the at-a-glance summaries of the differential diagnosis (TABLE 1)^2-5 and treatment options (TABLE 2),^3,6-25 can help you quickly get patients the relief they need to return to running.

TABLE 1
Differential diagnosis for runners’ foot pain^2-5

TABLE 2
Diagnosing and treating common runners’ injuries

Metatarsalgia: Pain on the plantar surface

Typically associated with a recent increase in activity or change in footwear, metatarsalgia is defined by pain on the plantar surface of the forefoot in the area of the metatarsal heads. The second, third, and fourth metatarsals are the most common offenders, and the pain may or may not be accompanied by swelling, bruising, or deformity.

Mechanical irregularities in the foot are thought to contribute to the development of metatarsalgia, which is typically inflammatory in nature. Physical exam often reveals tenderness at the affected metatarsal heads, with or without pain in the corresponding metatarsophalangeal joint, and occasionally, with overlying edema or hyperkeratosis.

Tuning fork test. Commonly used but weakly supported, this diagnostic test is performed by applying a vibrating tuning fork to a site of possible fracture. If the maneuver produces focal pain, the test is positive and may be helpful in ruling in metatarsal stress fractures.²⁶

Treatment: Change shoes, consider NSAIDs. Treatment for metatarsalgia begins conservatively, with a change in footwear. High heels or pointy-toed shoes should be avoided, and metatarsal pads (FIGURE 1) can be placed inside the shoes to help off-load the metatarsal head.⁶ The pads come prefabricated or can be custom made, and are typically placed by physical therapists to ensure proper placement. Orthotics should also be considered, as they can help normalize abnormal foot mechanics that may contribute to metatarsalgia.^7,8 (See “A word about runners’ footwear”.^9,27-31)

Metatarsalgia is believed to be an inflammatory process, and NSAIDs may be helpful. Contrast baths—alternately submerging the affected foot in a basin of hot (but not scalding) water for 1 to 2 minutes, then immersing it in cold water for 30 to 60 seconds and repeating the process for about 20 minutes once or twice daily—may be helpful. Magnetic insoles are not recommended, as they have been found to be no better than sham insoles.³² Rarely, surgical repair of underlying mechanical abnormalities is indicated for treatment of refractory metatarsalgia.

CASE On examination, Jim F has no swelling, but some hyperkeratosis overlying the second and third metatarsal heads. He has tenderness to palpation at these heads as well as the corresponding metatarsophalangeal joints, and a negative tuning fork test.

You advise Jim that he has metatarsalgia, educate him about the pathophysiology of this condition, and give him a prescription for a nonsteroidal anti-inflammatory drug. You suggest he use contrast baths—and explain how this is done—once or twice a day and refer him to physical therapy for proper placement of metatarsal pads in his shoes, and schedule an appointment for a 6-week follow-up.

Return to running. There is no firm recommendation regarding abstaining from running with metatarsalgia. Advise patients to use pain as a guide in determining the intensity and duration of activity.

FIGURE 1
Treatment for metatarsalgia is conservative

Stress fracture: Tenderness and pain of insidious onset

Stress fractures of the foot (SFF)—overuse injuries also known as fatigue fractures—are common in recreational runners. They are thought to result from microtraumas, which alone are not sufficient to break bone but together overwhelm the bone’s natural ability to remodel and recover over time. SFF are characterized by tenderness and pain of insidious onset, and typically occur when more than one training variable (eg, frequency, duration, and intensity) is changed simultaneously. SFF can also result from a change in exercise mechanics, such as foot strike.

Stress fractures can occur in any bone in the foot, but are most common in the metatarsal bones, specifically the mid or distal portion of the second or third metatarsal, or the tarsal navicular.^2,33 On examination, the patient will have tenderness to palpation, often well localized. A positive tuning fork test (see page 647) is highly suggestive of a stress fracture.

FAST TRACK

Some studies suggest that barefoot running or barefoot running shoes improve running mechanics; other studies have had unfavorable or inconsistent results.

In female runners, stress fractures may be associated with the female athlete triad—osteoporosis or osteopenia, disordered eating (specifically caloric deficiency and low BMI), and amenorrhea. In addition to the major long-term health problems that may result from even one component of the triad, SFF may be a short-term consequence.³⁴

Although SFF is a clinical diagnosis, x-rays—including 3-view plain films of the foot, with the area of concern clearly noted on the order—are recommended. Magnetic resonance imaging may be used for secondary imaging if doubt about the source of the pain remains.³⁵

Of note: Occasionally, a metatarsal stress fracture progresses to a frank fracture, specifically of the metaphyseal-diaphyseal junction of the fifth metatarsal—known as a Jones fracture. This type of fracture has a high rate of malunion or nonunion.³⁶ If there is any suspicion of a fracture in this area, consider a referral to a sports medicine specialist or orthopedic surgeon.

Treatment: Icing, analgesics, and a boot. Standard treatment for SFF includes icing for 15 to 20 minutes up to 3 times a day for a minimum of 72 hours after injury, but may be continued throughout the healing period. Analgesics such as acetaminophen and a walking boot for 3 to 4 weeks, with follow-up at 3 weeks, should also be implemented. Recent evidence suggests that NSAIDs may hinder the bone healing process, and their use in treating SFF is controversial.^10-12

Weaning from the boot can begin when the patient is pain free with the boot on, usually by 3 to 4 weeks. Patients often progress quickly from wearing the boot at all times to wearing it only outside of the house, to not wearing it at all. Advise patients who need to walk long distances for a good portion of the day to keep the boot nearby and to put it on if the pain returns.

Once weaning from the boot begins, physical therapy (PT) should be considered to help the patient regain foot and ankle range of motion (ROM), proprioception, and strength. Once he or she learns the exercises, rehabilitation can be accomplished with a home exercise program. Foot deformities, such as pes planus or pes cavus, may indicate a need for orthotics. A well-structured athletic shoe may help to prevent future injury.^7,8

Return to running. Once adequate ROM and strength in the foot and ankle are recovered, the patient can begin to resume activity, starting with a low-impact cross-training exercise, such as a stationary bike or elliptical, for a week or 2. A patient who remains pain free can progress from cross-training to running on a treadmill for another week or 2, then gradually switch to outdoor running.

Plantar fasciitis: Heel pain with an insidious onset

Plantar fasciitis is one of the most common causes of heel pain in athletes (primarily runners) and nonathletes alike. Plantar fasciitis may be associated with acute trauma, but is more commonly insidious in onset. The diagnosis is clinical and rarely requires imaging.

Pain associated with plantar fasciitis may be described as sharp and stabbing or dull and aching. It is on the plantar surface of the heel, sometimes radiating to the arch, and may localize to the insertion of the plantar fascia on the medial calcaneal tubercle (FIGURE 2). The pain is typically most severe with the first few steps in the morning or after other periods of prolonged rest. It usually improves after a few steps, but may return later in the day. Plantar fasciitis does not cause paresthesias or other neurologic symptoms, so their presence is suggestive of a different diagnosis, such as nerve entrapment, compartment syndrome, or tarsal tunnel syndrome.^3,5

Treatment: It’s multifactorial. NSAIDs are commonly used. Relative rest is recommended, but cross training may be considered to maintain fitness.³⁷ Short-term PT is also recommended to teach the patient proper stretching and strengthening techniques in the form of a home exercise plan. Modalities such as iontophoresis (a system of transdermal delivery of medication with the use of electrical currents), Graston (a form of instrument-assisted soft tissue mobilization), and taping may be incorporated into PT, as well.¹³

Night splinting may also be used to keep the foot in a dorsiflexed position. A splint can be purchased without a prescription and prevents the plantar fascia from shortening overnight by providing a continuous passive stretch, thus reducing pain with first steps.¹⁴

Orthotics may also help to reduce symptom severity and duration, and studies have found no difference in outcomes with prefabricated vs custom-made devices.¹⁵ Another treatment to consider, particularly for recalcitrant cases of plantar fasciitis, is extracorporeal shock wave therapy, which has been studied for more than a decade with conflicting results.¹⁶ Corticosteroid injection may also be used for treatment-refractory plantar fasciitis, but caution is required, as the injection may increase the risk of rupture of the plantar fascia.^17,18

Return to running. There are no set guidelines for when an athlete with plantar fasciitis can return to running. Typically, after 2 to 4 weeks of relative rest and other treatments, the runner can begin to transition from cross-training to treadmill running.

FIGURE 2
Severe pain with first steps of the day

Achilles tendinopathy: An overuse injury

Achilles tendinopathy (AT) is typically an overuse injury incurred by athletes, although it is sometimes seen in patients who are sedentary and overweight. With a prevalence among runners of approximately 11%, AT is sometimes called the “runners’ disease.”⁴

Tendinopathy is a more accurate description than tendonitis, as histologic studies of affected Achilles tendons suggest that AT is a degenerative, rather than an inflammatory, condition.³⁸ A diagnosis of AT can be further classified as midportion or insertional.

Midportion Achilles tendinopathy (MAT), characterized by pain that occurs in the body of the Achilles tendon and worsens with activity, is often a clinical diagnosis. Physical findings suggestive of MAT are tenderness to palpation of the midportion of the Achilles tendon, with thickening of the tendon, warmth, crepitus, or palpable nodules in the tendon body. Onset is insidious and is commonly associated with an increase in activity.

Treatment: Orthotics or a heel lift. Like that of plantar fasciitis, treatment of midportion Achilles tendinopathy is primarily conservative. The use of orthotics, or a heel lift, is one of the most cost-effective interventions, and they are widely used, despite limited evidence of efficacy.³⁹ Custom orthotics are costly, and patients often benefit from trying prefabricated orthotics first to determine whether they will help.

Eccentric exercises. One of the most studied interventions for MAT is eccentric exercise training. Studies of eccentric exercises have been very favorable, and the exercises can be taught during routine PT sessions.^19-22 Modalities such as ultrasound therapy and extracorporeal shock wave therapy (ESWT) have also been studied. But because results have been inconsistent, they are generally reserved for treatment-refractory cases.²³

In patients with no contraindications, NSAIDs may be a good choice for pain management with relatively favorable results in the literature.²⁴ Corticosteroid injections should not be used, as they have been directly linked to rupture of the Achilles tendon.²³

Other interventions, such as plasma-rich protein injections and prolotherapy—a technique in which an irritant is injected into the tendon in an attempt to create an inflammatory reaction, thus increasing local blood flow and healing—are being studied for the treatment of AT, but are not routinely used or covered by insurance for this purpose. Surgical intervention may be considered for patients whose symptoms last for more than 3 to 6 months despite conservative treatment.

Insertional Achilles tendinopathy (IAT) can be clinically differentiated from MAT by the location of symptoms and tenderness to palpation at the insertion site of the Achilles into the calcaneous. Like MAT, IAT is exacerbated by activity. Other conditions that may contribute to, or be mistaken for, IAT are a Haglund deformity and retrocalcaneal bursitis.

Treatment: Footwear modification. Treatment of IAT, like that of MAT, is primarily conservative. Orthotics or heel lifts are commonly used. However, there is greater emphasis on footwear modification due to the mechanical irritation and resultant posterior heel swelling often associated with IAT. While eccentric exercises play a role in IAT treatment, the benefits are limited.²⁵

As with MAT, corticosteroid injections are contraindicated due to the risk of tendon rupture. Modalities such as ultrasound, ESWT, plasma-rich protein, and prolotherapy lack sufficient evidence to be widely recommended.

For refractory cases of IAT, surgical intervention often relieves the pain.

Return to running. After an initial rest of 2 to 4 weeks, patients may return to running while completing therapy. It’s not necessary to wait until the patient is completely pain free, but pain should be used to guide decisions about intensity and duration of activity.

CASE When Jim returns 6 weeks later, he reports that he took 3 weeks off from running because of the pain. Initially, he used contrast baths daily, Jim says, but now he uses them only when he is symptomatic, and he discontinued the NSAID a few weeks ago. Jim tells you he went to the local running store for a new pair of running shoes and that he is now able to run at his previous pace while remaining relatively pain free.

CORRESPONDENCE Jessica Favero Butts, MD, One American Square, Suite 185, Indianapolis, IN 46282; [email protected]

CASE Jim F, 40 years old and overweight (BMI=28 kg/m²), has come to see you because of foot pain that began shortly after he took up running. Jim tells you that turning 40 was “an eye opener” that prompted him to “get healthy.” He says that while he was a competitive athlete in high school, he never ran regularly—until he embarked on a running program 3 months ago.

Jim denies acute injury, bruising, swelling, redness, fever, or chills, but states that the pain, which he describes as dull and achy, is gradually getting worse. It hurts the most when he stands for long periods of time. He says that he occasionally takes ibuprofen for the foot pain, but has not tried icing or stretching. When you ask him what kind of sneakers he wears during his runs, Jim reports that his running shoes—purchased at a discount store—are about 5 years old.

Participation in running has grown by more than 40% in the United States in the past decade.¹ As a result, patients like Jim are bound to have their share of aches, pains, and injuries that prompt them to visit their family physician. And that’s where this review can help. This rundown of the most common foot pain diagnoses, as well as the at-a-glance summaries of the differential diagnosis (TABLE 1)^2-5 and treatment options (TABLE 2),^3,6-25 can help you quickly get patients the relief they need to return to running.

TABLE 1
Differential diagnosis for runners’ foot pain^2-5

TABLE 2
Diagnosing and treating common runners’ injuries

Metatarsalgia: Pain on the plantar surface

Typically associated with a recent increase in activity or change in footwear, metatarsalgia is defined by pain on the plantar surface of the forefoot in the area of the metatarsal heads. The second, third, and fourth metatarsals are the most common offenders, and the pain may or may not be accompanied by swelling, bruising, or deformity.

Mechanical irregularities in the foot are thought to contribute to the development of metatarsalgia, which is typically inflammatory in nature. Physical exam often reveals tenderness at the affected metatarsal heads, with or without pain in the corresponding metatarsophalangeal joint, and occasionally, with overlying edema or hyperkeratosis.

Tuning fork test. Commonly used but weakly supported, this diagnostic test is performed by applying a vibrating tuning fork to a site of possible fracture. If the maneuver produces focal pain, the test is positive and may be helpful in ruling in metatarsal stress fractures.²⁶

Treatment: Change shoes, consider NSAIDs. Treatment for metatarsalgia begins conservatively, with a change in footwear. High heels or pointy-toed shoes should be avoided, and metatarsal pads (FIGURE 1) can be placed inside the shoes to help off-load the metatarsal head.⁶ The pads come prefabricated or can be custom made, and are typically placed by physical therapists to ensure proper placement. Orthotics should also be considered, as they can help normalize abnormal foot mechanics that may contribute to metatarsalgia.^7,8 (See “A word about runners’ footwear”.^9,27-31)

Metatarsalgia is believed to be an inflammatory process, and NSAIDs may be helpful. Contrast baths—alternately submerging the affected foot in a basin of hot (but not scalding) water for 1 to 2 minutes, then immersing it in cold water for 30 to 60 seconds and repeating the process for about 20 minutes once or twice daily—may be helpful. Magnetic insoles are not recommended, as they have been found to be no better than sham insoles.³² Rarely, surgical repair of underlying mechanical abnormalities is indicated for treatment of refractory metatarsalgia.

CASE On examination, Jim F has no swelling, but some hyperkeratosis overlying the second and third metatarsal heads. He has tenderness to palpation at these heads as well as the corresponding metatarsophalangeal joints, and a negative tuning fork test.

You advise Jim that he has metatarsalgia, educate him about the pathophysiology of this condition, and give him a prescription for a nonsteroidal anti-inflammatory drug. You suggest he use contrast baths—and explain how this is done—once or twice a day and refer him to physical therapy for proper placement of metatarsal pads in his shoes, and schedule an appointment for a 6-week follow-up.

Return to running. There is no firm recommendation regarding abstaining from running with metatarsalgia. Advise patients to use pain as a guide in determining the intensity and duration of activity.

FIGURE 1
Treatment for metatarsalgia is conservative

Stress fracture: Tenderness and pain of insidious onset

Stress fractures of the foot (SFF)—overuse injuries also known as fatigue fractures—are common in recreational runners. They are thought to result from microtraumas, which alone are not sufficient to break bone but together overwhelm the bone’s natural ability to remodel and recover over time. SFF are characterized by tenderness and pain of insidious onset, and typically occur when more than one training variable (eg, frequency, duration, and intensity) is changed simultaneously. SFF can also result from a change in exercise mechanics, such as foot strike.

Stress fractures can occur in any bone in the foot, but are most common in the metatarsal bones, specifically the mid or distal portion of the second or third metatarsal, or the tarsal navicular.^2,33 On examination, the patient will have tenderness to palpation, often well localized. A positive tuning fork test (see page 647) is highly suggestive of a stress fracture.

FAST TRACK

Some studies suggest that barefoot running or barefoot running shoes improve running mechanics; other studies have had unfavorable or inconsistent results.

In female runners, stress fractures may be associated with the female athlete triad—osteoporosis or osteopenia, disordered eating (specifically caloric deficiency and low BMI), and amenorrhea. In addition to the major long-term health problems that may result from even one component of the triad, SFF may be a short-term consequence.³⁴

Although SFF is a clinical diagnosis, x-rays—including 3-view plain films of the foot, with the area of concern clearly noted on the order—are recommended. Magnetic resonance imaging may be used for secondary imaging if doubt about the source of the pain remains.³⁵

Of note: Occasionally, a metatarsal stress fracture progresses to a frank fracture, specifically of the metaphyseal-diaphyseal junction of the fifth metatarsal—known as a Jones fracture. This type of fracture has a high rate of malunion or nonunion.³⁶ If there is any suspicion of a fracture in this area, consider a referral to a sports medicine specialist or orthopedic surgeon.

Treatment: Icing, analgesics, and a boot. Standard treatment for SFF includes icing for 15 to 20 minutes up to 3 times a day for a minimum of 72 hours after injury, but may be continued throughout the healing period. Analgesics such as acetaminophen and a walking boot for 3 to 4 weeks, with follow-up at 3 weeks, should also be implemented. Recent evidence suggests that NSAIDs may hinder the bone healing process, and their use in treating SFF is controversial.^10-12

Weaning from the boot can begin when the patient is pain free with the boot on, usually by 3 to 4 weeks. Patients often progress quickly from wearing the boot at all times to wearing it only outside of the house, to not wearing it at all. Advise patients who need to walk long distances for a good portion of the day to keep the boot nearby and to put it on if the pain returns.

Once weaning from the boot begins, physical therapy (PT) should be considered to help the patient regain foot and ankle range of motion (ROM), proprioception, and strength. Once he or she learns the exercises, rehabilitation can be accomplished with a home exercise program. Foot deformities, such as pes planus or pes cavus, may indicate a need for orthotics. A well-structured athletic shoe may help to prevent future injury.^7,8

Return to running. Once adequate ROM and strength in the foot and ankle are recovered, the patient can begin to resume activity, starting with a low-impact cross-training exercise, such as a stationary bike or elliptical, for a week or 2. A patient who remains pain free can progress from cross-training to running on a treadmill for another week or 2, then gradually switch to outdoor running.

Plantar fasciitis: Heel pain with an insidious onset

Plantar fasciitis is one of the most common causes of heel pain in athletes (primarily runners) and nonathletes alike. Plantar fasciitis may be associated with acute trauma, but is more commonly insidious in onset. The diagnosis is clinical and rarely requires imaging.

Pain associated with plantar fasciitis may be described as sharp and stabbing or dull and aching. It is on the plantar surface of the heel, sometimes radiating to the arch, and may localize to the insertion of the plantar fascia on the medial calcaneal tubercle (FIGURE 2). The pain is typically most severe with the first few steps in the morning or after other periods of prolonged rest. It usually improves after a few steps, but may return later in the day. Plantar fasciitis does not cause paresthesias or other neurologic symptoms, so their presence is suggestive of a different diagnosis, such as nerve entrapment, compartment syndrome, or tarsal tunnel syndrome.^3,5

Treatment: It’s multifactorial. NSAIDs are commonly used. Relative rest is recommended, but cross training may be considered to maintain fitness.³⁷ Short-term PT is also recommended to teach the patient proper stretching and strengthening techniques in the form of a home exercise plan. Modalities such as iontophoresis (a system of transdermal delivery of medication with the use of electrical currents), Graston (a form of instrument-assisted soft tissue mobilization), and taping may be incorporated into PT, as well.¹³

Night splinting may also be used to keep the foot in a dorsiflexed position. A splint can be purchased without a prescription and prevents the plantar fascia from shortening overnight by providing a continuous passive stretch, thus reducing pain with first steps.¹⁴

Orthotics may also help to reduce symptom severity and duration, and studies have found no difference in outcomes with prefabricated vs custom-made devices.¹⁵ Another treatment to consider, particularly for recalcitrant cases of plantar fasciitis, is extracorporeal shock wave therapy, which has been studied for more than a decade with conflicting results.¹⁶ Corticosteroid injection may also be used for treatment-refractory plantar fasciitis, but caution is required, as the injection may increase the risk of rupture of the plantar fascia.^17,18

Return to running. There are no set guidelines for when an athlete with plantar fasciitis can return to running. Typically, after 2 to 4 weeks of relative rest and other treatments, the runner can begin to transition from cross-training to treadmill running.

FIGURE 2
Severe pain with first steps of the day

Achilles tendinopathy: An overuse injury

Achilles tendinopathy (AT) is typically an overuse injury incurred by athletes, although it is sometimes seen in patients who are sedentary and overweight. With a prevalence among runners of approximately 11%, AT is sometimes called the “runners’ disease.”⁴

Tendinopathy is a more accurate description than tendonitis, as histologic studies of affected Achilles tendons suggest that AT is a degenerative, rather than an inflammatory, condition.³⁸ A diagnosis of AT can be further classified as midportion or insertional.

Midportion Achilles tendinopathy (MAT), characterized by pain that occurs in the body of the Achilles tendon and worsens with activity, is often a clinical diagnosis. Physical findings suggestive of MAT are tenderness to palpation of the midportion of the Achilles tendon, with thickening of the tendon, warmth, crepitus, or palpable nodules in the tendon body. Onset is insidious and is commonly associated with an increase in activity.

Treatment: Orthotics or a heel lift. Like that of plantar fasciitis, treatment of midportion Achilles tendinopathy is primarily conservative. The use of orthotics, or a heel lift, is one of the most cost-effective interventions, and they are widely used, despite limited evidence of efficacy.³⁹ Custom orthotics are costly, and patients often benefit from trying prefabricated orthotics first to determine whether they will help.

Eccentric exercises. One of the most studied interventions for MAT is eccentric exercise training. Studies of eccentric exercises have been very favorable, and the exercises can be taught during routine PT sessions.^19-22 Modalities such as ultrasound therapy and extracorporeal shock wave therapy (ESWT) have also been studied. But because results have been inconsistent, they are generally reserved for treatment-refractory cases.²³

In patients with no contraindications, NSAIDs may be a good choice for pain management with relatively favorable results in the literature.²⁴ Corticosteroid injections should not be used, as they have been directly linked to rupture of the Achilles tendon.²³

Other interventions, such as plasma-rich protein injections and prolotherapy—a technique in which an irritant is injected into the tendon in an attempt to create an inflammatory reaction, thus increasing local blood flow and healing—are being studied for the treatment of AT, but are not routinely used or covered by insurance for this purpose. Surgical intervention may be considered for patients whose symptoms last for more than 3 to 6 months despite conservative treatment.

Insertional Achilles tendinopathy (IAT) can be clinically differentiated from MAT by the location of symptoms and tenderness to palpation at the insertion site of the Achilles into the calcaneous. Like MAT, IAT is exacerbated by activity. Other conditions that may contribute to, or be mistaken for, IAT are a Haglund deformity and retrocalcaneal bursitis.

Treatment: Footwear modification. Treatment of IAT, like that of MAT, is primarily conservative. Orthotics or heel lifts are commonly used. However, there is greater emphasis on footwear modification due to the mechanical irritation and resultant posterior heel swelling often associated with IAT. While eccentric exercises play a role in IAT treatment, the benefits are limited.²⁵

As with MAT, corticosteroid injections are contraindicated due to the risk of tendon rupture. Modalities such as ultrasound, ESWT, plasma-rich protein, and prolotherapy lack sufficient evidence to be widely recommended.

For refractory cases of IAT, surgical intervention often relieves the pain.

Return to running. After an initial rest of 2 to 4 weeks, patients may return to running while completing therapy. It’s not necessary to wait until the patient is completely pain free, but pain should be used to guide decisions about intensity and duration of activity.

CASE When Jim returns 6 weeks later, he reports that he took 3 weeks off from running because of the pain. Initially, he used contrast baths daily, Jim says, but now he uses them only when he is symptomatic, and he discontinued the NSAID a few weeks ago. Jim tells you he went to the local running store for a new pair of running shoes and that he is now able to run at his previous pace while remaining relatively pain free.

CORRESPONDENCE Jessica Favero Butts, MD, One American Square, Suite 185, Indianapolis, IN 46282; [email protected]

CASE Jim F, 40 years old and overweight (BMI=28 kg/m²), has come to see you because of foot pain that began shortly after he took up running. Jim tells you that turning 40 was “an eye opener” that prompted him to “get healthy.” He says that while he was a competitive athlete in high school, he never ran regularly—until he embarked on a running program 3 months ago.

Jim denies acute injury, bruising, swelling, redness, fever, or chills, but states that the pain, which he describes as dull and achy, is gradually getting worse. It hurts the most when he stands for long periods of time. He says that he occasionally takes ibuprofen for the foot pain, but has not tried icing or stretching. When you ask him what kind of sneakers he wears during his runs, Jim reports that his running shoes—purchased at a discount store—are about 5 years old.

Participation in running has grown by more than 40% in the United States in the past decade.¹ As a result, patients like Jim are bound to have their share of aches, pains, and injuries that prompt them to visit their family physician. And that’s where this review can help. This rundown of the most common foot pain diagnoses, as well as the at-a-glance summaries of the differential diagnosis (TABLE 1)^2-5 and treatment options (TABLE 2),^3,6-25 can help you quickly get patients the relief they need to return to running.

TABLE 1
Differential diagnosis for runners’ foot pain^2-5

TABLE 2
Diagnosing and treating common runners’ injuries

Metatarsalgia: Pain on the plantar surface

Typically associated with a recent increase in activity or change in footwear, metatarsalgia is defined by pain on the plantar surface of the forefoot in the area of the metatarsal heads. The second, third, and fourth metatarsals are the most common offenders, and the pain may or may not be accompanied by swelling, bruising, or deformity.

Mechanical irregularities in the foot are thought to contribute to the development of metatarsalgia, which is typically inflammatory in nature. Physical exam often reveals tenderness at the affected metatarsal heads, with or without pain in the corresponding metatarsophalangeal joint, and occasionally, with overlying edema or hyperkeratosis.

Tuning fork test. Commonly used but weakly supported, this diagnostic test is performed by applying a vibrating tuning fork to a site of possible fracture. If the maneuver produces focal pain, the test is positive and may be helpful in ruling in metatarsal stress fractures.²⁶

Treatment: Change shoes, consider NSAIDs. Treatment for metatarsalgia begins conservatively, with a change in footwear. High heels or pointy-toed shoes should be avoided, and metatarsal pads (FIGURE 1) can be placed inside the shoes to help off-load the metatarsal head.⁶ The pads come prefabricated or can be custom made, and are typically placed by physical therapists to ensure proper placement. Orthotics should also be considered, as they can help normalize abnormal foot mechanics that may contribute to metatarsalgia.^7,8 (See “A word about runners’ footwear”.^9,27-31)

Metatarsalgia is believed to be an inflammatory process, and NSAIDs may be helpful. Contrast baths—alternately submerging the affected foot in a basin of hot (but not scalding) water for 1 to 2 minutes, then immersing it in cold water for 30 to 60 seconds and repeating the process for about 20 minutes once or twice daily—may be helpful. Magnetic insoles are not recommended, as they have been found to be no better than sham insoles.³² Rarely, surgical repair of underlying mechanical abnormalities is indicated for treatment of refractory metatarsalgia.

CASE On examination, Jim F has no swelling, but some hyperkeratosis overlying the second and third metatarsal heads. He has tenderness to palpation at these heads as well as the corresponding metatarsophalangeal joints, and a negative tuning fork test.

You advise Jim that he has metatarsalgia, educate him about the pathophysiology of this condition, and give him a prescription for a nonsteroidal anti-inflammatory drug. You suggest he use contrast baths—and explain how this is done—once or twice a day and refer him to physical therapy for proper placement of metatarsal pads in his shoes, and schedule an appointment for a 6-week follow-up.

Return to running. There is no firm recommendation regarding abstaining from running with metatarsalgia. Advise patients to use pain as a guide in determining the intensity and duration of activity.

FIGURE 1
Treatment for metatarsalgia is conservative

Stress fracture: Tenderness and pain of insidious onset

Stress fractures of the foot (SFF)—overuse injuries also known as fatigue fractures—are common in recreational runners. They are thought to result from microtraumas, which alone are not sufficient to break bone but together overwhelm the bone’s natural ability to remodel and recover over time. SFF are characterized by tenderness and pain of insidious onset, and typically occur when more than one training variable (eg, frequency, duration, and intensity) is changed simultaneously. SFF can also result from a change in exercise mechanics, such as foot strike.

Stress fractures can occur in any bone in the foot, but are most common in the metatarsal bones, specifically the mid or distal portion of the second or third metatarsal, or the tarsal navicular.^2,33 On examination, the patient will have tenderness to palpation, often well localized. A positive tuning fork test (see page 647) is highly suggestive of a stress fracture.

FAST TRACK

Some studies suggest that barefoot running or barefoot running shoes improve running mechanics; other studies have had unfavorable or inconsistent results.

In female runners, stress fractures may be associated with the female athlete triad—osteoporosis or osteopenia, disordered eating (specifically caloric deficiency and low BMI), and amenorrhea. In addition to the major long-term health problems that may result from even one component of the triad, SFF may be a short-term consequence.³⁴

Although SFF is a clinical diagnosis, x-rays—including 3-view plain films of the foot, with the area of concern clearly noted on the order—are recommended. Magnetic resonance imaging may be used for secondary imaging if doubt about the source of the pain remains.³⁵

Of note: Occasionally, a metatarsal stress fracture progresses to a frank fracture, specifically of the metaphyseal-diaphyseal junction of the fifth metatarsal—known as a Jones fracture. This type of fracture has a high rate of malunion or nonunion.³⁶ If there is any suspicion of a fracture in this area, consider a referral to a sports medicine specialist or orthopedic surgeon.

Treatment: Icing, analgesics, and a boot. Standard treatment for SFF includes icing for 15 to 20 minutes up to 3 times a day for a minimum of 72 hours after injury, but may be continued throughout the healing period. Analgesics such as acetaminophen and a walking boot for 3 to 4 weeks, with follow-up at 3 weeks, should also be implemented. Recent evidence suggests that NSAIDs may hinder the bone healing process, and their use in treating SFF is controversial.^10-12

Weaning from the boot can begin when the patient is pain free with the boot on, usually by 3 to 4 weeks. Patients often progress quickly from wearing the boot at all times to wearing it only outside of the house, to not wearing it at all. Advise patients who need to walk long distances for a good portion of the day to keep the boot nearby and to put it on if the pain returns.

Once weaning from the boot begins, physical therapy (PT) should be considered to help the patient regain foot and ankle range of motion (ROM), proprioception, and strength. Once he or she learns the exercises, rehabilitation can be accomplished with a home exercise program. Foot deformities, such as pes planus or pes cavus, may indicate a need for orthotics. A well-structured athletic shoe may help to prevent future injury.^7,8

Return to running. Once adequate ROM and strength in the foot and ankle are recovered, the patient can begin to resume activity, starting with a low-impact cross-training exercise, such as a stationary bike or elliptical, for a week or 2. A patient who remains pain free can progress from cross-training to running on a treadmill for another week or 2, then gradually switch to outdoor running.

Plantar fasciitis: Heel pain with an insidious onset

Plantar fasciitis is one of the most common causes of heel pain in athletes (primarily runners) and nonathletes alike. Plantar fasciitis may be associated with acute trauma, but is more commonly insidious in onset. The diagnosis is clinical and rarely requires imaging.

Pain associated with plantar fasciitis may be described as sharp and stabbing or dull and aching. It is on the plantar surface of the heel, sometimes radiating to the arch, and may localize to the insertion of the plantar fascia on the medial calcaneal tubercle (FIGURE 2). The pain is typically most severe with the first few steps in the morning or after other periods of prolonged rest. It usually improves after a few steps, but may return later in the day. Plantar fasciitis does not cause paresthesias or other neurologic symptoms, so their presence is suggestive of a different diagnosis, such as nerve entrapment, compartment syndrome, or tarsal tunnel syndrome.^3,5

Treatment: It’s multifactorial. NSAIDs are commonly used. Relative rest is recommended, but cross training may be considered to maintain fitness.³⁷ Short-term PT is also recommended to teach the patient proper stretching and strengthening techniques in the form of a home exercise plan. Modalities such as iontophoresis (a system of transdermal delivery of medication with the use of electrical currents), Graston (a form of instrument-assisted soft tissue mobilization), and taping may be incorporated into PT, as well.¹³

Night splinting may also be used to keep the foot in a dorsiflexed position. A splint can be purchased without a prescription and prevents the plantar fascia from shortening overnight by providing a continuous passive stretch, thus reducing pain with first steps.¹⁴

Orthotics may also help to reduce symptom severity and duration, and studies have found no difference in outcomes with prefabricated vs custom-made devices.¹⁵ Another treatment to consider, particularly for recalcitrant cases of plantar fasciitis, is extracorporeal shock wave therapy, which has been studied for more than a decade with conflicting results.¹⁶ Corticosteroid injection may also be used for treatment-refractory plantar fasciitis, but caution is required, as the injection may increase the risk of rupture of the plantar fascia.^17,18

Return to running. There are no set guidelines for when an athlete with plantar fasciitis can return to running. Typically, after 2 to 4 weeks of relative rest and other treatments, the runner can begin to transition from cross-training to treadmill running.

FIGURE 2
Severe pain with first steps of the day

Achilles tendinopathy: An overuse injury

Achilles tendinopathy (AT) is typically an overuse injury incurred by athletes, although it is sometimes seen in patients who are sedentary and overweight. With a prevalence among runners of approximately 11%, AT is sometimes called the “runners’ disease.”⁴

Tendinopathy is a more accurate description than tendonitis, as histologic studies of affected Achilles tendons suggest that AT is a degenerative, rather than an inflammatory, condition.³⁸ A diagnosis of AT can be further classified as midportion or insertional.

Midportion Achilles tendinopathy (MAT), characterized by pain that occurs in the body of the Achilles tendon and worsens with activity, is often a clinical diagnosis. Physical findings suggestive of MAT are tenderness to palpation of the midportion of the Achilles tendon, with thickening of the tendon, warmth, crepitus, or palpable nodules in the tendon body. Onset is insidious and is commonly associated with an increase in activity.

Treatment: Orthotics or a heel lift. Like that of plantar fasciitis, treatment of midportion Achilles tendinopathy is primarily conservative. The use of orthotics, or a heel lift, is one of the most cost-effective interventions, and they are widely used, despite limited evidence of efficacy.³⁹ Custom orthotics are costly, and patients often benefit from trying prefabricated orthotics first to determine whether they will help.

Eccentric exercises. One of the most studied interventions for MAT is eccentric exercise training. Studies of eccentric exercises have been very favorable, and the exercises can be taught during routine PT sessions.^19-22 Modalities such as ultrasound therapy and extracorporeal shock wave therapy (ESWT) have also been studied. But because results have been inconsistent, they are generally reserved for treatment-refractory cases.²³

In patients with no contraindications, NSAIDs may be a good choice for pain management with relatively favorable results in the literature.²⁴ Corticosteroid injections should not be used, as they have been directly linked to rupture of the Achilles tendon.²³

Other interventions, such as plasma-rich protein injections and prolotherapy—a technique in which an irritant is injected into the tendon in an attempt to create an inflammatory reaction, thus increasing local blood flow and healing—are being studied for the treatment of AT, but are not routinely used or covered by insurance for this purpose. Surgical intervention may be considered for patients whose symptoms last for more than 3 to 6 months despite conservative treatment.

Insertional Achilles tendinopathy (IAT) can be clinically differentiated from MAT by the location of symptoms and tenderness to palpation at the insertion site of the Achilles into the calcaneous. Like MAT, IAT is exacerbated by activity. Other conditions that may contribute to, or be mistaken for, IAT are a Haglund deformity and retrocalcaneal bursitis.

Treatment: Footwear modification. Treatment of IAT, like that of MAT, is primarily conservative. Orthotics or heel lifts are commonly used. However, there is greater emphasis on footwear modification due to the mechanical irritation and resultant posterior heel swelling often associated with IAT. While eccentric exercises play a role in IAT treatment, the benefits are limited.²⁵

As with MAT, corticosteroid injections are contraindicated due to the risk of tendon rupture. Modalities such as ultrasound, ESWT, plasma-rich protein, and prolotherapy lack sufficient evidence to be widely recommended.

For refractory cases of IAT, surgical intervention often relieves the pain.

Return to running. After an initial rest of 2 to 4 weeks, patients may return to running while completing therapy. It’s not necessary to wait until the patient is completely pain free, but pain should be used to guide decisions about intensity and duration of activity.

CASE When Jim returns 6 weeks later, he reports that he took 3 weeks off from running because of the pain. Initially, he used contrast baths daily, Jim says, but now he uses them only when he is symptomatic, and he discontinued the NSAID a few weeks ago. Jim tells you he went to the local running store for a new pair of running shoes and that he is now able to run at his previous pace while remaining relatively pain free.

CORRESPONDENCE Jessica Favero Butts, MD, One American Square, Suite 185, Indianapolis, IN 46282; [email protected]