Remor, the most common movement disorder in the general population, is an involuntary
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- DIFFERENTIAL DIAGNOSIS FOR MOVEMENT DISORDERS
- CLINICAL CLASSIFICATION OF TREMOR
- EVALUATION OF THE PATIENT WITH TREMOR
- Figure 1.
- CLINICAL FEATURES OF DISORDERS ASSOCIATED WITH TREMOR Essential Tremor
- Etiology and pathogenesis.
- PHARMACOLOGIC MANAGEMENT OF TREMOR
- Treatment of Other Tremors
- SURGICAL MANAGEMENT OF TREMORS
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remor, the most common movement disorder in the general population, is an involuntary, rhythmic, oscillatory movement of a body part. It is produced by activation of reciprocally innervated, antagonistic muscle groups, which leads to their repeated contractions. 1 Tremors can lead to social and physical deterioration and may be a harbinger of a complex medical syndrome. Although many forms of tremor may begin earlier in life, they progress with time and often do not come to the attention of a physi- cian until a patient is elderly. In one study, 98% of a multiethnic cohort of normal older adults had a mild detectable tremor on testing; in one third of the cases, the tremor worsened with activity. 2 Many patients feel that tremors are a part of aging and fail to report them to their physicians, which denies them adequate treatment. Under the current health care system, most patients with tremors are like- ly to initially present to their primary care physician. A study by Marttila et al 3 showed that 25% of the patients diagnosed by nonneurologists to have Parkinson’s disease actually had essential tremor. This illustrates the importance of clinicians recognizing tremors and their underlying causes in order to man- age them successfully. The 3 most common forms of tremor in the elderly population are essential tremor, parkinsonian tremor, and cerebellar tremor. This article reviews the clinical characteristics, etiology and pathogenesis, and treat- ment of these types of tremor. The clinical features and management of several other types of tremor are addressed, as well. DIFFERENTIAL DIAGNOSIS FOR MOVEMENT DISORDERS It is important to differentiate tremor from other involuntary movements, including choreiform move- ments, athetosis, dystonia, myoclonic movements, and tics. Choreiform movements are involuntary and rapid but jerky in nature, rather than rhythmic. They are prominent in the face and distal extremities and give the patient a fidgety appearance. Chorea present- ing in elderly patients is generally either senile chorea (which is not an inherited disorder) or, rarely, chorea following a cerebrovascular accident. Although Syd- enham’s chorea and Huntington’s chorea are rare in older persons, Huntington’s chorea always must be ruled out. 4 Athetosis constitutes slow writhing movements of the arms and legs that commonly occur on movement. It may be associated with hemiplegia and often occurs in children secondary to birth trauma. Dystonic movements are slow, prolonged move- ments of either the trunk muscles or a distal muscle group. They may be associated with tremors of the affected part (dystonic tremor). Examples of dystonia include spasmodic torticollis involving the neck mus- cles, writer’s cramp due to spasm of the shoulder mus- cles, and blepharospasm, a form of dystonia that con- sists of involuntary, repeated eye closure and is seen in elderly women. Blepharospasm is worsened by stress and can be confused with early Parkinson’s disease. Patients with blepharospasm may also have twitching of oral or facial muscles, which is known as Meige’s syndrome. 4 Myoclonic jerks are sudden, brief, and shock-like and lack the rhythmicity of tremors. In adults and the elderly, myoclonus is rare and occurs in association with Creutzfeldt-Jakob disease, uremia, hypomagne- semia and liver failure. 4 Tics are brief contractions of a muscle, which may be confused with tremors due to their repetitive nature. Tics commonly occur in chil- dren and can produce features such as sniffing, grunt- ing, pouting, and grimacing. CLINICAL CLASSIFICATION OF TREMOR Tremors may be classified based on their clinical fea- tures (Figure 1). Most tremors can be characterized as either a resting tremor or an action tremor. Resting tremor occurs in a limb or body part that is completely supported against gravity with absolutely no contraction T Dr. Bhagwath is an internist at St. Louis Internal Medicine, St. Louis, MO. www.turner-white.com Hospital Physician December 2001 31 C l i n i c a l R e v i e w A r t i c l e Tremors in Elderly Persons: Clinical Features and Management Gayathri Bhagwath, MBBS of the skeletal muscle. 5 If the limb is not supported, its muscles will be expending energy to maintain position; the tremor present in such a condition is an action tremor. For example, essential tremor is a type of action tremor that may be mistaken for a resting tremor if the affected limb is not completely at rest during examina- tion. Resting tremor is best observed when the patient is distracted. In Parkinson’s disease, the physician may observe mild tremor in the arm contralateral to the one he or she has asked the patient to swing, even if the patient is unaware of the tremor. 4 Action tremor includes postural, kinetic, and iso- metric tremors. 6 Postural tremor occurs when a body part is voluntarily held motionless against gravity—for example, pointing at an object or protruding the tongue. 7
ment of a body part. An intention tremor is a kinetic tremor that worsens during the completion of a visual- ly guided, goal-directed movement (eg, pouring tea into a cup). 6 Task-specific tremor occurs during com- plex tasks such as writing or playing a musical instru- ment. Simple kinetic tremor occurs with acts such as a simple turning of the wrist or foot. Isometric tremor occurs when a voluntary muscle contraction is op- posed by a stationary force. It can be elicited by having the subject make a fist or push against a wall or other stationary object.
A wide range of disorders cause resting and action tremor (Table 1), and some can manifest both types of tremor activity. As laboratory tests are not available for the diagnosis of many common causes of tremor, a de- tailed physical examination is a physician’s best diag- nostic tool. Information regarding the patient’s cur- rent and past medical history, as well as any family history of tremors, should be obtained. All medications used currently and in the past must be listed. A detailed neurologic examination to evaluate motor and sensory nervous systems, the extrapyramidal sys- tem, and cerebellar function is required. Careful observation during the performance of each neurologic test can yield invaluable information. For example, during a finger-to-nose test, a cerebellar action tremor manifests during the terminal part of the test, just before the finger touches the nose. In con- trast, a parkinsonian tremor may either disappear with the onset of finger-to-nose testing or may remain con- stant throughout the range of motion.
Other tremor syndromes: Dystonic tremor Isolated chin tremor Isolated voice tremor Indeterminate tremor syndrome Intention tremor Task-specific tremor Simple kinetic tremor Resting
tremor Postural
tremor Isometric tremor
Med 2000;160:2438–44.) Table 1. Causes of Tremors in the Elderly Action Tremor Resting Tremor Parkinsonism Parkinsonism Essential tremor Alcohol withdrawal Cerebellar disease Essential tremor* Holmes’ tremor Neurosyphilis Physiologic tremor Drugs (except those causing parkinsonism) *Although essential tremor is predominantly an action tremor, rarely, in advanced conditions, it may have a resting component. (Elble RJ. Diagnostic criteria for essential tremor and differential diagnosis. Neurology 2000;54[11 Suppl 4]:S2–6.) Data from Patten JP, editor. Neurological differential diagnosis. 2nd ed. London: Springer Publication;1998. Tremor Action
tremor Kinetic
tremor CLINICAL FEATURES OF DISORDERS ASSOCIATED WITH TREMOR Essential Tremor Essential tremor is the most common cause of tremor in elderly patients. It has a bimodal peak of onset in the second and sixth decades of life. 7 Also
known as senile tremor, it constitutes a mixture of pos- tural and kinetic tremors. It is generally bilateral and is gradually progressive. It affects upper limbs in 95% of cases, the head in 34%, lower limbs in 20%, the voice in 12%, the face in 5%, and the trunk in 5%. 7 A con- siderable number of patients with mild essential tremor (up to 50%) 8 may be unaware of their tremor, and it does not come to the attention of their physi- cian. Some patients may present with only isolated head tremor. Although benign, essential tremor in its severe form can cause functional and social impairment, titubation, and a tremulous voice. Severe essential tremor may be accompanied by cogwheel rigidity. If the postural form of essential tremor is mistakenly characterized as rest- ing tremor, the patient’s condition may be wrongly diagnosed as Parkinson’s disease, especially if cogwheel rigidity is present. However, in essential tremor, muscle tone and strength are normal. The clinical features of essential tremor and parkinsonian tremor are com- pared in Table 2. Essential tremor has been observed to be precipitat- ed and alleviated by several factors (Table 2). It improves with alcohol consumption but is generally not suspected to cause alcoholism in patients. 5 Typically, there is an absence of signs of other neuro- logic disorders, although essential tremor may coexist with Parkinson’s disease. Etiology and pathogenesis. The etiology and patho- physiology of essential tremor have not been elucidat- ed. At least 50% of patients with essential tremor have a positive family history. The familial form is an autoso- mal dominant disease with variable penetrance. 1 Autopsies of persons who had essential tremor revealed no histologic abnormalities. 9 Routine computed tomog- raphy and magnetic resonance imaging scans are typi- cally normal. 1 It has been proposed that enhanced oscillations in the olivocerebellar to rubrothalamic pathways are the cause of essential tremor. 9 Increased glucose metabolism in the olivary nuclei and increased blood flow in the red nucleus, cerebellum, and thala- mus have been observed bilaterally on positron emis- sion tomography of patients with essential tremor. 10 In
produced on stimulation of olivary nuclei with the alka- loid harmaline and serotonergic drugs, 11 lending fur- ther support to the involvement of this site in the gene- sis of tremor. Cerebellar Tremor Cerebellar tremor is a pure action tremor that is absent at rest. On examination, a combination of termi- nal intention tremor and some postural tremor can be seen. Dysmetria (ie, difficulty alighting on the target during voluntary movement) also characterizes cerebel- lar lesions. This manifests in the finger-to-nose test as “past-pointing.” Other features include ataxia (uncoor- dinated or inaccurate movement), nystagmus, muscular hypotonia, decreased reflexes, and dysdiadochokinesia (ie, an inability to perform rapid alternating move- ments). Titubation (head nodding) may be present when the patient is upright but not on supination. 12
www.turner-white.com Hospital Physician December 2001 33 Table 2. Comparison of Essential Tremor and Parkinsonian Tremor Characteristic Essential Tremor Parkinsonian Tremor Type of tremor Action, usually symmetrical Rest and action, initially unilateral Agents or states that improve Alcohol, relaxation; voluntary Sleep; voluntary suppression is the tremor suppression is possible not possible Agents or states that worsen Excitement, anger, fatigue, fear, Emotional stress, excitement, the tremor caffeine, nicotine, β-agonists fatigue Other findings Occasional cogwheel rigidity Bradykinesia, cogwheel rigidity, gait disturbance, depression, cognitive decline Head involvement Titubation commonly present Titubation is usually absent; chin, jaw, and lip tremor may be present Voice involvement Tremulous voice Low-volume voice Involvement of the laryngeal muscles leads to an unco- ordinated voice, but unlike in parkinsonism, the voice is of normal volume.
The cerebellum receives input from the motor cortex regarding the next intended movement of the limbs and the trunk. 4 The
cerebellum also receives sensory information from the peripheral nerves regarding limb position and move- ment. Under normal circumstances, the cerebellum uses the information from these sources to anticipate and prevent the occurrence of movement errors, such as tremors. 13 Vascular accidents, malignancy, and chronic alcohol or drug abuse 4 may cause a lesion in the deep cerebellar nuclei (ie, the dentate, globose, or emboliform nuclei) or in their connections to the con- tralateral thalamus via the brachium conjunctivum. Such a lesion disrupts the sensorimotor feedback loop between the limb and the motor cortex, which is oscil- latory in nature, and tremor results. Parkinsonism Parkinsonism is a movement disorder that can lead to severe physical and emotional disability. Although tremor is a hallmark of parkinsonism, it is not the cause of physical limitation in patients with the disease. Rather, functionality is severely limited by the bradyki- nesia, rigidity, and postural instability that are also char- acteristic of the disease. Both resting and action tremor (kinetic type) can be present in this disease, and it is commonly unilateral in the early stages (Table 2). In Parkinson’s disease of elderly onset (idiopathic Parkinson’s disease), resting tremor may be an uncommon initial symptom. 14 The same may hold true for drug-induced parkinsonism (DIP).
4 Common causes of DIP include neuroleptic agents, calcium channel blockers, valproic acid, tacrine, bethanechol chloride, reserpine, and methyldopa. 15 Lower-potency neuroleptics or novel neuroleptics (eg, clozapine) that lack prominent striatal receptor block- ade are less likely to cause DIP. 16 Clinically, DIP cannot be distinguished from idiopathic Parkinson’s disease; however, DIP develops subacutely within the first weeks of drug introduction or an increase in drug dosage. Tremor may be a simple oscillatory movement or it may be compound, such as a pill-rolling movement. The tremor affects the distal extremities (especially the hands) and the facial, jaw, and tongue muscles. Anxiety, emotional upset, and fatigue exacerbate the tremor, and it disappears during sleep. Cogwheel rigid- ity may be present and the voice volume is low. Monosymptomatic resting tremor is a predominant- ly resting tremor (occasionally with a postural compo- nent) that occurs in the absence of other parkinsonian features such as bradykinesia and rigidity. 5,6 It must be of 2-year duration to fit the diagnostic criteria and may be a form of Parkinson’s disease. Etiology and pathogenesis. The anatomy of the structures involved in production of parkinsonian tremor is briefly described. 17 Subcortical grey matter is grouped into nuclei known as basal ganglia, which include the striatum, globus pallidus, subthalamic nucleus, and substantia nigra. Nerve cells in the sub- stantia nigra pars compacta of the midbrain produce dopamine. Dopamine is transported along the axons to the caudate nucleus and the putamen, which col- lectively form the striatum. Dopamine helps modu- late the inhibitory output of the striatum to the globus pallidus interna and substantia nigra pars reticulata. These 2 nuclei, in turn, inhibit certain thal- amic nuclei that have a stimulatory influence on the cerebral cortex. In patients with Parkinson’s disease, dopamine is depleted as a result of the death of dopaminergic cells in the substantia nigra. In patients with neuroleptic drug–induced parkinsonism, dopaminergic D 2 recep-
tor blockade results in decreased dopamine activity. Both conditions can lead to disinhibition of the globus pallidum, causing suppression of the thalamic nuclei, which results in reduced excitation of the motor cor- tex. Because the motor cortex depends on the basal ganglia to facilitate movements generated by the cor- tex, the outcome of this depletion or underactivity of dopamine is a movement disorder. This pathway does not explain the origin of the rest tremor seen in parkinsonism. In Parkinson’s disease, it is known that the death of nigrostriatal neurons leads to abnormal intermittent oscillations in the neurons of the motor cortex, basal ganglia, and thalamus and that these abnormal oscillations can produce tremor. 9 The
exact cause of the oscillations is unclear, however. The cerebellum is involved in control of the parkinsonian rest tremor. 18
Drugs are associated with other types of tremor besides DIP. Long-term use of antipsychotic agents can also cause a postural tremor called tardive tremor. It is a low frequency murmur that is usually postural but may occur at rest or with movement. 6 Even short-term use of intravenous high-dose haloperidol (> 240 mg) has been associated with tremors, rigidity and dyskinesia. 19 Sympathomimetic agents, cyclosporine, lithium, and tri- cyclic antidepressants are known to enhance physiolog- ic tremor. 15 Lithium overdose produces ataxia, tremor, 34 Hospital Physician December 2001 www.turner-white.com B h a g w a t h : T r e m o r s i n E l d e r l y P e r s o n s : p p . 3 1 – 3 7 , 4 9 confusion, cardiac arrhythmias, gastrointestinal distress, muscle twitching, and fasciculations. It can be diag- nosed by measuring serum levels of lithium. 20 Tremors are one of the common clinical features of serotonin syndrome, which is most commonly caused by interaction between serotonergic agents and monoamine oxidase inhibitors. Symptoms resolve after the discontinuation of the serotonergic drugs. 21 Barbiturate withdrawal can produce anxiety, restless- ness, delirium, seizures, and tremor. 22 Abstinence from ethanol can produce similar symptoms within the first few days; when severe, this can lead to delirium tremens, which consists of gross tremor, altered senso- rium, fever, and tachycardia. Benzodiazepine withdraw- al leads to anxiety, nausea, vomiting, tremor, hallucina- tions, and seizures. Tremors may also be caused by hallucinogen use and may accompany phencyclidine (PCP) withdrawal. 22 Chronic exposure to metallic mercury produces an intention tremor that can be accompanied by erethism (memory loss, excitability, insomnia, and delirium). This may be observed in workers in the felt-hat indus- try and sometimes in dentists. 23 Acute exposure to mer- cury or its vapors can also lead to tremors. Physiologic Tremor Normal individuals can manifest an action tremor, especially while fatigued or experiencing emotions such as fear, anxiety, or stress. 6 Physiologic tremor can also result from medical conditions such as hypother- mia, hypoglycemia, pheochromocytoma, thyrotoxico- sis, and alcohol withdrawal. 5 A characteristic feature of physiologic tremor is the disappearance of the tremor on removal of the precipi- tating agent or resolution of the underlying state. In a patient with alcoholism, physiologic tremor should be differentiated from asterixis (repetitive partial flexion of the wrists during sustained wrist extension). Asterixis is a sign of metabolic encephalopathy and accompa- nies other signs of liver failure in these patients.
Patients with dystonia may have a localized tremor that can occur in a part affected by dystonia (eg, tremu- lous writer’s cramp) or in an unaffected part (eg, pos- tural arm tremor in a patient with cervical dystonia). This tremor is irregular in nature and is accompanied by abnormal posturing. When it involves the head, dys- tonic tremor may be confused with titubation (senile tremor). It may be distinguished from titubation by hav- ing the patient turn the head opposite to the direction of the dystonic pull; worsening of the tremor indicates dystonic tremor rather than titubation. 1 If the voice is affected, it is either crackling or breath-like in nature. Psychogenic Tremor Also called hysterical or functional tremor, psy- chogenic tremor is characterized by sudden onset and remission 5 and changes in severity over time. A history of mental illness and unrelated neurologic signs may be present. Tremor amplitude typically decreases with distraction.
Holmes’ tremor (red nuclear tremor) presents as a terminal intention tremor or resting tremor that is vio- lent in nature. Even a slight attempt to move a limb can lead to severe jerking movements that may lead to injury. Voice involvement can lead to inarticulate speech. 4
ated with certain tasks, such as writer’s tremor. 5 Palatal tremor includes symptomatic palatal tremor, which manifests as rhythmic movements of the soft palate and is usually associated with a brainstem or cerebellar lesion, and essential palatal tremor, which manifests as rhythmic ear clicks and is not associated with the pres- ence of a brain lesion. 24 Certain neuropathies, including chronic inflammatory demyelinating neuropathy, Guillain-Barré syndrome, and dysgammaglobulinemic neuropathy, are also associated with tremor. 6 The term “indeterminate tremor syndrome” is assigned to a condi- tion in which the patient has essential tremor along with certain neurologic signs that are insufficient to make a diagnosis of any neurologic syndrome. 6
Control of tremor is not always essential. Many patients with mild essential tremor do not feel the need to bring the tremor to the attention of their physicians, let alone get treatment for it.
β-Adrenergic blockers (eg, propranolol) and the anticonvulsive agent primidone are the mainstays of treatment for essential tremor (Table 3). β-Blockers can cause confusion and dizziness in elderly patients. Furthermore, they must be used cautiously in patients with asthma, heart failure, or diabetes. When essen- tial tremor is induced by a drug that is medically nec- essar y, β- blockers may be used to suppress the tremor.
15 Primidone has a response rate of up to 75% 25
stead of β-adrenergic blockers. B h a g w a t h : T r e m o r s i n E l d e r l y P e r s o n s : p p . 3 1 – 3 7 , 4 9 www.turner-white.com Hospital Physician December 2001 35 Gabapentin is well tolerated by older patients. 1 Benzodiazepines may be used to control the anxiety that enhances tremor. Severe drowsiness and confusion may occur in the elderly with their use. Calcium channel blockers are not very effective for the treatment of tremor, but they may be tried if other agents fail. 1 The alternative agents acetazolamide 26 and metazo- lamide 27
essential tremor. A double-blind placebo-controlled study showed no benefits with acetazolamide but found alprazolam effective in essential tremor treatment. 26 Patients may use alcohol to self - treat essential tremor; however, this practice should be discouraged, and the patient should be monitored because of the potential risk of alcoholism. Long-term use of alcohol is not beneficial because of the development of toler- ance. In older patients, alcohol use can lead to falls, drowsiness, and drug interactions. Botulinum toxin is a new treatment mode that is cur- rently under investigation. A randomized, double-blind trial evaluated the use of botulinum toxin type A in 133 patients. 28 Although postural hand tremor was signifi- cantly reduced, kinetic hand tremor showed no long-term improvement. Improved functional ability was not ob- served, probably owing to the dose-dependent hand weak- ness caused by the toxin itself. Botulinum toxin type A has produced a modest response in patients with head and voice tremor but carries the risk of producing dysphasia. 1 Strength training programs have been shown to decrease the magnitude of essential tremor but did not improve functional ability. 29
In patients with early Parkinson’s disease in whom tremor is the only manifestation, there is no function- al limitation; the use of medication is thus essential only when other symptoms are present. 12 All anti- parkinsonian drugs must be started at a small dose and gradually increased in strength and frequency. Anticholinergic agents constitute a reasonable first line of treatment in Parkinson’s disease (Table 4). 12 Potential adverse effects include urinary retention, confusion, and hallucinations; they also can worsen glaucoma in older patients. When anticholinergic agents are inadequate, amantadine can be added. If maximum tolerable dosages of both drugs are unsuc- cessful in treating the patient, they are discontinued and levodopa-carbidopa is begun. One of the prob- lems of using levodopa-carbidopa is the fluctuation between high and low blood levels of the drugs, lead- ing to on-off phenomenon and dyskinesia. To avoid this, smaller doses can be given at regular intervals. Bromocriptine can help in the management of on-off phenomenon and decrease the dose of levodopa. Recent studies have found apomorphine and clozap- ine useful in the treatment of parkinsonian tremor. 30,31
While most drug-induced tremors disappear after discontinuation of the drug, drug-induced parkinson- ian tremor may persist for years after discontinuation. 15 Treatment of drug-induced parkinsonian tremor is similar to that of Parkinson’s disease. Withdrawal symptoms produced by sedatives such as barbiturates and benzodiazepines are treated by substi- tuting related shorter-acting drugs given in tapering doses. Alcohol withdrawal symptoms can be treated with benzodiazepines. Delirium tremens is best managed by adequate sedation of affected patients and supportive treatment. 22 Antipsychotic agents should be avoided in these patients because these agents lower the seizure 36 Hospital Physician December 2001 www.turner-white.com B h a g w a t h : T r e m o r s i n E l d e r l y P e r s o n s : p p . 3 1 – 3 7 , 4 9 Table 3. Pharmacologic Agents for Treatment of Essential Tremor β-Adrenergic blockers Metoprolol Propranolol Benzodiazepines Clonazepam Diazepam Botulinum toxin injection Calcium channel blockers Gabapentin Primidone Data from Habib-ur-Rehman. Diagnosis and management of tremor. Arch Intern Med 2000;160:2438–44. Table 4. Pharmacologic Agents for Treatment of Parkinsonian Tremor Amantadine Anticholinergic agents Benztropine mesylate Biperiden Trihexyphenidyl Bromocriptine mesylate Levodopa-carbidopa Data from Evidente VG. Understanding essential tremor. Differential diagnosis and options for treatment. Postgrad Med 2000;108: 138–40, 143–6, 149. threshold. Hallucinogen and PCP users can be man- aged with supportive care and benzodiazepines. Frank psychosis can occur with PCP use and requires treat- ment with antipsychotic agents. Acute inorganic mercury exposure is treated with dimercaprol. 23 Chronic mercury poisoning is treated with N- acetyl penicillamine. 23 Lithium intoxication is treated with gastrointestinal decontamination, intra- venous hydration, diuresis, urine alkalinization, and supportive treatment. Hemodialysis may be required for severe cases. 20
Cerebellar tremors are extremely difficult to treat. Some progress has been reported with clonazepam and ondansetron. 32,33 Holmes’ tremor has shown some response to levodopa. 34 Physiologic tremor is best treated by removal of the causative agent or resolution of the pre- cipitating state. Small doses of β- blockers may also help. 6 Dystonic head tremors respond to botulinum toxin injec- tions. 35 Propranolol, primidone, alcohol, and botulinum toxin may be beneficial in the treatment of task-specific tremor.
25 Neuropathic tremor does not always improve with resolution of the underlying neuropathy and may respond to propranalol. 5 Palatal tremors occasionally respond to local botulinum toxin injection. 5
Surgical treatment is considered only for severe dis- abling tremors after medical treatment has failed. Two procedures used in the treatment of Parkinson’s dis- ease and essential tremor are thalamotomy and thala- mic stimulation targeting the ventralis intermedius nucleus of the thalamus. Thalamotomy is performed via thermocoagulation. Thalamic stimulation is per- formed by local implantation of a pulse generator. 6 These procedures, when performed on one side of the brain, improve symptoms on the contralateral side. Thalamic stimulation has the advantage of being feasi- ble bilaterally; however, a bilateral thalamotomy may lead to bulbar neurologic deficits (ie, dysphagia and dysarthria) and cognitive neurologic deficits, as well as visual field defects and hemiparesis. 6 These procedures improve tremor in 80% to 90% of patients with Parkinson’s disease. Although thalamo- tomy improves essential tremor in 69% to 93% of patients, 36 thalamic stimulation is preferred because of the bilateral nature of the disease. One-year follow-up of patients with disabling essential tremor treated with bilateral thalamic stimulation showed reduced tremor and better functional ability. 37 Thalamic surgery may be beneficial in Holmes’ tremor but is not usually performed because of the risks involved and the possibility of spontaneous remission. 5
Because of their frailty and coexistent medical prob- lems, geriatric patients are at high risk of morbidity and mortality when afflicted by a movement disorder such as tremor. Elderly patients may also be at risk of developing multiple forms of tremor (eg, resting and action). Because the presence of tremors is often con- sidered a part of aging, many patients may not benefit from the treatment opportunities available. In the evaluation of tremor, particular attention must be paid when the tremor is sudden in onset, occurs in uncommon sites (eg, the lower extremities, tongue, or chin), is preceded by a neurologic event, or is associated with other signs of neurologic dysfunc- tion. Careful assessment and the judicious use of med- ication, when needed, will help these patients retain their physical independence longer.
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