TREMOR

Etiologies

†††† Tremors are a type of movement disorder which are frequently encountered in clinical medicine.† They refer to repeated involuntary movements of a rhythmic oscillating nature around a fixed axis involving agonist and antagonist muscles.† Tremor may be a manifestation of an underlying illness such as the pill rolling tremor of Parkinsonís disease, or they may be without any underlying illnesses such as with essential tremors.† Tremors may be further classified as resting (occurring when the affected limb is not engaged in voluntary action), postural (occurring when the affected limb is maintaining posture in a gravity defying position), or action/intention (occurring when the affected limb is engaged in voluntary activity) tremors.† The upper extremities are most commonly affected; however, symptoms may also manifest in the legs, chin, neck, head, and voice.† Tremors subside during sleep.† It may be necessary to question the patientís bed partner for a reliable history.† Also ask the patient if the tremor has affected the patientís ability to perform tasks of daily living.

†††† A review of the patientís medications for a possible etiology should always be part of the initial evaluation.† If possible, discontinue any medication suspected of causing or exacerbating the tremor and reevaluate the patientís symptoms in several weeks.† Medications which are known to cause tremor include beta agonists, theophylline, aminophylline, corticosteroids, cyclosporine, amiodarone, caffeine, nicotine, calcium channel blockers, prochlorperazine, lithium, metoclopramide HCl, neuroleptics, reserpine, sympathomimetics, tricyclic antidepressants, and valproate sodium.† Specifically, question the patient regarding their intake of alcohol or caffeine, and if either of these are the suspected etiology, have the patient abstain and see if the tremor resolves.† Alcohol withdrawl is often associated with a severe transient tremor. If patients relate that alcohol lessens the tremor, then consider essential tremor as the most likely etiology.

†††† As stated above, a good neurologic exam is essential.† A handwriting sample should be taken from the patient at the initial visit (micrographia is seen with Parkinsonís disease) as this can be used to compare with future samples to evaluate the efficacy of various forms of therapy.† The exam should specifically evaluate for cogwheel rigidity, bradykinesia, impaired postural reflexes, masked facies, simian posturing, and Kayser-Fleischer rings.

†††† The differential diagnosis of tremor includes: chorea, tics, focal seizures, myoclonus, or asterixis.† Certain tremors display characteristics which may identify the underlying etiology.† The characteristic tremor of Parkinsonís disease is described as a unilateral resting tremor of an upper extremity.† It is a ďpill rollingĒ tremor on the order of 5 to 7 cycles per second that lessens or resolves with voluntary movements of the affected limb.† Essential tremor may be familial, and occurs during adolescence or adulthood with peaks in the second and sixth decades.† The hands and fingers are often first affected with later involvement of the head and neck, and the tremor may occur in a symmetric or asymmetric manner.† It may remain stable for prolonged periods but eventual progression is the norm.† Cerebellar tremors are described as a course side-to-side movement during voluntary activity of the affected limb or during sustained posture.† The finding of associated cerebellar symptoms (dysmetria, dyssynergia, hypotonia, dysarthria, and nystagmus) will help identify this type of tremor.† Unilateral cerebellar tremors may be secondary to mass lesions or strokes; whereas, bilateral tremors of the cerebellum may be secondary to cerebellar degeneration, metabolic or toxic encephalopathies, Wilsonís disease, infections, or multiple sclerosis.† There are no effective therapies for cerebellar tremors; therefore, identifying and treating the underlying etiology is imperative.† Physiologic tremors may be secondary to thyrotoxicosis, pheochromocytoma, hypoglycemia, emotional stress or exercise.† Rubral (midbrain) tremor refers to a low-frequency tremor that is present during rest and intentional movements.† There may also be a postural component.† Rubral tremors are often resistant to medical therapy.

†††† Therapy involves treating the underlying illness for secondary tremors.† Essential tremors may respond to beta-adrenergic antagonist therapy (propranolol, metoprolol, atenolol, etc), low dose primidone (25 to 250 mg/day) and/or benzodiazepines (diazepam, lorazepam, clonazepam, alprazolam, etc).† Other potential therapeutic options include acetazolamide, methazolamide, mirtazapine, and gabapentin.† Initially, theophylline may worsen essential tremor; however, chronic therapy after 2 to 4 weeks may actually help control tremor.† Refractory cases may require neurosurgical intervention (ventrolateral thalamotomy or thalamic deep brain stimulation).† The tremor associated with Parkinsonís disease may respond to carbidopa/levodopa combination therapy.† If not, specific therapies for tremor may be more effective such as benztropine (2-4 mg/day), trihexylphenidyl (8-12 mg/day) or amantadine (100 mg PO BID).† For refractory cases, neurosurgical intervention may be indicated.† Cerebellar tremors may respond to therapy with beta blockers, clonazepam, carbamazepine, tetrahydrocannabinol, trihexyphenidyl, or ondansetron HCl.† Rubral tremors which are frequently refractory to medical therapy, may respond to treatment with levodopa or anticholinergic agents.† Surgical therapies for refractory tremors include stereotactic thermocoagulation, thalamotomy, pallidotomy and high-frequency deep-brain stimulation.