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ULY CLINIC

19 Septemba 2025, 04:19:42

Tremors

Tremors are involuntary, rhythmic oscillatory movements resulting from alternating contraction of opposing muscle groups. They are the most common type of involuntary movement and often indicate extrapyramidal, cerebellar, or metabolic disorders, or may be induced by certain drugs.

Tremors are classified by timing and context:

Resting tremor: occurs when a limb is at rest; classic in Parkinson’s disease (pill-rolling tremor).
Intention tremor: appears only with purposeful movement, disappears at rest; seen in cerebellar disorders.
Postural (action) tremor: occurs while maintaining a posture; includes essential tremor.

Tremor-like movements may also include asterixis, a flapping tremor seen in hepatic failure. Tremors can be aggravated by stress or emotional upset, and alcohol may reduce postural tremors.

Pathophysiology

Extrapyramidal dysfunction: degeneration of basal ganglia circuits produces resting tremors (e.g., Parkinson’s disease).
Cerebellar lesions: impair coordination, causing intention tremors.
Metabolic disturbances: hypoglycemia, thyrotoxicosis, alkalosis, or hypercapnia can induce fine or coarse tremors.
Drug-induced: antipsychotics, sympathomimetics, and lithium may cause tremors via dopaminergic or adrenergic pathways.
Familial or idiopathic causes: genetic predisposition to essential tremor.

History and Physical Examination

History

Onset (sudden vs gradual), duration, progression, and symmetry.
Aggravating/alleviating factors (stress, activity, posture, drugs, alcohol).
Interference with daily activities (writing, eating, walking).
Associated symptoms: weakness, sensory changes, cognitive decline, behavioral changes.
Past medical history: neurologic disorders, endocrine or metabolic diseases.
Family history: tremor, Parkinsonism, essential tremor.
Medications: especially phenothiazines, lithium, metoclopramide, sympathomimetics.

Physical Examination

General observation: note posture, gait, and mental status.
Musculoskeletal: assess range of motion, muscle tone, strength.
Neurologic exam: identify chorea, athetosis, dystonia, or other involuntary movements.
Reflexes: deep tendon reflexes, Babinski, clonus.
Tremor characterization: type (resting, intention, postural), frequency, amplitude, symmetry.
Gait: observe for ataxia, shuffling, or propulsive gait.
Systemic exam: thyroid enlargement, signs of liver disease, or other organ involvement.

Medical causes

Cause	Onset	Key Features	Associated Signs	Pathophysiology	Management
Alcohol withdrawal syndrome	Acute, 7–48 h after last drink	Resting/intention tremor	Anxiety, tachycardia, diaphoresis, hypertension, insomnia, nausea, vomiting, severe: agitation, confusion, hallucinations, seizures	CNS hyperexcitability due to abrupt alcohol cessation	Benzodiazepines, supportive care, hydration
Alkalosis	Acute	Intention tremor, muscle twitching	Carpopedal spasm, agitation, paresthesia, hyperventilation	Increased neuronal excitability	Correct underlying alkalosis, supportive care
Benign familial essential tremor	Early adulthood	Bilateral postural tremor of hands/fingers; may spread to head, jaw, lips, tongue	Quavering voice if laryngeal involvement	Genetic, idiopathic	Beta-blockers, primidone, occupational therapy
Cerebellar tumor	Gradual	Intention tremor	Ataxia, nystagmus, incoordination, muscle weakness, hypoactive reflexes	Cerebellar dysfunction	Surgical resection, radiotherapy if malignant
Graves’ disease / thyrotoxicosis	Gradual	Fine tremor of hands/fingers	Nervousness, palpitations, heat intolerance, weight loss, dyspnea, goiter, exophthalmos	Excess thyroid hormones increase beta-adrenergic activity	Antithyroid drugs, beta-blockers, radioactive iodine, surgery
Hypercapnia	Acute/subacute	Rapid, fine intention tremor	Headache, fatigue, blurred vision, decreasing LOC	CNS effects of elevated CO₂	Treat underlying respiratory failure, oxygen therapy
Hypoglycemia	Acute	Rapid fine tremor	Confusion, diaphoresis, tachycardia, hunger, visual disturbances	Low glucose → impaired CNS function	Rapid glucose administration, monitor blood sugar
Multiple sclerosis	Gradual, relapsing	Waxing/waning intention tremor	Visual/sensory impairment, ataxia, nystagmus, spasticity, hyperreflexia, dysphagia, dysarthria	Demyelination of CNS pathways	Disease-modifying therapy, symptomatic management
Parkinson’s disease	Gradual	Resting tremor, pill-rolling, fingers → hand → foot/jaw/tongue	Rigidity, bradykinesia, masked facies, drooling, dysarthria, propulsive gait	Degeneration of dopaminergic neurons in substantia nigra	Dopaminergic therapy, physical therapy, supportive care
Thalamic syndrome	Acute/subacute	Contralateral ataxic tremor	Sensory loss, hemiballismus, hemichoreoathetosis, oculomotor palsy	Midbrain/thalamic lesions affecting motor/extrapyramidal pathways	Symptomatic, treat underlying stroke/lesion
Wernicke’s disease	Subacute	Intention tremor	Ataxia, ocular abnormalities, confusion, apathy, hypotension	Thiamine deficiency	IV thiamine, supportive care
West Nile encephalitis	Acute	Tremor, myoclonus	Fever, headache, rash, weakness, altered LOC, seizures	Viral CNS infection	Supportive care, monitor for complications
Drug-induced tremor	Variable	Resting/postural tremor	Dose-related, may include pill-rolling	Phenothiazines, lithium, metoclopramide, sympathomimetics	Dose adjustment, drug discontinuation, symptomatic therapy

Special considerations

Severe tremors may interfere with activities of daily living (ADLs).
Ensure safety during walking, eating, and self-care.
Monitor for falls, injuries, or functional decline.
Adjust medications if tremor is drug-induced.

Patient counseling

Educate about nature and cause of tremor.
Reinforce independence, suggest assistive devices if needed.
Advise on avoiding tremor triggers: stress, caffeine, certain medications.
Encourage adherence to treatment plans for underlying disorders.

Pediatric pointers

Normal neonates may show coarse tremors or hypocalcemic startle reflex.
Pathologic tremors may occur in cerebral palsy, fetal alcohol syndrome, or maternal drug exposure.
Evaluate for metabolic disturbances, congenital neurologic disorders, or developmental delays.

References

Berkowitz CD. Berkowitz’s Pediatrics: A Primary Care Approach. 4th ed. American Academy of Pediatrics; 2012.
Buttaro TM, Tybulski J, Bailey PP, Sandberg-Cook J. Primary Care: A Collaborative Practice. Mosby Elsevier; 2008.
McCance KL, Huether SE, Brashers VL, Rote NS. Pathophysiology: The Biologic Basis for Disease in Adults and Children. Mosby Elsevier; 2010.
Sommers MS, Brunner LS. Pocket Diseases. F.A. Davis; 2012.
Buttaro TM, Tybulski J, Bailey PP, Sandberg-Cook J. Primary Care: A Collaborative Practice. St. Louis, MO: Mosby Elsevier; 2008.
Lehne RA. Pharmacology for Nursing Care. 7th ed. St. Louis, MO: Saunders Elsevier; 2010.
McCance KL, Huether SE, Brashers VL, Rote NS. Pathophysiology: The Biologic Basis for Disease in Adults and Children. Maryland Heights, MO: Mosby Elsevier; 2010.
Sommers MS, Brunner LS. Pocket Diseases. Philadelphia, PA: F.A. Davis; 2012.
Jankovic J. Parkinson’s Disease and Movement Disorders. 6th ed. Philadelphia, PA: Wolters Kluwer; 2015.
Koller WC. Tremor: Diagnosis and Management. Philadelphia, PA: Lippincott Williams & Wilkins; 2010.