Flapping tremor

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Flapping tremor (asterixis) is a coarse, irregular, non-rhythmic tremor caused by brief lapses in sustained posture, classically seen in hepatic encephalopathy. Now searching the medical library for detailed content.
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Flapping Tremor (Asterixis)

Definition and Nomenclature

Asterixis (from the Greek a- = without, sterixis = fixed position) is the correct term for what is clinically called "flapping tremor." The name is somewhat misleading - it is not a true tremor (which requires rhythmic oscillation), but rather a negative myoclonus: a sudden, brief, arrhythmic lapse in sustained posture caused by involuntary interruption of muscle contraction.
  • In hepatic failure, it is also called the "liver flap"
  • Adams and Foley first described it in patients with hepatic encephalopathy
"Asterixis differs physiologically from both tremor and myoclonus... it had incorrectly been referred to as a 'negative tremor' or 'negative myoclonus.'" - Adams and Victor's Principles of Neurology, 12e

Pathophysiology

The underlying mechanism involves a cortically generated event:
  1. A sharp wave originating in the motor cortex precedes a sudden burst of EMG silence lasting 35-200 ms
  2. This interruption causes the antigravity muscles to briefly lose tone
  3. Gravity (or muscle elasticity) produces a sudden downward movement - the "flap"
  4. The patient then corrects the position, sometimes with overshoot
  5. This cycle repeats arrhythmically, once or several times per minute
This distinguishes it from:
  • True tremor: rhythmic oscillation from alternating agonist/antagonist contractions
  • Myoclonus: brief jerk from active muscle contraction (asterixis is the opposite - from inhibition)
  • Adams and Victor's Principles of Neurology, 12e

How to Elicit (Clinical Examination)

The classic test:
  • Ask the patient to hold arms outstretched with wrists dorsiflexed (hands extended, fingers spread) for 15-30 seconds
  • Alternatively: rest forearms on bed/chair arms and dorsiflex the hands
  • Observe for irregular, arrhythmic downward flapping movements of the hands/wrists
Other methods:
  • Ask patient to protude the tongue - it darts in and out
  • Ask patient to close the eyelids - irregular fluttering
  • Ask patient to hold flexed trunk muscles
  • Place hand flat on table and raise the index finger
  • In unresponsive patients: hip flexion-abduction against gravity (hip adductors contract, asterixis becomes prominent)
  • Adams and Victor's Principles of Neurology, 12e; Localization in Clinical Neurology, 8e

Causes

Asterixis is a marker of metabolic or toxic encephalopathy - it is not specific to any single cause.

Classic Causes:

CauseContext
Hepatic encephalopathyMost classic; "liver flap"
Uremia (uremic encephalopathy)CKD/AKI - accompanies fine tremor, myoclonus, hyperreflexia
HypercapniaType 2 respiratory failure, CO2 narcosis
Drug toxicityPhenytoin, other antiepileptics at toxic levels; some antibiotics; metoclopramide; phenothiazines; gabapentin; opioids (especially meperidine in CKD)
Metabolic acidosisIndistinguishable encephalopathy
AlcoholIn context of ALD and hepatic failure
Wilson's disease / other metabolicWhen encephalopathic

Focal/Structural (Unilateral Asterixis):

Unilateral asterixis (affecting arm and leg on one side) localizes to a contralateral structural lesion:
  • Anterior thalamic infarction or small hemorrhage (most common)
  • Frontal lobe lesion (ACA infarction)
  • Upper midbrain lesion
  • Parietal lobe lesion
  • Post-stereotaxic thalamotomy
  • Usually transient after stroke
  • Adams and Victor's Principles of Neurology, 12e; Localization in Clinical Neurology, 8e

Asterixis in Hepatic Encephalopathy (Most Important Context)

Hepatic encephalopathy is graded as follows (West Haven Criteria):
GradeFeatures
ISleep reversal, mild confusion, irritability, tremor, asterixis
IILethargy, disorientation, inappropriate behavior, asterixis
IIISomnolence, severe confusion, aggressive behavior, asterixis
IVComa - asterixis absent (wanes as coma deepens)
Key teaching point: Asterixis is present in grades I-III but disappears in grade IV coma - it requires some degree of voluntary muscle contraction to be present.
EEG in hepatic encephalopathy shows slow, high-amplitude triphasic waves.
  • The Washington Manual of Medical Therapeutics

Precipitating Factors for Hepatic Encephalopathy:

  • GI bleeding (nitrogen load)
  • Infection/sepsis
  • Constipation, high-protein diet
  • Diuretics (hypokalemia, alkalosis)
  • Opioids or sedatives
  • Azotemia / dehydration
  • Medication non-compliance (lactulose)
  • TIPS / portosystemic shunts
  • Progressive hepatocellular dysfunction

Key Differentials

FeatureAsterixisTremorMyoclonus
MechanismEMG silence (negative)Rhythmic oscillationBrief muscle contraction (positive)
RhythmArrhythmicRhythmicArrhythmic
Provoked bySustained posturePosture/rest/actionAction/stimulus
ContextMetabolic encephalopathyEssential, Parkinson's, etc.Anoxic injury, epilepsy
When mild and low-amplitude, asterixis can resemble 5-6 Hz postural tremor - EMG helps differentiate. - Bradley and Daroff's Neurology in Clinical Practice

Uremic Encephalopathy Context

In CKD/uremic encephalopathy, asterixis accompanies:
  • Fine action tremor
  • Myoclonus
  • Hyperreflexia
The distinction between asterixis and myoclonus in uremia is less clinically important than identifying the metabolic cause, as both can coexist in toxic-metabolic encephalopathy. - Comprehensive Clinical Nephrology, 7e

Summary Points

  1. Flapping tremor = asterixis = negative myoclonus - not a true tremor
  2. Mechanism: cortical sharp wave → 35-200 ms EMG silence → gravity pulls limb down → correction → repeated arrhythmically
  3. Elicited by: wrists extended, arms outstretched (hold 30 seconds)
  4. Most classic cause: hepatic encephalopathy (liver flap) - but seen in any metabolic/toxic encephalopathy
  5. Other causes: uremia, hypercapnia, drug toxicity (antiepileptics, antibiotics, opioids)
  6. Unilateral asterixis → contralateral structural lesion (most often thalamic stroke)
  7. Present in hepatic encephalopathy grades I-III; absent in grade IV coma
  8. EEG in hepatic encephalopathy: triphasic waves
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