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:

A sharp wave originating in the motor cortex precedes a sudden burst of EMG silence lasting 35-200 ms
This interruption causes the antigravity muscles to briefly lose tone
Gravity (or muscle elasticity) produces a sudden downward movement - the "flap"
The patient then corrects the position, sometimes with overshoot
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:

Cause	Context
Hepatic encephalopathy	Most classic; "liver flap"
Uremia (uremic encephalopathy)	CKD/AKI - accompanies fine tremor, myoclonus, hyperreflexia
Hypercapnia	Type 2 respiratory failure, CO2 narcosis
Drug toxicity	Phenytoin, other antiepileptics at toxic levels; some antibiotics; metoclopramide; phenothiazines; gabapentin; opioids (especially meperidine in CKD)
Metabolic acidosis	Indistinguishable encephalopathy
Alcohol	In context of ALD and hepatic failure
Wilson's disease / other metabolic	When 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):

Grade	Features
I	Sleep reversal, mild confusion, irritability, tremor, asterixis
II	Lethargy, disorientation, inappropriate behavior, asterixis
III	Somnolence, severe confusion, aggressive behavior, asterixis
IV	Coma - 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

Feature	Asterixis	Tremor	Myoclonus
Mechanism	EMG silence (negative)	Rhythmic oscillation	Brief muscle contraction (positive)
Rhythm	Arrhythmic	Rhythmic	Arrhythmic
Provoked by	Sustained posture	Posture/rest/action	Action/stimulus
Context	Metabolic encephalopathy	Essential, 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

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

This is a shared conversation. Sign in to Orris to start your own chat.