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Drop attacks
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Drop attacks
Contributors
Douglas J Lanska MD MS MSPH, contributing editor. Dr. Lanska of the Great
Lakes VA Healthcare System at the VA Medical Center in Tomah, Wisconsin, has
no relevant financial relationships to disclose.
Publication dates
Originally released December 28, 2004; last updated March 6, 2014; expires
March 6, 2017
Folder Path
Neurology > Neuro-otology
> Drop attacks
Quick Reference
Sections of Summary
- Historical note and
nomenclature
- Clinical manifestations
- Clinical vignette
- Localization
- Pathophysiology
- Differential diagnosis
Key points
• Drop attacks are sudden falls without loss of consciousness that are not
precipitated by a specific stimulus, occur with abrupt onset and without warning,
and are followed by a rapid return to baseline.
• The term “drop attack” has subsequently been used to encompass a wide
variety of sudden falls with or without existing conditions known to increase the
risk of falls, with or without provocation by a specific stimulus, with or without
loss of consciousness, and with or without significant baseline abnormalities.
• A range of localizations for drop attacks is possible, but most commonly lower
brainstem or spinal cord structures are implicated.
• Drop attacks generally indicate transient impairment of bilateral central
nervous system structures involved in maintenance of postural muscle tone and
balance.
• Tumarkin otolithic catastrophes (or crises) are drop attacks without
associated autonomic or neurologic symptoms in patients with severe vestibular
disease, usually due to Ménière disease.
- Diagnostic workup
- Prognosis and
complications
- Management
Supplemental Content
- Associated disorders
- Related summaries
- Differential diagnosis
- Demographics
References
- References cited
Web Resources
Guidelines
- AAN: Assessing Patients in
a Neurology Practice for
Risk of Falls
- NICE: Epilepsy (U.K.)
Historical note and nomenclature
Drop attacks are sudden falls without loss of consciousness that are not
precipitated by a specific stimulus, occur with abrupt onset and without warning,
and are followed by a rapid return to baseline (Sheldon 1960). Initially these
events were described in otherwise healthy elderly people (Sheldon 1960), but
the term “drop attack” has subsequently been used to encompass a wide variety
of sudden falls with or without existing conditions known to increase the risk of
falls, with or without provocation by a specific stimulus, with or without loss of
consciousness, and with or without significant baseline abnormalities. For the
purposes of this chapter, drop attacks do not include so-called epileptic “drop
attacks” or other seizure-related falls (Rathore et al 2007; Abd-El-Barr et al
2010), presyncope or syncope, stimulus-sensitive loss of muscular tone, or falls
in patients with marked nonparoxysmal leg weakness, ataxia, postural instability
(eg, Parkinson disease, progressive supranuclear palsy), or sensory loss.
- AAN: Epilepsy
Clinical Trials
- NIH: Epilepsy
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Clinical manifestations
Table 1. Clinical Criteria for Drop Attacks
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Sudden falls while standing or walking
Onset
• abrupt
• no aura or warning
• not provoked by specific stimulus
Event
• brief (seconds to a few minutes)
• no loss of consciousness
• no evidence of seizure (eg, tonic or clonic activity)
• may be accompanied by transient neurologic signs and symptoms
Post-event
• fully alert
• not confused
• rapidly returns to baseline
• may have transient difficulty standing
Baseline
• no severe leg weakness, ataxia, postural instability, or sensory loss
Tumarkin's otolithic catastrophes (or crises) are drop attacks without associated
autonomic or neurologic symptoms in patients with severe vestibular disease,
usually due to Ménière disease (Tumarkin 1936; Black et al 1982; Janzen and
Russell 1988; Odkvist and Bergenius 1988; Baloh et al 1990; Ishiyama et al
2001; 2003; Kentala et al 2001; Lee et al 2005; Timmer et al 2006; Ozeki et al
2008; Perez-Fernandez et al 2010; Huang and Young 2012). Rarely vestibular
drop attacks may be the presenting sign of Ménière disease (Baloh et al 1990).
Patients frequently report the sensation of being pushed, thrown, or knocked to
the ground (Tumarkin 1936; Baloh et al 1990; Ishiyama et al 2003). Many have
a subjective tilt of the environment concurrently with the fall (Ishiyama et al
2003). Although occurring in patients with Ménière disease, vestibular drop
attacks are not generally associated with the simultaneous occurrence of
symptoms of typical attacks of Ménière disease (ie, aural fullness, tinnitus,
fluctuating hearing loss, or vertigo) (Tumarkin 1936). Patients with vestibular
drop attacks can stand up immediately after a fall, whereas patients with drop
attacks from other causes may require several minutes to stand independently.
Similar events may occur in patients without Ménière syndrome, but with a
personal and family history of migraine and with typical migraine triggers for
their drop attacks (eg, alcohol, lack of sleep, emotional stress, and menses) (Lee
et al 2000; Ishiyama et al 2003). Patients with Ménière disease who develop
Tumarkin attacks are more disabled, have more severely impaired hearing in the
asymptomatic ear, especially at low frequencies, and experience autonomic
symptoms that are more severe and more frequent than those without Tumarkin
attacks (Perez-Fernandez et al 2010).
Clinical vignette
A 70-year-old man presented with drop attacks (Ishiyama et al 2001). The
events occurred without warning and were characterized by a feeling of being
pushed to the left with sudden loss of postural tone and abrupt falls, but no loss
of consciousness, no associated focal neurologic findings, and no residual
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weakness. He had 4 falls over the previous year. He had a 2-year history of
recurrent vertigo several times a week, lasting from 10 minutes to several hours,
but without meeting criteria for Ménière syndrome (ie, no aural fullness, change
in tinnitus, or fluctuation in hearing loss accompanying the vertigo). He also had
a history of (sudden?) profound right-sided hearing loss 8 years previously.
Neurologic examination, MRI with gadolinium, carotid ultrasound, and
electroencephalography were unrevealing. A presumptive diagnosis of atonic
seizures was made, but there was no improvement after treatment with
phenytoin. Audiograms demonstrated a profound right-sided sensorineural
hearing loss, and caloric testing demonstrated a complete right caloric paresis. A
presumptive diagnosis of “vestibular Ménière disease” was apparently made and
he was treated with a low-salt diet and diuretics without benefit. He ultimately
underwent a right transmastoid labyrinthectomy and was able to walk unassisted
by 3 weeks after surgery. He remained free of vertigo and drop attacks 3 years
after surgery.
Localization
A range of localizations for drop attacks is possible, but most commonly lower
brainstem or spinal cord structures are implicated. In patients with Ménière
disease, vestibular drop attacks (Tumarkin's “otolithic catastrophes”) probably
result from mechanical deformation of the otolithic membrane of the utricle or
saccule (Tumarkin 1936; Baloh et al 1990; Timmer et al 2006; Huang and Young
2012). Less commonly, hemispheric motor outflow tracts (eg, acute
hydrocephalus with third ventricular cysts, or bilateral anterior cerebral artery
ischemia) have been implicated. Transient dysfunction of these areas can disrupt
muscle tone bilaterally without affecting consciousness.
Pathophysiology
Drop attacks generally indicate transient impairment of bilateral central nervous
system structures involved in maintenance of postural muscle tone and balance.
In patients with cryptogenic drop attacks, a delay in long-loop (transcortical)
reflexes may produce inadequately rapid adjustments in postural tone to
maintain the erect posture under certain circumstances (Greenwood and Hopkins
1982).
Differential diagnosis
Conditions that may cause drop attacks include cervical cord compression,
including foramen magnum lesions (Maurice-Williams 1974; Straus et al 2009);
vertebrobasilar ischemia (Kameyama 1965; Brust et al 1979; Welsh et al 2004);
inner ear disorders (eg, Ménière disease and likely migrainous vertigo)
(Tumarkin 1936; Black et al 1982; Janzen and Russell 1988; Odkvist and
Bergenius 1988; Baloh et al 1990; Lee et al 2000; 2005; Ishiyama et al 2001;
2003; Kentala et al 2001; Brantberg et al 2005; Huang and Young 2012);
hydrocephalus and intraventricular tumors (Criscuolo and Symon 1986; Pollack
et al 1995; Kumar et al 2010); posterior fossa lesions (Lee et al 1994);
subclavian steal syndrome (Osiro et al 2012); and reportedly myxedema
(Kramer and Achiron 1993).
In elderly patients with sudden falls and presumed drop attacks, the absence of
a history of loss of consciousness is unreliable (Dey et al 1997). More than two
thirds of such patients are in fact found to have forms of cardiovascular syncope,
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including carotid sinus syndrome, orthostatic hypotension, and vasovagal
syncope (Dey et al 1997). Other causes in elderly patients include vestibular
disorders (Lee et al 2005) and cerebrovascular disorders.
Drop attacks due to vertebrobasilar insufficiency are typically accompanied by
other event-related neurologic manifestations (eg, visual loss, diplopia, vertigo,
numbness, etc.) in addition to the sudden loss of postural tone in the legs, but
rarely cases of sudden unexpected falls without associated clinical manifestations
are attributable to vertebrobasilar insufficiency (Brust et al 1979). Drop attacks
have often been attributed to vertebrobasilar insufficiency without sufficient
clinical support, making some authorities question the role of vertebrobasilar
insufficiency as a common cause of drop attacks; however, a large proportion of
older individuals with drop attacks have multiple areas of arterial occlusion,
stenosis, or hypoplasia in the regional hindbrain circulation (Welsh et al 2004).
Cryptogenic drop attacks are relatively common, represent a large proportion of
drop attacks in case series, and mainly affect women (Stevens and Matthews
1973). Some of these cases may be due to autoimmune disorders. Drop attacks
have been reported in 2 women with facio-brachio-crural dystonic episodes
associated with antibodies to leucine-rich glioma-inactivated 1, presumably an
autoimmune encephalitis (Maramattom et al 2013). In both cases, prolonged
EEG monitoring and brain MRI studies were normal, and neither responded to
conventional anticonvulsants. One case apparently responded to corticosteroid
treatment with intravenous methylprednisolone, whereas the other improved
spontaneously over 6 months.
Drop attacks can be confused with the falls caused by atonic seizures (Obeid
and Mikati 2007), cataplexy and other stimulus-induced drop episodes,
movement disorders (eg, asterixis, chorea, myoclonus) (Massey et al 1988), and
syncope. In children and young adults, it is important to distinguish spontaneous
drop attacks with preserved consciousness from atonic seizures (with transient
loss of consciousness) and stimulus-induced drop episodes. In older adults, it is
particularly important to distinguish spontaneous drop attacks from syncope (for
which the loss of consciousness may be transient and unrecognized).
The term “epileptic drop attacks” is actually a misnomer as these events are
actually generalized seizures with brief loss of consciousness. So-called epileptic
“drop attacks” occur with myoclonic-atonic seizures (also called astatic or
myoclonic-astatic seizures), Lennox-Gastaut syndrome, or other symptomatic
generalized epilepsies associated with brief rapidly generalized seizures
manifesting transient loss of consciousness and sudden atonic falls without
protective reflexes (Pazzaglia et al 1985; Fukushima et al 1993; Oguni et al
1993; 1997; Gambardella et al 1994; Lin et al 1995; Guerrini et al 1998; Tinuper
et al 1998; Maehara and Shimizu 2001; Rathore et al 2007). The loss of muscle
tone is brief and may include head drop, jaw droop, dropping of a limb, or loss of
all muscle tone and a fall (often with resulting head and facial injuries). Epileptic
“drop attacks” occur most commonly in young children but may begin in
adolescence and rarely in adults. Such epileptic falls are physically dangerous
and are often refractory to medical and surgical therapy. Interictal
electroencephalograms are usually abnormal and may include slow spike-wave
complexes, rhythmic slow activity, polyspike and wave activity, temporal or
frontal spikes, and bilateral synchronous spike activity during sleep.
Stimulus-induced sudden loss of muscular tone occurs most commonly as
cataplexy in patients with narcolepsy (OMIM #161400, #605841, and #609039),
but can also occur as a mono-symptomatic familial disorder (Gelardi and Brown
1967), and in certain degenerative conditions, such as Niemann-Pick type C
disease (Turpin et al 1991; Zafeiriou et al 2003) and Coffin-Lowry syndrome
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(Fryns and Smeets 1998; Nakamura et al 1998; Freesia et al 2002;Grau et al
2003; Nelson and Hahn 2003; Vankova et al 2003), and in certain uncommon
stimulus-sensitive reflex syncopes, such as stretch syncope (Sarrigiannis et al
2011). Cataplexy is often triggered by laughter, but can be triggered by surprise,
anger, or other emotional stimuli. Consciousness is retained but the patient loses
muscular tone with somewhat variable motor manifestations ranging from
complete postural collapse with a fall to relatively mild weakness with head
droop, jaw drop, and buckling of the knees. The duration of hypotonia in
cataplexy ranges from several seconds to several minutes, and recovery is
complete.
In patients with narcolepsy, cataplexy occurs as part of a constellation of
manifestations that include excess sleepiness, sleep attacks, hypnagogic and
hypnopompic hallucinations, and sleep paralysis. Although not all of the classic
features of narcolepsy may be present in all patients, cataplexy rarely precedes
the onset of hypersomnolence. About two thirds of patients with narcolepsy as
associated with cataplexy.
Niemann-Pick type C disease (OMIM #257220 and #607625) is an autosomal
recessive disorder with highly variable clinical manifestations and age of onset.
Onset of neurologic signs may be from infancy through adulthood, but is rare
after the age of 30 (Lanska and Lanska 1993). Clinical features may include
cataplexy as well as abnormal behavior, developmental delay, dementia,
psychosis, seizures, vertical gaze palsy, dysarthria, dysphagia, dystonia,
myoclonus, spasticity, ataxia, and hepatosplenomegaly (Grau et al 2003;
Vankova et al 2003; Zafeiriou et al 2003). Cataplexy occurs most commonly in
the juvenile forms, but may also occur in adults (Turpin et al 1991). Bone
marrow examination shows sea-blue histiocytes and may show foam cells, which
contain polymorphic cytoplasmic inclusions. Cholesterol esterification studies
show accumulation of unesterified cholesterol in lysosomes and low intracellular
esterification of exogenously supplied lipoprotein-derived cholesterol in cultured
fibroblasts (Lanska and Lanska 1993). Niemann-Pick type C disease should be
considered when progressive neurologic symptoms develop with either
organomegaly or a history of nontraumatic splenectomy (Lanska and Lanska
1993).
Coffin-Lowry syndrome (OMIM #303600) is characterized by mental
retardation, small stature, facial dysmorphism, skeletal deformities, and tapering
digits (Coffin et al 1966; Lowry et al 1971; Temtamy et al 1975; Fryns and
Smeets 1998; Nakamura et al 1998; Fryssira et al 2002; Nelson and Hahn
2003). In patients with Coffin-Lowry syndrome, “stimulus-induced drop episodes”
are characterized by sudden loss of muscular tone induced by sensory stimuli,
such as loud noises, visual threat, or unexpected light tactile stimulation (Fryns
and Smeets 1998; Nakamura et al 1998; Freesia et al 2002;Nelson and Hahn
2003). Consciousness is retained, and recovery is immediate. These episodes are
not associated with epileptiform activity on electroencephalography. During
spells, tonic electromyographic activity may be lost (as in cataplexy) or increased
(as in hyperekplexia), even in the same patient (Nelson and Hahn 2003).
Stretch syncope may be difficult to distinguish from epilepsy (Sarrigiannis et al
2011). Episodes are initiated with stretching associated with neck torsion and
breath holding, which may be followed by loss of consciousness and in more
prolonged episodes by asymmetric, recurrent facial and upper limb jerks.
Stretching may be associated with sinus tachycardia, followed by rhythmic
generalized slow wave abnormalities on EEG in attacks with associated
impairment of consciousness. Transcranial doppler studies showed a marked
drop in middle cerebral artery perfusion during the episodes.
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Diagnostic workup
A thorough history and examination are appropriate in patients with presumed
drop attacks, with careful attention in the history to any warning or aura,
precipitating factors (including emotional stimuli), loss of consciousness, or ictal
manifestations. Observations from witnesses can be particularly helpful in
clarifying the features of the episodes and in focusing the differential diagnosis.
Prior cardiovascular disease, palpitations, strokes or transient ischemic attacks,
movement disorders (including Parkinson disease, progressive supranuclear
palsy, myoclonus, ataxia, and asterixis), presyncope or syncope, headaches,
amaurosis, aural fullness, hearing loss, tinnitus, vertigo, cervical
spondyloarthropathy, and any severe orthopedic problems or peripheral vascular
disease involving the legs should be noted. Medications should be thoroughly
reviewed, with particular attention to agents that may precipitate seizures,
orthostatic hypotension, or sedation. Examination should identify any signs of
raised intracranial pressure (including papilledema), evidence of previous
strokes, movement disorders affecting postural tone or producing abnormal
movements of the legs or trunk, myelopathy, ataxia, postural instability, leg
weakness or spasticity, severe sensory loss in the legs, or mechanical/orthopedic
leg dysfunction.
Evaluation should include assessment or orthostatic pulse and blood pressure
(ie, supine, standing, and standing after 3 minutes). Depending on the clinical
circumstances, various studies may be necessary, including electrocardiography,
Holter monitoring, cervical spine imaging, brain imaging, vascular imaging (eg,
Doppler ultrasonography, magnetic resonance angiography, CT angiography, or
traditional angiography), electroencephalography, audiograms,
electronystagmography or video nystagmography, and vestibular evoked
myogenic potential testing.
Prognosis and complications
Injuries are common with drop attacks, because the falls are unexpected, rapid,
with inadequate opportunity for self-protective responses. Long-term prognosis
depends on the underlying condition. Some previous studies of prognosis have
included patients with cardiovascular syncope, epilepsy, and other conditions
that would not meet criteria for true drop attacks. However, such patients are
labeled, those with baseline significant neurologic findings, cardiac arrhythmias,
and congestive heart failure have a worse prognosis (Meissner et al 1986).
Patients with an isolated drop attack who have unrevealing medical and
neurologic evaluations have a favorable long-term outcome (Meissner et al
1986).
Management
With a varied constellation of causes, no single therapy is appropriate for all
drop attacks. Therapy is instead directed at treatment of the underlying cause.
Treatment is not generally indicated for individuals with an isolated drop attack
and unrevealing medical and neurologic evaluations (Meissner et al 1986).
Some authorities advocate conservative management of otolithic crises,
particularly given that many cases have a flurry of episodes followed by
remission (Janzen and Russel 1988; Baloh et al 1990). However, the events can
be associated with significant injuries and for some patients the attacks are so
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dangerous or intractable that surgery is indicated (Baloh et al 1990). Otolithic
crises have been treated successfully with either surgical ablation
(labyrinthectomy) or trans-tympanic gentamicin therapy in the absence of
serviceable hearing, or middle fossa vestibular nerve section to preserve
serviceable hearing (Black et al 1982; Odkvist and Bergenius 1988; Ishiyama et
al 2001). Even older patients can be successfully treated with ablative surgery
with excellent compensation and no vertigo or falls up to 10 years after surgery
(Ishiyama et al 2001). Vestibular nerve section is usually recommended only for
patients who have had symptoms for at least 5 years, unless the patient is
severely incapacitated or is in danger of severe bodily harm because of otolithic
crises (Black et al 1982).
In a small series of 10 patients, surgical decompression of Chiari I malformation
had a high success rate (70%) for clinical improvement in patients with drop
attacks (Straus et al 2009). Tilt table testing had poor predictive value in judging
the clinical response to surgical decompression and was useful in guiding surgical
decision- making.
A cardiac pacemaker has been anecdotally reported to resolve drop attacks
associated with ictal asystole in a patient with partial complex seizures (Zubair et
al 2009).
Miglustat, a reversible inhibitor of the enzyme glucosylceramide synthase, has
been anecdotally reported to resolve secondary cataplexy after 6 months of use
in a patient with Niemann-Pick disease type C (Zarowski et al 2011).
In patients with repeated falls, steps should be taken to minimize the risk of
injury. Clinicians should discuss and address modifiable risk factors for fractures
(as appropriate to the clinical situation):
• Excess alcohol intake (more than 2 drinks a day)
• Cigarette smoking
• Frail body habitus (weight less than 127 pounds or body mass index less than
20)
• Inadequate diet
• Estrogen deficiency
• Impaired eyesight
• Medications that facilitate development of osteomalacia (eg, phenytoin)
• Unsafe footwear (heels more than a quarter inch; loose heels; strap sandals;
smooth, hard soles; etc.)
• Sedentary lifestyle
• Home safety concerns (loose rugs, uneven surfaces, inadequate grab rails in
the bath tub, etc.)
Older adults, particularly those with falls, should undergo assessment of bone
mineral density by dual energy x-ray absorptiometry (DEXA) of the distal
forearm, lumbar spine, and proximal femur. Screening DEXA scans of the heels
can also be informative, but the results of heel DEXA studies do not correlate
perfectly with DEXA studies of the areas most likely to be fractured with falls (ie,
the wrist and femoral neck). According to World Health Organization criteria, Tscores above -1 are normal, T-scores between -1 and -2.5 indicate osteopenia
and a moderately increased risk of fracture, and T-scores below -2.5 are
indicative of osteoporosis (or severe osteomalacia) and a severely increased risk
of fracture. Significantly abnormal values (ie, generally T-scores less than -1.5 in
the presence of other risk factors for osteoporosis or falls with injury, or less
than -2.0 in the absence of other risk factors) should generally be managed with
calcium and vitamin D supplementation, and bisphosphonate therapy (eg,
alendronate).
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Associated disorders
None identified
Related summaries
Atonic seizures
Lennox-Gastaut syndrome
Neurocardiogenic syncope
Syncope
West syndrome
Differential diagnosis
cervical cord compression
foramen magnum lesions
vertebrobasilar ischemia
inner ear disorders
Ménière disease
migrainous vertigo
hydrocephalus
intraventricular tumors
posterior fossa lesions
myxedema
cardiovascular syncope
carotid sinus syndrome
orthostatic hypotension
vasovagal syncope
vertebrobasilar insufficiency
visual loss
diplopia
vertigo
vertebrobasilar insufficiency
multiple areas of arterial occlusion
stenosis
hypoplasia in the regional hindbrain circulation
falls caused by atonic seizures
cataplexy
other stimulus-induced drop episodes
movement disorders
asterixis
chorea
myoclonus
preserved consciousness from atonic seizures (with transient loss of
consciousness)
stimulus-induced drop episodes
syncope (for which the loss of consciousness may be transient and unrecognized)
generalized seizures with brief loss of consciousness
myoclonic-atonic seizures
astatic or myoclonic-astatic seizures
Lennox-Gastaut syndrome
stimulus-induced sudden loss of muscular tone
cataplexy
mono-symptomatic familial disorder
Niemann-Pick type C disease
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Coffin-Lowry syndrome
narcolepsy
excess sleepiness
sleep attacks
hypnagogic
hypnopompic hallucinations
sleep paralysis
organomegaly
nontraumatic splenectomy
stimulus-induced drop episodes
hyperekplexia
Demographics
For more specific demographic information, see the Epidemiology, Etiology, and
Pathogenesis and pathophysiology sections of this clinical summary.
Age
02-05 years
06-12 years
13-18 years
19-44 years
45-64 years
65+ years
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