Medical terminology knows 5 reasons for people to fall unaided: common fall, syncope, collapse, seizure and drop attack.
A drop attack consist of the loss of lower extremity tone, leading to collapse, but decidedly without disturbance of consciousness (as opposed to syncopes) and without accompanying neurological or other signs or symptoms, in particular without dizziness or faintness, diplopia etc. Peculiarly, the attacks occur while walking, not standing or sitting. They seem to be quite prevalent, constituting a significant percentage of falls in the elderly.
The concept of drop attacks is very old and yet, there is not much published about it. As far as I got in my literature review, a 1986 series in Neurology has the most modern data (an astonishing 108 patients!). Apart from that you have to work through case reports and chapters in neurology textbooks, such as Neurological Differential Diagnosis – a cased-based approach.
The prototypical patient is a woman over forty who reports falling forward while hurriedly walking on the pavement, as if someone had pushed her, without warning, the legs giving way. She might even have injured herself. Once down, she could get up again after a few seconds, without feeling dizzy, nauseus or unsteady.
The differential diagnosis is huge, since so many diseases have been associated with drop attacks, and in some cases falsely so.
Take vertebrobasilar ischemia, for instance. Before the advent of MRI and CTA, many anomalies in the posterior circulation were interpreted as evidence of pathology, such as hypoplastic posterior communicating arteries, asymmetry of one vertebral artery or hypoplastic V4 segments. In practice, it seems to be nearly impossible to get isolated drop attacks (without vertigo!) from a hemodynamic basilar compromise. In a series of 83 proven basilar artery occlusions from basilar stenoses, prodromi included “drop attacks” in only 4 cases and these were accompanied by vertigo in 3 (Ferbert, Stroke 1990). Similarly rare, yet pathophysiologically more reasonable, is the case of a high grade carotid artery stenosis with contralateral hypoplastic A1-segment – when the compromised ICA supplies both anterior cerebral arteries.
It is interesting to note that the stroke rate of people with drop attacks was not increased as compared to age-matched controls in the 1986 series.
Systemic hypoperfusion (aka syncope without dizziness)
The classical mechanisms of syncope (orthostatic, neurocardiogenic etc., aortic stenosis) practically always lead to disturbance of consciousness or at least dizziness. There is just one exception: rhythmogenic drop attacks (Adam-Stokes attacks). In the above mentioned case series this constituted a sizable percentage (13%). Although I would think that a careful reevaluation reduce that number considerably, I concede that an event recorder is a reasonable investment for recurring drop attacks, not the least, because the gadgets have become so simple to implant.
A special case is carotid hypersensitivity syndrome, where a vagal mechanism due to head rotation or local pressure is usually hypothesized. To be honest, I haven’t seen many cases of this, despite the fact that I am working in a neurovascular lab much of my spare time, so it can’t be that frequent.
Atonic (or astatic) seizures are well-known phenomena in pediatric neurology, arising in Lennox-Gastaut-syndrome, Doose syndrome and other epilepsies. It is rare as a manifestation of adult onset epilepsy, all the less in the elderly, yet the classical temporal lobe epilepsy can lead to temporal lobe syncopes or temporal lobe drop attacks in this age group as in any.
In these modern times of weird autoimmune encephalitis variants, LGI1-antibody encephalitis has been reported to cause drop attacks even before it’s more typical facio-brachio-crural dystonic seizures.
In (advanced) Parkinson’s you can be attacked by drops, usually with polypharmacy and fluctuating clinical course (on/off phenomena, freezing). Patients with Progressive Supranuclear Palsy tend to fall backward rather than forward, yet this can be described as a drop attack as well. Both diseases should present with clinical hints at the movement disorder.
Paroxysmal kinesiogenic dystonia has been proposed as an imitator of epilepsy and you could assume that this can lead to drop attacks as well, although I could not find a case report of this. At any rate of occurrence, a family history should help.
This can be an expression of epilepsy (particularly, if focal as in benign partial epilepsy, see above) or a more generalized encephalopathy such as hepatic or toxic, leading to Asterixis (think of Pregabalin, Oxcarbazepine and toxic doses of any central acting drug). History, a hunt for the “flapping tremor” and lab works should rule this out.
Vestibular drop attacks
An acute and temporary disturbance in otolith function can lead to drop attacks. This has been eponymized by Tumarkin who coined the term otolith crisis in the thirties. The attacks are not the correlate of an acute Meniere’s endolymphatic hydrops, but due to unstable otolith function. In contrast to most other drop attacks there ought to be a sensation of vertigo, i.e., of movement of the outer world, yet only few patients can actually report this.
Theoretically, other vestibular disorders, in particular superior canal dehiscence syndrome, should be able to provoke vestibular drop attacks as well, yet there are no case reports.
Quite a few diseases of the cervical myelon and the craniocervical junction can lead to temporary compression or dysfunction of either the pyramidal tract or the dorsal column afferent fibres, thus leading to either loss of tone or loss of feeling in the legs, hence the drop attack.
- Posterior fossa tumors
- Subacute combined degeneration (Vitamin B12)
- Chiari Type I
- Cervical spinal canal stenosis and other causes of cord compression
Other rare causes
- Third ventricle tumors (colloid cyst, pineal cyst) – usually with postural headache
- Isolated cataplexy as an abortive variant of narcolepsy
- Coffin-Lowry-syndrome – stimulus-induced drop events