Drop attacks

splash-water-1362224788t1gMedical 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.

Hemodynamic ischemia

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.

Movement disorders

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.

Negative myoclonus

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.

(Cranio-)Cervical dysfunction

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


Roughly each one to two years, a new antiepileptic is introduced. Since only about half of them actually survives the academic (Pregabalin) and the economic (Trobalt) scrutiny of time, it might be too early to study those drugs before they have become established. On the other hand, we might be confronted with any of those drugs and then hard-pressed to decide whether to continue them or not in, say, status therapy. So we discuss the one scenario in which perampanel has actually been investigated (add-on therapy in focal epilepsy), think about how AEDs are escalated in general and then use the drug information as well as a recent article to understand possible places for this new drug in our approach to epilepsy (and maybe status). This all with the caveat that Fycompa might actually be turned down by the GBA (a german institution that regulates reimbursement). 

Status therapy

As with many neurocritical care topics, there is no big evidence for status therapy, which is why the various guidelines differ dramatically, if only in the dose of drugs to be used. Since the german guidelines have just been released (though not online yet – hate them for it), it is time to review the basic steps (all the following is for Germany, only):

  • Status is when seizures take longer than 5 minutes (all guidelines agree on this, all original papers use different definitions)
  • If in doubt, give Thiamine 100 mg, Glucose (say 2-4 ampules of 40% dextrose) and (this is my personal recommendation and not really the guidelines) an ampule of Mg.
  • Monitor and ensure monitoring.
  • Make sure that an adequate dose of benzoshas been given
    • Lorazepam is preferred (0,05 mg/kg, at most twice)
    • Diazepam is mostly used by the Notarzt, because it needn’t be cooled – 0,15 mg/kg < 10 mg, at most twice
    • Midazolam 0,2 mg/kg can be given im or buccaly or any other way
  • If this fails, hit them with a non-sedating antiepileptic
    • Valproate 20-30 mg/kg (may be repeated with 10 mg/kg after 10 min) with 10mg/kg/min (an ampule of 300 mg a minute is ok)
    • Phenytoin 20 mg/kg (may be repeated with 10 mg/kg) with only 50 mg/min (which is why we rarely use it – takes over half an hour to be completed)
    • Levetiracetam 30-60 mg/kg (may be repeated full dose after 10 min)
    • Lacosamid is offered as an option with 5 mg/kg over 15 mins (too slow for my taste)
  • Next step, narcotic anticonvulsants(intubate, EEG controlled – Burst suppression)
    • Midazolam bolus 0,2 mg/kg, continuous infusion with 0,1-0,5 mg/kg/h
    • Disoprivan bolus 2 mg/kg, continuous infusion with 4-10 mg/kg/h
    • Thiopental bolus 5 mg/kg, continuous infusion with 3-7 mg/kg/h

All this should happen in less than an hour in the case of generalized or complex partial convulsive status epilepticus.
For non-convulsive, things go a bit slower, preferably with less sedating agents and without intubation, if possible.
Personally I often omit step 1 if the beginning of status lies back more than 15 mins (as usually is the case in the ER) as benzos probably don’t work so well then (due to internalization of GABA_A-receptors).

As last resort, our guidelines offer the following

  • Ketamine (good idea because of Glutamate antagonism) bolus of about 1 mg/kg, then 0,3-5,8 mg/kg/h
  • Magnesium
  • Lidocaine bolus 1-2 mg/kg, 1-4 mg/kg/h
  • Dexamethasone (how much?)
  • Sevoflurane and other inhalational anaesthetics


Juvenile myoclonic epilepsy

Starting with a 19 yo patient with first ever generalized tonic clonic seizure in bed we discuss the management of first seizure, why it is necessary to perform an EEG early even if a possible trigger can be found and why idiopathic generalized epilepsy can still manifest first in more adult patients. It is actually quite hard to find good data about adults with generalized epilepsy, but some original research points out that quite a few of them can first manifest in higher ages – up to 75 years in small series.

Treatment is slowly changing, now that Levetiracetam is becoming a first line drug in idiopathic generalized epilepsy and there is also Zonisamide which proved efficacy in small series; otherwise valproate, lamotrigine and topiramate remain.

As for reviews, I found this, yet any good book on epilepsy does the job.


We do learn a lot about new inventions such as Zebinix, Trobalt and Lyrica, yet nearly forgot the age old knowledge about the good ole antiepileptic drugs, such as Carbamazepine and Valproate. We recapitulate the history of CBZ’s development, the chemical peculiarities (it is an oligocyclic with all the problems of tricyclic agents), pharmacokinetics and practical aspects. Did you know that most of the pharmacodynamics of CBZ is not really well understood – except perhaps for its Na-channel modifications?

As for literature, I am hard pressed. Most of my knowledge stems from standard textbooks, such as Engel’s textbook.

Epilepsy versus Pregnancy

Starting with a 30 yo patient that developed a protracted seizure as first manifestation of a frontal brain injury induced symptomatic epilepsy that clearly states her wish of becoming pregnant eventually we discuss the interaction between child, mother and epilepsy as well as detailed data on the various AEDs for pregnancy:

  • What the AEDs do to the fetus (neural tube defects, delayed development, …)
  • What the pregnancy does to AEDs (necessity to increase LTG and so on)
  • What delivery does to epilepsy
  • What is it with breastfeeding on AEDs?

We use this brilliant recent article available on medscape:

  • Managing Epilepsy in Pregnancy. Expert Reviews in Obstetrics and Gynecology. 2011