1. ELSEVIER
Inhibitory Motor Status: Two New Cases and a Review
of Inhibitory Motor Seizures
Ross Fine Smith, Orrin Devinsky, and Daniel Luciano
Transient paralysis is an uncommon seizure symptom. We report two new
cases of inhibitory motor status and review 24 previously cases of inhibitory
seizures. Among the 22 adult patients, 14 (64%) had a frontoparietal lesion
(tumor, 7; stroke, 7); 5 (23%) had mesiotemporal sclerosis (MTS), and 3 (14%)
had no identified lesion. In contrast, all 4 pediatric patients had no identified
brain lesions. Inhibitory motor seizures were associated most commonly with
lesions in frontoparietal primary and supplementary motor-sensory area and,
less often, in the mesial temporal lobe. Inhibitory motor seizures arising from
frontoparietal foci are often more prolonged (>2-3 min) than those arising
from the mesial temporal area (<1.5 min). Patients with temporal lobe seizure
foci manifest ictal flaccidity of an extremity during a complex partial seizure
(CPS), which may represent motor neglect rather than ictal weakness since
strength cannot be accurately assessed when consciousness is impaired. In-
hibitory motor seizures from sensorimotor cortex seizure foci are probably
more common than is recognized. Key Words: Seizures--Epilepsy--
Inhibition. 9 1997 by Elsevier Science Inc. All rights reserved.
Inhibitory motor seizures are manifested as a
paroxysmal paralysis of the face, arm, leg, or hemi-
body and were first described by Gowers (1) as a
"paroxysmal appearing palsy of an epileptic ori-
gin." Consciousness typically is not impaired, and
full function of the paretic extremity returns. Inhibi-
tory motor seizures have been periodically de-
scribed by a variety of terms, including nonconvul-
sive seizure paralysis (2), hemiparetic seizures (3),
Received February 1, 1996; accepted August 22, 1996.
From the Department of Neurology, New York Uni-
versity School of Medicine, Hospital for Joint Diseases,
New York, NY, U.S.A.
Address correspondence and reprint requests to Dr.
Orrin Devinsky at Department of Neurology, Hospital
for Joint Diseases, School of Medicine, 301 East 17th
Street, New York, NY 10003, U.S.A.
ictal hemiparesis (4,5), ictal paralysis (6,7), and in-
hibitory epilepsy (8-10). Fisher (2) suggested the
following diagnostic criteria: (a) focal paralysis oc-
curring before convulsive movements in a limb, (b)
a similar deficit without convulsive movements, (c)
a convulsive seizure in one limb concomitant with
paralysis in another limb without convulsive move-
ments, (d) paralytic episodes preceding other epi-
leptic seizures, (e) a seizure discharge in the EEG
during the paralytic episodes, (f) episodes of pa-
ralysis in a clinical situation in which a seizure
rather than another type of episode is expected, (9)
episode resolution with antiepileptic drugs (AEDs)
but persistence with other therapeutic measures,
and (h) absence of other conditions accounting for
transient attacks of focal weakness. The mechanism
probably involves an epileptic focus inhibiting de-
J. Epilepsy1997;10:15-21
9 1997by ElsevierScienceInc.All rights reserved.
655 Avenue of the Americas,New York,NY 10010
0896-6974/97/$17.00
Pit 50896-697-t(96)00072-2

2. R. F. SMITH ET AL.
scending motor tracts, rather than stimulating
them, as in convulsive seizures (11).
Although partial seizures with inhibitory motor
phenomena such as speech arrest are not rare
(3,4,6), only sporadic cases and small series of ictal
paralysis of the face, appendicular, or truncal
muscles have been reported. We report two adult
cases exhibiting inhibitory motor seizures mani-
fested as prolonged focal weakness.
tient was given 10 mg intravenous diazepam
(DZP), which resulted in resolution of the semi-
rhythmic activity in 1 rain (Fig. 1B). Within 10 rain
of DZP injection, left upper and lower extremity
strength increased to 3-4/5. Phenytoin (PHT) was
initiated, and at a 3-month follow-up visit, his
strength remained 3--4/5.
Case 2
Case Reports
Case 1
A 25-year-old right-handed man presented with
progressive left hemiparesis I year after resection of
a right frontal astrocytoma and completion of
whole brain radiation and chemotherapy. Postop-
eratively, typical seizures consisted of eye and head
deviation to the left, progressing to left-sided clonic
activity. These occurred approximately once a
week. There was no postictal weakness. Follow-up
computed tomography (CT) scan showed a slight
increase in tumor size with right frontal edema. The
patient developed a complete left hemiplegia over
the course of several days, and the EEG showed
semirhythmic delta activity in the right central re-
gion (Fig. 1A). There was no improvement after the
administration of dexamethasone 20 mg followed
by 6 mg four times daily (q.i.d.) for 3 days. The
hemiplegia had persisted for days before the pa-
A 31-year-old left-handed woman with a recur-
rent left frontoparietal anaplastic astrocytoma was
evaluated for right focal motor seizures. The tumor
was partially resected in 1988, followed by radia-
tion therapy. After initial surgery and radiation, she
continued to have right focal motor seizures begin-
ning in the lower or upper extremity. These sei-
zures did not secondarily generalize. In 1993, sei-
zure frequency increased to three times a week de-
spite supratherapeutic levels of PHT and
therapeutic levels of phenobarbital (PB). She had
previously failed to respond to carbamazepine, val-
proate and primidone. Magnetic resonance imaging
(MRI) scan showed local tumor recurrence. After
debulking surgery, she continued to have right fo-
cal motor seizures, lasting 1-3 min and occurring
two to three times a week. She had a persistent
right-sided hemiparesis (proximal upper extremity
3/5, distal upper extremity 1-2/5, proximal lower
extremity 2-3/5, distal lower extremity 1-2/5). The
hemiparesis was clinically stable for more than 6
weeks. There was a mild worsening in the baseline
FP 1 - F 7
F 7 - T 3
T 3 - 1"5
Ts- 01
FP 2- F s
F~-T,
T4"Ts
FP1 -F7 ~
T 6 - 0 2
FP 1 - F 3
F 3 - T 4
T 4 - T 6
FT-T3
T3-'rs
Ts-O,
F P ~ - F s ~
F 8 - T 4
T,'T s
Te-O 2 ~ ~
FP,-F ~ , . - , . _ . _ ~
F 3 - T4
T,-T~
Figure 1. A: EEG during hendplegia showing right frontotemporal delta activity. B: EEG 20 s after intravenous diazepam
administration showing marked reduction in right-sided delta activity.
16 J EPILEPSY, VOL. 10, NO. 1, 1997

3. right hemiparesis for 15-30 min after simple partial
motor seizures. A trial of dexamethasone (10 mg
intravenously and 4 mg every 6 h for I week) failed
to improve strength. The EEG showed delta and
theta range slowing in the left centroparietal and
temporal regions.
Clobazam (CLB) 10 mg was initiated at night and
PB was reduced by 15 mg at night. Initial improve-
ment was observed the morning after she received
the first bedtime dose. In the next 4 days, her
strength improved to ~4/5 in all right-sided
muscle groups and remained at this functional level
for more than 6 months. She received no glucocor-
ticoids during this period. She remained seizure-
free with PHT, CLB, and reduced PB dose for more
than 6 months.
Literature Review
We reviewed the English language literature to
identify reported cases of inhibitory motor seizures.
The first source was a computerized Medline search
of the years 1978 to 1994 utilizing the following
keywords; epileptic paralysis, ictal hemiparesis,
nonconvulsive seizure, hemiparetic seizure, partial
paralysis, focal inhibitory seizure, unilateral atonic
seizure, and inhibitory motor seizure. Seizure and
hemiplegia were also cross-referenced. The second
source comprised references from previous case re-
ports and our review of more than 40 neurology
and epilepsy texts published before 1950.
Inclusion Criteria
Case reports with insufficient data or phenomena
that did not meet criteria were not reviewed. These
included reports of brief atonia of childhood (12)
and negative myoclonus (6). These episodes re-
quired an antecedent motor stimulus and lasted
only 100-500 ms. In addition, other negative ictal
phenomenon, including ictal-associated sensory
deficits and speech arrest, were not reviewed.
Results
Table I summarizes the characteristics of case re-
ports described in the literature. The two cases in
the current report are included.
Age and Sex
There was no predilection for sex (11 males, 10
females) or age (range 4 months to 79 years), in-
cluding our two cases (ages 25 and 31 years).
INHIBITORY MOTOR STATUS
Clinical Manifestations
All patients developed episodic weakness that
typically lasted 2-30 min and recurred. The weak-
ness usually progressed to paralysis and, after the
seizure, power of the involved extremities returned
to baseline.-Five patients reported an aura of numb-
ness in the involved areas, and two patients re-
ported lightheadedness. In only two previous cases
(Cases 12 and 15) was prolonged weakness re-
ported. Such prolonged ictal episodes constitute in-
hibitory motor status. In Case 12 the symptoms
lasted 14 h, and in Case 15 the symptoms lasted 3
days and did not resolve until DZP was adminis-
tered. The cases we report also manifested inhibi-
tory motor status, which resolved with the admin-
istration of intravenous DZP (in ~10 min) or oral
CLB (improvement in 410 h).
Underlying Disease
The cases reported in the literature and our 2
cases include various neuropathologic lesions. An
etiology was determined in all but 5 of the adult
cases. In 17 of 22 (77%) adult cases, an anatomic
lesion was detected on neuroimaging or autopsy [7
tumor, 5 mesiotemporal sclerosis KMTS),4 stroke].
Three other cases had evidence of at least one pre-
vious stroke and speculated an additional stroke
may have been responsible for the epileptic focus.
EEG Abnormalities
EEG abnormalities were detected in 23 of the 26
(88%) cases. No EEG reported in Case 4. In the 4
pediatric cases, no anatomic lesions were detected
and there was no evidence of underlying disease.
However, all 4 had abnormal EEGs and 2 patients
had abnormal single photon emission computed to-
mography scans that corresponded to the cortically
represented area of the paresis.
Lesion Localization
In 4 of the 7 tumor cases lesion location was re-
ported. All 4 tumors were located in the frontopa-
rietal region. In 3 of the 4 (75%) cases documented
strokes were located in the posterioinferior frontal
area, corresponding to the focal EEG abnormalities.
The 5 cases of MTS were documented by neuro-
pathological examination; 4 were left-sided.
J EPILEPSY,VOL. 10, NO. 1, 1997 17

4. R. F. SMITH ET AL.
~
t~
Q)
0
U-1
I-r.l
g-.
e~
o
o ~ "~
o,.~
Z
o O ~ ~ o ~ o o "~ o "~ U :~[~ ~
o .-~ ~ ~ ~ "~,
~o~ ~ ,- ~ ~ ~ .. ~ ~.
Z
u
cJ
o ~ ~ ~ "~ ~: ~ ~: '~ ~'
~ ~ ~ 0 ~ 0 ~-~ ~ r ~ 0 01-,
~ ,,., ,.~ ~ ~ ~ .~ 0 ~ ~ ~ ~ "~.
~~
~Lr) C',I
u'3 c~
r
0"3 '~
c',l
c,,I o
0
oc~
..-2
",,o
c,.-~
Ob-~ '~ "~
18 ] EPILEPSY, VOL. 10, NO. 1, 1997

5. E
t~
t~
E
~ u
<
0
I-=l
U.I
~=.0 o")
~o~
<
(_)
u
t'-:
u
r~
[--,
0
".~
"~,
.~o
0
U U U O ~
ooog.~
r4~.
o~
9r.~ ~'~
,-..1
== r o
~ ~ o
0 It') ,.~ "~
0
t'N
o~
O
0
,.;_,
e~
0
u
r
~o~
N O~..,
0"~ ~
i,,
.~ ~'~
~r)
0 0 ~
.'d~
P.
INHIBITORY MOTOR STATUS
Discussion
Inhibitory motor seizures have received rela-
tively little attention since their original description
by Gowers in 1881 (1). However, epileptic seizures
that cause negative symptoms are not rare. These
include ietal speech arrest (13-16), amaurosis
(17,18), amnesia (19-21), numbness or deafness (22),
neglect (23), and alien hand syndrome (24). In pa-
tients also experiencing partial motor seizures, the
inhibitory phenomena may be difficult to differen-
tiate from a Todd's paralysis. Such differentiation
requires a detailed history of the events and appro-
priate interpretation of the studies, which makes
evaluation of the other reported cases difficult.
Partial seizures that inhibit motor activity are
rarely reported but should be considered in the dif-
ferential diagnosis of transient weakness. Unlike
other partial seizure symptoms which usually last
less than 3 rain, ictal focal motor inhibition can last
relatively longer, often more than 5 min. The pri-
mary seizure localization associated with inhibition
of appendicular musculature is the frontoparietal
sensorimotor cortex. Such seizures can cause an ic-
tal paralysis that lasts more than 3 min. In contrast,
ictal paralysis associated with video-EEG docu-
mented temporal lobe seizures and pathologically
verified MTS typically lasts less than I rain (14). The
motor inhibition is the primary ictal manifestation
in the frontoparietal foci. In patients with mesio-
temporal foci, impaired consciousness and automa-
tisms are the primary ictal features and flaccidity of
an extremity is often subtle and not reported by the
patient or witnesses. Focal appendicular flaccidity
during complex partial seizures could result from
either active inhibition of motor cortex or areas me-
diating attention to motor (i.e., motor neglect).
In our two cases, the paresis persisted 2 to 42
days, most likely from continuous or intermittent
ictal discharges that directly inhibited motor activ-
ity, with Todd's paralysis or structural defect as
secondary mechanisms. Active inhibition is sup-
ported by the following observations: (a) both pa-
tients responded quickly to an AED; (b) Patient 1
had a documented ictal discharge that responded,
together with the hemiparesis, to intravenous DZP;
(c) weakness did not improve in either patient with
dexamethasone therapy administered before ben-
zodiazepines (BZDs); (d) follow-up neuroimaging
studies in both cases showed no evidence of re-
duced tumor size to account for improved strength;
and (e) no other etiology for change in power was
identified. The improved strength induced with
AED treatment would not be expected if weakness
J EPILEPSY, VOL. 10, NO. 1, 1997 19

6. R.F. SMITH ET AL.
resulted solely from a Todd's paralysis. Further-
more, the rhythmic EEG changes consistent with an
ictal discharge would not be expected to improve
with BZDs if Patient 1 was in a postictal state (i.e.,
Todd's paralysis). In these cases, the focal paresis
appeared to be a manifestation of partial status,
similar to that in the 63-year-old woman reported
by Fisher (2) and the 12-year-old boy reported by
Hanson and Chodos (3).
Both our patients had frontoparietal tumors,
whereas Fisher's case had a left inferior parietal in-
farct on neuropathological examination and no
cause was identified in the case of Hanson and Cho-
dos. The case of Hanson and Chodos predated the
magnetic resonance imaging (MRI) era, however,
and CT scans were not obtained, but the patient did
have an abnormal EEG and ictal [99mTc]-
pertechnetate brain scan. Brain tumors and strokes
have been previously associated with prolonged
partial seizures (25-27). Although weakness of ap-
pendicular and axial muscles has rarely been re-
ported to result from epileptic status, other inhibi-
tory seizure symptoms such as speech arrest and
aphasia are well documented in epileptic status
(13,28,29).
Hanson and Chodos (3) reported increased up-
take on [99mTc]-pertechnetate brain scans during in-
hibitory motor seizures in two patients. After AED
administration, brain scans became normal, epilep-
tiform activity resolved, and strength gradually re-
turned in the paretic limbs, which supports the con-
cept that weakness resulted from an inhibitory mo-
tor seizure; i.e., epileptiform activity reduced motor
strength. In the first case we described, the abnor-
mal EEG consistent with an ictal discharge resolved
with BZD administration and correlated with clini-
cal improvement, which further supports the rela-
tion between the electrophysiological seizure activ-
ity and the paralysis. The right-sided weakness in
the second case also improved shortly after the ad-
ministration of CLB.
Penfield and Jasper (15) reported that electrical
stimulation in the perisylvian language areas and
supplementary motor cortex could cause speech ar-
rest. Furthermore, stimulation of the human premo-
tor cortex could impair the ability to perform spe-
cific voluntary movement or to sustain a voluntary
contraction (30); L/iders et al. noted this defect in 17
of 42 patients undergoing premotor cortical stimu-
lation and suggested that the premotor areas di-
rectly inhibit primary motor cortex or are involved
in voluntary movement integration and cannot
function during electrical stimulation. Wilson (31),
in discussing inhibitory motor seizures, provided
20 J EPILEPSY, VOL. 10, NO. 1, 1997
several useful postulates: The cerebrum is a con-
tinuously interacting balance of excitation and in-
hibition and seizures distort this balance, with focal
ictal paralysis reflecting activation of inhibitory
mechanisms.
These cases suggest several clinical caveats. In-
hibitory motor seizures should be considered in pa-
tients with frontoparietal lesions who develop
acute motor deficits. In such patients, if neuroim-
aging studies fail to disclose progression of the le-
sion or if the other disorders are excluded (e.g.,
transient ischemic attack), evaluation with an EEG
may be revealing. A brief trial of a BZD should be
considered if other etiologies have been excluded,
especially if the EEG is abnormal. Patients with
temporal lobe seizures causing transient focal
weakness should be evaluated with coronal T1-
weighted MRI to exclude MTS or other structural
lesions.
References
1. Gowers WR. Epilepsy and other chronic convulsive disease.
New York: Williams Wood & Company, 1885.
2. Fisher CM. Transient paralytic attacks of obscure nature: the
question of nonconvulsive seizure paralysis. Can J Neurol
Sci 1978:5;267-73.
3. Hanson PA, Chodos R. Hem~paretic seizures. Neurology
1978;920-3.
4. Walker E, Sharbrough FW. The significance of lateralized
ictal paresis occurring during complex partial seizures. Epi-
lepsia 1988;29:665.
5. Globus M, Lavi E, Fich E, Abramsky O. Ictal hemiparesis.
Eur Neurol 1982:21;165-8.
6. Cirignotta F, Lugaresi E. Partial motor epilepsy with "nega-
tive myoclonus." Epilepsia 1991;32:54-8.
7. Tinuper P, Anguglia U, Laudadio S, Gastaut H. Prolonged
ictal paralysis: Electroenecphalographic confirmation of its
epileptic nature. Clin Electroencephalog 1987:18;12-4.
8. Kofman O, Tasker R. Ipsilateraland focal inhibitoryseizures.
Neurology 1967:17;1082-6.
9. Lee H, Lerner A. Transient inhibitory seizures mimicking
crescendo TIAs. Neurology 1990;40:165--6.
10. Sinniah D, Lin H, Loh T. Inhibitoryepilepsy.Aust NZ J Med
1979:9;448-50.
11. Efron R. Post-epilepticparalysis: theoretical critique and re-
port of a case. Brain 1961:84;381-94.
12. Oguni H, Sato F, Hayashi K, Wang PJ, Fukuyama Y. A study
of unilateral brief focal atonia in childhood partial epilepsy.
Epilepsia 1992;33:75--83.
13. Marrosu F, Brundu A, Rachele MG, Marrosu G. Epileptic
aphasia: first onset of monosymptomatie status epilepticus
in adults. Arch Neurol 1980;37:419-22.
14. Oestreich LJ, Berg MJ, Bachmann DL, et al. Ictal contrapare-
sis in complex partial seizures. Epilepsia 1995;36:671-5.
15. Penfield W, Jasper H. Epilepsy and the functional anatomy
of the human brain. Boston: Little Brown, 1954.
16. Cascino GD, Westmoreland BF, Swanson TH, Sharbrough

7. FW. Seizure-associated speech arrest in elderly patients.
Mayo Clin Proc 1991;66:254-8.
17. Gastaut H. A new type ofepilepsy: benignpartial epilepsyof
childhood with occipital spike-waves. Clin Electroencepha-
logr 1982;13:13-22.
18. Gilliam F, Wyllie E. Ictal amaurosis: MRI,EEG, and clinical
features. Neurology 1995;45:1619-21.
19. Prtichard PB, Holmstrom VL, Roitzsch JC, Giacinto J. Epi-
leptic amnesicattacks: benefitfrom antiepilepticdrugs. Neu-
rology 1985;35:1188-9.
20. Palmini AL, Gloor P, Jones-Gotman M. Pure amnestic sei-
zures in temporal lobe epilepsy. Brain 1992;115:749-69.
21. Melo TP, Ferro JM, Paiva T. Are brief or recurrent transient
global amnesiasofepileptic origin?J Neurol Neurosurg Psy-
chiatry 1994;57:622-5.
22. Devinsky O, Feldmann E, Bromfield E, et al. Structured in-
terview for partial seizures: clinical phenomenologyand di-
agnosis. J Epilepsy 1991;4:107-16.
23. Heilman KM, Howell GJ. Seizure-induced neglect. J Neurol
Neurosurg Psychiatry 1980;43:1035--40.
24. Leiguarda R, Starkstein S,Nogues M, Berthier M, ArbelaizR.
27.
28.
INHIBITORY MOTOR STATUS
Paroxysmal alien hand syndrome. J Neurol Neurosurg Psy-
chiatry 1993;56:788-92.
25. Juulqensen P, Denny-BrownD. Epilepsia partialis continua.
Arch Neurol 1966;6:23-9.
26. Bancaud J, Bonis A, Tailarach J, et al. Sydrome de Kojewni-
kow et acces somatomoteurs (6tude clinique EEG, EMG,
SEEG). Encephale 1970;59:391-438.
DePasquet E,GaudinE, BianchiA, De MendilaharuSA. Pro-
longed and monosymptomaticdysphasic status epilepticus.
Neurology 1976;26:244-7.
Racy A, Osborn MA, Vern BA,MolinariGF. Epileptic apha-
sia: first onset of monosymptomatic status epilepticus in
adults. Arch Neurol 1980;37:419-22.
29. Dinner DS, Li.ieders H, Lederman R, Gretter TE. Aphasic
status epilepticus: a case report. Neurology 1981;31:888-91.
30. Lfiders HO, Lesser RP, Dinner DS, et al. A negative motor
response elicited by electrical stimulationof the human fron-
tal cortex. In: (Advances in neurology;vo157.)Chauvel P, et
al., eds. New York: Raven Press, 1992:149-57.
31. Wilson KS. Modern problems in neurology. New York:
William Wood & Company, 1928:42-50.
J EPILEPSY, VOL. 10, NO. 1, 1997 21