Inhibitory motor seizures

Henry Hasson MD

Epilepsy & Seizures

Updated 01.07.2024
Released 08.20.2013
Expires For CME 01.07.2027

Inhibitory motor seizures

Author: Henry Hasson MD

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Editor: Solomon L Moshé MD

Inhibitory motor seizures

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Introduction

Overview

Inhibitory motor seizures are ictal motor epileptic events of central paresis usually unilateral mono- or hemiparesis while consciousness is intact. They are reported under a number of different names, which may be confusing. Inhibitory motor seizures are contralateral to the epileptogenic region, and they are usually associated with other subjective or objective manifestations (predominantly sensory or motor clonic), which mainly precede but may also occur concurrently with the paresis. The paresis is pyramidal in the majority of cases. Seizures last around 5 minutes, but may also progress into inhibitory motor status epilepticus of many hours or days. Sometimes ictal hemiparesis may take a progressive course following frequent ipsilateral clonic seizures. Nearly all patients also suffer from focal motor (mainly clonic) or focal sensory seizures, which affect the same parts of the body and are more frequent than the inhibitory motor seizures of the same patient. Inhibitory motor seizures affect mostly adults (median of 36 years) with brain structural lesions (mainly tumors). The diagnosis is based on thorough clinical assessment and confirmed with ictal EEG. Brain imaging is mandatory in view of the high incidence of brain structural pathology. Inhibitory motor seizures should be differentiated from nonepileptic attacks, transient ischemic attacks, postictal (Todd) paresis, negative myoclonus, and atonic seizures. Prognosis and management depends on etiology. In this article, the author provides a thorough review of historical aspects and details, nomenclature and classification (which is often problematic), clinical manifestations, pathophysiology, EEG, neuroimaging, and optimal management of patients with inhibitory motor seizures.

Key points

	• Inhibitory motor seizures commonly start in middle-aged patients, mainly with structural frontoparietal brain lesions.
	• They manifest with paresis/paralysis of one side of the body (hemiplegia with or without facial involvement) or one extremity (upper or lower monoplegia). These are often preceded by other objective or subjective ictal symptoms, which may also occur concomitantly with the paresis or independently.
	• The seizures last around 5 minutes, but may also progress into inhibitor motor status epilepticus.
	• Inhibitory motor seizures are diagnosed with thorough clinical assessment, though documentation is only achieved with ictal EEG.
	• Inhibitory motor seizures should be differentiated from postictal (Todd) paresis and nonepileptic transient attacks of paresis. They are also different from negative myoclonus and atonic seizures.

Historical note and terminology

The first reference to ictal paralysis is attributed to Gowers (21; 22), who was of the opinion that “weakness associated with epileptoid seizures may in minor attacks be due to inhibition of the same centres as are discharged in severer attacks” and mentioned a case of Jacksonian epilepsy (typical, right-sided) in which “minor fits consisted of inability to speak or move the right arm or leg, there being no convulsion.” He also described a 40-year-old woman with attacks that

begin with “ticking in the right ear,” and this is followed by a painful sensation “like hot needles running into the skin,” which passes down the side to the leg and foot and, after reaching the toes, returns up the leg and side and is felt in the arm, hand, and tongue. She mumbles and cannot speak for half an hour. There is no motor spasm, but as soon as the sensation is felt in the leg and arm the side becomes extremely weak, so that, although ordinarily able to walk well, she becomes unable to stand and scarcely able to raise the arm (21; 22).

In another 48-year-old patient, “the attacks consisted in ‘pins and needles’ in the left thumb, which passed up the arm to the shoulder and left scapula, with a sense of contraction in the arm. This became powerless, so that she dropped anything that was in the hand” (21; 22).

Jackson refers to Gowers’ view of ictal paralysis, but takes no definite position on it (27):

Post-epileptiform paralysis has been ascribed to inhibition by some medical men whose hypotheses deserve respectful consideration. Gowers believes that discharges in epileptic fits sometimes inhibit; he thinks that temporary paralysis is found in some cases after a purely sensory discharge which does not next discharge motor centres, but inhibits them. In some cases of epileptiform seizures the patient tells us that his arm ‘falls dead,’ there being no spasm in it, whilst the face of the same side is being convulsed. This, so far as I can learn, is a paroxysmal, not a post-paroxysmal paralysis, but possibly it remains for a short time after the convulsion of the face has ceased. I express no decided opinion as to the validity of the inhibition hypotheses. I think it possible that there may be discharge spreading slowly in a motor centre of the middle level, excessive enough: to cause slight after-exhaustion of some of its elements, although not one strong enough to overcome the resistance of lowest motor centres and thereby to produce actual convulsion.

Higier described a patient with ictal hemiparesis and suggested that in certain circumstances the cortical inhibition may predominate over the excitation (24). He later coined the term "status hemiparalyticus" a "paralytic equivalent of epilepsy without disturbance of consciousness” (23).

Holmes reported many cases of negative phenomena in focal epilepsies, mainly in visual epileptic seizures (24). Relevant to inhibitory motor seizures is the following extract of his work:

An interesting fact, not generally recognized, is that convulsive attacks are occasionally replaced by other manifestations, the most common of which is a sudden but transient paresis of that portion of the limb which in other attacks is involved in the clonic spasms. Usually the primary paresis appears in the part in which the spasms commence, but it may affect another region the cortical representation of which is adjacent to the site of discharge; in a case recorded by Hughlings Jackson, for instance, clonic movements of the face were immediately followed by paralysis of the hand of the same side. The following case is a good example of one in which at times defect or negative symptoms only occurred. The patient received a gunshot wound at his head in the region of the posterior end of the second left frontal convolution. Some months after being wounded he began to have epileptiform seizures of the Jacksonian type. …. Sometimes, however, attacks occurred in which there were neither tonic nor clonic spasms, or movements of any kind; he simply lost power suddenly and without any warning in the hand. If reading, his book might fall unexpectedly, or his cane might drop from his hand as he walked. The loss of power was complete for a time, but after a few minutes voluntary movement returned and gradually reached the normal. I have seen several other patients with Jacksonian motor epilepsy who were subject to similar sudden transient palsies of the limb or segment of the limb in which at other times the convulsion commenced. The immediate cause of this palsy is doubtful. Higier, who described one case, suggests that in certain circumstances the cortical inhibition of the antagonists may predominate over the excitation. It is difficult to explain it by this hypothesis; it seems more likely that it is due to a primary inhibition instead of waves of excitation spreading over the cortical motor elements, a change perhaps similar to that which causes loss of consciousness in epilepsy and the sudden relaxations of the muscles leading to "falls," which often occur in it. Such observations show that a local lesion producing a functional instability of part of the so-called motor cortex of the brain may, in addition to predisposing to local epileptiform phenomena, which are frequently followed by temporary loss of power in the convulsed part, be the immediate cause of such negative symptoms as a primary transient paralysis of regions of the body represented in its neighbourhood.

SAK Wilson (better known for his eponymous “Wilson disease”) is probably the first to use the name “inhibitory epilepsy” and meticulously described one of his patients during repetitive attacks of transient left-sided sensory loss and hemiparesis (62):

The attack commences by a sensation of tingling, of formication, of ‘wires’ in the left fingers and hand… At the same time as the numbness appears patient loses all power in his arm and leg. Anything he has in his hand be will let drop; he will be unable to pick anything up with the fingers. In a second or two the loss of power in the left arm and hand is absolute and he is quite unable to move it. Similarly with the leg, he is completely unable to move it at any joint… The duration of this combined numbness and loss of power may be merely a minute or two, or as long as 20 minutes. When the attack passes off recovery of power is usually simultaneous in arm and leg.

Lennox and Lennox described an

11-year-old boy who began to have seizures at the age of 8 months. Following a different type of seizure initially, the boy had seizures commencing with a “queer smile,” slumping to the right with weakness or paralysis of the right arm, and in some attacks inversion of the right eye. Puffiness of the right face might precede an attack… The right-sided weakness would persist for 15 minutes to several hours during which he would appear dazed or be briefly unconscious... A convulsion or convulsive movements never preceded the paresis (34).

However, it was Penfield and his associates (44; 46; 45) and later the investigators of the Cleveland Clinic Foundation in Ohio (36; 35; 37; 40) who documented various types and aspects of negative responses and their localization in patients undergoing neurosurgical assessment.

Nomenclature and classification. There is a significant confusion of the nomenclature used to describe inhibitory motor seizures, a matter that has to be addressed by the International League Against Epilepsy (ILAE). By definition, these should be epileptic seizures of central origin that manifest with inhibition (weakness) of motor activity. Inhibitory motor seizures are not synonymous with negative motor seizures, negative myoclonic seizures (negative myoclonus), atonic seizures, or postictal (Todd) paresis. Negative motor seizures manifest with motor arrest defined only by the inability to conduct voluntary movements or praxis, even though muscle power and tone, consciousness, and cognitive functions are relatively intact (ictal apraxia) (25). Arrest of movements predominantly caused by weakness and atonia of the affected limbs is not considered a negative motor seizure. The name negative motor seizures has been coined because of its similarity with the negative motor response, which consists of cessation of the voluntary tonic muscle contraction or the rapid alternating movements (wiggling of the tongue from side-to-side, rapid alternating horizontal or vertical eye movements, rapid alternating hand or foot movements) without loss of awareness, produced by means of high-frequency electric cortical stimulation of the frontal lobe negative motor areas (25).

Inhibitory motor seizures are also different from atonic seizures, which by definition are a manifestation of loss or diminution of muscle tone only.

See MedLink Neurology articles on Atonic seizures, Myoclonic-atonic seizures, Acute hemiplegia in childhood, Myoclonus, and Hemiplegic migraine. Inhibitory motor seizures are not mentioned in most of the ILAE classifications, including the more recent reports (04; 11; 17; 18; 51). Only the ILAE Task Force classifies them under focal neocortical seizures without spread (Table 1) and clarifies: “Inhibitory motor seizures are not a unique seizure type. The clinical manifestation merely represents the function of the involved cortex, just as focal motor seizures and unformed visual hallucinations reflect seizures in precentral gyrus and calcarine cortex” (15).

Table 1. Focal Motor Seizures

	• With elementary clonic motor signs • With asymmetric tonic motor seizures (eg, supplementary motor seizures) • With typical (temporal lobe) automatisms (eg, mesial temporal lobe seizures) • With hyperkinetic automatisms • With focal negative myoclonus • With inhibitory motor seizures
From: (15)

Also, inhibitory motor seizures are not specifically cited in the ILAE glossary (07). The only possible reference to them is the following:

MOTOR: Involves musculature in any form. The motor event could consist of an increase (positive) or decrease (negative) in muscle contraction to produce a movement. Unless noted, the following terms are adjectives modifying “motor seizure” or “seizure” (eg, “tonic motor seizure” or “dystonic seizure”), and whose definitions can usually be understood as prefaced by “refers to.”

According to the 2014 ILAE “Epilepsy diagnosis” manual, a negative motor feature is characterized by reduced motor activity (11).

	• A negative myoclonic feature involves an interruption in normal tonic muscle activity for 500 milliseconds or less, without evidence of preceding myoclonus.
	• An atonic feature involves sudden loss or diminution of muscle tone without apparent preceding myoclonic or tonic activity. This lasts greater than 500 milliseconds but less than 2 seconds. It may involve the head, trunk, jaw, or limb musculature.
	• A hypomotor feature involves a decrease in amplitude, or rate or arrest of ongoing motor activity.

The instruction manual for the ILAE 2017 operational classification of seizure types proposes that the term “akinetic” (arrest of movement) should be characterized as “focal behavior arrest, generalized absence” (17).

Furthermore, in the updated ILAE report of definition and classification of status epilepticus, “ictal paresis (ie, focal inhibitory status epilepticus)” is listed as a type of focal motor status epilepticus with no details (59).

Author’s comment. This article is a thorough and objective review of inhibitory motor seizures. Emphasis is on focal inhibitory motor seizures. Because of the significant confusion on nomenclature and classification, detailed clinical vignettes from the literature are presented and exact quotations of published reports are given. Inhibitory motor seizures are described and reported under a number of different names, such as “nonconvulsive seizure paralysis,” “hemiparetic seizures,” “ictal hemiparesis,” “ictal paralysis,” “inhibitory epilepsy,” “akinetic seizures,” “negative” or “atonic seizures,” and so forth. As an example of misperception, the characterization of these seizures as “atonic seizures” is unjustifiable because in a significant number of patients with ictal hemiparesis, there is cortical pyramidal hemiparesis as documented by the involvement of the face (paresis of the lower facial muscles) and ipsilateral increase of tendon reflexes (31). This also has significant implications on pathophysiology, which appears to be different between ictal focal paresis and atonic seizures as indicated by the different populations affected. Atonic seizures (loss of tone) occur mainly in children with epileptic encephalopathies, whereas hemiparetic seizures occur mainly in adults with focal brain structural lesions. Also, the term akinetic (inability to move) should be abandoned because akinesia may be due to many causes of epileptic or nonepileptic origin. Finally, this article is not an attempt to classify them in accordance with their different types based on focal/generalized and mechanistic criteria, which may be considered by the ILAE Commissions on Classification and nomenclature.

Clinical manifestations

Presentation and course

Inhibitory motor seizures commonly:

	• start in middle-aged patients, mainly with structural frontoparietal brain lesions
	• last around 5 minutes, but may also progress into inhibitor motor status epilepticus
	• manifest with paresis/paralysis of one side of the body (hemiplegia with or without facial involvement) or one extremity (upper or lower monoplegia) (53).

Focal inhibitory seizure

A picture taken during a focal inhibitory seizure. The patient was asked to hold up her arms, but could not raise the right arm. During the interictal state, she had normal muscle strength. (Courtesy of Dr. CT Skidmore).

Age at onset. In 31 reported patients reviewed by the author for the purposes of this article, the age at onset varied from 4 months to 78 years of age with a median of 36 years (average ± SD=39±21). Only seven patients were younger than 12 years of age, and five patients were 70 years of age or older.

Ictal clinical manifestations. Hemiparesis (with or without facial involvement) is the commoner clinical symptom followed in prevalence by monoparesis of the upper or lower extremity (20; 12; 49; 53; 10). Axial (trunk) paralysis is rare. The paresis is probably pyramidal in the majority of cases. These inhibitory motor symptoms are contralateral to the epileptogenic focus, and they are usually associated with other subjective or objective manifestations (predominantly sensory), which mainly precede but may also occur concurrently with the paresis. Paresis alone without other symptoms is rare. Consciousness is intact or mildly cloudy. Duration ranges from 2 minutes (average 5 minutes) to sometimes hours or days (inhibitory motor status epilepticus). Sometimes ictal hemiparesis may take a progressive course following frequent ipsilateral clonic seizures (10).

Focal inhibitory seizure

Other types of seizure. Significantly, nearly all patients also suffer from focal motor (mainly clonic) or focal sensory seizures, which affect the same parts of the body and are more frequent than the inhibitory motor seizures of the same patient.

Smith and associates reviewed inhibitory motor seizures in 26 well-selected cases published between 1978 and 1997 (54). All patients developed episodic weakness that typically lasted around 5 minutes (range 2 to 30 min) and recurred. The weakness usually progressed to paralysis, and, after the seizure, power of the involved extremities returned to baseline. Five patients reported an aura of numbness in the involved areas, and two patients reported lightheadedness. Inhibitory motor status epilepticus lasting from 10 hours to 3 days, usually terminating with intravenous diazepam, occurred in two of 26 patients.

Kovac and Diehl reviewed 18 patients with “definite atonic seizures” (excluding focal atonic seizures of rolandic epilepsy) with ictal EEG documentation (31). Though the authors categorized these seizures as “atonic seizures,” these were most likely inhibitory motor seizures. Paresis affected the upper limb in 12 (67%) patients, lower limb in two (11%) patients, both limbs of one side (hemiparesis) in three (17%) patients, and involved trunk muscles in one (6%) patient. Paresis as the only presentation of a seizure was rare—only three cases (17%). Usually, paresis was embedded in a seizure that also presented with positive motor and or sensory signs. Positive motor signs in the same seizure were found in 11 (61%) cases. An aura preceding paresis was reported in nine (50%) patients. In four patients, this was a somatosensory aura involving the limb that presented with paresis, whereas the aura consisted of an alien limb sensation, a discomfort in the chest, or was unspecific in the other five cases. The duration of paresis ranged from several seconds to hours, with most of the cases presenting with paresis that lasted several minutes. Scalp EEG recordings were available in 15 patients, whereas EEG was recorded with subdural electrodes in three cases. Ictal scalp EEG findings pointed to the central region in many cases. However, midline and parietal and temporoparietal localizations were also observed. Invasive EEG recordings identified the mesial frontal region and the precentral gyrus as ictal generators. Imaging identified a lesion in 10 cases (56%). In addition these authors identified seven patients in whom:

…ictal atonia was present but coincided with some degree of impairment of consciousness. These seizures do not fulfill the strict criteria of atonic seizures. Interestingly in those seizures, trunk or generalized atonia occurred more frequently and in many of these patients during the seizure periodic lateralized epileptiform discharges were observed in EEG indicating a more widespread brain pathology.

Bilateral inhibitory (akinetic) motor seizures have also been described. Toledano and associates analyzed clinical and EEG characteristics of bilateral akinetic seizures of patients retrospectively identified from 1858 consecutive video-EEG studies (58). All patients had ictal video-EEG, comprehensive clinical evaluation, neuropsychological testing, and brain magnetic resonance imaging. Ten patients (nine men) were identified; mean age was 22.5 years (range 0.3-71 years) at the time of epilepsy onset and 34.9 years (range 5-73 years) at the time of evaluation. Bilateral akinetic seizure was the only seizure type in four patients. Bilateral akinetic seizures consisted of sudden speech and motor arrest in eight patients, whereas in two patients seizures were characterized by abrupt freezing precipitated by gait initiation. Startle precipitated bilateral akinetic seizures in four patients. MRI showed mesial frontal lobe lesions in six patients. Epileptiform activity was restricted to the frontal midline electrodes in all patients, with variable extension to frontal regions. In five patients, bilateral akinetic seizures were initially misdiagnosed as generalized seizures or nonepileptic events. The authors concluded that bilateral akinetic seizures should be considered in the differential diagnosis of patients reporting paroxysmal inability to move with preservation of awareness, bearing in mind that these seizures can occur spontaneously or be precipitated by startle. The diagnosis can be achieved with video-EEG monitoring, showing stereotyped semiology and distinctive EEG abnormalities, and is often supported by the presence of lesions involving the frontal lobes (58).

Ictal paresis in limbic (complex) focal seizures. Oestreich and associates reported that five (5.3%) of 94 consecutive patients with focal epilepsy had ictal unilateral arm and hand paresis during 27 of 34 limbic focal seizures (42). This was always contralateral to an epileptogenic temporal lobe abnormality, as determined by video-EEG monitoring and surgical outcome. When examined, the paretic arm and hand were flaccid. None of these patients had postictal Todd paralysis. In most of the seizures, the arm ipsilateral to seizure onset had simultaneous purposeful movements or automatisms, sometimes with awkward posturing. However, as pointed out by Noachtar and Luders:

…only 2 of the 5 patients in this study were actually tested during the seizures to prove the loss of electromyographic tone. In the other 3 patients a retrospective video analysis showed unilateral automatisms without contralateral dystonic posturing of the arm. It is unclear if in these patients the lack of movement was due to paresis or a mild tonic increase in muscle tone (40).

Bleasel and colleagues found that unilateral immobile limb occurred in 12% of 34 patients with temporal lobe epilepsy and none in 20 patients with extratemporal lobe epilepsy (14 frontal, three parietal, and three occipital) (05). However, the distinction between focal paresis and lack of motor activity due to mild tonic posturing (which is a common feature in motor seizures arising from the temporal lobes) is often difficult (40).

Inhibitory motor status epilepticus. Lengthy inhibitory motor seizures constituting inhibitory motor (nonconvulsive) status epilepticus have been well reported (54; 02; 08). It occurred in two of the 26 reviewed cases and in an additional two detailed patients (54).

Armon and associates reported five patients who, 2 to 4 days after an intracranial neurosurgical procedure, developed new persistent focal neurologic deficits attributed to inhibitory focal (nonconvulsive) status epilepticus lasting for days, which resolved with antiepileptic treatment (02). Only one of these patients had pure inhibitory motor status epilepticus (left hemiparesis); two had right hemiparesis and aphasia, and the remaining two had aphasia only. The age range of the five patients was 15 to 74 years. The operations were aneurysm clippings (three patients) and resections of an oligodendroglioma and a cavernous hemangioma (one patient each). EEG showed, in all patients, continuous or intermittent focal seizure activity arising from cortex regionally relevant to the clinical dysfunction. Subtle positive epileptic phenomena (jerking) occurred intermittently in three patients as a late concomitant. Administration of antiepileptic drugs resulted in significant improvement within 24 hours in four patients, with parallel resolution of ictal EEG activity. The fifth patient improved more slowly. Two patients relapsed when antiepileptic drug concentrations fell, and improved again when they were raised. Similarly, a 45-year-old patient developed prolonged episodes with flaccid paralysis of the left arm after surgical drainage of a right frontoparietal subdural hematoma (60). Video-EEG recording showed clear-cut epileptic ictal discharges involving the right perirolandic cortical areas. Inhibitory motor status epilepticus has also been detailed in a report of two other cases (08).

Prognosis and complications

The overall prognosis depends on the cause, though seizures may respond adequately to antiepileptic drugs.

Clinical vignette

Clinical vignette 1. Wilson meticulously described a historical and didactic case of ictal hemiparesis and provided a neurologic assessment of the attacks (62). Note that during the ictal hemiparesis there were definite signs of pyramidal involvement.

A 24-year-old man always has had good health. Six months ago, without any apparent cause, the patient began to suffer from curious attacks of tingling in the left hand and arm, and left side of the body, which have continued steadily and are now becoming more frequent. At first these occurred perhaps one or two in a fortnight, but now every two or three days. They may come at any time, but as far as he knows not during the night. In the attacks he never loses consciousness but he feels queer and “regular knocked.”

Aura: Of this a very definite description is given, and it has always been the same. It begins by his eyes becoming “misty,” not one eye more than the other, or before the other. He can see his way about but he cannot distinguish the forms of objects. He has noticed that the mistiness is chiefly on looking downwards; on looking to either side he sees constant “bright flashing stars” in the outer parts of the field. They are not coloured. This mistiness of vision and these subjective visual phenomena continue for about 15 to 20 minutes before the attack proper commences.

Character of the attack: The attack commences by a sensation of tingling, of formication, of “wires” in the left fingers and hand. This is variously described by patient—it is as if “he had his hand in a stocking”; as if “it were entangled in string”. In the earliest attacks the sensation did not pass the wrist, and patient was able to abate it by putting his hand into water, rubbing it, etc. But all the other attacks have been wider in range. The sensation passes up the left arm in a few seconds, then down the left side of trunk rapidly into leg and foot and toes; it then appears (in the more recent attacks) in the left side of the face (lower division). It plays along the lower jaw on the left side, and makes the left half of the tongue tingle. The duration of the sensation varies from only a few seconds to some minutes. When it is over, it leaves arm, leg and face quite numb and “dead.” At the same time as the numbness appears patient loses all power in his arm and leg. Anything he has in his hand he will let drop; he will be unable to pick anything up with the fingers. In a second or two the loss of power in the left arm and hand is absolute and he is quite unable to move it. Similarly with the leg, he is completely unable to move it at any joint. The duration of this combined numbness and loss of power may be merely a minute or two, or as long as 20 minutes. When the attack passes off recovery of power is usually simultaneous in arm and leg. He thinks there is little if any loss of power in the left face; it feels as though it were being stretched or dragged up, but it is not so powerless as the limbs.

Sequelae: Usually has headache (temporal and frontal) after the fit, and this may last a whole day. There is no sickness or vomiting. Patient thinks that the left side, arm especially, is becoming rather weak, but in any ease the degree is slight. Otherwise, feels perfectly well.

State on admission: No indication of abnormality in circulatory, respiratory, or alimentary systems.

Cerebral: Attention, memory, intelligence, excellent. Is not conscious of any mental change. Not emotional. Apart from fits, no headache or giddiness. Speech, taste, smell, hearing, unaffected.

Cranial: No cranial tenderness. 2. V.A. 6/6 R. and L. No restriction of fields, rough test.

O.D.: L, appears normal, though rather high-coloured. R, definitely high-coloured; veins full. 3, 4, 6. No diplopia, no ptosis, strabismus or nystagmus. No ophthalmoplegia. Pupils regular, equal, medium size; reactions normal. 5-12. No impairment observed in the function of these nerves. No facial asymmetry or weakness. No defect in phonation, articulation, or deglutition. No defect of palatal movement. Pharyngeal reflex present. No facial hypaethesia or anaesthesia. Tongue protruded straight.

Motor system: General muscular nutrition and development good. There is some general flabbiness of the muscles more marked in the left arm than in the right. No particular difference in legs. No incoordination of any kind. No involuntary movements. Patient is right-handed. There is perhaps just a little relative weakness of the left arm as a whole. No difference in power of legs, which is good. All voluntary movements good in range.

Sensory system: No objective changes of any kind detected. No astereognosis. No atopognosis. No loss or diminution in sense of position or passive movement. No diminution of muscle pain sense.

Reflexes: Abdominal and epigastric present and equal; brisk. Knee jerks, arm jerks, brisk; no apparent difference between the two sides. No ankle clonus. Double flexor response. No organic reflex impairment.

Wilson described the fits as observed by himself as follows (62):

(1) 12.40 p.m.—When I saw the patient he was lying on his right side, with his legs drawn up, right not so much as left, and with his left arm flexed at the elbow and extended at the wrist. The left foot was distinctly inverted and toes were pointing downwards. He said that at that moment the whole of his left side felt numb, including the lower part of his face and round the nose on the left side. He further declared that the sensation had come on when his legs happened to be drawn up, and that he could not move his left leg. When I tested him, he was unable to move the leg at all, and could move the arm only at the shoulder and elbow, and that very slightly.

Patient had no appearance of distress, no difficulty in speaking, no twitching, and was absolutely conscious and coherent the whole time.

Testing him quickly, it was seen that his arm was rather rigid at the shoulder and elbow, and that the wrist and fingers were quite flaccid. The resistance to passive movement seemed to be due to defective inhibition of antagonists, a phenomenon well seen in the left leg. The leg was resistant to passive movement, more proximally than distally, and immobile. His face on the left side was distinctly affected, especially in the lower division, for both volitional and emotional movements. His lower maxilla was “chattering” and he was unable to control this. He remarked then that his tongue on the left side, and the parts underneath his tongue, were numb.

Tested quickly for sensation, there was anaesthesia of the hand and wrist, and of the leg. The limits were undefined. There was astereognosis in the left hand, and also very considerable diminution of the sense of passive movement and of position. There was very little if any diminution in appreciation of painful stimuli. All the tendon jerks on the left side were exaggerated, but I failed to elicit an extensor response on the left. The abdominal reflexes were diminished on the left.

12.46.—By this time there was some return of movement in the arm, and also in the leg. He could slowly push his leg down, though he could not lift it off the bed. He was able to flex and extend at wrist and could move the fingers slightly. The position of the foot was maintained. In the attempt to move the leg, defective inhibition of antagonists was particularly well seen. Thus as he slowly extended, the hamstrings were seen and felt to contract spasmodically. The same thing was noticed in the gastrocnemius when he tried to dorsiflex the foot.

Spontaneous left patellar clonus commenced at this point, and when the left knee jerk was elicited there was prolonged patellar clonus. Ankle clonus was likewise obtained, but it was not so well sustained. There was a left flexor response at this stage. The numbness was gradually disappearing from leg and face, but it persisted in the arm and hand. When I was testing his sensation for touch, he remarked that the touch of my finger on his leg and arm and hand gave rise to a feeling of pins and needles at the spot touched.

The facial asymmetry was absent now, and his tongue was protruded straight, although it was tremulous. There was no defect of jaw movement. The jaw clonus had disappeared.

The loss of sensation to touch remained, and stereognosis was still inaccurate.

12.55.—In the attempt to close his hand, there was some irregular twitching of the forearm muscles, chiefly of the antagonists to the movement. Diminution of muscle sense was not now so marked. By this time the movements of his legs were normal in range but not of normal strength. He complained that where his limbs had been numb they were now cold, but to my hand there was no actual difference in the temperature of the two sides.

1.02.—Asked to hold his arms out it was seen that the left arm was oscillating very slightly and irregularly, but he was able to hold it as well as the right. The reflexes on the left side were now distinctly less brisk than a few minutes ago, although patellar clonus was still obtained. On stimulating the sole of the left foot, there was flexion—though very slight—of the great toe, and extension of the small ones. Left abdominal reflex less marked than right.

There was still slight persisting anaesthesia of the fingers, left, but not elsewhere.

1.08.—All movements on the left were now good in range, but there was slight weakness generally at all joints. The anaesthesia had disappeared.

(2) Patient again seen in a fit one week later.—When I saw him, he was lying on his bed with his clothes on. He was perfectly conscious, a little pale, and his lower jaw was chattering incessantly. His left arm and leg were helpless. The arm was flexed at the elbow, and lying across his body. On request, he was unable to lift the hand or arm off his body. Neither limb was at all stiff or rigid; on the contrary they were completely flaccid. He complained that all the feeling had left the limbs on that side, and that the numbness was extending to the left side of his face. The numbness and coldness began in the fingers and passed up the arm and down the trunk to the leg.

On the left side the jerks were unusually brisk; there was definite though not well- sustained ankle clonus. Also there was apparently a left extensor response, though this was difficult to be sure of; sometimes there was no movement of the toe in response to the stimulus. The left arm jerks were also exaggerated. Both abdominal reflexes were active at this stage.

A minute or so later there was slight return of power in the limbs, distal more than proximal, and more in arm than leg. At this point sensation was rapidly tested, when it was found there was no diminution of appreciation of pain on the left side, but considerable diminution of tactile acuity.

Topognosis also was tested, when there was seen to be definite preaxial localisation.

Patient then remarked that the numbness had spread to the inside of the left cheek and under the tongue on the same side. The chattering of the jaw was less, but he said that he had a disagreeable feeling in his throat, as though he were “swallowing a sob.”

His sense of position and of passive movement was then tested in the left hand, and it was found that when his third finger was moved he referred it to the first, his fourth to his third, his second to his second. The diminution in sensation continued.

When I was testing his sense of pain again, in the left hand, he said that a prick felt hot as well as sharp. His fingers still felt numb, but the numbness was passing from the rest of him. From this point his left grasp began rapidly to improve, but it was noticed that he could not sustain it owing to defective innervation of the synergic and defective inhibition of the antergic muscles.

A few minutes later the subjective sensations had almost disappeared, except in the fingers. The jerks remained very brisk. The power of the limbs was returning.

(3) Six days later, a third fit was observed in part. It had begun with a sensation “like a battery” starting in the left hand and running quickly up the left arm and down the left side into the leg and foot, as well as into the tongue and face (left), and this was succeeded by numbness in the same left-sided distribution. When I saw him, he said he had lost all power over the left limbs. I found that the left side of the face moved less well than the right, and that the tongue was protruded distinctly to the left. The left limbs were limp and useless; voluntary power was practically nil, though there were just the slightest movements possible of finger flexion.

While I was conducting this brief examination, the clinical condition changed before my eyes (as on previous occasions). The left limbs became rather rigid, the arm moved (involuntarily) into a position of slight flexion at elbow and adduction at shoulder while the fingers partially closed. At the same time the left leg flexed slightly at hip and knee, extended at ankle, and assumed a position of adduction.

Within a minute or two power commenced to return; movements of the left arm increased in strength and were associated with a sort of coarse tremor or oscillation of the left arm at the shoulder—an internal and external rotation of the upper arm in succession. Passive movement of the left leg evoked a kind of spasmodic alternation of extension and flexion at hip and knee through a very limited range.

The deep reflexes were exaggerated on the left side, but both plantars were in flexion, and both abdominals were present and active. Sustained ankle clonus was readily elicited on the left side.

Some ten minutes after the commencement of the attack the patient was rapidly recovering both movement and sensibility, and in a quarter of an hour altogether the above-described symptoms and signs had vanished.

The hyperaemic condition of the optic discs eventually changed into a slight papilloedema, and the question of operation was broached. The patient refused to consider this, and passed from my observation.

Clinical vignette 2. O’Donovan and colleagues described a case of inhibitory motor seizures of early onset (41). Note ictal ipsilateral tendon hyperreflexia and coexisting gait apraxia.

A 6-year-old Caucasian girl developed episodic left hemiparesis at 1 year of age. Her developmental milestones had been normal and the pregnancy was uncomplicated. A first cousin had seizures. Her episodes of left sided weakness occurred mainly on awakening but occasionally at other times throughout the day. The left sided weakness was more obvious in the leg than the arm, and typically lasted 5-30 min. During the episodes, she had gait apraxia that was not apparent at other times. She did not have incontinence, convulsions, or loss of consciousness. Brain MRI was normal. The episodes did not improve on valproic acid or on carbamazepine. Her neurologic examination was normal between episodes, but during the event she had 4/5 motor strength of left leg. Heel knee-shin testing on the left was dysmetric and there was an apraxia of gait during the ictus. The left patellar and ankle jerks were hyperreflexic. These abnormalities persisted for an hour, after each seizure. Her baseline EEG was significant for interictal segments of spike and wave activity lasting up to 5 s with phase reversal at the vertex. During three recorded episodes of hemiparesis, spike and wave discharges of 15 s duration were seen at the vertex electrodes. Montage reformatting and source analysis of scalp ictal EEG did not appear to provide additional localizing information. Ictal SPECT was normal and baseline SPECT was not performed. Her events subsequently responded to treatment with levetiracetam.

Clinical vignette 3. Smith and colleagues described a case of inhibitory motor status epilepticus (54).

A 25-year-old right-handed man presented with progressive left hemiparesis 1 year after resection of a right frontal astrocytoma and completion of whole brain radiation and chemotherapy. Postoperatively, 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 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 region. There was no improvement after the administration of dexamethasone 20 mg followed by 6 mg four times daily for 3 days. The hemiplegia had persisted for days before the patient was given 10 mg intravenous diazepam, which resulted in resolution of the semi rhythmic activity in 1 min. Within 10 min of diazepam injection, left upper and lower extremity strength increased to 3-4/5. Phenytoin was initiated, and at a 3-month follow-up visit, his strength remained 3-4/5.

Clinical vignette 4. Dale and Cross described a case of ictal hemiparesis progressively evolving together with frequent ipsilateral motor clonic seizures (12).

A girl of 2 years 4 months of age presented with a 30-minute afebrile generalized seizure followed by transient left-sided weakness. The girl was born uneventfully at term. She had two episodes of transient eye deviation to the left at 4 months of age, which was thought at the time not to be significant. Her subsequent development was normal and she developed a left-hand preference. Over the months succeeding her initial presentation, she had daily seizures that involved eye deviation to the left, eye blinking, left facial twitching, and left arm jerking. Her mother also noted a progressive disuse of her left hand, which did not appear to fluctuate.

Examination revealed a developmentally normal child, with a head circumference on the 90th centile and no neurocutaneous stigmata. She had a mild left facial weakness and a marked right-hand preference, with reluctance to use her left arm. Her left hand had poor fine motor movements but no reflex asymmetry. Her lower limbs were normal. Interictal EEG at presentation showed right temporal slow waves with occasional sharp discharges, suggesting the presence of a space-occupying lesion. However, neuroimaging with both CT and MRI revealed no structural brain abnormality.

Carbamazepine monotherapy (up to 20mg/kg/day) was commenced, which had no impact on the seizure frequency. Sodium valproate was added and within 1 month the patient was seizure free. Once the seizures were controlled, the girl’s left-sided weakness gradually resolved and neurologic examination 2 weeks after seizure arrest revealed no focal deficit.

The subject remained on dual therapy for the next 3 years, during which time she remained seizure free and retained her normal neurologic and cognitive function, although she remains right-handed. An attempt at weaning her off carbamazepine led to reemergence of transient episodes of left-arm weakness not associated with clonic movements nor change in awareness. Repeat MRI led no demonstrable change from the original scan. Control of these transient monoplegic episodes was regained with lamotrigine. The girl remained on sodium valproate, but carbamazepine was discontinued.

Clinical vignette 5. Lee and Lerner described a 70-year-old man with inhibitory motor seizures initially misdiagnosed as crescendo transient ischemic attacks (33).

A 70-year-old right-handed man had episodes of right arm numbness and paralysis. The episodes began approximately 10 days before admission. Initially, he described only several episodes a day, increasing in frequency to approximately 15 a day over the past several days before admission. During the episodes, he became weak in the right arm and would drop items from his right hand. The episodes would last 3 to 5 minutes. There were no headaches, aura, or precipitating factors. He was also slightly confused and had some difficulty speaking during the episodes. Between episodes he was asymptomatic. The patient was admitted to the intensive care unit with a diagnosis of crescendo transient ischemic attacks. Despite being fully anticoagulated with heparin, the patient continued to experience three to four episodes of right arm paralysis per hour. An EEG was obtained during an episode. Immediately prior to an episode, the patient complained of discomfort involving the right arm, followed by flaccid paralysis of the arm with no weakness of the leg or face. No gross tonic-clonic activity was noted. The episode lasted approximately 2 minutes. During the episode the patient was alert but had some mild word-finding problems. EEG during the episode showed high-amplitude rhythmic slow-wave activity of 2 to 3 Hz in the posterior parietal region bilateral and intermixed spike- and sharp-wave activity in the left parietal region. With return of motor function, the EEG returned to normal. Due to the paroxysmal nature of the EEG, the patient was given phenytoin, and heparin was discontinued. He was given a loading dose of 1000 mg over a period of 12 hours. Over the next several days, the episodes decreased in number and ceased. The patient’s mild right-arm weakness resolved and has remained asymptomatic in the ensuing 6-month follow-up (33).

Clinical vignette 6. Ictal hemiparesis with a progressive course following frequent ipsilateral clonic seizures (10).

A 39-year-old man with neurofibromatosis 2 had recurrent stereotyped episodes of weakness affecting his right leg, with sudden onset of weakness and numbness of the whole leg, reaching a maximum over 30 seconds, and lasting for 30 minutes, followed by almost complete and rapid resolution over a minute. There was a residual abnormal feeling for about 24 hours but he would feel otherwise well. During these episodes, his right arm felt slightly weak and uncoordinated. On one occasion, he was woken from sleep by momentary cramping in the right leg before the onset of weakness and numbness. There had been three such episodes over 6 months, but before his clinic appointment there had been a cluster of four attacks within 24 hours, requiring hospital admission. Brain MRI showed numerous meningiomas, the largest of which was near the vertex, adjacent to the left side of the falx. He started on levetiracetam, with no subsequent attacks (10).

Biological basis

Localization. Findings from intracranial recording of spontaneous inhibitory motor seizures and cortical stimulations from patients undergoing neurosurgical assessments have provided significant insights into the neuronal activity underlying inhibitory and negative ictal motor phenomena. However, the exact mechanisms are not yet fully understood and it is likely that localization and pathophysiology are different from inhibitory, negative, and atonic seizures.

Inhibitory motor seizures. The role of primary motor and sensorimotor areas. The exact cortical site that the epileptic discharge must activate to give rise to inhibitory motor seizures manifesting with paresis has not been well established (40). It is likely that their main localization is the contralateral primary motor cortex in the precentral gyrus because inhibitory hemiplegia often involves the lower facial muscles, and it is associated with increased tendon reflexes. The implication of the primary sensorimotor cortical areas is also indicated because (1) nearly half of these patients experience some kind of somatosensory sensation or clonic convulsions before or at onset of the focal paresis in the same body region or side, (2) frequent occurrence of structural abnormalities in these areas, and (3) improvement of seizures after ablation of the offending lesion (30).

Matsumoto and colleagues obtained an ictal electrocorticogram with chronically implanted subdural electrodes from a 30-year-old man with a low-grade glioma in the right postcentral gyrus who had a focal inhibitory seizure of the left arm (38). During the ictal paresis, the authors observed epileptic discharges in the positive arm motor area of the right precentral gyrus and in its rostral area, but not in the negative motor area. Interestingly, this area showed positive motor responses when electrically stimulated. The epileptic activity likely inhibited the spinal motoneuron pool without eliciting excitatory activity in the corticospinal pathway.

Shi and Zuo described a child with focal inhibitory motor seizures, with the seizure focus in the primary motor cortex (52). Seizures were characterized by ictal paralysis of the contralateral limbs without loss of consciousness. The seizure focus and progression were examined using long-term video EEG monitoring and MRI Invasive recordings of the ictal EEG revealed spike rhythms arising from the primary motor cortex, suggesting that seizures associated with paralysis can arise from hyperactivity in either positive or negative motor areas. Resection of the cortical area related to ictal onset resulted in a seizure-free status for the last 3 years (52).

Negative motor responses have also been linked to the primary motor and sensorimotor cortex. Ikeda and associates studied three patients with medically intractable focal epilepsy (two with frontal lobe epilepsy and one with parietal lobe epilepsy) (26). All patients underwent chronic long-term video-EEG monitoring, cortical mapping by 50 Hz electric cortical stimulation, and recording of cortical somatosensory-evoked potentials with chronically implanted subdural grid electrodes to map both epileptogenic and functional zones. After these clinical evaluations, cortical stimulation by single electric pulse (0.3 ms duration, 1 Hz) was carried out through pairs of subdural electrodes located at the primary sensorimotor area, pre-supplementary motor area, and lateral negative motor area, whereas surface EMG was recorded from the muscles of the contralateral hand. The results showed the following:

(A) In all subjects, single pulse stimulation of primary sensorimotor area elicited a motor evoked potential followed by a silent period in the contralateral distal hand muscles, the latter lasting 300 ms after the stimulus. The duration of the silent period was proportional to the size of the preceding motor evoked potential. In one subject, a silent period without any preceding motor evoked potential was elicited, and, in another subject, there was a short silent period immediately before motor evoked potential in the contralateral thenar muscle.

(B) Following the stimulation of either pre-supplementary motor area or lateral negative motor area, no silent period was observed.

The authors concluded that the inhibitory mechanism within the primary sensorimotor area (but probably not in the nonprimary motor areas) is either closely linked to or completely independent of excitation, most likely plays an important role in eliciting brief negative motor phenomena such as cortical negative myoclonus or silent period (26).

Also, the excitability state of the primary motor cortex has been studied with transcranial magnetic stimulation. It elicits an excitatory motor evoked response, followed by a brief (50 to 100 ms) interruption or a silent period of the ongoing muscle activity (61). Such a silent period is reflexively induced by spinal inhibition and eventually enhances the movement induced by the preceding myoclonus (55). A silent period without a preceding myoclonus can also produce a jerk (negative myoclonus) due to a sudden interruption of the ongoing muscular activity, and is related to a mechanism of supraspinal inhibition and lasts from 100 to 500 ms (57).

Negative motor responses and negative motor seizures. The role of the negative motor areas in the lateral (posterior inferior frontal gyrus) and mesial (posterior mesial superior frontal gyrus in front of the supplementary sensorimotor area proper) aspects of the frontal lobes. In patients undergoing presurgical evaluation for intractable epilepsy, high frequency (50 Hz) cortical electrical stimulation of the negative motor areas through subdural electrodes produced predominantly contralateral and, to a lesser extent, ipsilateral negative motor responses and probably negative motor seizures, predominantly of limb and tongue muscles (46; 45; 40). Thus, these may be the primary localizations responsible for negative motor response, negative motor seizures, and, to a larger extent, negative myoclonus (25). However, it was postulated that the inhibitory motor seizures of a man with neurofibromatosis 2 were related to a meningioma overlying the supplementary negative motor area in the mesial superior frontal gyrus (10).

Epileptic negative myoclonus. Neuroimaging and neurophysiologic investigations, including intracerebral recordings and electrical stimulation procedures in patients with epilepsy, suggest the participation of premotor, primary motor, primary sensory, and supplementary motor areas in the pathophysiology of negative myoclonus (48).

Atonic seizures. Role of corticoreticulospinal pathways. The pathophysiology of focal and generalized atonic seizures and the atonic components of seizures are largely unknown; cortical and subcortical mechanisms have been implicated to explain the loss of muscle tone (56). Blume postulated that discharges in the premotor cortex and other areas, as reflected by spikes and troughs of bisynchronous spike-and-wave discharges, descend to excite the pontine and medullary reticular formation, which inhibits spinal motor neurons, thereby producing sudden hypotonia of axial muscles (06). Bilateral ictal atonia of limbs has been shown in focal seizures in cases with bilateral lesions or evidence of caudal propagation to brainstem structures or contralateral hemisphere seizure spread (50).

In the brainstem, the direct or indirect (via the corticoreticular efferents) activation of the pontine reticular formation, which is responsible for atonia or inability to move in REM sleep and in cataplexy, could produce a motor inhibition and underlie at least generalized atonic seizures. For example, there are indications that cortical activation of fast corticoreticular pathways produces marked inhibition of postural tone, particularly of the axial musculature (47; 32). However, it is not clear whether this mechanism, which could explain generalized atonic seizures, plays a role in the generation of focal inhibitory motor seizures.

As reviewed by Kovak and Diehl, the brain areas involved in bilateral, predominantly proximal loss of muscle tone are distinct nuclei in the pons and the medulla oblongata (31). Corticoreticular neurons project ipsilateral to the upper portion and bilateral to the lower portion of these nuclei, and, therefore, unilateral activation of the pathway in animals leads to bilateral muscle tone loss. The good results of callosotomy in the treatment of epileptic atonic drop attacks in the context of focal epilepsies suggest that bilateral synchronization of the epileptic discharge via the corpus callosum is a crucial mechanism. Whether this may lead to a bilateral activation of inhibitory cortical areas or of cortical regions projecting downward to brainstem structures is not known.

See also Localization and pathophysiology in the MedLink Neurology article, Atonic seizures.

Etiology and pathogenesis

The main etiology of inhibitory motor seizures is any type of structural lesion that primarily affects the frontal lobes and their vicinity. Predominantly, these are brain tumors and, less often, malformation of cortical development, strokes, and hematomas.

Differential diagnosis

Confusing conditions

Thorough clinical history and detailed clinical examination is the basis for correct diagnosis, which is confirmed with EEG (preferably video-EEG) and EMG. Unfortunately, many reports in the literature do not include details of the clinical examination during the ictus or ictal EEG/EMG recordings. The result is avoidable diagnostic uncertainties.

Nonepileptic transient paretic attacks. Inhibitory motor seizures should first be differentiated from nonepileptic attacks of paresis such as transient ischemic attack, hemiplegic migraine, alternating hemiplegia, and psychogenic seizures (14; 13). Such cases of inhibitory motor seizures imitating transient ischemic attacks have been published (33; 19). The differential diagnosis is even more demanding when the attacks appear with a sudden increase in severity of a preexisting unilateral paresis as in Sturge-Weber syndrome (28; 03). Inhibitory motor seizures are more likely to be associated with a short temporary speech disturbance and partial amnesia for the event (14).

In children, recurrent alternating hemiplegia associated with paroxysmal movements such as dystonic attacks and nystagmus may be misdiagnosed as ictal hemiparesis (43).

EEG is mandatory in any case of transient imitators of inhibitory motor seizures.

Postictal paralysis (Todd paralysis). Postictal paralysis should be thoroughly considered, mainly in patients who also have focal convulsive seizures and particularly when positive motor symptoms are embedded with the paretic manifestations. It is easily conceivable that mild clonic movements preceding the focal paresis may have been overlooked and that the paresis occurred postictally. In a large number of reported ictal paretic episodes, the diagnosis of “ictal” (versus postictal) was based on the response of the hemiparesis to antiepileptic drugs, particularly benzodiazepines (16; 12).

Purely atonic seizures without weakness. Attempts to separate inhibitory motor seizures from purely atonic seizures may require simultaneous recording of the EEG and preferably also the EMG.

See MedLink Neurology articles: Atonic seizures, Myoclonic-atonic seizures, Acute hemiplegia in childhood, Myoclonus, and Hemiplegic migraine.

Associated and underlying disorders

Inhibitory motor seizures mainly occur in structural focal epilepsies affecting the frontal and, less often, the parietal and temporal lobe.

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Contributors

All contributors' financial relationships have been reviewed and mitigated to ensure that this and every other article is free from commercial bias.

Author

Henry Hasson MD

Dr. Hasson of Albert Einstein College of Medicine has no relevant financial relationships to disclose.
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Editor

Solomon L Moshé MD

Dr. Moshé of Albert Einstein College of Medicine has no relevant financial relationships to disclose.
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Former Authors

C P Panayiotopoulos MD PhD
Jerome Engel Jr MD PhD

Patient Profile

Age range of presentation: 2 to 65+ years65+ years
Sex preponderance: Female = male
Heredity: None
Population groups selectively affected: None
Occupation groups selectively affected: None

ICD & OMIM codes

ICD: Epilepsy and recurrent seizures: 345

Localization-related (focal) (partial) epilepsy and epileptic syndromes with complex partial seizures: 345.4

Localization-related (focal) (partial) epilepsy and epileptic syndromes with simple partial seizures: 345.5

Epilepsy, unspecified: 345.9

Epilepsy: G40

Localization-related (focal)(partial) symptomatic epilepsy and epileptic syndromes with simple partial seizures (which can evolve to secondarily generalized seizures): G40.1

Localization-related (focal)(partial) symptomatic epilepsy and epileptic syndromes with complex partial seizures (which can evolve to secondarily generalized seizures): G40.2

Other epilepsy: G40.8

Epilepsy, unspecified: G40.9

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Inhibitory motor seizures

Associated Disorders

Rolandic epilepsy
Structural focal epilepsies

Differential Diagnosis

postictal (Todd) paresis
nonepileptic transient attacks of paresis
negative myoclonus
atonic seizures
transient ischemic attacks
- myoclonus
- hemiplegic migraine

Also Relevant

Atonic seizures
Benign childhood epilepsy with centrotemporal spikes
Epilepsy with myoclonic-atonic seizures
Focal clonic seizures
Myoclonic-atonic seizures

Inhibitory motor seizures

Inhibitory motor seizures

Introduction

Overview

Key points

Historical note and terminology

Table 1. Focal Motor Seizures

Clinical manifestations

Presentation and course

Prognosis and complications

Clinical vignette

Biological basis

Etiology and pathogenesis

Epidemiology

Differential diagnosis

Confusing conditions

Associated and underlying disorders

Diagnostic workup

Management

Outcomes

Special considerations

Media

References

Contributors

Author

Editor

Former Authors

Patient Profile

ICD & OMIM codes

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Also in This Category

Anti-LGI1 encephalitis

Self-limited (familial) neonatal epilepsy

Alcohol withdrawal seizures

Epileptic lesions due to malformation of cortical development

Epileptic spasms

Sleep and epilepsy

Neocortical temporal lobe seizures

Jacksonian seizures

Inhibitory motor seizures

Introduction

Overview

Key points

Historical note and terminology

Table 1. Focal Motor Seizures

Clinical manifestations

Presentation and course

Prognosis and complications

Clinical vignette

Biological basis

Etiology and pathogenesis

Epidemiology

Differential diagnosis

Confusing conditions

Associated and underlying disorders

Diagnostic workup

Management

Outcomes

Special considerations

Media

References

Contributors

Author

Editor

Former Authors

Patient Profile

ICD & OMIM codes

This is an article preview. Start a Free Account to access the full version.

Questions or Comment?

Also in This Category

Anti-LGI1 encephalitis

Self-limited (familial) neonatal epilepsy

Alcohol withdrawal seizures

Epileptic lesions due to malformation of cortical development

Epileptic spasms

Sleep and epilepsy

Neocortical temporal lobe seizures

Jacksonian seizures

This is an article preview.
Start a Free Account
to access the full version.