Online newspaper of professor Yasser Metwally

The author: Professor Yasser Metwally

http://yassermetwally.com

INTRODUCTION

It was stated that a spike focus does not necessarily denote a stable epileptogenic focus; benign Rolandic epilepsy stands as the epitome of the truth of this statement. Zones of cortical hyperexcitability (hyperirritability) may behave like a focus in the EEG, but these dysfunctions may burn themselves out with advancing age. Not so an epileptogenic focus which is based on cerebral pathology. Most of this pathology is residual, while the possibility of a space-occupying lesion must always be kept in mind. But are residual epileptogenic lesions quiet residues of a bygone active disease? Modern electromicroscopic work has shown that “residual” gliosis is a very active process, which provides a better understanding for the epileptic irritation of neurons. In this chapter we will discuss the electroclinical criteria of some focal epilepsies.

TEMPORAL LOBE EPILEPSY

• Introductory Remarks

The temporal lobe is far more often than any other areas the seat of an epileptogenic focus. What renders the temporal lobe so prone to harbor epileptogenic foci? The answer probably lies in 1) special anatomo-physiological properties of the limbic (arche- and palcocortical) portion of the temporal lobe, and 2) a certain vulnerability of neocortical and limbic parts of the temporal lobe to some forms of pathology.

Seizures arising from the temporal lobe have captivated the interest of epileptologists, electroencephalographers, neurologists, neurosurgeons, and even psychiatrists during the past decades. The impressive multitude of temporal lobe functions in the human are reflected by the enormous variety of seizure patterns. Temporal lobe functions are in part higher cortical functions; they are also functions of the limbic system with its crossroads of autonomic nervous system regulations and emotionality.

• Terminology

The term “temporal lobe epilepsy” is correct as far as “seizures arising from the temporal lobe” are concerned. It should not be used as a synonym for psychomotor (complex partial) seizures, since 1) not all seizure manifestations of the temporal lobe fall into this category (many patients also have grand mal seizures and a few have grand mal only) and 2) psychomotor (complex partial) seizures may occasionally originate from the vicinity of the temporal lobe, usually as extensions of the limbic system into the fronto-orbital region. The reader will find more information and details on the historical development in the section on types of psychomotor seizures.

• Clinical Ictal Manifestations

The wide variety of seizure manifestations is presented in the section on types of psychomotor seizures.

• Ictal EEG Manifestations

See the section on types of psychomotor seizures.

• Interictal EEG Manifestations

The anterior temporal spike or, more often, sharp wave discharge, randomly firing, is the classical EEG finding in the interseizure interval. With the use of the International Electrode System, this discharge is recorded from the F7, or F8, electrode, which is essentially frontobasal and slightly in front of the tip of the temporal lobe. Sleep EEG studies are highly important in demonstrating anterior temporal spiking otherwise anterior temporal spiking might be missed in a tracing obtained solely in the waking state.

Figure 1. Typical anterior temporal spikes in a patient with temporal lobe epilepsy

The spike (sharp wave) discharge is bilateral in about 25 to 35% of the cases. Patients with bilateral anterior temporal spikes (sharp waves) are more likely to have both psychomotor and grand mal seizures. Sleep has an important role in the facilitation of temporal spikes.

Bilateral anterior temporal spiking may be bilateral independent or synchronous. Bilateral synchrony has been divided into real synchrony and discharges transmitted from one side to the other. The spike discharge occurs over one temporal lobe only in 34%, while transmission from side to side is noted in 24%, synchrony in 19%, and bilateral independence in 23%.

Brain tumor is rarely discovered in patients with bilateral independent temporal spikes. Patients with unilateral spikes often prove to have mesial temporal sclerosis; the superior aspects of the temporal lobe showed a maximum of corticographic spike activity. Patients with lesions of the basomesial surface and the tip of the temporal lobe revealed spikes transmitted secondarily to the opposite side or bilateral synchronous spiking. These patients may show less prominent or even equivocal scalp EEG findings.

The paroxysmal EEG abnormalities may exceed the boundaries of the temporal lobe. Psychomotor or complex partial seizures are more likely to occur when focal EEG abnormalities are limited to the temporal lobe.

In some patients, anterior temporal spikes are scanty, while consistent focal slowing is present over this area. This pattern is usually not good evidence for a space-occupying lesion unless progression of the focal slow (mainly polymorphic delta) activity is demonstrable.

Children and young adolescents with temporal lobe epilepsy and unequivocal complex partial seizures often have inconclusive EEG findings. Spikes or sharp waves may be over midtemporal or central regions (thus falsely suggestive of benign Rolandic epilepsy) or diffuse. Even generalized spike wave discharges may occur and slow spike wave complexes may overshadow all other abnormalities when one deals with a case of Lennox-Gastaut syndrome giving rise to psychomotor seizures.

It evidently takes a while until the classical anterior temporal spike (sharp wave) focus is fully developed. Very rarely, the opposite happens with anterior temporal spiking being just a form of benign midtemporal spiking (even without any seizures and with full EEG normalization at age 11 yr). With advancing age, the anterior temporal spike focus increasingly becomes the impressive hallmark of temporal epilepsy, until an overabundance of this discharge occurs. Above age 50-60 yr, the anterior temporal spike or sharp wave is, in most cases, a simple exaggeration of temporal minor sharp activity, which is extremely common in elderly patients with mild or moderate degrees of cerebrovascular disorder and no seizure disorder whatsoever. In epileptics above age 50, temporal lobe spiking is a very common finding, but this does not necessarily mean that one is dealing with a temporal lobe epileptic; on the contrary, grand mal seizures outnumber psychomotor seizures by a wide margin.

The combination of total absence of paroxysmal discharges, marked unilateral temporal polymorphic delta activity, and recent onset of psychomotor seizures is very suggestive of a rapidly growing temporal lobe tumor. Very slowly growing tumors such as certain astrocytomas may show EEG patterns undistinguishable from those of temporal lobe epileptics with mesial temporal sclerosis. Meningiomas of the medial sphenoid wing position and psychomotor seizures may have very little or no EEG abnormality.

Small sharp spikes (see chapter on abnormal paroxysmal patterns) may appear over the temporal region and its neighborhood in early sleep as forerunners of typical large anterior temporal sharp waves, giving support to the diagnosis of temporal lobe epilepsy. The occurrence of small sharp spikes alone, however, contributes nothing to this diagnosis. These small discharges arise from a wide region, including deep structures and might indicate only some degree of neuronal hyperexcitability.

An unusual EEG pattern in temporal lobe epileptics might take the form frontal midline theta activity with an average frequency of 5.78/sec in 36% of these patients.

Table 1 Electroclinical characteristic of temporal lobe epilepsy.

Unfortunately, it must be conceded that a fair number of patients with unequivocal psychomotor (complex partial) seizures show normal EEG tracings awake, asleep, and with activations, not only once but repeatedly. The availability of a CT scan, MRI is particularly important, since certain deep seated tumors impinging on the medial portions of the temporal lobe may give rise to seizures without inter-ictal EEG abnormalities. Sleep deprivation may occasionally bring the EEG abnormalities into the open. A sharp reduction of anticonvulsants usually has a remarkable effect, but, as a conscientious physician, one uses this form of activation with great reservation and reluctance. The epileptic rebound may lead to more widespread or even generalized seizure discharges, thus masking the focal character of the seizure disorder, or, much worse, the patient will have numerous seizures; worst of all, a dreadful status epilepticus grand mal may develop.

The addition of nasopharyngeal leads improves very slightly the chances of demonstrating a temporal lobe epileptogenic focus. In addition to the artifact-proneness of these leads, the electrodes may easily cross over to the side contralateral to the nostril of insertion. Sphenoidal leads are more likely to yield valuable additional information from the anterior portion of the temporal lobe; the invasive character of their insertion has discouraged most electroencephalographers from using these electrodes.

• Age and Prevalence

Temporal lobe epilepsy spans a period from early childhood to senility but, as was pointed out, classical cases are usually found in older adolescents and in young and middle-aged adults; childhood and senium tend to dilute the clinical and EEG semiology.

• Psychological and Psychiatric Features

A review of the copious literature on this subject could fill a monograph; in this context, we have to confine ourselves to a few basic statements. According to personal impression, the most common psychological features are irritability and hyposexuality; these data were derived from patients considered candidates for temporal lobectomy because of the severity of their seizure disorder.

A constant state of irritability renders these patients more volatile; some of them exhibit hostility and are prone to aggressive acts, but it must be stated very clearly that these cases are exceptional and not the rule. In recent decades, the conjunction of acts of violence or crime and temporal lobe epilepsy has been widely accepted without sufficient support from clinical data. Single observations of aggressive acts must be considered exceptional. Studies of large patient groups have clearly shown the rarity of aggressive acts in patients with temporal lobe epilepsy. Hyposexuality has been confirmed in these patients.

Patients with major psychomotor epilepsy are subject to an increased risk of psychiatric disturbance but that, except the immediate postictal psychotic state, the risk appears to reflect the site and extent of brain damage and the individual’s psychosocial history and opportunities more than a diagnosis of epilepsy.” This author also feels that “. . . temporal lobe epilepsy makes a very small contribution to the pool of psychiatric disturbances, including violence.”

Relationships to the schizoid personality have been frequently reported and combination with overt schizophrenia is well known, though not common.

The electroencephalographer will occasionally find that patients with temporal lobe epilepsy and schizophrenia show marked EEG improvement or completely normal tracings when the psychiatric condition is at its worst, while the patient is practically seizure-free, and vice versa (enhanced seizure disorder, massive spiking and psychiatric improvement). This “seesaw phenomenon” has been observed (“forced normalization”).

A comparison of left- and right-sided temporal epilepsies (dominant versus nondominant temporal lobe) has shown some psychological-psychiatric differences. Epileptogenic foci in the temporal lobe in the dominant hemisphere are more likely to be associated with aggressive behavior.

The causes of temporal lobe epilepsy are as follows (in order of frequency)

• No histopathological abnormality, the most common

• Unspecified minor abnormalities

• Cortical neuronal loss and gliosis

• Gliomas and ganglioglioma

• Cortical neuronal loss, gliosis and hippocampal sclerosis

• Meningo-cerebral cicatrix and remote contusion

• Vascular formation of brain and/or pia

• Hamartomas

• Tumors other than gliomas

• Residuum of brain abscess

• Post-meningitic cerebral atrophy

• Tuberous sclerosis and formes frustes

• Subacute and chronic encephalitides

• Ulegyria

• Anomalous cases

• Residuum of old infarct

The higher incidence of tumors deserves special attention when one considers their progressive and eventually life threatening nature. A sizeable portion of these tumors, however, are of very mildly progressive nature and almost behave like a nontumoral lesion. Small tumors as the cause of seizures are found mainly in the mesio-inferior areas such as an uncus and amygdaloid region. Temporal lobe seizures may also be caused by a pituitary tumor with a large supradiaphragmatic portion and, furthermore, by lipomas of the corpus callosum.

• Neurophysiological Mechanisms

Limbic and neocortical portions of the temporal lobe (and, not seldom, of the adjacent fronto-orbital region) are actively involved in the ictal and inter-ictal epileptic phenomena of temporal lobe epilepsy. The uncinate region, comprising the amygdaloid complex, uncinate gyrus, and anterior-insular and peninsular portions of the temporal lobe, appears to be mostly involved in typical psychomotor automatisms, whereas the lateral temporal neocortex appears to be most active in experienced psychomotor seizures.

The role of the hippocampus remains enigmatic. Hippocampic electrical stimulation in man almost never results in afterdischarges or seizures this structure is more likely to be secondarily involved. Its role …… “to consolidate memory traces”, is often jeopardized in ictal activity. It must be added that the left and right hippocampus apparently serve special memory functions, with verbal memory on the dominant and nonverbal visual memory on the nondominant side. Amygdalo-hypothalamic connections are likely to account for emotional responses, in normal physiology as well as, in a morbid and exaggerated form, during ictal activity. Connections between amygdala and basal ganglia (putamen, globus pallidus, putamen) might serve the behavioral-motor component of temporal lobe seizures. Autonomic manifestations are probably served by the amygdala through the hypothalamus or originate from the insular cortex. Bilateral temporal lobe involvement is very common.

• Course and Therapy

Until a few years ago, 4 principal medications were used for partial seizures: phenytoin, carbamazepine, valproate, and phenobarbital. In recent years, a number of newer medications have been approved by the FDA. These newer AEDs have not been evaluated in double-blind trials as monotherapy, so how they compare to the older AEDs is not known. The initial choice of medication depends on side-effect profile, cost considerations, and dosage schedule. The major VA trials did not show any significant difference in seizure control among the 4 older AEDs. Adverse effects were greater with phenobarbital and with valproate.

Single-drug therapy is the goal, and the dosage of each medication prescribed should be increased until either seizures are controlled or adverse effects occur.

Temporal lobe epilepsy is a serious seizure disorder. Good therapeutic responses to first line medications are the exception rather than the rule.

It is saddening to see a large number of patients remain unresponsive to any medication. These patients are candidates for surgical treatment by temporal lobectomy. The facilities for seizure surgery are limited and the selection of patients is beset with psychological problems. Not every suitable candidate is sufficiently motivated to give his consent for this operation. In well screened material, about 40% of the patients will become seizure-free after temporal lobectomy.

The electroencephalographer is often amazed at the minor effects of temporal lobectomy on the EEG as such; such changes are often limited to local voltage depression corresponding to the cortical removal. The excision of this sizeable portion of brain tissue usually produces less EEG effect than a diagnostic cortical biopsy, which is often followed by marked local delta activity for a period of time. Persisting seizure discharges are likely to change their spatial distribution to some extent; previous anterior temporal spike activity may move to the midtemporal region.

FRONTAL LOBE EPILEPSY

• Introduction

Frontal lobe epilepsy is much less common than temporal lobe epilepsy. Moreover, frontal lobe epilepsy is less significant as an epileptological entity. Frontal lobe seizures often consist of immediate grand mal attacks, thus obscuring any focal initiation, has been widely confirmed.

• Seven different clinical seizure patterns are distinguished:

1. Immediate unconsciousness followed by a grand mal with minimal or no lateralizing signs.

2. Immediate unconsciousness associated with initial turning of the head and eyes (sometimes of the body) to the opposite side, promptly followed by a grand mal, probably originating from the anterior third or fourth of the frontal lobe contralateral to the adversive movement.

3. Initial adversion of head and eyes to the opposite side, preserved consciousness, and conscious adversive (contraversive) attack which, after 5 to 20 sec may or may not be followed by a grand mal. The origin usually lies in the convexity of the intermediate frontal region.

4. Posturing movement of the body with tonic elevation of the contralateral arm, downward extension of the ipsilateral arm, and turning of head away from the side of the lesion as if looking at the raised hand. This type of seizure arises from the medial aspect of the intermediate frontal region in the vicinity of the supplementary motor region. This type of seizure has also been described as “mesiofrontal epilepsy”and was attributed to the supplementary motor region within the interhemispheric fissure.

5. Brief attacks of “dizziness,” a “flush,” or “weak” feeling. This vague sensation may stop after a few seconds or it may be followed by brief arrest of activity, confusion, and staring. This attack imitates the petit mal absence clinically and even electroencephalographically. In contrast with true petit mal absences, these attacks may be followed by a grand mal.

6. Sudden alteration of thought processes, such as “forced thinking” (“my thoughts suddenly became fixed”). This may be followed by a petit mal-like absence or by a grand mal.

7. Seizures arising from the fronto-orbital cortex are practically undistinguishable from temporal lobe epilepsy. Petit mal absence status-like ictal symptomatology due to a left frontal epileptogenic focus is occasionally demonstrated.

• More frequently occurring seizure manifestations are listed in the following table.

Table 2. Subdivision of Frontal Lobe Seizures.

• EEG Observations

Frontal lobe spiking may be found in various forms. Spike activity is particularly scarce and the search for an EEG focus often elusive in mesiofrontal (interhemispheric) foci. If demonstrable at all, spikes are found over the superior frontal or frontal midline region; their size is small.

Large and somewhat blunted sharp waves are found in cases of presumed fronto- orbital epilepsy. Generalized synchronous spike wave bursts are found in patients with bilateral synchrony. In some of the cases, only depth EEG can demonstrate the primary focus. The ictal patterns of frontal lobe epilepsy are not basically different from other forms of neocortical focal seizure disorders.

• Course and Therapy

Anticonvulsants indicated for use in partial seizures are the medical treatment of choice. Patients will generally require many years of treatment, so consideration of side effects is important. While most of the anticonvulsants are in pregnancy category C or D, the risk of medication to the fetus must be weighed against the risk of maternal seizures to the fetus. Due to the risk of level fluctuations, patients should not switch between brand and generic anticonvulsants, and if a generic is used, patients should receive the same generic formulation consistently.

ROLANDIC (SENSORIMOTOR) EPILEPSY

• Introductory Remarks

This subsection essentially pertains to Rolandic epilepsies of adult life; benign Rolandic epilepsy of childhood and rare cases of progressive Rolandic epilepsy in children have been presented in the chapter on age-determined epileptic conditions.

Focal motor seizures arising from the pre-central motor region have been well known. These seizures beautifully reflect the somatotopic arrangement of the motor cortex. Jackson (1870) made a clear distinction between seizures starting with twitching of facial and glossal muscles and those starting with finger, hand, or foot movements of the opposite side.

The somatotopic arrangement of the motor cortex must not be conceived of as a mosaic in which the smallest focus of epileptic irritation will give rise to contralateral twitching of extremely small corresponding muscular segments. In other words, there does not seem to be full equality among the cortical segments. Areas with a large cortical-Rolandic representation also have low thresholds for electrical stimulation (index finger, thumb, then face and foot). This is probably also true for the less commonly focal sensory seizures arising from the post-central gyrus.

• Clinical-ictal Manifestations

Clonic twitching of contralateral muscle segments with preserved consciousness is the principal manifestation of Cortical motor Rolandic epilepsy. This clonic activity may a) remain localized, b) spread over the rest of the contralateral half of the body, and c) eventually culminate in a grand mal seizure. The spread of clonic activity from one body region to another is widely known as “Jacksonian march”.

Focal Rolandic motor seizures usually last from 10 see to several minutes. Attacks exceeding a duration of 30 min must be regarded as a focal motor status or even as epilepsia partialis continua or Koshevnikov syndrome. Most attacks started in the hand, followed by mouth, arm, fingers, foot, face, and leg. Involvement of trunk muscles was uncommon.

As to epileptic manifestations of the sensory Rolandic cortex (post-central gurus), a variety of paresthesias or dysesthesias have been observed. “Formication,” or the sensation of running ants, is the most common symptom, followed by numbness, pain, and sensations of heat or cold. Pain as a sensoricortical ictal symptom is more common than one would expect from experimental data concerning pain perception and the post-central gyrus.

Focal motor or sensory attacks can stop at any stage. Sensory focal attacks are usually quickly associated with focal motor activity. Uncontaminated sensory cortical seizures are so rare that one should thoroughly rule out possibilities such as ischemic cerebral attacks or peripheral neuritic pain.

Bilateral focal motor seizures are extremely rare. In such cases, the clonic motions spread from one side gradually to the other half of the body.

Post-epileptic paralysis (Todd’s paralysis) has been known since the original observations of Todd (1856). Post-ictal paresis of the ictally involved muscle segments has been thought to be caused by metabolic exhaustion but, in recent years, the concept of active inhibition has prevailed. Postictal motor deficits are more common in active pathology such as vascular lesions, AV malformations, or tumors. In general, these motor deficits are more common in children and last for minutes, hours, or a few days.

• EEG Findings

The ictal EEG shows astounding variations. Lack of ictal EEG changes is a well known weakness of electroencephalography, probably due to the smallness of the cortical spiking. In the majority of the cases, ictal repetitive spiking is present over the affected motor cortex. Interictal spike activity also shows variations ranging from absence to pronounced focal spiking, which, incidentally, is most common in children with benign Rolandic epilepsy. In patients with acute watershed-type infarctions, focal motor seizures are often accompanied by PLED.

• Neurophysiological Considerations

Focal motor seizures are usually strictly cortical, but the structural lesion causing the seizures may not be precisely located in the Rolandic region. Neighboring lesions may cause the pre-central cortex to erupt in epileptic discharges due to its low threshold.

• Etiology

Onset of focal motor or focal sensory seizures in adult life must always raise the suspicion of a tumor involving or in the vicinity of the Rolandic cortex. Arteriovenous malformations should also be considered one of the more common causes of focal motor seizures. Post-traumatic epilepsy and cerebral arteriosclerosis are also common causes; neurosyphilis and tuberculoma previously ranked high in the list of causes.

• Prevalence

Prevalence is probably between 3 and 10% of a population of epileptics, depending on the sampling.

• Therapy and Course

Therapy and course depend strongly on the type of underlying pathology. In general, focal motor and sensory seizures show a good to very good response to first line anticonvulsants. Surgical interventions are limited by the threat of subsequent catastrophic motor deficits. Removal of parasagittal meningiomas is usually followed by excellent results.

PARIETAL LOBE EPILEPSY

Epileptic phenomena of parietal origin do not form a well defined epileptological entity. Parietal lobe functions are complex; functional differences between the dominant and the nondominant parietal lobe compound the problems of parietal lobe function.

There is, therefore, no typical parietal lobe seizure symptomatology. In most cases, the seizures affect visual functions and a variety of complex visual disturbances may be found, such as scintillation or oscillopsia. Short attacks of extremely severe vertigo may occur. Automatisms and ictal tonic postural changes of the upper limbs is reported as parietal lobe phenomena.

Trauma is the most common cause of these seizures. Post-traumatic epilepsy caused by lacerating wounds from high velocity projectiles and shell fragments most often affects the centroparietal region.

OCCIPITAL LOBE EPILEPSY

Epileptic phenomena of the occipital lobe are not common. When the attacks originate from the calcarine fissure, elementary visual sensations such as bright light, sparks, or a ball of fire are experienced. The sensations may move across the visual field or remain stationary for the duration of the seizure. Spread from a temporal lobe focus into the occipital region with elementary visual ictal sensations has been reported.

Attacks of blindness may be accompanied by generalized spike wave activity. Bilateral synchronous occipital spike wave activity has been reported during visual hallucinations. Epileptic nystagmus, also called oculocionic seizures, may occur during occipital lobe seizures. It is interesting to note that occipital lobe epilepsy tends to occur in acute or subacute cerebral disorders. Occipital lobe epilepsy must be carefully distinguished from migrainous or ischemic disturbances.

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