Focal sensory seizures with elementary symptoms …

Epilepsy & Seizures

Updated 03.07.2024
Released 03.07.2024
Expires For CME 03.07.2027

Focal sensory seizures with elementary symptoms

Authors: K P Vinayan MD DM, Soumya V Chandrasekharan MD DM

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Editor: Jerome Engel Jr MD PhD

Focal sensory seizures with elementary symptoms

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Introduction

Overview

Aura is part of a seizure that occurs before consciousness is impaired and for which memory is later retained. It reflects involvement of the non-silent cortex at seizure onset and remains a useful indicator for epileptogenic zone localization (01). Auras arising from the primary sensory cortex closely mirror its functions and are referred to as elementary symptoms; they carry the best localization value during presurgical evaluation. Hence, identifying this phenomenon in seizure semiology is of prime importance. Auras include somatosensory, visual, auditory, olfactory, and gustatory symptoms.

Key points

	• Auras are often underrecognized in clinical practice but have prime importance in seizure localization.
	• Elementary auras arise from primary sensory cortices, and as the seizure involves associated areas, they become more complex.
	• Medical management of elementary auras is the same as for focal seizures.
	• Prompt consideration of alternate clinical possibilities is required to avoid inappropriate treatment.
	• Identification of the red flags in the localization of aura, along with proper correlation to the EEG and radiological data, is mandatory to improve seizure outcomes after surgery in drug-resistant focal epilepsies.

Historical note and terminology

The term aura refers to “breeze” and originates in Roman and Greek mythology. “Aura” was a Goddess who was raped by Dionysus and became the mother of twins. She kept rage in mind throughout pregnancy, tried to kill her children, and murdered one of them. After a sequence of suicide attempts, she jumped into the river Sangarius and was transformed into a spring.

The first description of aura in literature came as early as the 2nd century AD in the work of a physician, Aretaeus of Alexandria, who described a wide variety of auras associated with epilepsy, including olfactory, vertiginous, visceral, visual, auditory, and gustatory auras (25). Later descriptions of the phenomenon came from Galen, one of Aretaeus’ contemporaries, around 200 AD.

Clinical manifestations

Presentation and course

Elementary symptoms are commonly associated with focal seizures with preserved awareness. However, auras can occur before focal seizures with impaired awareness and even generalized seizures (13). Auras can be experienced as negative or, more commonly, positive sensory symptoms. Based on the primary sensory cortex involved, elementary symptoms can be subclassified as follows.

Somatosensory symptoms. Somatosensory symptoms are abnormal sensations experienced as tingling or numbness limited to a well-defined region of the body, which localize the symptomatogenic zone to the contralateral primary sensory cortex. They are unilateral and distal in distribution and exhibit Jacksonian march. Elementary sensory symptoms can be bilateral and more widespread due to activation of the supplementary sensorimotor area or secondary somatosensory area (28). Stimulation of the secondary somatosensory area can also result in unpleasant sensations of heat or pain (32).

Visual symptoms. Commonly, elementary visual symptoms are perceived as stereotyped, multi-colored, and circular flashes appearing on the edge of a temporal hemifield or of both eyes; they multiply in number and size and move horizontally toward the other side. Usually, they develop within seconds and generally last up to 1 to 3 minutes (11). The symptomatogenic zone is identified as the primary visual cortex (Broadmann’s area 17 and 18) without a clear lateralization. Occasionally, lateralization to one visual field may be noted, which localizes the symptomatogenic zone to the contralateral primary visual cortex. Further localization to the upper or lower visual field may also be noted rarely. Not infrequently, patients report amaurosis during or after the ictus (17). As the visual stream projects to associated areas (parieto-temporal cortices through dorsal and ventral streams), more complex visual hallucinations like visual disequilibrium, autoscopy, or nondescribable visual phenomenon may be seen (05).

Auditory symptoms. Elementary sounds and noises in the form of buzzing indicate proximity to the primary auditory cortex in the superior temporal gyrus in the transverse gyrus of Heschl. Elementary auditory auras have poor lateralizing value (15). Auditory symptoms are also seen in a small proportion of patients with mesial temporal lobe epilepsy (03). The presence of auditory auras is a poor prognostic factor for seizure outcomes after anterior temporal lobectomy and amygdalohippocampectomy (04). Ictal deafness has been described from the dominant temporal lobe in the anterolateral part of Heschl’s gyrus (21). Complex auditory phenomena, such as music, relate to auditory association areas in the contiguous temporal neocortex. More complex auditory auras, such as illusions, have been associated with the posterior insula and frontal operculum (36).

Olfactory symptoms. Elementary olfactory hallucinations are usually of sudden onset, lasting 5 to 30 seconds, and may be unpleasant (burnt, chemical, or sickening sensation), neutral, or pleasant (flowers, grilled meat, pistachio); most commonly, they are unpleasant. They are localized to the primary olfactory cortex and have no lateralizing value (34). The anterior olfactory nucleus, piriform cortex, olfactory tubercle, and lateral entorhinal cortex constitute the primary olfactory cortex (26). Tumors in the orbitofrontal region, which is the secondary olfactory cortex responsible for odor discrimination, have been associated with olfactory aura (41).

Gustatory symptoms. Unpleasant taste can be a manifestation of focal seizures. The exact localization is controversial. Cortical stimulation studies have found insulo-opercular regions to be the symptomatogenic zone (19; 32). Gustatory auras have no lateralizing value.

Prognosis and complications

Medical management of elementary aura is not separate from that of focal epilepsy. As aura in focal epilepsy has good localizing value comparable to routine electrophysiological and imaging studies, identifying auras in focal epilepsy is associated with good surgical outcomes in refractory epilepsies. Among the elementary symptoms, the presence of somatosensory, visual, and auditory auras are the most valuable tools in identifying epileptogenic foci. The prognostic value and surgical outcomes of auras were extensively studied in mesial temporal lobe epilepsies. The presence of auditory and vertiginous auras has been associated with a poor seizure outcome after anterior temporal lobectomy and amygdalo-hippocampectomy (04). Moon and colleagues studied the surgical prognostic value of auras in 300 patients who underwent resective surgeries. A total of 225 patients had auras, of which 65 had elementary sensations. The presence of auditory auras was associated with a poor surgical outcome. Inducing habitual auras via intracranial electrical stimulation during presurgical evaluation had no bearing on surgical outcomes (23).

Biological basis

Localization

Elementary somatosensory aura is localized to the contralateral primary sensory cortex and is located in the anterior part of the parietal lobe, which constitutes the postcentral gyrus. Somatosensory auras, which are more widespread or bilateral, are localized to the supplementary sensorimotor area, which is located anteriorly to the primary sensory cortex in the precentral gyrus. The secondary somatosensory area is another localization for widespread somatosensory aura and is located in the superior bank of the Sylvian fissure or the posterior insula. The presence of somatosensory aura in presumed temporal lobe epilepsy raises the question of potential extratemporal seizure onset, which compromises the chances of seizure freedom following standard anterior temporal resection (27).

Elementary visual aura arises from the contralateral primary visual cortex (V1), in close proximity above and below the calcarine fissures. The superior portion of the calcarine fissure corresponds to the inferior visual field, whereas the inferior portion corresponds to the superior field. The primary function of the visual cortex is to process visual information, and it is stratified into six layers: V1 to V5 and the inferior temporal cortex. V1 is the first stop for the visual inputs and, as the visual information is passed along subsequent layers of visual cortex, becomes more specialized. V1 is constituted by simple cells and responds to specific visual cues, such as orientation of edges and lines in a single receptive visual field. V1 through V3 have more complex cells, which respond to edges and orientations of summation of several receptive fields along with movement in specific directions (16). More complex visual hallucinations are localizable to visual association areas and their projections along the dorsal and ventral streams of the visual recognition pathway.

Elementary auditory auras arise from Heschl's gyrus in the superior temporal lobe, which is the primary auditory area involved in auditory processing. Leftward asymmetries in volume of Heschl's gyrus, which is a normal variation in the human adult brain, are due to greater myelination attributed to its specialization for handling fast temporal information (24). On the other hand, the dense, highly interconnected columnar structure in the right auditory cortex makes it effective in fine frequency distinctions (31), thus, the left Heschl's gyrus processes rapidly changing auditory stimuli and the right cortex processes spectrally complex stimuli (40). Also, the processing complexity increases in the superficial layers of Heschl's gyrus (22). Diffusion tensor imaging studies have identified five tracts that pass through Heschl's gyrus fiber intersection area, including the anterior segment of the arcuate fasciculus, middle longitudinal fasciculus, acoustic radiation, inferior fronto-occipital fasciculus, and optic radiation, which are important in higher-order auditory processing, auditory visual association, and auditory learning (12). The affection of some of these fibers results in complex auditory perceptual alterations as seen in frontal opercular epilepsies (36).

Elementary olfactory auras are localized to the anterior olfactory nucleus, piriform cortex, olfactory tubercle, or lateral entorhinal cortex, which are the components of the primary olfactory cortex. Three olfactory areas have been identified in the human brain. The medial olfactory area is the primitive olfactory system located in the midbasal portions of the frontal lobe anterior to the hypothalamus. It connects to the hypothalamus and limbic system and is concerned with basic olfactory reflexes. The lateral olfactory area consists of the prepyriform and pyriform cortex and amygdala and is important in liking healthy foods and disliking unhealthy foods. The newer olfactory area, which is concerned with conscious perception and analysis of olfaction, is connected to the orbitofrontal cortex via the thalamus. The first and second olfactory areas are concerned with elementary olfactory, and the third area with complex auras (34).

Gustatory auras are less well studied and mostly arise from insulo-opercular regions.

Etiology and pathogenesis

The International League Against Epilepsy classified the etiology of seizures and epilepsy syndromes into six categories (13). Etiologies for focal seizures with preserved awareness under these categories include:

	(i) Structural causes like stroke, trauma, infection, tumor, or focal cortical dysplasia.
	(ii) Genetic causes like mutations in RELN1 or LGI1 genes and often dysregulation in the mechanistic target of rapamycin complex 1 (mTORC1) pathway are associated with autosomal dominant lateral temporal epilepsy.
	(iii) Infectious etiologies include tuberculosis, neurocysticercosis, and cytomegalovirus.
	(iv) Metabolic causes for focal epilepsies commonly include mitochondrial encephalopathy with lactic acidosis and stroke-like episodes, peroxisomal disorders, and pyridoxine-dependent epilepsy.
	(v) Immune-mediated focal epilepsy syndromes include Rasmussen encephalitis, antineuronal nuclear antibody type 1 (anti-Hu) encephalitis, anti-N methyl-D-aspartate (anti-NMDA) receptor encephalitis, anti-leucine-rich glioma inactivated 1 (anti-LG1) encephalitis, contactin-associated protein-like 2 (CASPR2) encephalitis, and glutamic acid decarboxylase 65-antibody (GAD65) encephalitis.
	(vi) The etiology is unknown in a third of focal epilepsies, as seen in self-limited focal epilepsies of childhood.

Pathophysiology

Epileptogenesis results from the transformation of a normal neuronal network into a chronically hyperexcitable one is a dynamic process that establishes critical interconnections and results in structural changes like neurogenesis, gliosis, axonal damage, sprouting, dendritic plasticity, blood-brain barrier damage, recruitment of inflammatory cells into brain tissue, reorganization of the extracellular matrix, and reorganization of the molecular architecture of individual neuronal cells. Excitatory potentials result in ictogenesis by the generation of paroxysmal depolarization shifts in individual neurons, synchronization of epileptiform discharges, and setting off slow depolarization and burst discharges. The major neurotransmitter involved is glutamate.

Differential diagnosis

Confusing conditions

Migraine with aura. Migraine is a close differential diagnosis of focal sensory seizures with elementary symptoms, the commonest being migraine with visual aura. Migraine and epilepsy often co-exist in the same individual. The prevalence of migraine among persons with epilepsy ranges from 8% to 24% (37) and has been studied extensively in temporal lobe epilepsy and juvenile myoclonic epilepsies (30). The most common type of aura in migraine is visual aura (87.1%), followed by sensory (38.5%) and speech and language auras (15.6%). Olfactory auras are rare in migraine and may be seen in around 3.9% of cases (33; 02). Visual disturbances in migraine aura develop slowly over 4 to 60 minutes and are mainly uncolored or black-and-white patterns, although colorful aura is seen in up to 40% (29). They appear in the center of the visual field and move peripherally. Scintillating scotoma and blurry vision are the most frequent visual symptoms in children, followed by tunnel vision and zig-zag lines. Visual perception abnormalities are seen in adults (18). Migraine aura rarely has accompanying neurologic symptoms like tonic deviation of the eyes and alterations in consciousness. Multiple auras, including somatosensory, auditory, and olfactory hallucinations, can also co-occur in migraine.

Transient ischemic attacks. Transient ischemic attacks are often difficult to differentiate from epileptic auras clinically but are more prolonged (minutes to hours). The phenomenology is mostly negative with a loss of elementary sensory perception like loss of vision or field cuts; positive sensory phenomena are very rare in transient ischemic attack MRI, and EEG might often be normal in both situations.

Psychiatric disorders. Hallucinations have been reported in a variety of psychiatric disorders like schizophrenia, bipolar disorder, severe depression, mania, and substance abuse (10). Seventy percent of patients with schizophrenia experience hallucinations, most commonly auditory but also visual. Auditory hallucinations are typically third-person hallucinations. Visual hallucinations have a predominance of denatured people, body parts, or unidentifiable things. Severe depression is sometimes accompanied by auditory hallucinations, which are usually transient and consistent with the patient's depressed mood. Auditory hallucinations may also occur in mania. Negative hallucinations have been reported in depression.

Associated and underlying disorders

Focal sensory seizures with elementary symptomatology are seen in both self-limited and structural focal epilepsies with foci closer to the primary sensory areas. Evaluation should be directed toward identifying the focus and the underlying structural lesion. Autoimmune and genetic epilepsies may also present with focal sensory seizures with elementary symptomatology.

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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.

Authors

K P Vinayan MD DM

Dr. Vinayan of the Amrita Institute of Medical Sciences has no relevant financial relationships to disclose.
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Soumya V Chandrasekharan MD DM

Dr. Chandrasekharan of Lisie Hospital in Kochi, India, has no relevant financial relationships to disclose.
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Editor

Jerome Engel Jr MD PhD

Dr. Engel of the David Geffen School of Medicine at the University of California, Los Angeles, has no relevant financial relationships to disclose.
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Patient Profile

Age range of presentation: 0-65+ years
Sex preponderance: No sex preponderence
Heredity: Autosomal dominant in subset of neocortical temporal epilepsies with auditory aura
Population groups selectively affected: No population groups selectively affected
Occupation groups selectively affected: No occupation group selectively affected

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Focal sensory seizures with elementary symptoms

Associated Disorders

Self-limited focal epilepsies of childhood
Childhood occipital visual epilepsy
Autosomal dominant lateral temporal epilepsy

Differential Diagnosis

Migraine with aura
Transient ischemic attacks
Psychiatric disorders
Psychogenic nonepileptic events

Also Relevant

Aura continua
Childhood occipital visual epilepsy
EEG in epilepsy
Focal seizures with experiential symptoms
Frontal lobe seizures
- Migraine and epilepsy
- Migraine aura without headache
- Migraine with brainstem aura

Clinical Categories

Epilepsy & Seizures

Focal sensory seizures with elementary symptoms …

Focal sensory seizures with elementary symptoms

Introduction

Overview

Key points

Historical note and terminology

Clinical manifestations

Presentation and course

Prognosis and complications

Biological basis

Localization

Etiology and pathogenesis

Pathophysiology

Epidemiology

Prevention

Differential diagnosis

Confusing conditions

Associated and underlying disorders

Diagnostic workup

Management

Special considerations

Pregnancy

Anesthesia

References

Contributors

Authors

Editor

Patient Profile

ICD & OMIM codes

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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

Focal sensory seizures with elementary symptoms

Introduction

Overview

Key points

Historical note and terminology

Clinical manifestations

Presentation and course

Prognosis and complications

Biological basis

Localization

Etiology and pathogenesis

Pathophysiology

Epidemiology

Prevention

Differential diagnosis

Confusing conditions

Associated and underlying disorders

Diagnostic workup

Management

Special considerations

Pregnancy

Anesthesia

References

Contributors

Authors

Editor

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.