| Aura Continua Heinz Gregor Wieser Date of submission: May 4, 2001 Date of Update: September 17, 2003 Medline SEARCH DATE: September 17, 2003 |
|
Acknowledgements
and disclosures Please disclose any financial or other conflicts of interest that might bias your contributions, or give rise to the perception of such bias. Relevant financial ties can include consultantships, memberships in speaker's bureaus, grants, research support, salaries, royalties, ownership, equity positions, stock options, or other financial arrangements wherein you stand to gain substantially from an increase of stock value or corporate revenues. Disclosures and acknowledgements will be linked to the author name(s) and will display along with appointments and affiliations. Disclosures, acknowledgements, and affiliations can be entered and updated via the "Update My Profile" link in the Online Submission System. Alternatively, you may send such information along with your updated manuscript. Thumbnail So that MedLink Corporation can highlight your clinical summary and your authorship on the MedLink Neurology home page and in our weekly email to subscribers, we ask that you provide here a brief overview of your subject (about 50 to 100 words) aimed at enticing readers to view this clinical summary. For updates, please include a sentence that refers to something new you have added. Refer to yourself in the 3rd person (eg, Dr. Doe of Superior Institution explains the basics…). For more information and examples of thumbnails, please see the Instructions to Authors, which can be downloaded from your "My Writing Assignments" page in the Online Submission System (http://www.medlinkoss.com). Current thumbnail: Aura continua is an intriguing condition of epileptic nature. The reason long-lasting seizure discharges remain restricted to a circumscribed area of the brain is not completely understood. However, new insights emerge from animal models of epilepsy and, in particular, from studies of network disturbances seen in cortical dysgenesis. Aura continua has been observed with a variety of clinical signs and symptoms that depend on the localization of the epileptic discharge and reflect the functional organization of the brain. In this clinical summary, Heinz-Gregor Wieser, MD, of the Universitatssipital in Zurich, Switzerland, reviews the most fascinating phenomena described within the context of aura continua. These phenomena include ictal psychic phenomena with perceptual hallucinations, mnemonic, emotional, and other rare misperceptions, such as depersonalization, distortion of body image, and heautoscopy. HISTORICAL NOTE AND NOMENCLATURE It is interesting to
note that Alexander von Tralleis (6th century) recommended that in
patients with such an aura, the therapy should also be directed to the
organ affected by the aura. He described a patient in whom he had
successfully treated his epilepsy by local application of capsicum to his
involved foot (Heintel 1975). John Hughlings Jackson (1835-1911) then described masterly what was
later on called psychomotor attack by Gibbs and colleagues and
Dämmerattacke (twilight attack) by Meyer-Mickeleit (Gibbs et al 1937;
Meyer-Mickeleit 1950). Jackson’s concept of "a particular variety of
epilepsy" (Jackson 1889), the "uncinate fits" also had forerunners. In
1748 Robert Whyatt had described such a condition with gelastic seizures
and olfactory aura (Whyatt 1765). Anderson as well as Jackson and Beevor
had noted the association of temporal lobe tumors with olfactory
hallucinations and dreamy states (Jackson and Beevor 1890; Anderson 1996).
However, it was the post mortem finding of a small cystic lesion
restricted to the uncinate gyrus in a patient who had suffered from
seizures with dreamy states, elaborated automatisms, and amnesia (Jackson
and Colman 1898) that led Jackson and Stewart to the concept of "uncinate
fits" with "origin of the discharge lesion . . . made up of some cells,
not of the uncinate gyrus alone, but of some cells of different parts of a
region of which this gyrus is part . .“ (Jackson and Stewart 1899). Modern
neurology and epileptology is proud of its achievements, but it is
difficult to add much to the early description of Jackson and Stewart:
The term "aura" is usually referred to that portion of a seizure experienced before loss of consciousness occurs and for which memory is retained. In the case of simple partial seizure, the aura is the entire seizure; but where consciousness is subsequently lost, the aura is, in fact, the first symptom of a psychomotor or complex partial seizure (Dreifuss 1997). To the best of my knowledge, Scott and Masland first described somatosensory hallucinations as a "continuous symptom" of an "aura continua” (Scott and Masland 1953). The term "aura continua" can be found in Karbowski as a synonym for continuous psychomotor status (Karbowski 1985; Wieser 2001). Wolf used it as synonym for "status epilepticus of focal sensory seizures" or for hallucinosis (Wolf 1970; 1980; 1982). On the other hand, in a recent glossary of epilepsy terminology (Kaplan et al 1995) under the term “aura,” one can read, "Although commonly used this term has been ‘officially’ discarded since 1973. . ." Wieser describes the problems with the terminology of nonconvulsive status epilepticus, including aura continua (Wieser 2001). Aura continua is a subtype of nonconvulsive status epilepticus and is synonymous with simple partial status epilepticus. CLINICAL MANIFESTATIONS Long-lasting epileptic phenomena can be motor, nonmotor, or both (Blum 2002). Although it is reasonable to assume that all types of simple partial status epilepticus (SPSE) with motor phenomena are associated with some kind of somatosensory phenomena, we feel that the term aura continua should be restricted to those subjective feelings without visible motor phenomena because the involuntary movement is sensed. Thus, we exclude here SPSE with motor phenomena or any other objective phenomena such as aphasia. Dysphasic or aphasic SPSE and the syndrome of acquired epileptic aphasia (Landau-Kleffner syndrome) and its relationship with electrical status epilepticus during slow sleep in children is now listed under "epilepsy with continuous spike-waves during slow wave sleep” (Wieser 2001). From a clinical point of view, aura continua can be classified into 4 types: (1) somatosensory (ie, dysesthesia phenomena that involve the trunk, head and extremities); (2) aura continua that involve the special senses (ie, visual, auditory, vertiginous, gustatory and olfactory); (3) aura continua with predominantly autonomic symptoms; and (4) aura continua with psychic symptoms (VanNess et al 1997). A special subtype in children, the so-called abdominal aura continua (abdominal epilepsy, recurring abdominal pain) has been described (Schaeffler and Karbowski 1981; Mitchell et al 1983; Peppercorn and Herzog 1989). Finally, the French authors have used a category "erratic.” Under this category, rare other manifestations and boundary conditions can be summarized (Wieser 1997). Although well localized (or hemi-) dysesthesia as a cortical phenomenon of ongoing ictal discharges is likely to exist; convincing evidence (ie, support by clear-cut EEG findings) is scanty. Pain as an epileptic aura (Whitty 1953), and painful epileptic seizures are likewise uncommon but are described (Wilkinson 1973; Young and Blume 1983; Siegel et al 1999). Direct evidence that long-lasting pain occurs as aura continua (ie, as a special form of partial status epilepticus) is also scanty, but this possibility should not be discarded. Certain forms of pain per se might be closely linked to epileptic basic phenomena (Fromm et al 1987), and the positive therapeutic effect of antiepileptic drugs in such circumstances is well-known. Aura continua with elementary visual phenomena has been encountered by Gastaut, and prolonged complex visual hallucinations were described by Gastaut, and Sowa and Pituck (Gastaut 1983; Sowa and Pituck 1989). Status epilepticus amauroticus has been described by Barry and colleagues, and ictal visual hallucinations with reversible postictal hemianopia with anosognosia by Barry and colleagues, and Spatt and Mamoli (Barry et al 1985; Spatt and Mamoli 2000). Sheth and Riggs reported an unusual case of a clinically silent occipital electrographic status epilepticus persisting for more than 3 years in a 13-year old girl (Sheth and Riggs 1999). Hadjikoutis and Sawhney (Hadjikoutis and Sawhney 2003) described a case with occipital seizures presenting with bilateral visual loss. Schiffter and Straschill as well as Wieser described aura continua musicalis (Schiffter and Straschill 1977; Wieser 1980). Our patient was published under the heading psychomotor status epilepticus because eventually, the aura continua with musical hallucinations (the patient experienced a song well-known and familiar to her) in "endless repetition" and with stereo-EEG documented restricted epileptiform discharges near Heschl's gyrus spread to the ipsilateral mesiobasal limbic structures, accompanied by alteration of consciousness. The beginning of this electrical epileptiform status activity was accompanied by musical hallucinations only. Most cases with simple auditory hallucinations described in literature do not fulfill the criteria of an aura continua (Penfield and Perot 1963; Karbowski 1980). Blanke and colleagues (Blanke et al 2003) described a patient with epilepsy (secondary to left parieto-temporal brain damage) suffering from the paroxysmal unilateral experience of hearing a person in her near extrapersonal space associated with a deficit in spatial auditory perception and other paroxysmal disorders of somatognosia. Limbic status with olfactory symptoms has been documented (Wieser 1982). A "gustatory aura continua" was the leading symptom of case 4 in our 1985 paper (Wieser et al 1985), with left hippocampal status activity in the depth EEG. It was also associated with subtle higher cognitive deficits detected with a tachistoscopically presented lexical decision task. The main clinical features of autonomic seizures are abdominal sensations, apnea, arrhythmias and bradyarrhythmias, chest pain, cyanosis, erythema, flushing, genital sensations and orgasm, hyperventilation, lacrimation, miosis/mydriasis/hippus, palpitations, perspiration, pilomotor excitation ("gooseflesh"), tachycardia, urinary urgency and incontinence, and vomiting. Psychomotor partial seizures with autonomic symptoms as the leading feature are well known (Wieser and Williamson 1993). Under the category nonconvulsive status epilepticus, Rabending and Fischer (Rabending and Fischer 1986) describe ictal bradycardia and asystole. Nishiguchi and colleagues (Nishiguchi et al 2002) described a boy with occipital lobe epilepsy showing prolonged QTc in the ictal ECG. Zijlmans and colleagues (Zijlmans et al 2002) determined the prevalence of heart rate changes and ECG abnormalities during epileptic seizures in 281 seizures in 81 patients. ECG abnormalities were found in 26% of seizures (44% of patients) and long seizure duration increased the occurrence of ECG abnormalities. Umbilical sensations in children (VanBuren 1963), long-lasting borborygmi, widened pupils, pilomotor phenomena, goose-flesh or periodically shivering, etc. have been described (Brody et al 1960; Wieser 1979; 1981; 1983a; 1983b; 1988; 1991; Wieser et al 1981; Stodieck and Wieser 1986). Certain peculiarities of personality and behavior are often associated with such conditions and, therefore, we have described such conditions in the context of "limbic dyscontrol syndrome" (Girgis and Kiloh 1980; Wieser and Landis 1983). It is our belief that autonomic phenomena usually are associated with overt or subtle behavioral changes such as irritability, fear, panic, and, sometimes, existential emptiness, or some other form of pathological self-perception. A particularly rare ictal or status symptom is aggression (Delgado-Escueta et al 1981). Ictal depression and anxiety in temporal lobe epilepsy is far more frequent (Weil 1956); Henriksen as well as McLachlan and Blume described a status with fear as the outstanding clinical expression (Henriksen 1973; McLachlan and Blume 1980). A large amount of literature exists on this topic (Trimble and Bolwig 1992; Smith et al 1991). Ictal laughter (Mueller and Mueller 1980) is usually associated with hypothalamic pathology, mainly hamartoma, in which gelastic seizures are the hallmark. A rare ictal phenomenon is "hemicrania epileptica" (Isler et al 1984; Andermann and Lugaresi 1987), which may last longer than 30 minutes and, therefore, can then be labeled as a form of status epilepticus. Hemicrania continua is a primary headache disorder that is characterized by a continuous unilateral headache of moderate severity, exacerbations of severe pain and complete responsiveness to indomethacin. In hemicrania continua, visual auras may precede or accompany the pain exacerbations (Peres et al 2002). Psychic seizures were referred to by Jackson as so-called dreamy state including deja vu as well as ictal reminiscences (Jackson 1875; 1890; 1898; 1899). He subsequently referred to such events as "psychical.” Gowers reported 25 patients with "psychical auras" with 10 having an "emotional aura"; all of these had fear (Gowers 1881). Penfield introduced the term "experiential" to describe such mental phenomena and divided the patients’ past experience into illusions and hallucinations, which could be predominantly visual, auditory, or both, or an "unclassified" experience such as a dream, a flashback, or a memory without further description. Lennox referred to 3 categories of "psychic seizures,” which are (1) dream states, feeling of unreality or illusions; (2) hallucinations; and (3) mild confusion or disorientation, a feeling of strangeness without loss of memory and consciousness. Experiential means that the mental phenomena have a relevance to the patients past; Gloor specified that they typically combine elements of perception, memory, and affect (Gloor 1990). Mesial temporal lobe seizures may present as anxiety disorders (Young et al 1995). The principal ictal "psychic phenomena" may be listed as follows (Fish 1997):
LOCALIZATION Theoretically, each part of the cortex, and probably deep nuclei as well (Wieser et al 1998), can give rise to long-lasting localized epileptiform discharges. According to their functional specialization, the epileptic dysfunction of a localized ganglionic structure of the brain may give rise to "positive" or "negative" symptoms of a particular quality. The understanding is that the symptoms and signs are often the result of the interpretation of the not discharging "healthy" brain, which is confronted with a pathological "bombardment" or an epileptic dysfunction of a part of itself. This implies that the localization of the cortex where symptoms are produced (the "symptomatogenic zone") and the localization where seizures are generated (the primary "epileptogenic zone") are not necessarily concordant. The most common localization of sensory seizures that involve the trunk, head, and extremities (somatosensory) as well as the special senses (visual, auditory, vertiginous, gustatory and olfactory) are listed in Table 1 together with some references. Table 1. Principal Ictal “Psychic Phenomena”
An intriguing question is whether certain brain regions predispose more than others for such a circumscribed and long-lasting discharge behavior. By analogy with epilepsia partialis continua (Wieser 2001) and psychomotor or limbic status epilepticus (Wieser 2001), it is reasonable to assume that certain brain regions are, in fact, predisposed to this discharge behavior. From posttraumatic epilepsy, it is well-known that the central and mesiotemporal lobe cortices are more seizure-prone than other cortices, but it is less clear whether region-specific differences exist to limit seizure discharges in time. PATHOPHYSIOLOGY An "aura continua" reflects the intrinsic epileptogenic properties of a discharging epileptogenic focus that remains "well controlled". Obviously, in such a condition there is no further progression or recruitment (ie, no relevant increase of the number of epileptically involved neurons). Metaphorically spoken, the "critical mass" necessary for the spread of the discharge is not reached. To a certain degree, however, waxing and waning occurs. The aura content is the product of the "interpretive cortex" (Penfield 1959) dealing with this discharging focus. Several of our patients who underwent selective amygdalohippocampectomy (Wieser and Yasargil 1982) because of drug-resistant mesial temporal lobe epilepsy, and in whom this operation was successful with no further habitual seizures, experienced persisting auras in the first months after this operation. Moreover, a few patients claimed that the feeling of an impending seizure would, with some fluctuation of its intensity, persist for hours or even days, and thus mimic an "aura continua.” In such cases, it is likely to assume that the removal of amygdala and hippocampus led to a suppression of the full blown psychomotor seizures, but that the temporal and insular neocortex were still epileptically disturbed and able to produce prolonged aura phenomena. The so-called "running down" phenomenon of such postoperatively persisting auras lends further support to the idea that for the full expression of psychomotor seizures, both the mesial limbic and the neocortical cortices are necessary. DIFFERENTIAL DIAGNOSIS An ongoing continuous or recurrent intermittent epileptic discharge might be suspected, and consequently proven, with EEG and response to antiepileptic drug treatment in an epileptic person with known focal pathology and prolonged aura symptoms consisting of phenomena that fit well with the localization of the epileptic discharge. However, in the absence of clear-cut EEG findings, an aura continua in particular (if expressing itself with strange and unusual phenomena) might be difficult to diagnose. Not infrequently convincing ictal discharges cannot be detected without intracranial recordings. Such techniques, of course, are only justified in the context of surgical epilepsy therapy. Long-lasting autonomous, emotional, and psychic phenomena and personality, in which the mesial temporal lobe (in particular the amygdala) and the insular and frontal cortices are candidate areas for suspected discharges, pose a problem. Discharges at such a localization are difficult to detect in routine scalp EEG. Autonomic signs and symptoms occur in simple partial seizures and are frequent in complex partial seizures. Prolonged autonomic ictal features can mimic psychiatric, endocrine, cardiac, and gastrointestinal disorders (Devinsky et al 1986). Cardiovascular and thoracic symptoms are not specific for temporal lobe seizures, but are also seen in frontal lobe seizures, and probably more commonly so. Pupillary dilatation is thought by some authors to be a sign of hypothalamic seizure spread. Table 2 lists the most important differential diagnosis of autonomic phenomena. Table 2. Differential Diagnosis of Autonomic Aura Continua
(Liporace and Sperling 1997) Table 3. Differential Diagnosis of Aura Continua with Psychic Phenomena and Psychic Seizures
(Liporace and Sperling 1997) DIAGNOSTIC WORKUP To diagnose aura continua, two principal requirements have to be fulfilled: (1) some clinically evident alteration in mental status such as hallucinations and illusions or behavior from baseline; and (2) seizure activity on the EEG. Correlating mental, autonomic or emotional changes from baseline with EEG evidence of ongoing epileptic activity is essential to diagnose aura continua. Polygraphic recordings, such as electrocardiography, respiration, and electrodermal skin responses are helpful for detecting and quantifying autonomic phenomena. If inaccessible for routine scalp electrodes, and if depth recording is not available, ictal SPECT or ictal PET are helpful for the diagnosis. Ictal SPECT and ictal PET are easy to obtain in a status condition. Finally, the prompt response to antiepileptic drugs might be important for the diagnosis. Since the majority of aura continua phenomena are associated with some kind of lesion, a thorough examination of the patient, including neurologic, neuropsychologic examinations, and MRI, PET, or SPECT in the ictal and interictal state is essential. Polygraphic video-EEG documentation is recommended.
SYNDROMES AND DISEASES IN WHICH THE SEIZURE TYPE OCCURS According to the literature, partial status epilepticus (Shorvon 1994)
is reported to be controlled by diazepam in 88% (of 67 patients). Clobazam
(Corman et al 1998), midazolam, an imidazobenzodiazepine, and lorazepam
(Mitchell 1996) are considered antiepileptic drugs of first choice;
midazolam is short acting and, therefore, can be well titrated on
prolonged infusion if necessary. Paradoxical response to diazepam and
midazolam in partial status epilepticus has been rarely observed (Al Tahan
2000). In children with Ohtahara-like syndromes and serial partial
seizures associated with cortical dysplasia, pyridoxal phosphate showed
good therapeutic efficacy (Ohtsuka et al 2000). Aminoff MJ. Do nonconvulsive seizures damage the brain--no. Controversies in neurology. Arch Neurol 1998;55:119-21. Andermann F, Lugaresi E, editors. Migraine and epilepsy. Boston: Butterworth, 1987. Anderson J. On sensory epilepsy: a case of basal cerebral tumor, affecting the left temporo-sphenoidal lobe, and giving rise to a paroxysmal taste-sensation and dreamy state. Brain 1996;9:385-95. Barry E, Sussmann NM, Bosley TM, et al. Ictal blindness and status epilepticus amauroticus. Epilepsia 1985;26:577-84. Blanke O, Ortigue S, Coeytaux A, Martory MD, Landis T. Hearing of a presence. Neurocase. 2003;9(4):329-39. Blum AS. Focal status epilepticus [eMedicine Clinical Knowledge Base]. April 9, 2002. Available at: http://www.emedicine.com. Accessed September 2003. Bogousslavski J, Martin R, Regli F, Despland PA, Bolyn S. Persistent worsening of stroke sequela after delayed seizures. Ann Neurol 1992;49:385-8. Brody JA, Odom GL, Kunkle EC. Pilomotor seizures: report of a case associated with a central glioma. Neurology 1960;10:993-7. Brugger P, Agosti R, Regard M, Wieser HG, Landis T. Heautoscopy, epilepsy, and suicide. J Neurol Neurosurg Psychiatry 1994;57(7):838:9. Cockerell OC, Walker MC, Sander JW, Shorvon SD. Complex partial status epilepticus: a recurrent problem. J Neurol Neurosurg Psychiatry 1994;57:835-7. Corman C, Guberman A, Benavente O. Clobazam in partial status epilepticus. Seizure 1998;7:243-7. Delgado-Escueta AV, Mattson RA, King L, et al. The nature of aggression during epileptic seizures. N Engl J Med 1981;305:711-6. Devinsky O, Price BH, Cohen SI. Cardiac manifestations of complex partial seizures. Am J Med 1986;80(2):195-202. Dreifuss F. Classification of epileptic seizures. In: Engel J Jr, Pedley TA, editors. Epilepsy; A comprehensive textbook. Philadelphia: Lippincott-Raven Publishers, 1997:517-24. Engel J Jr, Ludwig BJ, Feteli M. Prolonged partial complex status epilepticus: EEG and behavioral observations. Neurology 1978;28:863-9. Fish DR. Psychic seizures. In: Engel J Jr, Pedley TA, editors. Epilepsy; A comprehensive textbook. Philadelphia: Lippincott-Raven Publishers, 1997:543-8. Fromm GH, Faingold C, Browning RA, Burnham WM, editors. Epilepsy and the reticular formation. Neurology and neurobiology. Vol 27. New York: Alan R. Liss Inc, 1987. Galen. In: Kühn CG, editor. Opera omnia: de locis affectis III. Vol 8. Leipzig, 1821;11:194. Gastaut H. Classification of status epilepticus. In: Delgado-Escueta AV, Wasterlain CG, Treimann DM, Porter RJ, editors. Status epilepticus. Advances in neurology. Vol 34. New York: Raven Press, 1983:15-35. Gibbs FA, Gibbs EL, Lennox WG. Epilepsy: a paroxysmal cerebral dysrhythmia. Brain 1937;60:377-88. Girgis M, Kiloh LG, editors. Limbic epilepsy and the dyscontrol syndrome. Developments in Psychiatry. Vol. 4. Amsterdam: Elsevier/North-Holland Biomed Press, 1980. Gloor P. Experiential phenomena of temporal lobe epilepsy: facts and hypotheses. Brain 1990;113:1673-94. Gloor P, Olivier A, Quesney LF, Andermann F, Horowitz S. The role of the limbic system in experiential phenomena of temporal lobe epilepsy. Ann Neurol 1982;12:129-44. Gowers WR. Epilepsy and other convulsive diseases: their causes, symptoms and treatment. London: J and A. Churchill, 1881. Gupta AK, Jeavons PM, Hughes RC, Covanis A. Aura in temporal lobe epilepsy: clinical and electrographic correlation. J Neurol Neurosurg Psychiatry 1983;46:1079-83. Hadjikoutis S, Sawhney IM. Occipital seizures presenting with bilateral visual loss. Neurol India. 2003;51(1):115-6. Hausser-Hauw C, Bancaud J. Gustatory hallucinations in epileptic seizures. Brain 1987;110:339-59. Heintel H. Quellen zur Geschichte der Epilepsie. In: Ackerknecht EH, Buess H, editors. Hubers Klassiker der Medizin und Naturwissenschaften. Vol. XIV. Bern: Hans Huber Verlag, 1975. Henriksen GF. Status epilepticus partialis with fear as clinical expression. Report of a case and ictal EEG-findings. Epilepsia 1973;14:39-46. Isler HR, Wieser HG, Egli M. Hemicrania epileptica. In: Rose FC, editors. Progress in migraine research 2. London: Pitman Books, 1984:69-82. Jackson JH. On temporary mental disorders after epileptic paroxysms. In: Taylor J, editor. Selected writings of John Hughlings Jackson. Vol 1. London: Staples Press, 1875:119-34. Jackson JH. On a particular variety of epilepsy ("intellectual aura"), one case with symptoms of organic brain disease 1889. In: Taylor J, editor. Selected writings of J.H. Jackson. Vol 1. New York: Basic Books Inc, 1958:308-17, 385-405. Jackson JH, Beevor C. Case of tumor of the right temporo-sphenoidal lobe, bearing on the localization of the sense of smell and on the interpretation of a particular variety of epilepsy. Brain 1890;12:346-57. Jackson JH, Colman WS. Case of epilepsy with tasting movements and "dreamy state": Very small patch of softening in the left uncinate gyrus. Brain 1898;21:580-90. Jackson JH, Stewart P. Epileptic attacks with a warning of crude sensation of smell and with intellectual aura (dreamy state) in a patient who had symptoms pointing to gross organic disease of the right temporo-sphenoidal lobe. Brain 1899;22:334-549. Jordan KG. Nonconvulsive status epilepticus in acute brain injury. J Clin Neurophysiol 1999;16:306-13. Kaplan PW. Nonconvulsive status epilepticus in the emergency room. Epilepsia 1996;37:643-50. Kaplan PW, editor. Nonconvulsive status epilepticus. J Clin Neurophysiol 1999;16:323-60. Kaplan PW, Loiseau P, Fischer RS, Jallon P. Epilepsy A to Z. A glossary of epilepsy terminology. New York: Demos Vermande, 1995. Karbowski K. Auditive und vestibuläre Halluzinationen epileptischer Genese. In: Karbowski K, editor. Status psychomotoricus und seine Differentialdiagnose. Bern: Hans Huber Verlag, 1980:39-71. Karbowski K. Epileptische Anfälle. Heidelberg: Springer, 1985. Lende RA, Popp AJ. Sensory jacksonian seizures. J Neurosurg 1976;44:706-11. Liporace JD, Sperling MR. Simple autonomic seizures. In: Jengel J Jr, Pedley TA, editors. Epilepsy: a comprehensive textbook. Philadelphia: Lippincott-Raven Publishers, 1997:549-55. Mayeux R, Lueders H. Complex partial status epilepticus: Case report and proposal for diagnostic criteria. Neurology 1978;28:957-61. McLachlan RS, Blume WT. Isolated fear and complex partial status epilepticus. Ann Neurol 1980;8:639-41. Meyer-Mickeleit R. Ueber die sogenannten psychomotorischen Anfälle, die Dämmerattacken der Epileptiker. 65. Wandersammlung der südwestdeutschen Neurologen und Psychiater 10.-11.06.1949, Badenweiler. Arch Psychiat Nervenkr 1950;184:271. Mikulecka A, Krsek P, Hlinak Z, Druga R, Mares P. Nonconvulsive status epilepticus in rats: impaired responsiveness to exteroceptive stimuli. Brain Res 2000;117:29-39. Mitchell WG. Status epilepticus and acute repetitive seizures in children, adolescents, and young adults: etiology, outcome, and treatment. Epilepsia 1996;37(Suppl 1):74-80. Mitchell WG, Greenwood RS, Messenheimer JA. Abdominal epilepsy. Cyclic vomiting as the major symptom of simple partial seizures. Arch Neurol 1983;40:251-2. Mueller D, Mueller J. Lachen als epileptische Manifestation. VEB G. Fischer: Jena, 1980. Nishiguchi M, Shima M, Takahashi Y, et al. [A boy with occipital lobe epilepsy showing prolonged QTc in the ictal ECG] No To Hattatsu 2002;34(6):523-7. Ohtsuka Y, Sato M, Sanada S, Yoshinaga H, Oka E. Suppression-burst patterns in intractable epilepsy with focal cortical dysplasia. Brain Dev 2000;22:135-8. Penfield W. The interpretive cortex. Science 1959;129:1719-25. Penfield W, Jasper HH. Epilepsy and functional anatomy of the human brain. Boston: Little Brown, 1954. Penfield W, Perot P. The brain's record of auditory and visual experience. A final summary and discussion. Brain 1963;86:596-696. Penfield W, Rasmussen T. The cerebral cortex of man. A clinical study of localization and function. New York: MacMillan, 1957. Peppercorn MA, Herzog AG. The spectrum of abdominal epilepsy in adults. Am J Gastroenterol 1989;84:1294-6. Peres MF, Siow HC, Rozen TD. Hemicrania continua with aura. Cephalalgia 2002;22(3):246-8. Prensky AL. An approach to the child with paroxysmal phenomenon with emphasis on nonepileptic disorders. In: Dodson WE, Pellock JW, editors. Pediatric epilepsy: diagnosis and therapy. New York: NY Demos Publication, 1992. Rabending G, Fischer W. [Epileptic psychosis and nonconvulsive status epilepticus with ictal bradycardia and asystole] Psychiatr Neurol Med Psychol (Leipz) 1986;38(4):184-8. Russel WR, Whitty CM. Studies in traumatic epilepsy. 2. Focal motor and somatic sensory fits. A study of 85 cases. J Neurol Neurosurg Psychiatry 1953;16:73-97. Russel WR, Whitty CM. Studies in traumatic epilepsy. 3. Visual fits. J Neurol Neurosurg Psychiatry 1955;18:79-96. Salanova V, Andermann F, Olivier A, Rasmussen T, Quesney LF. Occipital lobe epilepsy: electroclinical manifestations, electrocorticography, cortical stimulation and outcome in 42 patients treated between 1939 and 1991. Brain 1992;115:1655-80. Schaeffler L, Karbowski K. Recurring paroxysmal abdominal pains of cerebral origin. Schweiz Med Mochenschr 1981;111:1352-60. Schiffter R, Straschill M. Aura continua musicalis - Bericht über einen Krankheitsfall mit sensorischem Status epilepticus. Nervenarzt 1977;48:321-35. Scott JS, Masland RL. Occurrence of "continuous symptoms" in epilepsy patients. Neurology 1953;3:297-301. Sheth RD, Riggs JE. Persistent occipital electrographic status epilepticus. J Child Neurol 1999;14:334-6. Shorvon S. Status epilepticus. Cambridge: University Press, 1994:382. Siegel AM, Williamson PD, Roberts DW, Thadani VM, Darcey TM. Localized pain associated with seizures originating in the parietal lobe. Epilepsia 1999;40:845-55. Slater E, Beard AW. The schizophrenia-like psychoses of epilepsy. Br J Psychiatry 1963, 109:95-150. Smith DB, Treiman DM, Trimble MR, editors. Neurobehavioral problems in epilepsy. Advances in neurology. Vol 55. New York: Raven Press, 1991. Sowa MV, Pituck S. Prolonged spontaneous complex visual hallucinations and illusions as ictal phenomena. Epilepsia 1989;30:524-6. Spatt J, Mamoli B. Ictal visual hallucinations and post-ictal hemianopsia with anosognosia. Seizure 2000;9:502-4. Stodieck SR, Wieser HG. Autonomic phenomena in temporal lobe epilepsy. J Autonom Nerv Syst 1986;(Suppl):611-21. Treiman DM, Delgado-Escueta AV. Complex partial status epilepticus. In: Delgado-Escueta AV, Wasterlain CG, Treimann DM, Porter RJ, editors. Status epilepticus. Advances in neurology. New York: Raven Press, 1983;34:15-35. Trimble MR, Bolwig TG, editors. The temporal lobes and the limbic system. Petersfield, UK: Wrightson Biomed Publ, 1992. Uematsu S, Lesser RP, Fischer RS, et al. Motor and sensory cortex in humans: topography studied with chronic subdurale stimulation. Neurosurgery 1992b;31:59-72. Uematsu S, Lesser RP, Gordon B. Localization of sensorimotor cortex: the influence of Sherrington and Cushir on the modern concept. Neurosurgery 1992a;30:904-13. VanBuren JM. The abdominal aura: a study of abdominal sensations occurring in epilepsy and produced by depth stimulation. Electroenceph Clin Neurophysiol 1963;15:1-19. VanNess PC, Lesser RP, Duchowny MS. Simple sensory seizures. In: Engel J Jr, Pedley TA, editors. Epilepsy: a comprehensive textbook. Philadelphia: Lippincott-Raven Publishers, 1997:533-42. Waterhouse EJ, Vaughan JK, Barnes PY, et al. Synergistic effect of status epilepticus and ischemic brain injury on mortality. Epilepsy Res 1998;29:175-83. Weil AA. Ictal depression and anxiety in temporal lobe disorders. Am J Psychiatry 1956;113:149-57. Whitty CW. Causalgic pain as an epileptic aura. Epilepsia 1953;2:37-41. Whyatt R. Observations on the nature, causes and cure of those disorders which have been commonly called nervous, hypochondriac, or hysteric: to which are prefixed some remarks on the sympathy of the nerves. 2nd ed. Edinburgh, 1765:146. Wieser HG. "Psychische Anfälle" und deren stereoelektroenzephalographisches Korrelat. Z EEG-EMG 1979;10:197-206. Wieser HG. Temporal lobe of psychomotor status epilepticus: a case report. Electroencephalogr Clin Neurophysiol 1980;48:558-72. Wieser HG. Stereoelektroenzephalographisches Korrelat motorischer Anfälle. Z EEG-EMG 1981;12:1-13. Wieser HG. Zur Frage der lokalisatorischen Bedeutung epileptischer Halluzinationen. In: Karbowski K, editor. Halluzinationen bei Epilepsien und Differentialdiagnose. Bern: Hans Huber Verlag, 1982:67-92. Wieser HG. Electroclinical features of the psychomotor seizure. A stereo-electroencephalographic study of ictal symptoms and chronotopographical seizure patterns including clinical effects of intracerebral stimulation. Stuttgart-London: Fischer-Butteworths, 1983a:242. Wieser HG. Depth recorded limbic seizures and psychopathology. Neurosci Biobehav Rev 1983b;7:427-40. Wieser HG. Spontane und evozierte Spitzentätigkeit im Tiefen- und Oberflächen-EEG. EEG-Labor 1988;10:8-30. Wieser HG. Ictal manifestation of temporal lobe seizures. In: Smith DB, Treiman D, Trimble M, editors. Neurobehavioral problems in epilepsy. Advances in neurology. Vol 55. New York: Raven Press, 1991:301-15. Wieser HG. Simple partial status epilepticus. In: Engel J Jr, Pedley TA, editors. Epilepsy: a comprehensive textbook. Philadelphia: Lippincott-Raven Publishers, 1997:709-23. Wieser HG. Epilepsia partialis continua. In: Gilman S, editor. MedLink neurology. 3rd ed. San Diego: MedLink Corporation, 2001. Wieser HG, Hailemariam S, Regard M, Landis T. Unilateral limbic epileptic status activity: stereo EEG, behavioral, and cognitive data. Epilepsia 1985;26:19-29. Wieser HG, Hajek M, Constantinopol D, Siegel AM, Yonekawa Y, Wichmann W. Symptomatische Epilepsien bei Läsionen des Hirnstamms, des Dienzephalons und des Thalamus. Klinische Neurophysiologie 1998;29:10-21. Wieser HG, Landis T. Is the "interictal behaviour syndrome of temporal lobe epilepsy" really an "interictal" phenomenon? Neurol Psychiatr 1983;6:70-8. Wieser HG, Siegfried J, Bernoulli C. Corrélations stéréo-electroencéphalographiques des manifestations psychiatriques dans l'épilepsie. Méd et Hyg 1981;39:1920-8. Wieser HG, Williamson PD. Ictal semiology. In: Engel J Jr, editor. Surgical treatment of the epilepsies. 2nd ed. New York: Raven Press, 1993:161-71. Wieser HG, Yasargil MG. Selective amygdalohippocampectomy as a surgical treatment of mesiobasal limbic epilepsy. Surg Neurol 1982;17:445-57. Wilkinson HA. Epileptic pain. An uncommon manifestation with localizing value. Neurology 1973;23(5):518-20. Wolf P. Zur Klinik und Psychopathologie des Status psychomotoricus. Der Nervenarzt 1970;41:603-10. Wolf P. Systematik von Status kleiner Anfälle in psychopathologischer Hinsicht. Mit Kasuistiken einiger seltener Zustandsbilder. In: Wolf P, Köhler GK, editors. Psychopathologische und pathogenetische Probleme psychotischer Syndrome bei Epilepsie. Bern. Hans Huber Verlag, 1980:32-52. Wolf P. Halluzinationen im Rahmen epileptischer Psychosen. In: Karbowski K, editor. Halluzinationen bei Epilepsien und ihre Differentialdiagnose. Bern: Hans Huber Verlag, 1982:58-66. Young G, Blume WT. Painful epileptic seizures. Brain 1983;106:537-54. Young GB, Chandarana PC, Blume WT, McLachlan RS, Munoz DG, Girvin JP. Mesial temporal lobe seizures presenting as anxiety disorders. J Neuropsychiatry Clin Neurosci 1995;7:352-7. Zijlmans M, Flanagan D, Gotman J. Heart rate changes and ECG abnormalities during epileptic seizures: prevalence and definition of an objective clinical sign. Epilepsia 2002;43(8):847-54. ILAE Abbreviations NCSE:nonconvulsive status epilepticus SPSE:simple partial status epilepticus Synonyms Simple partial status epilepticus Subtopics Epileptic hallucination and illusions Prolonged autonomic and psychic phenomena Subclinical status epilepticus Major keyword descriptors autonomic changes EEG seizure pattern electroencephalographic status epilepticus epileptic productive symptoms focal sensory seizures hallucinoses limbic system nonconvulsive status epilepticus seizure discharges seizures simple partial status epilepticus somatosensory hallucinations status epilepticus status hallucinosis temporal lobe uncinate fits waxing and waning Minor keyword descriptors alteration in mental status behavioral change cognitive abnormalities depth recording ictal activity loss of consciousness ongoing discharge Age of presentation 06-12 years 13-18 years 19-44 years 45-64 years 65+ years Age of typical presentation 06-12 years 13-18 years 19-44 years 45-64 years Permuted topic, synonyms, variants Aura continua continua, Aura illusions, Epileptic hallucination hallucination and illusions, Epileptic phenomena, Prolonged autonomic and psychic psychic phenomena, Prolonged autonomic and autonomic and psychic phenomena, Prolonged status epilepticus, Subclinical epilepticus, Subclinical status partial status epilepticus, Simple status epilepticus, Simple partial epilepticus, Simple partial status Related topics Absence status epilepticus Diazepam Electrical status epilepticus during slow sleep Epilepsy Limbic status epilepticus (psychomotor status) Typical absence seizures Differential diagnosis psychiatric disorders endocrine disorders cardiac disorders gastrointestinal disorders cardiovascular symptoms thoracic symptoms papillary dilation carcinoid pheochromocytoma hypoglycemia organic gastrointestinal disease panic attacks paroxysmal autonomic dysfunction
|
|||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||