The Tohoku Journal of Experimental Medicine
Online ISSN : 1349-3329
Print ISSN : 0040-8727
ISSN-L : 0040-8727
Volume 161, Issue Supplement
Displaying 1-20 of 20 articles from this issue
  • EIJIRO SATOYOSHI
    1990 Volume 161 Issue Supplement Pages 1-19
    Published: 1990
    Released on J-STAGE: March 14, 2011
    JOURNAL FREE ACCESS
    Various types of the distal myopathy except Welander's late distal myopathy of Swedish type were described. There were many reports in the past concerning the varieties of the distal myopathy. Distal myopathy is a rather rare disorder and it may be difficult to diagnose these cases. Among these various distal myopathy, an emphasis was made upon the clinical and pathological characteristics of the diseases, particularly distal muscular dystrophy of Miyoshi, Distal myopathy with rimmed vacuolear formation of Nonaka and ours, and Oculopharyngo-distal myopathy. All these diseases show the distal muscle involvement but the clinical features, heredity, course and pathological features are quite different, and prognosis is also different. Accordingly when we examined these distal myopathy cases, clinical characteristics and histo-pathological findings should be carefully studied. It shoud be also emphasized that the level of serum CPK dose not indicate the severity of the myopathy. In muscluar dystrophy or myositis, serem CPK elevates remarkably and we can consider the level of CPK as a sign of the severity or condition of the disease. However, in myopathy as “rimmed vacuolar distal myopathy” serem CPK remains in normal level even though weakness is severe. This is due to absence of the membrane abnormalities of muscle cells. Leakage of the CPK from muscle cells, therefore, does not reflect the degree of the cell destruction. In this point we have to remember the fact that serum CPK is not a indicator of all muscle diseases and even if the CPK is normal, we have to consider the presence of myopathy.
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  • OLAF B. PAULSON
    1990 Volume 161 Issue Supplement Pages 21-27
    Published: 1990
    Released on J-STAGE: March 14, 2011
    JOURNAL FREE ACCESS
    Movements disorders are prominent symptoms in many neurological diseases, especially with affection of the basal nuclei. Several of these diseases have characteristic symptoms and signs, whereas clinical diagnosis is more difficult in other diseases. The various movement disorders, hypokinesia, hyperkinetic syndrome, tremor etc. are defined and described, and clinical features of the various diseases were commented on.
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  • KAZUO HASEGAWA
    1990 Volume 161 Issue Supplement Pages 29-38
    Published: 1990
    Released on J-STAGE: March 14, 2011
    JOURNAL FREE ACCESS
    The dementing disorder constitute the largest single problem because of the state of extreme helplessness that characterizes its advanced stages. The clinical psychiatry have to face with this disabling disease, for which the adequate treatment or strategies have not been established. Firstly the author describes the size of the problem by introducing our recent epidemiological study on age-related dementia in Kanagawa Prefecture. The result of the study revealed that the prevalence of dementia was 4.8% and it increased with age. The other recent epidemiological study also showed similar findings. One of the common findings in these studies was that the prevalence of senile dementia was much lower than that of vascular dementia and apparently indicated the reverse tendency reported in the traditional studies in Europe and USA. Secondly the author discusses the diagnostic criteria of dementia as well as the differential diagnosis. Thirdly he describes the validity study of Hasegawa's dementia scale which is widely used as the screening instrument of the demented aged in Japan. The author also describes the Hasegawa's scale was applicable for research tool for the measurement of cognitive decline of the very old aged by introducing the centenarian study. Lastly the author states the issues of family care status of the demented elderly and emphasized the importance of caring the care-givers in the family.
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  • HIDEO TOHGI
    1990 Volume 161 Issue Supplement Pages 39-47
    Published: 1990
    Released on J-STAGE: March 14, 2011
    JOURNAL FREE ACCESS
    Vascular dementia is almost always associated with organic brain lesions due to ischemia, not with arteriosclerossis alone. In Japan, more than 50% of dementia in population older than 65 years are of vascular origin. Vascular dementia occurs with diffuse vascular lesions in the cerebral white matter or circumscribed lesions in particular areas such as the thalamus, anterior limb of the internal capsule, and cingulate gyrus, all of which constitute the ascending activating system or the limbic system. Vascular dementia is clinically characterized by stepwise progression, fluctuating course and predominant deterioration of intelligence with relative preservation of personality. Reversibility, disproportionate impairment of intelligence and personality, and dementia caused by a focal lesion observed in vascular dementia pose problems with regard to the classical concept of dementia. The similarity and difference between remitting dementia and disturbance of consciousness remain to be scrutinized.
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  • SHIGENOBU NAKAMURA
    1990 Volume 161 Issue Supplement Pages 49-60
    Published: 1990
    Released on J-STAGE: March 14, 2011
    JOURNAL FREE ACCESS
    Neurotransmitters including acetylcholine, dopamine, norepinephrine, serotonin, GABA and vasopressin were examined in control subjects and patients with Alzheimer-type dementia, involving presenile and senile dementia. Neurotransmitters exhibited various mode of changes with aging. Abnormalities found in senile or presenile dementia were not always parallel to the age-related changes. These results suggest that Alzheimer-type dementia cannot be understood as an accerelated senescence, but other etiological factors might be introduced for the manifestation of the dementia. Moreover, the disturbance in neurotransmitters revealed a difference between presenile Alzheimer's disease and senile dementia, indicating that further studies should be carried out taking the age of onset into consideration.
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  • MAKOTO IWATA
    1990 Volume 161 Issue Supplement Pages 61-78
    Published: 1990
    Released on J-STAGE: March 14, 2011
    JOURNAL FREE ACCESS
    Visual information processings are realized by the posterior association cortex spreading in front of the striate and parastriate areas from which two major visual association pathways arise. The dorsal or the occipito-parietal pathway which transmits the inputs from the peripheral as well as the central visual field to the parietal association cortex is responsible for the visuospatial analysis of the visual informations. The occipito-temporal or the ventral pathway originates only from the foveal vision area, and sends the visual inputs to the inferior temporal lobe which engages in visual pattern or whole gestalt recognition of the visual informations. In addition to this dichotomous disposition of the dorsal and the ventral visual association pathways in each cerebral hemisphere, there is another type of functional specialization which is hierarchical rather than dichotomous. In the left cerebral hemisphere, the collateral pathways arise from both dorsal and ventral main streams and engage in the process of reading, or the verbal mode of visual information processing.
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  • EIICHI IWAI, MASAO YUKIE, JOJI WATANABE, SHIGEYA YAGINUMA, YASUTAKA OS ...
    1990 Volume 161 Issue Supplement Pages 79-93
    Published: 1990
    Released on J-STAGE: March 14, 2011
    JOURNAL FREE ACCESS
    To investigate the nature underlying the process of pattern discrimination learning, a series of seven experiments on seven working assumptions were undertaken. The main findings are as follows. The pattern discrimination learning consists of two time-dependent stages: The initial or first learning stage is the period of performance at chance, and the succeeding or second stage is the period of performance from just above the chance to a criterion level. The duration of the first stage is dependent on the degrees of cue-response separations, whereas that of the second stage is independent of. During the first stage, monkeys do not attend to the discriminative cue even at small cue-response separations, whereas during the second stage, they achieve pattern discrimination, or pattern perception and cognition, regardless of cue-response separations. After having learned the first pattern task with a cue-response separation, they learned new pattern tasks by means of the second stage, showing marked saving of the duration of the first stage. The findings in the present studies indicate that the first stage of learning is predominantly involved in the process of attending to the discriminative cues remote from the response site (a selective attention to the cue), whereas the second stage is concerned with the process of perception and cognition of the discriminative cue.
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  • EIICHI IWAI, MASAO YUKIE, JOJI WATANABE, KAZUO HIKOSAKA, HIDEO SUYAMA, ...
    1990 Volume 161 Issue Supplement Pages 95-120
    Published: 1990
    Released on J-STAGE: March 14, 2011
    JOURNAL FREE ACCESS
    To elucidate the role of the amygdala in visual perception and cognition, the effects of ablations of the amygdala and inferotemporal cortex on several visual tasks were compared with each other, and also the distribution patterns of the projections between them were investigated. The findings indicate that the inferotemporal cortex plays a critical role in visual perception, cognition and memory, whereas the amygdala is involved fundamentally in controlling emotional and motivational behavior. However, the amygdala is concerned with vision in the following ways: It receives neutral visual information highly processed in the visual cortex, invests the information with emotional and motivational significance through interactions with the cortical and subcortical systems of emotion and motivation, and then it returns the information coded to the visual areas to be re-processed; to be consciously perceived in area TEO, and to be meaningfully cognized, recognized and memorized in areas TE and TEG. Therefore, two channel model regarding the mechanism of visual information processing in the inferotemporal cortex is proposed: A first channel is concerned with processing neutral information, while the second one, with processing meaning information coded emotionally and motivationally in the amygdala. In addition, the present studies demonstrate that area TEG, which is cytoarchitectur ally a transitional area between areas TE and TG and whose functional significance has remained unclear, is involved significantly in visual cognition rather than visual perception.
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  • KEVIN W. WALSH
    1990 Volume 161 Issue Supplement Pages 121-130
    Published: 1990
    Released on J-STAGE: March 14, 2011
    JOURNAL FREE ACCESS
    Of the higher disorders associated with posterior cerebral lesions two have received considerable attention in the past decade. These are prosopagnosia, the so-called agnosia for faces, and alexia without agraphia. Major aspects of these disorders are reviewed briefly.
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  • MASAAKI NAGAFUCHI
    1990 Volume 161 Issue Supplement Pages 131-138
    Published: 1990
    Released on J-STAGE: March 14, 2011
    JOURNAL FREE ACCESS
    Right unilateral spatial neglect (USN) was investigated on three left brain-damaged patients suffering from the right homonymous hemianopsia and hemiplegia. A test battery consisted of visuo-constructive praxis; 1) putting blocks into a box, 2) bisecting a horizontal line, 3) figure drawing, 4) drawing of a dial plate and 5) copying drawing. The investigation revealed that USN of left brain-damaged patients resulted from 1) generally impaired mental function, 2) right unilateral sensory deprivation and 3) right hemiplegia. It was guessed that, as for a patient with right homonymous hemianopsia and hemiplegia, his attention would be attracted toward the left hand, and then he would be apt to neglect the right side. Right USN was not so prominent compared with the left one of right hemispheric lesion. However, it is suggested that if clinicians examine carefully the visuo-constructive function in addition to aphasia on left brain-damaged patients, right USN appears greater in some cases.
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  • KOICHI TAGAWA, Ken NAGATA, FUMIO SHISHIDO
    1990 Volume 161 Issue Supplement Pages 139-153
    Published: 1990
    Released on J-STAGE: March 14, 2011
    JOURNAL FREE ACCESS
    Even though the PET study revealed a total infarct in the territory of the left PCA in our 3 cases of pure alesia, it is still obscure which part of the left occipital lobe is most closely associated with the occurence of the pure alexia. In order to elucidate the intralobar localization of the pure alexia, it is needed to have an ideal case who shows an pure alexia due to the localized lesion within the left occipital lobe. Furthermore, high-resolution PET scanner will circumvent the problem in detecting the metabolism and blood flow in the corpus callosum which plays an important role in the pathogenesis. We have shown that the occlusion of the right PCA also produced a left unilateral agnosia which is one of the common neurological signs in the right MCA infarction. To tell whether the responsible lesion for the unilateral spatial agnosia differs between the PCA occlusion and the MCA occlusion, the correlation study should be carried out in a greater number of the subjects. Two distinctive neuropsychological manifestations, cerebral color blidness and prosopagnosia, have been considered to be produced by the bilateral occipital lesion. The PET studies disclosed reduction of blood flow and oxygen metabolism in both occipital lobes in our particular patient who exibited cerebral color blindness and posopagnosia.
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  • ITARU KIMURA, AYUMU OHNUMA, HARUAKI SEKI, SHUN-ICHI SASO, KYUYA KOGURE
    1990 Volume 161 Issue Supplement Pages 155-165
    Published: 1990
    Released on J-STAGE: March 14, 2011
    JOURNAL FREE ACCESS
    Motor impairment, clinically defined as bradycinesia has been considered as resulting only from motor system problems. Combined analysis of cognitive function and dynamic characteristics was studied in 20 patients with Parkinson's disease by a simple aiming task on visuomotor performance system. The dynamic characteristics in a Parkinson's disease patient was evaluated by two parameters: decreased amplitude of the voluntary movement (=low gain constant) and delayed initiation of voluntary movement (=long reaction time). The visual event-related potential elicited in a target detection paradigm (P300 component) was recorded in 12 patients with Parkinson's disease. P300 latency was significantly prolonged in the patient group than in the normal control group (p<0.05). P300 has been shown to be intimately related to the cognitive process in the human brain and might well serve as a tool to monitor and evaluate the cognitive state in a clinical situation. The main cause of cognitive involvement in Parkinson's disease may include coexisting dementia and defective motivation. This type of cognitive disturbance may also serve partly as a cause of bradycinesia.
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  • PETER MARX
    1990 Volume 161 Issue Supplement Pages 167-182
    Published: 1990
    Released on J-STAGE: March 14, 2011
    JOURNAL FREE ACCESS
    The progress of clinical and experimental neuro-ophthalmology during the last two decades was reviewed. The ocular motor system in the brain stem was described firstly based on anatomical, neuro-physiological and clinical evidences. Clinical syndromes in cerebrovascular brain stem impairments which present ocular motor dysfunction were analyzed briefly.
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  • HIROKO NAKAMURA
    1990 Volume 161 Issue Supplement Pages 183-202
    Published: 1990
    Released on J-STAGE: March 14, 2011
    JOURNAL FREE ACCESS
    We investigated the relationship between language disturbances and the impairment of rhythmic capabilities (temporal perception & expression) in the patients with thalamic hemorrhage and compared them to patients with cortical lesions to probe the relationship of the thalamus to the mechanism of aphasic symptoms. 101 right-handed individuals, including 12 with thalamic hemorrhage, were studied to analyze language (verbal) and rhythmic (non-verbal) functions. Comparison of left- and right-hemisphere damaged patients revealed significant hypofunction of language and rhythmic capabilities in the group with lesions of left hemisphere. Some correlation could be seen between the rhythm disturbance and the language impairments in terms of severity and types. In contrast, the patients with thalamic hemorrhage showed a dissociation between the severely abnormal rhythm (non-verbal) and milder language (verbal) impairments. The language function values were constantly higher in the cases with thalamic hemorrhage than with cortical damages, while rhythmic capabilities were reduced, a tendency unlike that of the group with cortical damages. These findings suggest that language is primarily a function of the cerebral cortex of the dominant hemisphere, and that the thalamic area, necessary for the timing mechanism (rhythmic function), plays a part in the overall mechanism of aphasic symtomatology.
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  • Mechanisms Affecting Limbic Function
    ALAN H. LOCKWOOD
    1990 Volume 161 Issue Supplement Pages 203-211
    Published: 1990
    Released on J-STAGE: March 14, 2011
    JOURNAL FREE ACCESS
    Disorders of metabolism are the most common cause of coma of unknown etiology. Hyperammonemia is important as an etiologic factor in the development of hepatic encephalopathy, operating via direct and indirect mechansims that affect the function of the limbic system. The entry of ammonia into the brain is controlled by blood-brain pH gradients, and cerebral blood flow, coupled with regional variations in the capillary surface area-permeability product. In the brain, ammonium ions may inhibit the generation of action potentials, by substituting for potassium and sodium in current generation, and interfere with the chloride pump, producing a reversible depolarizing shift of the inhibitory post synaptic equilibrium potential toward the equilibrium potential. Ammonia entering the brain is quickly trapped by the ATP-consuming glutamine synthetase reaction leading to energy depletion in the reticular activating system. Ammonia may also interfere with ATP production due to a suspected inhibition of the malate aspartate shuttle, the mechanism for moving reducing equivalents into mitochondria for oxidative phosphorylation. Ammonia also depletes glutamate, causing a potential dysruption of glutamatergic neurotransmission. We recently evaluated the effects of chronic portacaval shunts (PCS) and ammonia on regional brain glucose metabolism using the 14C-deoxyglucose technique and found important direct and indirect effects on the limbic system. After a PCS, glucose metabolism was significantly increased in all 20 brain regions that were sampled, with the smallest increase in the cortex and the greatest increase in the reticular activating system. The pattern of glucose metabolism appeared to be different in the two groups, an impression that was confirmed by multivariate statistical analytical techniques. Assuing that differences in metabolic rate are linked to differences in function, we hypothesized that the hyperammonemia associated with a PCS causes a functional reorganization of the brain that may be responsible for the development of HE. When intracarotid infusions of ammonia were given, glucose metabolism in the ventromedial nucleus of the hypothalamus was activated. Since stimulation of this nucleus inhibits feeding behaviors, we postulated that ammonia's action on satiety centers is directly responsible for appetite loss and the development of cachexia, important elements of chronic liver disease. Since skeletal muscle is an important organ in the maintenance of ammonia homeostasis, reducing skeletal muscle bulk will predispose to additional episodes of hyperammonemia, perpetuation the cycle. Theories developed during the study of HE, including functional cerebral reorganization and selective effects on specific nuclei, may be of conceptual importance in the consideration of other forms of metabolic encephalopathy and the production of characteristic neurological signs and symptoms. -; ;
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  • HIDEO TOHGI, YOSHIYUKI KUROIWA, TOSHIAKI KONNO, HITOSHI MADARAME
    1990 Volume 161 Issue Supplement Pages 213-229
    Published: 1990
    Released on J-STAGE: March 14, 2011
    JOURNAL FREE ACCESS
    The mode of cerebral representation for each half of the body is various according to the functions that are represented; contralateral, ipsilateral and bilateral. We reviewed, and discussed the meaning of, such different patterns of cerebral representation for somatic and autonomic functions.
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  • Correlations between Neurological Deficits and Radiological Localizations
    HIROSHI MOCHIZUKI, HIROSHI SAITO
    1990 Volume 161 Issue Supplement Pages 231-239
    Published: 1990
    Released on J-STAGE: March 14, 2011
    JOURNAL FREE ACCESS
    In order to detect the functional subsets of the mesial frontal lobe, 26 patients with lesions involving mesial frontal lobe were investigated. The results were summarized as follows; (1) Hemiparesis predominantly in lower extremity was common motor deficit in patients with mesial frontal motor cortices. Four patients with supplementary motor damage sparing motor cortex showed long lasting hemiparesis. (2) Verbal adynamia was common symptom due to left supplementary motor and superior prefrontal damage. Transient mutism was found in two patients with superior prefrontal damage without the involvement of supplementary motor cortex. (3) Emotional disturbance char acterized by depressed motivation was also common. No hemispheric laterality could be detected in these patients. (4) Dementia and memory disturbance related to the pole and anterior area of superior prefrontal damage. (5) Transient urinary incontinence was presented only by right superior prefrontal damage, and permanent incontinence related with bilateral damage. (6) Akinetic mutism was related with bilateral large damage including cingulate. (7) Motor neglect and dressing apraxia possibly due to programing disturbance related to lesions in right hemisphere.
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  • SADAO ICHIJOH
    1990 Volume 161 Issue Supplement Pages 241-251
    Published: 1990
    Released on J-STAGE: March 14, 2011
    JOURNAL FREE ACCESS
    In benign childhood epilepsy, EEGs often show spikes in the mid-temporal region although there is no evidence of brain lesions in this region. In this study, mid-temporal spikes are classified into four types with regard to scalp distribution, and it is hypothesized that these spikes may originate in the hippocampus and then spread to the scalp, mainly by volume conduction. The subjects were 50 children (epileptic and non-epileptic), 2 to 15 years of age, with mid-temporal spikes in EEGs: type 1, unilateral mid-temporal spikes (25 cases); type 2, bilateral synchronous spikes (8 cases); type 3, bilateral synchronous spikes with the two sides having opposite polarities (2 cases); and type 4, bilateral asynchronous spikes (15 cases). Because the pyramidal cells are arranged in the form of a “C” in transverse sections of the hippocampus, scalp distribution of spikes might be explained as follows. If the axis of electrical dipoles in the hippocampus is oblique, the electrical potential will spread unilaterally; if the anxis is vertical, the potential will spread bilaterally; if the axis is horizontal, the two sides will have opposite poles. With regard to bilateral asynchronous spikes, the two hippocampi may be involved in generation of the spikes. It is thought that the mid-temporal spikes may be non-specific phenomena resulting from various etiologies.
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  • Kindling Studies in Cats
    MITSUMOTO SATO
    1990 Volume 161 Issue Supplement Pages 253-271
    Published: 1990
    Released on J-STAGE: March 14, 2011
    JOURNAL FREE ACCESS
    Among many factors linked to an intractability of partial seizure secondarily generalized, changes in the brain resulting from repeated epileptic seizures are discussed mainly in light of our evidence obtained from kindling studies in cats. In addition, the literatures on biological mechanisms of the kindling effect are reviewed briefly. The evidence demonstrated and reviewed here indicates that: 1) limbic structure is not susceptable to develop generalized convulsions initially, 2) repeated attacks of limbic seizures result in a profound reduction in seizure threshold at the primary epileptogenic focus in the limbic structures, 3) once a limbic seizure developed to secondarily generalized convulsion, it seldom changes into the original partial seizure, 4) kindled events in the limbic structures are more profound and persistent than that in the cerebral cortex, and 5) repetition of focal cortical or limbic seizures may eventually produce spontaneous convulsive seizures originating in the limbic structures. These findings strongly suggest that the limbic system, rather than the cerebral cortex, is more susceptible to a lasting functional change resulted from seizure repetition, which can lead to an intractability of epilepsy with partial seizure. Lasting changes in the cell membrane including long-lasting enhancement of inositol phospholipid hydrolysis of the amygdala stimulated by excitatory amino acid appear important for development of trans-synaptic changes underlying the kindling-induced seizure susceptibility.
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  • Its Pathogenesis and Clinical Significance
    KEIJI SANO, TAKAAKI KIRINO
    1990 Volume 161 Issue Supplement Pages 273-295
    Published: 1990
    Released on J-STAGE: March 14, 2011
    JOURNAL FREE ACCESS
    Sclerosis of the cornu Ammonis or Ammon's horn sclerosis (AHS) is an “often-described, yet hitherto enigmatic phenomen” as Spielmyer put it in 1927. It has been found in cases with ischemia, anoxia or hypoglycemia and in more than half of the epileptic brains examined at autopsy. Various theories about its pathogenesis have been propunded. Among them, the “Pathoklise” theory of the Vogts and the vascular theory of Spielmeyer and his associates were prevailing until recently. In 1953, two articles were published to contribute to the pathogenesis of ictal automatism (a type of complex partial or temporal lobe seizures). One is the incisural sclerosis theory by Penfield and his associates and the other is the Ammon's horn sclerosis theory by Sano and Malamud. The former authors described a diffuse sclerosis of the infero-mesial temporal structures without, however, specifically relating it to AHS. They considered it was the result of localized anoxia of that portion of the brain caused by incisural herniation occurring during parturition. Sano and Malamud maintained that AHS is a result of convulsions, a distinct scar adjacent to which epileptogenic foci may develop in the course of time to cause ictal antomatism. The latter theory was corroborated by Sano, Falconer and others. Falconer expanded the theory to the assertion that not only ictal automatism but other types of intractable epilepsy may be due to “mesial temporal (Ammon's horn) sclerosis”. The most recent development in the pathogenesis of AHS is the excitotoxicity theory. Namely, AHS is caused by excessive excitation of neurons, probably by putative excitatory neurotransmitters, especially, glutamate. For this theory, there is a significant body of evidence. The problem of AHS, an old research subject and a matter of long-lasting controversy, has now been updated and become one of the newest topics in the field of experimental neurobiology.
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