Temporal lobe ictal behavioral patterns in hippocampal sclerosis and other structural abnormalities

Kutlu, Gülnihal; Bilir, Erhan; Erdem, Atilla; Gömceli, Yasemin Bıçer; Leventoğlu, Alev; Kurt, G. Semiha; Karataş, Ayşe; Serdaroğlu, Ayşe

doi:10.1016/j.yebeh.2004.12.013

Cited by 12 publications

(10 citation statements)

References 23 publications

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“…Moreover, up-regulated Drd2 expression may reflect compensatory decreased signaling through the Drd2. We also show that loss of the Drd1aϩ population results in spontaneous stereotyped seizures with features reminiscent of human complex partial seizures of temporal lobe origin where ictal hand automatisms are typically seen (30,31). The seizures are likely to be related to hippocampal rather than striatal pathology.…”

Section: Discussionmentioning

confidence: 63%

Ablation of D1 dopamine receptor-expressing cells generates mice with seizures, dystonia, hyperactivity, and impaired oral behavior

Gantois

Fang

Jiang

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

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Huntington's disease is characterized by death of striatal projection neurons. We used a Cre/Lox transgenic approach to generate an animal model in which D1 dopamine receptor (Drd1a)؉ cells are progressively ablated in the postnatal brain. Striatal Drd1a, substance P, and dynorphin expression is progressively lost, whereas D2 dopamine receptor (Drd2) and enkephalin expression is up-regulated. Magnetic resonance spectroscopic analysis demonstrated early elevation of the striatal choline/creatine ratio, a finding associated with extensive reactive striatal astrogliosis. Sequential MRI demonstrated a progressive reduction in striatal volume and secondary ventricular enlargement confirmed to be due to loss of striatal cells. Mutant mice had normal gait and rotarod performance but displayed hindlimb dystonia, locomotor hyperactivity, and handling-induced electrographically verified spontaneous seizures. Ethological assessment identified an increase in rearing and impairments in the oral behaviors of sifting and chewing. In line with the limbic seizure profile, cell loss, astrogliosis, microgliosis, and down-regulated dynorphin expression were seen in the hippocampal dentate gyrus. This study specifically implicates Drd1a؉ cell loss with tail suspension hindlimb dystonia, hyperactivity, and abnormal oral function. The latter may relate to the speech and swallowing disturbances and the classic sign of tongueprotrusion motor impersistence observed in Huntington's disease. In addition, the findings of this study support the notion that Drd1a and Drd2 are segregated on striatal projection neurons. striatum ͉ Cre ͉ Huntington's disease T he nigrostriatal pathway projects from the midbrain substantia nigra pars compacta to innervate the dorsal striatum. Dopamine is released from dopaminergic terminals in the striatum to regulate motor activity and eating behavior (1). Early studies suggested that dopamine D1 (Drd1a) and D2 receptors (Drd2) are segregated on striatal projection neurons; the Drd1a is expressed on substance P and dynorphin-positive striatal neurons, which project directly to the substantia nigra pars reticulata/entopeduncular complex (known as the direct pathway), whereas Drd2 is preferentially expressed on enkephalin-positive striatopallidal projecting neurons (2). Neurons within the globus pallidus then project to the subthalamic nucleus, which in turn relays to the substantia nigra pars reticulata/entopeduncular complex (known as the indirect pathway). Dopamine also modulates the activity of glutamatergic corticostriatal input on striatal projection neurons.Idiopathic Parkinson's disease is characterized by the death of dopaminergic neurons; however, rare Parkinsonian syndromes have been identified in which the defect is associated with cell death in the dopamine-responsive neurons in the striatum (3-6). Huntington's disease (HD) (7-10), a neurodegenerative condition with motor, cognitive, and psychiatric disturbances, also involves death of dopamine receptor-expressing striatal projection neurons. Several ...

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Section: Discussionmentioning

confidence: 63%

Ablation of D1 dopamine receptor-expressing cells generates mice with seizures, dystonia, hyperactivity, and impaired oral behavior

Gantois

Fang

Jiang

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

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“…An alternative explanation was that mutated channels are differentially expressed at GABAergic neurons, then provoking inhibition of these neurons that could lead to network disinhibition and seizures. In MTLE, seizures originate in the hippocampus para-hippocampal areas (partial seizures) with secondary generalization in some cases (Arabadzisz et al, 2005;Bernasconi et al, 2005;Cavazos and Cross, 2006;Kutlu et al, 2005). Therefore, the role of BK channel dysfunction will probably be different in generalized epilepsy with thalamo-cortical involvement.…”

Section: Discussionmentioning

confidence: 99%

Down-regulation of BK channel expression in the pilocarpine model of temporal lobe epilepsy

Otalora¹,

Hernandez²,

Arshadmansab³

et al. 2008

Brain Research

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In the hippocampus, BK channels are preferentially localized in presynaptic glutamatergic terminals including mossy fibers where they are thought to play an important role regulating excessive glutamate release during hyperactive states. Large conductance calcium-activated potassium channels (BK, MaxiK, Slo) have recently been implicated in the pathogenesis of genetic epilepsy. However, the role of BK channels in acquired mesial temporal lobe epilepsy (MTLE) remains unknown. Here we used immunohistochemistry, laser scanning confocal microscopy (LSCM), western immunoblotting and RT-PCR to investigate the expression pattern of the alpha-pore forming subunit of BK channels in the hippocampus and cortex of chronically epileptic rats obtained by the pilocarpine model of MTLE. All epileptic rats experiencing recurrent spontaneous seizures exhibited a significant down-regulation of BK channel immunostaining in the mossy fibers at the hilus and stratum lucidum of the CA3 area. Quantitative analysis of immunofluorescence signals by LSCM revealed a significant 47% reduction in BK channel in epileptic rats when compared to age-matched non-epileptic control rats. These data correlate with a similar reduction in BK channel protein levels and transcripts in the cortex and hippocampus. Our data indicate a seizure-related down-regulation of BK channels in chronically epileptic rats. Further functional assays are necessary to determine whether altered BK channel expression is an acquired channelopathy or a compensatory mechanism affecting the network excitability in MTLE. Moreover, seizure-mediated BK down-regulation may disturb neuronal excitability and presynaptic control at glutamatergic terminals triggering exaggerated glutamate release and seizures.

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“…Various previous studies could not determine the lateralizing values of auras [20,22,27]. Guptka et al, however, claimed that autonomic and psychic auras are associated with a right temporal focus [28].…”

Section: Discussionmentioning

confidence: 95%

“…Information on whether patients had auras and the types of auras (abdominal, auditory, autonomic, gustatory, olfactory, psychic, somatosensory, and visual) that they had were gathered from the patient descriptions on video-EEG monitoring and from medical records. Ictal behavioral characteristics mentioned in the previous literature [2,3,20,21] including behavioral arrest, oroalimentary and genital automatisms, dystonic or tonic limb posturing, versive or nonversive head deviation, postictal nose wiping, ictal vocalization or speaking, periictal vegetative signs (vomiting, urinary urge, coughing, thirst/ drinking), ictal emotional signs (laughing, crying, fear), unilateral eye blinking, last clonic jerk, ictal spitting, ictal aphasia, and postictal paresis were observed in video recordings. Among these, ictal/postictal aphasia, postictal paresis, and ictal eye blinking were not observed as it was not possible to assess these three signs accurately though video-EEG records.…”

Section: Methodsmentioning

confidence: 99%

An evaluation of lateralizing signs in patients with temporal lobe epilepsy

Ataoglu

Yıldırım

Bilir

2015

Epilepsy & Behavior

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Temporal lobe ictal behavioral patterns in hippocampal sclerosis and other structural abnormalities

Cited by 12 publications

References 23 publications

Ablation of D1 dopamine receptor-expressing cells generates mice with seizures, dystonia, hyperactivity, and impaired oral behavior

Ablation of D1 dopamine receptor-expressing cells generates mice with seizures, dystonia, hyperactivity, and impaired oral behavior

Down-regulation of BK channel expression in the pilocarpine model of temporal lobe epilepsy

An evaluation of lateralizing signs in patients with temporal lobe epilepsy

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