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Genetically Epilepsy-Prone Rats
Published in Carl L. Faingold, Gerhard H. Fromm, Drugs for Control of Epilepsy:, 2019
Phillip C. Jobe, Pravin K. Mishra, John W. Dailey
Increasing degrees of tonic seizure involvement are indicated by scores of 4 and above. Class 4 and 5 convulsions are characterized by tonic ventriflexion of the trunk and neck, tonic extension of the forelimbs, and tonic flexion of the hindlimbs. Class 6 and 7 convulsions are similarly characterized except that the pelvic limbs have succeeded to partial extension. Class 8 and 9 seizures go one step further by featuring complete tonic extension of the pelvic limbs.
Audiogenic Seizures in Mice and Rats
Published in Steven L. Peterson, Timothy E. Albertson, Neuropharmacology Methods in Epilepsy Research, 2019
Audiogenic seizure susceptibility in the DBA/2 occurs during a limited period of development.5 A low incidence of the initial audiogenic seizure response, wild running, occurs at 13 d of age.15 Audiogenic seizure incidence and severity rapidly increase with age, reaching 100% incidence by 17 d of age, with a 90% incidence of tonic seizures. It should be noted that tonic seizures in this report included both tonic hindlimb flexion and hindlimb extension and thus do not represent a 90% incidence of a maximal audiogenic seizure response (hindlimb extension).15 In another report, peak incidence of audiogenic seizures occurs at 21 d of age in which over 91% of the mice exhibited either clonic or tonic seizures.16 Again the data presentation does not reveal the actual incidence of hindlimb extension. Still another report indicates an 87% incidence of the “most severe form of the seizure, i.e., the full clonic-tonic seizure,” occurs at 21 d of age.17 Presumably this description is referring to hindlimb extension as the most severe form of audiogenic seizure. These three reports are illustrative of the confusion that exists in the audiogenic seizure literature due to inconsistent or incomplete descriptions of seizure responses. However, there is general consensus that audiogenic seizures in DBA/2 mice peak in incidence and severity between 16 and 21 d of age.5
Cortico-cortical evoked potentials
Published in Hans O Lüders, Deep Brain Stimulation and Epilepsy, 2020
Riki Matsumoto, Dileep R Nair, Eric LaPresto, Imad Najm, William Bingaman, Hans O Lüders
A 33-year-old right-handed man with medically intractable partial epilepsy since age 7 underwent invasive video-EEG monitoring with subdural electrodes placed at the lateral frontoparietal and lateral and basal temporal areas. Habitual seizures started with an aura consisting of a tingling sensation in his chest, spreading to his arms and legs. Seizures were then followed by a left face tonic seizure, finally evolving into a generalized tonic-clonic seizure. While interictal epileptiform discharges were widely spread over the right hemisphere, the EEG seizures started with an electrodecremental pattern in the lateral and basal temporal areas, followed in 2 seconds by a paroxysmal fast activity in Plate D maximum at electrode D1. Standard 50 Hz electrical stimulation at electrode D1 elicited a habitual aura. Bipolar stimulation of electrodes D1 and D2 were performed to investigate cortico-cortical connections in the temporal area in an attempt to better understand the spike propagation. CCEPs were recorded from the basal and lateral temporal areas (Figure 9.1). Stimulation of electrodes D1 and D2 elicited CCEPs from the adjacent electrodes with its maximum at electrode D5/6, peaking latency at 12 ms. CCEPs were also recorded from Plate E with its maximum at E4, though with smaller amplitude and longer peak latency. No clear focal potentials were recorded from the lateral temporal area at Plate B. To investigate short and long cortico-cortical connections in the frontoparietal area, pairs of electrodes in Plate C were stimulated. CCEPs were recorded from the posterior half of Plate C in the inferior frontal gyrus (IFG) and from a part of Plate A in the inferior parietal area (Figure 9.2). In Plate C, large short-latency CCEPs were recorded from the electrodes close to the pair of stimulation (Figure 9.2). The largest CCEPs were obtained from electrodes adjacent to the pair of stimulation with a peak latency of 12–14 ms. With regards to long cortico-cortical connections, stimulation at Pair 3 in the posterior part of inferior frontal gyrus elicited CCEPs in the posterior part of the inferior parietal area with the first negative peak at 25-37 ms followed by a larger late negative potential. On the other hand, no clear activity was recorded when the anterior part of inferior frontal gyrus (Pair 1) was stimulated. These studies showed the presence of the interconnection within the ventral prefrontal/premotor area (by short cortico-cortical connections) and the fronto-parietal circuit between the ventral prefrontal/premotor and posterior inferior parietal areas (by long cortico-cortical connections).
Unilateral cerebral cortical encephalitis with epilepsy: a possible special phenotype of MOG antibody-associated disorders
Published in International Journal of Neuroscience, 2020
Ran Tao, Chuan Qin, Man Chen, Hai-Han Yu, Long-Jun Wu, Bi-Tao Bu, Dai-Shi Tian
Case 2. A 28-year-old man was admitted to a local hospital with headache and fever in Sept 2017. During hospitalization, the patient experienced a consciousness disturbance and a generalized tonic seizure. CSF analysis demonstrated marked pleocytosis (520*10∧6 cells/L). He was diagnosed with encephalitis and treated with anti-infective therapy. The symptoms of headache and fever disappeared. However, he developed visual loss in his left eye and then transferred to our hospital. Neurologic examination showed impaired visual acuity of the left eye and neck stiffness. CSF analysis revealed pleocytosis (105*10∧6 cells/L), normal glucose and protein and microbiological results were negative. The MOG antibody test in the serum was positive (1:10). Autoimmune encephalitis-related autoantibodies, including NMDAR-Abs, CASPR2 antibodies, LGI1 antibodies, AMPAR antibodies, GABA receptor antibodies, were negative both in serum and CSF. Brain MRI revealed unilateral hemispheric cortical hyperintense lesions in FLAIR imaging, with slightly leptomeningeal enhancement (Figure 2). Orbital MRI showed bilateral optic nerves thicken near the eyeball, especially on the left side (Figure 2). The patient was diagnosed with MOG antibody-associated encephalitis, and treated with high-dose intravenous corticosteroids and antiepilepsy drugs. He recovered quickly and his visual acuity improved completely.
The antiepileptic and neuroprotective effect of the Buxus hyrcana Pojark hydroethanolic extract against the pentylentetrazol induced model of the seizures in the male rats
Published in International Journal of Neuroscience, 2018
Vahid Azizi, Farzin Allahyari, Abdolkarim Hosseini
This study adopted a double-blind procedure (the operator was unaware of the animal categorization to any particular group). The animals were randomly divided into seven groups of six as follows: (1) the negative control group received normal saline (0.25 ml kg−1), (2) the positive control group received PB (30 mg kg−1 B.W.), (3, 4, 5, 6, 7) and the experimental groups received the ethanol extract (BHP: 150, 300, 450, 600 and 750 mg kg−1 B.W., respectively). Thirty minutes after the intra-peritoneal injection, the animals were challenged with PTZ (70 mg kg−1 B.W.; single dose). In order to record and measure seizure behavior, the animals were transferred individually into the transparent plastic boxes; quickly after the PTZ challenge, the seizure behavior was observed for 1 h and was recorded and stored in the computer through the connected camera. The onset time of the threshold or tonic seizure delay, the onset of the tonic and clonic seizures and also the total time of the tonic–clonic seizures were measured [14].
Sub-chronic boldine treatment exerts anticonvulsant effects in mice
Published in Neurological Research, 2018
Leila Moezi, Siranoush Yahosseini, Akram Jamshidzadeh, Mona Dastgheib, Fateme Pirsalami
The convulsive dose of PTZ inducing a clonic seizure in 97% of the animals called CD97. In this experimental model, single intraperitoneal injection of PTZ (85 mg/kg, CD 97) is used for induction of generalized tonic–clonic seizure. Following seizure induction, the incidence and the latency for the onset of the generalized tonic seizure and the death incidence were evaluated. Immediately after PTZ injection, the animal was transferred to an open field (50 cm in diameter) and observed for 30 min for the occurrence of convulsion or death. Time latencies for the appearance of the first myoclonic jerk and generalized clonus were measured following PTZ administration. Latency is defined as the time between PTZ injection and the onset of myoclonic and clonic seizures. Myoclonus was defined as sudden jerks. Generalized clonus was described as the involvement of all four limbs and tail rearing, wild running and jumping, sudden loss of upright posture and autonomic sign such as hypersalivation and defecation. The incidence of tonic seizure and death was also recorded. Tonic seizure was described as a full tonic hind limb extension (THE) when the angle off the hind limbs to the torso exceeded 90° (usually 180°)