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To change line appearance, select the element in which you want to format a line, look to the properties for the parameters, and change the appropriate settings for the line The corresponding section in the chart is highlighted so that you can see what is going to be changed Because the change itself is on a line and not on an area or object, you have to look closely to see the change appear on the screen You also can change the line type of a chart that has at least one data series of the type profile or line You do this by selecting the property Data Series Format | <name of data series> and then choosing the entry from the Line Type list

Just why the neurons in or near a focal cortical lesion discharge abnormally is not fully understood Some of the electrical properties of a cortical epileptogenic focus suggest that its neurons have been deafferented Such neurons are known to be hyperexcitable, and they may remain so chronically, in a state of partial depolarization, able to re irregularly at rates as high as 700 to 1000 per second The cytoplasmic membranes of such cells appear to have an increased ionic permeability, which renders them susceptible to activation by hyperthermia, hypoxia, hypoglycemia, hypocalcemia, and hyponatremia as well as by repeated sensory (eg, photic) stimulation and during certain phases of sleep (where hypersynchrony of neurons is known to occur) As an example, epileptic foci induced in the animal cortex by the application of penicillin are characterized by spontaneous interictal discharges, during which the neurons of the discharging focus exhibit large, presumably Ca-mediated paroxysmal depolarizing shifts (PDSs), followed by prolonged after-hyperpolarizations (AHPs) The latter also are due in part to Ca-dependent K currents but are better explained by enhanced synaptic inhibition The PDSs occur synchronously in the penicillin focus and summate to produce surface-recorded interictal EEG spikes; the AHPs correspond to the slow wave of the EEG spike-and-wave complex (Engel) The neurons surrounding the epileptogenic focus are hyperpolarized from the beginning and are inhibitory and release gamma aminobutyric acid Seizure spread probably depends on any factor or agent that activates neurons in the focus or inhibits those surrounding it The precise mechanisms that govern the transition from a circumscribed interictal discharge to a widespread seizure state are not understood Biochemical studies of neurons from a seizure focus have not greatly clari ed the problem Levels of extracellular K are found to be elevated in glial scars near epileptic foci, and a defect in voltage-sensitive Ca channels has also been postulated Epileptic foci are known to be sensitive to acetylcholine and to be slower in binding and removing it than is normal cerebral cortex A de ciency of the inhibitory neurotransmitter GABA, increased glycine, decreased taurine, and either decreased or increased glutamic acid have been variously reported in excised human epileptogenic tissue, but whether these changes are the cause or result of seizure activity has not been determined The interpretation of reported abnormalities of GABA, biogenic amines, and acetylcholine in the cerebrospinal uid (CSF) of epileptic patients poses similar dif culties Concurrent EEG recordings from an epileptogenic cortical focus and subcortical, thalamic, and brainstem centers in the animal model have enabled investigators to construct a sequence of electrical and clinical events that characterize an evolving focal seizure Firing of the involved neurons in the cortical focus is re ected in the EEG as a series of periodic spike discharges, which increase progressively in amplitude and frequency Once the intensity of the seizure discharge exceeds a certain point, it overcomes the inhibitory in uence of surrounding neurons and spreads to neighboring cortical regions via short corticocortical synaptic connections If the abnormal discharge remains con ned to the cortical focus and the immediate surrounding cortex, there are probably no clinical symptoms or signs of seizure, and the EEG abnormality that persists during the interseizure period re ects this restricted type of abnormal cortical activity A provocative new nding, based on sophisticated mathematical analysis of EEG tracings, demonstrates subtle electrographic changes up to several minutes before the ictal discharge (see LeVan Quyen.

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