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et al) This suggests that seizures are triggered either by a change in central thalamic rhythm generators or a subtle change in the electrical activity in the region of a focal lesion The clinical utility of this nding has not been determined Even more provocative are the ndings of Litt and colleagues; using complex techniques in a small number of patients, they have detected prolonged bursts of seizure-like activity days before the onset of temporal lobe seizures Their unconventional proposal is that these events cause a cascade of electrophysiologic changes that very gradually culminate in a seizure If unchecked, cortical excitation spreads to the adjacent cortex and to the contralateral cortex via interhemispheric pathways and also to anatomically and functionally related pathways in subcortical nuclei (particularly the basal ganglionic, thalamic, and brainstem reticular nuclei) It is at this time that the clinical manifestations of the seizure begin, the initial signs and symptoms depending on the portion of the brain from which the seizure originates The excitatory activity from the subcortical nuclei is fed back to the original focus and to the other parts of the forebrain, a mechanism that serves to amplify their excitatory activity and to give rise to the characteristic high-voltage polyspike discharge in the EEG There is propagation downward to spinal neurons as well, via corticospinal and reticulospinal pathways, yielding a generalized tonic-clonic convulsion The spread of excitation to the subcortical, thalamic, and brainstem centers is thought to correspond to the tonic phase of the seizure and loss of consciousness as well as to the signs of autonomic nervous system overactivity (salivation, mydriasis, tachycardia, increase in blood pressure) Vital functions may be arrested, but usually for only a few seconds In rare instances, however, death may occur owing to a sustained cessation of respiration, a derangement of cardiac action, or some unknown cause The development of unconsciousness and the generalized tonic contraction of muscles is re ected in the EEG by a diffuse high-voltage discharge pattern appearing simultaneously over the entire cortex Soon after the spread of excitation, a diencephalocortical inhibition begins and intermittently interrupts the seizure discharge, changing it from the persistent discharge of the tonic phase to the intermittent bursts of the clonic phase Electrically, a transition occurs from a continuous polyspike to a spike-and-wave pattern The intermittent clonic bursts become less and less frequent and nally cease altogether, leaving in their wake an exhaustion (paralysis) of the neurons of the epileptogenic focus and a regional increase in permeability of the blood-brain barrier An overshoot of these inhibitory mechanisms is thought to be the basis of Todd s postepileptic paralysis (and of postictal stupor, sensory loss, aphasia, hemianopia, headache, and diffuse slow waves in the EEG, as described earlier) and regional edema in T2-weighted MR images Plum and associates have observed a two- to threefold increase in glucose utilization during seizure discharges and suggested that the paralysis that follows might be due to neuronal depletion of glucose and increase in lactic acid However, inhibition of epileptogenic neurons may occur in the absence of neuronal exhaustion The exact roles played by each of these factors in postictal paralysis of function are not settled Bilaterally synchronous three-per-second high-voltage spikeand-wave discharges and seizures resembling absence attacks have been produced in animals by a number of experimental procedures The spike-and-wave complex, which represents brief excitation followed by slow-wave inhibition, is the type of EEG pattern that. barcode font for excel free download Using the Barcode Font in Microsoft Excel (Spreadsheet)
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To insert bar codes into a Microsoft Excel document please follow these steps: characterizes the clonic (inhibitory) phase of the focal motor or grand mal seizure By contrast, this strong element of inhibition is present diffusely throughout an absence attack, a feature that perhaps accounts for the failure of excitation to spread to lower brainstem and spinal structures (tonic-clonic movements do not occur) However, the absence seizure can also at times activate the mechanism for rhythmic myoclonus, probably at an upper brainstem level Current physiologic data indicate that the characteristic EEG patterns of both generalized forms of epilepsy (ie, tonic or tonicclonic and absence) are generated in the neocortex and are enhanced by the synchronizing in uences of subcortical structures In both instances, the generalization of the clinical and electrical manifestations depends upon activation of a deep, centrally located physiologic mechanism, which, for reasons outlined in Chap 17, includes the midbrain reticular formation and its diencephalic extension, the intralaminar and nonspeci c thalamic projection systems (originally referred to by Pen eld as the centrencephalon ) There is no evidence, however, that seizure activity originates in these deep activating structures; therefore the term centrencephalic epilepsy has been replaced by corticoreticular epilepsy Complex partial seizures are almost always of temporal lobe origin, arising in foci in the medial temporal lobe, amygdaloid nuclei, and hippocampus Only rarely do they originate in the convexity of the temporal lobe and propagate to the amygdaloid nuclei, hippocampus, and posteroinferior parts of the frontal lobe Electrical stimulation in these areas reproduces feelings of depersonalization, emotionality, and automatic behavior, the characteristic features of psychomotor epilepsy The automatic behavior appears to be a direct effect of the temporal lobe discharge in some instances and a postexcitatory or inhibitory effect in others Loss of memory for the events of the episode may be due to the paralytic effect of the discharge on neurons of the hippocampus Of theoretical importance is the observation that a seizure focus, if active for a time, may sometimes establish, via commissural connections, a persistent secondary focus in the corresponding cortical area of the opposite hemisphere (mirror focus) The nature of this phenomenon is obscure; it may be similar to the kindling phenomenon mentioned earlier in animals, where a repeated nonconvulsive electrical stimulation of normal cortex induces a permanent epileptic focus No morphologic change is visible in the mirror focus, at least by light microscopy The mirror focus may be a source of confusion in trying to identify the side of the primary lesion by EEG, but there is little evidence that it can produce chronic seizures in humans Similarly, there are no rm data supporting a role for kindling in the diagnosis and management of patients with epilepsy (Goldensohn) Severe seizures may be accompanied by a systemic lactic acidosis with a fall in arterial pH, reduction in arterial oxygen saturation, and rise in PCO2 These effects are secondary to the respiratory arrest and excessive muscular activity If prolonged, they may cause hypoxic-ischemic damage to remote areas in the cerebrum, basal ganglia, and cerebellum In paralyzed and arti cially ventilated subjects receiving electroconvulsive therapy, these changes are less marked and the oxygen tension in cerebral venous blood may actually rise Heart rate, blood pressure, and particularly CSF pressure rise briskly during the seizure According to Plum and colleagues, the rise in blood pressure evoked by the seizure usually causes a suf cient increase in cerebral blood ow to meet the increased metabolic needs of the brain. how to make barcodes in excel MS Excel Inventory Management System download | SourceForge.net
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