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which the EEG abnormalities are less regularly of a 3-per-second spike-and-wave type (they may occur at the rate of 2 to 25 per second or take the form of 4- to 6-Hz polyspike-and-wave complexes) Atypical petit mal is a term that was coined to describe long runs of slow spike-and-wave activity, usually with no apparent loss of consciousness External stimuli such as asking the patient to answer a question or to count will interrupt the run of abnormal EEG activity About one-third of children with absence attacks will, in addition, display symmetrical or asymmetrical myoclonic jerks without loss of consciousness, and about half will also at some time have major generalized (tonic-clonic) convulsions As described further on, a common and relatively benign variety of myoclonic seizure occurs in late childhood and adolescence (juvenile myoclonic epilepsy) In sharp contrast to the aforementioned epilepsies is a form that has its onset between 2 and 6 years of age and is characterized by atonic, or astatic, seizures (ie, falling attacks), often succeeded by various combinations of minor motor, tonic-clonic, and partial seizures and by progressive intellectual impairment in association with a distinctive, slow (1- to 2-Hz) spike-and-wave EEG pattern This is the Lennox-Gastaut syndrome Often it is preceded in earlier life by infantile spasms, a characteristic EEG picture (3-Hz hypsarrhythmia ), and an arrest in mental development, a triad sometimes referred to as the West syndrome (see further on) The early onset of atonic seizures with abrupt falls, injuries, and associated abnormalities nearly always has a grave implication namely, the presence of serious neurologic disease Prematurity, perinatal injury, and metabolic diseases of infancy are the most common underlying conditions This is essentially a symptomatic generalized epilepsy, in contrast to the foregoing idiopathic types The LennoxGastaut syndrome may persist into adult life and is one of the most dif cult forms of epilepsy to treat The notion that absence, myoclonic, and akinetic seizures constitute a petit mal triad, as originally proposed by Lennox, has been generally abandoned Akinesia (motionlessness) is not unique to any seizure type The typical absence, with or without myoclonic jerks, rarely causes the patient to fall and should be considered a separate entity because of its relative benignity.

The phenomenon of myoclonus has already been discussed in Chap 6, where the relationship to seizures was indicated Characterized by a brusque, brief, muscular contraction, some myoclonic jerks are so small as to involve only one muscle or part of a muscle; others are so large as to implicate a limb on one or both sides of the body or the entire trunk musculature Many are brief, lasting 50 to 100 ms They may occur intermittently and unpredictably or present as a single jerk or a brief salvo As mentioned earlier, an outbreak of several small, rhythmic myoclonic jerks may appear with varying frequency as part of absence seizures and as isolated events in patients with generalized clonic-tonic-clonic or tonic-clonic seizures As a rule, these types of myoclonus are quite benign and respond well to medication In contrast, disseminated myoclonus (polymyoclonus), having its onset in childhood, raises the suspicion of acute viral encephalitis, the myoclonus-opsoclonus-ataxia syndrome of Kinsbourne, lithium or other drug toxicity, or, if lasting a few weeks, subacute sclerosing panencephalitis Chronic progressive polymyoclonus with dementia characterizes the group of juvenile lipidosis, Lafora-

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type familial myoclonic epilepsy, certain mitochondrial disorders, or other chronic familial degenerative diseases of unde ned type (paramyoclonus multiplex of Friedreich, dyssynergia cerebellaris myoclonica of Ramsay Hunt) In middle and late adult years, disseminated myoclonus joined with dementia usually indicates the presence of so-called Creutzfeldt-Jakob disease (page 653) and rarely of Alzheimer disease A few late-onset cases of Lafora disease have been reported (Messouak et al), but this remains mainly a childhood process, autosomal recessive in transmission, characterized by a triad of progressive dementia, myoclonus, and episodes of generalized seizures, some of which are visual in nature Intraneuronal cortical inclusions of amyloid are found, and similar inclusions are found in muscle, liver, and skin (polyglucosan body disease is another process associated with these changes) Myoclonus is usually the main manifestation of juvenile myoclonic epilepsy, as discussed below Uremia at any age gives rise to myoclonus, twitching, and sometimes seizures The large number of diseases causative of myoclonus and seizure disorders are discussed in Chaps 33, 37, and 39 Juvenile Myoclonic Epilepsy This is the most common form of idiopathic generalized epilepsy in older children and young adults It begins in adolescence, typically about age 15, with a range that essentially spans all of the teenage years The patient comes to attention because of a generalized seizure, often upon awakening or because of myoclonic jerks in the morning that involve the entire body; sometimes absence seizures are prominent The family reports that the patient has occasional myoclonic jerks of the arm and upper trunk that become prominent with fatigue, during early stages of sleep, or after alcohol ingestion A few patients in our experience have had only the myoclonic phenomena and rare absence seizures that persisted unnoticed for years The EEG characteristically shows bursts of 4- to 6-Hz irregular polyspike activity A linkage has been established to chromosome 6 in some cases of this illness and in some other forms of juvenile-onset epilepsy, but no mendelian pattern of inheritance has been established The disorder does not impair intelligence and tends not to be progressive, but a proclivity to infrequent seizures usually continues throughout life Valproic acid in particular and some other anticonvulsants have been highly effective in eliminating the seizures and myoclonus; they should be continued inde nitely.

Completing this initial basic line chart simply required adding some minor text to the chart Most of the time was spent creating the query to support this chart With the appropriate data available, a reasonable chart can be created almost immediately To create this chart, I adjusted the default chart type from column to line by right-clicking on the Chart Web item and choosing Edit from the context menu and I then chose basic lines rather than the dimensional options, as shown in the following illustration

Somatic motor Jacksonian (focal motor) Prerolandic gyrus Masticatory, salivation, Amygdaloid nuclei, opercular speech arrest Simple contraversive Frontal Supplementary motor cortex Head and eye turning associated with arm movement or athetoiddystonic postures Somatic and special sensory (auras) Somatosensory Contralateral postrolandic Unformed images, lights, Occipital patterns Auditory Heschl s gyri Vertiginous Superior temporal Olfactory Mesial temporal Gustatory Insula Visceral: autonomic Insular-orbital-frontal cortex Complex partial seizures Formed hallucinations Temporal neocortex or amygdaloid-hippocampal complex Illusions Dyscognitive experiences (deja vu, dreamy states, ` depersonalization) Temporal Affective states (fear, depression, or elation) Automatism (ictal and Temporal and frontal postictal) Absence Frontal cortex, amygdaloidhippocampal complex, reticular-cortical system Bilateral epileptic myoclonus Reticulocortical, frontocentral

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