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By U. Innostian. University of California, Los Angeles.

They may obscure normal sleep architecture and buy cheap alesse 0.18 mg on-line birth control wiki, while not the pattern of electrographic status epilepticus of sleep (ESES) order alesse 0.18 mg otc birth control free, may occupy up to 50% of the recording. Generalized spikes, and in some patients multifocal spikes, can be seen throughout the recording. Neuropsychologic Disturbances Mental retardation is almost universal in LGS, with fewer than 10% of patients pre- serving near-normal intellectual functioning. Children may appear normal or near normal at onset with an abrupt deterioration following the onset of uncontrolled sei- zures, or may have a preceding encephalopathy, including infantile spasms. Overall, cognition progressively deteriorates, compounded by repeated trauma from falls and the effects of multiple anticonvulsants. Behavior problems abound and include autis- tic spectrum disorders, aggressiveness, and hyperactivity. EVALUATION—ETIOLOGY The differentiation of LGS from other catastrophic onset childhood epilepsies is important for prognosis and management. The seizure pattern may not appear char- acteristic initially and suggestive EEG patterns may not appear for several months. Therefore, it is not unreasonable to pursue diagnostic testing that may be suggested by the individual’s presentation—for example, that of progressive myoclonic epi- lepsy in a patient in whom the initial presentation includes myoclonic seizures. Very few patients with LGS, however, have documented abnormalities of metabolism. Concerns that LGS may be related to a developmental channelopathy or be an immune-mediated process have yet to be substantiated. In some series, 17–30% of patients with LGS have a history of infantile spasms. Therefore, central nervous system insults known to predispose to infantile spasms have been implicated in the pathogenesis of LGS. These include congenital infec- tions, sequela of neonatal hypoglycemia, hypoxic–ischemic encephalopathy, and traumatic brain injury. Lennox–Gastaut Syndrome 81 Structural abnormalities are the most common underlying etiology of sympto- matic LGS. Rarely, brain tumors have been known to cause LGS, although this raises the difficulty of differentiating true LGS from secondary bilateral synchrony. Tuberous sclerosis or other neurocutaneous syndromes are found in children with LGS, but not as frequently as in association with infantile spasms. Developmental brain malformations are the most common structural lesion to be reported in LGS, especially subcortical band heterotopia, bilateral perisylvian syndrome, and focal cortical malformations. It is therefore important to perform magnetic reso- nance imaging when considering the diagnosis of LGS, as there are reported cases of seizure reduction with focal surgical resection of lesions. Other types of neuroima- ging, including PET and SPECT scans, have not been uniformly helpful and are cur- rently better research than diagnostic tools. The majority of cases of LGS remain cryptogenic despite extensive metabolic evaluation and neuroimaging. Evaluation aimed at maximizing supportive care, such as neuropsychological assessment to identify baseline neurodevelopmental state and aid in appropriate educational placement are also important. It is helpful to differentiate LGS from other seizure syndromes, especially from myoclonic astatic epilepsy (Doose syndrome), that may have a more favorable prog- nosis. Children with myoclonic astatic epilepsy have the occurrence of multiple types of generalized seizures suggestive of LGS (i. However, it is always idiopathic, axial tonic seizures are rare or absent, onset is younger than in LGS (typically between 18 months and 4 years), EEG demonstrates photosensitivity, and there is a strong genetic predisposition. Prognosis for seizure control and devel- opmental outcome is more benign than in LGS. Similarly, an entity named atypical benign partial epilepsy of childhood occurs in children between 2 and 6 years, with prominent nocturnal partial seizures, myoclonic, and atonic seizures without tonic seizures. Electroencephalogram is remarkable for diffuse slow spike and wave in sleep and 3-Hz spike wave in the waking record.

It was in this type bilitation commission was established in New of surgery that his tools were most useful and Jersey in 1919 purchase alesse 0.18mg without prescription birth control nexplanon. This was quite different from any in London buy alesse 0.18mg otc birth control hormone imbalance, at the International Congress of Med- other type that had been done before. It was a V- icine at the Royal National Orthopedic Hospital, shaped fore-and-aft wedge. Albee felt strongly he demonstrated his bone-grafting techniques that, since one could not duplicate in the human with his motor-driven saw. In 1914, 4 months knee the normal gliding mechanism of the 6 Who’s Who in Orthopedics articular bone surfaces, a wedge type of arthro- plasty that provided both mobility and stability was to be preferred. As an interposing membrane in arthroplasties, he always used the facial fat graft advocated by Murphy. Winnett Orr, in Lincoln, NE, Albee became very much interested in osteomyelitis. He was convinced that the reason for the success of the closed plaster method of Orr in the infected com- pound fracture and the old osteomyelitic case was the spontaneous development within the host of a substance that thrived on virulent pathogenic bacteria and completely destroyed them. This substance, in 1921, had been called a “bacteriophage” by D’Herelle, of Yale. Albee was able to show a phage appearing in 94% of 100 cases of acute and chronic osteomyelitis. His Lewis ANDERSON treatment was to clean the infected material out of the wound completely and then inject a bacteri- 1930–1997 ophage solution into osteomyelitic wounds. In 1933 Albee described a rather ingenious Lewis Anderson was born in Greensboro, arthroplasty of the elbow in which, after he had Alabama, on October 13, 1930. He attended reconstructed the joint, he lengthened the olecra- Emory University in Atlanta from 1947 through non with its triceps attached—in some ways a 1949 and received his MD degree from the Uni- comparable operation with his kinesiology lever versity of Pennsylvania in Philadelphia in 1953. Anderson served In 1934 he became greatly interested in low- as an intern at the Hospital of the University of back pain. Myofascitis, he said, was the principal Pennsylvania in 1953 and 1954 and then began a cause. This he described as a low-grade inflam- residency in general surgery at the same institu- matory change in the muscles and the fascia, with tion. His training was interrupted by 2 years of the fascial insertions of the muscle to bone active duty in the United States Naval Medical becoming hypersensitive because of toxic inflam- Corps, during which he served as the senior matory or metabolic changes. His treat- subsequently completed his residency at the ment for this condition was, first, the removal Hospital of the University of Pennsylvania. He emphasized colonic received his orthopedic training at the Campbell irrigation and the introduction of Bacillus aci- Clinic in Memphis from 1957 through 1960. Truly, he was an out- ate professor, and, from 1971 to 1977, as Profes- standing personality in the most progressive era sor of Orthopedic Surgery at the University of orthopedic surgery of all time. He once wrote, of Tennessee Center for Health Sciences in “I have never liked looking back. Although the bones did not heal faster with these techniques, he noted that immobility of adjacent joints, joint stiffness, malreduction, and nonunion—all well-known complications of 7 Who’s Who in Orthopedics closed treatment of fractures—often were American Academy of Orthopedic Surgeons, the avoided and that the overall rate of morbidity and American Orthopedic Association, the American complications was greatly reduced with early Medical Association, the Southern Medical Asso- motion, which could be used in conjunction with ciation, Alpha Omega Alpha, and numerous other rigid internal fixation. Anderson was an American– author of more than 60 articles that were pub- Canadian Exchange Traveling Fellow, along with lished in medical journals and of more than 20 Dr. III, demonstrated tremendous energy and good reported on his pioneering work in a paper enti- nature. He became a leader early in his career and tled “Compression-Plate Fixation in Acute was the model of a true “southern gentleman. Not only did this MD, died at the age of 67 in Mobile, Alabama, change in technology have a dramatic effect on after a brief illness. Anderson was asked to review all three editions of the Manual of Inter- nal Fixation, by the AO Group, for The Journal of Bone and Joint Surgery; the reviews appeared in 1971, 1980 and 1992. Anderson became the first Profes- sor and Chairman of the Department of Orthope- dic Surgery at the University of South Alabama in Mobile. In 1989, he was named the Louise Lenoir Locke Distinguished Professor of Ortho- pedics. He served as President of the Board of Directors of the University of South Alabama Health Sciences Foundation from 1979 through 1982 and again in 1985, as Secretary–Treasurer of the Medical Staff of the University of South Alabama Medical Center in 1979, and as Presi- dent of the Professional Medical Staff of the University of South Alabama from 1980 through 1982. In 1986, he was appointed Interim Dean of the University of South Alabama College of Med- Nicolas ANDRY icine.