EEG features of the appalic syndrome resulting from cerebral anoxia

Matsuo, Fumisuke

doi:10.1016/0013-4694(85)91049-1

Cited by 6 publications

(2 citation statements)

References 28 publications

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“…5 Epilepsy, anoxia, and depression have all been noted to cause slow-wave sleep attenuation. 6,7,8 Moreover, as we age, sleep becomes less robust, more fragmented, and attenuated, which is part of natural EEG deterioration. 9 Aside from these medical conditions, external environmental stressors, such as "the first-night effect" can play a role in the manipulation of sleep by decreasing the amount of slow-wave sleep.…”

Section: What Is the Diagnosis?mentioning

confidence: 99%

Loss of Slow-Wave Sleep

Eljammal

Valladares

Irwin

2006

Journal of Clinical Sleep Medicine

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A 40-year-old Hispanic American male, who weighed 165 lb and was 5'11" tall, consented to participate in a 3-day sleep protocol and was admitted to the UCLA General Clinical Research Center. The patient complained of fatigue during the day and difficulty initiating sleep, along with 3 to 4 awakenings per night. He denied snoring and having any difficulty breathing during sleep. A 2-week sleep diary confirmed his sleep-wake pattern. The patient also denied any history of head injury, epilepsy, or anoxia and the use of any over-the-counter or prescription medication use for the previous month. A diagnosis of current depression was ruled out, though he reported having been treated for depression with Paxil 2 years ago, when he took his last dose of Paxil. The patient reported alcohol consumption of 10 drinks per day, 12 days per month, with last his drink 18 days prior to study admission to the research center. Sleep StudyOvernight polysomnography was carried out over 3 nights using a computerized system (Somnologica, Flaga hf, Medical Devices, Iceland). The first night assessed the presence of sleep apnea and nocturnal myoclonus. The patient's apnea-hypopnea index was within normal limits (< 1.5/h), as was his periodic leg movement index (< 10/h). Oxygen saturation fluctuated between 91% and 95% throughout the night. During the third night, polysomnography showed that the patient slept for 403.5 minutes, with a sleep onset of 39.9 minutes and an overall sleep efficiency of 84.1%. Out of his total sleep time, he spent 12.1% (49 minutes) in stage 1, 61.7% (249 minutes) in stage 2, and 26% (105.5 minutes) in rapid eye movement sleep (Figure 1). No stage 3 or 4 sleep was noted. The patient experienced spontaneous arousals and microarousals throughout the night, with an index of 7.2. Disclosure StatementThis was not an industry supported study. Drs. Eljammal, Valladares, and Irwin have indicated no financial conflicts of interest.

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Section: What Is the Diagnosis?mentioning

confidence: 99%

Loss of Slow-Wave Sleep

Eljammal

Valladares

Irwin

2006

Journal of Clinical Sleep Medicine

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“…Patienten im apallischen Syndrom bzw. im PVS eine durch ihre Uneinheitlichkeit gekennzeichnete Vielzahl von Befunden erhoben worden.Die im Schrifttum publizierten EEG-Resultate weisen (auch bei Kindern) ein Kontinuum auf, das von Nonnalbefunden (41, 141, 159) über wohl am häufigsten manifeste diffuse Frequenz-und Amplitudenminderungen(46,52,59,65,99,101, Ill,127,150,159) bis hin zum isoelektrischen EEG(25,41,46,75) reicht. Der letztgenannte Befund ist vor allem bei Patienten im "kompletten apallischen Syndrom" nach hypoxischer Hirnschädigung beschrieben, wohingegen die anderen Konstellationen keine Beziehung zur Ätiologie erkennen lassen.…”

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Das ,,apallische Syndrom" - zu Notwendigkeit und Konsequenzen einer Begriffsklärung

Kallert¹

1994

Fortschr Neurol Psychiatr

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Starting from the increasing clinical requirement to make grave decisions (e.g. discontinuation of treatment) during hospitalisation of patients in an apallic syndrome, problems of defining the "apallic syndrome"--compared with the Anglo-American term "persistent vegetative state"--are reviewed. Besides conceptual criticism based on pathogenetic considerations and neuropathological findings the author especially demonstrates the varying inclusion criteria of the clinical syndrome concerning the apallic syndrome as well as the persistent vegetative state. Furthermore attempts to introduce more precisely defined subgroups (e.g. complete apallic syndrome) and new competing terms are shown. Referring to clinical diagnosis the low value of technical studies resulting from a great range of--sometimes controversial--findings contrasts with the high importance of identifying clinically related syndromes. Recent prognostic data that apply to judging the permanence of an apallic syndrome or persistent vegetative state are discussed. From this follows that they are of limited validity for the single patient. Finally it is attempted to work out some implications for clinical proceedings that should enable to meet a situation afflicted with diagnostic and prognostic uncertainties according to the present medical knowledge.

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Cerebrale Grenzsituationen

Pichlmayr¹,

Lehmkuhl²

1988

EEG -Überwachung Des Intensivpatienten

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EEG features of the appalic syndrome resulting from cerebral anoxia

Cited by 6 publications

References 28 publications

Loss of Slow-Wave Sleep

Loss of Slow-Wave Sleep

Das ,,apallische Syndrom" - zu Notwendigkeit und Konsequenzen einer Begriffsklärung

Cerebrale Grenzsituationen

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