Sleep study in SSPE (first results)

Petre-Quadens, O; Sfaello, Z; Bogaert, Lies; Moya, Gloria Jiménez

doi:10.1212/wnl.18.1_part_2.060

Cited by 14 publications

(4 citation statements)

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“…shown by Quadens (31) and also found by us, would accord with a cortico-orbital destruction or with an impairment of the thalamiccortical conduction system. So far the origin of the complexes has not been elucidated, and we agree with Quadens (31) that probably both cortex and thalamus are important, and therefore the hypothesis that a thalamo-cortical system is responsible cannot be excluded.…”

Section: Discussionsupporting

confidence: 68%

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EEG Findings in Subacute Sclerosing Panencephalitis

Uribe¹,

Londoño²

1972

Clinical Electroencephalography

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Section: Discussionsupporting

confidence: 68%

“…Sleep studies done by Quadens et al (31 ) distinguished two different sleep stages: one characterized by low voltage fast waves, with or without sleep spindles, and the other characterized by high voltage slow waves. During the high voltage slow wave stage, the "S.S.P.E.…”

Section: Discussionmentioning

confidence: 99%

EEG Findings in Subacute Sclerosing Panencephalitis

Uribe¹,

Londoño²

1972

Clinical Electroencephalography

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“…Some patients have n o change in the frequency or periodicity of complexes during sleep [3, 41. In some patients periodic complexes disappear during sleep [5,61, while other patients show an increased frequency of the periodic complexes during sleep [4,[7][8][9][10][11]. A few reports describe periodic complexes occurring predominantly during the sleep recording [12, 131.…”

Section: Discussionmentioning

confidence: 99%

Activation of periodic complexes of subacute sclerosing panencephalitis by sleep

Westmoreland¹,

Gómez²,

Blume³

1977

Annals of Neurology

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Three patients with clinically proved subacute sclerosing panencephalitis (SSPE) had electroencephalograms i n which periodic stereotyped complexes characteristic of SSPE were apparent d u r i n g sleep b u t were not observed d u r i n g the initial awake recordings. The first patient had periodic complexes only d u r i n g sleep. The second and third patients had complexes that were inconstant and sporadic during the awake recordings b u t regular and periodic d u r i n g sleep. Although sleep c a n have a variable effect on t h e electroencephalographic pattern in SSPE, it may facilitate elicitation of typical periodic complexes In questionable cases of SSPE.Westmoreland BF, Gomez MR, Blume W T Activation of periodic complexes of subacute sclerosing panencephalitis by sleep Ann Neurol 1 [185][186][187] 1977 The electroencephalogram in subacute sclerosing panencephalitis (SSPE) shows a characteristic pattern of periodic stereotyped complexes that is usually diagnostic for SSPE. The patient, however, may n o t always present with t h e typical EEG pattern. T h i s r e p o r t describes 3 patients i n whom the characteristic periodic pattern of SSPE became apparent only w h e n a sleep recording was performed. Case ReportsThe first patient, a 13-year-old boy, was well until five months before being seen at our clinic, when he had the onset of progressive deterioration in intellect and behavior and episodes of falling to the ground without warning. Laboratory studies showed increased protein in the cerebrospinal fluid, with an elevated gamma globulin level and measles antibody titer. The initial EEG showed 6 to 7 Hz slowing with frequent trains of generalized and bilaterally synchronous 2 to 2.5 Hz spike-and-wave discharges. O n the following day a second tracing was obtained during which the patient was given 10 mg of diazepam intravenously; 15 minutes later he fell asleep, and generalized, periodic, and stereotyped slow waves at intervals of 2 to 3 seconds appeared ( Figure). This periodic pattern persisted throughout the sleep recording. After the patient woke up the periodic complexes disappeared, and the EEG again showed diffuse theta slowing. (This patient has been reported in more detail elsewhere [I]). In the second patient, a 13-year-old girl, progressive ataxia, deterioration in intellectual functioning, dysarthria, and athetoid movements of the extremities had developed four months before she was seen at our clinic. Laboratory studies showed elevated protein in the cerebrospinal fluid with an increased gamma globulin level and an elevated measles antibody titer. The awake EEG showed diffuse 4 to 6 Hz slowing with occasional sporadic, higher-amplitude, 2 to 3 Hz waveforms. During the recording the patient spontaneously wenr to sleep, at which timegeneralized, periodic, stereotyped slow-wave complexes, recurring every 1 0 seconds, became apparent. These were present throughout the sleep recording but disappeared after arousal from sleep. Four days later, periodic complexes were present during the awake...

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“…The hypotheses put forward can be classified into three groups: 1. The complexes originate in the cerebral cortex (Lesse et al 1958, Bogacz et al 1959, van Leeuween 1964, Passonant et al 1970); 2. the periodicity of the complexes ari-ses from subcortical structures, that is from the thalamus, the midbrain or the bulbo-pontine reticular formation {Rademecker 1960, Petsche et al 1961, Fenyo andHasznos 1964, Cobb 1966, Lombroso 1968, Petre-Quadens et al 1968); 3. the appearance of the complexes is an effect of severe impairment of both cortical and subcortical structures (Celesta 1973).…”

Section: Introductionmentioning

confidence: 99%

Polygraphic Recordings in Subacute Sclerosing Panencephalitis – A Study of the Pathophysiology of the Periodic EEG Complexes

Hg¹,

Pl²,

Reimer³

1976

Neuropediatrics

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Polygraphic whole night recordings were performed in 10 patients with SSPE. In most cases sleep states could not be classified according to the usual criteria, but two different states with differing EEG patterns were always seen. A significant correlation was obtained between EEG complexes and phase of the respiratory cycle in 8 out of 9 patients, irrespective of the sleep state. Slowing of heart rate for one R-R interval was observed to occur during the onset of the complex in 7 patients in both sleep states, and in 2 patients only in one state. Periodic occurrence of complexes was stable throughout the night. This stability seems to be maintained by a mechanism regulating the duration of an interval according to the duration of the preceding one. It is suggested that diffuse involvement of subcortical structures rather than a localized change is responsible for the generation of the EEG complexes in SSPE.

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Sleep study in SSPE (first results)

Cited by 14 publications

References 0 publications

EEG Findings in Subacute Sclerosing Panencephalitis

EEG Findings in Subacute Sclerosing Panencephalitis

Activation of periodic complexes of subacute sclerosing panencephalitis by sleep

Polygraphic Recordings in Subacute Sclerosing Panencephalitis – A Study of the Pathophysiology of the Periodic EEG Complexes

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