[Patient complains about sleep disorders: place "restless legs" therein].
Explore the source record for details and available documents.
Adult↗
Biomedical subjects
I Eisensehr
Publications and source records attributed to I Eisensehr.
[Epilepsy and sleep disorders].
Sleep disorders often occur in patients with epilepsy. Every neurologist is familiar with the postictal drowsiness after tonicoclonic convulsions and likewise with the provocation of an attack after sleep deprivation that is often combined with alcohol consumption. It is more difficult to differentiate between motor disturbances and epileptic episodes during sleep. For example, nocturnal paroxysmal dystonia, which are frequently an expression of frontal lobe epilepsy, are long not recognized as non-epileptic, sleep-associated attacks. In addition, nocturnal episodes in context of a REM sleep behavioral disturbance can occasionally be differentiated from frontal lobe epileptic seizures only with great difficulty. A clear differential diagnostics between epileptic and non-epileptic attacks during sleep is, however, a requirement for a selective treatment.
Anticonvulsants↗
Alteration of the striatal dopaminergic system in human narcolepsy.
Striatal D2/D3 dopaminergic receptors have been proposed to play a role in cataplexy. The authors studied the striatal presynaptic dopamine transporter and postsynaptic D2-receptors in seven patients with narcolepsy and seven control subjects using [123I](N)-(3-iodopropene-2-yl)-2beta-carbomethoxy-3beta-(4-chlorophenyl)tropane and [123I](S)-2-hydroxy-3-iodo-6-methoxy-([1-ethyl-2-pyrrolidinyl]methyl)benzamide SPECT. D2-receptor binding was elevated in narcolepsy (p = 0.017) and correlated with the frequency of cataplectic and sleep attacks (R > or = 0.844, p < or = 0.017). The human striatal dopaminergic system is altered in vivo in narcolepsy/cataplexy.
Aged↗
Hypersomnia associated with bilateral posterior hypothalamic lesion. A polysomnographic case study.
We examined an obese 58-year-old patient with a bilateral posterior hypothalamic lesion of unknown etiology. A 24-hour polysomnography revealed a markedly increased total sleep time (17.6 h). During daytime, only 3 continuous wake phases occurred. REM periods occurred only between 5 p.m. and 6 a.m. We conclude from our results that, similar to the results from animal experiments, the posterior hypothalamus in humans plays a critical role in the maintenance of wakefulness.
Antigen-Antibody Reactions↗
Normal IPT and IBZM SPECT in drug-naive and levodopa-treated idiopathic restless legs syndrome.
Fourteen drug-naive and 11 levodopa-treated patients with idiopathic restless legs syndrome (RLS), and 10 controls age-matched to each RLS group separately were examined with polysomnography (PSG), [(123)I]-(N)-(3-iodopropen-2-yl)-2beta-carbomethoxy-3beta-(4-chlorophenyl) tropane ((123)I-IPT) SPECT, and [(123)I]-(S)-2-hydroxy-3-iodo-6-methoxy-[(1-ethyl-2-pyrrolidinyl)methyl] benzamide ((123)I-IBZM) SPECT. Drug-naive and levodopa-treated patients with RLS and controls showed similar striatal dopamine transporter and dopamine D(2)-receptor binding, the latter declining with age. The authors conclude that striatal dopamine transporter and receptor density is normal in drug-naive and levodopa-treated patients with RLS.
Aged↗
Normal plasma levels of orexin A (hypocretin-1) in narcoleptic patients.
Deficient orexin signaling has been shown to cause narcolepsy-like conditions in animals. In human narcolepsy, CSF levels of orexin A (hypocretin-1) were reported to be low in most cases. The authors measured CSF and plasma orexin A levels in patients with narcolepsy and in controls. Confirming earlier studies, they found CSF orexin A levels to be extremely low in patients with narcolepsy. However, plasma orexin A levels did not differ from those observed in controls. These results suggest that orexin deficiency in patients with narcolepsy is a phenomena restricted to the CNS.
Adult↗
REM sleep behavior disorder in sleep-disordered patients with versus without Parkinson's disease: is there a need for polysomnography?
We reviewed the polysomnograms (PSGs) of 292 consecutive patients with sleep disorders (Parkinson's disease (PD), n=19, other sleep disorders, n=273) to investigate the sensitivity and specificity of the clinical diagnosis of rapid eye movement behavior disorder (RBD) compared with polysomnographic diagnosis. Patients with dementia, multiple system atrophy, or any other neurodegenerative disease were excluded. RBD was diagnosed clinically if the minimal criteria, according to the guidelines given in the International Sleep Disorders Classification, were fulfilled. The following PSG criteria were required for diagnosis of RBD: REM sleep without muscle atonia seen in PSG associated with motor behavior visible in the PSG-synchronized videotape. Nine of nineteen PD patients (47%) had RBD. RBD occurred in only four patients without PD (1.8%). The sensitivity of specialized interviews for identifying RBD clinically was good in non-PD patients (sensitivity: 100%, specificity: 99.6%). However, the sensitivity was poor (33%) with a specificity of 90%, in patients with PD. We conclude that the diagnosis of RBD in patients with PD requires PSG, whereas interviews are sufficient for diagnosing RBD in non-PD patients.
Aged↗
[Obstructive sleep apnea syndrome. Which therapy for which patients].
Obstructive sleep apnea syndrome is defined by the American Academy of Sleep Medicine as a combination of at least five obstructive events per hour of sleep and such other symptoms as daytime sleepiness, ischemic heart disease and stroke. In addition to weight reduction, the use of oral appliances, and continuous positive airway pressure (CPAP), a number of surgical interventions such as uvulopalatopharyngoplasty and maxillomandibular advancement are also available for the treatment of sleep apnea. Since no prolongation of life has yet been shown for most of the therapeutic options, treatment needs to be individualized on the basis of symptoms, clinical findings and compliance.
Humans↗
Sleep in Lennox-Gastaut syndrome: the role of the cyclic alternating pattern (CAP) in the gate control of clinical seizures and generalized polyspikes.
Non-rapid eye movement (NREM) sleep contains periods of arousal instability (cyclic alternating pattern or CAP) and periods of arousal stability (non-CAP). During CAP, arousal oscillates between higher (phase A) and lower (phase B) levels of activation. We evaluated the relationship between CAP and the occurrence of epileptic events, i.e. clinical seizures and generalized interictal discharges, during sleep in 10 patients with Lennox-Gastaut syndrome (LGS). The macro- and microstructure of sleep of 10 attended overnight polysomnograms were analyzed. Compared with 10 age- and gender-matched controls, patients with LGS had significantly less stage 2 and REM sleep and higher amounts of CAP rate (68% vs. 33%; P<0.0001). The number of generalized polyspike bursts per hour of sleep was highest in slow wave sleep (226.5+/-57.6) and lowest in REM sleep (3.9+/-1.5). The polyspike burst frequency was significantly greater (P<0.017) during CAP (213.2+/-60.1) than during non-CAP (100.3+/-40), and within CAP, generalized polyspikes occurred more often (P=0.005) during phase A (461.1+/-127.2) than during phase B (6.1+/-1.9). The total amount of generalized polyspike bursts identified in NREM sleep correlated positively both with the number of A phases containing at least one generalized polyspike (P=0.005) and with the mean number of polyspikes within each of these A phases (P<0.0001). Nocturnal clinical seizures occurred in 8 of the 10 patients and showed a similar trend. We conclude from our results that CAP modulates the occurrence of both clinical seizures and generalized epileptic discharges in LGS by means of a gate-control mechanism: an independent spike generator is inhibited in phase B and non-CAP and bursts with its intrinsic activity in phase A.
Adolescent↗
Haematological aspects of obstructive sleep apnoea.
Obstructive sleep apnoea (OSA) is associated with increased cardiovascular morbidity and mortality. Several studies indicate an influence of OSA on haematological features. There is evidence of elevated platelet activation and increased haematocrit in OSA. Studies investigating the underlying cause of polycythaemia in OSA reveal different results: increased haematocrit in OSA might be due to enhanced erythropoietin excretion and/or plasma volume dysregulation based on altered release of volume-regulating hormones such as atrial natriuretic peptide (ANP). This review addresses haematological issues associated with OSA, especially platelet function, haematocrit and haemoconcentration. 2001 Harcourt Publishers Ltd
Journal Article↗
Absence of nystagmus during REM sleep in patients with vestibular neuritis.
Saccades, including fast phases of nystagmus, disappear during drowsiness and non-rapid eye movement (NREM) sleep, but are present during the alert state and REM sleep. The purpose of this study was to determine whether spontaneous nystagmus is present in patients with vestibular neuritis during REM sleep. Eight patients with spontaneous nystagmus due to vestibular neuritis and eight control patients without any nystagmus underwent at least one night of polysomnography. Fast phases of nystagmus were analyzed. The number of right and left horizontal saccades were counted, first during 3-5 minute samples of the awake state before sleep onset, then during the first REM episode and the last REM episode of nocturnal sleep, and finally during the alert state in the morning after nocturnal sleep. All patients with vestibular neuritis showed significantly more saccades (fast phases) towards the side contralateral to their vestibular lesion in the awake state before and after the polysomnography. This reflects their spontaneous nystagmus. By contrast, during REM sleep the patients with vestibular neuritis showed no preponderance in saccade direction. The eye movement pattern in REM was the same for patients and controls. In conclusion, peripheral vestibular imbalance producing nystagmus in vestibular neuritis in the awake state is not active at the brain stem level during REM sleep.
Aged↗
[REM sleep behavior disorder].
Rapid eye movement sleep behavior disorder (RBD) is a rare but clinically distinct disorder which is easily overlooked. It commonly occurs in older men and, because of its similarity to epileptic seizures, is often misdiagnosed. The etiology of RBD is still unknown. However, there is an interesting association with Parkinson's disease which presents some pathophysiological hypotheses. Treatment is usually successful with clonazepam.
Aged↗
Reduced striatal dopamine transporters in idiopathic rapid eye movement sleep behaviour disorder. Comparison with Parkinson's disease and controls.
Rapid eye movement (REM) sleep behaviour disorder (RBD) is characterized by complex behaviour during REM sleep. The aetiology of this disorder is still unknown, but a recent study showed an association between RBD and Parkinson's disease. We therefore studied striatal postsynaptic dopamine D2 receptor density with [123I](S)-2-hydroxy-3-iodo-6-methoxy-(1-ethyl-2-pyrrolidinylmethyl ) benzamide ([123I]IBZM) and the striatal presynaptic dopamine transporter with (N)-(3-iodopropene-2-yl)-2beta-carbomethoxy-3beta-(4-chlorop henyl) tropane ([123I]IPT) using single-photon emission computed tomography (SPECT) in patients with idiopathic RBD. We compared the [123I]IPT-SPECT results of five patients with polysomnographically confirmed idiopathic RBD with the [123I]IPT-SPECTs of seven age- and sex-matched controls without a history of sleep disorders, and of 14 patients with Parkinson's disease (Hoehn and Yahr stage I). All RBD patients had significantly reduced striatal [123I]IPT binding compared with the controls (RBD: right, 2.94 +/- 0.32, left, 3.03 +/- 0.41; controls: right, 4.41 +/- 0.17, left, 4.34 +/- 0.21; P = 0.003), but significantly higher striatal [123I]IPT binding compared with the striatum contralateral to the symptomatic body side of the Parkinson's disease patients (Parkinson's disease: ipsilateral, 3.17 +/- 0.36, P = 0.298; contralateral, 2.51 +/- 0.31, P = 0.019). Uptake of [123I]IBZM was not significantly different in the RBD group compared with the controls. This study demonstrates that [123I]IPT-SPECT is a useful diagnostic tool in RBD and that reduced striatal dopamine transporters may be a pathophysiological mechanism of idiopathic RBD. (Results are given as mean +/- standard deviation.)
Adult↗
Valproate for sleep consolidation in periodic limb movement disorder.
In this study, open-label valproate (VPA) was administered to patients as a treatment for periodic limb movement disorder (PLMD). Six patients aged 28 to 62 years with complaints of sleep disturbance and at least five periodic limb movements (PLMs) per hour of sleep underwent polysomnograms (PSGs) with and without low-dose VPA treatment (125-600 mg at bedtime). After a baseline PSG, patients received VPA therapy from 2 weeks to 14 months, until the time of the follow-up PSG on VPA (median, 5 months; mean, 6 months). All six patients experienced subjective improvement in daytime alertness. Sleep efficiency was improved from 76% to 88% (p = 0.003), stage 1 (light) sleep decreased from 26% to 13% (p = 0.04), stage 3 and 4 (deep) sleep increased from 19% to 30% (p = 0.01), and rapid eye movement sleep was unchanged. There was a trend toward a reduction in the number of PLMs per hour of sleep and in the percentage of arousals associated with PLMs. All of the patients continued taking VPA after the PSGs were completed. One patient discontinued VPA 1 month after completion of the last PSG because of short-term side effects, and one patient stopped VPA 22 months after the last PSG because of weight gain. Thus, these data indicate that VPA has a long-term beneficial effect on sleep consolidation in patients with PLMD.
Adult↗
[Myasthenia gravis. Opportunistic cytomegalovirus infection after long-term azathioprine therapy].
Opportunistic infections after long-term treatment with azathioprine (AZA) have not been noted in patients with myasthenia gravis (MG). We report on a 56-year-old woman with generalized MG who presented with cytomegalovirus infection after being treated with AZA for 17 years. The indication for immunosuppressive treatment in MG should be regularly reconfirmed, particularly since at least 50% of patients can discontinue AZA after two to four years without risk of exacerbation.
Azathioprine↗
Platelet activation, epinephrine, and blood pressure in obstructive sleep apnea syndrome.
OBJECTIVE: There is an increased risk of patients with obstructive sleep apnea syndrome (OSAS) to have stroke or cardiac infarcts. Besides hypertension, epinephrine-induced platelet activation could be a further reason for the increased cardiovascular morbidity and mortality in OSAS. METHODS: During a 4-month period (August 1994 to December 1994) we recruited prospectively 76 patients referred for polysomnograms because of a suspected sleep disorder such as OSAS. RESULTS: Fifty patients had no respiratory events during sleep (non-OSAS), 19 patients had more than five but less than 50 obstructive apneas or hypopneas per hour of total sleep time (mild-to-moderate OSAS group), and seven patients had an apnea hypopnea index of more than 50 per hour of total sleep time (severe OSAS group). Blood pressure, plasma epinephrine levels, and P-selectin expression (as a marker for platelet activation) were measured in every patient at 9 PM and 6 AM (before and after the polysomnogram). There was a significant correlation of the apnea hypopnea index with 9 PM and 6 AM systolic and diastolic blood pressure, with 9 PM platelet activation, and with 6 AM epinephrine levels mainly due to high values in the severe OSAS group. CONCLUSIONS: Our results suggest that platelet activation, epinephrine, and high blood pressure play a role in the high prevalence of cerebrovascular and cardiovascular events in patients with OSAS.
Adult↗