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C L Bassetti

Publications and source records attributed to C L Bassetti.

12 recordsLinked to original sources
PubMed2007

[Sleep and movement disorders].

The three different states of being (wakefulness, NREM and REM sleep) are associated with profound neurophysiological and neurochemical changes in the brain. These changes explain the existence of movement disorders appearing only or preferentially during sleep, and the effects of sleep on movement disorders. Sleep-related movement disorders are of clinical relevance for multiple reasons: 1) high frequency (e.g. restless legs syndrome (RLS)); 2) diagnostic relevance (e.g. REM sleep behavior disorder (RBD) as first manifestation of Parkinson disorder); 3) diagnostic uncertainty (e.g. parasomnias vs nocturnal epilepsy); 4) association with injuries (e.g. RBD, sleepwalking), sleep disruption/daytime sleepiness (e.g. RLS), and psycho-social burden (e.g. enuresis); 5) requirement of specific treatments (e.g. nocturnal epilepsy, stridor, RBD). This article gives an overview on clinical manifestations, pathophysiology, work-up and treatment of sleep-related movement disorders (e.g. RLS, bruxism), parasomnias (e.g. sleepwalking, RBD), sleep-related epilepsies, and on sleep-associated manifestations of movement disorders (e.g. Parkinson disease, multiple system atrophy).

Adult↗
PubMed2006

Practice parameter: prediction of outcome in comatose survivors after cardiopulmonary resuscitation (an evidence-based review) [RETIRED]: report of the Quality Standards Subcommittee of the American Academy of Neurology.

OBJECTIVE: To systematically review outcomes in comatose survivors after cardiac arrest and cardiopulmonary resuscitation (CPR). METHODS: The authors analyzed studies (1966 to 2006) that explored predictors of death or unconsciousness after 1 month or unconsciousness or severe disability after 6 months. RESULTS: The authors identified four class I studies, three class II studies, and five class III studies on clinical findings and circumstances. The indicators of poor outcome after CPR are absent pupillary light response or corneal reflexes, and extensor or no motor response to pain after 3 days of observation (level A), and myoclonus status epilepticus (level B). Prognosis cannot be based on circumstances of CPR (level B) or elevated body temperature (level C). The authors identified one class I, one class II, and nine class III studies on electrophysiology. Bilateral absent cortical responses on somatosensory evoked potential studies recorded 3 days after CPR predicted poor outcome (level B). Burst suppression or generalized epileptiform discharges on EEG predicted poor outcomes but with insufficient prognostic accuracy (level C). The authors identified one class I, 11 class III, and three class IV studies on biochemical markers. Serum neuron-specific enolase higher than 33 microg/L predicted poor outcome (level B). Ten class IV studies on brain monitoring and neuroimaging did not provide data to support or refute usefulness in prognostication (level U). CONCLUSION: Pupillary light response, corneal reflexes, motor responses to pain, myoclonus status epilepticus, serum neuron-specific enolase, and somatosensory evoked potential studies can reliably assist in accurately predicting poor outcome in comatose patients after cardiopulmonary resuscitation for cardiac arrest.

Cardiopulmonary Resuscitation↗
PubMed2006

Sleep-wake disturbances in sporadic Creutzfeldt-Jakob disease.

BACKGROUND: The prevalence and characteristics of sleep-wake disturbances in sporadic Creutzfeldt-Jakob disease (sCJD) are poorly understood. METHODS: Seven consecutive patients with definite sCJD underwent a systematic assessment of sleep-wake disturbances, including clinical history, video-polysomnography, and actigraphy. Extent and distribution of neurodegeneration was estimated by brain autopsy in six patients. Western blot analyses enabling classification and quantification of the protease-resistant isoform of the prion protein, PrPSc, in thalamus and occipital cortex was available in four patients. RESULTS: Sleep-wake symptoms were observed in all patients, and were prominent in four of them. All patients had severe sleep EEG abnormalities with loss of sleep spindles, very low sleep efficiency, and virtual absence of REM sleep. The correlation between different methods to assess sleep-wake functions (history, polysomnography, actigraphy, videography) was generally poor. Brain autopsy revealed prominent changes in cortical areas, but only mild changes in the thalamus. No mutation of the PRNP gene was found. CONCLUSIONS: This study demonstrates in sporadic Creutzfeldt-Jakob disease, first, the existence of sleep-wake disturbances similar to those reported in fatal familial insomnia in the absence of prominent and isolated thalamic neuronal loss, and second, the need of a multimodal approach for the unambiguous assessment of sleep-wake functions in these patients.

Aged↗
PubMed2006

Hypocretin (orexin) deficiency predicts severe objective excessive daytime sleepiness in narcolepsy with cataplexy.

Cerebrospinal fluid (CSF) hypocretin-1 deficiency is associated with definite ("clear cut") cataplexy in patients with narcolepsy. The relationship between CSF hypocretin-1 levels and other narcoleptic symptoms (including excessive daytime sleepiness, EDS) is not properly understood. In a consecutive series of 18 subjects with narcolepsy and definite cataplexy, patients with undetectable CSF hypocretin-1 (n = 12) were found to have significantly lower mean sleep latencies (p = 0.045) and a higher frequency of sleep onset REM periods (SOREMPs, p = 0.025) on multiple sleep latency test than patients (n = 6) with detectable levels. Conversely, Epworth sleepiness scale scores, the frequency of hallucinations/sleep paralysis, and the frequency and severity of cataplexy were similar in both groups. These results suggest that hypocretin deficiency identifies a homogenous group of patients with narcolepsy characterised by the presence of definite cataplexy, severe EDS, and frequent SOREMPs.

Adolescent↗
PubMed2005

Hypocretin-1 (orexin A) deficiency in acute traumatic brain injury.

Hypocretin-1 is involved in the regulation of the sleep-wake cycle. The authors prospectively assessed CSF hypocretin-1 levels in 44 consecutive patients with acute traumatic brain injury (TBI). Compared with controls, hypocretin-1 levels were abnormally lower in 95% of patients with moderate to severe TBI and in 97% of patients with posttraumatic brain CT changes. Hypocretin-1 deficiency after TBI may reflect hypothalamic damage and be linked with the frequent development of posttraumatic sleep-wake disorders.

Adolescent↗
PubMed2005

Post-ischemic delivery of the 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor rosuvastatin protects against focal cerebral ischemia in mice via inhibition of extracellular-regulated kinase-1/-2.

After recent clinical trials, statins have gained increasing significance in secondary stroke prevention. From experimental studies, it is well established that statins have beneficial action when delivered prophylactically prior to a stroke. Conversely, much less is known about the effects of statins on injury development when delivered after ischemia. We here examined the effects of a post-ischemic delivery of rosuvastatin (0.5, 5 or 20 mg/kg, administered i.p. immediately after reperfusion onset), a potent 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor, on brain injury and cell signaling after focal cerebral ischemia, induced by 90 min of intraluminal middle cerebral artery occlusion in mice. In animals receiving normal saline, 0.5 or 5 mg/kg rosuvastatin, middle cerebral artery occlusions resulted in reproducible brain infarcts at 24 h after reperfusion onset, which did not differ in size. However, rosuvastatin, administered at higher doses (20 mg/kg), reduced infarct volume at 24 and 48 h after ischemia (by 34+/-16% and 18+/-3%, respectively, P<0.05). Western blots revealed that rosuvastatin decreased phosphorylated extracellular-regulated kinase-1/-2 and reduced activated caspase-3 levels in ischemic brain areas, while endothelial NO synthase expression, p38 and Jun kinase phosphorylation were not influenced by the 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor. Rosuvastatin also significantly diminished expression levels of inducible NO synthase in the ischemic brain. Our results indicate that rosuvastatin may have utility not only as stroke prophylaxis but also as acute therapy inhibiting executive cell death pathways.

Animals↗
PubMed2003

Diffusion-weighted MRI in acute spinal cord ischaemia.

Acute spinal cord ischaemia is often undetectable with conventional MRI. Diffusion-weighted MRI (DWI) has been difficult to use in the spine because of susceptibility artefacts. We assessed the diagnostic value of echoplanar DWI for early confirmation of spinal cord ischaemia. We performed conventional MRI and DWI in two men and three women, aged 54-75 years with clinically suspected acute spinal cord ischaemia. Imaging was performed 9-46 h after the onset of symptoms, and 2-9 days later to assess the extent of ischaemic signal change. Spatial resolution of DWI within the spine using standard equipment was poor, but in all patients, early DWI revealed areas of high signal indicating decreased diffusion, confirmed by measurement of apparent diffusion coefficients. Follow-up MRI showed high signal on T2-weighted images and contrast enhancement at the expected levels. Neurological deficits corresponded with radiological findings in four patients: various syndromes, including isolated bilateral weakness or sensory change and combined deficits, were found. Echoplanar DWI may be helpful for confirmation of spinal cord ischaemia in the acute stage, but follow-up T2-weighted images have superior spatial resolution and correlation with clinical findings and lesion extent.

Acute Disease↗
PubMed2003

CSF hypocretin-1 levels in narcolepsy, Kleine-Levin syndrome, and other hypersomnias and neurological conditions.

OBJECTIVE: To determine the role of CSF hypocretin-1 in narcolepsy with and without cataplexy, Kleine-Levin syndrome (KLS), idiopathic and other hypersomnias, and several neurological conditions. PATIENTS: 26 narcoleptic patients with cataplexy, 9 narcoleptic patients without cataplexy, 2 patients with abnormal REM-sleep-associated hypersomnia, 7 patients with idiopathic hypersomnia, 2 patients with post-traumatic hypersomnia, 4 patients with KLS, and 88 patients with other neurological disorders. RESULTS: 23 patients with narcolepsy-cataplexy had low CSF hypocretin-1 levels, while one patient had a normal hypocretin level (HLA-DQB1*0602 negative) and the other two had intermediate levels (familial forms). One narcoleptic patient without cataplexy had a low hypocretin level. One patient affected with post-traumatic hypersomnia had intermediate hypocretin levels. The KLS patients had normal hypocretin levels while asymptomatic, but one KLS patient (also affected with Prader-Willi syndrome) showed a twofold decrease in hypocretin levels during a symptomatic episode. Among the patients without hypersomnia, two patients with normal pressure hydrocephalus and one with unclear central vertigo had intermediate levels. CONCLUSION: Low CSF hypocretin-1 is highly specific (99.1%) and sensitive (88.5%) for narcolepsy with cataplexy. Hypocretin ligand deficiency appears not to be the major cause for other hypersomnias, with a possible continuum in the pathophysiology of narcolepsy without cataplexy and idiopathic hypersomnia. However, partial hypocretin lesions without low CSF hypocretin-1 consequences cannot be definitely excluded in those disorders. The existence of normal hypocretin levels in narcoleptic patients and intermediate levels in other rare aetiologies needs further investigation, especially for KLS, to establish the functional significance of hypocretin neurotransmission alterations.

Adolescent↗
PubMed2002

Power and coherence of sleep spindle frequency activity following hemispheric stroke.

Brainstem and thalamic structures are known to play a critical role in modulating sleep-wake cycles, but the extent to which the cerebral hemispheres are involved remains unclear. To study the role of the cerebral hemispheres in generating sleep EEG patterns, all-night polysomnographic recordings were collected in subjects with brain damage (n = 30) caused by hemispheric stroke and in hospitalized controls (n = 12). Recordings were made in the acute (< or =10 days post-stroke), subchronic (11-35 days post-stroke) and chronic (>60 days post-stroke) phases of stroke. Bipolar and referential EEG derivations were recorded. Standard sleep stage scoring was conducted using the referential derivation placed opposite the lesion. Sleep stage 2 power and coherence spectra were calculated based on recordings from bipolar derivations. In the mean spectra, the highest spindle frequency peak was identified and its size was calculated relative to the background spectrum. Analysis of visually scored EEG data indicated that, compared with controls, acute phase brain-damaged subjects had lower sleep efficiency and increased waking after sleep onset. The durations of rapid eye movement and non-rapid eye movement sleep stages did not differ significantly between brain-damaged subjects and hospitalized controls. Spectral analyses revealed that, compared with hospitalized controls, brain-damaged subjects had significantly reduced spindle peak sizes in the power and coherence spectra from derivations ipsilateral to the lesion. Within-subject comparisons across time demonstrated that the power and coherence of sleep spindle frequency activity increased significantly from the acute to the chronic phases of stroke, suggesting that plastic mechanisms allowed the possibility of recovery. Our findings provide novel evidence that the cerebral hemispheres are important in generating coherent sleep spindles in humans, and they are consonant with prior empirical and theoretical evidence that corticothalamic projections modulate the generation of synchronous spindle oscillations. Because spindle oscillations are thought to be involved in blocking sensory input to the cortex during sleep, the decrease in synchronous spindle frequency activity following hemispheric stroke may contribute to the observed reduction in sleep continuity.

Adolescent↗
PubMed2001

Restless legs syndrome: a clinical study of 55 patients.

BACKGROUND: Restless legs syndrome (RLS) is a common sleep disorder. In 1995, clinical criteria for the diagnosis of RLS were defined. OBJECTIVE: To describe the clinical spectrum in a series of unselected RLS patients meeting the new diagnostic criteria. METHODS: We prospectively assessed by questionnaire and clinical assessment the characteristics of 55 consecutive RLS patients (35 women, 20 men; mean age = 62 +/- 16 years). RESULTS: In 27% of the patients, RLS started before the age of 20 years (early-onset RLS). Sensory disturbances were painful in 56% of patients and felt in legs (98%), arms (35%), and 'internally' (45%). Motor disturbances included 'dyskinesias while awake' (36%). Insomnia (58%) was commoner than hypersomnia (24%). In 67% of the patients, no etiology of RLS was found (idiopathic RLS). Early-onset RLS was more commonly familial (p = 0.01) and associated with 'growing pains' (p = 0.005) than late-onset RLS. Patients with RLS and hypersomnia were younger (p = 0.01) and less commonly had painful sensations (p = 0.04) than patients with RLS and insomnia. Patients with idiopathic RLS were younger (p = 0.004), and less commonly had insomnia (p = 0.01) than patients with symptomatic RLS. CONCLUSIONS: RLS is a clinically pleomorphic syndrome, reflecting the contribution of multiple genetic and acquired factors in the pathogenesis of RLS.

Adult↗