1/62. circadian rhythm sleep disorder associated with pontine lesion.A 55-year-old man presented with excessive daytime sleepiness and a circadian rhythm sleep disorder. magnetic resonance imaging of the brain revealed a pontine lesion distinguishable from major cerebrovascular disease, demyelination and neoplasm. benzodiazepines, antidepressants, methylcobalamine and thyroxine failed to synchronize the circadian rhythm. Antiepileptic drugs aggravated the condition, while melatonin and protireline partially relieved the patient from poorly controlled sleep disorder. A pontine lesion appeared to be related to the circadian rhythm sleep disorder of the patient.- - - - - - - - - - ranking = 1keywords = brain (Clic here for more details about this article) |
2/62. Genetic factors in human sleep disorders with special reference to Norrie disease, prader-willi syndrome and Moebius syndrome.Sleep-wake problems are common in specific inborn errors of metabolism and structure of the central nervous system. Psychological factors, behavioural difficulties, metabolic disturbances, and widespread rather than focal damage to the nervous system are present in many of these diseases and all influence the sleep-wake cycle. However, a number of conditions cause relatively focal damage to the neuroanatomical substrate of sleeping and waking. These include fatal familial insomnia, with involvement of the prion protein gene on chromosome 20, Norrie disease, the prader-willi syndrome and the Moebius syndrome. The last three important conditions, although rare, are considered in detail in this review. They result in sensory deprivation, hypothalamic and mid-brain damage, and involve the X-chromosome, chromosome 15, and chromosome 13, respectively. These conditions cause a wide variety of sleep disturbance, including parasomnias, daytime sleepiness, and a condition like cataplexy. The place of the relevant gene products in normal sleep regulation needs further exploration.- - - - - - - - - - ranking = 1keywords = brain (Clic here for more details about this article) |
3/62. Peduncular hallucinosis: an unusual sequel to surgical intervention in the suprasellar region.Peduncular hallucinations are formed visual images often associated with sleep disturbance, and are caused by lesions in the midbrain, pons and diencephalon. In the present study, we report two patients who developed peduncular hallucinations following surgery in the suprasellar region. In one of these, the peduncular hallucinations were a sequel to endoscopic third ventriculostomy, while in the other, they were due to diencephalon and mid-brain compression by a postoperative clot following excision of a hypothalamic astrocytoma.- - - - - - - - - - ranking = 2keywords = brain (Clic here for more details about this article) |
4/62. Posttraumatic delayed sleep phase syndrome.circadian rhythm sleep disorders may occur after traumatic brain injury. We describe a 48-year-old man who presented with sleep onset insomnia and cognitive dysfunction after a car accident. A diagnosis of delayed sleep phase syndrome (DSPS) was confirmed by sleep logs and actigraphy, which revealed sleep onset in the early morning hours and awakening around noon.- - - - - - - - - - ranking = 9.7291041379284keywords = brain injury, traumatic brain, brain, injury, trauma (Clic here for more details about this article) |
5/62. Is the delayed sleep phase syndrome a physical or psychological disease? A case report of disappearance following a change of latitude.The delayed sleep phase syndrome is characterized by an abnormally late sleeping and arousal time. Among several available treatments, chronotherapy, light therapy and melatonin administration strongly suggest a frequently recurring disturbance of the brain's circadian clock. However, several studies show psychological disturbances, which are either potentially a consequence or a cause or only fortuitously associated. The first case of disappearance of the disturbance after a move to a tropical latitude does not determine the main responsible factor.- - - - - - - - - - ranking = 1keywords = brain (Clic here for more details about this article) |
6/62. The pathology of rem sleep behavior disorder with comorbid Lewy body dementia.A patient with rem sleep behavior disorder who subsequently developed probable Lewy body dementia is now reported to have a definite pathologic diagnosis of Lewy body dementia. Examination of brain revealed lewy bodies as well as marked neuronal loss in brainstem monoaminergic nuclei-particularly locus coeruleus and substantia nigra-that inhibit cholinergic neurons in the pedunculopontine nucleus mediating atonia during REM sleep.- - - - - - - - - - ranking = 2keywords = brain (Clic here for more details about this article) |
7/62. Morvan's syndrome: peripheral and central nervous system and cardiac involvement with antibodies to voltage-gated potassium channels.Morvan's 'fibrillary chorea' or Morvan's syndrome is characterized by neuromyotonia (NMT), pain, hyperhydrosis, weight loss, severe insomnia and hallucinations. We describe a man aged 76 years with NMT, dysautonomia, cardiac arrhythmia, lack of slow-wave sleep and abnormal rapid eye movement sleep. He had raised serum antibodies to voltage-gated K( ) channels (VGKC), oligoclonal bands in his CSF, markedly increased serum norepinephrine, increased serum cortisol and reduced levels and absent circadian rhythms of prolactin and melatonin. The neurohormonal findings and many of the clinical features were very similar to those in fatal familial insomnia, a hereditary prion disease that is associated with thalamic degenerative changes. Strikingly, however, all symptoms in our MFC patient improved with plasma exchange. The patient died unexpectedly 11 months later. At autopsy, there was a pulmonary adenocarcinoma, but brain pathology showed only a microinfarct in the hippocampus and no thalamic changes. The NMT and some of the autonomic features are likely to be directly related to the VGKC antibodies acting in the periphery. The central symptoms might also be due to the direct effects of VGKC antibodies, or perhaps of other autoantibodies still to be defined, on the limbic system with secondary effects on neurohormone levels. Alternatively, changes in secretion of neurohormones in the periphery might contribute to the central disturbance. The relationship between VGKC antibodies, neurohormonal levels, autonomic, limbic and sleep disorders requires further study.- - - - - - - - - - ranking = 1keywords = brain (Clic here for more details about this article) |
8/62. Sleep-wake schedule disorder disability: a lifelong untreatable pathology of the circadian time structure.Certain sleep-wake schedule disorders (SWSDs) cannot be successfully managed clinically using conventional methods of sleep therapy. We describe two cases of SWSD, the first following head trauma and the second originating during childhood, that had been misdiagnosed by physicians for many years. After conventional treatment for SWSD with light therapy and melatonin failed to bring about substantial improvement, it was determined that they were suffering from an incurable disability. Hence, we propose new medical terminology for such cases--SWSD disability. SWSD disability is an untreatable pathology of the circadian time structure. patients suffering from SWSD disability should be encouraged to accept the fact that they suffer from a permanent disability, and that their quality of life can only be improved if they are willing to undergo rehabilitation. It is imperative that physicians recognize the medical condition of SWSD disability in their patients and bring it to the notice of the public institutions responsible for vocational and social rehabilitation.- - - - - - - - - - ranking = 0.0025491630316979keywords = trauma (Clic here for more details about this article) |
9/62. Prognostic value of evoked potentials and sleep recordings in the prolonged comatose state of children. Preliminary data.OBJECTIVES: Sleep recordings and evoked potentials (EPs) were used in five comatose children to evaluate their predictive value for outcome following a severe comatose state. methods AND SUBJECTS: The protocol included EEG, Brainstem Evoked Responses (BERs), Somatosensory evoked potentials (SEPs) and polysomnography. From 10 to 15 days post-coma (D10 to D15), EEG and clinical examinations were carried out every second day, then one day in four from 15 to 30 days post-coma (D15 to D30), and one day in seven from D30 to six months (M6). evoked potentials and polysomnography were recorded on D10-D15 or D30 in the second month (M2) and in M6. Of the five children, three were in anoxic coma and two in traumatic coma. All had extensive lesions and a glasgow coma scale (GCS) score of less than five. The results of the EEG, polysomnographic and EP recordings were compared to the clinical outcome. RESULTS AND CONCLUSION: In the three anoxic comas we observed BER abnormalities and the absence of SEP N20 associated with wide cortical lesions with brainstem extension. Sleep recordings showed major alterations of the wake-sleep cycle without any improvement in M6. Abnormalities included loss of the normal REM-sleep pattern associated with alteration of NREM sleep and periods of increase in motor activity without EEG arousal. This sleep pattern appeared to be associated with involvement of the brainstem. In the two traumatic comas, alterations of the early cortical SEP responses were less severe and the BERs were normal. Some sleep spindles were observed as well as the persistence of sleep cycles in the first weeks post-coma. The combined use of EEG, EPs and polysomnography improved the outcome prediction in comparison with the use of just one modality. EPs and sleep recordings were far superior to clinical evaluation and to GCS in the appreciation of the functional status of comatose children. The reappearance of sleep patterns is considered to be of favorable prognosis for outcome of the coma state, as is the presence of sleep spindles in post-trauma coma. This study showed that EPs and sleep recordings help to further distinguish between patients with good or bad outcomes.- - - - - - - - - - ranking = 2.0076474890951keywords = brain, trauma (Clic here for more details about this article) |
10/62. Secondary causes of paroxysmal dyskinesia.PxD are sudden, episodic, involuntary movement disorders that may include any combination of dystonia, chorea, athetosis, or ballism. The majority of reported cases are familial or idiopathic; however, there have been several reports of secondary PxD. We report 20 new cases of secondary, non-psychogenic PxD, and review 130 cases reported in the literature. The results suggest that although PxD is a rare disorder, secondary forms may be more common than previously recognized, accounting for 26% of all cases in our series. Secondary cases are notable for their variability in age of onset, the presence of both kinesigenic and non-kinesigenic symptoms in some patients, the prevalence of sensory precipitants, and most importantly, the reversal of symptoms when the underlying etiology is treated in some patients. In addition to MS, other causes to be considered in patients presenting with PxD include cerebral vascular insufficiency and stroke, trauma, metabolic abnormalities, and CNS infections. awareness of the association of these etiologies with secondary PxD will permit prompt diagnoses and appropriate interventions. Potential pathophysiologic mechanisms including loss of inhibition or primary neuronal hyperactivity are discussed. In addition, recent hypotheses regarding channelopathies in relation to PxD are presented.- - - - - - - - - - ranking = 0.0025491630316979keywords = trauma (Clic here for more details about this article) |
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