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Query: UMLS:C0917801 (insomnia)
 10,606 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Tick-borne encephalitis is transmitted by the tick ixodes ricinus. After the second world war an increase in the number of cases of encephalitis was observed and the neurotropic virus was isolated for the first time in 1948. Reservoir animals are mouse-like wild animals and also agricultural domestic animals. The infection is transmitted to humans through tick bites. It becomes apparent subjectively in headaches, vomiting, tiredness, giddiness and insomnia, and objectively in meningeal symptoms, extrapyramidal tremor, cerebellar ataxia, vestibular nystagmus and paresis. The treatment consists of strict rest in bed for 10 days at least and symptomatic support of the general health. Good results are obtained with antiedematous therapy with hydrocortisone or pyritinol.
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PMID:[Clinical picture of Central European tick-borne encephalitis (author's transl)]. 82 10

An 18-year-old female had common cold and insomnia in early March 1987. Later, abnormal speech and behavior, emotional incontinence, anorexia and consciousness disturbance appeared. On March 19, she was admitted to our hospital in semi-comatose state. Myoclonus-like movement on hands was observed, and epileptic attacks with tonic and clonic convulsions occasionally occurred. There were no neurological findings that suspected cerebral focal lesions. The respiration was assisted through tracheal intubation. Laboratory examinations showed inflammatory reactions (CRP+2, WBC 10,600) and transient high levels serum CK (6,215 IU). As she had bradycardia (30-40/min) with complete AV block on ECG, the pacemaker was implanted. The complication of myocarditis was suspected. EEG showed bilateral slow waves (3-6Hz), dominantly in frontal areas. Brain CT and CSF examinations were normal. After the combined administration of ara-A, dexamethasone and anti-convulsant, the consciousness level was recovered within a month. The serum antibody against coxsackie virus B4 alone was significantly increased. We concluded that coxsackie virus B4 caused acute encephalitis with mental symptoms and myocarditis with AV block. Recently, cytomegalovirus was reported to be the causative virus in a young female with non-HSV encephalitis who showed mental symptoms with good prognosis, but coxsackie virus B4 should also be considered as one of the causative viruses.
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PMID:[Coxsackie virus B4 encephalitis in a young female who developed mental symptoms, and consciousness disturbance, and completely recovered]. 959 14

We reported a 5-year-old boy with acute encephalitis due to suspected herpes simplex infection, who developed confusion, agitation and insomnia during intravenous administration of acyclovir. He recovered from these neuro-psychiatric symptoms two days after the cessation of acyclovir. The same symptoms recurred two days after its re-administration and resolved on the next day of the second cessation of the drug. Electroencephalogram (EEG) showed periodic lateralized epileptiform discharges (PLEDs) on hospital day 16, which disappeared on hospital day 27, suggesting that neurotoxicity of acyclovir may induce PLEDs. Although acyclovir is useful for the treatment of herpes simplex and varicella-zoster virus infections, we have to pay attention to its neurotoxicity.
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PMID:[A case report of acute encephalitis with neuro-psychiatric side-effects of acyclovir]. 969 30

Dreams appear to be generated in the process of reinforcing memory circuits of the brain, as circuits are activated by self-generated electrical slow waves, with dream contents reflecting information stored in activated circuits. Illusory dreams and other healthy delirious states appear to occur when activated memory circuits are incompetent, containing synapses whose efficacies deviate from their 'dedicated' values. Organic delirium and some other mental disorders may have their basis in brain pathologies that alter reinforcing slow waves, causing synaptic efficacies to depart from dedicated values. Activation of these incompetent circuits leads to recall of faulty memories--a substrate for delirium. In treatment of organic delirium by electroconvulsive therapy (ECT), the electric shock temporarily suppresses abnormal slow-wave regimes, allowing remedial reinforcement regimes to resume. These restore dedicated synaptic efficacies, temporarily alleviating the delirium. The action of ECT shocks appears to parallel closely that of cardiac defibrillating shocks. Greater than normal amounts of circuit reinforcement protect sensory circuitry in fatal familial insomnia, and cognitive circuitry in encephalitis lethargica.
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PMID:Mental malfunction and memory maintenance mechanisms. 1085 64

In 1916, von Economo first described encephalitis lethargica (EL), a CNS disorder presenting with pharyngitis followed by sleep disorder, basal ganglia signs (particularly parkinsonism) and neuropsychiatric sequelae. Since the 1916-1927 epidemic, only sporadic cases have been described. Pathological studies revealed an encephalitis of the midbrain and basal ganglia, with lymphocyte (predominantly plasma cell) infiltration. The EL epidemic occurred during the same time period as the 1918 influenza pandemic, and the two outbreaks have been linked in the medical literature. However, von Economo and other contemporary scientists thought that the 1918 influenza virus was not the cause of EL. Recent examination of archived EL brain material has failed to demonstrate influenza RNA, adding to the evidence that EL was not an invasive influenza encephalitis. By contrast, the findings of intrathecal oligoclonal bands (OCB) and beneficial effects of steroid treatments have provoked the hypothesis that EL may be immune-mediated. We have recently seen 20 patients with a similar EL phenotype, 55% of whom had a preceding pharyngitis. The patients had remarkable similarity to the historical descriptions of EL: sleep disorder (somnolence, sleep inversion or insomnia), lethargy, parkinsonism, dyskinesias and neuropsychiatric symptoms. CSF examination commonly showed elevated protein and OCB (75 and 69% respectively). Investigation found no evidence of viral encephalitis or other recognized causes of rapid-onset parkinsonism. MRI of the brain was normal in 60% but showed inflammatory changes localized to the deep grey matter in 40% of patients. We investigated the possibility that this phenotype could be a postinfectious autoimmune CNS disorder, and therefore similar to Sydenham's chorea. Anti-streptolysin-O titres were elevated in 65% of patients. Furthermore, western immunoblotting showed that 95% of EL patients had autoantibodies reactive against human basal ganglia antigens. These antibodies were also present in the CSF in four patients tested. By contrast, antibodies reactive against the basal ganglia were found in only 2-4% of child and adult controls (n = 173, P < 0.0001). Rather than showing polyspecific binding, these antibodies bound to common neural autoantigens of molecular weight 40, 45, 60 and 98 kDa. Regional tissue comparisons showed that the majority of these autoantigens were specific to or enriched in CNS tissue. Immunohistochemistry with secondary staining localized antibody binding to neurons rather than glial populations. Further investigation is required to determine whether these antibodies affect neuronal function (i.e. whether they are pathogenic anti-neuronal antibodies). Histopathology in one case demonstrated striatal encephalitis with perivenous B- and T-lymphocytic infiltration. We believe an EL-like syndrome is still prevalent, and propose that this syndrome may be secondary to autoimmunity against deep grey matter neurons.
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PMID:Encephalitis lethargica syndrome: 20 new cases and evidence of basal ganglia autoimmunity. 1467 31

An adult case of suspected recurrent measles encephalitis with psychiatric symptoms is reported. A 46-year-old woman developed measles encephalitis presenting as schizophreniform disorder and recovered three months after onset. However, approximately two years later, she suffered a relapse of encephalitis presenting with psychiatric symptoms (auditory hallucination, cenesthopathy, insomnia, depressive mood) and became comatose. Following ten days of symptomatic treatment, her clinical symptoms gradually improved. Three months later, she made a remarkable recovery without neurological sequelae. Since then, she has maintained good condition for six years. The diagnosis of suspected recurrent measles encephalitis was made on the basis of the change of anti-measles IgM antibody titers. Acute relapse of disseminated encephalomyelitis (ARDEM) and multiple sclerosis (MS) were ruled out due to no abnormal finding of cerebral white matter on MRI. Six years after the recurrent episode, the titers of anti-measles IgM antibodies (EIA) in the serum were still high, suggesting that she was suffering from a chronic measles virus infection. This patient should be followed up for a longer time because there is a possibility that she might be in the latent period of subacute sclerosing panencephalitis (SSPE).
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PMID:[An adult case suspected of recurrent measles encephalitis with psychiatric symptoms]. 1467 80

This study was conducted to clarify the clinical and neurophysiologic characteristics of patients with Morvan syndrome, and to compare and contrast this syndrome with other forms of autoimmune encephalitis. A retrospective chart review of the clinical features and neurophysiologic studies of two cases of Morvan syndrome seen at the Mayo Clinic was performed. Neurophysiologic studies included polysomnography, comprehensive autonomic testing, MRI, positron emission tomography, EEG, and single-photon emission computed tomography. In two cases of Morvan syndrome, the clinical features, electrophysiologic findings, and immunologic studies (high levels of voltage-gated potassium channel antibodies) were consistent with previously reported findings. Several novel observations were made. Autonomic testing demonstrated peripheral autonomic neuropathy in addition to autonomic hyperactivity. Polysomnography showed complete absence of sleep. Neuroimaging study findings were largely normal. Morvan syndrome is an autoimmune disorder affecting both the peripheral and central nervous system. Neurophysiologic studies demonstrate hyperexcitability of peripheral nerves, autonomic dysfunction, and severe insomnia. The absence of abnormalities on imaging studies suggests that central nervous system symptoms are related to functional rather than structural disruption of neural networks.
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PMID:Neurophysiologic studies in Morvan syndrome. 1562 31

In case a pre-senile patient presented subacutely progressive dementia, secondary dementia, such as paraneoplastic neurological syndrome (PNS), hypothyroidism, confusion, early phase of primary degenerative dementia and prion diseases are to be considered. It is a case of pathologically confirmed, and clinico-pathologically assessed limbic encephalitis with cerebellar degeneration. The patient was a 63-year old male, with a well followed up medical history of gastric cancer 8 years earlier. Four weeks after he presented himself at our hospital his memory and disorientation progressively declined. A neurological examination revealed gaze nystagmus, with potential secondary dementia. However, no abnormal findings were detected from systemic radiological examination, or from chemical analyses. Two months later, after the onset of the disease, he presented additional symptoms, including seizure, gait disturbance, and insomnia. On admission, neurological examinations revealed gaze nystagmus and progression of dementia; however, his thought process was relatively preserved. No paroxysmal synchronized discharge was seen on electroencephalogram. Chest X-rays showed an inflammatory infiltration. In spite of anti-biotic medication, he died due to respiratory failure. The autopsy was limited to the brain. Histologically, limited lymphocytic infiltration into the hippocampus through the entorhinal cortex, with marked neuronal loss and gliosis was observed. Neuronophagia, microglial nodules, and perivascular lymphocytic infiltration were also seen. Additionally, most of the Purkinje cells in the cerebellum were lost, with Bergmann's gliosis and sparse lymphocytic infiltration. No tumor was observed in the brain. Pathological findings of the brain were compatible with paraneoplastic limbic encephalitis and cerebellar degeneration, though no neoplasm, clinically or pathologically, was detected in this patient. Consequently, it is suggested that when a senile patient presents sub-acute onset of progressive dementia, with a variety of neurological symptoms, paraneoplastic syndrome is to be taken into consideration, even if a tumor or an auto-antibody is not detected since the resection of the tumor is still the best therapeutic means. Otherwise immuno-suppressive and steroid therapies should be used.
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PMID:A pre-senile case of limbic encephalitis and cerebellar degeneration, with subacute onset of progressive dementia. 1567 63

A major controversy over REM sleep's role in memory processing may owe to inadequate allowances for the highly conservative nature of evolutionary adaptations. The controversy hinges on whether NREM sleep, alone, retains primitive memory processing capabilities. The selective pressure for primitive sleep, is thought to have been the need to obviate conflicts between enormous neural processing requirements of complex visual analysis and split-second control of movements, on the one hand, and memory processing, on the other. The most efficient memory processing during mammalian and avian sleep appears to be a two-step process: synapses in individual component circuits of events are reinforced primarily by slow brain waves during NREM sleep, with the reinforced components temporally bound by fast waves, and manifested as dreams, during REM sleep. This dual action could account for partitioning of sleep periods into multiple NREM-REM cycles. It is proposed that in the absence of REM sleep, all needed memory processing can be accomplished by NREM sleep, alone, though less efficiently. Many symptoms of fatal familial insomnia are attributed to subnormal nightly reinforcement of brain circuitry because of almost total loss of sleep, and compensatory responses thereto during waking. During this disorder, sensory circuitry seemingly is spared by virtue of its supernormal reinforcement during almost continuous waking. Contrariwise, sparing of an adult's 'higher faculties' in encephalitis lethargica appears to owe to supernormal circuit reinforcement during almost continuous sleep.
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PMID:Evolutionary approaches to understanding sleep. 1573 92

The study, and the preceding companion article, reviews the pioneering contributions of Constantin von Economo (1876-1931) to Neuroscience in a modern context. The neurological studies of von Economo include the discovery of a new nosological entity, encephalitis lethargica, with which his name is forever linked ('von Economo disease'). Based on a percipient analysis of pathoanatomical material from patients with encephalitis lethargica who manifested with either insomnia or somnolence, von Economo deduced the existence of distinct centres in the brain for the regulation of sleep and wakefulness. He presented a synthesis of his ideas in a series of lectures in New York in 1929 and at the First International Neurological Congress held in Berne in 1931. Constantin von Economo was nominated three times for the Nobel Prize in Physiology or Medicine for the discovery of encephalitis lethargica. As those studies have exerted and continue to exert the highest impact among von Economo's publications, the present article examines the spectrum of his observations on encephalitis lethargica and the cerebral control of sleep, documented in 63 published works--including post-humous translations into French and English of original German texts; complete bibliographic information is given. His remaining 76 works of an annotated total of 139 scientific publications deal with brain structure, evolution and intelligence, as well as general works on nervous and mental pathology and form the focus of the preceding article.
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PMID:The percipient observations of Constantin von Economo on encephalitis lethargica and sleep disruption and their lasting impact on contemporary sleep research. 1656 19


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