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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Paramedian thalamic stroke (PTS) is a cause of organic hypersomnia, which in the absence of systematic sleep-wake studies has been attributed to disruption of ascending activating impulses and considered a "dearoused" state. However, an increasing mount of data suggests a role of the thalamus in sleep regulation and raises the possibility that a sleep disturbance contributes to hypersomnia in PTS. We evaluated 12 patients with magnetic resonance imaging-proven isolated PTS and hypersomnia with 10 to >20 hours of sleep behavior per day. Nocturnal polysomnographic findings paralleled the severity of hypersomnia. All subjects had increased stage 1 NREM sleep, reduced stage 2 NREM sleep, and reduced numbers of sleep spindles. In patients with severe hypersomnia, slow-wave (stages 3-4) NREM sleep was often reduced, but there were no major REM sleep alterations. Daytime sleep behavior was associated mostly with stage 1 sleep by electroencephalogram; there was no correlation between hypersomnia and results of nap tests. We conclude that hypersomnia following PTS is accompanied by deficient arousal during the day and insufficient spindling and slow-wave sleep production at night. These observations support the hypothesis of a dual role of the paramedian thalamus as "final common pathway' for both maintenance of wakefulness and promotion of NREM sleep.
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PMID:Hypersomnia following paramedian thalamic stroke: a report of 12 patients. 861 25

Proximal myotonic myopathy (PROMM) is an autosomal dominantly inherited multisystemic disorder characterized by myotonia, proximal muscle weakness, and cataracts. This disorder is not linked to the gene locus of myotonic dystrophy (DM). We describe three new families with PROMM. In all patients, CTG repeats of the DM gene in DNA from blood leukocytes were normal. MRI of the brain revealed a consistent pattern of marked white matter hyperintensity on T2-weighted images in four patients; two additional patients had similar but mild to moderate MRI abnormalities. The morphology of these abnormalities is unknown. Clinical symptoms of brain disease were not consistent and included mental changes with hypersomnia, parkinsonian features, stroke-like episodes, and seizures. The causative relationship of these clinical features with the MRI white matter abnormalities remains to be established. Our observations suggest that PROMM may involve the brain.
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PMID:Proximal myotonic myopathy with MRI white matter abnormalities of the brain. 900 90

The paramedian thalamus is believed to play an important role in the regulation of sleep, and disturbances of sleep regulation are known to occur in paramedian thalamic stroke (PTS). We examined 12 consecutive patients with PTS and sleep disturbance by MRI. Two distinct groups of patients could be defined: six presenting with severe hypersomnia (group 1) and six with slight sleepiness (group 2). On MRI, all patients had ischaemic lesions involving the paramedian thalamic nuclei, the centre of the lesions being the dorsomedial and centromedial thalamic nuclei. In group 1 the lesions were bilateral, butterfly-shaped infarcts involving the paramedian nuclei (three cases); or unilateral with an extension into the subthalamic nuclei. In group 2 the lesions were unilateral and limited to the paramedian nuclei, mainly the dorsomedial nucleus. Bilateral lesions can be attributed to a common origin in some cases for both paramedian thalamic arteries and the mesencephalic arteries.
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PMID:MRI of paramedian thalamic stroke with sleep disturbance. 935 Nov 3

We present a comprehensive review of sleep studies performed in patients with brain lesions complemented by 16 additional personal selected cases and by discussion of the corresponding animal data. The reader is cautioned about the risk of establishing an erroneous correlation between abnormal sleep and a given disorder due to the important inter and intra variability of sleep parameters among individuals. Salient points are stressed: the high frequency of post-stroke sleep breathing disorders is becoming increasingly recognised and may, in the near future, change the way this condition is managed. Meso-diencephalic bilateral infarcts induce a variable degree of damage to both waking and non-REM sleep networks producing and abnormal waking and sometimes a stage 1 hypersomnia reduced by modafinil or bromocriptine, which can be considered as a syndrome of cathecholaminergic deficiency. Central pontine lesions induce REM and non-REM sleep insomnia with bilateral lateral gaze paralysis. Bulbar stroke leads to frequent sleep breathing disorders. Polysomnography can help define the extent of involvement of various degenerative diseases. Fragmented sleep in Parkinson's disease may be preceded by REM sleep behavioural disorders. Multiple system atrophies are characterised by important sleep disorganization. Sleep waking disorganization and a specific ocular REM pattern are often seen in supra-nuclear ophtalmoplegia. In Alzheimer patients, sleep perturbations parallel the mental deterioration and are possibly related to cholinergic deficiency. Fronto-temporal dementia may be associated with an important decrease in REM sleep. Few narcoleptic syndromes are reported to be associated with a tumour of the third ventricle or a multiple sclerosis or to follow a brain trauma; all these cases raise the question whether this is a simple coincidence, a revelation of a latent narcolepsy or, as in non-DR16/DQ5 patients, a genuine symptomatic narcolepsy. Trypanosomiasis and the abnormal prion protein precociously after sleep patterns. Polysomnography is a precious tool for evaluating brain function provided it is realised under optimal conditions in stable patients and interpreted with caution. Several unpublished cases are presented: one case of pseudohypersomnia due to a bilateral thalamic infarct and corrected by modafinil, four probable late-onset autosomal recessive cerebellar ataxias without sleep pattern anomalies, six cases of fronto-temporal dementia with strong reduction in total sleep time and REMS percentage on the first polysomnographic night, one case of periodic hypersomnia associated with a Rathke's cleft cyst and four cases of suspected symptomatic narcolepsy with a DR16-DQ5 haplotype, three of which were post-traumatic without MRI anomalies, and one associated with multiple sclerosis exhibiting pontine hyper signals on MRI.
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PMID:Sleep and brain lesions: a critical review of the literature and additional new cases. 1181 Sep 86

The evolution of subjective sleep and sleep electroencephalogram (EEG) after hemispheric stroke have been rarely studied and the relationship of sleep variables to stroke outcome is essentially unknown. We studied 27 patients with first hemispheric ischaemic stroke and no sleep apnoea in the acute (1-8 days), subacute (9-35 days), and chronic phase (5-24 months) after stroke. Clinical assessment included estimated sleep time per 24 h (EST) and Epworth sleepiness score (ESS) before stroke, as well as EST, ESS and clinical outcome after stroke. Sleep EEG data from stroke patients were compared with data from 11 hospitalized controls and published norms. Changes in EST (>2 h, 38% of patients) and ESS (>3 points, 26%) were frequent but correlated poorly with sleep EEG changes. In the chronic phase no significant differences in sleep EEG between controls and patients were found. High sleep efficiency and low wakefulness after sleep onset in the acute phase were associated with a good long-term outcome. These two sleep EEG variables improved significantly from the acute to the subacute and chronic phase. In conclusion, hemispheric strokes can cause insomnia, hypersomnia or changes in sleep needs but only rarely persisting sleep EEG abnormalities. High sleep EEG continuity in the acute phase of stroke heralds a good clinical outcome.
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PMID:Evolution of sleep and sleep EEG after hemispheric stroke. 1246 1

Sleep-disordered breathing (SDB) and sleep-wake disturbances (SWD) are frequent in stroke patients. They deserve attention, because they may significantly influence rehabilitation process and functional outcome. In addition, SDB may increase the risk of stroke recurrence. More than 50% of stroke patients have SDB, mostly obstructive sleep apnea (OSA). In some patients, stroke recovery is accompanied by an improvement of SDB. The treatment of choice for OSA is continuous positive airway pressure. Oxygen, theophylline, and other forms of ventilation may be helpful in patients with other forms of SDB (eg, Cheyne-Stokes breathing). In at least 20% to 40% of stroke patients, SWD are present, mainly in form of increased sleep needs (hypersomnia), excessive daytime sleepiness, or insomnia. Depression, anxiety, SDB, stroke complications (eg, nocturia, dysphagia, and urinary or respiratory infections), and drugs may contribute to SWD and should be addressed first. In patients with SWD of primary neurologic origin, treatment with stimulants or dopaminergic drugs and hypnotics or sedating antidepressants, respectively, can be attempted.
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PMID:Sleep Apnea and Other Sleep-Wake Disorders in Stroke. 1267 Apr 13

More than 50% of stroke patients have sleep-disordered breathing (SDB), mostly in the form of obstructive sleep apnea (OSA). SDB represents both a risk factor and a consequence of stroke. The presence of SDB has been linked with poorer long-term outcome and increased long-term stroke mortality. Continuous positive airway presure is the treatment of choice for OSA. Oxygen and other forms of ventilation may be helpful in other (e.g., central) forms of SDB. SDB can improve spontaneously after stroke. About 20 to 40% of stroke patients have sleep-wake disorders (SWD), mostly in form of insomnia, excessive daytime sleepiness/fatigue, or hypersomnia (increased sleep needs). Depression, anxiety, SDB, stroke complications, and medications may contribute to SWD and should be addressed first therapeutically. Brain damage per se, often at thalamic or brainstem level, can be also a cause of persisting SWD. In these patients, hypnotics, dopeminergic agents, and stimulants (e.g., modafinil) can be attempted.
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PMID:Sleep and stroke. 1579 34

Three months previously, a 17-year-old girl had complained of right-hand side hemiparesis, and her brain magnetic resonance imaging (MRI) showed a signal change in the left temporoparietooccipital area. The 3243A>G mutation was found in mitochondrial DNA. She was diagnosed with mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS) and was prescribed dichloroacetic acid to treat lactic acidosis. Her health improved. Two months later, she developed drowsiness and generalized weakness. A New lesion was not found on brain MRI, and electrodiagnostic findings were compatible with acute motor sensory axonal neuropathy. Her negative symptoms, such as depressed mood, loss of interest in activities, psychomotor retardation, and hypersomnia, were aggravated. She was prescribed antidepressants and psychostimulants by a psychiatrist after diagnosis of severe depression episode with catatonic features. One month later, her catatonic condition had improved with medication. Our experience shows that psychiatric diagnostic evaluation of abruptly regressed neurologic and clinical features is important, even in a patient with devastating underlying disease.
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PMID:Depressive episode with catatonic features in a case of mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS). 1945 Dec 68

The paramedian thalamic arteries can arise as a pair from each P1 of the posterior cerebral artery, but they may also arise equally from a common trunk off one P1, thus supplying thalamus bilaterally. Such a common trunk is called the artery of Percheron and supplies the mesial aspects of both thalami and the rostral midbrain. This is a retrospective review of 1,253 consecutive patients with ischemic stroke enrolled in a stroke registry within an 8-year period (January 2001-December 2008). All were evaluated with detailed clinical and neuropsychological evaluation, magnetic resonance imaging (MRI), blood studies, electrocardiogram, and transthoracic echocardiography. All standard risk factors were recorded in these patients. Ten patients (0.7%) in this series presented with a first-ever thalamic stroke demonstrating bilateral paramedian thalamic lesions on MRI. The main cause of bilateral paramedian thalamic infarctions was small artery disease (60%), followed by cardioembolism (40%). A well-defined clinical picture is shown in bilateral paramedian thalamic artery infarcts. These patients had disorder's consisting of consciousness, memory dysfunctions, various types of vertical gaze paresis, and psychological changes. Although neurologic deficits and hypersomnia recovered to large extent in patients with paramedian thalamic infarcts, cognitive deficits that were mainly linked with bilateral and left-sided lesions often persisted. Vertical gaze paresis tended to improve and never seriously disturbed the patient's activities. We believe that these kinds of strokes have been commonly overlooked, especially without widespread use of MRI.
J Stroke Cerebrovasc Dis
PMID:Bilateral paramedian thalamic artery infarcts: report of 10 cases. 2061 Jan 85

We describe a unique patient who developed hypersomnia as the sole presenting symptom of bilateral thalamic infarcts.
J Stroke Cerebrovasc Dis 2012 Feb
PMID:Isolated hypersomnia due to bilateral thalamic infarcts. 2085 35


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