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Biomedical subjects

M S Aldrich

Publications and source records attributed to M S Aldrich.

At least 19 recordsLinked to original sources
PubMed1992

Dopamine-receptor autoradiography of human narcoleptic brain.

Although the pathology of human narcolepsy is unknown, studies of human and canine narcolepsy have suggested that dopamine metabolism may be disturbed. We used quantitative autoradiography to assess dopamine D1- and D2-receptor binding in basal ganglia and amygdala of five narcoleptic and 17 control human brains. In caudate, narcoleptic brains had a statistically significant increase of 57% in D1-receptor binding, and large but not significant increases of 54% in medial globus pallidus D1 binding, 63% in caudate D2-receptor binding, 95% in lateral globus pallidus D2 binding, and 93% in lateral amygdala D2 binding. We found no major changes in the putamen or in the basal or accessory basal nuclei of the amygdala. These results suggest that narcolepsy is associated with upregulation of dopamine receptors in specific areas of the brain, although medications used prior to death may have contributed to the findings.

Adult↗
PubMed1992

Sleep disorders.

Advances in knowledge of brain regulation of sleep and wakefulness have led to greater understanding of the effects of such diseases as narcolepsy and sleeping sickness on brain function. Treatment of the two most common sleep disorders, insomnia and obstructive sleep apnea syndrome (OSAS), is often but not always effective; promising new approaches are under investigation.

Brain↗
PubMed1992

Narcolepsy.

Narcolepsy is a chronic neurologic disorder characterized by excessive daytime sleepiness, cataplexy, and premature onset of rapid eye movement sleep. It can be differentiated from other disorders causing daytime drowsiness by its clinical symptoms and by sleep laboratory studies. The disorder usually begins in adolescence and remains present throughout life. Genetic susceptibility to narcolepsy is closely associated with specific HLAs that indicate the existence of a gene in the region of the major histocompatibility complex on chromosome 6 that increases susceptibility to narcolepsy. Neurochemical studies of human and canine narcolepsy have demonstrated disturbed monoaminergic and cholinergic function that may account for impaired regulation of rapid eye movement sleep, but the link between these abnormalities and the genetic factors is still unknown. Treatment of sleepiness with stimulants and cataplexy with tricyclic antidepressants leads to substantial improvement but does not fully resolve symptoms in most patients.

Arousal↗
PubMed1991

The neurobiology of narcolepsy.

Narcolepsy is characterized by excessive sleepiness and abnormal manifestations of rapid eye movement (REM) sleep. Neurochemical studies of human and canine narcolepsy have demonstrated disturbed monoaminergic and cholinergic function and suggest that deficits of noradrenaline availability in specific brain regions may account for much of its disordered pathophysiology. Genetic susceptibility to narcolepsy is closely linked to a specific region of the major histocompatibility complex on chromosome 6 and an important direction for future research will be to unravel the relationship between this gene region and the neurochemical abnormalities of narcolepsy.

Animals↗
PubMed1991

Diagnostic value of video-EEG polysomnography.

To investigate the diagnostic value of video-EEG polysomnography (VPSG), we reviewed our experience in 122 patients with suspected parasomnias who underwent one or two nights of VPSG. Of 86 patients without known epilepsy, VPSG provided useful diagnostic information for 41 (69%) of those with a history of prominent motor activity during sleep and for 11 (41%) of those with a history of minor motor activity during sleep. Two children and one adult with clinical histories suggestive of sleep terrors had unequivocal partial seizures during VPSG. Of 36 patients with known epilepsy, VPSG was useful diagnostically in 28 (78%). VPSG is superior to standard polysomnography for the evaluation of parasomnias because of the increased capability to identify and localize EEG abnormalities and to correlate behavior with EEG and polysomnography. VPSG may also be a suitable alternative to intensive inpatient monitoring for some patients with known or suspected epilepsy who have frequent undiagnosed nocturnal spells.

Electroencephalography↗
PubMed1990

Narcolepsy.

Explore the source record for details and available documents.

Adolescent↗
PubMed1990

Epileptiform abnormalities during sleep in Rett syndrome.

We recorded all-night electroencephalograms (EEGs)/polysomnograms on 2 consecutive nights from 4 children (ages 4-11 years) with Rett syndrome. The first 10 sec of each 60 sec epoch were analyzed with counts of left and right hemisphere spikes and correlated with sleep stage. Spike counts were lowest during wakefulness. Spikes were most frequent over parasagittal regions during all sleep stages and varied from 0.28 +/- 0.03 to 40.4 +/- 0.7 (mean +/- S.E.M.) spikes/hemisphere/min. Spike counts were 51-109% higher during NREM sleep than during REM sleep. In 3 of 4 subjects, spikes were most frequent during light NREM sleep. Spikes increased in frequency during the second half of the night. We conclude that in Rett syndrome, epileptiform activity is maximally expressed in stage 1-2 NREM sleep and during the early morning hours. Sleep EEG features may be useful in the diagnosis of Rett syndrome.

Child↗
PubMed1990

Preliminary findings in the treatment of obstructive sleep apnea with transtracheal oxygen.

The effects of continuous low flow oxygen via transtracheal oxygen delivery (TTOD) were assessed in four patients with obstructive sleep apnea (OSA) and daytime hypersomnolence who were unable to tolerate continuous positive nasal airway pressure (CPAP). The overall quality of sleep, sleep fragmentation, pattern of respiration, and nocturnal oxygen saturations were evaluated with the patients receiving 2 to 3 L/min of oxygen by TTOD, and the results were compared to polysomnograms with and without nasal cannula oxygen. The mean respiratory disturbance index (apneas plus hypopneas/hour of sleep) was improved by TTOD compared to no therapy or nasal cannula oxygen, and improvement in sleep disturbance was associated with improvement in overall nocturnal oxygen saturation. The mean apnea duration was not increased by TTOD and the duration of the longest apneic spells was decreased by 33 to 85% with this therapy. These improvements in respiratory status were accompanied by symptomatic improvement in daytime sleepiness, and there were no significant side effects. These findings suggest that TTOD may be a safe and effective alternative treatment of OSA for some patients who are unable to tolerate nasal CPAP therapy.

Adult↗
PubMed1990

Sleep disorders and airway obstruction in newborns and infants.

For most infants with a disorder of breathing control or airway obstruction, cause and management can be defined with a careful history and a few simple diagnostic tests. Pneumograms and multichannel studies can identify patterns of apnea and associated hypoxemia and can be used to assess therapeutic efficacy. For the majority of infants with disordered breathing, the outcome is favorable and conservative management is appropriate. More extensive diagnostic evaluation is reserved for infants with severe apnea or those with evidence of a significant contributing underlying disease. For these infants, management should be directed at the underlying cause and at identifying and preventing severe, life-threatening events.

Airway Obstruction↗
PubMed1990

Neurologic aspects of sleep apnea and related respiratory disturbances.

Several types of neurologic diseases can contribute to disturbed respiration during sleep. Abnormal function of respiratory and upper airway muscles can occur with neuromuscular diseases and lead to upper airway obstruction and alveolar hypoventilation during sleep. Central nervous system disorders that cause dysarthria and dysphagia can also lead to obstructive and central sleep apnea, even in the absence of the usual anatomic deformities associated with OSA. Appropriate treatment requires an understanding of the effect of the underlying disease process on upper airway and respiratory function.

Airway Resistance↗
PubMed1990

Are morning headaches part of obstructive sleep apnea syndrome?

To determine whether morning headaches are a consistent symptom in sleep apnea, we reviewed clinical and polysomnographic data of 304 patients with sleep apnea and compared the findings with normal control subjects and with three other groups of patients seen at a sleep disorders center. Eighteen percent of patients with sleep apnea had frequent morning headaches compared with 21% to 38% in the other groups of patients and 6% of control subjects. In patients with sleep apnea, morning headaches were most common in those with mild predominantly nonobstructive apnea. Polysomnographic characteristics of patients with moderate to severe sleep apnea did not significantly differ between patients with frequent headaches and those without such headaches. Frequent morning headaches are a nonspecific symptom in patients with sleep disorders and are not a consistent or reliable symptom of sleep apnea syndrome.

Adult↗
PubMed1989

Sleep abnormalities in progressive supranuclear palsy.

We studied sleep patterns for three nights in 10 subjects with moderate to severe progressive supranuclear palsy and correlated the findings with disease severity using quantitative measures of motor, cognitive, and eye movement impairment. All subjects had severe insomnia, spending 2 to 6 hours awake per night; the mean time awake per night for the group was more than 4 hours. Sleep latency became shorter and the number of awakenings increased with greater motor impairment, and total sleep time declined as dementia worsened. These findings indicate that in progressive supranuclear palsy insomnia is related to disease severity. Insomnia associated with progressive supranuclear palsy appears to be worse than the insomnia of Parkinson's disease or Alzheimer's disease and may be due to degenerative changes in brain structures responsible for sleep maintenance.

Aged↗
PubMed1989

Exacerbation of human cataplexy by prazosin.

A middle-aged woman with narcolepsy developed a pronounced exacerbation of cataplexy within 3 days of beginning treatment for hypertension with prazosin, an alpha 1-adrenoceptor antagonist. At times, episodes of cataplexy were virtually continuous (status cataplecticus), and there was only partial amelioration with tricyclic antidepressants. Cataplexy improved when prazosin was discontinued. These findings are similar to the reported effects of prazosin on cataplexy in narcoleptic dogs; they support a role for altered alpha 1-adrenoceptor function in narcolepsy.

Cataplexy↗
PubMed1989

Automobile accidents in patients with sleep disorders.

Sleep-related motor vehicle accidents are a serious safety hazard both for the driver who falls asleep and for others on the road. Sleep disorders may be significant contributing factor in some of these accidents. We reviewed data on sleep-related accidents from 70 control subjects and 424 adults with four categories of sleep disorders: sleep apnea, narcolepsy, other disorders of excessive sleepiness, and sleep disorders without excessive sleepiness. The proportion of individuals with sleep-related accidents was 1.5-4 times greater in the hypersomnolent patient groups than in the control group. In patients with hypersomnia, the incidence of sleep-related accidents per year of excessive sleepiness was 3-7%. Although the proportion of patients with sleep-related accidents was highest in narcoleptics, apneics were involved in more sleep-related accidents because of their greater number. Apneics and nacroleptics accounted for 71% of all sleep-related accidents. The proportion of severe apneics who had sleep-related accidents was almost twice that of patients with mild or moderate apnea. Mean sleep latency by Multiple Sleep Latency Test did not differ significantly in patients with accidents and those without. Patients with a wide variety of sleep disorders appear to be at increased risk for sleep-related accidents. The severity and duration of hypersomnia are probably not the only factors that contribute to that risk. These findings have implications for the management of patients with sleep disorders.

Accidents, Traffic↗
PubMed1989

Narcolepsy associated with lesions of the diencephalon.

Although symptomatic narcolepsy, or narcolepsy due to identifiable brain lesions, was once thought to be common, there are few well-documented reported cases since the discovery of the association of REM sleep abnormalities with narcolepsy. Even fewer such reports have been accompanied by human leukocyte antigen (HLA) testing. We report 3 patients who fulfill criteria for symptomatic narcolepsy, 1 with a craniopharyngioma, the 2nd with a hypothalamic syndrome of unknown etiology, and the 3rd with obstructive hydrocephalus and a sarcoid granuloma in the region of the 3rd ventricle. The first 2 were positive for HLA-DR2 while the 3rd was negative for the HLA-DR2 and HLA-DQwl antigens. These findings suggest that diencephalic lesions can be associated with signs and symptoms of narcolepsy that are clinically indistinguishable from those of idiopathic narcolepsy, and that the HLA-DR2 antigen is not required in all cases of symptomatic narcolepsy.

Adult↗
PubMed1989

Failure of cholinergic agonist RS-86 to improve cognition and movement in PSP despite effects on sleep.

Postmortem studies of patients with progressive supranuclear palsy (PSP) have demonstrated loss of cholinergic neurons in the striatum, nucleus basalis of Meynert, and the pedunculopontine nucleus. These findings suggest that cholinergic drugs might be an effective treatment for this disease. We studied the efficacy of RS-86, a direct cholinergic agonist, upon motor abilities, eye movements, and psychometric performance in 10 patients with PSP during a 9-week placebo-controlled, double-blinded, crossover trial. Glycopyrrolate, a peripheral anticholinergic drug, was given throughout the trial to minimize cholinergic side effects. We used changes in rapid eye movement (REM) sleep to assess the degree of cholinergic activation achieved by treatment. Despite the enhancement of cholinergic activity in the CNS as indicated by increases in REM sleep latency and REM sleep time, RS-86 did not improve motor signs, eye movements, or cognition. Pharmacologic replacement of the cholinergic deficits in PSP does not result in significant clinical benefit.

Aged↗
PubMed1988

Intracerebral hemorrhage complicating intravenous tissue plasminogen activator treatment.

Tissue plasminogen activator's thrombolytic action is relatively specific for fibrin; however, systemic bleeding can occur in patients, especially when heparin is simultaneously administered. We describe two cases of intracerebral hemorrhage from a cohort of 450 patients (0.44%) treated at one institution with tissue plasminogen activator and heparin for acute myocardial infarction. A pooled worldwide review of 5258 cases from several clinical protocols for treatment of acute myocardial infarction, using tissue plasminogen activator from one source, revealed a similar overall incidence of 0.68%. The incidence of intracerebral hemorrhage may be reduced by lowering the total dose of tissue plasminogen activator or by reducing the infusion rate and duration. The incidence of central nervous system hemorrhage with tissue plasminogen activator is within the range reported with streptokinase, but because equal coronary artery thrombolytic doses are not known, no definitive comparison is possible.

Aphasia↗