Search

We report on a 30-year-old patient with isolated, left-sided hypoglossal nerve palsy after uncomplicated, presumably streptococci-induced tonsillitis. Needle electromyography (EMG) of the tongue showed denervation changes in the muscles supplied by the left hypoglossal nerve. Cranial CT and MRI, CSF examination, Doppler sonography, visual evoked potential (VEP), and auditory evoked potential (AEP) showed no abnormalities and, in particular, no signs of the carotid artery dissection or brainstem lesion. The symptoms and signs resolved within a few weeks after penicillin V treatment. We suppose that the hypoglossal affection of the uncomplicated tonsillitis in this case was due to an aberrant position of the nerve.

There exist a variety of American and European recommendations regarding treatment with hypnotics, especially the duration of treatment. The German Sleep Society now publishes its own view to help physicians to cope with these different recommendations, some of which are contradictory. Therapy with hypnotics must include substantial information on the type of drug, dose, timing and duration as well as information about the possibility of interval treatment. Agonists at the benzodiazepine receptor, like the conventional benzodiazepines and zopiclone or zolpideme, are indicated in short-lasting adjustment insomnia as well as in long-lasting psychophysiological insomnia. Regarding the duration of prescription the German Sleep Society recommends a period of 14 days in de novo patients, which can be repeated once only. In persisting insomnias further approaches should disregard benzodiazepine receptor agonists, but rely on other classes of substances such as tricyclic antidepressants instead. If such approaches are ineffective, the intake of benzodiazepine receptor agonists may be extended to 6 months, when a sleep log and objective observations have documented a true sleep deficit, when daytime impairment arises, when daytime impairment arises, when rebound insomnia, organic or mental insomnias and dependencies have been excluded, and when the indication is monitored at 14-day intervals. If the insomnia persists, during and in spite of therapy a specialist in sleep medicine should be consulted. If therapy is still ineffective after 3 months of daily treatment, a sleep laboratory should be consulted.

Circadian modulation of seizure threshold is subjected to a multitude of periodical, aperiodical and stochastical influences. Epilepsies on the other hand influence the biological rhythms themselves. Epileptic seizures are activated during transient sleep stages. Nocturnal seizures lead to severe sleep disorders and therefore to hypersomnia. Partial and generalized epilepsies have a different sleep profil even without seizure manifestation. Finally antiepileptic drugs may interfere with circadian rhythms. Knowing the chronobiological context a differentiation of epileptic seizures from nonepileptic parasomnias may succeed more easily. To ensure the appropriate diagnostical proceeding multichannel EEG should be used in every polysomnography with neurological topics.

In a randomized, double-blind, parallel group study in private practice, zopiclone given for 28 days was compared with flunitrazepam, triazolam and placebo in its effect on quality of sleep and daytime well-being in 1507 patients suffering from insomnia. For quantitative assessment, patients were defined as responders according to either a shortening of sleep latency by at least 15 min, or prolongation of total sleep time by at least 20%, or reduction of the number of nocturnal awakenings to three or less and a fresh feeling in the morning, as well as lack of impairment in daytime well-being as a result of tiredness or anxiety. The responder rate tended to be higher with zopiclone (37.4%) than with flunitrazepam (30%) and triazolam (32.2%) and was significantly greater (p = 0.0017) than with placebo (26.8%). Daytime well-being was particularly responsive to zopiclone and most responsive in severe insomniacs. With the exception of those to triazolam, rates of response were most pronounced in patients with insomnia of a short duration (< or = 1 year) than in those with insomnia of a longer duration (> or = 1 year). Following discontinuation of treatment, all groups showed a moderate reduction in therapeutic effect, but no rebound insomnia occurred.

1. The procedure described--the immediate data transfer and entry system (ITES)--is suitable to improve the quality of data collected in multicentre studies in private practice. 2. The results of the study show that regarding influence on sleep quality and daytime well-being the non-benzodiazepine Z is significantly superior to placebo and slightly superior to the benzodiazepines F and T. 3. The advantage of Z treatment is the better daytime well-being after taking the hypnotic for sleep induction the night before. 4. This study shows that a quality standard equal to that in clinical practice may be achieved in private practice.

A total of 181 human immunodeficiency virus (HIV)-seropositive hemophiliacs and 28 hemophilic controls were evaluated by psychometric tests and by electroencephalogram (EEG). Patients were classified from stages 1-6 according to the immunological criteria of the Walter Reed staging system. Statistical analysis of psychometric data showed an effect of the stage of the disease on test performances, indicating a decline in attention, accumulation of perceptual interferences, decline in visuoperceptual speed and visuomotor response speed and reduced verbal memory performance, especially in stage 6 patients. Comparison of performance levels with normative test data already revealed cognitive deficits in about 20-30% of the patients in stages 2-5. As regards verbal memory, especially learning and recognition of new verbal information were impaired. In contrast, there was no significant deficit for nonverbal memory processing. Compared with the controls, patients exhibited an increasing number of abnormal EEG findings in stages 2-6. As a conclusion, in the stages before acquired immunodeficiency syndrome (AIDS) develops, EEG findings as well as psychometric findings indicate central nervous system involvement of AIDS in about 20-30% of cases, whereas in full-blown AIDS there is a marked increase to 80%. Besides a more general deficit of attention and psychomotor speed as is seen in subcortical dementia, there is evidence for a particular verbal learning disorder, suggesting additional selective impairment of the brain.

A case report describing destructive osteolytic changes in the cervical spine in a patient with ankylosing spondylitis and a partial transverse lesion. The differential diagnosis is discussed with reference to the literature. The possibility of surgical stabilization - which in this case was successful - to achieve relief from pain and improved mobility is pointed out.

The diagnostic classification of arthralgia and non-characteristic neurological deficit is a challenge for the neurologist and the internist if both symptoms arise simultaneously or in combination. Diseases with the combined appearance of both symptoms are grouped into those with early and more or less simultaneous onset, those starting with arthralgias followed by neurological deficits, neurogenic arthropathies, and those presenting both symptoms as complications of ongoing internal disease. A diagnostic procedure is set out and recommended.

An all-night polygraphic study of sleep was carried out in 6 healthy volunteers acutely medicated with clonidine (225 micrograms), yohimbine (15 mg), a combination of both drugs or with placebo at random order under simple blind conditions. The conventional scoring of sleep stages was extended by an on-line analysis of the EEG according to Hjorth. Clonidine, an agonist at alpha2 receptors, induced increases of the stages 2 and 3 + 4 but a decrease of REM sleep; the reduction of the parameters mobility and complexity during non-REM sleep signified synchronization of the EEG. Yohimbine, an antagonist at the same receptor sites, enhancing noradrenaline release, increased stage 1 and REM sleep, but decreased the stages 2 and 3 + 4; increases of mobility during REM and non-REM sleep signified desynchronization. The combined treatment with clonidine + yohimbine reduced REM sleep, but not as extensively as clonidine alone; the Hjorth parameters were without significant alterations compared to placebo. The physiological hypotonia was enhanced by clonidine and the combined treatment with clonidine + yohimbine. These results favour the hypothesis of a noradrenergic facilitation of REM sleep.

Human immunodeficiency virus (HIV)-seropositive patients show involvement of the central and/or peripheral nervous system. We present here the results of electroencephalographic (EEG) findings in stage WR 1-5 HIV-seropositive hemophiliacs from a total of 184 who attended our clinic prior to October 1987.

In order to further clarify the involvement of serotonin in the control of secretion of pituitary lactogens, diurnal and sleep prolactin (PRL) and growth hormone (GH) profiles were investigated in healthy subjects treated with ergot and non-ergot serotonin antagonists. A group of 10 subjects received a single oral dose of 2 mg each of pizotifen, methysergide, and the dopaminergic drug bromocriptine as reference substance, in comparison with placebo. Blood was collected at hourly intervals for 6 h. Another group of 10 individuals received either a placebo, 2.5 mg bromocriptine (n = 6) twice daily for 4 days or pizotifen (n = 10) 0.5 mg 3 times daily for 12 days before undergoing EEG recording and blood sampling during night sleep. The diurnal plasma profiles of PRL and GH were not modified by pizotifen, a non-ergot drug. Methysergide and bromocriptine, two ergot derivatives, significantly (P < 0.01 and P < 0.001 respectively) suppressed the basal secretion of PRL throughout the trial and increased plasma GH significantly (P < 0.01). The sleep profile of PRL was not modified by pizotifen but there was a moderate reduction in GH reaching the level of significance (P < 0.02) between hours 1 and 2 of sleep. Bromocriptine suppressed completely PRL secretion throughout the entire sleep period and significantly (P < 0.05) prolonged the secretory profile of GH. The results indicate the presence in the ergot molecule of a dopaminergic moiety responsible for PRL inhibition and GH stimulation. This effect is independent of the serotonin active component of the drug.

The pharmacokinetics and the endocrine profile of a new low molecular somatostatin derivative, SMS 201-995, were investigated in a group of 35 normal subjects. Clearance studies (n = 6) for this peptide showed a prolonged half-life in plasma, 113 min, following single sc injections of 50 or 100 micrograms. Arginine stimulation tests (n = 6) were conducted immediately and 180 min after sc injection of 50 micrograms of SMS 201-995. The stimulatory effect of arginine on GH and insulin was counteracted by the peptide at the P less than 0.001 and P less than 0.02 significance level, respectively. Delayed arginine stimulation revealed a persistent blockade of the GH release (P less than 0.02), whereas a recovery of the insulin response was observed. Plasma glucagon increments following a standard protein meal (n = 10) were significantly (P less than 0.001) inhibited by previous sc injection of 50 micrograms of SMS 202-995. Pretreatment with 50 and 100 micrograms of SMS 202-995 sc (n = 9) inhibited (P less than 0.001) the stimulatory effect of TRH (200 micrograms iv) on TSH without modifying basal levels. The injection of 100 micrograms/h during sleep completely abolished the nocturnal GH peak in 4 volunteers. No rebound rise after decline of the suppressive action on GH was recorded in any of the trials. Safety chemistries and blood coagulation studies remained normal and no side-effects or untoward reactions were recorded throughout the investigation.(ABSTRACT TRUNCATED AT 250 WORDS)

At the age of 22 years, identical twin brothers simultaneously developed symptoms of intracranial pressure. Radiological investigation revealed cerebellar midline tumors with occlusive hydrocephalus of the third and lateral ventricles. At operation, subependymomas with identical histological features were found in the fourth ventricle in both twins. This is the first report of subependymomas in identical twins. The clinical data suggest that this tumor type is of maldevelopmental origin.

A 31-year-old man with histologically documented pulmonary sarcoidosis developed a severe hypokinetic rigid syndrome with a supranuclear gaze palsy following recurrent lymphocytic meningitis and occlusive hydrocephalus. Magnetic resonance imaging (MRI) showed multiple hyperintense foci in the CNS, not detectable by computed tomography (CT). Long-term steroid therapy led to clinical complete remission.

Niflumic acid and indomethacin showed to be inhibitors of catecholamine--uptake into rat striatal and hypothalamic synaptosomes. Whereas the inhibition by niflumic acid was non-competitive for both amines at similar Ki values, the action of indomethacin displayed differences between areas as well as amines: the potency of inhibition by indomethacin was greater in striatal than in hypothalamic synaptosomes irrespective of the amine; the type of inhibition by indomethacin was non-competitive for norepinephrine, but competitive for dopamine regardless of the brain area.