Search PubMed⌕ Search

Biomedical subjects

E Niedermeyer

Publications and source records attributed to E Niedermeyer.

At least 19 recordsLinked to original sources
PubMed1998

Frontal lobe functions and dysfunctions.

Frontal lobe syndromes with personality change are well known for about 150 years but mysteries of their underlying anatomophysiological mechanisms have started to unfold in recent years. The frontal lobe accommodates an extension of the primary motor (precentral) cortex, the premotor region and the interhemispherically located supplementary motor region, both of them forming area 6 and its subdivisions. The anterior and inferior frontal structures (and also the eye field, area 8) belong to the prefrontal region. The prefrontal cortex is also involved in motor action: in its initiation, planning, designing and sequencing rather than its mere execution. This requires drive and initiative to move, their deficits resulting in moderate to extreme apathy. Forces of motivation are likely to be mediated via the fronto-orbital cortex (known as an extension of the temporo-limbic system) which also exerts inhibitory influences on prefrontal functioning, and disinhibitory frontal lobe syndromes (from tactlessness to aggression) are the result of frontobasal impairment. A special form of frontal-motor cortex disconnection may occur in childhood: in the rare Rett syndrome and, with limitation to the prefrontal cortex, in the common Attention Deficit Hyperactivity Disorder (ADHD). The initiation of movement is based upon the constant influx of afferent-sensory messages from posterior cerebral regions and strong mesiodorsal thalamic connections, providing information for each following initiatory prefrontal motor impulse which depends on such information from the past moment. This "Working Memory" appears to be the keystone of mental and motor prefrontal function. Becoming unnecessary in the next moments, the afferent signals undergo immediate extinction due to inhibitory fronto-orbital impulses. It is assumed that the classical absence attack with generalized spike-waves of frontal onset causes a "suspension of the working memory" and thus permits immediate postictal recuperation of frontal functions. The gap between afferent and efferent signals in the working memory is likely to permit neurocognitive-processes and, in Homo sapiens, a widened gap is thought to provide a basis for reflection and cogitation uniquely human properties.

Attention Deficit Disorder with Hyperactivity↗
PubMed1997

Alpha rhythms as physiological and abnormal phenomena.

There are three physiological alpha rhythms in mature healthy humans: (a) the classical posterior alpha; (b) the Rolandic mu rhythm and (c) the midtemporal 'third rhythm'. The classical posterior alpha rhythm develops out of a 4/s rhythm appearing at age 4 months and gradually reaches the alpha frequency band around age 3 years. The mature frequency around 10/s is subject to subtle physiological changes and grossly decelerates in the face of pathology. No posterior alpha rhythm may be detectable in a minority of healthy adults with an inherited low voltage fast EEG. One is tempted to speculate that these individuals may have a hidden alpha rhythm in neuronal level and defective mechanisms of synchronization. Alpha blocking with visual stimuli (eye opening) is a classical response; responses to mental stimuli (mental arithmetic) are inconsistent, presumably due to the involvement of higher cognitive functions. The Rolandic my rhythm is found with scalp EEG in a minority of subjects but there is good reason to presume that all healthy adults have this rhythm. A particularly powerful mu rhythm reaches the scalp but this could be also an indicator of a mild CNS dysfunction. There is even a relationship between mu rhythm and the central spike activity in children with benign Rolandic epilepsy. The midtemporal third rhythm is not detectable in the scalp EEG unless there are local bone defects. Its functional significance is debatable; its blocking responses encompass various higher cognitive tasks and are inconsistent; responses to auditory stimuli do occur but appear to be of secondary significance. This rhythm arises from midtemporal structures which by far exceed the borders of the auditory cortex. Abnormal rhythmical alpha activity-above all the alpha coma in life-threatening cerebral anoxia -is discussed in order to deepen our understanding of the physiological alpha rhythms. Severe cortical de-afferentation may give rise to cortical autorhythmicity-either in alpha frequency or in other frequency bands. Physiological alpha rhythms are likely to have closer relationships to 'events' than one might have thought earlier. The demonstration of event-related desynchronization and synchronization (in Pfurtscheller's work) clearly underscores this view.

Alpha Rhythm↗
PubMed1997

Unusual EEG theta rhythms over central region in Rett syndrome: considerations of the underlying dysfunction.

In 10 female patients (age 2-26 years) with clinical evidence of Rett Syndrome (RS), unusual and prominent rhythmical theta activity (4-5/sec or 5-6/sec) proved to be the outstanding EEG feature. This pattern was present in waking state and/or sleep. When it was noted in the waking state, the localization (vertex, central region and vicinity) and blocking responses to active or passive movements suggested a slow equivalent of Rolandic mu rhythm (in two patients associated with a posterior 10-12/sec alpha rhythm). In sleep, rhythmical theta activity was either Rolandic or more diffuse, sometimes independently occurring with central spikes. The prominent rhythmical 4-5/sec or 5-6/sec activity and its relationship to Rolandic mu rhythm suggest a dysfunction of the motor cortex in RS. This would be congruent with the frequent observation of central spikes. EEG evidence of motor cortex dysfunction might be helpful in the understanding of this enigmatic disorder and conducive to the following hypothesis: RS is characterized by motor cortical dyscontrol due to primary frontal lobe dysfunction. The usefulness of EEG, however, is limited to insights into the (secondary) motor-cortex dysfunction.

Adolescent↗
PubMed1997

Attention-deficit hyperactivity disorder (ADHD) and frontal-motor cortex disconnection.

Attention-Deficit Hyperactivity Disorder (ADHD) is a very common pediatric-neuropsychiatric entity of still unknown etiology, and is thus a topic of controversy. A neurological concept is presented in order to attain a better conceptualization of ADHD. This concept focuses on the frontal lobe as the inhibitor of excessive motor activity. This inhibitory function is presumed to be most active during childhood. The concept of a disturbed frontal-motor cortex connection was first developed in view of a completely different and rare disorder of childhood: Rett Syndrome (RS) with smallness of the frontal lobe, excessive motor activity and EEG abnormalities often confined to the Rolandic region. Accordingly, what is due to structural damage in RS, might be caused by simple dysfunction in ADHD under essential ly benign circumstances. Not a damaged but a "lazy" frontal lobe results in disinhibited motor activity and also in disturbed attention ( a predominantly frontal lobe function). In the light of this concept, the calming effect of methylphenidate in ADHD is quite logical (frontal stimulation improving motor inhibition) and not paradoxical. It is the "lazy" frontal lobe that responds to "the whip" whereas a truly sick frontal lobe as in RS would be unable to respond.

Attention Deficit Disorder with Hyperactivity↗
PubMed1996

Primary (idiopathic) generalized epilepsy and underlying mechanisms.

Primary Generalized Epilepsy (PGE) has been more hotly debated over the past decades than other forms of epileptic seizure disorder. The sudden synchronous appearance of bilateral spikes and spike-waves (mainly with myoclonus resp. absence) used to perplex the earliest generation of electroencephalographers, and the enigmatic genesis of these discharges (and seizures) has not ceased to fascinate the investigators of this phenomenon. A "centrencephalic" concept with paroxysmal discharges arising from thalamic structures and "projecting" to the cortex was championed for many years and eventually laid aside. More recently, the role of the thalamic level has been re-emphasized, mainly on the basis of experimental work. In this article, the bulk of experimental work is critically reviewed: the simian model (Papio papio), the feline, and the rodent models (Wistar rat, tottering mouse). Stress is being laid on fundamental differences between all of these models and human PGE. EEG evidence indicates a superior frontal origin of bilateral-synchronous spikes and spike-waves; depth EEG recordings in patients have failed to demonstrate primary thalamic spike generation. The heart of the matter in PGE appears to be the mechanism underlying paroxysmal discharges; above all the role of arousal. It is not awakening from sleep but the ensuing period that is critical in its epileptogenic thrust caused by alternating periods of return to drowsiness and arousing stimuli. This biphasic process gradually escalates EEG bursts to myoclonus (or absences) and possibly to a generalized tonic-clonic convulsion. Most conducive to this crescendo is the state of tiredness following a night of poor sleep. Bilateral synchrony is not precise and small time differences exist. The line between primary and secondary bilateral synchrony (with a primary cortical focus) can become blurred. Genetic predisposition to generalized paroxysms must always be considered, even in the face of a primary focus with secondary bilateral synchrony. Photosensitivity is a second paroxysm-inducing mechanism in PGE; it is much less common than the abnormal arousal ("dyshormia"); both mechanisms can be present in the same patient. Therapy and prevention of seizures in PGE are finally discussed. The concept of abnormal arousal mechanisms can be put into practice in order to prevent seizures: avoidance of sleepless nights, not always an easy task in adolescents and young adults.

Animals↗
PubMed1996

Dipole theory and electroencephalography.

Dipole theory has become a centerpiece of modern discussions regarding the nature of EEG phenomena. Along with dipole theory, the role of volume conduction and, in particular, the inverse problem have gained a powerful position in the modern approach to EEG. An attempt is being made to explore the origins of these concepts. Their advent and rise to a dominant position has been the expression of a new wave of biophysical approaches to EEG. These new trends started in the 1970's and have gradually overshadowed the classical neurophysiological-neurobiological approach. Electrogenesis in cerebral structures and propagation of EEG signals along pathways characterize the "old" EEG theory. It is being pointed out that dipole theory is indeed theory; it is based on spherical models of homogeneous fluid. Attempted adjustments to the brain and its anatomy have been made. Microdipoles at the neuronal level (an essential part of electrogenesis) are plausible; major problems exist as far as macrodipoles are concerned. Differences between the dipole theory in EEG and MEG are discussed. The modern search for the source of a given EEG potential (inverse problem) depends on dipole theory and may be quite misleading. Spread by volume conduction is likely to be vastly exaggerated. A plea is made for mutual understanding and tolerance.

Biophysical Phenomena↗
PubMed1996

Chronic steroid-responsive encephalitis without autoantibodies to glutamate receptor GluR3.

Autoantibodies to GluR3, an AMPA glutamate receptor subtype, may be a cause of chronic unilateral encephalitis (Rasmussen's syndrome). We report a woman with chronic left hemisphere encephalitis whose partial seizures, aphasia, and motor weakness are highly responsive to intermittent steroids and cyclophosphamide. Her serum and CSF were negative for antibodies to GluR3 by both immunoblot and immunocytochemical analysis of cells transfected with GluR3 cDNA, indicating that separate immune-mediated processes may be involved in some cases of chronic encephalitis.

Adult↗
PubMed1994

Consciousness: function and definition.

The term "consciousness" plays an enormous role in the clinical assessment of patients and also in psychophysiological considerations. It has often been said that consciousness is a term that defies definition. This lack of definability, however, might be more apparent than real. In the multitude of facets, three main components can be singled out: a) vigilance, b) mental contents and c) selective attention. Vigilance, not to be equated with consciousness, is most amenable to electrophysiological studies. The stages of sleep have fairly well standardized EEG correlates, unlike the comatose states. The overflowing wealth of mental contents is constantly adjusted to momentary needs by the mechanism of selective attention. Awareness is a subcomponent and differs from both vigilance and consciousness. Emotionality is particularly important among the variety of further subcomponents. The time factor must be taken into account in order to understand the dynamics and fluctuations of consciousness.

Animals↗
PubMed1994

High frequency bursting during rapid finger movements in an unusual case of epilepsia partialis continua.

Myoclonic activity was analyzed in a 25-year-old male patient suffering from epilepsia partialis continua in his right finger and hand extensors and flexors. The involuntary tremorlike regular muscle jerks occurred at an average rate 7.7/s under resting conditions. Bursting frequency did not change during smooth ramp movements but increased up to 25/s during rapid extensions of the fingers. The EEG showed trains of sharp waves over the left temporoparietal and the midcentral regions but backaveraging did not yield reproducible jerk-related potentials. Somatosensory evoked potentials were not enhanced. It is suggested that the observed pattern of muscle jerks resulted from a spontaneous bursting behaviour of motor cortical neurones.

Adult↗
PubMed1993

Migraine-triggered epilepsy.

Eight young adult patients are reported, referred because of generalized tonic-clonic seizures with unsatisfactory treatment response. All of them had migraine. The major convulsions were preceded by a typical visual prodroma in 6 out of 8 patients, and a full-blown migraine attack followed the convulsion in all patients. Clinical findings were unremarkable, the EEG was mostly normal or slightly abnormal without typical paroxysmal findings, and CT scan and MRI were normal. All patients also had independent migraine attacks without convulsions; all of them had a positive family history of migraine. The response to antimigrainous and/or antiepileptic medication was sluggish or disappointing in most cases. A correction of the patient's life style proved to be the most effective approach.

Adult↗
PubMed1993

An unusual paroxysmal EEG pattern in mixed focal/generalized epilepsies.

This report focuses on an unusual paroxysmal discharge: "compounded sharp waves," focal and mostly over frontotemporal regions, of high voltage, occurring mainly in sleep tracings of children with epileptic seizures. The duration of compounded sharp waves exceeds by far the maximum duration of classical sharp waves. In all of the three reported cases, there were also generalized-synchronous paroxysmal bursts and two children had spike-wave absences. The clinical significance of the focal discharge (in association with generalized bursts) remains unclear.

Adolescent↗
PubMed1993

[Subacute encephalopathy with seizures in chronic alcoholism].

We report a case of subacute encephalopathy with seizures in chronic alcoholism (age 34 years). This syndrome clearly differs from the known neurological complications of chronic alcoholism. One of the authors has observed (and reported) such cases in the Baltimore area. Subacute encephalopathy is characterized by lethargy, confusion and neurological deficits such as hemiparesis, homonymous hemianopsia and aphasia. Epileptic seizures (generalized tonic-clonic, focal) are obligatory. The EEG shows very prominent slowing and periodic lateralized paroxysmal discharges (PLEDs). The condition is complicated by a variety of internal-medical complications. Structural neuroradiological tests are either normal or irrelevant. The cause and pathogenesis remain obscure. The subacute course ends with gradual resolution.

Adult↗
PubMed1992

Dextromethorphan and high-dose benzoate therapy for nonketotic hyperglycinemia in an infant.

To test the hypothesis that nonketotic hyperglycinemia causes overstimulation of the excitatory N-methyl-D-aspartate receptor by allosteric glycine activation, and that reduction of glycine and blocking of the cation channel coupled to the receptor would be beneficial, we administered benzoate and dextromethorphan, a blocker of the N-methyl-D-aspartate channel to an infant with nonketotic hyperglycinemia. Therapy with benzoate, 500 mg/kg per day, was started on day 5, and the dosage was increased to 750 mg/kg per day on day 8, with prompt normalization of the neurologic and electroencephalographic findings. The glycine concentrations in both plasma and cerebrospinal fluid were substantially reduced. Dextromethorphan was added to the regimen on day 12. The electroencephalogram remained normal until the infant was 8 months of age, when diffuse slowing became apparent. Serial brain magnetic resonance imaging showed delayed myelination. At 12 months of age, physical examination findings and growth were normal except for hypotonia. The developmental quotient was approximately 60, and the child was free of seizures. This outcome, although not ideal, is better than that typical for nonketotic hyperglycinemia. Our results suggest that trials with additional patients and other N-methyl-D-aspartate cation channel blockers are warranted.

Benzoates↗
PubMed1992

Asymptomatic HIV infection does not cause EEG abnormalities: results from the Multicenter AIDS Cohort Study (MACS)

We conducted EEG testing in 200 asymptomatic homosexual men, half of whom were HIV seropositive. We chose to include half of the subjects because they were rated as impaired on a neuropsychological screening test. We used both traditional visual EEG interpretation and quantitative EEG analysis. Abnormal EEGs and borderline degrees of EEG slowing occurred in 32% of these men. These EEG changes were not related to HIV serostatus. EEG changes did correlate with the impaired neuropsychological test performance. Clinicians faced with abnormal EEG results or borderline EEG slowing in an asymptomatic HIV-seropositive patient should not attribute the EEG change to effects of the serostatus itself but should look for other causes.

Acquired Immunodeficiency Syndrome↗
PubMed1991

Electroencephalogram and seizures in chronic alcoholism.

CNS complications of chronic alcoholism are frequently difficult to assess due to the variety of direct and secondary conditions which can result from alcoholic drinking and lifestyles. The influence of alcoholism and alcohol-related factors on the EEG of patients with chronic alcoholism was studied in 213 patients (15.4% of all adults who had EEGs) using visual analysis. The influence of a variety of alcohol-related factors - drinking history, clinical complications, traumatic head injuries, head CT findings and laboratory results - on the EEG and alcohol-related seizures was studied. The effect of EEG results on the decision to treat alcohol-related seizures was also assessed. 152 of the patients had seizures, mostly (90% of those with defined seizure types) generalized tonic-clonic seizures. 53% of all seizures occurred in the early withdrawal period (8 h to 7 days abstinence). A history of partial seizures was significantly associated with findings of focal EEG abnormalities, a history of head injuries and structural lesions on CT. The clinical significance of these findings was unclear, however, as the majority of patients who had focal EEG abnormalities or structural brain lesions still appeared to have generalized withdrawal seizures. The EEG and CT appeared to be complementary tests: for most patients, focal abnormalities were demonstrated on only one of the two tests. The majority of patients (56%) with normal EEGs had predominantly low voltage recordings (less than 25 muV), compared with 13.9% of 1167 patients without a history of alcoholism (P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Crossover phenomena in epileptic syndromes of childhood.

Benign Rolandic epilepsy (BRE) and primary generalized epilepsy (PGE) are found at about the same period of childhood. Crossover from PGE to BRE and vice versa may occur; two short case reports provide further evidence for this development. Hence, transitions from a primarily generalized to a focal (partial) epileptic seizure disorder and vice versa is a possibility. Both PGE and BRE are based upon states of hyperexcitability, i.e. dysfunctional rather than structural abnormalities that are capable of changing their spatial distribution.

Child↗