Hippocampic theta rhythm.

A prominent theta rhythm dominates the EEG of rodents such as rabbits, rats and mice. This rhythmical activity is preponderant in the hippocampus and may become quite widespread; it is usually arousal-related and generated by cholinergic mechanisms. This pattern has been intensively studied by experimental neuroscientists but is rather little known in circles of clinical electroencephalographers. Hippocampic theta rhythm is also found in canines and felines but at a clearly lesser degree and is practically absent in monkeys and humans. An olfactory memory of the macrosmatic rodents helps us understand "the world in which they live," their EEG patterns being an objective sign of their neuropsychology.

Vertebrobasilar artery insufficiency and electroencephalogram.

This is a renewed diagnostic approach to vertebrobasilar artery insufficiency (VBI)--a condition which stood in the focus of this author's interest several decades ago. The time for a revisitation has come. The EEG findings consist mainly of generally reduced voltage output and enhanced photic driving response. There is also some theta activity over anterior temporal and midtemporal region, but this finding is common in the early stage of all cerebrovascular disorders. Dysfunction of the pontine portion of the ascending reticular formation might be the cause of the lowered voltage output. The enhanced photic driving might be due to very light hypoxia of the visual cortex.

Akinesia and the frontal lobe.

A report of severe akinetic episodes in patients with Parkinson disease (PD) has been the stimulus for the following discussion of akinesia and its variants. Severe persistent akinesia may occur in frontal lobe impairment. Therefore, it is likely that extension of the Parkinsonian dysfunction into the frontal lobe causes severe akinesia which should be separated from the very common Parkinsonian hypokinesia. Another very common clinical phenomenon of PD is sudden freezing. Hence the frontal lobe--hardly regarded as a region of special interest in the realm of PD--can be the cause of severe and dangerous complications of PD. The term "arrest reaction" or "motor arrest" denotes a similar freezing. It is recommended to restrict these terms to certain forms of frontal lobe epilepsy. This discussion of hypokinetic and akinetic states should also include catatonia: a form of schizophrenia with a special type of akinesia. Though without major neuropathological substratum, this condition can, in extremely rare cases, lead to severe hyperthermia and fatal outcome (presumably via hypothalamic dysfunction).

Alzheimer disease: primary ischemia concept and promising therapy.

The important role of cerebral blood flow (CBF) in Alzheimer disease (AD) has been increasingly recognized in recent years. An abundance of data (The Rotterdam Study, see text) has shown the decline of CBF velocity with transcranial Doppler, confirming earlier data obtained with the xenon133 method. In spite of these data, AD is still considered a neurodegenerative disorder with secondary CBF changes. This work is a critical evaluation of earlier literature because of cogent reasons for the adoption of a new concept of AD as a primary ischemic disorder. Reports of lacking correlation between severity of CBF defi cit and degree of tissue damage or clinical fi ndings serve as evidence for primary ischemia because of the incompatibility with the concept of secondary ischemia.The CBF defi cit is thought to be due to the human upright gait in here dopredisposed individuals. As to therapy and prevention, a very simple, cheap and promising treatment is suggested (head-down-therapy).

Considerations of the ischemic basis and therapy of Alzheimer Disease.

A recently presented concept of Alzheimer disease (AD) is based on a primarily ischemic (rather than degenerative) type of brain disease. Etiologically, this new concept is presumed to be related to the human upright gait along with individual predisposition. The proposed treatment--head-down therapy (HDT) --is the centerpoint of this presentation: a simple and generally accessible type of therapy, with monitoring by neuropsychological questioning, electroencephalography, and transcranial Doppler. As a treatment of AD (limited to stage 1), HDT is expected to be helpful. It is possible, however, that its prophylactic use may be of even greater importance.

Alzheimer disease: caused by primary deficiency of the cerebral blood flow.

Alzheimer's disease (AD) is associated with considerably decreased cerebral blood flow (CBF) thought to be secondary, since dead neurons do not need oxygen and glucose. This view, however, needs to be critically re-examined. The role of CBF in AD was submitted to a thorough analysis, raising the question: "Is there really a lack of demand in the presence of undisturbed blood supply?" CBF decline is present in AD while the number of affected CNS systems is still quite small. The step-by-step evolution of AD mirrors a brain that progressively becomes ischemic. Areas related to memory function (hippocampus, temporal lobe cortex and vicinity) are bound to suffer first because of their particularly vulnerable blood supply. This is the scenario of a disorder caused by primary and not by secondary CBF deficiency--a deficiency perhaps attributable to the upright gait of homo sapiens. This new approach also opens new avenues for treatment and prevention, which will be briefly discussed.

Ultrafast EEG activities and their significance.

The true frequency range of the EEG is much broader than it has been assumed and taught for decades. The EEG apparatuses with inkwriting pens recording on paper are incapable of giving us trustworthy tracings beyond 80/sec. With the introduction of digital EEG machines, the exploration of the 60 to 1000 Hz range has already begun in the past few years (but, strangely enough, had been in use during the pioneer age when short photographic EEG recordings were made). The new wave of ultrafast recording began in the domain of somatosensory evoked potentials (SSEP). In the field of EEG (strictly speaking), research work started very recently. Ultrafast EEG activity promises new insights into the electrophysiological basis of epileptic phenomena. Activities from 150- to 500/sec have been noted in recent studies (including personal work). Faster frequencies (500-1000/sec) are likely to play a major role in the electrophysiology of neurocognition and motor initiation. Such EEG-based neurocognitive studies will provide us with in-real-time data and thus outperform PET scanning and functional MRI. Even ultrafast EEG activity has its limitation, which appears to lie around 1000/sec. Faster frequencies (1000-3000 Hz)--recorded mainly with cathode ray oscillography--are probably incompatible with the shortest duration of true field potentials and might be nothing but "neuronal chatter."

Clinical and EEG features of patients with EEG wicket rhythms misdiagnosed with epilepsy.

BACKGROUND: EEG wicket rhythms are 6- to 11-Hz medium-to-high voltage bursts that are sometimes misidentified as epileptogenic activity. The authors determined the clinical and EEG features of patients with wicket rhythms who had been incorrectly diagnosed with epilepsy. METHODS: Electroencephalographers at an epilepsy center re-read EEGs for patients referred for epilepsy management and identified patients with wicket rhythms. On further evaluation, the majority (54%; 25/46) of these patients were found not to have epilepsy. The authors compared the clinical and EEG features for the 25 patients with wickets and nonepileptic episodes with those of age- and sex-matched patients with partial-onset epilepsy using univariate and multivariate analysis. RESULTS: Several features distinguished patients with EEG wicket patterns and nonepileptic episodes (n = 25) from age- and sex-matched patients with epilepsy (n = 25): mid-adult age at onset of episodes (mean 38.4 years vs 19.8 years), prolonged clinical episodes (mean 155 minutes vs 2.3 minutes), and long duration of EEG wicket patterns (mean 0.66 seconds vs 0.11 second spikes). After controlling for other factors, patients without major confusion during episodes were unlikely to have epilepsy. CONCLUSION: Wicket patterns are often interpreted as epileptogenic. This distinctive EEG pattern should be considered in patients with clinical episodes atypical for epilepsy.

"Mu rhythm status" and clinical correlates.

Rolandic mu rhythm is usually limited to brief stretches of 0.5 to 2 sec duration. Two observations of status-like enhancement of mu rhythm have prompted this report. In both cases, 4-hour EEG-Video-Monitoring was used. Clinically, the reported cases differed considerably. Case 1 showed nearly continuous mu activity associated with general motionlessness: akinesia/amimia but without rigidity, caused by frontal lobe impairment due to multiple sclerosis. In Case 2, an impressive mu-status started in drowsiness and was presumably attributable to levitiracetam (which had rendered seizure-free the patient's formerly severe case of temporal lobe epilepsy). Mu rhythm status, thus far, is an unknown EEG entity. It can be caused by impaired fronto-motor input and may also constitute a medication-effect (levitiracetam).

The electrocerebellogram.

A revisitation of EEG studies derived experimentally from the cerebellum confirms the predominance of ultrafast activities but also shows various degrees of underlying slower frequencies (from the beta down to the delta range). Earlier personal work was based upon recording from the human cerebellum (and especially from fastigial and dentate nucleus) in connection with therapeutic cerebellar electrical stimulation. These patients suffered from intractable seizures (advanced cases of Lennox-Gastaut syndrome). Naturally, our recording technique in 1974 excluded the ultrafast range above 80/sec but failed to show activities in the upper beta range. In these cases, the severity of the seizure disorder caused structural impairment and ictal activity invaded the cerebellum. The electrocerebellogram is still insufficiently understood. An attempt at an analysis of known facts is being made. Further research in this field is needed.

The clinical relevance of EEG interpretation.

There is need nowadays to re-emphasize the capabilities of electroencephalography: a method representing the extremely important function/dysfunction-orientation in neurological thinking and practice. Valuable and relevant messages to the clinician naturally require solid EEG training and the resulting expertise. The idea that valuable EEG information is limited to the field of epileptology is erroneous. A plethora of clinically relevant messages can be derived from the EEG in nonepileptic conditions and, above all, in metabolic (and so called "mixed") encephalopathies where neuroimaging has almost nothing to offer. The discussion of EEG and epileptology only skirts pediatric conditions (and most of the epileptic syndromes). It is shown that EEG reading in epileptology is a lot more than simply "hunting spikes." A strong plea is being made against the presently fashionable overuse of the term "non-convulsive status epilepticus." Continuing neglect of functional/dysfunctional orientation can seriously endanger the entire field of Neurology.

Electrophysiology of the frontal lobe.

The electrophysiology of the frontal lobe appears to be unimpressive when the view is limited to the routine EEG recording of a healthy waking adult. There is usually low voltage fast activity, which becomes more pronounced when recorded with depth leads. Three special EEG patterns of marginal to slightly abnormal character are discussed: a) rhythmical midfrontal 6-7/sec activity of juveniles, b) rhythmical midfrontal sharp 4-6/sec activity of infancy and early childhood with arousal from sleep, and c) frontal intermittent rhythmical delta activity (FIRDA) in waking adults with frontopolar maximum, possibly related to thought processes under abnormal conditions. With extension of the frequency range, ultraslow (DC-like) as well as fast beta (gamma, 40-80/sec) and ultrafast activity (80-1000/sec) are found particularly over the frontal lobes. Ultraslow baseline shifts are arousal-related and mixed with overlying ultrafast waves. Attention control and the "working memory" involve chiefly the dorsolateral prefrontal cortex, investigated with P300 responses and likely to show ultrafast spectra. Perception-related 40-80/sec gamma activity has been thought to be associated with the entrance into consciousness. Initiation and design of motor activity spreads from prefrontal to the frontomotor cortex, associated with powerful event-related potentials: contingent negative variation (CNV) and "Bereitschafts potential" ("readiness potential," RP). Neuroscientific research of the highest frontal lobe functions has become a very active domain of neuroimaging. With the use of the extended frequency range, EEG and also evoked potential studies could add further information with acquisition in real time. Ultrafast frequency ranges presented in computerized frequency analysis and mapping might show impressive correlates of highest frontal lobe functions.

Mario Gozzano: the work of an EEG pioneer.

The study of the early history of electroencephalography can yield fascinating insights and surprises. A revisit to the work of Mario Gozzano (1898-1986) has proved to be particularly stimulating. His EEG study of 1935 is a classic and should be resurrected from the graveyard of history. Gozzano was an eminent clinical neurologist-epileptologist and chairman of the neurological-psychiatric university departments in Cagliari, Pisa, Bologna and, from 1951 to his retirement, in Rome. He quickly recognized the significance of EEG and produced his major experimental EEG work in the wake of a stay at the Berlin-Buch Brain Institute. His prolonged corticograms of various regions in the rabbit demonstrated striking differences between various cortical areas. Topical cortical strychnine produced spikes (a barely known phenomenon at that time) and the evolution from interictal to ictal spiking. Spikes induced by visual stimuli may be regarded as precursors of evoked potentials. While Hans Berger was a holist ("the brain working as a whole"), Gozzano (influenced by Vogt and Kornmueller) provided EEG support for the localizationists.

The epileptic pre-aura.

The term "pre-aura" is used for the designation of earliest pre-ictal manifestations that escape detection by conventional EEG and both objective and subjective behavioral signs. Fairly recent reports have indicated earliest pre-ictal vascular changes (perifocal ischemia and hyperemia) and also changes found in various methods of quantified EEG. These changes may precede the seizure onset (in conventional terms) by 1 to 20 minutes. There is good reason to assume that pre-auras are limited to focal epilepsies and do not occur in the various subforms of primary generalized epilepsy. The electrodecremental type of seizure onset, mostly found in the frontal region, could also denote a pre-aura in the earliest decremental phase. The very earliest pre-aura phenomena are most likely to be neuronal rather than vascular. Further proof could come with the use of ultrafast EEG frequency recordings.

Ultrafast frequencies: a new challenge for electroencephalography, with remarks on ultraslow frequencies.

EEG frequencies are not limited to the usual 0.5-70/sec (or 0.3-100/sec) range. In recent years, ultrafast activities between 100 and 1000/sec have been the topic of various studies with regard to physiological and paroxysmal conditions. Personal work on ultrafast frequencies in deep structures (elicited with pentylenetetrazol in rats) is mentioned in passing and will be the object of a special study. Other work focusing on the sensorimotor cortex and thalamocortical connections has proved to be seminal for ultrafast EEG research in conjunction with evoked responses (N20 response, SSEP) and experimental neurophysiological studies of afferent volleys, including those causing paroxysmal cortical responses. The well known decremental seizures with initially flat tracings require clarification with ultrafast recordings. In the physiological-neurocognitive domain, Pfurtscheller's event-related desynchronization might also benefit from the use of ultrafast recording. A plea for additional ultraslow recording (DC recording) is also being made, since paroxysmal flattening (electrodecrement) may be associated with an ultraslow negative baseline deflection. The combination of ultrafast (facilitated by digital technique) and ultraslow (technically difficult in patients, easier in experimental animals) would finally denote the frequency-wise complete EEG.

Frontal lobe disinhibition, Rett syndrome and attention deficit hyperactivity disorder.

Motor cortex hyperexcitability in Rett Syndrome (RS) has been ascribed to the failure of an inhibiting system arising from the frontal lobes, a system needed in childhood and early adolescence. It is also presumed that, on a virtually dysfunctional (nonstructural) basis, motor cortex hyperexcitability in ADHD is also due to insufficient frontal lobe inhibition ("lazy frontal lobe"). A series of schematic illustrations is added for the sake of easier comprehension of the presented concept.

Considerations of nonconvulsive status epilepticus.

The original concepts of absence status (AS) and complex partial status (CPS) are critically reviewed. This review has been prompted by a modern concept of nonconvulsive status epilepticus (NCSE), portrayed as a rather common condition occurring chiefly in the critically ill elderly with high morbidity and mortality. This new view is a striking departure from the original concepts of AS and CPS as rare protracted epileptic events occurring usually in temporarily confused but otherwise satisfactorily healthy and ambulatory patients. This new trend appears to have been caused by a misinterpretation of EEG findings: prominent generalized spike activity is in reality the expression of a very severe encephalopathy rather than of NCSE, most often caused by an anoxic episode. The role of EEG is emphasized but a valuable interpretation depends on an expert integration of EEG and clinical data. A brief discussion of epileptic twilight states further stresses the difficult differential diagnosis.

Absence seizures and the frontal lobe.

There is no doubt that the frontal lobe plays a major role in the 3/sec spike-wave absence seizure. It is pointed out initially that the controversies of cortical vs. thalamic origin of the spike-waves and the associated absence can be laid at rest as far as human absence seizures and human primary generalized epilepsy (PGE) are concerned: their origin is cortical with maximal frontal lobe involvement. Experimentally-induced spike-wave bursts or spontaneous spike-waves in animals pertain to other forms of epileptic seizure disorder. The frontal maximum of the 3/sec spike-wave pattern indeed indicates maximal frontal lobe involvement including both prefrontal and frontomotor portions. The absence as such is presumed to be a suspension of the working memory--an eminently frontal lobe function. This explains the immediate restoration of ictally-impaired neurocognitive functions right at the termination of the seizures. This concept can be applied not only to the classical absence occurring in PGE but also to the rare cases of secondary bilateral synchrony with a primary frontal epileptogenic focus leading to true (though very slightly different) absences.

The burst-suppression electroencephalogram.

The burst-suppression (BS) pattern of the EEG occurs in a rather limited number of conditions. It has been observed in deep stages of general anesthesia and in conjunction with sedative overdoses. It is also known to occur in the wake of cardiorespiratory arrest. Undercutting of the cortex has been found to result in BS activity. Rare neonatal epileptic encephalopathies also give rise to BS. Our personal interest was prompted by the consistent finding of BS activity in rats following cerebral anoxia (nitrogen inhalation, airway obstruction): after periods of EEG flatness, BS activity developed, followed by periodic bursts and diffuse slowing. On the other hand, earlier literature (before 1960) showed virtually no observation of BS, neither in anoxic patients, nor in animal experiments. It is likely that the introduction of modern intensive care treatment has engineered episodes of BS activity, probably due to modifications of the anoxic cerebral pathology.

Slow sharp waves.

Slow sharp waves (SSHW) are of longer duration (around 200 msec and longer) than typical sharp wave discharges (70 to 200 msec). This pattern is not merely of academic interest, as the electroclinical correlation showed that SSHW were found in 23 patients, mostly above age 50 years, with serious illnesses of various etiologies. Epileptic seizures occurred in a minority of the cases. The electrophysiological basis remains unclear and there is no answer to the question, "what causes the relatively long duration of these discharges?"