Biomedical subjects
Publications and source records attributed to D W Klass.
Focal cerebral lesions are often associated with voltage asymmetry of sleep spindles, usually with depressed voltage on the side of the lesion. In this report, we document a case in which a brain tumor was associated with a frequency asymmetry in addition to a voltage asymmetry of sleep spindles. The slower frequency spindles occurred on the side of the lesion.
We have studied 120 patients with EEGs that show defective reactivity of alpha activity in which one side fails to attenuate during the performance of mental arithmetic. The side of defective reactivity was the right side in 74 patients and the left in 46. A similar asymmetric reactivity of alpha activity to eye opening (Bancaud phenomenon) was seen in 32 patients. Also, 113 patients had lateralized EEG abnormalities on the side of defective reactivity and on the side in which cerebral lesions or disorders of cerebral function were present. The unilateral failure of alpha attenuation with mental concentration represents a subtle lateralized electrographic manifestation of cerebral dysfunction on the side of defective reactivity.
Since 1981, when we first described a group of patients with subclinical rhythmic electrographic discharge of adults (SREDA), we have seen 108 patients with SREDA. Nineteen of these patients had unusual or atypical features of SREDA. The typical pattern consists of a non-evolving theta rhythm occurring in a widespread manner but maximal over the parietal and posterior temporal regions and lasting for a few seconds to a minute without clinical manifestations or symptoms. The unusual variants consist of predominantly delta frequencies, notched waveforms, a frontal or more focal distribution, a more prolonged duration, and presence during sleep. There was no significant difference in the patient group that had the atypical pattern compared with those with the typical pattern. Although the mechanism of the SREDA is unclear, it appears to represent a benign EEG phenomenon that has little diagnostic significance and should be distinguished from seizure discharges.
Angelman's syndrome is a rare genetic disorder characterized by developmental delay, craniofacial abnormalities, ataxia, paroxysmal laughter, and seizures. The diagnosis is suspected in infants who have the characteristic clinical features and electroencephalographic (EEG) abnormalities and is confirmed by the genetic identification of a maternally derived 15q11-13 deletion. We report on 3 patients with genetically confirmed Angelman's syndrome who had the characteristic clinical and EEG features. The EEGs demonstrated high-amplitude 2- to 3-Hz delta activity, with intermittent spike-and-slow-wave discharges maximal in the occipital region in 2 patients and generalized sharp-and-slow-wave discharges, occipital spikes, and electrographic status epilepticus during slow-wave sleep in the other patient. The findings of generalized high-amplitude delta slowing and occipital spike-and-wave discharges, facilitated by eye closure, in children with developmental delay and seizures suggest the diagnosis of Angelman's syndrome and should lead to genetic testing.
A burst-suppression pattern on the EEG following anoxic insult is usually associated with a poor prognosis. Myoclonic jerks may accompany the electrographic burst. On rare occasions oral, ocular, or appendicular movements can be associated with bursts of EEG activity recorded following cerebral anoxic insult. At times these movements may cause confusion about the patient's state of consciousness or the purposefulness of the movements; they may mimic volitional movements in response to external stimuli. To better describe the variety of movements that may accompany bursts of EEG activity in comatose patients, we review 12 cases where movements occurred in association with the electrographic bursts.
Five patients had electroencephalograms (EEGs) that showed periodic epileptiform discharges in the midline (PEDIM); other than location, this activity has the same characteristics as periodic lateralized epileptiform discharges (PLEDs). All 5 patients had acute onset of partial motor seizures involving the lower extremity. The location of the PEDIM corresponded to the seizure type and focal neurologic deficits. All 5 patients had sustained a cerebrovascular insult, either old or new, and the PEDIM and seizures suggested an origin from the watershed area between the anterior, middle, and posterior cerebral arteries, involving predominantly the parasagittal region of the cerebral hemisphere.
We have identified a previously unreported subtype of periodic lateralized epileptiform discharge (PLED) characterized by periodic discharges arising from ipsilateral independent foci. All 4 patients had acute cerebral lesions, and 3 of them had focal motor seizures with secondary generalization. The site of localization of the PLEDs corresponded to the boundaries of the underlying structural lesion or lesions, and this, together with the variable temporal relationship between them, supports a cortical origin for PLEDs associated with underlying lesions. the spatial and temporal independence of these periodic discharges in combination with their association with (1) acute cerebral lesions. (2) altered consciousness and seizures, and (3) resolution with time leads us to propose the term "IpsiIPs" to describe this subtype of PLEDs.
PURPOSE: Episodic loss of consciousness presents a diagnostic challenge to the neurologist. A perhaps underrecognized cause of episodic loss of consciousness, which we call the ictal bradycardia syndrome, occurs when epileptic discharges profoundly disrupt normal cardiac rhythm, resulting in cardiogenic syncope during the ictal event. We attempt to determine whether the presence of the ictal bradycardia syndrome provides localizing information regarding the site of seizure onset and to describe the demographics of patients with this syndrome. We also discuss difficulties in diagnosis and treatment. METHODS: We review 23 cases of the ictal bradycardia syndrome from the literature and present four additional cases. Brief histories are provided for the four previously unreported cases. Where data are available, cases are analyzed with respect to age, sex, and site of seizure onset. RESULTS: Patients with the ictal bradycardia syndrome ranged from 4 months to 72 years (mean 39 years). There was an approximately 5:1 ratio of males to females. Twenty of the 23 patients (87%) whose site of ictal onset could be localized had temporal lobe epilepsy, although no clear lateralizing predominance was apparent. CONCLUSIONS: The ictal bradycardia syndrome should be considered in patients with unusual or refractory episodes of syncope, or in patients with a history suggestive of both epilepsy and syncope. It suggests seizure onset in temporal lobe, and is more commonly diagnosed in males. Diagnosis may be aided by ambulatory EEG/ECG monitoring. Cardiac pacemaker implantation along with antiepileptic drug therapy may be necessary to minimize the possibility of death.
We reviewed two series of patients with the phi rhythm (posterior rhythmic slow waves occurring after eye closure) to determine its characteristics and clinical significance. Phi rhythm was defined as a minimum of three consecutive monomorphic posterior delta waves occurring within 2 sec of eye closure on at least two occasions during electroencephalography. Group 1 consisted of 30 patients (16 male and 14 female) with a mean age of 11.6 +/- 8.4 years (range, 3 to 46 years) who were evaluated between 1978 and 1993. Phi rhythm most commonly occurred when the patient was alert and after concentrated visual attention, such as reading or picture or pattern scanning. Seventeen of these patients had epilepsy (11 generalized, 3 focal, 1 both, and 2 unclassified). The frequency of epilepsy was not significantly different from that of a control group of 60 patients matched for age and sex; however, generalized epilepsies were more common in the phi group (P = 0.008). Group 2 consisted of a previously unreported series of 121 patients evaluated between 1960 and 1962. A diverse range of underlying clinical diagnoses was evident in both groups. The mechanism of the phi rhythm is unknown, but the findings suggest that the origin is subcortical and that the presence of this activity should not be considered diagnostic of a seizure disorder.
The clinical and EEG findings in 20 patients with reading epilepsy (RE) diagnosed at the Mayo Clinic, Rochester, Minnesota, between 1949 and 1989 are documented in this study. Sixteen patients were followed for more than 10 years. The age at onset of RE ranged from 10 to 46 years (median 17.5 years). Precipitating factors other than reading, involving linguistic or non-linguistic higher cognitive processes, occurred in nine patients. Spontaneous myoclonus affecting the upper extremities, especially in the morning, indicated co-occurrence of juvenile myoclonic epilepsy (JME) in four patients. A positive family history for seizures (including one person with RE) was obtained for four patients. Interictal EEG abnormalities were present in 12 patients (60%). Ictal EEG findings were generalized and symmetric in 75% of patients, with a strictly focal (temporoparietal) discharge occurring in only two patients. Of the 11 patients who were alive and for whom recent information regarding seizure status was available, only three were symptom-free without anticonvulsant medication. Our data indicate resemblance of the clinical manifestations of RE with JME and other cognitive function-related seizures and point toward an overlap with them. We propose a classification for higher cognitive function-related epilepsies in general and RE in particular to explain the electrographic heterogeneity and clinical overlap observed. A hypothetical model to explain the ictogenesis and to encompass the electroclinical heterogeneity in RE is suggested.
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Temporal intermittent rhythmic delta activity (TIRDA) has been reported to be highly specific for diagnosing complex partial epilepsy. Of 12,198 electroencephalographic (EEG) recordings performed at the Mayo Clinic between May 1, 1990 and May 1, 1991, 33 records from 27 patients (18 women and nine men; mean age, 41.5 years; range, 13-82 years) showed TIRDA. Clinical seizures were diagnosed in all patients, and complex partial epilepsy was well documented in 23. In a control group of 100 patients without TIRDA and matched for age and sex, generalized seizures were diagnosed in 25 and partial seizures in 15. Differences between TIRDA and control groups were highly statistically significant. Focal temporal sharp waves or spikes occurred in 23 patients with EEG recordings that contained TIRDA; three of these patients also exhibited generalized atypical spike-and-wave discharges. Four patients had TIRDA but no other epileptiform activity, although earlier EEGs of three of these patients contained spikes or sharp waves. These findings confirm earlier work, and we conclude that TIRDA represents an important epileptogenic abnormality.
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Midazolam hydrochloride, a water-soluble benzodiazepine for intravenous injection, is frequently used to provide sedation to mechanically ventilated patients in the critical-care unit. Although the effects of midazolam on the electroencephalograms (EEGs) of healthy volunteers have been reported previously, to our knowledge such effects in ill patients have not been documented. Herein we describe the effects of intravenously administered midazolam on the EEGs of eight seriously ill patients (age range, 49 to 80 years; mean, 69 years). The EEGs showed drug-induced relatively fast (alpha or beta) frequency activity superimposed on delta slowing in six patients and mild to moderate voltage attenuation in three patients. An alpha frequency coma pattern, a transient burst-suppression pattern, and a spindle coma pattern were also seen. Thus, the effects of intravenously administered midazolam on the EEGs of seriously ill patients are similar to those noted after the administration of other benzodiazepines. These potential effects should be considered when their EEG tracings are interpreted.
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Some of the unusual patterns that can be encountered on the EEG are described briefly. The patterns are grouped according to the predominant frequencies involved and/or by distinctive morphology or distribution. Those involving predominantly the alpha frequency range are alpha squeak, retained alpha, alpha-delta sleep, unilateral decrease in reactivity of alpha activity, and extreme spindles. The patterns involving the beta frequency range are the fast alpha variant, posterior temporal fast activity in children, the fast spiky spindle variant, central fast activity, and diffuse paroxysmal or continuous fast activity. The patterns of predominant theta frequencies are the slow alpha variant, frontal arousal rhythm, rhythmic temporal theta activity of drowsiness, midline theta rhythms, and focal parietal theta activity. Activity in the delta range includes the transient rhythmic slowing occurring after eye closure and the more continuous posterior rhythmic slowing. Patterns with a distinct morphology or distribution include the breach rhythm, wicket spikes, zeta waves, periodic frontal sharp complexes, subclinical rhythmic electrographic discharge of adults, and the EEG pattern of holoprosencephaly.
Loss of consciousness is rare in the absence of transient or persistent insult to the diencephalon or mesencephalon. We found three patients with severe atherosclerotic stenosis or occlusion of both internal carotid arteries who experienced brief loss of consciousness. Common characteristics were the absence of clinical or electroencephalographic seizure activities, significant cardiovascular disease, or a history suggestive of vasovagal syncope. Angiographically, the patients had widely patent vertebrobasilar circulation and collaterals from vertebrobasilar to carotid circulation. Episodic loss of consciousness disappeared after carotid endarterectomy. We concluded that bilateral hemispheric ischemia caused brief loss of consciousness, but selective focal ischemia in the subcortical structures superimposed on widespread bihemispheric ischemia may have been responsible. Since loss of consciousness is rare in carotid occlusive diseases, systemic and vertebrobasilar causes must be carefully ruled out in each instance.
Acute encephalopathy and an abnormal electroencephalogram with a periodic sharp wave pattern developed in a 58-year-old woman shortly after she received a few doses of baclofen. The clinical and electroencephalographic abnormalities improved promptly after the medication was discontinued.