Jack D. Grabow

SEIZURES AFTER HEAD TRAUMA: A POPULATION STUDY

A cohort of 2747 patients with head injuries was followed for 28,176 person-years to determine the magnitude and duration of the risk of posttxaumatic seizures. Injuries were classified as severe (brain contusion, intracerebral or intracranial hematoma, or 24 hours of either unconsciousness or amnesia), moderate (skull fracture or 30 minutes to 24 hours of unconsciousness or amnesia), and mild (briefer unconsciousness or amnesia). The risk of posttraumatic seizures after severe injury was 7.1% within 1 year and 11.5% in 5 years, after moderate injury the risk was 0.7 and 1.6%, and after mild injury the risk was 0.1 and 0.6%. The incidence of seizures after mild head injuries was not significantly greater than in the general population.

The incidence, causes, and secular trends of head trauma in Olmsted County, Minnesota, 1935–1974

Records in the Mayo Clinic linkage system were reviewed to determine the incidence of head trauma in Olmsted County, Minnesota, from 1935–1974. Minimum criteria for inclusion—loss of consciousness, posttraumatic amnesia, or skull fracture—were met by 3587 cases. During the decade from 1965–1974, the age-adjusted incidence rates per 100,000 population were 270 in males and 116 in females. The rate was highest—658—in males aged 15 to 24, but it was at least 50 in all age and sex groups. Major causes of head injury were automobile accidents (37%) and falls (2%). The incidence of head injuries related to automobiles and recreation has been increasing, whereas most other categories have remained stable or have declined. Of all cases, 446 were fatal, the average annual incidence being 32 per 100,000 in males and 9 per 100,000 in females. Among the groups at high risk of head trauma are those who have had head trauma previously.

Head trauma and subsequent brain tumors.

A long term study of 2,953 persons with 29,859 person-years of follow-up after head injury provided an opportunity to investigate the long-debated association between head trauma and subsequent intracranial tumor. In this series the observed number of cases of subsequent brain tumor did not differ from the number we expected. Because brain tumors are relatively rare, the results of this large series cannot absolutely refute the possibility that head trauma predisposes to brain tumor, but the individual risk is very small, and the weight of evidence does not support an etiological association. The occurrence of subsequent brain tumors in this series was not associated with the severity or location of the head injury. Head trauma does not seem to be a significant etiological factor in meningioma; that tumor has a higher incidence in females, whereas males have 2- to 3-fold greater incidence of head trauma. If any association between head trauma and subsequent brain tumor does exist, it is extremely small or occurs only in the presence of other factors, which themselves must be rare.

California arbovirus encephalitis in children.

UNTIL RECENT YEARS three principal arboviruses, Eastern, Western, and St. Louis, have been associated with human encephalitis in the United States. Since 1964, a considerable number of symptomatic cases of encephalitis associated with California encephalitis virus (C.E.V.) infections have been reported from this country, primarily from Wisconsin and other Midwestern states. It has been the most common arthropod-borne viral infection found in Wisconsin residents. This paper reports clinical and follow-up studies of 35 children with central nervous system disease associated with California encephalitis group virus infection.

A comparison of EEG activity in the left and right cerebral hemispheres by power-spectrum analysis during language and non-language tasks

In 10 female subjects, power-spectrum analysis was performed on the alpha activity elicted during the resting state, 4 right hemispheric tasks, and 3 left hemispheric tasks. The data were treated in 3 ways: approach 1, comparing the right and left hemispheric alpha activity; approach 2, comparing the right and left hemispheric alpha activity adjusted for the resting state; and approach 3, comparing the right and left hemispheric alpha activity adjusted for the previous task. Approaches 1 and 2 revealed few significant differences in the alpha activity of the hemispheres, but approach 3 provided data that better fit the theory of decreased power spectrum of attenuation of activity in the activated hemisphere. Thus, approach 3 may be useful in developing an electroencephalographic test for determining cerebral dominance for language.

Summated potentials evoked by speech sounds for determining cerebral dominance for language.

Ten normal adult right-handed subjects receive phonemic combinations (/epik/, /epak/, /a/, /pi/, /pa/) and pure tones (2500 and 8000 Hz) binaurally through matched earphones. Fifty responses from electrodes at P5, P6, C5, C6, F7 and F8 (referenced to linked mastoids) were summated, and evoked potentials from homologous areas were measured separately and superimposed in order to observe differences. Visual inspection of superimposed responses showed no consistent gross asymmetries that lateralized to either hemisphere. Comparison between amplitude of evoked potentials (N1, P2) at P5 and P6 were not significant (P < 0.05; paired t test). We suggest that our technique may not be a useful clinical test for cerebral dominance.

Transmissible mink encephalopathy agent in squirrel monkeys: Serial electroencephalographic, clinical and pathologic studies

A p ogressive neuro logic disease in squirrel, rhesus and stumptail monkeys has been produced by means of a transmissible mink encephalopathy (TME) agent.’.’ Gibbs and associates” have tentatively classified this agent as a member of the subacute spongiform viral encephalopathy agents, which also include those that produce scrapie in sheep and kuru and Jakob-Creutzfeldt disease in man. The disease in mink was originally described in Wisconsin4 and subsequently has been reported in Idaho,s Ontario6 and East germ an^.^ It is characterized by a 9 to 12 month incubation period and progressive cen tral nervous system disturbances. The elect roencephalographic (EEG) evidence o f disease in mink precedes the clinical onset by 39 days (mean) and consists of a slowing of the normal ( 5 o r 6 H z ) background activity to between 2.5 and 5 Hz.” N o periodic complexes are seen. Histologically, the lesions are limited to the central nervous system and consist of diffuse vacuolation of the gray matter, astrocytosis, and varied degrees of neuronal degeneration .* No inflammatory response o c Neurology / Volume 23 /August 1973 820 curs in tissues, and no specific antibody response in serum has been found. Serial EEG studies done in a small series of primates inoculated with the TME agent revealed that generalized slowing of the background activity preceded clinical signs of disease.z No periodic complexes were seen in this group. Due to lack of immune response, serial EEG studies have been the most reliable clinical method of evaluating the onset of preclinical encephalopathy in animals susceptible to the TME agent. To develop a single primate model for a comparative study of neurologic, pathologic and immunochemical responses to different slow-virus agents affecting man, we initiated a more extensive EEG and clinical investigation of squirrel monkeys. We reviewed 562 EEG

Posterior cerebral epilepsy: special considerations

Abstract Surgical treatment for epileptic seizures emanating from the posterior cerebral cortex (occipital, parietal, posterior temporal areas) is less common than for seizures from the anterior temporal and frontal regions. The diagnosis entails integrating the combination of clinical, electrographical, neuropsychological, and imaging studies. Extremely important is the knowledge of the pathways of possible suprasylvian spread anteriorly toward the central sulcus of the frontoparietal cortex (producing focal sensory/motor symptoms) or to the midline, reaching the supplementary motor regions (postural, bilateral asymmetrical limb girdle, focal tonic, vocalization, speech arrest, etc.). There can be infrasylvian spread to the lateral temporal cortex or, very frequently, to the mesial temporal regions such as the hippocampus and amygdala (expressing experiential phenomena and automatisms). For a patient with a single occipital lobe focus suggested by a visual aura or hemianopic field defect, for example, the anterior spread could follow different pathways and gives a clinical and electrographic appearance suggesting multiple focal seizures, thus causing confusion for less informed epileptologists. The problem of anterior spread has been known since the pioneering days of epilepsy surgery by the late Wilder Penfield, Herbert Jasper, and associates at the Montreal Neurological Institute (see case studies in the 1954 text Epilepsy and the Functional Anatomy of the Human Brain) and the extensive metrazol activation studies by Ajmone-Marsan and Ralston [C. Ajmone-Marsan, B.L. Ralston, The Epileptic Seizure: Its Functional Morphology and Diagnostic Significance. A Clinical–Electrographic Analysis of Metrazol-Induced Attacks, Charles C. Thomas, Publisher, Springfield, 1957]. These concepts have been rediscovered and elaborated upon by several investigators. In the past, as emphasized by Penfield, Jasper, and their associates, the epileptic focus was excised along with all or most of the lesion, depending on the proximity to vital cortex such as speech and motor areas. Various lesions, including tumors, cortical dysplasias, gliosis, angioma, and hippocampal sclerosis, can produce an epileptic focus, and the exact mechanism for lesion-induced epileptogenesis is still unknown. In recent years, lesionectomy alone has been performed by some investigators without searching for and excising the epileptogenic focus. These procedures have been enhanced by the development of stereotactic surgery with computer-assisted procedures. With the patients head fixed in a frame, refined imaging studies can display on a screen three-dimensional views of the brain, vasculature, and lesion. The best results have shown a significant reduction in the number of seizures or even no seizures in about 90% of patients, but longer follow-up is needed. In some reports, patients presented with complex partial seizures, and anterior temporal lobectomy was performed to remove the secondary epileptogenic activity within the hippocampus and amygdala, structures that frequently are the destination for spread from more posterior lesions. To improve seizure control, a second surgical procedure was often necessary to remove the posterior lesion and epileptic surround. At times, intracranial electrode grids and strips were inserted during a previous craniotomy, which meant that some patients had up to three surgical procedures. In planning posterior surgery for epilepsy, it is important to individualize each case rather than follow fixed ideas about surgical management emphasized by each major epilepsy center. The following case serves as an example. While I was temporarily at the University of Washington after retiring from the Mayo Clinic, a neurologist in Spain referred a 16-year-old girl to me. The imaging studies showed a left posterior lesion (occipital, parietal, and posterior temporal). On scalp EEG recordings, a recorded seizure emanated from that area. However, the patient also had complex partial epilepsy (CPE), and interictal EEGs showed anterior temporal spikes as well as temporal intermittent rhythmic delta activity (TIRDA), which has a very high specificity for CPE [Can. J. Neurol. Sci. 16 (1989) 398]. The neuropsychological and intracarotid amobarbital studies for language and memory performed by Dr. Dodrill showed left cerebral dominance for language and no contraindications for surgery. Craniectomy was performed by Dr. George Ojemann. After the eloquent cortex for language and motor function were identified with cortical mapping procedures, electrocorticography was performed. Multicontact strip electrodes recorded epileptiform activity from the hippocampus as well as the TIRDA pattern there. Surgical resection included the left anterior temporal lobe and hippocampus. Most of the gliotic lesion was excised by tunneling from the mesial temporal region toward the lesion, preserving the convexity of the posterior cerebral cortex. This single surgical procedure tailored to the individual patient reduced postoperative morbidity and was successful because after 7 years of follow-up, there is excellent control of seizures. She recently graduated from college, drives an automobile, and has taken an internship in theater as a preliminary step toward employment. This report emphasizes both the primary focus (the posterior lesion) and the possible spread anteriorly to a secondary focus. On the basis of the clinical, imaging, electrographical, neuropsychological, and amobarbital findings, the surgical treatment should be individualized with the goal of removing, when possible, both the lesion with its primary focus and the secondary focus, optimally during a single craniotomy. “For every complex problem, there is a solution that is simple, neat, and wrong”. H.L. Mencken (1880–1956)