Biomedical subjects
Publications and source records attributed to K Elisevich.
Cranial settling and basilar invagination with medullospinal compression is believed to have resulted in the production of a syrinx in a case of Paget's disease of the cranium. This mechanism of compression at the craniovertebral junction resembles the development of syringomyelia in Chiari malformations presenting in adult life.
Injections of combined lectin-conjugated and unconjugated horseradish peroxidase were made in the dorsal (d) and ventral (v) divisions of the paramedian reticular nucleus (PRN), a precerebellar relay nucleus, of the cat. The origins of supramedullary afferent projections to the PRN were identified in the pons, midbrain and cerebral cortex using the transverse plane of section. The data indicate a segregation of input from a number of sites to the dPRN and vPRN. The interstitial nucleus of Cajal projects bilaterally to the dPRN and predominantly to the ipsilateral side. The vPRN receives only a unilateral projection from the ipsilateral nucleus of Cajal. Major afferent projections to the vPRN arise from the ipsilateral nucleus of Darkschewitsch and the intermediate layer of the contralateral superior colliculus. Neither of these sites projected to the dPRN. The raphe nuclei and medial reticular formation of the pons and midbrain contribute a moderate input to both divisions of the PRN. A moderate bilateral cerebral cortical projection arises from the first somatomotor area (SMI). The ventral coronal and anterior sigmoid gyri project mainly to the dPRN and vPRN respectively. Smaller afferent projections arise from the posterior sigmoid gyri and area 6 of Hassler and Mühs-Clement (1964) in the medial wall of the anterior sigmoid gyrus. Inputs from the accessory oculomotor nuclei, tectal regions and the first somatomotor cortex suggest a role in postural control for the PRN which may underlie its involvement in mediating orthostatic reflexes.
Seventy-eight carotid endarterectomy specimens were reviewed microscopically for the presence of mural capillary atheromatous emboli. Twelve specimens (15%) were found to contain these emboli. An attempt to correlate this finding with clinical and radiologic data yielded no evidence of an increased predisposition to recurrent transient ischemic attacks or stroke in the affected patients even in the absence of ulceration. Nevertheless, further attention must be given to defining the drainage patterns of such embolized mural capillaries and elucidating their role, if any, in the pathophysiology of stroke.
A 53-year-old woman with assimilation of the atlas to the occiput presented with paraesthesiae in the right half of her tongue and ipsilateral neck pain aggravated by head turning. After being intermittent for several years, the symptoms eventually became persistent and increasingly incapacitating. At operation, the C2 spinal nerves were found to be compressed by protuberant atlanto-axial joints, particularly on the right side. The superficial parts of the resected C2 spinal nerves showed a loss of both myelinated and unmyelinated nerve fibres. After operation, the patient experienced partial relief of her symptoms.
Intracranial tuberculomas may imitate, both clinically and radiologically, the more commonly observed intracranial tumors. This case report outlines the development of such a lesion masquerading as a typical meningioma of the frontal fossa. Discussion of intracranial tuberculomas follows, with special reference to clinical and radiological findings.
The messenger ribonucleic acid (mRNA) of gap junction protein connexin 43 was quantified in the tetanus toxin rat model of focal epilepsy following injection of toxin into the left amygdala. Animals were monitored electrographically at weekly intervals with bilateral amygdala electrodes. Cohorts of 3 rats were sacrificed at weeks 1, 2, 3, 4, 6, 8, and 10, and bilateral regions containing the amygdala and posterior cerebral cortex were sampled, frozen, and later pooled for northern blot analysis. Spike generation was manifest in all animals during the first 4 wk followed by variable attenuation and cessation by 10 wk. Electrode implantation alone was shown by regression analysis to cause significant (p < 0.05) elevation of connexin mRNA in weeks 1-4. Injection of toxin diminished connexin mRNA expression in the amygdala when compared to electrode implantation alone. No trend in connexin mRNA expression was established over time in either amygdala or cerebral cortex in the acute epileptic or chronic postepileptic phase. No association between connexin 43 mRNA expression and the development of epileptogenicity was found in the context of a self-limiting animal model of focal epilepsy.
The expression of mRNA for connexin 43, a gap junction protein putatively found in astrocytes, is studied in two experimental models of epilepsy: the electrically kindled rat and the tetanus-toxin-injected rat. Rats were kindled by electrical stimulation of the amygdala to Racine class 5 seizures and divided into cohorts of three to undergo 3, 6, or 10 such events, respectively. Another two cohorts of rats received injections of tetanus toxin at strengths of 3 and 9 MLD50, respectively, into the amygdala. Features of epileptogenicity were identified electrographically in both cohorts during the first 4 wk following toxin injection with spontaneous ictal events recorded in the latter cohort. All rats were sacrificed 4 wk after electrode or cannula implantation, except for two toxin-injected cohorts that were sacrificed at wk 8 or 10. The epileptogeonic area in the region of the amygdala was harvested and pooled by cohort for Northern blot analysis. These were compared with control nonimplanted tissues. In the tetanus-toxin-injected animals, at time-points of 4, 8, and 10 wk, connexin 43 mRNA expression in epileptogenic tissues is found to be decreased or unchanged relative to control cases. Kindled rats demonstrated reductions of connexin mRNA with a trend toward normalizing levels with increasing numbers of stimulations when compared to control animals. Connexin 43 immunostained sections of the basolateral amygdala showed a similar trend in protein expression. Both experimental models of epilepsy show no connexin 43 mRNA upregulation despite varying degrees of epileptogenicity. This study therefore does not support the hypothesis that an increase in transcription is the basis for any proposed increase in gap junction communication involving connexin 43 in the context of epileptogenicity or as a reaction to increased neuronal excitability.
Empirical evidence in the clinical literature suggests that ionizing radiation influences human epileptic behavior. A group of patients with tumor-associated epilepsy, biopsy-proven malignancy, and primary antineoplastic treatment with ionizing radiation was selected to evaluate this observation. The antiepileptic effect of ionizing radiation was examined in 9 patients presenting with malignant cerebral tumor and medically refractory partial seizures during at least 2 months. Tissue diagnosis was obtained by stereotactic biopsy without further surgery. Histological categories included anaplastic astrocytoma (5 cases), glioblastoma (2), lymphoma (1), and metastatic non-small cell carcinoma of the lung (1). All patients had medically refractory simple partial seizures with or without secondary generalization with frequencies of 3/week to 8/day for 2-7 months before completion of therapy. Fractionated radiation therapy by parallel opposed fields was delivered with a cumulative dose range of 3,000-6,600 cGy. One patient also had 125I brachytherapy with implant removal after 6 months. Five patients had a seizure-free outcome for periods lasting 2-12 months, whereas the remainder experienced a reduction in frequency of greater than 75% during a follow-up period of 3 months to 6 years. One patient with a glioblastoma remained seizure-free for 3 months and experienced 2 generalized seizures during tumor progression and clinical deterioration but otherwise remained under good anticonvulsant control until his death after 1 year. This review of cases of partial seizures attributable to an unresected malignant cerebral tumor indicates that ionizing radiation may have a favorable effect upon medically refractory partial seizures with significant reduction or elimination of seizures. Moreover, the effect lasts beyond the immediate and early postradiation period. The therapy may thus also lessen the propensity for cerebral tissue towards later epileptogenicity that gives rise to a partial seizure disorder.