Debra Elliott

Seizures caused by nontraumatic parenchymal brain hemorrhages.

Seizures occurred in 15% of patients with parenchymal brain hemorrhage (early in 12% and delayed in 3%). Seizures were most frequent with lobar hemorrhages and uncommon with deep subcortical hemorrhages. Lobar hemorrhages in the frontal, parietal, or temporal region were more commonly associated with seizures, whereas occipital hemorrhages were not. Seizures were most common if the hemorrhage was due to an aneurysm, angioma, or neoplasm and less common if hypertensive or spontaneous. If the patient had recurrent seizures or developed delayed seizures, CT showed that the hemorrhage evolved to a hypodense appearance; if the seizure did not recur, CT showed that the hemorrhage evolved to an isodense appearance.

Quaternary Epitope Specificities of Anti-HIV-1 Neutralizing Antibodies Generated in Rhesus Macaques Infected by the Simian/Human Immunodeficiency Virus SHIVSF162P4

ABSTRACT Monoclonal antibodies (MAbs) that neutralize human immunodeficiency virus type 1 (HIV-1) have been isolated from HIV-1-infected individuals or animals immunized with recombinant HIV-1 envelope (Env) glycoprotein constructs. The epitopes of these neutralizing antibodies (NAbs) were shown to be located on either the variable or conserved regions of the HIV-1 Env and to be linear or conformational. However, one neutralizing MAb, 2909, which was isolated from an HIV-1-infected subject, recognizes a more complex, quaternary epitope that is present on the virion-associated functional trimeric Env spike of the SF162 HIV-1 isolate. Here, we discuss the isolation of 11 anti-HIV NAbs that were isolated from three rhesus macaques infected with the simian/human immunodeficiency virus SHIVSF162P4 and that also recognize quaternary epitopes. A detailed epitope mapping analysis of three of these rhesus antibodies revealed that their epitopes overlap that of the human MAb 2909. Despite this overall similarity in binding, however, differences in specific amino acid and glycosylation pattern requirements for MAb 2909 and the rhesus MAbs were identified. These results highlight similarities in the B-cell responses of humans and macaques to structurally complex neutralization epitopes on related viruses, HIV-1 and SHIV.

Intracerebral hemorrhage following electroconvulsive therapy

Muscle relaxants and anesthetic agents are given with electroconvulsive therapy (ECT) to prevent traumatic injuries during convulsion. Cardiovascular or cerebrovascular complications may develop in high-risk patients who are hypertensive or have other cardiac disorders and undergo ECT.’ We now report a patient who developed an intracerebral hemorrhage (ICH) during ECT. Case report. A 69-year-old woman was admitted for ECT. She had several recent episodes of depression that had responded to antidepressant medication; however, recent depression had lasted 4 months without improvement despite treatment with amitriptyline, imipramine, lithium, fluoxetine, and alprazolam. She was nonfunctional and required hospitalization. The patient had no family history of dementia or psychiatric illness, had no recent head trauma, was not hypertensive, and had no prior cerebrovascular symptoms. She did not drink alcohol. When initially admitted to the hospital, her mental state was consistent with severe depression. She had no memory impairment or clinical dementia. Chest radiograph and ECG were normal. Laboratory studies, including complete blood count, platelet count, prothrombin time, partial thromboplastin time, and erythrocyte sedimentation rate, were normal. ECT was performed on four occasions. The patient was induced with etomidate, and succinylcholine was used for muscle relaxation. Following the first three treatments, the patient had confusion for 15 minutes. After the fourth ECT, confusion lasted 4 hours. She also reported that her vision became blurred and she bumped into objects on her right side. She reported no headache or nausea. Neurologic examination showed right homonymous hemianopia, right pronator drift, right-sided Babinski’s sign, and recent memory impairment. During ECT, her b l d pressure was recorded at 120 to 135 mm Hg systolic and 60 to 80 mm Hg diastolic. She had no signs of head injury. Laboratory studies, including complete blood count, coagulation profile, collagen vascular studies, ECG, and echocardiogram, were normal. CT showed a left parieto-occipital hemorrhage with no abnormal enhancement (figure, A). Four days later, she awakened from sleep feeling “strange,” and she had bitten her tongue. EEG showed left posterior hemisphere slow-wave activity without spike discharges. Anticonvulsant therapy was initiated with phenytoin for a presumed seizure, and no further seizures occurred. One week later, CT showed that the hemorrhage was resolving. MRI showed the hemorrhage with surrounding edema, but there was no evidence of neoplasm or arteriovenous malformation (figure, B). Four months later, she had no more seizures and visual field examination showed improvement. Depression was markedly improved, and she had no cognitive or memory impairment. No further ECT had been performed. She now lives independently. Discussion. The well-described adverse effects of ECT are acute confusion and memory impairment.’ It is controversial whether ECT causes structural brain damage.2-4 There have been reports of localized edema, gliosis, and petechial hemorrhages located directly underneath the electrode site.* The most common systemic complications of ECT are cardiovascular. When the electrical stimulus is applied without atropine pretreatment, there is vagal activation which causes bradycardia and hypotension. When the electrical seizure occurs, there is increased sympathomimetic activity, causing increased arterial blood pressure and tachycardia.’ This patient was not hypertensive and had no other cardiovascular disease, however, during the course of ECT she developed a lobar hemorrhage. The CT and MRI findings showed no characteristics to indicate traumatic hemorrhagic contusion or hemorrhagic infarction from a potential cardiac embolism. Without angiography, we cannot rule out an “occult” vascular malf~rmation.~ The blood coagulation profile showed no evidence of coagulopathy. The etiology of the ICH could not be determined. When an elderly normotensive patient develops a nontraumatic lobar ICH, the possibility of cerebral amyloid angiopathy (CAA) should be ~onsidered.~,~ There was no documented evidence of acute hypertensive episodes during ECT however, it is probable that CAA patients have fragile vessels that are particularly sensitive to even mild blood pressure elevations that may have occurred during ECT. In summary, we describe an elderly normotensive woman who developed medically refractive depression and suffered nontraumatic parieto-occipital hemorrhage following ECT. Since CAA is an increasingly recognized cause of behavioral change in elderly patients, it is important to consider this condition as a cause of ICH in elderly patients, especially if ECT is being considered.

Putaminal hemorrhage: clinical-computed tomographic correlations.

SummaryNinety-two percent of 100 patients with putaminal hemorrhage were hypertensive. Of the eight normotensive patients, seven were substance abusers or had bilateral putaminal hemorrhages. The one other normotensive patient was less than 40 years old. The 100 hemorrhages had the following locations: 1. medial putaminal (17 cases; six were normotensive and less than 40 years old and five were substance abusers); 2. lateral putaminal extending through the external capsule (eleven cases); 3. putaminal-capsular and subcortical white matter (32 cases); 4. putaminal cerebral hemispheric (19 cases); 5. putaminal-thalamic (19 cases); 6. bilateral (two cases). A disproportionate number of black patients suffered hematoma extension to the cerebral hemispheres or thalamus (46%) compared to Caucasians (23%). Overall mortality was 20% (17 blacks and three Caucasians) and occurred in patients with hematoma extension to the thalamus or cerebral hemispheres. Contrast-enhanced CT was performed in all 100 patients and provided no additional diagnostic yield. This indicates limited use for enhanced CT in hypertensive patients with putaminal hemorrhage who have a characteristic appearance of the acute hemorrhage on the nonenhanced CT.

Intraventricular hemorrhage in adults : clinical-computed tomographic correlations

The clinical and computed tomographic (CT) findings in 100 consecutive adult nontraumatic intraventricular hemorrhage (IVH) cases are analyzed. There were 74 parenchymal brain hemorrhages with secondary ventricular extension. The ventricles were filled with blood and asymmetrically enlarged. If the hemorrhage involved putamen, cerebellum, pons, or subcortical cerebral hemispheric white matter, IVH was associated with large parenchymal hematomas; these patients had poor clinical outcome. With thalamic or caudate hematomas, IVH frequently occurred with large hematomas but may occur with small hematomas. The small hematomas were located directly contiguous to the ventricular walls and caused extensive ventricular blood. Patients with small thalamic and caudate hemorrhage with intraventricular blood had good clinical outcome; whereas patients with large hematomas had poor outcome. Primary IVH occurred in 24 cases. In these cases, blood was seen in all ventricular chambers. Aneurysms involving the anterior cerebral-anterior communicating artery region were the most common etiology for primary IVH.

St. Louis Encephalitis with Focal Neurological Signs

St. Louis encephalitis (SLE) is a form of epidemic encephalitis named for a 1993 outbreak in that Missouri city when 11000 cases occurred; the fatality rate during this epidemic was ∼20% [1]. Although it is the most common type of viral encephalitis, !1% of patients present for medical attention [2]. Symptoms are usually nonspecific and consistent with those of viral meningitis. The virus causing SLE is distributed throughout the United States, and similar viruses exist worldwide. The disease is spread by Culex species mosquitoes, hence the primary risk factor is mosquito exposure. Focal neurological signs are extraordinary: to our knowledge, there are no previous reports of SLE with focal neurological signs in the medical literature. Here we report the case of a young man who presented with delirium and focal neurological signs attributable to SLE. A 33-year-old man was admitted to the hospital with weakness and delirium. Two days before admission, the patient complained only of dizziness. On the day before admission, he had a right footdrop. He was seen at an emergency department and was discharged. He woke up the next morning with right lower extremity paralysis and was admitted to another institution. The patient had no significant medical history and had not traveled for several months from northern Louisiana. He regularly abused alcohol and occasionally abused illicit (not intravenous) drugs. His temperature was 38.47C. He was anxious and agitated but cooperative. The right lower extremity strength was graded 1/5 with areflexia; the left lower extremity strength was graded 2/5 with hyporeflexia. The remainder of the physical examination was unremarkable. Pertinent findings included a negative urine toxicology screen, and the serum chemistry analysis was normal. Lumbar puncture revealed CSF with a WBC count of 484/mm (75% lymphocytes, 23% polymorphonuclear cells, and 2% monocytes), an RBC count of 21/mm, a glucose level of 48 mg/dL, and a protein level of 87 mg/dL. CT of the head and spine with contrast medium was unremarkable. On hospital day 2, the patient became delirious. Thereafter, his condition was stable for 10 days, and he was transferred to our hospital. At that time, all cultures and an ELISA for HIV were negative. At our institution, his mental status varied. The right lower extremity was paralyzed with areflexia; the left leg had 2/5 strength with hyporeflexia. Results of the remainder of the physical examination were normal. Magnetic resonance imaging of the head and spine with contrast medium was unre-

Massive putaminal-thalamic nontraumatic hemorrhage

Fourteen patients developed massive putaminal-thalamic hemorrhage. All patients were young black men. They were hypertensive but without chronic hypertensive vascular changes. They had been treated with antihypertensive medication for less than 3 yr. All patients presented with a prodromal headache beginning 18-30 h before the brain hemorrhage. Initial clinical signs were heralded by a change in the headache pattern and vomiting. All patients became comatose and hemiplegic within 4-12 h. CT showed a hyperdense putaminal-thalamic hemorrhage which was 60 to 86 mm in maximal diameter. There was marked mass effect with secondary intraventricular extension. All patients died within 72 h, despite rapid and adequate blood pressure control and maximal medical treatment of cerebral edema and increased intracranial pressure.

Nontraumatic temporal subcortical hemorrhage

SummaryThirty patients with temporal hematomas were analyzed. Four with frontal extension survived. Of 6 with ganglionic extension, three had residual deficit. Of 8 with parietal extension, 4 had delayed deterioration and died, two patients recovered, and two with peritumoral hemorrhage due to glioblastoma multiforme died. Five patients with posterior temporal hematomas recovered. In 7 patients with basal-inferior temporal hematomas, angiography showed aneurysms in 3 cases, angiomas in 2 cases and no vascular lesion in 2 cases. Of 23 cases with negative angiography and no systemic cause for temporal hematoma, 12 patients were hypertensive and 11 were normotensive. Ten hypertensive patients without evidence of chronic vascular disease had the largest hematomas, extending into the parietal or ganglionic regions. Seven of these patients died; 3 had residual deficit. Eleven normotensive and two hypertensive patients with evidence of chronic vascular change had smaller hematomas. They survived with good functional recovery.

Nontraumatic posterior temporal lobe hemorrhage: Clinical computed tomographic correlations

Ten patients with nontraumatic posterior temporal hematomas were analyzed. These hemorrhages were spontaneous (four cases) or hypertensive (six cases). With right posterior temporal hematomas, headache and confusion of sudden onset were the initial common characteristic clinical signs. The absence of prominent lateralizing neurological deficit simulated a diffuse toxic or metabolic encephalopathy. With left-sided hematomas, Wernicke-type aphasia was the initial feature. The 10 hematomas were 1.8 to 2.8 cm in maximal diameter. In these 10 cases, clinical outcome was good, as all patients survived and the hematoma resolved spontaneously.

Eclampsia: A Pediatric Neurologic Problem

Eclampsia is a syndrome of hypertension, proteinuria, edema, and neurologic manifestations such as seizures, focal deficits, or blindness occurring during pregnancy, mainly in primigravidas. Although it is not seen often in the pediatric population, it occurs with greater frequency among pregnant patients under the age of 15 than in the general population. Serious sequelae can be prevented with prompt and adequate treatment, including termination of pregnancy. (J Child Neurol 1989;4:55-60).