Biomedical subjects
Publications and source records attributed to F T Nichols.
We undertook a prospective study of consecutive patients to determine the frequency of elevated IgG and IgM anticardiolipin antibodies in transient ischemic attack and ischemic stroke and found elevated IgG antibodies in 8.2% (9 of 110) and IgM in 9.1% (10 of 110), only the former being significantly greater than in a healthy control population. We suggest that anticardiolipin screening be concentrated on the young.
Ischemic stroke is a common and disabling complication of sickle cell disease (Hb SS). Most infarctions occur in the presence of intracranial stenotic lesions of the large vessels of the circle of Willis. Transcranial Doppler (TCD), by measuring flow velocity in these arterial segments, can detect focal stenosis on the basis of elevated flow velocity. We report the preliminary results of a prospective study to develop criteria for detection of stenotic lesions based on TCD and identification of patients with Hb SS at risk for stroke. Comparing the TCD findings from six patients with lesions demonstrated by angiography to those from 115 Hb SS children without stroke, we conclude: (a) middle cerebral (MCA), anterior cerebral (ACA), or internal carotid (ICA) artery mean velocities greater than 190 cm/s strongly suggest focal stenosis; (b) MCA or ACA mean velocities of 150 to 190 cm/s suggest abnormality but at present cannot be considered diagnostic of stenosis; (c) mean velocities up to 150 cm/s are possibly due to the effects of low hematocrit and/or young age, and cannot as yet be distinguished from velocity elevations due to vessel stenosis.
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Although a number of reports are available on the occurrence of headache in patients with ischemic cerebrovascular disease, most studies have recorded the frequency but not the specific sites of the pain. We report 18 patients who underwent balloon inflation in the distal internal carotid artery and middle cerebral artery stem during embolization therapy for intracerebral arteriovenous malformations. Eleven patients had reproducible patterns of headache during balloon inflation. Inflation in the proximal middle cerebral artery stem produced pain primarily in the ipsilateral temple, that in the middle of the middle cerebral artery stem produced pain referred primarily retro-orbitally, and inflation in the distal middle cerebral artery stem produced pain referred primarily to the forehead. Experimental studies have demonstrated similar patterns of referred pain. The fact that these areas of referred pain are so reproducible is of potentially great clinical importance in the approach to management of patients with cerebrovascular disease.
We studied heart rate following unilateral hemispheric inactivation by intracarotid amobarbital in 25 patients undergoing preoperative evaluation for epilepsy surgery. Heart rate increased after left hemisphere inactivation, but decreased following right hemisphere inactivation. The results are consistent with differential left/right cerebral hemispheric effects on autonomic function, and appear related to functional and anatomic asymmetries in both the central and peripheral nervous systems.
Clinical and necropsy findings in 11 patients with sickle cell anemia (SS) indicate that intracranial hemorrhage (IH) is a delayed sequela of the same vasculopathy that causes cerebral infarction during childhood. Evidence of prior cerebral infarction during childhood included hemiparesis, seizures, an episode of coma, or mental retardation. Computerized tomography (CT) scans showed cerebral infarcts with lucent areas and dilated ventricles or cerebral atrophy. CT or magnetic resonance imaging (MRI) scans after the intracranial hemorrhage demonstrated intraventricular or intracerebral hemorrhages. Angiography or autopsy in seven patients showed widespread vascular occlusion and narrowing of arterial vessels. Moyamoya with internal carotid artery occlusion was identified in two cases. At the time of the IH, three patients were being treated with prophylactic transfusion regimens. We hypothesize that the central nervous system vasculopathy progresses over time and that arterial narrowing in both large and small vessels secondary to endothelial hyperplasia is followed by neovascularization and hemorrhage. Recognition of this pattern of delayed intracranial hemorrhage following cerebral infarction should encourage more intensive evaluation aimed at developing rational interventional therapy prior to a terminal intracranial hemorrhage.
To investigate left/right asymmetries in cerebral gaze mechanisms, eye deviation was evaluated in 90 patients following intracarotid sodium amylobarbitone injections. For right-handed subjects with left cerebral language dominance, the occurrence and severity of eye deviation were greater for right versus left hemisphere injections. In contrast, subjects with mixed cerebral dominance for language/handedness exhibited no left/right difference in the incidence of eye deviation. The results are consistent with right cerebral dominance for attentional/intentional mechanisms directed at external space. Further analysis suggests that the cerebral asymmetry for gaze may be due to an evolutionary loss of attentional/intentional mechanisms by the left cerebral hemisphere as language function developed.
Takayasu arteritis, an occlusive arteritis usually involving the aorta and its major branches, occurs most commonly in young oriental women. The authors report the case of a 54-year-old caucasian woman with Takayasu arteritis who initially presented with the inflammatory manifestations of fever and markedly accelerated erythrocyte sedimentation rate. Over 2 months she developed evidence of vascular insufficiency with arm claudication, diminished radial pulses, and decreased blood pressure in the arms, suggestive of an occlusive arteritis. Arteriography revealed the typical findings of Takayasu arteritis, which involved the brachial and axillary arteries but spared the aorta and its major branches. Changes in the patient's clinical course were correlated with sedimentation rate, angiography, and Duplex sonography.
Bibrachial palsy is a distinctly unusual pattern of muscular weakness. We have described a woman who had a slowly progressive clinical course, with profound bibrachial palsy and neurogenic respiratory failure, but neurologically normal lower extremities. Autopsy revealed encephalomyelitis and a small previously undetected oat cell carcinoma with inflammatory infiltration. The pathologic features are consistent with an autoimmune process.
We investigated the relation of plasma lipids to the risk for ischemic stroke by comparing clinical and biochemical characteristics of survivors of cortical (n = 48) and lacunar (n = 36) brain infarction. By analysis of variance, no differences were observed in the concentrations of total cholesterol, triglycerides, low density lipoprotein cholesterol, very low density lipoprotein cholesterol, or apoproteins A1 and B. Patients with lacunar infarction, however, had higher concentrations of high density lipoprotein (HDL)-cholesterol than patients with cortical stroke. This HDL-cholesterol difference was due primarily to a strikingly low HDL-cholesterol content in white patients with cortical stroke. These data suggest that previously demonstrated differences in HDL-cholesterol concentrations between patients with ischemic stroke and control subjects without stroke may apply to patients with cortical but not lacunar infarction. Separation of cerebral infarction into subtypes based on mechanism may help clarify lipid-related risk factors in cerebrovascular disease.
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The P3 evoked potential has been linked to memory mechanisms, but its neuronal generators are uncertain. Transient global amnesia (TGA) is a disorder of recent memory that has been postulated to result from ischemia or focal seizures in the medial temporal lobes and/or thalamus. To our knowledge, this is the first report of a recording of P3 evoked potential and sphenoidal electroencephalogram during TGA. The tonal P3 was not decremented in comparison to P3 recordings one month and two years after recovery. Sphenoidal electroencephalogram was normal. The results suggest that the neuronal networks which generate the tonal P3 are not involved in the part of the memory system affected by TGA.
Virgil Sydenstricker was a member of a notable American family which included authoress Pearl S. Buck and the eminent epidemiologist Edgar Sydenstricker. Dr. Sydenstricker's contributions in the fields of hematology and nutritional disease are legion. His landmark work in sickle cell anemia characterized a definite symptom complex with specific hematologic findings and inheritance pattern. He wrote on the complications of malnutrition and attempted to delineate the specific effects of individual nutritional factors. Dr. Sydenstricker and his associate H. M. Cleckley first described the syndrome of niacin deficiency encephalopathy. Today, the syndrome is still occasionally reported. Niacin deficiency should be considered when unexplained acute confusional states or neurologic deficits occur in the setting of malnutrition, antituberculous drug use, or chronic partial nutritional deficiency with acute increase in metabolic demand.
We describe a case of homozygous sickle cell anemia in which noninvasive transcranial Doppler ultrasonography and magnetic resonance imaging were used to detect angiographically documented occlusive lesions of intracranial arteries.
Unilateral hyperhidrosis occurred contralateral to acute cerebral infarctions in six patients. Two patients had localized infarctions of opercular cortex, while the other four had large strokes involving both superficial cortical and deep subcortical structures. The unilateral hyperhidrosis typically involved the face and arm and was transient, lasting 1 to 3 days. No other autonomic dysfunction occurred. One patient died, and the others had significant residual neurologic disability, thus indicating poor prognosis when this sign is present. Disruption of a pathway of cortical origin, inhibitory to contralateral sweating, is a proposed mechanism for the hyperhidrosis seen contralateral to acute cerebral infarction in these patients.
We studied 25 patients with sickle cell anemia and cerebral infarction. We classified lesions as to probable mechanism (large versus small vessel disease) based on the CT/MRI appearance of established infarction. Most patients had CT/MRI patterns of major cerebral vessel occlusion (41%) or border-zone (distal insufficiency) infarcts (31%) best explained by large cerebral vessel vasculopathy. Seven of 25 (28%) had either isolated subcortical (12%) or small cortical branch occlusion (16%) consistent with other mechanisms such as small vessel occlusion or embolism. These results suggest that most clinically recognized cerebral infarctions in sickle cell anemia are caused by large vessel disease, but this mechanism may not account for symptoms of cerebral ischemia in all cases.
Although hemichorea is often ascribed to a vascular lesion, generalized chorea of adult onset is often thought to be due to degenerative diseases. We describe a 74-year-old woman with generalized chorea that was diagnosed at autopsy as due to multiple lacunar infarcts in the basal ganglia. Generalized chorea in adults may be caused by vascular disease of the basal ganglia.
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