Biomedical subjects

C M Filley

Publications and source records attributed to C M Filley.

64 records · Page 4Linked to original sources

PubMed1986

Neurologic sequelae of chronic solvent vapor abuse.

Neurologic abnormalities were seen in 13 of 20 patients with a history of chronic solvent vapor (primarily toluene) abuse for 2 or more years. The patients were evaluated after an abstinence period of at least 4 weeks, to avoid neurologic effects of acute intoxication. Neurologic signs included cognitive (60%), pyramidal (50%), cerebellar (45%), and brainstem/cranial nerve (25%) findings. Eight of nine CTs revealed diffuse atrophy of cerebral hemispheres, cerebellum, and brainstem. BAERs were abnormal in three of four patients, and EEG abnormalities were seen in three of seven patients. Chronic exposure to solvent vapor may cause persistent neurologic impairment.

Adolescent↗

PubMed1985

Education provides no protection against Alzheimer's disease.

It has been suggested that educational achievement confers protection against dementia. We examined educational level and age of onset in 28 patients with Alzheimer's disease, and assessed the progression of dementia over a mean period of 28 months using both a measure of neurobehavioral status and an index of functional impairment. No protective effect of education was found in either early- or late-onset dementia.

Alzheimer Disease↗

PubMed1984

Neuromyelitis optica in the elderly.

Blindness and quadriparesis developed in an elderly woman whose symptoms began at the age of 69 years. Postmortem examination revealed extensive demyelinative lesions in the optic nerves and spinal cord. The clinical and pathologic findings were consistent with the diagnosis of neuromyelitis optica ( NMO ). This case serves to document that NMO and presumably typical multiple sclerosis can occur initially at an advanced age.

Age Factors↗

PubMed1984

Brain infarction and hemorrhage in young and middle-aged adults.

Of 131 young (17 to 44 years) and middle-aged (45 to 55 years) adults who had brain infarction or hemorrhage, the most common etiologic factors were rheumatic heart disease, migraine and oral contraceptive use among the younger group. In contrast, atherosclerotic, hypertensive and diabetes-associated cerebrovascular were the most common causes in the middle-aged group. Patients who have a stroke before age 45 should have prompt, complete laboratory and radiologic testing to define a possible treatable cause.

Adolescent↗

PubMed1982

Neurologic manifestations of podophyllin toxicity.

A young woman presented with podophyllin intoxication following topical application of podophyllin resin to genital condylomata acuminata. The disorder was marked by hallucinatory psychosis, bone marrow depression, and mild hepatic dysfunction. The psychosis and systemic disturbances resolved within 3 weeks, but were followed by autonomic and sensorimotor peripheral neuropathy. This case illustrates the transient central neurotoxicity and persistent peripheral neurotoxicity of podophyllin.

Adult↗

PubMedDate not supplied

Central nervous system effects of chronic toluene abuse--clinical, brainstem evoked response and magnetic resonance imaging studies.

We describe the results of neurological evaluation, magnetic resonance imaging (MRI) of the brain and brainstem auditory evoked response (BAER) testing in 11 chronic toluene vapor abusers. Neurological abnormalities were seen in four of 11 individuals and included cognitive, pyramidal, cerebellar and brainstem findings. MRI of the brain was abnormal in three of 11 individuals and revealed the following abnormalities: 1) Diffuse cerebral, cerebellar, and brainstem atrophy; 2) Loss of differentiation between the gray and white matter throughout the CNS; and 3) Increased periventricular white matter signal intensity on T2 weighted images. BAERs were abnormal (control mean +/- 3 S.D.) in five of 11 individuals. As a group, the latency of V (p less than 0.01), the III-V interpeak (p less than 0.05) and the I-V interpeak latencies were prolonged compared to controls. All three individuals with abnormal MRI scans also had abnormal neurological examinations and BAERs. Two of five individuals with abnormal BAERs, however, had normal neurological examinations and MRI scans. Our data support previous findings of diffuse white matter involvement in chronic toluene abusers and suggest that BAERs may detect early CNS injury from toluene inhalation even at a time when neurological examination and MRI scans are normal. BAERs, therefore, may be a sensitive screening test to monitor individuals at risk from toluene exposure (either abusers or industrially exposed individuals) for early evidence of CNS injury.

Adult↗

PubMedDate not supplied

Neurocysticercosis in the United States: 35 cases and a review.

Neurocysticercosis has become more prominent in the United States in recent years because of an increase in immigration from endemic regions and because of improved ease of diagnosis with computed tomography (CT). Neurocysticercosis should be suspected in any patient from a high-risk region who has symptoms or signs of a central nervous system disorder, especially seizures, headaches, or signs of increased intracranial pressure. The best diagnostic test is CT of the head, which usually shows a combination of multiple punctate calcifications; hydrocephalus; and parenchymal, subarachnoid, or intraventricular cysts with and without contrast enhancement. Cysticercosis is confirmed serologically by measurement of cysticercosis antibody titers in serum or cerebrospinal fluid and histologically by biopsy of a lesion. Treatment with praziquantel and dexamethasone is usually sufficient, but ventricular shunting or surgical removal of intraventricular or spinal cysts may be necessary. Whenever a case is identified, other household members should be examined for symptoms and signs of neurocysticercosis and screened for active Taenia solium infection.

Brain Diseases↗

PubMedDate not supplied

MR enhancing brain lesions in methanol intoxication.

Methanol intoxication can cause necrosis of the putamen and subcortical white matter that is evident on neuroimaging. We report a 47-year-old man with significant methanol intoxication who had enhancing lesions in the caudate nuclei, putamina, hypothalamus, and subcortical white matter by MRI. This case demonstrates that contrast enhancement of brain lesions can be observed after methanol poisoning.

Brain Diseases↗

PubMedDate not supplied

Toxic leukoencephalopathy.

The white matter of the brain is vulnerable to a wide variety of toxins. Leukoencephalopathy is being increasingly recognized in a number of different patient populations. The detection of early and subtle toxin effects has been facilitated by the advent of magnetic resonance imaging, which offers better resolution of white matter than other neuroimaging methods. Neuropathologic features of leukoencephalopathy are also becoming more completely elucidated. Injury to white matter has been described from cranial irradiation and cancer chemotherapeutic drugs, and from a number of other therapeutic agents, drugs of abuse, and environmental toxins. Many patients have reversible leukoencephalopathy, whereas others experience a progressive and irreversible course. Leukoencephalopathy is associated with neurobehavioral manifestations that may be subtle or devastating, and the syndrome of white matter dementia may result. The pathogenesis of toxic leukoencephalopathy remains largely unknown, and treatment is limited in most cases to prevention by avoidance or minimization of the toxin exposure. However, the prognosis for this syndrome may be relatively favorable because of the frequent sparing of axons even when myelin is affected. Toxic leukoencephalopathy is an emerging clinical disorder that presents the opportunity for improving clinical outcomes in a number of patient groups and for achieving a deeper understanding of the role of white matter in cognitive and emotional function.

Air Pollutants↗

PubMedDate not supplied

Non-Alzheimer fronto-temporal degenerative dementia. A neurobehavioral and pathologic study.

In contrast to Alzheimer's disease (AD), which predominantly affects the limbic system and association neocortex, degenerative dementias have been identified that show greatest damage in frontal and temporal neocortex. This "lobar atrophy" was first described by Arnold Pick over 100 years ago. We present four autopsy-documented, non-AD cases of fronto-temporal degeneration (FTD), each with neurobehavioral assessment. Three of the patients presented with personality change and the fourth with non-fluent aphasia; memory was initially preserved in all, and only later did dementia become evident. At autopsy, the hippocampi were relatively spared in all cases. One patient had classic Pick-body temporal lobe Pick's disease (PD), 2 had frontal lobe-predominant atrophy with severe degeneration of caudate and substantia nigra (so-called "generalized Pick's"), and the fourth had temporal lobe degeneration without Pick bodies or cells. We propose that subgroups of FTD be categorized both by microscopic features and gross patterns of atrophy, and that subgroups of FTD be kept separate for neurochemical and genetic studies. Neurobehavioral and neuropsychological evaluation early in the course of unusual degenerative dementia can aid in distinguishing FTD cases from AD patients for clinical and drug studies.

Adult↗