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Biomedical subjects

J C Brust

Publications and source records attributed to J C Brust.

At least 19 recordsLinked to original sources
PubMed2001

Music and the neurologist. A historical perspective.

Neurological disorders affecting musical function can produce either positive or negative symptoms. Positive phenomena include musicogenic epilepsy (seizures triggered by music), musical partial seizures (hallucinated music as the expression of the seizure), musical release hallucinations (nonepileptic musical hallucinations, usually associated with impaired hearing), and synesthesia (hallucinated colors triggered by musical tones). Negative phenomena comprise the amusias, which can be receptive, expressive, or both, and can selectively involve particular components of musical processing, including pitch, interval, contour, rhythm, meter, timbre, and emotional response. Amusia is often accompanied by aphasia, but each can occur in the absence of the other. Neurological disorders provide evidence that musical processing is multimodal and widely distributed in both cerebral hemispheres.

Aphasia↗
PubMed2001

Acute ventricular hemorrhage in adults with hydrocephalus managed by corpus callosotomy and fenestration of the septum pellucidum. Report of three cases.

Three patients with hypertension-induced basal ganglia or thalamic hemorrhage and ventricular rupture underwent corpus callosotomy and fenestration of the septum pellucidum. A patient with a left thalamic hemorrhage underwent surgery on an emergency basis and made a complete physical recovery, although she retained mild psychomotor deficits. Another patient with a large right basal ganglia hemorrhage who also underwent surgery on an emergency basis retained a spastic left hemiparesis without evident psychomotor deficits. The third patient with a left thalamic and basal ganglia hemorrhage, who was initially awake and then lapsed into stupor days later, underwent surgery, but did not recover consciousness. Hydrocephalus was reversed and effectively controlled in all three patients without having to perform a shunt placement procedure.

Adult↗
PubMed1999

Leukoencephalopathy and raised brain lactate from heroin vapor inhalation ("chasing the dragon")

BACKGROUND: Inhalation of heated heroin vapor ("chasing the dragon"), which is gaining popularity among drug users seeking to avoid the risks of parenteral drug administration, can produce progressive spongiform leukoencephalopathy. METHODS: We studied the clinical phenotype and course, MRI, MRS, and brain pathology in the first American patients described with this syndrome. RESULTS: Two of the three heroin users studied inhaled heroin pyrolysate together daily over the course of 2 weeks. They developed ataxia, dysmetria, and dysarthria. Patient 1 progressed to an akinetic mute state with decorticate posture and subsequent spastic quadriparesis. Patient 2 developed a mild spastic quadriparesis and gait freezing. Patient 3 was asymptomatic following less heroin exposure. Brain MRI showed diffuse, symmetrical white matter hyperintensities in the cerebellum, posterior cerebrum, posterior limbs of the internal capsule, splenium of the corpus callosum, medial lemniscus, and lateral brainstem. MRS showed elevated lactate. Brain biopsy (Patient 1) showed white matter spongiform degeneration with relative sparing of U-fibers; electron microscopy revealed intramyelinic vacuolation with splitting of intraperiod lines. Progressive deterioration occurred in Patients 1 and 2 over 4 weeks. Both were treated with antioxidants including oral coenzyme Q, and clinical improvement occurred. Patient 1 recovered nearly completely over 24 months. Patient 2 improved, but developed a delayed-onset cerebellar hand tremor. Both still have white matter abnormalities on MRI and MRS. CONCLUSIONS: Elevated lactate in white matter and the possible response to antioxidants suggests mitochondrial dysfunction in progressive spongiform leukoencephalopathy following inhalation of heated heroin vapor.

Administration, Inhalation↗
PubMed1999

Dose-response effect of fetal cocaine exposure on newborn neurologic function.

BACKGROUND: Studies of fetal cocaine exposure and newborn neurologic function have obtained conflicting results. Although some studies identify abnormalities, others find no differences between cocaine-exposed and cocaine-unexposed infants. To determine the effects of prenatal cocaine exposure on intrauterine growth and neurologic function in infants, we prospectively evaluated 253 infants shortly after birth. METHODS: Women who delivered a live singleton >36 weeks by dates were eligible for enrollment. Maternal exclusionary criteria were known parenteral drug use, alcoholism, and acquired immunodeficiency syndrome; infant exclusionary criteria were Apgar scores </=4 at 5 minutes, obvious congenital malformations, seizures, or strokes. A total of 98% of infants were evaluated between 1 to 7 days of age. Newborns were assessed with the Neurological Examination for Children (NEC) by a pediatric neurologist (C.A.C.) who was blinded to exposure status. Gestational age was determined by Ballard's examination. Cocaine exposure was determined for the last trimester by radioimmunoassay of maternal hair (RIAH). Exposure values ranged from 2 to 4457 ng/10 mg hair. Infants were excluded if a maternal hair sample was missing (N = 13). The sample comprises 240 woman and infant pairs-104 cocaine-exposed and 136 cocaine-unexposed. RESULTS: Compared with unexposed controls, cocaine-exposed infants exhibited higher rates of intrauterine growth retardation (24% vs 8%), small head circumference ([HC] <10th% percentile) (20% vs 5%) and neurologic abnormalities: global hypertonia (32% vs 11%), coarse tremor (40% vs 15%), and extensor leg posture (20% vs 4%). We found increasing odds (odds ratio) of growth and neurologic impairment with increasing level of cocaine exposure in stratified analyses. The odds ratio associated with three levels of cocaine exposure (no exposure, low exposure = RIAH 2-66 ng/mg; and high exposure = RIAH 81-4457 ng/mg) respectively are: 1.0, 3.3, and 6.1 for small head size (chi2 for trend); 1.0, 3. 3, and 4.3 for global hypertonia (chi2 for trend); 1.0, 3.4, and 7.4 for extensor leg posturing (chi2 for trend); and 1.0, 3.8, and 3.8 for coarse tremor (chi2 for trend). Significant associations between cocaine exposure and neurologic signs were found in logistic regression equations that controlled for 20 or more variables. CONCLUSION: We conclude that adverse neonatal effects associated with fetal cocaine exposure follow a dose-response relationship: newborns with higher levels of prenatal cocaine exposure show higher rates of impairments in fetal head growth and abnormalities of muscle tone, movements, and posture. Significant relationships between cocaine exposure and these outcomes remain in controlled analyses.

Adult↗
PubMed1998

Acute neurologic complications of drug and alcohol abuse.

Recreationally abused substances include both legal and illegal agents, broadly classified as opioids, psychostimulants, sedatives, cannabis (marijuana), hallucinogens, inhalants, dissociative anesthetics (phencyclidine), anticholinergics, ethanol, and tobacco. These substances are associated with an array of neurological emergencies resulting from overdose, withdrawal, and other medical and neurological complications.

Alcohol Drinking↗
PubMed1997

Vasculitis owing to substance abuse.

The term drug dependence refers to psychic dependence (addiction), physical dependence, or both, in someone who administers a drug periodically or continuously. Recreational drug abusers are at risk for occlusive and hemorrhagic stroke of diverse cause. Although sometimes over diagnosed, cerebral vasculitis has been historically verified in users of legal and illegal drugs.

Adult↗
PubMed1995

Neurological correlates of fetal cocaine exposure: transient hypertonia of infancy and early childhood.

OBJECTIVE: To assess whether prenatal cocaine exposure has any long-term effects on neurodevelopment. DESIGN: A prospective cohort study with examiners blind to drug exposure and human immunodeficiency virus (HIV) status. SUBJECTS: Of 144 high-risk infants enrolled in a perinatal HIV neurodevelopmental study, 119 (83%) infants with both neurological and urine toxicology measures were followed up to age 24 months. METHODS: Neurological and developmental assessments were analyzed at 6-month intervals grouped according to the presence of cocaine in urine toxicology: 51 infants were cocaine-positive. Adjusted odds ratios (ORs) and 95% confidence interval (CI) were obtained by logistic regression equations that adjusted for perinatal variables, including measures of fetal growth, gestation, HIV status, and infant toxicology results. SETTING: Harlem Hospital Center from 1988 to 1992. RESULTS: At age 6 months, 21 of 51 (41%) cocaine-positive children exhibited hypertonia of any type (hypertonic tetraparesis, hypertonic diparesis, and hypertonic hemiparesis) compared with 17 of 68 (25%) cocaine-negative infants (OR = 2.1, CI = 1.0-4.6). Cocaine-positive infants were four times more likely to show hypertonic tetraparesis (HTP) than cocaine-negative infants (OR = 4.0; CI = 1.5-10.8). The association remained significant in multivariate analyses. Hypertonia, consistent with cerebral palsy, diminished over time in both groups. In 97% of affected infants hypertonia resolved by 24 months. Arm hypertonia abated first; leg hypertonia remained in some children up to age 18 months. No differences in development scores between cocaine-positive and cocaine-negative were noted at any age interval. However, among cocaine-positive infants those with early HTP showed significantly lower mean developmental scores at 6 and 12 month compared to infants without HTP. CONCLUSION: Cocaine positivity urine toxicology at birth is associated with hypertonia during infancy. Such cocaine-induced effects are usually symmetrical, transient, and the majority of exposed children outgrow hypertonia by 24 months of life. Among cocaine-positive infants, HTP may be a marker for later developmental impairments.

Adult↗
PubMed1994

Focal myopathy induced by chronic intramuscular heroin injection.

A patient developed focal fibrotic myopathy after many years of intramuscular heroin use. While such changes have been associated with chronic intramuscular injections of pentazocine and meperidine, a similar myopathy resulting from chronic intramuscular heroin has not been convincingly described.

Heroin↗
PubMed1993

Hypertension and the risk of new-onset unprovoked seizures.

We tested the a priori hypothesis that hypertension can lead to seizures through vascular brain damage that might or might not involve manifest stroke. A case-control study with 227 patients admitted for a first unprovoked seizure and 294 acute surgical controls was carried out at Harlem Hospital Center, New York City, between 1981 and 1984. History of hypertension was significantly associated with unprovoked seizures, even after adjustment for antecedent stroke and other potential confounders (adjusted odds ratio [OR] = 1.57; 95% confidence limit [CL], 1.0 to 2.44). There was marked synergism between history of stroke and history of hypertension; subjects with a history of both had a fourfold increase in seizure risk compared with subjects with neither (adjusted OR = 4.07; 95% CL, 1.50 to 11.0). In these data, history of hypertension appears to be an independent risk factor for new-onset unprovoked seizures, especially, but not only, in conjunction with a history of stroke.

Adult↗
PubMed1993

Other agents. Phencyclidine, marijuana, hallucinogens, inhalants, and anticholinergics.

Acute phencyclidine intoxication causes psychosis and a myriad of other symptoms and signs, some life-threatening. Anticholinergic poisoning is also a medical emergency, often requiring an intensive care unit. Marijuana and hallucinogens have rarely, if ever, resulted in direct overdose death, but intoxication can result in accidents or self-injury. Inhalants cause death from cardiac arrhythmia, suffocation, or accident. Each of these agents is associated with a variety of medical and neurologic complications, some of which are discussed at greater length elsewhere in this issue.

Hallucinogens↗
PubMed1993

Hospital-acquired morbidity on a neurology service.

Clinical services must monitor hospital-acquired morbidity, but what rates are expected specifically for neurology inpatients is not evident from published studies. We studied prospectively 1317 consecutive admissions to a neurology service in a university-affiliated city hospital from 1987 to 1990 and recorded all nosocomial infections, nosocomial pneumonia, and decubitus ulcers of stage III or IV. Over the 3-year period, 6.8% of patients had > or = 1 nosocomial infection (and almost half of these had a nosocomial bloodstream infection); 3.1% had > or = 1 case of nosocomial pneumonia; 1.2% developed severe decubitus ulcers, and 8.4% had one or more of the three complications. The incidence of nosocomial infection exceeds that expected from multihospital studies. How much of the excess is peculiar to neurology patients and how much can be attributed to factors in our community and at our hospital cannot be determined from this study. Furthermore, our statistics are not meant as norms, but as initial estimates for quality assurance.

Cross Infection↗
PubMed1992

Charles Loomis Dana.

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History, 19th Century↗