Biomedical subjects
Publications and source records attributed to J C Brust.
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.
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.
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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.
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.
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.
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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.
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.
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Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
An elderly woman developed humeral subluxation secondary to syringomyelic neuroarthopathy. Atypical features included her advanced age, the unilaterality of sensory symptoms and signs, the nearly normal motor function, and the absence of long tract signs. Magnetic resonance imaging confirmed the presence of a cervical syrinx, and electrodiagnostic studies suggested superimposed compressive brachial plexopathy. This case suggests that syringomyelia may be underdiagnosed in patients with atypical presentations.
We reviewed 153 episodes of cobalamin deficiency involving the nervous system that occurred in 143 patients seen over a recent 17-year period at 2 New York City hospitals. Pernicious anemia was the most common underlying cause of the deficiency. Neurologic complaints, most commonly paresthesias or ataxia, were the first symptoms of Cbl deficiency in most episodes. The median duration of symptoms before diagnosis and treatment with vitamin B12 was 4 months, although long delays in diagnosis occurred in some patients. Diminished vibratory sensation and proprioception in the lower extremities were the most common objective findings. A wide variety of neurologic symptoms and signs were encountered, however, including ataxia, loss of cutaneous sensation, muscle weakness, diminished or hyperactive reflexes, spasticity, urinary or fecal incontinence, orthostatic hypotension, loss of vision, dementia, psychoses, and disturbances of mood. Multiple neurologic syndromes were often seen in a single patient. In 42 (27.4%) of the 153 episodes, the hematocrit was normal, and in 31 (23.0%), the mean corpuscular volume was normal. Neutropenia and thrombocytopenia were unusual even in anemic patients. In nonanemic patients in whom diagnosis was delayed, neurologic progression frequently occurred although the hematocrit remained normal. In 27 episodes, the serum cobalamin concentration was only moderately decreased (in the range of 100-200 pg/ml) and in 2 the serum level was normal. Neurologic impairment, as assessed by a quantitative severity score, was judged to be mild in 99 episodes, moderate in 39 and severe in 15. Severity of neurologic dysfunction before treatment was clearly related to the duration of symptoms prior to diagnosis. In addition, the hematocrit correlated significantly with severity, independent of the longer duration of symptoms in nonanemic patients. Four patients experienced transient neurologic exacerbations soon after beginning treatment with cyanocobalamin, with subsequent recovery. Followup evaluation was adequate to assess the neurologic response to vitamin B12 therapy in 121 episodes. All patients responded, and in 57 (47.1%), recovery was complete, with no remaining symptoms or findings on examination. The severity score was reduced by 50% or greater after treatment in 91% of the episodes. Residual long-term moderate or severe neurologic disability was noted following only 7 (6.3%) episodes. The extent of neurologic involvement after treatment was strongly related to that before therapy as well as to the duration of symptoms. The percent improvement over baseline neurologic status after treatment was inversely related to duration of symptoms and hematocrit. Some evidence of response was always seen during the first 3 months of treatment.(ABSTRACT TRUNCATED AT 400 WORDS)
Cocaine, especially in its alkaloidal or "crack" form, has been increasingly associated with cerebrovascular disease. Before the crack epidemic, cocaine hydrochloride (HCl) was also implicated as a cause of stroke. However, less is known about the differences in stroke subtypes, age at stroke onset, or presence of underlying structural cerebrovascular disease with different forms of cocaine use. We compared 26 patients (previously reported) from our four institutions plus 16 cases reported in the literature of stroke associated with alkaloidal cocaine to 63 (57 reported in the literature and six not previously reported from our four institutions) cases of stroke associated with cocaine HCl. Ischemic and hemorrhagic strokes are equally likely after alkaloidal cocaine use, whereas cocaine HCl is more likely (approximately 80% of the time) to cause hemorrhagic stroke, with approximately half the intracranial hemorrhages occurring from ruptured cerebral saccular aneurysms or vascular malformations. The presence of an underlying cerebral aneurysm was more common among patients with cocaine HCl-associated strokes than alkaloidal cocaine-associated strokes. Cerebral infarction was significantly more common among the alkaloidal cocaine users than in all the cocaine HCl users, and this was also true when alkaloidal cocaine users were compared with parenteral cocaine HCl (intravenous and intramuscular) users. Only hemorrhagic stroke has been reported with intravenous cocaine HCl use. We conclude that the pathogenesis of cocaine-related stroke is heterogeneous, and depends, in part, on the form of cocaine used.
BACKGROUND AND METHODS: The use of cocaine, especially one of its alkaloidal forms ("crack"), has been increasingly associated with cerebrovascular disease. To clarify the clinical, radiologic, and pathological features of the events associated with cocaine use, we identified 28 patients at four medical centers who had stroke temporally related to the use of alkaloidal cocaine (during or within 72 hours of use). RESULTS: The 28 patients had the following types of cerebrovascular event: cerebral infarction (n = 18 [2 hemorrhagic; 1 fatal]) in the areas supplied by the middle cerebral artery (n = 10), anterior cerebral artery (n = 3), posterior cerebral artery (n = 1), and vertebrobasilar arteries (n = 4); subarachnoid hemorrhage (n = 5); intraparenchymal hemorrhage (n = 4); and primary intraventricular hemorrhage (n = 1). Eighteen patients (64 percent) had acute neurologic symptoms immediately or within one hour of using cocaine. Fifteen patients (45 percent) with either occlusive or hemorrhagic strokes had sever headache as an early symptom. Vasculitis was not suggested by radiography in any patient, nor was it identified on pathological examination in one patient who died. All the patients were young (mean age, 34 years; range, 23 to 49) and had no other apparent, direct cause of stroke. Other risk factors for stroke among the patients included mild mitral-valve prolapse (n = 4), hypertension (n = 4), cigarette smoking (n = 8), and regular alcohol use (n = 6). CONCLUSIONS: There is a strong temporal association of the use of alkaloidal cocaine with both ischemic and hemorrhagic cerebrovascular events. Cocaine-related stroke probably has many causes. A thorough history focusing on the use of cocaine and toxicologic screening of urine and serum should be part of the evaluation of any young patient with a stroke.
Previous studies of human immuno-deficiency virus-related neurologic disease have been either retrospective or have included mostly homosexual patients. We sought to determine (1) the true prevalence of neurologic abnormalities in patients with acquired immunodeficiency syndrome or lymphadenopathy acquired immunodeficiency-related complex, and (2) whether differences in prevalence or type of neurological abnormality exist between parenteral drug abusers and non-parenteral drug abusers. We prospectively evaluated 190 adult inpatients with either acquired immunodeficiency syndrome (129) or lymphadenopathy acquired immunodeficiency-related complex (61); 151 (80%) were parenteral drug abusers, and 172 patients (91%) had neurologic symptoms or signs. There was no significant difference in prevalence of neurologic disease between parenteral drug abusers and non-parenteral drug abusers, or between patients with acquired immunodeficiency syndrome and those with lymphadenopathy acquired immunodeficiency-related complex. The prevalence of neurologic symptoms in these patients with lymphadenopathy acquired immunodeficiency-related complex and acquired immunodeficiency syndrome is the highest reported to date and appears to reflect the prospective nature of the study.