Neurological complications of substance abuse.
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Alcoholism↗
Biomedical subjects
J C Brust
Publications and source records attributed to J C Brust.
Syringomyelia presenting as shoulder dysfunction.
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.
Aged↗
Neurologic aspects of cobalamin deficiency.
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)
Adolescent↗
A comparative study of the cerebrovascular complications of cocaine: alkaloidal versus hydrochloride--a review.
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.
Administration, Intranasal↗
Cerebrovascular complications of the use of the "crack" form of alkaloidal cocaine.
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.
Adult↗
Neurologic disease in human immunodeficiency virus-infected drug abusers.
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.
AIDS-Related Complex↗
The diagnosis and treatment of cerebral mycotic aneurysms.
Seventeen patients were treated for 28 documented cerebral mycotic aneurysms. Initial neurological symptoms were attributable to aneurysm rupture in only 7 patients, and in 3 of them symptoms did not suggest subarachnoid hemorrhage. Six patients presented with embolic infarction and 1 with meningitis; in 3 patients it was uncertain if aneurysm rupture occurred. Four patients had rupture of at least one aneurysm while receiving appropriate antibiotic treatment and another had rupture at the conclusion of therapy. Of 20 aneurysms followed angiographically or with computed tomography during medical treatment, 10 became smaller or disappeared and 10 remained unchanged or enlarged, 1 with fatal rupture. Eight ruptured aneurysms were surgically excised; 2 of the patients with ruptured aneurysms died and 2 had residual aphasia or cognitive impairment. All 4 patients whose only surgery was for an unruptured aneurysm made uneventful recoveries. Recognizing the retrospective and anecdotal nature of our data and the differing views of previous investigators, we recommend: (1) that careful neurological examination, computed tomography, and (unless contraindicated) lumbar puncture be performed on any patient with endocarditis; (2) that those with neurological abnormalities not attributable to systemic toxicity, including pleocytosis in the cerebrospinal fluid or apparent infarction on computed tomographic scans, undergo four-vessel cerebral angiography; (3) that single accessible mycotic aneurysms in medically stable patients be promptly excised, with individualization of multiple or proximal aneurysms; and (4) that repeat angiography be performed at the conclusion of antibiotic therapy in patients requiring long-term anticoagulation.(ABSTRACT TRUNCATED AT 250 WORDS)
Adolescent↗
Illicit drug use and the risk of new-onset seizures.
The authors studied the use of heroin, marijuana, and cocaine before the onset of a first seizure in 308 patients with seizures and 294 controls at Harlem Hospital Center, New York City, between 1981 and 1984. Heroin use, both past and present, appeared to be a risk factor for all first seizures (adjusted odds ratio = 2.80, 95% confidence interval (CI) 1.53-5.74). For unprovoked seizures, the adjusted odds ratio was 2.58 (95% CI 1.36-4.90) for ever heroin use and 4.70 (95% CI 0.86-25.78) for heroin use within 24 hours of hospitalization. For provoked seizures, respective adjusted odds ratios were 3.65 (95% CI 1.54-8.65) and 27.74 (95% CI 3.57-215.52). Marijuana use appeared to be a protective factor against first seizures in men. For men with unprovoked seizures, the adjusted odds ratio was 0.42 (95% CI 0.22-0.82) for ever marijuana use and 0.36 (95% CI 0.18-0.74) for marijuana use within 90 days of hospitalization. For men with provoked seizures, respective adjusted odds ratios were 1.03 (95% CI 0.36-2.89) and 0.18 (95% CI 0.04-0.84). Cocaine use, while common among study subjects, was not shown to be a significant risk factor either for all first seizures or for subgroups of seizures, regardless of the time of last use. The authors conclude that heroin use is a risk factor and marijuana use a protective factor for new-onset seizures.
Adult↗
Embolic stroke after smoking "crack" cocaine.
A 39-year-old woman had an embolic upper division middle cerebral artery branch occlusion 3 hours after smoking the free base of cocaine ("crack"). Radionuclide ventriculography demonstrated cardiomyopathy, and echocardiography documented a left atrial thrombus. This case demonstrates that embolism is one mechanism of ischemic stroke after cocaine use, and that cardiomyopathy, possibly cocaine induced, may be the source of embolus. A cardiac source of embolus should be sought in patients with cocaine-associated cerebral infarction.
Adult↗
Labelling 'unexpected' deaths on a neurology service.
We wrote a list of descriptive phrases to dichotomize admissions to a neurology service by a priori perceptions of risk of death within 30 days as "higher than average" versus "lower than average." In 500 consecutive admissions, the higher-risk list carried a 17-fold relative risk of death for the 20% of admissions so classified. The list is a valid and informative predictor of 30-day outcome that supports a classification of deaths as "expected" or "unexpected."
Cause of Death↗
Direct dyslexia. Preserved oral reading of real words in Wernicke's aphasia.
A 70-yr-old man was able to read aloud, without comprehending what he read, following a stroke that caused Wernicke's aphasia with severely impaired comprehension of speech. Tested on admission, and at 3 and 9 months, he could read aloud both orthographically simple and orthographically complex real words, and showed neither semantic errors, preference for nouns, nor difficulty with function words. He could not, however, read aloud orthographically simple nonwords. His disorder thus appears to be the first pure example of 'direct dyslexia', which, in contrast to previously well-documented examples of 'deep' and 'surface' dyslexia, implies the existence in reading of a direct route, independent of phonology or semantics, between visual and oral word representations.
Aged↗
The EEG response to diffuse and patterned photic stimulation during acute untreated alcohol withdrawal.
We studied the responses to diffuse and patterned stroboscopic light stimulation prospectively in 49 individuals during acute alcohol withdrawal prior to pharmacologic treatment. Photomyogenic responses (PMR) occurred in only two (4%) of those tested, and photoparoxysmal responses (PPR) never occurred. These findings suggest that PMR occur far less often during alcohol withdrawal than previously thought and that PPR may not be a direct manifestation of alcohol withdrawal.
Adult↗
Alcohol consumption and withdrawal in new-onset seizures.
We studied alcohol use before the onset of a first seizure in 308 patients with seizures and 294 controls. The risk of seizures increased with increasing current alcohol use. For unprovoked seizures (i.e., seizures occurring without an antecedent event, such as a recent stroke), the adjusted odds ratios rose from 3-fold at intakes of 51 to 100 g of ethanol per day (95 percent confidence limits, 1.3 and 6.3), to 8-fold at 101 to 200 g per day (95 percent confidence limits, 3.3 and 18.7), and to almost 20-fold at 201 to 300 g per day (95 percent confidence limits, 6.1 and 6.2). For provoked seizures, the odds ratios were lower and statistically significant only above 200 g per day (odds ratio, 10.1; 95 percent confidence limits, 2.3 and 43.8 at 201 to 300 g per day; odds ratio, 7.4; 95 percent confidence limits, 1.8 and 30.5 above 300 g per day). Among ex-drinkers (abstention greater than or equal to 1 year), no increased risk was detected. Alcohol withdrawal was not associated with the onset of seizures in this study; 16 percent of first seizures in drinkers fell outside the conventionally defined withdrawal period, and the remainder exhibited a seemingly random timing after the last drink. We conclude that the relation of seizures to alcohol use is dose dependent and appears to be causal, and that seizures can be interpreted as a disorder induced by the ingestion of alcohol, independently of alcohol withdrawal.
Adult↗
Neuropsychiatric disorders caused by cobalamin deficiency in the absence of anemia or macrocytosis.
Among 141 consecutive patients with neuro-psychiatric abnormalities due to cobalamin deficiency, we found that 40 (28 percent) had no anemia or macrocytosis. The hematocrit was normal in 34, the mean cell volume was normal in 25, and both tests were normal in 19. Characteristic features in such patients included paresthesia, sensory loss, ataxia, dementia, and psychiatric disorders; longstanding neurologic symptoms without anemia; normal white-cell and platelet counts and serum bilirubin and lactate dehydrogenase levels; and markedly elevated serum concentrations of methylmalonic acid and total homocysteine. Serum cobalamin levels were above 150 pmol per liter (200 pg per milliliter) in 2 patients, between 75 and 150 pmol per liter (100 and 200 pg per milliliter) in 16, and below 75 pmol per liter (100 pg per milliliter) in only 22. Except for one patient who died during the first week of treatment, every patient in this group benefited from cobalamin therapy. Responses included improvement in neuropsychiatric abnormalities (39 of 39), improvement (often within the normal range) in one or more hematologic findings (36 of 39), and a decrease of more than 50 percent in levels of serum methylmalonic acid, total homocysteine, or both (31 of 31). We conclude that neuropsychiatric disorders due to cobalamin deficiency occur commonly in the absence of anemia or an elevated mean cell volume and that measurements of serum methylmalonic acid and total homocysteine both before and after treatment are useful in the diagnosis of these patients.
Adolescent↗
Granulomatous angiitis of the brain. An inflammatory reaction of diverse etiology.
Granulomatous angiitis of the brain (GAB) is defined histologically by granulomatous inflammation of intracranial blood vessels. We have studied four patients with autopsy-proved GAB who had, respectively, Hodgkin's lymphoma, herpes zoster, neurosarcoidosis, and no associated illness. Headache, fever, or mental change was followed by hemiparesis or quadriparesis, coma, and death in all four patients. There were no diagnostic findings from cerebral computed tomograms, cerebrospinal fluid, or cerebral angiograms; the diagnosis was established only by postmortem examination. Vasculitis was limited to the brain in all four patients, and involved large arteries, small arteries and veins, or both large and small vessels. Differences in etiology and different particulars of the pathologic conditions imply that GAB is a nonspecific reaction, not a unique disease. The diagnosis, moreover, cannot be proved without histologic confirmation. A biopsy specimen is the only way to ascertain the diagnosis in living patients.
Adult↗
Vascular dementia is overdiagnosed.
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Brain Ischemia↗
Alcohol, seizures, and epilepsy.
Seizures, epilepsy, and alcohol are complexly interrelated. Although it is commonly perceived that patients with epilepsy experience problems with seizure control if they use alcohol, this is not confirmed by the few experimental studies that have tested the hypothesis. The last 30 years have emphasized the role of withdrawal from alcohol as a mechanism of seizure production. However, this is but one of many potential mechanisms by which seizures and epilepsy may be related to alcohol use and abuse. The rare but clear situations in which alcohol can act as a convulsant drug need further study, and mechanisms by which the long-term neurotoxic effects of alcohol lead to chronic epilepsy also need further elucidation.
Alcoholic Intoxication↗
Global aphasia without hemiparesis: multiple etiologies.
Acute global aphasia without hemiparesis has been considered pathognomonic of embolic stroke. During 1 year, we encountered six patients with this syndrome. Two had multiple strokes, probably embolic. One had atrial fibrillation; at autopsy, there were metastases as well as multiple infarcts in the left hemisphere. One had a single large infarct in the territory of an anterior branch of the middle cerebral artery (MCA), one had subarachnoid hemorrhage of unknown origin, and one had a sylvian fissure hematoma with intraparenchymal extension from a ruptured MCA aneurysm. Nonembolic etiologies are therefore also possible and include conditions that bar anticoagulation.
Aged↗