[Superior sagittal sinus thrombosis: clinical picture and computed tomographic findings].
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Biomedical subjects
Publications and source records attributed to E Melamed.
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Twenty-six patients with recently diagnosed leptomeningeal metastases underwent multiple diagnostic procedures in order to assess possible cerebral parenchymal involvement. Pretreatment studies included detailed neurological examination, computed tomographic scan, electroencephalogram, neuropsychological assessment, psychiatric evaluation, and measurement of regional cerebral blood flow (rCBF) using the xenon 133 inhalation technique. At diagnosis 50% of the patients had symptoms and signs of cerebral dysfunction. Computed tomographic scanning and electroencephalography detected abnormalities in 42% and 58%, respectively. Scoring was abnormally low on at least three neuropsychological tests in 93% of the patients. The mean rCBF was reduced in 88% of patients by 16.1 +/- 2.5% (mean +/- SEM; range, 8 to 45%) compared with age-matched controls (p less than 0.001). rCBF was reduced and cognition was impaired in patients with or without overt cerebral manifestations. Neuropsychological testing and rCBF measurement may be helpful in early detection of cerebral dysfunction in patients with leptomeningeal metastases.
Multiple parameters for brain volume and mass were studied in 85 parkinsonian patients and in 149 normal controls aged 24 to 84 using CT scanning. In controls there was reduction in brain substance with advancing age. Increased brain atrophy in patients with Parkinson's disease (PD) was mainly observed in the younger age group of 24 to 49. This included parameters evaluating the size of the lateral and third ventricles (P less than 0.05 and P less than 0.01 respectively) and the size of the subarachnoid space in the frontal interhemispheric and Sylvian fissures (P less than 0.005 and P less than 0.01). With computed canonical correlation analysis a formula was obtained which expressed the tendency of the atrophic process in PD to involve the areas surrounding the third ventricle and the mesial aspect of the frontal lobes more than during normal aging.
Patients with sepsis often manifest symptoms of encephalopathy similar to those observed in portasystemic encephalopathy. As a causal relationship has been demonstrated between hepatic encephalopathy and a deranged brain neurotransmitter profile, the catecholaminergic and serotoninergic brain neurotransmitter profile in a septic rat model was investigated. Septic animals exhibited lower levels of norepinephrine (NE), 3,4-dihydroxyphenylacetic acid, and homovanillic acid compared to normal controls. Severely septic animals with encephalopathy exhibited significantly lower levels of NE, dopamine, 5-hydroxytryptamine, and 5-hydroxyindoleacetic acid compared to rats only mildly septic with no encephalopathy. The infusion of branched chain amino acids during sepsis had no effect on this deranged brain neurotransmitter profile. Previous results of derangements in the blood-brain barrier transport mechanism combined with the present findings of a deranged brain amino acid and neurotransmitter profile during sepsis may be responsible, at least in part, for the metabolic encephalopathy observed during sepsis and might suggest a common etiology for septic, hepatic, and other metabolic encephalopathies.
In mice, long-term reductions in striatal DA produced by the neurotoxin MPTP were completely prevented by its combined administration with amphetamine. Depletion of DA from DA terminals by cotreatment with reserpine did not suppress but rather enhanced MPTP-induced DA decrements in striatum. Amphetamine protection against DA neurotoxicity of MPTP in mice is probably not due to increases in DA release and may be related to inhibition of MPTP transport into nigrostriatal terminals via the DA reuptake system.
In rats with partial, unilateral lesions of the dopaminergic nigrostriatal pathway, synthesis of dopamine (DA) per surviving neurone was assessed by measuring the ratio of DOPA accumulated after inhibition of aromatic amino acid decarboxylase to dopamine (DOPA/DA ratio). Release of DA per surviving neurone was assessed by measuring the ratios of the concentrations of 3,4-dihydroxyphenylalanine (DOPAC) and homovanillic acid (HVA) to DA. In striata ipsilateral to the lesion, the DOPA/DA ratio was elevated 4-fold, and the DOPA/DA and HVA/DA ratios were elevated 2-fold as compared to values in contralateral striata. Administration of gamma-butyrolacetone (750 mg/kg, 30 min), i.e. of a drug which accelerates synthesis of DA, further increased the DOPA/DA ratio in lesioned striata to levels 37 times higher than those measured on the control side of saline-injected controls. Morphine (20 mg/kg, 30 min) and haloperidol (2.5 mg/kg, 60 min), i.e. drugs known to accelerate the turnover and release of DA, further elevated the DOPAC/DA and HVA/DA ratios in lesioned striata to levels approx. 5 times higher than the ratios measured on contralateral sides of saline-treated controls. The data indicate that dopaminergic neurones surviving partial lesions of the nigrostriatal pathway synthesize and release DA at an elevated but submaximal rate. Synthesis and release of DA can be further enhanced to a large extent by drugs.
Pregnant HS/Ibg mice received 3 g/kg phenobarbital in their milled food; control dams received unadulterated milled food. Their offspring were tested on ages 22 and 50 days for norepinephrine (NE) and dopamine (DA) levels and DA turnover in the hypothalamus and striatum. Additional groups were tested on days 8, 22, and 50 for brain stem tryptophan hydroxylase (TPH) activity. Hypothalamic DA level among offspring with prenatal PhB exposure (B offspring) was 37% below control level on age 22 days and 61% below control on day 50 (p less than 0.001). Hypothalamic NE level of B offspring was reduced on age 50 days (52%, p less than 0.05) and not on day 22. DOPAC level and DA turnover did not differ among B and control groups. Prenatal exposure to PhB did not have a significant effect on TPH activity. The changes in catecholamines may mediate, at least in part, some of the early barbiturate induced neuromorphological and behavioral changes previously found in our laboratory.
N-methyl-4-phenyl-1,2,5,6-tetrahydropyridine (MPTP) is toxic to dopaminergic neurones in several mammalian species including mice. Combined treatment with phenylethylamine prevented in mice the long-term (30 days post-treatment) dopamine depletions in striatum induced by MPTP. Phenylethylamine, a naturally-occurring specific substrate of monoamine oxidase (MAO) type B, probably protects against effects of MPTP by competitively inhibiting the oxidative conversion of MPTP to its toxic metabolite N-methyl-4-phenylpyridinium ion catalysed by MAO-B.
Acute appearance of hemiparesis or hemiplegia with initial marked spasticity was observed in 8 stroke patients. All had intracerebral hematomas and in 7 it was located in the region of the basal ganglia. By contrast, none of 121 hemiplegic patients with hemispheric ischemic stroke hospitalized during the same period had increased muscle tone in the involved limbs at stroke onset. Study indicates that association of hemiplegia with immediate spasticity at stroke onset is a clinical clue to a possible deeply located intracerebral hematoma.
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In Parkinson's disease, there is high prevalence of dementia, reduction of the regional cerebral blood flow (rCBF), and neuronal loss and Alzheimer-like pathologic changes in cerebral cortex. Since rCBF is also decreased in Alzheimer's dementia, it is theoretically possible that both decreases in rCBF and cognitive impairment in parkinsonians are caused by a similar mechanism, eg, reduced metabolic demand or loss of cholinergic neurons innervating cortex and microvessels. We therefore measured rCBF using the 133Xenon inhalation technique and evaluated cognitive function with a detailed neuropsychological test battery in 48 patients with Parkinson's disease. Mean brain, hemispheric, and regional flows were decreased in parkinsonians as compared with those in age-matched controls. Most of the cognitive functions were impaired in patients as compared with those in normal subjects. However, there was no correlation between the magnitude of rCBF reduction and the presence and severity of intellectual deterioration in parkinsonians, suggesting that each may be caused by a different mechanism.
We quantitatively evaluated the computerized tomograms (CT) of 148 neurologically intact subjects, aged 28 to 84 years, to examine the effect of normal aging on the integrity of brain mass. Ten parameters were measured in each CT scan as indices for brain volume, including size of lateral, third and fourth ventricles, width of the sylvian and interhemispheric fissures, cortical sulci and the prepontine cistern. Most of these measurements showed that advancing age is associated with progressive loss of brain substance. Data show that the atrophy of brain during normal aging is both cortical and central and is not limited to the older population, but begins at a young age. These normative measurements may serve for comparison with data obtained from CT scans of patients with various neurological disorders.
Regional cerebral blood flow (rCBF) was measured by the 133xenon inhalation technique in 103 healthy, nonhospitalized subjects of whom 44 were less than 30 years of age. Mean brain and hemispheric flows and rCBF decreased with advancing age. Moreover, a steep decline in rCBF became apparent as early as the third decade of life. Our findings suggest that the decline of rCBF is not limited to healthy elderly subjects, but is a progressive phenomenon that begins at an earlier age.
To examine the pattern of retinal dopamine (DA) turnover during 24 h, DA and 3,4-dihydroxyphenylacetic acid (DOPAC) were measured at 2-h intervals in rats kept in a regular 12-h light-dark cycle. DA and DOPAC were higher during the light and lower during the dark hours. These rhythmic variations were abolished and DA and DOPAC remained low during 24 h of light deprivation. Findings indicate that DA turnover in the retina is accelerated during the light and suppressed during the dark phases of the diurnal light-dark cycle. These fluctuations in retinal DA neuronal activity are not truly circadian but are dependent on environmental lighting as an external stimulator.
Dementia and generalized myoclonic jerks were the only neurologic features in a patient with cryptococcal encephalitis. Despite the presence of numerous budding yeasts identified as Cryptococcus neoformans in the CSF, there was no inflammatory reaction. Protein and glucose levels were normal, with no pleocytosis.
Paroxysmal dystonia was the initial manifestation of multiple sclerosis (MS) in eight patients. The disorder was generally characterized by dystonic posturing of unilateral extremities, averaging less than one minute in duration. Facial grimacing and dysarthria occurred in two of the eight patients. This paroxysmal phenomenon was frequently the cause of diagnostic confusion. The time elapsing before other neurological symptoms of MS developed was as long as ten years.
In 42 patients with acute unilateral ischemic or hemorrhagic hemispheric stroke, conjugate eye deviation toward the lesioned side was usually of brief duration. It subsided within 48 hours in 24 patients (57%) and lasted no longer than 5 days in 38 patients (90%). Early disappearance of conjugate eye deviation was an isolated phenomenon and preceded any improvement in the other focal neurological deficits, which persisted in their initial severity. In 6 additional patients with stroke, conjugate eye deviation was remarkably prolonged, lasting from 13 to more than 43 days. In all 6 there was evidence for preexisting damage to the contralateral frontal region. Our study suggests that early recovery of conjugate eye deviation in patients with acute hemispheric stroke may be mediated by the contralateral unaffected frontal eye field.
Changes in corticotrophin (ACTH) and corticosterone (CS) serum levels, were examined in rats in which either 6-hydroxydopamine or vehicle were injected into the medial forebrain bundle (MFB) and which were sacrificed by decapitation 14 days later. The injection of the neurotoxin, which depleted very significantly the norepinephrine (NE) content of the mediobasal hypothalamus, elevated significantly the basal levels of serum ACTH and CS, but inhibited the rise in the levels of these hormones following photic stimulation. These results would suggest that the hypothalamic NE system has normally an inhibitory effect on basal ACTH and CS secretion and that the hormonal response to photic stimulation is mediated by that system and possibly by NE MFB fibers.