Enlargement Of Subarachnoid Spaces Research Articles

Épanchement péricérébral idiopathique du nourrisson: simple variante anatomique ou facteur de risque hémorragique?

Idiopathic subarachnoid space enlargement (ISSE) is usually regarded as a benign lesion. Two infants, 6 and 8 months old respectively, were hospitalized for neurological disorders revealing subdural hematoma. The first one was drowsy after an apparent life threatening event. The CT scan showed a recent subdural hematoma with ISSE. The outcome was spontaneously uneventful. The second patient presented a febrile hemiconvulsion preceding a status epilepticus. The diagnosis of empyema complicating subdural hematoma with ISSE was done on MRI. Recovery occurred after a 3 week course of parenteral antibiotics and 1 year of antiepileptic treatment. In these two cases, there was no history of head injury and the retrospective study of cranial perimeter growth curves showed acceleration before the acute event. The reputation of benignity is not asurped regarding the ISSE. Nevertheless, it must be recognized as a factor furthering emergence of subdural hematoma, even in absence of injury context.

Pericerebral Fluid Collection: Differentiation of Enlarged Subarachnoid Spaces from Subdural Collections with Color Doppler Us

Pericerebral Fluid Collection: Differentiation of Enlarged Subarachnoid Spaces from Subdural Collections with Color Doppler Us

Pericerebral fluid collection: differentiation of enlarged subarachnoid spaces from subdural collections with color Doppler US.

To determine if the cerebral cortical vain sign seen on magnetic resonance (MR) images can be used with color Doppler ultrasound (US) to differentiate enlarged subarachnoid space from subdural collection. Eighteen infants with pericerebral fluid collection were prospectively examined with color Doppler US and MR imaging. Patients were classified into two groups: group A, with positive cortical vein sign (visualization of color-coded cortical veins that cross fluid collections at cerebral convexities); and group B, without the sign. Positive cortical vein sign was seen at US in 12 patients (group A): nine with benign enlargement of subarachnoid spaces, two with brain atrophy, and one with meningococcal meningitis. The veins were displaced and embedded within the echogenic pia-arachnoid that surrounds the brain or were trapped in the subarachnoid spaces between the neo-membrane and cortical surface (group B, negative cortical vein sign) in four patients with meningitis, two victims of child abuse, and one patient with leukemia. Findings from subsequent MR imaging confirmed the color Doppler US findings. Color Doppler US depiction of the cortical vain sign appears to be as effective as MR imaging in differentiating enlargement of the subarachnoid fluid space from subdural effusion.

Extra-cerebral intracranial fluid collections in childhood: differentiation between benign subarachnoid space enlargement and subdural effusion using color-coded duplex ultrasound

Extracerebral fluid collections in infancy are a common diagnostic problem, because by noninvasive imaging studies (including cranial ultrasonography, CT and NMR), no definite differentiation between two distinct pathological conditions can be found until today: An enlargement of the subarachnoid spaces in children with macrocephaly is a frequent observation of mostly unknown etiology but is known to be associated with a good prognosis. If surgery is necessary in these patients, ventricular shunting is required. On the other hand subdural effusions are often of traumatic origin and require frequently neurosurgical intervention (subdural shunting). Most reports on extracerebral fluid collections in infancy have not differentiated between both pathological conditions and therefore reveal confusing results. Recent studies using magnetic resonance imaging have shown that vascular flow phenomena in the arachnoid space can be used to a reliable diagnosis, whereas previous noninvasive neuroimaging attempts including high resolution computerized tomography (CT) have been useless. We investigated a cohort of 20 patients aged 4 mths to 30 mths (mean 10.5 +/- 6.6 months) 16 with the history of macrocephaly and normal neurological development and 4 patients after head trauma and symptoms of an elevated intracranial pressure. In all 16 patients with the clinical diagnosis of benign subarachnoid space enlargement colour coded Doppler sonography detected archnoid vessels within the fluid collection, furthermore high resolution ultrasound demonstrated the dural border of of the arachnoidea as an echogenic membrane, an observation useful as a further sign of the subarachnoid location of the fluid collection. In the 4 patients with subdural hematoma the fluid collection showed an increased echogenity, no vascular structures and no surrounding border. Out of these observations we conclude that high resolution ultrasound and colour-Doppler sonography are able to reliably differentiate between a subdural and a subarachnoid fluid collection. An NMR investigation with its higher risks (sedation, anesthesia) focused on this target only seems therefore to be not necessary in these patients.

Anterior fontanelle pressure monitoring for the evaluation of asymptomatic infants with increased head growth rate.

We studied non-invasive intracranial pressure monitoring in 20 asymptomatic infants with increased head growth rate. Both basal anterior fontanelle pressure (AFP) traces and occurrence of pressure waves were analysed and compared with normal range values previously established. Eight recordings were classified as pathological; cerebral imaging showed subdural collections or ventricular dilatation in all cases. Five out of these eight infants further developed neurological deficits and/or increase of the ventricular size, and required neurosurgical procedures. Twelve infants had normal AFP traces; six of these had normal cerebral imaging and six showed enlargement of subarachnoid spaces with normal ventricles. All of these 12 patients normalised their head growth rate and remained asymptomatic. This observation suggests that AFP monitoring may be helpful in asymptomatic infants with increased head growth rate to identify a progressive intracranial process and the potential need for a neurosurgical procedure.

EEG in successful aging; a 5 year follow-up study from the eighth to ninth decade of life

Fifteen out of 25 successfully aged individuals completed a 5 year EEG follow-up study from the eighth to ninth decade of life with comprehensive neuropsychological investigation. One subject suffered from stroke and one developed symptoms of dementia during the follow-up. Of 13 subjects who completed the follow-up as being healthy, MRI showed subtle enlargement of ventricles or subarachnoid spaces and mild signal hyperintensities in a few regions in 2 subjects. General cognitive decline was not observed (WAIS-R IQ: 113.4 at entry, 114.3 five years later). There were no EEG dominant frequencies below 8 c/sec and no more background slowing than a few theta waves per 10 sec, either at entry or 5 years later. Intermittent slowing was observed in 9 subjects at entry and in 8 subjects 5 years later. The prevalence of intermittent slowing was suggested to increase with advancing age when compared to previous studies with younger elderly. However, intermittent slowing occurred only a few times in an EEG test and lasted for less than 2 sec. Moreover, the presence of intermittent slowing did not correlate with any neuropsychological decline or any MRI change. This type of intermittent slowing was regarded as non-specific and clinically silent.

Prospective measures of cerebral atrophy and perfusion among cognitively intact stroke patients

Cerebral atrophy, tissue densities, and local perfusions were measured prospectively utilizing computed tomography among 19 cognitively intact stroke patients and 24 age-matched cognitively and neurologically normal controls. Mean follow-up intervals were 27.0 months for stroke patients and 31.0 months for controls. Stroke patients were treated by controlling risk factors and antiplatelet drugs. Cognitive testing remained normal among patients and controls. Among stroke patients, annual rates for cerebral atrophic indices were +3.4%, for ventricular enlargement +6.9%, for subarachnoid space enlargement +0.1%, and for cortical atrophy -2.5%. Annual reductions in cerebral perfusion, per 100 g brain/min, for cortex were total, -2.3 ml; frontal -3.8 ml; temporal, -2.4 ml; occipital, 2.0 ml; basal ganglia, -2.3 ml; and thalamus -3.8 ml. Annual decreases in local Hounsfield unit (LHU) densities for cortex were total, -0.6 HU; frontal, -0.8 HU; and temporal, -0.4 HU. Among controls, annual rates for cortical atrophy were -1.0% and for declines in cerebral perfusion were -0.7 ml for total cortex, and -1.4 ml for temporal cortex. Annual decreases in HU densities were total cortex, -0.6 HU; frontal, -0.9 HU; and temporal -0.4 HU. Among cognitively intact stroke patients, annual rates for cerebral atrophy and reductions in cerebral cortical perfusion were accelerated by more than three times those seen among agematched controls but were significantly less than similar measures among stroke patients with dementia.

Extracerebral fluid collections in infancy: role of magnetic resonance imaging in differentiation between subdural effusion and subarachnoid space enlargement.

The pathological process of extracerebral fluid collections in infancy includes subdural effusion and enlargement of the subarachnoid spaces. Both conditions have traditionally been investigated as a single clinical entity, because of difficulty in differentiating between them. The prognosis of subdural effusion is not as benign as that of enlargement of subarachnoid spaces, requiring differential diagnosis between these disorders. The present study was conducted to elucidate whether this differentiation could be made on magnetic resonance (MR) images. The series consisted of 16 infants aged 10 months or younger, including eight with verified subdural effusion and eight in whom a diagnosis of enlargement of the subarachnoid spaces was achieved by neuroimaging studies other than MR imaging. In all eight patients with subdural effusion, the intensity of the fluid was greater than that of cerebrospinal fluid (CSF) in at least one of the sequences using T1-weighted, proton-density, and T2-weighted MR images. The flow-void sign, indicating vessels in the fluid spaces, was not seen in any of these eight patients. On the other hand, in all eight patients with enlargement of the subarachnoid spaces, the fluid was isointense in relation to CSF, and vascular flow-void areas were seen in at least one of the MR imaging sequences. Based on these observations, it is concluded that differentiation between subdural effusion and enlargement of the subarachnoid spaces can be established by focusing on two aspects of MR imaging findings: 1) the intensity of the fluid, which is either iso- or hyperintense relative to CSF, and 2) the presence or absence of vascular flow-void areas in the fluid spaces.

Developmental prognosis for infants with benign enlargement of the subarachnoid spaces.

The development of nine infants with enlarged subarachnoid spaces identified by specific CT-scan criteria was prospectively followed to two to three years of age. Infants with intracranial hemorrhage, CNS anomaly, microcephaly or other factors of potentially major negative impact on their development were excluded. All study infants had normal or only minimally increased ventricular size and none developed hydrocephalus. Head circumference was greater than or equal to 90th percentile in all cases, and six fathers also had a head circumference greater than or equal to 90th percentile. Six infants had gross motor delay and mild hypotonia in the first year. One, born at 30 weeks gestational age, had transient dystonia. At follow-up all the infants were developing normally, apart from four with minor concerns. Infants with macrocephaly or rapid head-growth, CT-scan findings of enlarged subarachnoid spaces and normal to minimally increased ventricular size, and who have a parent with macrocephaly, have a good developmental prognosis and a characteristic pattern of neuromotor development in the first year.

Neuronal ceroidlipofuscinosis: CCT findings in fourteen patients.

CCT was performed in 14 children/adolescents with juvenile ceroid lipofuscinosis (JNCL) at different stages of the disease. CCT was normal in 7 patients; mildly abnormal in 3, clearly abnormal in another 3 and severely abnormal in 1 patient. Characteristic findings were symmetrical enlargement of subarachnoid spaces and of the lateral and third ventricles. White matter showed no changes in density. In later stages also the fourth ventricle was enlarged and cerebellar atrophy was seen. CCT findings were not closely correlated with onset and/or severity of the neurological abnormalities. CCT findings were positively correlated with age of the patients: CCT was usually normal if patients were less than 10 years old, and usually abnormal if patients were more than 14 years old.

Computed tomography in the hydrocephalic patient after shunting.

The interpretation of postshunt computed tomographic (CT) scans of hydrocephalic patients presents numerous difficulties unless the interpreter has a thorough knowledge of the clinical symptoms, type and cause of hydrocephalus, preshunt morphology of ventricles and subarachnoid spaces, possible complications of shunt placement, and signs of shunt failure. A review of 368 scans from 108 hydrocephalic patients included subgroup statistical analysis of the development of ventricular asymmetry and of subarachnoid space changes after shunting. The situation and appearance of ventricular catheters were quite variable. Subarachnoid space enlargement after shunting usually was related to long-standing high-grade ventriculomegaly, and was observed most commonly in congenital or acquired nonneoplastic hydrocephalus with little relationship to the site of blockage. Ventricular asymmetry developed in one third of the cases and was related to the site of the shunt catheter tip. Preshunt asymmetry persisted in spite of shunt placement in the larger ventricle. Accurate diagnosis of shunt failure usually required baseline CT studies, correlation with clinical findings, and, in some cases, serial scans.

Cranial Computed Tomography (CCT) Findings in Children Treated with ACTH and Dexamethasone: First Results

8 children with different petit mal epilepsies were systematically treated with ACTH and dexamethasone. CCT examinations were performed before, during and after treatment. In all children severe cerebral changes. enlargement of ventricles and subarachnoid space developed during the initial phase of treatment with Depot-ACTH. Similar changes, but to a less severe degree, could be demonstrated during the phase of dexamethasone therapy thereafter. In all patients cerebral changes disappeared after hormonal treatment had ended. At this point many children had a developmental spurt, developmental relapses could not be observed. It is suggested that these reversible changes seen on CCT scans represent a form of morphological plasticity of brain structures. These results bear certain consequences as to the therapy of cerebral edema.

Cranial computed tomography findings in anorexia nervosa.

Four patients with anorexia nervosa were studied by cranial computed tomography (CT). Three of the four demonstrated abnormal enlargement of cortical sulci and subarachnoid spaces as compared with an age-matched control group. The relationship of this finding to established neuropathological changes in anorexia nervosa is discussed.

Computed tomography; the anatomic basis of the zone of diminished density surrounding meningiomas

Computed tomography of meningiomas often demonstrates a zone of diminished density surrounding the actual tumor. This zone may be related to widening of the subarachnoid space, cerebral edema, tissue necrosis, or demyelination. A case is presented in which the anatomic basis of the zone of diminished density was shown on pneumoencephalography and at surgery to be an enlarged subarachnoid space.