Hydrocephalus, congenital hydrocephalus. Aminal model: bovine hydrocephalus, congenital internal hydrocephalus, aqueductal stenosis.
Explore the source record for details and available documents.
SEARCH · PubMed Health
Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Explore the source record for details and available documents.
The coexistence of cerebrovascular disease leading to deep white matter infarction and normal-pressure hydrocephalus has been noted previously in clinical studies, as both diseases can present with the triad of gait disturbance, dementia, and incontinence. The purpose of this MR study was to determine if the two diseases demonstrated a statistical association. Evidence of patchy periventricular hyperintensity representing presumed deep white matter infarction was sought in 20 patients shunted for normal-pressure hydrocephalus and in 35 additional consecutive patients with clinical symptoms and MR findings consistent with normal-pressure hydrocephalus. Deep white matter infarction was also sought in 62 consecutive age-matched control subjects. There was a statistically significant (p less than .001) higher association (58%) of marked infarction in the 55 patients with normal-pressure hydrocephalus than in the age-matched controls (24%). MR findings of communicating hydrocephalus (ventriculomegaly and increased aqueductal CSF flow void) were sought in 78 consecutive patients with presumed deep white matter infarction, and the degree of severity of the two diseases was also found to be statistically significant (p less than .05). In view of this association, the possibility that the two diseases are related was considered. A potential mechanism is discussed whereby deep white matter infarction leading to decreased periventricular tensile strength could result in communicating hydrocephalus. It is plausible that normal-pressure hydrocephalus may result from a number of different insults to the brain.
This report describes the occurrence of rapid progression of hydrocephalus after discharge from the nursery in four of 48 infants who had had previous arrest of progression of post-hemorrhagic hydrocephalus, and at least partial resolution of ventriculomegaly. This later-onset hydrocephalus occurred at a mean age of seven months; the most consistent presenting clinical feature was rapid head growth. Three of the four infants required a ventriculo-peritoneal shunt and the fourth was treated with acetazolamide, with apparent resolution of the hydrocephalus. Newborn infants with post-hemorrhagic hydrocephalus should be followed carefully throughout the first year for prompt detection of later hydrocephalus.
The clinical features and pathophysiology of specific forms of hydromyelia are analyzed in this report together with the chronological changes of associated hydrocephalus. Nine patients were studied; all had hydromyelia with varying degrees of associated hydrocephalus. Clinically applicable classification systems were used to evaluate the progression of hydrocephalus (Stages I to IV) and to define the compartment isolated after shunting in the previously communicating cerebral ventricles (Types I to IV). Four patients had Stage IV disease (holoneural canal dilatation); one had Stage II and four had Stage I disease (both Stages I and II with supratentorial hydrocephalus). All patients were initially treated by ventriculoperitoneal shunting at an average age of 9.9 years. Five patients had progressive spinal symptoms before or after treatment of their hydrocephalus. Two patients had Type III isolation (an isolated rhombencephalic ventricle) with a functioning ventricular shunt; ventriculography confirmed a communication between the fourth ventricle and the hydromyelia, and both patients improved after placement of a shunt in the fourth ventricle. The remaining patients had Type IV isolation (isolated central canal dilatation) with a functioning ventricular shunt. This study indicates that in some cases the pathophysiology of hydromyelia is closely related to associated hydrocephalus. A new concept of the development of an isolated compartment after shunting is proposed to explain the progression of hydromyelia in these cases.
With the advent of computed tomography (CT) scan, much information has been obtained about the pathophysiology of hydrocephalus. It is now clear that hydrocephalus is not a disease entity but rather a syndrome or sign resulting from disturbances in the dynamics of cerebralspinal fluid (CSF) caused by various diseases. Consequently, it has become necessary to revise its definition and classification. In this paper, a contemporary definition and classification of hydrocephalus are presented. Also, a classification of "intractable hydrocephalus"--with its diagnostic criteria--which is a clinically unsolved problem, is attempted, bearing in mind its place in the clinical management and future investigation of the pathophysiology of hydrocephalus.
A review was made of experimental methods available to produce congenital hydrocephalus by teratogenic methods. Radiation, infections, trypan blue, hypervitaminosis A, salicylates and nutritional deficiencies were considered. In the course of prenatal zinc deficiency experiments, congenital hydrocephalus was frequently encountered and histologic sections were made of many representative specimens. Details of the findings are described, among them various types of aqueduct stenosis or obileration. Although these anomalies suggest that occlusion of the aqueduct is the cause of the enlargement of the ventricular system it was noted that there was also ventricular dilatation caudal to the stenotic point of the aqueduct. Hydrocephalus without aqueductal stenosis has also been observed in experimental animals. It seems possible that some cases of congenital hydrocephalus attributed to aqueductal stenosis are examples of hydrocephalus with secondary block of the aqueduct.
A total of 160 patients suspected of having acquired hydrocephalus were studied either by quantitative isotope ventriculography (QIV) or by lumbar isotope cisternography (LIC). Of these patients, 56 had hydrocephalus. Mental deterioration, gait disturbances, ataxia, spasticity, and incontinence were most frequently present in the hydrocephalic patients, but none of the signs or combinations thereof are pathognomonic of acquired hydrocephalus. These signs are independent of the intracranial pressure (ICP) and the type of hydrocephalus. Surgical shunt procedures were in most cases followed by the disappearance of mental deterioration, gait disturbances, ataxia, and spasticity.
It is intended for this research, to provide some basis for the understanding of the rational mechanics of the cranial content. There are many interesting and controversial facts derived from the experimental and clinical-pathological observations of hydrocephalus and increased intracranial pressure. For instance, in some patients a moderate increase of intracranial pressure is accompanied by hydrocephalus and mental changes, while in others, with high intracranial pressure, the ventricles and mental functions remain unaltered. What then is the parameter that changes the size of the ventricles and impairs brain function? It is shown how the transmission of intraventricular pressure throughout the brain parenchyma creates a stress distribution that varies in magnitude; how during the production, maintenance, and reversal of hydrocephalus, and normal pressure hydrocephalus the stress is distributed throughout the brain; and how in the presence of a sudden increase of intracranial pressure nature has arranged additional mechanisms for protecting the brain. It is important to recognize that some aspects of intracranial physiopathology can be explained through classical concepts of physics, prior to attempting to interpret such processes solely in terms of biological or auto-regulatory phenomena.
Dilation of the subarachnoid channels overlying the cerebral hemispheres, ie, external hydrocephalus, can be an early anatomic-radiologic finding in some infants with congenital communicating hydrocephalus. This structural change may progress to ventricular dilation or internal hydrocephalus. Enlargement of the subarachnoid channels appears to occur during the first stage in the development of congenital communicating hydrocephalus, which is to say that the subarachnoid compartment allows accumulation of CSF before there is significant ventricular distention, at least in some infants. When a pneumoencephalogram or a CT scan is performed at this stage, the findings may falsely suggest "cerebral atrophy." In six patients who received this grave neuroradiologic diagnosis, five subsequently developed normally and the sixth has static incoordination or clumsiness and mild intellectual deficiency.
To clarify the pathogenesis of normal pressure hydrocephalus (NPH), quantitative measurement of CSF dynamics was attempted using RI techniques. In this study results concerning RI ventriculography and RI transfer test from CSF to plasma were reported. "Barrier ratio" and regional cerebral blood flow study in NPH will be reported elsewhere. Fifty-three patients with chronic communicating hydrocephalus wer devided into two groups. Thus, twenty-seven cases were diagnosed as NPH according to clinical symptoms and signs, and others were considered as mere chronic communicating hydrocephalus without any NPH characteristics. Results are as follows: 1) 169Yb--DTPA ventriculography; In NPH group, there was longer retention of RI injected into lateral ventricle, and RI activity was not detected in the cisterna magna 60 minutes after the injection. These findings show remarkable delay of CSF flow in NPH patients. 2) Transfer test of 169Yb--DTPA from CSF to plasma; Immediately after the RI injection, Transfer ratio of RI activity from CSF to plasma was measured. It was revealed that intraventricular RI was more rapidly transfered to plasma in NPH group compared with in the control group, suggesting accelerated trans-ependymal absorption of RI in NPH group.
Transaxial CT scans of 100 patients with hydrostatic hydrocephalus and 50 patients with hydrocephalus ex vacuo have been reviewed with respect to measurements of: frontal horn ratio, width of the temporal horns, width of the third ventricle, width of cerebral fissures and sulci. The diagnosis of hydrostatic hydrocephalus is probable when (a) both temporal tips are visualized and measure 2 mm or greater in width and the sylvian and interhemispheric fissures and cerebral sulci are not visible, or (b) there is visualization of temporal horn tips measuring 2 mm or greater in width and the lateral ventricles are symmetrically enlarged with the frontal horn ratio 0.50 or more.
Visual evoked potentials (VEP) of 12 children with progressive hydrocephalus internus were studied. Depending on the severity of hydrocephalus internus VEP show remarkable changes. First of deformation of VEP occurs, than a slowing of latencies and finally an extreme increase of latencies combined with a further deformation of VEP. The whole duration of the VEP shows a marked prolongation.
Based on the results of quantitative isotope ventriculography (QIV) a group of 25 patients was divided into 17 hydrocephalic and 8 non- or doubtfully hydrocephalic patients. An atrio-ventricular shunt (A-V shunt) was inserted in all 25 patients. Eight of the hydrocephalic patients improved or became well, while nine hydrocephalic patients were unchanged, worse or dead at the time of follow-up. These nine patients suffered either from severe brain damage, chronic alcoholism over several years, arterial hypertension, severe diabetes, or acute meningo-encephalitis caused by a virus infection. None of the eight non- or doubtfully hydrocephalic patients improved after the operation. From this it was concluded that QIV is of considerable diagnostic value in acquired hydrocephalus.
Monoamine metabolites, cholinesterases and lactic acid in lumbar cerebrospinal fluid (CSF) were investigated on patients with the adult hydrocephalus syndrome (idiopathic normal pressure syndrome; AHS, n = 15), Alzheimer's disease (AD, n = 14), multi-infarct dementia (MID, n = 13) and controls (n = 21). Patients had clinical and CSF hydrodynamic investigations. Monoamine concentrations were determined by reversed-phase liquid chromatography, cholinesterases and lactate were determined photometrically. In the AHS patients, CSF monoamine concentrations were not significantly different compared with controls, AD or MID patients. AHS and AD patients showed a similar reduction of CSF acetylcholinesterase activity compared with controls. Positive correlations were found in concentrations of CSF homovanillic acid, CSF 5-hydroxyindoleacetic acid and CSF lactic acid versus CSF outflow conductance (that is, resistance against CSF outflow) in the AHS patients. A similar pattern was observed in a subgroup of MID patients characterised by dilated ventricles and disturbed CSF hydrodynamics. These data suggest that a low CSF outflow conductance may facilitate the clearance of acidic substances from the arachnoid space at the probenecid sensitive active transport site. Alternative explanations would be that a pathologically low CSF outflow conductance is accompanied by an inverse caudorostral flow of CSF or a compromised trans-ependymal diffusion.
Use of the miniature Ommaya's reservoir in the treatment of extremely low birth-infant (under 1,000 mg) with hydrocephalus was studied in a series of five patients. The reservoir has a small-caliber with a 3 cm ventricular catheter. For these infants, this miniature Ommaya's reservoir is extremely useful for protection of the cortical mantle until a definitive procedure can be carried out after increase of body weight. The clinical course in five cases are summarized.
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.