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Query: UMLS:C0024523 (malabsorption)
 7,319 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. Between 1965 and 1974 146 patients with unexplained tetraspasticity were admitted and examined. In 123 cases extended neuroradiologic examination with myelography of the cervical spinal canal was carried out. A space occupying lesion was found in 59 cases: narrow spinal canal, protruding discs. In 64 cases no pathologic processes were seen radiologically. Comparison of both groups: no differences in clinical signs, history or findings. 2. Tetraspasticity alone was the leading sign in 30 cases. The legs were always more severely involved than the upper limbs. In 70% spasticity was more severe on the right. Further clinical analysis depends on additional signs, particularly paresthesiae, pain, disturbed joint-sense. Among the patients with protruding discs heart-and circulatory insufficiency is a little more common, but in the group without protrusion exogenous/endogenous metabolic conditions(intoxication, malabsorption) and neoplasms. -Protein content of CSF is raised equally in both groups, particularly albumin. This is probably due to reduced circulation of CSF. In 6 patients an internal hydrocephalus was found. 3. No single active causative factor could be found nor any familial relationship. In spite of increasingly extended diagnostic techniques no underlying condition could be discovered. Tetraspastic is a "polygenetic" reaction of the central nervous system without a final common path. The cases show that mechanical factors (cervical myelopathy) predispose locally to non-mechanical injuries.
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PMID:[Unexplained tetraspasticity in adults (author's transl)]. 58 67

Although complication occasionally occur in the use of ventriculoperitoneal shunts (VP-shunt), the occurrence of intractable ascites and extracranial metastasis through the shunt are uncommon. Recently intractable ascites occurred in a two years old girl in whom a left VP-shunt had been placed before four month for obstructive hydrocephalus secondary to medulloblastoma. Paracentesis was performed with recovery of clear, straw-colored fluid with a specific gravity of 1012, a protein content of 0.3 gm/L and many of mononuclear cell on microscopic examination. Liver-scan and enzyme profile gave normal results. During 3 weeks, 6 times paracentesis were performed and total volumes of ascites were 3850 ml. At 5 and 6 times paracentesis, Carboquone 1 mg was injected into peritoneal cavity and 0.1 mg into ventricle cavity through flashing device. After these injection, intractable ascites were cured, no metastasis can be seen in peritoneal cavity when died 4 month later. No precise explanation can be offered for occurrence of this intractable ascites. It is said that chronic irritation of the visceral and parietal peritoneum or sub-clinical peritonitis may cause peritoneal malabsorption. In our case, antitumor agent was very effective, so this treatment will be recommended to try for intractable ascites.
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PMID:[Medulloblastoma with intractable ascites treated by carboquone--a complication of a ventriculoperitoneal shunt (author's transl)]. 59 23

Malabsorption of cerebrospinal fluid was made experimentally by the administration of neutral carbon black suspension into the lateral ventricles of 22 adult cats. The compartmental analysis of intracranial pressure at the intraventricular fluid and tissue pressure in the cerebral white matter was carried out in the early stage of the communicating hydrocephalus. Following results were obtained: 1) Cerebrospinal fluid pressure from the lateral ventricle was always significantly higher than that from the brain tissue during the process of ventricular expansion. 2) Water content in the cerebral white matter was correspondingly increased when the pressure difference with greater value in ventricular fluid pressure was maintained. However tissue water content was decreased definitively when such pressure values at two compartments were equalized due to augment of the tissue pressure component. 3) Decreasing of cerebral blood flow demonstrated in spite of relatively higher value of cerebral perfusion pressure. From these findings the authors speculated that a higher pressure in the ventricular system will be a driving force, by which the enlargement of ventricular system was induced.
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PMID:[Measurement of ventricular fluid pressure and brain tissue pressure in acute experimental communicating hydrocephalus (author's transl)]. 71 48

The syndrome of abasia (gait disorder) and incontinence in old age is aetiologically ambiguous. If it is combined with an internal communicating hydrocephalus, it is necessary to think of the syndrome of malabsorption hydrocephalus and consequently of a drainage of the cerebro-spinal fluid. The indication for a shunt is defined with a diagnostic lumbar puncture, a cerebrospinal fluid scan, and if it is still uncertain, by continuous cerebro-spinal fluid pressure records. In a well-defined indication with the shunt, more than half of the patients would improve and about one third of them would have a very good recovery. However, a shunt operation on a patient with hydrocephalus ex vacuo (from cerebral atrophy) should be avoided since it could worsen the patient's condition. Therefore it is essential to discriminate clearly between these two very different types of hydrocephalus.
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PMID:[Hydrocephalus. Abesia--dementia--incontinence. Drain or not?]. 409 77

The authors investigated the hydrodynamics in normal pressure hydrocephalus (NPH) and suggested surgical indication for identifying cases suitable for shunt operation. 48 patients with presumed NPH who underwent CT scanning, CT cisternography, and continuous monitoring of intracranial pressure for 24 hours were studied for assessing the correlation of incidence of B wave with clinicopathological features of the normal pressure hydrocephalus syndromes. The causes of NPH consisted of idiopathic of primary origin in 24 patients, subarachnoid hemorrhage in 9, head injury in 8, cerebrovascular occlusion in 3, meningitis in 2, intracerebral hematoma in one and craniotomy in one. The incidence of B waves in term of percentage of time with B waves did not correlate with the age of the patients and presence or absence of CT evidence of brain atrophy. There was a good correlation between incidence of B waves and the degree of ventriculomegaly, the presence of periventricular lucency on CT, and the grade of CSF circulation disturbance as evaluated by CT cisternography. The pathogenesis of B waves may be related to increased malabsorption of CSF in the major pathways and episodic pressure response promoting CSF absorption in the lesser pathways. Those patients who exhibit the type IV or type V on CT cisternography and B waves for more than 20% of the time monitored on continuous monitoring of intracranial pressure (ICP) responded to shunting in more than 90%. Patients showing type III-b on CT cisternography and B waves for more than 5% on ICP monitoring benefited from a shunt in about 70%. On the other hand, patients with type III-a on CTC and B waves for less than 5% of the time monitored could not be expected to respond to shunting. Incidence of B waves on continuous ICP monitoring correlated closely with response to CSF shunting. Therefore continuous ICP monitoring, combined with CT cisternography, provide a reliable indication of the potential of a patient with NPH to recover after shunting.
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PMID:[Continuous intracranial pressure monitoring in normal pressure hydrocephalus--with special reference to clinical significance of B wave and prognostic criteria for CSF shunting]. 684 9

A Bull Terrier that was continuously chasing its tail was examined clinically, electroencephalographically, and by computed tomography of the head. The dog was also given test treatments with an anticonvulsant (diazepam) and a pure opioid antagonist (naloxone). The dog appeared to be hysterical and dissociated from its surroundings. Electroencephalography revealed a seizure pattern that was most marked over the temporal lobe, and computed tomography revealed mild hydrocephalus. Diazepam effectively controlled tail chasing, whereas naloxone did not. The dog was discharged on anticonvulsant therapy but subsequently had to be euthanatized when aggression developed. Results of examination and treatment have led the investigators to propose a hereditary mechanism for tail chasing, perhaps related to zinc malabsorption.
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PMID:Tail chasing in a bull terrier. 845 9

The disease is named after George H. Whipple who, in 1907, was the first to describe an intestinal "lipodystrophy". Although Whipple's disease is generally recognized as a multisystem chronic granulomatous disease, primarily involving the digestive system, it can also appear as a primary neurological disorder in rare cases. Most often it is manifested with loss of weight, diarrhea, malabsorption, abdominal pain, lymphadenopathy, cardiopathy, hyperpigmentation and hypotension. The presence of periodic acid-Schiff (PAS)-positive macrophages in biopsy specimens (not only jejunal) and demonstration of "Whipple's bacilli" visible by electron microscopy, are diagnostic signs of active Whipple's disease. Whipple's disease confined to the CNS is rare. It is rarely found in the differential diagnosis of patients with progressive neurological deterioration. The most common neurological picture includes progressive dementia, external ophalmoplegia, myoclonus, seizures, ataxia, hypothalamic dysfunction (sleep disorders, hyperphagia, polydipsia) and meningitis. Oculofacial-skeletal myorhythmia as a movement disorder, associated with Whipple's disease, is reported. Fulminant course of cerebral Whipple's disease is unusual and unfavourable. The confusing and nonspecific clinical appearance is typical for primary CNS involvement. It has recently been suggested that CNS involvement occurs in all cases, although only 10-20% of patients may show it. The CNS is the most common site of disease relapse. The CT scans and MRI of the brain are often normal, but may show cortical/subcortical atrophy, hydrocephalus, focal or intracerebral mass lesions. The cerebrospinal fluid can sometimes contain PAS-positive macrophages. Brain biopsy is suggested as a diagnostic method in cases of high suspicion of CNS Whipple's disease. However, the lesions are frequently inaccessible and false negative. Without extended antibiotic therapy, the course of Whipple's disease is lethal. Now, the prognosis is good, although the optimal antimicrobial regimen is not clearly established. Initial parenteral therapy (tetracycline, penicilline, streptomycine, chloramphenicol, ampicilline) and peroral long-term treatment with trimetoprime-sulphametoxasole, are recommended. As CNS relapse of Whipple's disease may occur after several years, long-term treatment should include antibiotics that are able to cross the blood-brain barrier. The CNS relapse, in contrast to the systemic ones, is resistant to the treatment. Appropriate therapy instituted earlier in the course of the disease is associated with a better neurological outcome. Early recognition can be critical in Whipple's disease because of irreversible neurological sequelae seen later in the course of this potentially treatable condition. In cases with high clinical suspicion in which Whipple's disease cannot be diagnosed with procedures such as jejunal biopsy, antibiotic therapy is recommended. Recovery of an established neurological deficit may rarely occur. Longterm follow-up studies would help to identify the optimal antibiotic regimen and duration of treatment.
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PMID:[Neurologic disorders in Whipple's disease]. 910 28

Three unrelated infants presented with radiographic punctate calcifications, nasal hypoplasia, and abnormalities of the spine. Additional anomalies included cupped ears in 2 patients and one each with Dandy-Walker malformation with hydrocephaly, congenital cataracts, and peripheral pulmonary artery stenosis. The mothers of these 3 patients had chronic conditions associated with intestinal malabsorption requiring total parenteral nutrition for varying periods of time. The underlying causes of malabsorption were celiac disease, short bowel syndrome secondary to surgical resection, and jejuno-ileal bypass, respectively. Bleeding diathesis occurred in one mother requiring vitamin K supplementation during the second and third trimesters of pregnancy. We speculate that the chondrodysplasia punctata and other abnormalities in these children were caused by an acquired maternal vitamin K deficiency manifested during early pregnancy. However, the involvement of other vitamin deficiencies cannot be excluded. Thus, vitamin K deficiency of the embryo secondary to maternal malabsorption appears to be a third vitamin K-related mechanism leading to chondrodysplasia punctata in addition to warfarin embryopathy and epoxide reductase deficiency (pseudo-warfarin embryopathy).
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PMID:Vitamin K deficiency embryopathy: a phenocopy of the warfarin embryopathy due to a disorder of embryonic vitamin K metabolism. 938 32

The traditional theory of communicating hydrocephalus has implicated the bulk flow component of CSF motion; that is, hydrocephalus is generally understood as an imbalance between CSF formation and absorption. The theory that the cause of communicating hydrocephalus is malabsorption of CSF at the arachnoid villi is not substantiated by experimental evidence or by physical reasoning. Flow-sensitive MRI has shown that nearly all CSF motion is pulsatile, and there is substantial evidence that hyperdynamic choroid plexus pulsations are necessary and sufficient for ventricular dilation in communicating hydrocephalus. We have developed a model of intracranial pulsations based on the analogy between the pulsatile motion of electrons in an electrical circuit and the pulsatile motion of blood and CSF in the cranium. Increased impedance to the flow of CSF pulsations in the subarachnoid space redistributes the flow of pulsations into the ventricular CSF and into the capillary and venous circulation. The salient features of communicating hydrocephalus, such as ventricular dilation, intracranial pressure waves, narrowing of the CSF-venous pressure gradient, diminished cerebral blood flow, elevated resistive index and malabsorption of CSF, emerge naturally from the model. We propose that communicating hydrocephalus is the result of a redistribution of CSF pulsations in the cranium.
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PMID:A model of pulsations in communicating hydrocephalus. 1207 74

It is almost a century since Dandy made the first experimental studies on hydrocephalus, but its underlying mechanism has been unknown up to now. The conventional view is that cerebrospinal fluid (CSF) malabsorption due to hindrance of the CSF circulation causes either obstructive or communicating hydrocephalus. Analyses of the intracranial hydrodynamics related to the pulse pressure show that this is an over-simplification. The new hydrodynamic concept presented here divides hydrocephalus into two main groups, acute hydrocephalus and chronic hydrocephalus. It is still accepted that acute hydrocephalus is caused by an intraventricular CSF obstruction, in accordance with the conventional view. Chronic hydrocephalus consists of two subtypes, communicating hydrocephalus and chronic obstructive hydrocephalus. The associated malabsorption of CSF is not involved as a causative factor in chronic hydrocephalus. Instead, it is suggested that increased pulse pressure in the brain capillaries maintains the ventricular enlargement in chronic hydrocephalus. Chronic hydrocephalus is due to decreased intracranial compliance, causing restricted arterial pulsations and increased capillary pulsations. The terms "restricted arterial pulsation hydrocephalus" or "increased capillary pulsation hydrocephalus" can be used to stress the hydrodynamic origin of both types of chronic hydrocephalus. The new hydrodynamic theories explain why third ventriculostomy may cure patients with communicating hydrocephalus, a treatment incompatible with the conventional view.
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PMID:Radiological assessment of hydrocephalus: new theories and implications for therapy. 1601 May 78


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