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Query: UMLS:C0010200 (cough)
23,843 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

CSF pressure recordings have been taken from the lumbar region and the cisterna magna of 16 patients during coughing in the sitting position. Isolated coughs of low amplitude have been studied. The lumbar pressure waves occur sooner and lower. Thus there is a phase during which the lumbar pressure exceeds the cisternal, followed by one in which the cisternal exceeds the lumbar. These phenomena may be conveniently displayed on a differential trace. The phase during which the cisternal pressure exceeds the lumbar may be protracted. It is suggested that Froin's syndrome, central subarachnoid pouches and syringobulbia may be associated with upward pressure waves. Cough headache, the filling stages of communicating syringomyelia and tonsillar herniation may be associated with valve-like blockage at the foramen magnum which produces craniospinal pressure dissociation by interfering with downward or rebound pulsation. Decompensation of hydrocephalus after birth may be related to pulsation in association with crying; also after removal of a meningocele sac decompensation may be related to the effects of similar pulsation modified by changes in capacitance following operation. The cord destruction of syringomyelia, and the mechanisms which fill spinal subarachnoid cysts may be related to pressure waves directed both upwards and downwards. The merits and limitations of cough impulse as a clinical test for spinal blockage are discussed, and the suggestion is made that after further evaluation they may provide a more sensitive indication of spinal blockage than Queckenstedt's test.
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PMID:Cerebrospinal fluid pressure changes in response to coughing. 99 Sep

Herniation of the hindbrain occurs when the lowest parts of the cerebellum and sometimes part of the medulla are moved downwards through the foramen magnum, a pressure difference acting across the foramen magnum moulding the tissues into a plug. It is suggested that the clinical course in both adults and babies with spina bifida may be explained by the hindbrain hernia acting as a valve.The term 'Chiari Type I deformity' is commonly used for an abnormality in which the tonsils and lowermost parts of the cerebellar hemispheres are prolapsed through a normal foramen magnum. Acute herniation may occur as a result of space-occupying lesions. Chronic herniation may be morphologically identical although it tends to be more severe. Sometimes it will produce few symptoms which often may be delayed so that the original causative lesion may not be apparent. Causes include bone softening, tumour, or previous meningitis. Birth injury is probably the commonest cause of the deformity, which presents clinically in adults.In infants with severe forms of spina bifida a hindbrain herniation is present. This abnormality may be called 'Chiari Type II deformity' or Arnold-Chiari deformity and is an intra-uterine abnormality in which the fourth ventricle and medulla are grotesquely herniated before they are properly developed and the foramen magnum is enlarged.The commonest clinical presentation of Chiari Type I deformity is syringomyelia, which is usually not diagnosed until adult life. Other presentations include syringobulbia, headache, oscillopsia, attacks of giddiness, lower cranial nerve palsies, and ataxia. Particularly characteristic are cough headache and cough syncope. Syringomyelia and syringobulbia in particular may be irreversible by the time they are diagnosed. Nevertheless, surgical decompression may be successful in relieving symptoms of headache, cough syncope, and long-tract compression; most cases of syringomyelia show some improvement and in others progression of the disease is arrested. Operative techniques for hindbrain herniation are discussed.Chiari Type II deformity is probably responsible for the progression of hydrocephalus after birth in the majority of babies with spina bifida. Measurement of pressure in the cerebrospinal fluid above and below the foramen magnum shows that intermittent pressure difference is commonly present at times of neurological deterioration. Surgical decompression of the hernia in adults allows correction of the valvular effect, which may be monitored by pressure measurements. In babies the associated hydrocephalus is usually so gross that it requires separate treatment, but pressure monitoring may be of value in assessing the state of the disease.
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PMID:Chronic herniation of the hindbrain. 701 51

This is a case report of a male patient who presented with orofacial pain for a year as the only manifestation of syringobulbia-syringomyelia associated with Arnold-Chiari malformation. This article places emphasis on the clinical presentation and possible differential diagnoses. The pain was continuous and affected the left side of the face. It was exacerbated by coughing and physical effort, possibly as a consequence of an increase in intracranial pressure. Paroxysmal pain crises developed over this background of continuous pain, compatible with neurogenic trigeminal pain of the left second branch, together with pain episodes similar to cluster headache on the same side. The symptoms were resolved following neurosurgical management with amplification of the foramen magnum.
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PMID:Orofacial pain as the sole manifestation of syringobulbia-syringomyelia associated with Arnold-Chiari malformation. 1144 28

Syringomyelia is frequently accompanied by an extramedullary lesion at the foramen magnum, particularly a Chiari I malformation. Although syringomyelia associated with foramen magnum obstruction has characteristic clinical, radiological, and neuropathological features, its pathogenesis remains unclear. Currently prevalent hydrodynamical theories assert that obstruction of the subarachnoid space at the foramen magnum interferes with flow of cerebrospinal fluid (CSF) between the spinal and the intracranial subarachnoid compartments. As a result, spinal CSF is driven into the spinal cord through the perivascular spaces to form a syrinx. These theories are implausible biophysically because none postulates a pump adequate to drive fluid through these spaces. None of the theories can explain why syrinx pressure is higher than CSF pressure; why extensive gliosis, edema, and vascular wall thickening regularly occur; and why the composition of syrinx fluid is not identical with that of CSF. A new theory of pathogenesis is proposed to address these difficulties. In the presence of subarachnoid obstruction at the foramen magnum, a variety of activities, such as assuming the erect posture, coughing or straining, and pulsatile fluctuations of CSF pressure during the cardiac cycle, produce transiently higher CSF pressure above the block than below it. There are corresponding changes in transmural venous and capillary pressure favoring dilation of vessels below the block and collapse of vessels above the block. The spatially uneven change of vessel caliber produces mechanical stress on the spinal cord, particularly caudal to the block. The mechanical stress, coupled with venous and capillary dilation, partially disrupt the blood-spinal cord barrier, allowing ultrafiltration of crystalloids and accumulation of a protein-poor fluid. The proposed theory is consistent with the neuropathological findings in syringomyelia and with the pressure and composition of syrinx fluid. It also accounts for the prolonged course of syringomyelia and its aggravation by cough, strain, and assumption of an erect posture. It contributes to understanding the low incidence and the morphology of syringobulbia. It explains the poorly understood presentation of foramen magnum meningiomas with symptoms of a mid- to low-cervical myelopathy. The theory also affords an understanding of the late recurrence of symptoms in children with hydromyelia who are treated with a ventricular shunt.
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PMID:The pathogenesis of syringomyelia associated with lesions at the foramen magnum: a critical review of existing theories and proposal of a new hypothesis. 1514 May 99