22
that
are
crucial to the formation of cholesterol
stones
and
explain changes in frequency. As for prevention--one can only reinforce the currently fashionable counsel for the healthy lifestyle which attempts to keep us slim and avoid very large families. Jørgensen T. Abdominal symptoms and gallstone disease: an epidemiological investigation. Hepatology 1989; 9: 856-60. 2. Royal College of General Practitioners’ Oral Contraception Study. Oral contraceptives and gallbladder disease. Lancet 1982; ii: 957-59. 3. Watkinson G. The autopsy incidence of gallstones in England and Scotland. Proceedings Third World Congress of Gastroenterology, Tokyo, 1967; 4: 125-30. 4. Barker DJP, Gardner MJ, Power C, Hutt MSR. Prevalence of gallstones at necropsy in nine British towns: a collaborative study. Br MedJ 1979; 1.
ii: 1389-92.
There was unanimous agreement about the principles underlying the pathophysiology of NPH. Any defect in the main exit channels from the CSF pathways to the venous
circulation at the cranial arachnoid villi will cause an increase in resistance to outflow. Most fluid normally passes through extracellular intraendothelial clefts, but with increasing CSF pressures, micropinocytotic vesicles respond by enlarging and fusing to create transcellular channels. If the arachnoid space is contaminated by red cells as a result of head injury, surgery, or subarachnoid haemorrhage, fibrinogen is converted to fibrin, encouraging deposition of a protein net. This net impedes the circulation of CSF over the hemispheres and the villi become clogged. A substance present in whole blood and plasma but not in
NORMAL-PRESSURE HYDROCEPHALUS few neurological conditions for which the is simple and often dramatically effective but the methods of reaching the diagnosis remain controversial. Even the conventionally accepted name of normal-pressure hydrocephalus (NPH), introduced by Hakim in 1964, is misleading because hydrocephalus in the proven absence of a raised resting intracranial pressure is a feature of several other conditions-eg, cerebral atrophy, multiple infarcts, Alzheimer’s disease, and hypertensive encephalopathy. The classic triad of progressive dementia, gait disturbance, and urinary incontinence is as likely to occur in any of these more common disorders as in NPH, so differentiation on the basis of clinical criteria alone is most unwise. There
are
dialysate interrupts transendothelial
vesicular transport and further raises the overall outflow resistance. Pressure gradients are created between formation and absorption sites, and it is the transmantle gradient that may well contribute to the dilatation of the ventricles either acutely or several months later. Although villus changes occur after meningitis, structural changes have not been reported in idiopathic NPH and the defect in absorption remains a mystery. serum or
treatment
It is necessary to select a group of patients who would have a good chance of responding to permanent drainage of the cerebrospinal fluid (CSF) through a ventriculoatrial or ventriculoperitoneal shunt. With the introduction of higher definition computed tomographic scanning in the past decade, it had been hoped that recognition of periventricular translucency and disproportionately narrow surface sulci at the vertex of the hemispheres, in addition to the classic clinical features, would resolve the diagnostic difficulty. For a small subgroup of patients with a previous head injury, cranial surgery, subarachnoid haemorrhage, or a bout of meningitis and for another subgroup with a short history or radiological evidence of enlarging ventricles, this selection is believed by many to be acceptable, with over a 40% chance of successful response to a shunt. However, most patients referred to neurologists have a history of many months with two or three of the clinical triad, some of the radiological features of NPH, and no known relevant history. In such cases, the success rate of CSF drainage is less than 15 %, and just below the incidence of postoperative complications. Subjecting all these patients to a shunt procedure would be deemed indiscriminate.
Faced with this dilemma, a group of neurosurgeons in Copenhagen lately asked the Alfred Benzon Foundation to assemble a group of basic scientists and clinical researchers from nine countries to discuss openly the terminology, diagnosis, and treatment of this condition and to share their experiences of studying the disorders of CSF circulation implicated in this and other neurological conditions.!
Previously, isotope and pneumoencephalography were to demonstrate the supposed changes in CSF flow
used
patterns. Others have monitored intracranial pressure for 24 hours to observe the frequency of B waves, which are more common in these patients. Such indirect measurements do not add any diagnostic information to the clinical and features. At the Copenhagen symposium, the assembled company unanimously favoured estimating the influence of the pathological process on CSF circulation by measuring outflow resistance in patients with suspected idiopathic NPH. Most agreed that if the outflow resistance was less than 11 mm Hg/ml per minute, a shunt was unlikely to help. The higher the resistance above this level, the greater was the chance of clinical improvement with shunting, with probabilities ranging from 25% to 80%.
radiological
The methods of measurement used varied from centre to In one series of over 2000 patients, access to the CSF circulating system was by the lumbar route, but it was essential that the arachnoid should not be penetrated more than once to prevent extravasation of CSF during the test through previous puncture holes. Most workers preferred ventricular access, despite the slight risk of infection. A bolus technique is simple and quick, but in unanaesthetised patients the resistance is underestimated because the bolus causes a pressure overshoot due to transient vasodilatation, and reproduciblity is then poor. Continuous infusions of Ringer lactate to produce a series of steady states, either by constant flow or by constant pressure, proved very reproducible and compared favourably with the most complex technique, by which electronically regulated infusions were used to achieve rapid stabilisation, with computer modelling to allow volume accounting. centre.
Despite the general agreement on the practical issues relating to normal-pressure hydrocephalus, the thirty-one participants suggested thirty-one "more appropriate" alternative names for this syndrome. 1.
Gjerris F, Borgesen SE, Sorensen PS, eds. Outflow of cerebrospinal fluid. Alfred Benzon Symposium 27. Copenhagen: Munksgaard, 1989.
that
are
crucial to the formation of cholesterol
stones
and
explain changes in frequency. As for prevention--one can only reinforce the currently fashionable counsel for the healthy lifestyle which attempts to keep us slim and avoid very large families. Jørgensen T. Abdominal symptoms and gallstone disease: an epidemiological investigation. Hepatology 1989; 9: 856-60. 2. Royal College of General Practitioners’ Oral Contraception Study. Oral contraceptives and gallbladder disease. Lancet 1982; ii: 957-59. 3. Watkinson G. The autopsy incidence of gallstones in England and Scotland. Proceedings Third World Congress of Gastroenterology, Tokyo, 1967; 4: 125-30. 4. Barker DJP, Gardner MJ, Power C, Hutt MSR. Prevalence of gallstones at necropsy in nine British towns: a collaborative study. Br MedJ 1979; 1.
ii: 1389-92.
There was unanimous agreement about the principles underlying the pathophysiology of NPH. Any defect in the main exit channels from the CSF pathways to the venous
circulation at the cranial arachnoid villi will cause an increase in resistance to outflow. Most fluid normally passes through extracellular intraendothelial clefts, but with increasing CSF pressures, micropinocytotic vesicles respond by enlarging and fusing to create transcellular channels. If the arachnoid space is contaminated by red cells as a result of head injury, surgery, or subarachnoid haemorrhage, fibrinogen is converted to fibrin, encouraging deposition of a protein net. This net impedes the circulation of CSF over the hemispheres and the villi become clogged. A substance present in whole blood and plasma but not in
NORMAL-PRESSURE HYDROCEPHALUS few neurological conditions for which the is simple and often dramatically effective but the methods of reaching the diagnosis remain controversial. Even the conventionally accepted name of normal-pressure hydrocephalus (NPH), introduced by Hakim in 1964, is misleading because hydrocephalus in the proven absence of a raised resting intracranial pressure is a feature of several other conditions-eg, cerebral atrophy, multiple infarcts, Alzheimer’s disease, and hypertensive encephalopathy. The classic triad of progressive dementia, gait disturbance, and urinary incontinence is as likely to occur in any of these more common disorders as in NPH, so differentiation on the basis of clinical criteria alone is most unwise. There
are
dialysate interrupts transendothelial
vesicular transport and further raises the overall outflow resistance. Pressure gradients are created between formation and absorption sites, and it is the transmantle gradient that may well contribute to the dilatation of the ventricles either acutely or several months later. Although villus changes occur after meningitis, structural changes have not been reported in idiopathic NPH and the defect in absorption remains a mystery. serum or
treatment
It is necessary to select a group of patients who would have a good chance of responding to permanent drainage of the cerebrospinal fluid (CSF) through a ventriculoatrial or ventriculoperitoneal shunt. With the introduction of higher definition computed tomographic scanning in the past decade, it had been hoped that recognition of periventricular translucency and disproportionately narrow surface sulci at the vertex of the hemispheres, in addition to the classic clinical features, would resolve the diagnostic difficulty. For a small subgroup of patients with a previous head injury, cranial surgery, subarachnoid haemorrhage, or a bout of meningitis and for another subgroup with a short history or radiological evidence of enlarging ventricles, this selection is believed by many to be acceptable, with over a 40% chance of successful response to a shunt. However, most patients referred to neurologists have a history of many months with two or three of the clinical triad, some of the radiological features of NPH, and no known relevant history. In such cases, the success rate of CSF drainage is less than 15 %, and just below the incidence of postoperative complications. Subjecting all these patients to a shunt procedure would be deemed indiscriminate.
Faced with this dilemma, a group of neurosurgeons in Copenhagen lately asked the Alfred Benzon Foundation to assemble a group of basic scientists and clinical researchers from nine countries to discuss openly the terminology, diagnosis, and treatment of this condition and to share their experiences of studying the disorders of CSF circulation implicated in this and other neurological conditions.!
Previously, isotope and pneumoencephalography were to demonstrate the supposed changes in CSF flow
used
patterns. Others have monitored intracranial pressure for 24 hours to observe the frequency of B waves, which are more common in these patients. Such indirect measurements do not add any diagnostic information to the clinical and features. At the Copenhagen symposium, the assembled company unanimously favoured estimating the influence of the pathological process on CSF circulation by measuring outflow resistance in patients with suspected idiopathic NPH. Most agreed that if the outflow resistance was less than 11 mm Hg/ml per minute, a shunt was unlikely to help. The higher the resistance above this level, the greater was the chance of clinical improvement with shunting, with probabilities ranging from 25% to 80%.
radiological
The methods of measurement used varied from centre to In one series of over 2000 patients, access to the CSF circulating system was by the lumbar route, but it was essential that the arachnoid should not be penetrated more than once to prevent extravasation of CSF during the test through previous puncture holes. Most workers preferred ventricular access, despite the slight risk of infection. A bolus technique is simple and quick, but in unanaesthetised patients the resistance is underestimated because the bolus causes a pressure overshoot due to transient vasodilatation, and reproduciblity is then poor. Continuous infusions of Ringer lactate to produce a series of steady states, either by constant flow or by constant pressure, proved very reproducible and compared favourably with the most complex technique, by which electronically regulated infusions were used to achieve rapid stabilisation, with computer modelling to allow volume accounting. centre.
Despite the general agreement on the practical issues relating to normal-pressure hydrocephalus, the thirty-one participants suggested thirty-one "more appropriate" alternative names for this syndrome. 1.
Gjerris F, Borgesen SE, Sorensen PS, eds. Outflow of cerebrospinal fluid. Alfred Benzon Symposium 27. Copenhagen: Munksgaard, 1989.
