intracranial pressure and intraventricular haemorrhage

3
LE’ITTRS orientated and his speech was clear. He had asterixis (a sudden lapse of position of the limb, with prompt return to its original position), which started within one or two seconds of dorsiflexion of the right wrist, but only after a significant delay of 10 to 20 seconds on the left. Once started, the pattern was the same for both sides. Dorsiflexion of the feet produced asterixis concurrently on both sides, and closing his eyes tightly also induced symmetrical regular opening and closing. Tendon reflexes and power were considered to be equal on the two sides but the supinator jerk was not performed on the left as a period of dialysis had just been completed. The lapse of position in asterixis is associated with electrical silence, simultaneously in all the muscle groups contracting. It has been suggested that this is due to failure of temporal integration of proprioceptive information at a cerebral level2. However, the arteriovenous fistulae must have a local effect which results in brisk tendon reflexes and delay in onset of asterixis. Does a change in the chemical environment, as a result of the shunt, affect the sensitivity of muscle fibres and/or muscle spindles? Royal Hospital for Sick Children, Yorkhill, Glasgow G3 8SJ. RUTH E. DAY ANNA V. MURPHY 1. 2. REFERENCES Venables, G. S., Cartlidge, N. E. F. (1981) ‘Brisk reflexes in the limbs of patients with arteriovenous Tyler, R. H. (1968) ‘Neurological disorders in renal failure.’ American Journaloj’Medicine. 44, 734-748. fistulae.’ Lancer, I, 143. Intracranial Pressure and Intraventricular Haemorrhage SIR-An article by Keasley Welch entitled ‘The intracranial pressure in infants’’ has been brought to our attention subsequent to our submitting our own papers on the causation of intraventricular hemorrhage. We are pleased to find that another author has advanced the same hypothesis for causation as we have d ~ne~.~. Welch states: ‘the intriguing possibility arises that negative intracranial pressure is the force responsible for spontaneous intracranial bleeding in the newborn’. To support this view, he points out that intracranial hemorrhage is a familiar complication of lowered intracranial pressure, as it can occur from lumbar puncture for pneumoencephalography, spinal anesthesia, or diversion of CSF in the treatment of hydrocephalus. He refers also to an association between intraventricular hemorrhage and dehydration of the brain caused by hypernatremic hyperosmolality in infants and experimental animals. However, the subdural and subarachnoid hemorrhages Welch alludes to are different from intraventricular hemorrhage. Direct evidence is not given that germinal-matrix hemorrhage with or without intraventricular hemorrhage- the most common intracranial hemorrhage in the premature newborn-can be related to decreased intracranial pressure. It is disappointing that this author, although measuring intracranial pressure in small newborns prone to intraventricular hemorrhage during the first postnatal days, did not attempt to correlate the occurrence of intracranial hemorrhage with the measured pressures. It is astonishing that so obvious a pathogenetic mechanism as decreased intracranial pressure causing intracranial bleeding in the premature newborn has not received more attention in the literature. Welch was the first to mention it as a theoretical possibility’. We 8 19

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Page 1: Intracranial Pressure and Intraventricular Haemorrhage

LE’ITTRS

orientated and his speech was clear. He had asterixis (a sudden lapse of position of the limb, with prompt return to its original position), which started within one or two seconds of dorsiflexion of the right wrist, but only after a significant delay of 10 to 20 seconds on the left. Once started, the pattern was the same for both sides. Dorsiflexion of the feet produced asterixis concurrently on both sides, and closing his eyes tightly also induced symmetrical regular opening and closing. Tendon reflexes and power were considered to be equal on the two sides but the supinator jerk was not performed on the left as a period of dialysis had just been completed.

The lapse of position in asterixis is associated with electrical silence, simultaneously in all the muscle groups contracting. It has been suggested that this is due to failure of temporal integration of proprioceptive information at a cerebral level2. However, the arteriovenous fistulae must have a local effect which results in brisk tendon reflexes and delay in onset of asterixis. Does a change in the chemical environment, as a result of the shunt, affect the sensitivity of muscle fibres and/or muscle spindles?

Royal Hospital for Sick Children, Yorkhill, Glasgow G3 8SJ.

RUTH E. DAY ANNA V. MURPHY

1.

2.

REFERENCES Venables, G. S., Cartlidge, N. E. F. (1981) ‘Brisk reflexes in the limbs of patients with arteriovenous

Tyler, R. H. (1968) ‘Neurological disorders in renal failure.’ American Journaloj’Medicine. 44, 734-748. fistulae.’ Lancer, I , 143.

Intracranial Pressure and Intraventricular Haemorrhage

SIR-An article by Keasley Welch entitled ‘The intracranial pressure in infants’’ has been brought to our attention subsequent to our submitting our own papers on the causation of intraventricular hemorrhage. We are pleased to find that another author has advanced the same hypothesis for causation as we have d ~ n e ~ . ~ . Welch states: ‘the intriguing possibility arises that negative intracranial pressure is the force responsible for spontaneous intracranial bleeding in the newborn’. To support this view, he points out that intracranial hemorrhage is a familiar complication of lowered intracranial pressure, as it can occur from lumbar puncture for pneumoencephalography, spinal anesthesia, or diversion of CSF in the treatment of hydrocephalus. He refers also to an association between intraventricular hemorrhage and dehydration of the brain caused by hypernatremic hyperosmolality in infants and experimental animals. However, the subdural and subarachnoid hemorrhages Welch alludes to are different from intraventricular hemorrhage. Direct evidence is not given that germinal-matrix hemorrhage with or without intraventricular hemorrhage- the most common intracranial hemorrhage in the premature newborn-can be related to decreased intracranial pressure. It is disappointing that this author, although measuring intracranial pressure in small newborns prone to intraventricular hemorrhage during the first postnatal days, did not attempt to correlate the occurrence of intracranial hemorrhage with the measured pressures.

It is astonishing that so obvious a pathogenetic mechanism as decreased intracranial pressure causing intracranial bleeding in the premature newborn has not received more attention in the literature. Welch was the first to mention it as a theoretical possibility’. We

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Page 2: Intracranial Pressure and Intraventricular Haemorrhage

I)I V I I O P M I N l A l MI I)IC'INI ANI)C' I I I I I ) N I I ~ K O I O ( , Y 1981. 23

pursued the same idea independently, and were able to provide evidence supporting this hypothesis, summarised briefly as follows: ( 1 ) The brains of human infants born after 30 weeks gestation and dying with germinal- matrix and intraventricular hemorrhage are significantly less heavy, even with their massive intraventricular blood-clots, than the brains of their matched controls. I t is likely that this reduction in weight reflects reduced tissue water and tissue pressure'. (2) A close temporal relationship exists between the occurrence of postnatal head-shrinkage4, accompanied by a reduction of intracranial pressure in premature infants', and the occurence of intraventricular hemorrhage. (3) An association between intraventricular hemorrhage and plasma hyperosmolality6, the rapid injection of hyperosmolar solutions (alkali therapy7-"), and hypovolemia and hyp~ tens ion '* -~~ has been observed. I n all four of these circumstances the brain-tissue pressure is reduced; in the first two as a result of attraction of fluid from the brain into the vascular compartment, and in the last two as a result of reduction in perfusion pressure. (4) Bleeding into the ventricles takes place hours, or even days, after birth in most instance^'^"^. Such timing calls for a postnatal mechanism to account for the development of intraventricular hemorrhage. Impaired regulation of water balance leading to decreased cerebral-tissue pressure is prevented from occurring in the fetus in utero, but is recognized as a frequent problem i n small premature infants".

*Laboratory of Neuropathology, University of Cincinnati College of Medicine, Cincinnati, Ohio.

GABRIELLE M. DE COURTEN-MYEKS* THEODORE R ABI NOWlC'Zt

?Head of Division of Neuropathology, University Hospital Centre, Lausanne, Switzerland.

REFERENCES I . Welch, K. (19x0) 'The intracranial pressure in infants.' Journal of Neurosurgery. 52, 693-699. 2. de Courten, G. M., Rabinowicz, T. (1981) 'Intraventricular haemorrhage in premature infants:

reappraisal and new hypothesis.' Developmental Medicine and Child Neurology, 23, 389-403. 3. de Courten, G. M., Rabinowicz. T. (1981) 'Analysis of 100 infant deaths with intraventricular

haemorrhage: brain weights and risk factors.' Developmental Medicine and Child Neurologj', 23,

4. Williams, J., Hirsch, N. J., Corbet, A. J., Rudolf. A. J. (1977) 'Postnatal head shrinkage in small infants.' Pediatrics. 59, 619-622.

5. Welch, K. (1977) 'The emergence of hydrocephalus after ventricular hemorrhage and the estimation o f intracranial pressure in infants.' American .Journal of Diseases 01' Children. 131, 1203-1204.

6. Thomas. D. B. ( 1976) 'Hyperosmolality and intraventricular hemorrhage in premature babies.' Acta Paediatrica Scandinavica. 65, 429-432.

7. Simmons, M. A., Adcock. E. W., Bard, H.. Battaglia, F. C. (1974) 'Hypernatremia and intracranial hemorrhages in neonates.' New England Journal qf Medicine. 291, 6-10.

8 . Wigglesworth, J. S.. Keith, I . H.. Girling, D. J., Slade, S. A. (1976) 'Hyaline membrane disease, alkali. and intraventricular haemorrhage.' Archives qf Diseaw in Childhood, 51, 755-763.

9. Bland, R. D., Clarke, T. L.. Harden, L. B. (1976) 'Rapid infusion ofsodium bicarbonate into premature infants soon after birth: a controlled prospective trial.' American Journal@ Ob.s~et r icsand( ;~nera lu~~:

10. T'iipke, B., Menzel, K. (1977) 'Pufferbehandlung und intrakranielle Blutung bei untergewichtigen asphyktischen Neugeborenen.' fudiarrie und ihrer Grenzgebiete. 16, 9-15.

I I . Papile, L. A.. Burstein. J.. Burstein. R.. Koffler, H.. Koops. B. (1979) 'Relationship of intravenous sodium bicarbonate infusions and cerebral intraven tricular hemorrhage.' .Journal of Pediarrics. 93, 834-836.

287-295.

124, 263-267.

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Page 3: Intracranial Pressure and Intraventricular Haemorrhage

LETTERS

12. Krishnamoorthy, K. S.. Fernandez, R. A., Momose, K. J., de Long, G. R., Moylan, F. M. B., Todres, 1. D.. Shannon, D. C. (1977)‘Evaluation of neonatal intracranial hemmorage by computerized tomography.’ Pediatrics. 59, 165-1 72.

13. Moriette, G.. Relier, J. P., Larroche, J. C. (1977) ‘Les hkmorrhagies intraventriculaires au cours de la maladie des membranes hyalines.’ Archives Franpises de Pidiutrie. 34, 492-504.

14. Fujimura, M., Salisbury, D. M., Robinson, R. 0.. Howat, P., Emerson, P. M.. Keeling, J. W., Tizard, J. P. M. (1979) ‘Clinical events relating to intraventricular haemorrhage in the newborn.’ Archives of Disease in Childhood, 54, 409-414.

15. Dyer, N., Brill, A. B., Gutberlat, R., Raye, J., Faxelius, G., Swanstrom. S., Stahlman, M. (1971) ‘Timing of intracranial bleeding in newborn infants.’ Journal of Nuclear Medicine, 12, 353-354.

16. Tsiantos, A., Victorin, L., Relier, J . P.. Dyer. N., Sundell, H., Brill, A. B., Stahlman. M. (1974) ‘Intraventricular hemorrhage in the prematurely born infant.’ Journal of Pediatrics. 85, 854-859.

17. Roy, R. N., Sinclair, J. C. (1974) ‘Hydration of the low birthweight infant.’ Clinics in Perinutology. 2, 393-417.

Notices

‘Assessing Parental Capacity’ Wallingford. Oxfordshire, 20th-21st January I982

A course on ‘Assessing Parental Capacity-birth parents, substitute parents and local authorities’ will be held at Castle Priory College, Wallingford, Oxfordshire on 20th and 2 1st January 1982. This intensive two-day workshop is designed for experienced staff of all disciplines involved in the welfare of children who have sustained or are vulnerable to abuse. Further information from Mrs. J . W. Knowles, BA, Principal, Castle Priory College, Thames Street, Wallingford, Oxfordshire OX10 OHE. (Tel.: 0491 37551).

World Congress on Mental Retardation Toronto, Ontario, 22nd-26th August 1982

THE lnternational Association for the Scientific Study of Mental Retardation is to sponsor a world congress on mental retardation in Toronto, Canada, from 22nd to 26th August 1982. The theme will be Global Sharing and Learning-Through the 80s, with emphasis on local action. The congress will feature programmes at various levels for scientists, professionals, service providers and consumers, with a full range of topics in the field of developmental disability. Further information from World Congress, N l M R Kinsmen Building, York University Campus, 4700 Keele Street, Downsview, Ontario, Canada M3J 1P3.

European Society for Paediatric Neurosurgery Rennes, France, 27th-30th June I982

THE Eighth Congress of the European Society for Paediatric Neurosurgery will be held in Rennes, France, between 27th and 30th June 1982. Topics will include ‘Turnours of the cerebral hemispheres’, ‘Technical problems in the operating theatre and in the intensive care unit’ and free communications. Further information from Dr. C1. Le Berre, Congress Secretary, Neurosurgical Clinic, University of Rennes, H6pital de Pontchaillou, Rue H. Le Guillou, 3501 1 Rennes, France.

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