SUMMARY Three patients with subacute necrotising encephalolmyelopathy are reported, all of whose CT brain-scans showed areas of low attenuation in the basal ganglia, especially in the lenticular nucleus. The authors suggest that this brain-scan appearance may help in the diagnosis of this disorder during life.

ZUSAMMENFASSUNG C T Befunde hei suhakuter nekrotisierender Encephalomyelopathie Es wird iiber drei Patienten mit subakuter nekrotisierender Encephalomyelopathie berichtet, bei denen das Hirn CT hypodense Areale in den Basalganglien, insbesondere im Nucleus lenticularis, aufwies. Die Autoren sind der Meinung, dap dieser Befund beim Hirn C T die Diagnose dieser Erkrankung zu Lebzeiten erleichtern kann.

RESUMEN Aspect0 del scanner en la encefolomielopatia necrotizanre Tres pacientes con encefalomielopatia necrotizante subaguda mostraban en su scanner cerebral Areas de baja densidad en 10s ganglios basales, especialmente en el nucleo lenticular. Los auteres sugieren que esta imagen en el scanner puede ayudar al diagn6stico de esta enfermedad en vida.

References Aquilonius, J., Askmark, H., Enoksson, P.,

Lundberg, P. 0.. Mostrom, U . (1978) 'Com- puterized tomography in severe methanol in- toxication.' British Medical Journal, 1, 929-930.

Bertorini, T., Engel, W., Di Chiro, G., Dalakas, M. (1978) 'Leukoencephalopathy in oculocranio- somatic neuromuscular disease with ragged red fibers. Mitochondria1 abnormalities demonstrated by computerized tomography.' Archives of Neurology, 35, 643-647.

Ebels, E., Bloxzijl, E., Troelstra, J. (1965) 'A Wernicke-like encephalomyelopathy in children (Leigh), an inborn error of metabolism?' Ilelverica Paediatrica Acta, 3, 310-324.

Finelli, P. (1981) 'Changes in the basal ganglia following cyanide poisoning.' Journal of Computer Asrisred Tomography. 5 , 755-756.

Goutikres, F., Aicardi. J. (1982) 'Acute neurological dysfunction associated with destructive lesions of the basal ganglia in children.' Annals of Neurology. 12. 328-332.

Hall, K., Gardner-Medwin, D. (1978) 'CT scan appearances in Leigh's disease (subacute necro- tizing encephalomyelopathy).' Neuroradiology.

Hirabashi, S., Kitahara, T., Hishida, T. (1980) 'CT in perinatal hypoxic and hypoglycemic en- cephalopathy with emphasis o n follow-up studies.' Journal of Computer Assisted 7omogruphy. 4,

16, 48-50.

Peroneal Palsy Produced by Intravenous Fluid Infiltration in a Newborn

Karherine L. Kreusser 522 Joseph J. Volpe

45 1-456. Kendall. ,B., Claveria, L., Quiroga, W. (1977) 'CAT

scan i n leukodystrophies and neuronal de- generations.' In Boulay, G. (Ed.) The First European Seminar in C T Scan in Clinical Practice. Heidelberg: Springer. pp. 191-202.

Maki, Y., Akimoto, H., Enomoto, T. (1980) 'Injuries of basal ganglia following head trauma in children.' Child's Brain. 7, 1 13- 123.

Matsuo. F., Cummings, . I . , Anderson, R. (1979) 'Neurological sequelae of massive hydrogen sulfide inhalation.' Archives of Neurology. 36, 45 1-452.

McBurney, A,, Leigh, D., Mcllwain, H . (1980) 'Erythrocyte transketolase activity in suspected cases of Leigh's disease, or subacute necrotizing encephalom ye lo pa thy. ' Archives qf DOeuse in

Namiki, H . (1965) 'Subacute necrotizing encephalo- myelopathy.' Archives of Neurology, 12, 98-107.

Nelson, R. F., Guzman, D . A,, Grahovac. Z., Howse, D. (1979) 'Computerized cranial tomography in Wilson disease.' Neurology. 29, 866-868.

Swartz. W., Hutchinson, H., Berg. B. (1981) 'Com- puterized tomography in subacute necrotizing encephalomyelopathy (Leigh's disease).'.4nnuls qf Neurology, 10, 268-271.

Terrence, C. F.. Delaney, J. F., Alberts, M. C. (1977) 'Computed tomography for Huntington's disease.' Neuroradiolo,qy, 13, 173-1 75.

Childhood. 55. 789-794.

Focal peripheral-nerve disease in the newborn, causing restricted weakness, is often the result of traumatic injury during labor and delivery (Volpe 1981). Traumatic peripheral-nerve lesions occur more commonly in the upper extremity, but occasionally involve the lower extremity. We report a case of peroneal nerve palsy, with electrophysiological documentation o f the lesion and definition of a previously unrecorded cause.

Case report C.B. was the second child of a healthy 24-year-old

mother. whose pregnancy was complicated only by premature onset of labor after a 31-week gestation. Vaginal delivery with vertex presentation was unremarkable. Apgar scores were 3 and 8 at one and five minutes respectively. Birthweight was 1560g. Increasing respiratory distress, in spite of sup- plemental oxygen, led to the infant's transfer to St. Louis Children's Hospital. The infant was intubated immediately on arrival. Chest X-ray demonstrated severe hyaline membrane disease. Maximal ventilatory support was required by 12 hours of age. Because of agitation and difficulty in maintaining adequate ventilation, the infant was paralysed with pan- curonium for 12 hours. Lumbar puncture on the first day of life was unremarkable.

Cranial ultrasound scan on the third day of life demonstrated a left subependymal and moderate intraventricular hemorrhage. Neurological exam- ination o n the same day was notable only for mild stupor. Motility was normal throughout. Serial neurological examination over subsequent weeks revealed no abnormalities. Serial ultrasound scans showed mild ventricular dilatation, resolution of the left intraventricular hemorrhage, and the devel- opment of cystic changes in the region of the left caudate nucleus at the site of the previous subependymal hemorrhage.

At five weeks of age the infant weighed 1840g and had been weaned t o 26 per cent O?. delivered by hood. A 1 ' 5cm diameter area of ecchymotic discoloration and swelling was observed in the region distal to the right fibular head at the site of an infiltrated intravenous solution; the infiltration had occurred several days previously. Three days after the discoloration appeared a right foot-drop was noted. Neurological examination was notable for the absence of dorsiflexion a n d eversion of the right ankle. Plantar flexion was normal, and strength at all other major joints also was normal. T h e right ankle jerk was 3 t , and other tendon reflexes were 2+. Sensation to pin-prick was intact throughout.

Motor-nerve conduction velocity studies were performed at six weeks of age (37 weeks post- conception). Right peroneal-nerve conduction velocity was I 3 d s e c (popliteal space to ankle), with response voltage 0 ' 4 m V in the extensor digitorum brevis after stimulation in the popliteal space, and 0 .6mV after stimulation at the ankle. Right posterior tibial-nerve conduction velocity was 2 5 d s e c . with response voltage 5mV after stimulation in the popliteal space, and 9mV after stimulation at the ankle. The findings were consistent with a right peroneal-nerve lesion between the popliteal space and the ankle.

The infant was treated with a foot splint to maintain the ankle and forefoot in a neutral position, as well as with a range ofpassive motionexercises. By the time o f discharge at eight weeks of age there was only minimal spontaneous dorsiflexion. At follow-up examination at six months of age n o evidence of distal right lower-extremity weakness was observed.

SUMMARY

Discussion Foot-drop in the newborn has been reported to result from a number of etiological factors, including intramuscular gluteal injection of irritant substances resulting in sciatic neuropathy (Curtiss and Tucker 1960, Gilles and Matson 1970); umbilical arterial injection of vaso- constricting agents (Hudson et a/. 1950) and hypertonic glucose solutions (San Agustin et a/. 1962); amniotic bands (Hudson et af. 1950); reduction of dislocated hips (Hensinger and Jones 198 1); birth trauma, includingconstriction- ring dystocia (Craig and Clark 1958, Crumrine et af. 1975); and compression by footboard for intravenous therapy(Fischer and Strasburger 1982). An intravenous infiltration causing peroneal-nerve com- pression has not been cited previously as a cause of foot-drop. The clinical and electrophysiological data indicate a pero- neal-nerve lesion at the site of the infiltrated intravenous solution.

Maintaining intravenous access in premature infants who are treated increasingly frequently with peripheral hyperalimentation is a challenge, and the use of a variety of small superficial veins may be necessary. Indeed, the use of intravenous sites rarely used in older patients is relatively common in the care of small premature infants. Because of the ease of compressing critical subcutaneous structures such as nerves, care must be taken to avoid placing intravenous lines at certain vulnerable sites, e.g. the lateral region of the upper leg.

Acknowledpment We thank Dr. Richard Marshall for referring this patient to us.

Authors' Appointments Katherine L. Kreusser, M.D., Fellow in Pediatric Neurology, Instructor in Pediatrics; 'Joseph J. Volpe, M.D., Professor of Pediatrics, Neurology and Biochemistry; Stein Professor o f Developmental Neurology; Washington University School of Medicine, St. Louis, Missouri 63 178.

'Correspondence to second author.

A premature infant developed peroneal palsy a s a result of infiltration of intravenous fluids, a previously unrecognized cause. Electrophysiological evidence of peroneal-nerve injury is presented. Caut ion is advocated in the placement of intravenous lines in small infants.

Paraly.iie du SI'L par perfusion intraveineuse chez un nouveau-ne IJn premature a present6 unz paralysie du SPE a la suite d'une perfusion intraveineuse. ce qui etait

R i s u M t

a- m

i

2 -3 3 d

523

Y v1

d

524

anttrieurement une cause non reconnue. Les auteurs discutent les preuves electro-physiologiques de la ICsion du SPE et conscillent la prudence dans la mise en place des perfusions intraveineuses chez les petits nourrissons.

ZUSAMMENFASSUNG Peronaeus Lijhmung durch Infiltration intravenoser Fliissigkeit beim Neugeborenen Ein Friihgeborenes entwickelte nach Infiltration von intravenoser Fliissigkeit eine Peronaeus Lahmung, eine zuvor unbekannte Ursache. Die Autoren diskutieren iiber elektrophysiologische Hinweise auf eine Verletzung des N. peronaeus und empfehlen besondere Vorsicht beim Legen intravenoser Zugange beim Saugling.

RESUMEN Pardisis peronea producida por una infiltracidn de liquid0 endovenoso en el recikn nacido Un lactante prematuro desarroll6 una parilisis peronea como resultado de una infiltraci6n de liquidos endovenosos, mecanismo que al principio no fut reconocido. Los autores discuten la evidencia de la lesion del nervio peroneo y sugieren cautela al administrar tratamientos endovenosos en niiios pequeilos.

References Craig, W. S., Clark, J. M. P. (1958) ‘Of peripheral

nerve palsies in the newly born.’ Journal 01 Obstetrics and Gynaecology of the British Commonwealth, 65, 229-237.

Crumrine, P. K., Koenigsberger, M. R., Chutorian, A. M. (1975) ‘Footdrop in the neonate with neurologic and electrophysiologic data.’ Journal of Pediatrics, 86, 779-780.

Curt is , P. H., Tucker, H. J . (1960) ‘Sciatic palsy in premature infants.’ Journal of the American Medical Association. 174. 1586-1 588 .

Fischer, A. Q., Strasburger, M. D. (1982) ‘Footdrop in the neonate secondary to the use of footboards.’

Congen ita I Hydrocephalus Secondary to Intra-uterine Germinal Matr I n traven tr i c u I a I Haemorrhage

Alan Hill Bohdan Rozdilsky

Congenital hydrocephalus most commonly is a result of obstruction to the flow of cerebrospinal fluid at the aqueduct of Sylvius (Friede 1975). Obstruction may occur as an isolated cerebral lesion (e .g . primary aqueductal stenosis), or in association with other abnormalities (e.g. Arnold Chiari malformation). It may also occur as a result of aqueductal gliosis

Journal ofPediatrics. 101, 1003-1004. Gilles, F. H., Matson, D. D. (1970) ‘Sciatic nerve

injury following misplaced gluteal injection.’ Journal of Pediatrics, 16, 247-254.

Hensinger. R. N., Jones, E. T. (1981) Neonatal Orthopedics. New York: Grune & Stratton.

Hudson, F. R., McCandless, A., O’Malley, A. G. (1950) ‘Sciatic paralysis in newborn infants.’ British Medical Journal, 28, 223-225.

San Agustin, M., Nitowsky, H. M., Borden, J . N. (1962) ‘Neonatal sciatic palsy after umbilical vessel injection.’ Journal of Pediatrics. 60, 408-413.

Volpe, J . J. (1981) Neurology of the Newborn. Philadelphia: W . B. Saunders.

secondary to intra-uterine infection or intracranial haemorrhage (Sarnat et al. 1979, Zalneraitis et a/. 1979). Less commonly, it occurs as a sex-linked inherited disorder (Friede 1975).

In this report we describe a case in which hydrocephalus was present a t birth: subsequent neuropathological study dem- onstrated evidence of intra-uterine haem- orrhage of the subependymal germinal matrix, with extension into the ventricular system and subsequent aqueductal gliosis.

Case report The patient was born at term following an uncomplicated pregnancy. The fetal heart-rate was normal until t w o minutes before delivery, when it decreased to 70 beats per minute. Delivery was precipitous and the amniotic fluid contained meconium. The Apgar score was 3 at one minute, following which the infant was intubated and resuscitated. Birthweight was 3930g. The head circumference was 43cm (>97th percentile).

The infant was transferred to University Hospital, Saskatoon, on the first day of life. On arrival, the infant was hypertonic and had a large head. The anterior and posterior fontanelles were enlarged and full, and the cranial sutures were separated. CT scan of the head revealed enlargement of the lateral and third ventricles and a small fourth ventricle (Fig. la). The extent of ventricular dilatation and an area of low density in the left frontal periventricular region are shown in Figure I b. A ventriculo-peritoneal shunt