Vohtme 93 Number 2

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Quadriplegia and cortical blindness in Hemophilus influenzae meningitis Alonso L DeSousa, M.D., Martin B. Klelman, IM.D.,* and John Mealey, Jr., M.D., Indianapolis, Ind.

Q u A D R t P L E G I A and cortical blindness are rare complications of purulent meningitis. We present the first detailed description of a spinal cord syndrome resulting from Hemophihts influenzae meningitis.

showed improvement. Suspected cortical blindness was documented using visual evoked response. A computerized tomography scan at this time showed lucencies in both frontoparietal areas, felt to be consistent with small subdural fluid collections.

CASE REPORT A 3-year-old white female with fever, headache, and vomiting of 12 hours' duration became increasingly lethargic, developed seizures, and was taken to a local hospital. Lumbar puncture revealed cloudy cerebrospinal fluid which contained 4,400 white blood ceIIs/mm 3, 100% of which were poiymorphonuclear leukocytes. The concentration of glucose in the CSF was 6 mg/dl and of protein, 123 mg/dl. Gram-negative pleomorphic bacilli were seen on smear and were later identified as IL ba,fluenzae type B. Therapy was begun with chloramphenicol (100 mg/kg/24 hour) and ampicillin (400 mg/kg/24 hour) intravenously, and she was transferred to the James Whitcomb Riley ttospital for Children. On admission she was unresponsive and flaccid, tler pupils were mi0iic but reacted to light. The optic fundi were normal and reflex extraocular movements were full. Corneal reflexes were present. Shortly after admission she became apneic and was placed on mechanical ventilation. The CSF became sterile after 24 hours of treatment. She remained unresponsive for three days and then .became able to open her eyes and mouth on command. Spontaneous respiratory effort and movement of extremities were not observed during thi s time. After one week she continued to move the facial muscles purposefully but remained flaccid and had no respiratory effort. One week later she began to show reflex withdrawal of her extremities but made no effort to breathe. A spinal tap after eight days of treatment revealed 20 white blood cells with 5% polymorphonuclear leukocytes and 95% lymphocytes; CSF glucose and protein concentrations were normal. She was treated for a total of 15 days with chloramphenicol intravenously. Spinal taps done subsequently revealed nornfal CSF. An electromyogram at one month showed a denervation pattern in the left lower extremity with normal conduction velocity in the peroneal ne~'e. A repeat EMG one month later

From the Section of Neurological Surgery of the Department of Surgery and the Infectious Disease Section of the Department of Pediatrics, Indiana Universit)' School of Medichle. *Reprint address: Departmentof Pediatrics, Indiana Un(rersit)"School of Medicine, 1100 I1".Michigan St., Indianapolis, IN 46202.

0022-3476/78/0293-0253500.20/0

9 1978 The C. V,. Mosby Co.

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Abbreviation used CSF: cerebrospinal fluid

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Two months after the onset of illness she was alert, had good facial expression, and was able to move her head slightly. She reflexly withdrew all four extremities and had bilateral ankle clonus. Her deep tendon and superficial reflexes were absent, and muscle tone was improved. There was analgesia to pinprick in all areas except the trigem!nal, distribution, where sensation was normal. Touch sensation was intact, and localization of touch was preser,'ed to some degree in all extremities. Proprioceptive and vibratory sensations were intact. Phrenie nerve stimulation during fluoroscopy showe d adequate responses. Nine weeks after treatment was begun, spontaneous respiratory effort was noted as well as some voluntary movement of the left arm. At this time analgesia to the C2 level persisted and posterior column sensation remained normal. Visual evoked response at this time showed improvement. Spinal cord angiography was not performed. Five months after admission she breathed on he~"own and was able to lift her left arm and move her right arm slightly. Her sensory level for pain and temperature had descended to the C,.7 level and correlated With her motor improvement. She was able to see large moving objects and to differentiate colors. Stanford Binet intelligence testing using verbal items revealed intellectual function to be normal for age; she scored one to two years beyond her chronologic age in several areas tested. Eight months after the onset of her illness she remains hospitalized for treatment of frequent episodes of respirator)' insufficiency. DISCUSSION Apnea which was not associated with concomitant seizure activity probably resulted from injury to the upper cervical cord or the medulla. Vascular injury, perhaps including thrombosis o f the anterior spinal artery, is the most likely cause o f the quadriplegia. Clinical features supporting this hypothesis are the: (1) C._. sensory level with dissociation (posterior colunm sensation preserved); (2) flaccid (later spastic) quadriplegia with some minimal !mprovement in motor function; and (3) lack o f evidence for direct cord trauma or cord compression due to abscess,

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Brief clinical and laboratory observations

hematoma, or tumor. The clinical features are consistent with those described in the anterior spinal artery syndrome,' which is thought to result from occlusion of the anterior spinal artery. Although many etiologies have been implicated as initiating the vascular compromise, occlusion following Hemophihts i~uenzae infection has n o t previously been described. Few clinical reports document spinal cord injury after purulent meningitis. Conus medullaris syndrome due to intramedullary vasculitis has been described after meningococcal meningitis. -~ Cerebral angiography has demonstrated arterial Occlusion and resultant encephalomalacia ~ in patients with H. influenzae meningitis. We find no descriptions of the findings of spinal cord angiography. Although there is ample pathologic documentation of cerebral vascular involvement in purulent meningitis, pathologic descriptions of spinal cord lesions are comparatively few and generally predate the use of effective antibiotics. Vascular and perivascular inflammation , with or without capillary thrombosis or focal hemorrhages, have been described in the brain and spinal cord." ~ The upper cervical cord Was noted as the most frequent site of cord vascular injury in one report) Arterial thrombosis was rare in two autopsy series" '; however, these repoi'ts describe frequent arteritis and phlebitis accompanying tL influenzae meningitis. Cortical blindness in this child may have resulted from cerebral hypoxia due to apneic spells, convulsive episodes, or cerebral vasculitis. Cortical blindness is infrequently reported in patients with H. infl, enzae meningitis. ~ The occipital cortex, specifically laminas 3 and 4 of Brodmann, is thought to be the area most sensitive to hypoxic damage, since it represents a border zone in the distribution of major cerebral arteries. ~ The prognosis of cortical

The Journal of Pediatrics August 1978 blindness, regardless of the underlying condition, is generally good. +. . . . . Recovery of vision can be complete or partial and may occur over a period varying from several days to many months after onset. +Visual evoked response is useful for diagnosis and follow-up of cortical blindness.6, s

Clinical recognition of spinal cord injury in a critically ifl child with purulent meningitis is difficult. Clinicians should be aware of this entity, since it requires supportive treatment early in the illness. Although the ultimate prognosis is not clear, some improvement may be expected. REFERENCES 1. Steegmann AT: Syndrome of the anterior spinal artery, Neurology 2:15, 1952. 2. Gotschal RA: Conus medullaris syndrome after meningococcal meningitis, N Engl J Med 286:882, 1972. 3. James JE, Itodges FJ, Jordan CE, et al: Angiography and cysternography in acute meningitis due to tlemophilus influenzae, Radiology 103:601, 1972. 4. Turner JWA: Spinal cord lesions in cerebrospinal fever, Lancet 1:398, 1948. 5. BankstlS, .~nd McCartney JE: Meningococcal encephalitis, Lancet !:219, 1942. 6. Barnet AB, Manson JL, and Wilner E: Acute cerebral blindness in childhood, Ne/~rology20:1147, 1970. 7. Acers TE, and Cooper WC: Cortical blindness secondary to bacterial meningitis, Am J Ophthalmol 59:226, 1965. 8. Tepperberg J, Nussbaum E, and Feldman F: Cortical blindness following meningitis due to Hemophilus influenzae type B, J PEDL~'rR91:434, 1977. 9. Iloyt WF, and Walsh FB: Cortical blindness with partial recovery following acute cerebral anoxia from cardiac arrest, Arch Ophthalmol 60:1061, 1958. 10. Lorber J: Recovery ofvision following prolonged blindness in children with hydrocephalus or following pyogenic menihgitis, Clin Pediatr 6:699, 1967.

Catch-up brain growth--demonstration by CA T scan llarold G: Marks, M.D.,* Patricia Borns, M.D., Nina L. Steg, M.D., Susan B. Stine, M.D., Henry tl. Stroud, M.D., and Thomas S. Vates, M.D.~ Wilmington, Del.

IN ANIMALS, undernutrition during the entire period of rapid brain growth will result in a deficit in cell number and irreversible decrease in brain weight. If good nutrition is begun before the end of this period, the rate of cell From the Alfred L duPont Institute. *Reprint address: P.O. Box 269, IVilmington, DE 19899.

division may increase sufficiently to correct the deficit in cell number. Undernutrition after the period of rapid Abbreviation used CAT: computed axial tomography brain gro~.vth results in a decrease in cell size and a reversible decrease in brain weight.'

0022-347617810293-0254500.30/0 9 1978 The C. V. Mosby Co.

Quadriplegia and cortical blindness in Hemophilus influenzae meningitis.

Vohtme 93 Number 2 Brief clinical and laboratory observations 253 Quadriplegia and cortical blindness in Hemophilus influenzae meningitis Alonso L...
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