A case of calcification in the spinal arachnoid giving rise to spinal cord compression

Journal of the neurologicalSciences Elsevier Publishing Company, Amsterdam - Printed in The Netherlands

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Short Reports A Case of Calcification in the Spinal Arachnoid giving rise to Spinal Cord Compression INTRODUCTION Spinal a r a c h n o i d a l calcifications are n o t u n c o m m o n l y f o u n d o n n e u r o p a t h o l o g i c a l e x a m i n a t i o n b u t it is very rare for these to be a c c o m p a n i e d by neurological signs of spinal cord disease. We report below a single u n u s u a l case showing this association.

CASE REPORT A.M., a 52-year-old male patient was admitted to the neurosurgical service on July 1962, complaining of progressive weakness of the lower limbs which had started 1 year earlier. His previous history was unremarkable except for an episode of renal lithiasis treated 3 years earlier. The weakness of the lower limbs was more severe on the left side. Extensor hypertonus was present and the patient also expeiienced tingling in the feet, which subsequently extended up the lower limbs on to the abdomen. Both

Fig. 1. A drawing of the arachnoidal calcifications observed at operation. J. neurol. Sci. (1968) 7:381-384

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hands were subsequently affected and recently moderate weakness of the upper limbs had developed. The sphincters were normal. On neurological examination the patient was unable to stand alone. There was bilatelal spasticity of the lower limbs, worse on the left side; the lower limb reflexes were increased, there was ankle clonus, and bilateral Babinski signs. Cutaneous reflexes were reduced and there was moderate hypaesthesia for pain and temperature in the feet bilatet ally with bilateral reduction of vibration sense up to the iliae crests. Routine laboratory tests (including serum calcium and phosphorus) were normal. Radiography of

Figs. 2 and 3. The histological appearances of the calcified arachnoidal plaques. J. neurol. Sci. (1968) 7:381-384

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the spinal column was also normal. Lumbar puncture performed at the time of myelographyshowed a manometric block. The contrast medium was partially arrested at T6-%, where irregularities of the spinal canal were evident. The spinal fluid contained 180 mg protein/100 ml. An electroencephalogram and bilateral carotid arteriograms were normal. An exploratory operation was decided upon and a laminectomy was performed at T0-Tg. The bone appeared ivory hard. The dura was normal. The spinal cord was found to be wrapped by arachnoidal calcareous plaques (Fig. 1). The extent of this calcification was remarkable in that the plaques covered practically the whole spinal surface, particularly laterally. The plaques were easily removed; they were not apparently adherent to the cord or to the pial vessels. The vessels were poorly filled, resulting in a widespread whitish appearance of the spinal cord. Further surgical procedures were considered inadvisable and the wound was sutured in layers. The patient was dischargedafter a short post-operative course. His neurological state remained unchanged for about 3 years but then his symptoms increased and he developed a total paraplegia with sensory loss below T6. Histopathological examination of the plaques showed a meningeal fibrosis with collagen vortices. In some zones calcium pre-calcospherites were evident. At the outer border of the plaques the arachnoid was thickened, but no inflammatory changes were found (Figs. 2 and 3). DISCUSSION Discussion of the significance of spinal arachnoidal calcification will be found in the reports of ZANDA (1889), CUSHING AND WEED (1915), ELSBERG(1916), WEED (1920), MCKENDREE AND IMBODEN (1921), DANDY (1925), HERREN (1939), MORRISON et aL (1959), LOMBARDIAND PASSERINI(1955), TERRANOVA AND NICOLA (1959), SLAGER (1960), RETIF et al. (1964), ARENDAND FERENS(1961), GULATIet al. (1965), POMERANCE (1964), NISCH (1964), HASSLER(1967) and MORELLOet al. (1967). It seems wise to distinguish between asymptomatic and symptomatic cases of spinal arachnoidal calcification. Symptomatic cases in which neurological signs of spinal cord compression arise are rare (WISE AND SMITH 1965). Our report of such a symptomatic case demonstrated the following points: (1) There was no past history of any illness which could have resulted in the development of spinal arachnoidal calcification; (2) There was no histological evidence of an arachnoiditis which could have been responsible for the calcification; (3) The calcification was not accompanied by any apparent disorder of calcium and phosphorus metabolism. The importance of previous spinal haemorrhage as a possible aetiological factor was stressed by GATZKE et al. (1957). Spinal trauma (PuuSEPP 1931)or spinal anaesthesia have been implicated by others (CARBONE et al. 1954). It has never been proved that spinal haemorrhage can be followed by an arachnoidal reaction with subsequent calcification. Spinal trauma could certainly explain cases oflocalised calcification but could hardly explain widespread calcification such as that observed in the case of BIANCHIMAIOCCHI(1955). Not even in the 94 autopsied cases of spinal arachnoidal calcification reported by KNOBLICHAND OLSEN (1966) was there any clear correlation between the histological findings and the neurological symptoms. In fact, none of these patients complained, during life, of symptoms or signs of spinal cord disease, nor did their spinal cords show any microscopic abnormalities beneath the plaques. Histological data produced by KNOBLICHAND OLSEN(1966) suggested the hypothesis that calcification is probably an epiphenomenon which follows degenerative changes occurring in clusters ofarachnoidJ. neurol. Sci. (1968) 7:381-384

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al cells. Their findings would suggest that neurological s y m p t o m s c a n n o t be correlated with the extent a n d severltytof " q the calcification. Our experience, however, indicated that neurological signs, when present, can probably be ascribed to spinal cord compression. But in our case surgical treatment appeared to be unsuccessful in preventing a chronic paraplegia. We thus suggest that the rare symptomatic cases m a y represent p r i m a r y chronic myelopathies of u n k n o w n origin which are followed by secondary calcification in the arachnoid. A n exception could be the infrequent finding of localised calcification limited to an area previously subjected to t r a u m a . Neurosurgical Service, Neurological Clinic of the University Parma (Italy)

V. NIZZOLI C. TESTA

(Received 30 April, 1968) REFERENCES ALEM.~,G. (1967) Personal communication concerning two unpublished cases. AREND, R. AND Z. FERENS(1961) Blaski kostne (Wapniowe) w oponie pajeczej rdzenia kregowego, Neurol. Neurochir. Psychiat. pol., 11 : 781-791. BtANCm-MAIOCCHI,A. (1955) Un raro caso di calcificazioni diffuse dell' aracnoide spinale (aracnoidite calcarea), Arch. ortop. (Milano), 68 : 629-639. CARBON~,F., R. HASAERTSANDJ. CORDmR(1954) Ossification diffuse de l'arachnoide spinal. Pr6sentation d'un cas, Acta neurol, belg., 54: 183-191. CUSHING, H. AND L. H. WEED (1915) Studies on the cerebro-spinal fluid and its pathway, Part 9 (Calcareous and osseous deposits in the arachnoidea), Bull. Johns Hopk. Hosp., 26: 367-372. DANDY, W. E. (1925) The diagnosis and localization of spinal cord tumors, Ann. Surg., 81 : 223-254. ELSBERG,C. A. (1916) Diagnosis and Treatment of Surgical Diseases of the Spinal Cord and its Membranes, Saunders, Philadelphia, Pa. GATZK~,L. D., H. W. DODGEANO M. B. DOCKERTV(1957) Arachnoiditis ossificans. Report of two cases, Proc. Mayo Clin. , 32: 689-704. GULATI,H., G. BrtANDARIANDJ. MARI