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 »  Introduction
 »  Case report
 »  Discussion
 »  References

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Year : 2001  |  Volume : 49  |  Issue : 2  |  Page : 174-7

An oligo astrocytoma with widespread calcification along axonal fibres.


Department of Neurosurgery, G.B. Pant Hospital, New Delhi, 110 092, India.

Correspondence Address:
Department of Neurosurgery, G.B. Pant Hospital, New Delhi, 110 092, India.

  »  Abstract

A rare case of a young man with a diffusely calcified oligo astrocytoma in right parieto occipital region, which spread along the axonal fibres into right temporal lobe and to the left parietal lobe is presented. Computed tomography (CT) and magnetic resonance imaging (MRI) demonstrated the extent of the lesion. The mass was partially resected.

How to cite this article:
Gupta V, Singh D, Sinha S, Tatke M, Singh A, Kumar S. An oligo astrocytoma with widespread calcification along axonal fibres. Neurol India 2001;49:174


How to cite this URL:
Gupta V, Singh D, Sinha S, Tatke M, Singh A, Kumar S. An oligo astrocytoma with widespread calcification along axonal fibres. Neurol India [serial online] 2001 [cited 2020 Sep 25];49:174. Available from: http://www.neurologyindia.com/text.asp?2001/49/2/174/1270




   »   Introduction Top

Calcification is largely a sign of slow growth in gliomas. Approximately 10 to 15% of all intracranial tumours are sufficiently calcified to be recognised roentgenographically.[1],[2] Calcification within the neoplasm is the hall mark of oligodendrogliomas and the reported frequency varies with the sensitivity of the imaging techniques. On skull radiography, almost 47% of oligodendrogliomas gave discrenable calcification.[1] The frequency for detection of calcification rises to 91% on CT scan.[3] We describe a patient with extensive calcium deposits extending from right parieto occipital region to right temporal and left parietal lobe. The literature search revealed only one report so far.[4]


   »   Case report Top

A 35 year old male presented with one year history of left sided focal seizures involving left upper limb followed by left lower limb without secondary generalisation. Three months later, he started having bifrontal dull headache, not associated with vomiting. This was followed by weakness in left upper and lower limbs and facial asymmetry. General physical examination was normal. There was no positive family history suggestive of tuberculosis. Neurological examination revealed bilateral papilloedema with left sided supranuclear palsy. There was left hemiparesis, extensor plantar response, increased tone and hyperreflexia on left side. CT scan [Figure - 1] showed a irregular hyperdense calcified lesion in right parieto occipital region, with finger like calcification extending into temporal lobe. On contrast administration, [Figure - 2] there was minimal enhancement of the lesion on right side. The enhancement was seen in left parietal region as well. Magnetic resonance imaging (MRI) revealed hyperintense character of the mass on T1WI [Figure - 3]. On T2WI, [Figure - 4] the calcified lesion generated no signal and no surrounding oedema. A differential diagnosis of calcified arteriovenous malformation was also considered and hence a CT angiogram was done, which did not add to the available information.
A right parieto occipital craniotomy was done. Brain surface was tense on opening the dura. Tumour was found about a centimetre and half below cortical surface. It was a ill defined, non capsulated, greyish red mass, moderately vascular, with rubbery consistency. An intraoperative diagnosis on crush smear examination of the lesion was a low grade astrocytoma with foci of calcification. Sub total excision was done. Histopathological examination of the tumour tissue showed areas of low grade fibrillary astrocytoma with larger areas of oligodendroglioma with infiltration into the cortex. Focal calcification was seen in the tumour, both in the oligodendroglial and astrocytic components. The calcification was also seen around vessels, and in the tumour which had infiltrated the cortex. A final diagnosis of a grade II oligoastrocytoma was made.


   »   Discussion Top

In a study of 1608 histologically verified gliomas, Kalan and Burrows[1] found calcification in 149 cases (9.3%). Oligodendroglioma had discrenable calcification in 47% cases as compared to 6.3% in astrocytomas. Mork et al[5] found calcification in 28% of 192 histologically verified oligodendrogliomas on plain X-ray skull. With the advent of CT, the detection frequency of calcification has been reported to be upto 91%.[3] Calcification may be in the form of calcospherites or as deposits within the microvasculture of the neoplasm. Calcification can occur anywhere within neoplasm, but is especially common where the tumour has infilterated into the cortical gray matter, where it may form an irregular gyriform ribbon. Classically, four morphological types of glial pathological calcification may be distinguished on plain skiagraphy i.e. localised, diffuse, multiple scattered and multiple symmetric.[6] In oligodendrogliomas, calcification is typically seen as linear, wavy streaks on plain X-ray. It is uncommon for the diffuse calcium deposits to be located in the parietal, occipital and temporal lobes. On CT scan, oligodendrogliomas characteristically are heterogenous masses commonly seen as mixtures of hypodensity, isodensity, calcification and occassionally haemorrhage. Minimal mass effect may be seen. On contrast administration, there is heterogeneous enhancement, which may be thick, irregular and often at the periphery. This is sometimes described as 'connecting the dots'.[7] However, in our case on contrast adminstration there was no enhancement on right side where as lesion in left parietal region was enhancing and was located at the same level. These findings are not characteristic of oligodendrogliomas. On MRI, the oligodendroglioma characteristically presents as a mass that usually shows mixed heterogenous hypointensity on T1WI and hyperintensity on T2WI with better demarcated edges.[6] However, in our case, the lesion generated hyperintense signal on T1WI and T2WI . Usually, it is expected that calcium deposition would generate a dark signal on T1WI and T2WI sequences. Solid deposits of calcium may generate no signal as calcium ions do not contain mobile protons. However, on search of literature, we found that it is unusual for calcified lesion to appear hyperintense on T1WI.[6] Henkelman et al[8] reported on this finding and attributed it to some metabolic process, in which calcium is fixed to a protein. Dell et al[9] reported a case of pseudohypoparathyroidism with extensive calcifica-tion of basal ganglia on CT scan but with a hyperintense signal on T1WI.
The spread of tumour occurs locally through extensions of infiltrating tumour cells into normal brain, or more rarely through CSF dissemination along the neuroaxis and through shunts into pleural and peritoneal cavities.[10],[11] The invasive nature of malignant glioma cells enables them to penetrate normal brain barrier, rendering complete surgical extirpation difficult, focal radiation ineffective and relapse or recurrence at a later date. Increased understanding of the key roles played by the extra cellular matrix (ECM), proteases and cell adhesions have given newer insight in the process of glioma cell invasion. The ECM is the naturally occuring substrate upon which cells migrate, proliferate and differentiate in vivo.[12]
Tumour invasion in the brain occurs along basement membrane of blood vessels or the glial limitans externa, that contain extracellular matrix (ECM) proteins. Frequently invasive glioma cells are also found to migrate along myelinated fibre tracts of white matter, which seems to be the possibility in our case. Invasion follows the path of blood vessles and more prominently along myelinated axons, in which single glioma cells have shown intra fasicular, perifasicular and inter fibrillary migration.[12] Organelles in the cytoplasm has been shown to be moving down the axon toward the nerve terminal and back towards the cell body.[13] Axonal flow may also play an important part in tumour spread. MRI and CT have shown fibre tracts that allow the spread of oedema and tumour from one location to another, making possible rapid and remote spread of glioma.[14] Cowley[15] postulated that the major association bundles provide an anatomical substrate along which cerebral oedema and presumably even blood, tumour and other unencapsulated fluids, can spread in the cerebrum. Microscopic spread to contralateral hemisphere of malignant gliomas has been observed in 100 consecutive cases in one series.[16]
On the basis of these facts, we believe that in this case the spread of oligodendroglioma and calcification in such an extensive fashion could be due to spread along corpus callosum to opposite parietal lobe, although, the patients's motor, sensory and speech functions were largely spared. The favourable clinical course is attributable to the fact that the tumour grew slowly and directly involved only a small number of axonal fibres.

 

  »   References Top

1.Kalan C, Burrows EH : Calcification in intracranial gliomata. Br J Radiol 1962; 35 : 589-602.   Back to cited text no. 1    
2.Peterson HO, Keiffer SA : The skull. In : Introduction to neuroradiology. Book Harper and Row Publishers, Hagerstown, Maryland 1st edition. 1972; 10-18.   Back to cited text no. 2    
3.Vonofakas D, Marcu ID, Hacker H : Oligodendrogliomas : CT patterns with emphasis on features indicating malignancy. J Comput Assist Tomogr 1979; 3 : 783-788.   Back to cited text no. 3    
4.Okuchi K, Hiramatsu K, Morimoto T et al : Astrocytoma with wide spread calcification along axonal fibres. Neuroradiology 1992; 34 : 328-330.   Back to cited text no. 4    
5.Mork SJ, Lindegaard KF, Halvorsen TB et al : Oligodendroglioma; Incidence and biological behaviour in a defined population. J Neurosurg 1985; 63 : 881-889.   Back to cited text no. 5    
6.Taveras JM : General pathologic conditions. In : Neuroradiology (3rd edition) Williams and Wilkins Baltimore 1996; 79-154.   Back to cited text no. 6    
7.Howard Lee S, Rao CVGK. Zimmerman RA et al : Primary brain tumours. In : Cranial MRI and CT, Third edition Book. Mcgraw hill Inc New York 1981; 327-328.   Back to cited text no. 7    
8.Henkelman R, Watts t, Kuchrazyk W : High signal intensity on MRI of calcified brain tissue. Radiology 1991; 179-199.   Back to cited text no. 8    
9.Dell LA, Brown MS, Orisson WW et al : Physiologic intracranial calcification with hyperintensity on MR imaging : Case report and experimental model. AJNA 1988; 9 : 1145-1148.   Back to cited text no. 9    
10.Burst JC, Moiel RJ, Rosenberg RN : Glial tumour metastasis through a ventriculo pleural shunt, resulting massive pleural effusion. Arch Neurol 1968; 18 : 649.   Back to cited text no. 10    
11.Wakamastsu T, Matsuo t, Kawano S et al : Glioblastoma with extra cranial metastasis through ventriculo peritoneal shunts. J Neurosurg 1977; 34 : 697.   Back to cited text no. 11    
12.Giese A, Westphal M : Glioma invasion in the central nervous system. Neurosurgery 1996; 39 : 235-252.   Back to cited text no. 12    
13.Hammerschiag R, Brady ST : Axonal transport and the neuronal cytoskeletch. In : Basic neurochemistry : molecular cellular and medical aspects.4th edition. New York. 1989; 457-477.   Back to cited text no. 13    
14.Curnes JT, Burger PC, Djang WT et al : MRI of compact white matter pathways. AJNR 1988; 9 : 1061-1066.   Back to cited text no. 14    
15.Cowley AR : Influence of fiber tracts on the CT appearance of cerebral oedema. AJNR 1983; 4 : 915-925.   Back to cited text no. 15    
16.Matsukado Y, MacCarty CS, Kemohan JW : The growth of glioblastoma multiforme in neurosurgical practice. J Neurosurg 1961; 18 : 636-644.   Back to cited text no. 16    

 

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