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 »  Clinical data
 »  Pathology
 »  Discussion
 »  References

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Year : 1999  |  Volume : 47  |  Issue : 1  |  Page : 75-6

A case of 27 year old male with recurrent neurological deficit.


Department of Pathology and Neurology, Postgraduate Institute of Medical Education and Research, Chandigarh, U.T., 160012, India.

Correspondence Address:
Department of Pathology and Neurology, Postgraduate Institute of Medical Education and Research, Chandigarh, U.T., 160012, India.



How to cite this article:
Banerjee A K, Prabhakar S. A case of 27 year old male with recurrent neurological deficit. Neurol India 1999;47:75


How to cite this URL:
Banerjee A K, Prabhakar S. A case of 27 year old male with recurrent neurological deficit. Neurol India [serial online] 1999 [cited 2023 Jan 28];47:75. Available from: https://www.neurologyindia.com/text.asp?1999/47/1/75/1652




   »   Clinical data Top


First Admission
27 year male farmer was admitted with history of numbness of left side of face of six weeks duration, followed by weakness of left side of body a week later. He developed numbness and buring sensation of right side of body, tinnitus, diminished hearing from both ears, double vision and vertigo with in next two weeks. Weakness of left side progressed for 8 days and there after showed gradual improvement. There was history of dribbling of food from the leftside and unsteadiness of gait during walking. Examination revealed pulse of 82/mt. BP-130/70 mm Hg, cafe-au-lait spot over left gluteal region and multiple pigmented spots over right pectoral region. Higher mental functions were normal. Speech showed cerebellar dysathria. Visual acuity, fundus and visual fields, were normal. Pupils were equal and reactive to light. He had right internuclear ophthalmoplegia, left gaze palsy, vertical and horizontal nystagmus, left supranuclear facial palsy, left hearing loss and sluggish palatal movements on right side. There was no motor or sensory deficit, however, coordination was defective with left sided cerebellar signs. Investigation revealed normal haemogram, urine analysis, blood biochemistry, VDRL, CSF examination, chest X-ray and ECG. Visual evoked responses were normal. Brain stem auditory evoked responses were normal on right side. No wave was seen beyond I and II because of profound sensory neural hearing loss; he was started on prednisolone 60 mg daily. There was spontaneous improvement. Ataxia, ocular movements and paraesthesia improved. He recovered completely in two months

Second Admission : (17 Months later)

Admitted with history of sudden onset burning sensation over face of 45 days duration, weakness of all four limibs 4 days later and difficulty in speech a month later. He developed difficulty in swallowing, tinnitis, double vision and ataxia two days before admission. His neurological status was continuously deteriorating. Examination revealed pulse of 86/min., B.P.-120/70 mmHg., normal higher mental functions, scanning speech with dysarthria and dysphonia. Visual acuity, fundi and fields were normal. Eye movements were full ; however, he had jerky pursuit and coarse nystagmus on looking to right. He had diplopia on looking in all directions, left supranuclear facial palsy and absent gag and palatal reflexes. Left hypoglossal nerve was also involved. Tone was spastic in left limbs. There was left hemiparesis. Abdominal reflexes was absent. Left planter response was extensor. Pain, touch and temperature sensations were diminished on left half of body. Joint position and vibration sensations were absent over left ankle. He had bilateral cerebellar signs and gait ataxia. Investigation revealed normal haemogram, urine analysis, blood biochemistry, X-ray skull and chest. LE Cells, ANF and rheumatoid factor were negative. CSF examination was normal. CT or MRI could not be done because of technical reasons. A clinical diagnosis of multiple sclerosis was made.


   »   Pathology Top


A limited autopsy consisting of examination of the brain, spinal cord and the orbital contents was performed. The brain weighed 1125gm after fixation. The medulla was swollen to about twice its volume. Serial slicing showed effacement of normal architecture by a poorly outlined lesion involving the right half of the medulla [Figure. 1]. Microscopic examination showed dense perivascular infiltration by lymphoid cells [Figure. 2]. These cells were several layers thick around the blood vessels and also infiltrated the intervening parenchyma. The cells consisted of a mixed population of small and large lymphoid cells which were uniformly positive for B-cell marker CD 20 [Figure.3] and negative for T-cell markers. Reticulin preparations demonstrated the characteristic perivascular network of fibres enclosing these cells. Moderate degree of astrocytic proliferation was noted in these areas. Focal infiltration of the leptomenings was present. Adjacent sections showed the tumour extending downwards to the left half of lower medulla and upwards upto mid-pons and right cerebellar white matter.

A diagnosis of primary non-Hodgkin's lymphoma, B-cell type, of the brain was made. Although the extracranial organs were not examined, the possibility of extracranial lymphoma seems unlikely according to the clinical course.


   »   Discussion Top


Recent clinical and epidemiological studies indicate an increase in the incidence of primary CNS lymphoma. The increase is only partly due to its association with AIDS and other immunosuppressive states. During the last three decades we have observed a threefold increase in the number of such cases unassociated with immunodeficiency states. Similar observations have been made in centres dealing with large number of cases.[1] One interesting aspect of this case is the remarkable improvement and complete recovery following therapy with steroids. Such a responce is well known in CNS lymphoma and may be confused with other steroid responsive conditions like multiple sclerosis.[2]
 

  »   References Top

1.Miller DC, Hochperg Fh, Harris NI et al : Pathology with clinical correlations of primary central nervous system. Non-hodgkin's lymphoma the massalhusetts general hospital experience 1958-1989. Courier 1994; 74 : 1383-1397.   Back to cited text no. 1    
2.Geppert M, Ostertag CB, Seitz G et al : Glucocorticoid therapy obscures the diagnosis of cerebral lymphoma. Acta Neuropathol 1990; 80 : 629-634.  Back to cited text no. 2    

 

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