Primary CNS lymphoma (PCNSL) is defined (by Sierra del Rio et al.

) as an extranodal, nonHodgkins lymphoma arising within the brain, eyes, leptomeninges, or spinal cord in the absence of systemic lymphoma at the time of diagnosis. In immunocompetent individuals, PCNSL comprises only 3% of all primary brain tumors and only 1% of all non-Hodgkins lymphoma. However, it is the most common intracranial tumor in AIDS patients. Unlike in our patient, the vast majority, 95%, of PCNSL are diffuse, large B-cell lymphomas. The remaining 2-5% is primary T-cell lymphomas. Rarer still are the small, B-cell types such as follicular, lymphoplasmocytic or mucosa associated lymphoid tissue type. Most of the symptoms of PCNSL are behavioral and personality changes, cognitive dysfunction, psychomotor slowing. Symptoms of increased ICP occur in half. Unlike in other intracranial masses, cranial nerve dysfunction and seizures occur only in a minority. A peculiar presentation of PCNSL is the involvement of vitreous, retina, optic nerves in 10-15% of cases. The tumor in the occipital lobe resulted in compression of structures in the cranium causing cerebral edema, which blocked the normal circulation of the CSF thereby causing an increase in the intracranial pressure. This could then have caused the headache, vomiting, and visual disturbances of the patient. The visual changes could also be due to lymphoma encroaching on the retina. The pathogenesis of PCNSL is still not clear, however, there are two hypotheses as to the origin of the lymphoma cells. It has been found that T and B cells transit through the CNS and the lymphoma could arise from a benign inflammatory process that causes B cell proliferation within the CNS. Alternately, the lymphoma cells could be metastasis from sub-clinical systemic lymphoma. It could be that the body was able to eliminate the systemic lymphoma but some cells have escaped into the CNS. There are multiple risk factors for the development of PCNSL, as for the patient, he is a 29pack year smoker. This could have contributed to the development of his cancer. In addition, our patient also has psoriasis and diabetes. Both of these are chronic inflammatory states that can induce lymphomagenesis and this could have contributed to the development of the cancer, although we must emphasize that the link between psoriasis and lymphoma has only been established for Hodgkins Lymphoma and cutaneous T-cell types. There is growing evidence that diabetes is a risk factor for PCNSL and one proposed explanation is that insulin resistance leads to hyperinsulinemia causing increased levels of insulin-like growth factor, which promotes tumor growth while suppressing cellular apoptosis, both of which are involved in the development and progression of malignancies. DM type 2 is a common co morbid of psoriasis. We can explain this by observing that obesity is correlated with DM type 2 and psoriasis. Adipose cells secrete TNF- which is an inflammatory mediator in psoriasis and an inducer of insulin resistance. DM type 2 also weakens the immune system which predisposes the person to infections like TB and schistosomiasis. We have presumptive evidence for PTB based on chest X-ray and schistosomiasis based on liver UTZ.