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A previously well 35-year-old male presented with a one month history of generalized progressive headaches, mental status changes, and behavioral changes in the form of aggression and somnolence. His initial physical examination was unremarkable apart from bilateral papilledema and delirium. Investigations, including complete blood count (CBC), urea, creatinine, electrolytes, erythrocyte sedimentation rate (ESR), liver function tests (LFT), thyroid stimulating hormone (TSH), EKG, and chest x-ray, were within normal limits. An immediate computed tomogram (CT) scan of the head showed acute hydrocephalus. A shunt was inserted, and a CSF sample was obtained. It showed an elevated cell count (WBC 26x109 cells/L, 82% lymphocytes) and elevated protein (7.05 g/L). The CSF staining for AFB was negative, as were the bacterial and viral cultures. Cytological and fungal staining was also negative. Weighted with gadolinium, T1 and FLAIR MRI sequences displayed an extensive white matter abnormality with prominent meningeal and hypothalamic enhancement (Figure 1). Tuberculosis (TB) was the main diagnostic consideration. Sarcoidosis, lymphoma and lepto-meningeal metastasis were also considered. The CSF cytology was negative on two occasions, making a neoplastic cause less likely. Tuberculosis was felt to be the most likely etiological diagnosis, as there were no systemic findings of sarcoidosis on his initial presentation.
A 58-year-old male presented with a one-year history of low mood, early morning awakening from sleep, apathy, difficulty with memory, concentration and organization. This had been associated with intrusive concerns of a recent social stressor. He was no longer able to work and was on medical disability. Except for a 20kg weight loss there were no other constitutional or neurological symptoms. He had hypertension and hypercholesterolemia and was on atorvastatin and aspirin. He scored 28/30 on mini-mental status examination (MMSE) with errors on object recall; however he could recall forgotten items after cueing. He had difficulty with concentration, was apathic andhad a negative outlook to the future. His neurological examination and a detailed hematological work up including chemistry, cell counts, vitamin B12, folate, and renal, hepatic and thyroid function tests were normal. A brain magnetic resonance image (MRI) showed mild cerebral atrophy. Based on a formal neuropsychological assessment he was diagnosed with depression and started on Venlafaxine.
This chapter presents a case study of a 69-year-old right-handed man who was presented in June 2006 with a 1-year history of progressive word finding difficulties and mild phono-articulatory problems. It provides the general history, family history, examination, initial diagnosis and follow-up data of the patient. In a simple delayed recall test, he was able to remember five out of ten figures, which is considered slightly impaired. Based on the overall clinical, neuropsychological, language, and neuroimaging data, a diagnosis of Progressive Non-Fluent Aphasia (PNFA) was made. Duloxetine was started for the depressive symptoms with good clinical response. Primary progressive aphasia (PPA) is a clinical syndrome characterized by progressive dissolution of language with relative preservation of other cognitive abilities for at least 1 to 2 years. Recent studies have classified the clinical presentations of PPA into three main subtypes: agrammatic, logopenic, and semantic variant.