ABSTRACT:Background:Human immunodeficiency virus (HIV) infection frequently results in neurological complications but the impact of different neurological syndromes on patients' quality of life remains unknown.Methods:We investigated health-related quality of life (HRQoL) parameters among HIV/Acquired Immune Deficiency Syndrome (AIDS) patients with and without neurological disease, including 11 dimensions of HRQoL within the Medical Outcomes Short-form Health Survey-HIV.Results:Comparisons of sociodemographic and systemic clinical variables did not differ between HIV/AIDS patients with (n=94) and without (n=75) neurological disease. However, patients with neurological diseases exhibited significantly lower HRQoL scores compared to matched controls, which was most evident among HIV/AIDS patients with cognitive impairment and sensory neuropathy. Prospective analysis revealed diminishing HRQoL scores prior to neurological diagnosis followed by a progressive and sustained improvement in HRQoL scores after intervention over a 96-week period.Conclusions:These studies indicate that while HIV-related neurological diseases are associated with reduced HRQoL scores, enhanced neurological care has a positive impact on HIV/AIDS patients' overall well-being.
patients had higher rates of panic attacks than those of the nonrespiratory subtype, indicating greater sensitivity to CO 2 . The characterization of PD subtypes through CO 2 challenge may be useful in elucidating the biological features, course, and response to treatment of PD. The lifetime risk of depression in those with multiple sclerosis (MS) is very high, with some estimates exceeding 50% (1). In initial trials of interferon beta-1b, there were several suicide attempts and 1 completed suicide, compared with no suicides in the placebo group (2). Since that time, there has been concern that interferon treatment can cause depressive symptoms, and the product monograph suggests that patients treated with interferon beta-1b be "informed that depression and suicidal ideation may be a side effect of treatment" (3). Some recent studies have not confirmed this association. The following case suggests a causal link between interferon beta-1a treatment of MS and major depressive disorder. References Case ReportA The 5 point reduction in CES-D scores was modest, but there was a significant clinical reduction in depressive symptomatology, and she was able to continue with interferon beta-1a treatment. It has been shown that patients with MS who have depression often discontinue therapy (6); this patient felt well enough to continue with her prescribed diseasemodifying therapy.An analysis of depression data from the PRISMS clinical trial showed no evidence of increased depressive symptomatology associated with interferon beta 1a (the median change in CES-D score after 6 months of treatment was 0) (7). While the PRISMS trial provides evidence that depression must be a rare event during interferon treatment, clinicians should maintain an index of suspicion. If significant depressive symptoms arise, pharmacotherapeutic treatment appears to be an option. In our case, there was a beneficial response to selective serotonin reuptake inhibitor (SSRI) therapy (citalopram). Recent studies have shown that prophylactic treatment with paroxetine is an effective strategy to minimize depression induced by treatment with interferon alfa-2b for malignant melanoma (8). It is also evident that swift detection and treatment can reduce the impact of major morbidity associated with MS. Recently, there have been numerous case reports of glucose intolerability and diabetic ketoacidosis (DKA) associated with olanzapine. These cases are confounded by factors such as polypharmacy and comorbid medical illness. We report the case of a young healthy man on olanzapine monotherapy who developed DKA, and hyperglycemia when rechallenged. References
IntroductionAlthough vitamin B12 deficiency is a well-known cause of hematological and neuropsychiatric illness, the presentation of combined severe pancytopenia, demyelination and prominent psychiatric impairment is rare.Case presentationWe present a case of a previously healthy 55-year-old East African man with severe vitamin B12 deficiency (serum vitamin B12 22pmol/L) secondary to pernicious anemia. He had a severe hypoproliferative megaloblastic anemia with hemolysis (hemoglobin 61g/L, mean corpuscular volume 99fL, reticulocytes 0.8%, haptoglobin undetectable), leukopenia (2.7×109/L), thrombocytopenia (96×109/L), ataxia with central demyelination, and megaloblastic madness. The patient’s anemia, myelopathy and psychiatric condition responded well to parenteral vitamin B12 replacement therapy, with significant improvement seen within weeks.ConclusionHematological manifestations of vitamin B12 deficiency are typically inversely correlated with the presence and severity of neuropsychiatric impairment. Although uncommon, a presentation with severe hematological and neuropsychiatric disease can occur, as illustrated by this case. Its presence may help guide diagnosis as well as provide clinically important prognostic information.
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