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Cryptococcal Meningitis is a fungal infectious disease of worldwide distribution, primarily associated with underlying immunosuppression conditions such as HIV infection, glucocorticoid treatment, status post organ transplantation and oncological treatments. Prevalence is particularly high in third-world countries where it constitutes one of the primary causes of central nervous system infections and may carry fatal outcomes. We present two cases of Cryptococcal Meningitis that portray the vast spectrum of clinical presentations associated with Cryptococcal Meningitis as well as relevant diagnostic and therapeutic implications.
Case study - These adult otherwise healthy patients presented at a public urban university hospital in southern Colombia. Both had an unusual clinical course and suffered fatal outcomes despite being seemingly immunocompetent at baseline. A diagnosis of hepatic cirrhosis could have been considered a cause of immunosuppression in one of the patients and the diagnostic work-up for the other patient revealed no evidence of immunological deficiency.
Cryptococcal Meningitis affecting immunocompetent individuals has been increasingly reported in recent years. Furthermore, outcomes in this population are particularly worse than those generally affected by the disease. A review of the literature related to the possible immunological mechanisms’ underlying the presented clinical course is included. We emphasize the importance of considering Cryptococcus spp. as a possible etiologic agent among differential diagnoses upon encountering suggestive meningeal conditions in immunocompetent patients.
Major depressive disorder (MDD) is a highly prevalent and often debilitating condition with a vast impact on modern societies worldwide. Although it interferes significantly with functioning, MDD is frequently unresponsive to conventional treatment approaches and pharmacotherapy failure has been reported in approximately one third of patients. Current knowledge of the exact underlying disease mechanisms is insufficient, and may thus largely contribute to such therapeutic limitations. Optogenetics, a novel study field employing the expression of genetically-encodable light-sensitive proteins in specific cell types, circumvents the limitations of other forms of neuromodulation and enables temporally precise, bidirectional control of cellular activity in well-defined neuronal populations. This strategy has been used successfully to dissect neural pathways and circuitries involved in complex mental diseases such as MDD.
A systematic literature search was conducted using the terms “Optogenetics”, “Depression” and “Major depressive disorder” on the databases MEDLINE, LILACS, SciELO, Pubmed and BIREME. Inclusion criteria were adopted: articles published in the English language from 1971 (description of bacteriorhodopsin as a light-activated regulator of transmembrane ion flow) to 2017 and articles based on experimental studies were selected.
By using highly validated animal models based on the exposure of phenotypically susceptible rodents to different forms of chronic stress, researchers have been able to reproduce the hallmark symptoms of Depression as well as the histopathological abnormalities found in human brain specimens post-mortem. Several brain regions and neuron populations involved in MDD have been identified by use of a variety of molecular resources including viral vectors, genetically engineered animals, multiple promoters and bacterial opsins. Important areas of dysfunction underlying depression including the medial prefrontal cortex, the ventral tegmental area, the nucleus accumbens, the hippocampus and the basolateral amygdala have been investigated by using optogenetic neuromodulation, yielding new insights into the pathological processes underlying MDD. Researchers have been able to pinpoint affected circuitries and employ time-precise light modulation to successfully revert symptoms of MDD, restoring normal function. It is important to highlight that although promising, studies using optogenetics are controversial, largely due to the variable set tools, models and tests employed in research.
Light modulation using optogenetics has greatly aided to establish accurate models to unveil the neurobiological basis of Depression. Further research will continue to help build more complete pathophysiological constructs and pave the way for new treatment strategies.
The association of sleep disorders and post-traumatic stress disorder (PTSD) is almost universal. Nightmares are not only one of the most commonly associated but also featured as a diagnostic criterion for PTSD. PTSD-related nightmares are particularly distressing, may impair functioning and increase risk of suicide. No specific pharmacologic agent has been demonstrated to impair dreaming. Inhibition of PTSD-related nightmares with pramipexole has not heretofore been described. Such a case is presented.
Case study - This 60 year-old male with PTSD and trauma-related nightmares upon introduction of pramipexole 0.5mg PO qHS for Restless Leg Syndrome (RLS) had total elimination of dreams, which recurred upon discontinuation of this agent as a result of insomnia and increased anxiety. A lower dose of 0.375mg qHS provided optimal RLS-symptom control and overall improved tolerance despite nightmare recurrence.
Abnormalities on Neurological examination: Recent recall: 2 of 4 objects without improvement with reinforcement. Able to spell the word “world” forwards but not backwards. Abstract thought impaired. Chemosensory testing: Anosmia and normogeusia. Motor: Drift: mild right pronator drift with right cerebellar spooning and right abductor digiti minimi sign. Reflexes: 3+ brachioradialis and biceps bilaterally, absent ankle jerks. Other: CT scan with and without contrast: normal.
Nightmares related to PTSD may occur during Rapid Eye Movement (REM) sleep and non-REM sleep. Underlying sympathetic activation may lead to disruptive motor behavior similar to that seen in REM sleep behavior disorder. The exact mechanism of action by which inhibition of dreams occurred with use of pramipexole is unclear. Such a response is consistent with prior documented evidence of REM sleep suppression with low-dose pramipexole such as it‘s efficacy in reducing the intensity and frequency of nightmares and dream enactment related to REM sleep behavior disorder. Further research on therapeutic interventions that target nightmares directly may be beneficial for the management of patients with PTSD.
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