Background and Purpose-The fornix connects various structures involved in memory. We report a patient with anterograde amnesia after an acute ischemic infarct in the anterior fornix. Case Description-A 71-year-old female with acute-onset amnesia had neuroimaging studies showing ischemic infarction of both columns and the body of the fornix and the genu of the corpus callosum. Neuropsychological evaluation revealed anterograde amnesia without evidence of callosal disconnection. The patient showed marked improvement in her memory function on the follow-up visit. Conclusions-Amnesia in this case is likely due to infarction of the anterior fornix structures.
Introduction Insomnia is a widespread condition, especially in the elderly population. While the International Classification of Sleep Disorders (ICSD) third edition appropriately removed primary insomnia subtypes from the classification, our case illustrates the importance of these factors in considering a chronic insomnia disorder diagnosis. We present a case of severe subjective insomnia with no apparent objective findings, instead with evidence of excellent sleep efficiency on the contrary. Report of Cases: A 76-year-old male with a past medical history of anxiety and a recent diagnosis of early Parkinson's disease presented to the Sleep medicine clinic with two years of insomnia which started after his retirement. The patient felt difficulty with falling asleep every night. He underwent a sleep study and was found to have sleep-disordered breathing, which responded well to Bilevel positive airway pressure (BiPAP) therapy. However, insomnia symptoms persisted and were resistant to multiple medications, including Mirtazapine, Melatonin, and Suvorexant. He was referred for Cognitive Behavioral Therapy with minimal to no improvement in his symptoms. Conversely, a one-week Actigraphy recording on Bipap therapy surprisingly revealed an excellent sleep efficiency with near-continuous seven to eight hours of sleep every night. The etiology of chronic insomnia is poorly understood but is typically multifactorial, as described in the second edition of ICSD. In this case, paradoxical insomnia played a significant role in the patient's clinical presentation. Paradoxical insomnia is defined as thoughts or perceptions of time asleep as wakefulness, with objective measures documenting normative amounts of sleep. Previous work suggests that alterations in the sleep/arousal system may contribute to this apparent mismatch between conventional objective sleep measures and subjective reports. Conclusion This case demonstrates the challenge of effectively diagnosing and managing chronic insomnia. While the new classification guidelines from the ICSD appropriately remove insomnia subtypes from the diagnostic paradigm, familiarity with these previously described subtypes may aid clinical decisions. Crucial to this discussion is that previously described "secondary" or "subtypes" of primary insomnia may develop an independent clinical course that may require further attention. Support (If Any) ICSD 2nd,3rd editions.
Introduction The COVID-19 vaccines have documented transient side effects, including injection site soreness, redness, headache, fatigue, and fever. In addition, there have been few reported long-term side effects, including Guillain-Barre, pericarditis, and cerebral venous sinus thrombosis. We present a rare case of severe insomnia as a long-term side effect following COVID-19 vaccination. Report of Cases: A 59-year-old female with a past medical history of well-controlled hypothyroidism and migraine presented to the sleep center with four months of insomnia. She had a history of COVID infection in November 2020 with only mild symptoms of sore throat and fatigue. The patient finished her two-shot series of the Moderna COVID-19 vaccine in April 2021. Immediately following the vaccination, the patient had severe trouble falling and staying asleep. Her insomnia was resistant to multiple medications including zolpidem Immediate-release(IR), Controlled-release(CR) formulas, zaleplon, eszopiclone, trazodone, melatonin, clonazepam, suvorexant, and lemborexant. However, magnetic resonance imaging (MRI) brain imaging only showed nonspecific white matter disease. She had no mood disorders or psychosocial stressors, and the patient had excellent sleep hygiene measures. However, insomnia caused severe impairment of her daily life activities to a point where she was almost seeking inpatient admission for her insomnia. During the COVID-19 pandemic, the effects on sleep have been significant, particularly insomnia. Prescriptions for sleep medications have increased. Many have attributed the rise of insomnia to pandemic-related stress, disturbance of circadian rhythm from home confinement, and worsening mental health. Conclusion To our knowledge, there have not been documented side effects of insomnia on the COVID-19 vaccines, with some studies suggesting sleep deprivation reducing their effectiveness. As vaccination efforts continue worldwide, awareness of side effects from vaccines is paramount for clinicians facing the challenges in patient care.This case demonstrates that chronic insomnia can be a side effect of the COVID-19 vaccines. Therefore, further surveillance of patients and side effects from COVID-19 vaccination is warranted as insomnia can have significant clinical and psychosocial consequences. Support (If Any)
Introduction Alice in wonderland syndrome (AIWS), also known as Todd’s syndrome, is a neuropsychological condition that causes a set of symptoms with alteration of body image. These distortions include appearing smaller(micropsia) or larger(macropsia) or appearing to be closer or farther than they are. The exact cause of AIWS is currently unknown. Some associations include, migraine, temporal lobe epilepsy, brain tumors, psychoactive drugs or Epstein-Barr-virus. The treatment for this disease primarily aims at treating the underlying reason as to why the patient had the event. Report of case(s) 7-year-old boy presents to sleep clinic for nighttime hallucinations. Nightly episodes described as body parts that seem abnormally large or small and people talking very fast. Events lasted 15 minutes. Patient had full recall and developed anxiety when falling asleep. Medications at presentation: vitamins, melatonin, Montelukast. Montelukast was discontinued. Referred to neurology for video EEG, which was negative for frontal lobe seizures. Due to restless sleep and snoring, sleep study and ferritin was ordered. He was found to have mild OSA with an AHI of 2.2 and a ferritin level of 28. The patient was not considered a surgical candidate for his mild OSA; therefore, watchful waiting and re-initiation of montelukast proceeded with initiation of oral iron. At sleep clinic follow up, family noted improvement of hallucinations for 2-3 months and then restart, with worsening. Upon medication review, Montelukast was the inciting factor to the presence and resolution of hallucinations. Conclusion In this patient the montelukast seemed to be the triggering factor of AIWS. It has been suggested that the inhibition of leukotriene receptors in the brain could be responsible for this drug reaction. No other obvious triggers, or results of work up were able to better explain his resolution once he discontinued montelukast. This just further promotes close pharmacologic vigilance in the pediatric population. Support (if any)
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