Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0917801 (insomnia)
 10,606 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The objective of this clinical-pathologic study was to identify biomarkers for a pallidopontonigral degeneration (PPND) kindred of frontotemporal dementia and parkinsonism linked to chromosome 17 (FTDP-17) harboring the N279K tau mutation. Five affected subjects, one at-risk who later became symptomatic, and one at-risk asymptomatic mutation carrier, had abnormal (18)fluorodeoxyglucose PET demonstrating asymmetric temporal lobe hypometabolism. All except the asymptomatic mutation carrier had abnormal brain MRI. Parkinsonism, myoclonus, anosmia, insomnia, speech, and autonomic dysfunction were identified. Autopsy of six affected subjects showed frontotemporal degeneration with extensive tauopathy. Further studies of FTDP-17 patients are needed to replicate these findings.
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PMID:Clinical-pathologic study of biomarkers in FTDP-17 (PPND family with N279K tau mutation). 1719 72

Subfrontal schwannomas are rare lesions. They can be misdiagnosed as olfactory meningiomas or neuroblastomas. We report a case of giant schwannoma involving the anterior cranial fossa; the frontal and ethmoid sinuses and nasal cavities. The patient presented with a year-long history of increasingly severe headache associated with insomnia. Examination revealed no neurological deficit except for the anosmia. Magnetic Resonance Imaging revealed a 9x5x3 cm intranasal-subfrontal extraaxial mass. Nasal biopsy indicated the presence of a schwannoma. The lesion was totally removed through a bifrontal craniotomy and the skull base was repaired with periosteal flap, fibrin glue and a split craniotomy graft. In addition to the cosmetic advantages over standard transfacial approaches, the extended subfrontal approach also provides early dissection of neural tissues, avoiding an inadvertent cerebrospinal fluid leak.
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PMID:Nasal-subfrontal giant schwannoma. 1910 91

Patients suffering from Parkinson's disease (PD) will typically experience a range of motor and nonmotor symptoms during the course of their illness, each of which will affect a particular individual to varying degrees. However, patients' perceptions of troublesome symptoms often differ from the clinician's view, and these discrepancies can hamper effective management of PD. In this study, we have assessed 265 consecutive PD patients by asking them to rank their three most troublesome symptoms in the last 6 months, so to gain further insight from the impact of illness on patients' quality of life. Patients were divided into early (<6 years) and late PD groups (>/=6 years) from symptom onset. The division at 6 years was based on the mean time from symptom onset to the development of motor complications. In the early PD group, the 5 most prevalent complaints (ranked in descending order) are slowness, tremor, stiffness, pain, and loss of smell and/or taste. In the advanced PD group, fluctuating response to their medication (most common: wearing-off phenomenon followed by dyskinesia), mood changes, drooling, sleep problems (most common: middle and late night insomnia followed by daytime sleepiness), and tremor were the top 5. Our findings provide further evidence for the diversity of experience in PD and suggest that as the disease advances the most troublesome issues that patients perceive are the lack of response to medication and the nonmotor aspects of the disease, highlighting the importance of assessment and patient-centered management in the follow-up of these patients.
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PMID:Parkinson's disease symptoms: the patient's perspective. 2062 64

To date, no guidelines exist for the screening, evaluation, and management of nutritional status in PD. Dozens of studies demonstrate an association between diet in adulthood with subsequent risk of developing PD. Individuals with PD are at increased risk of malnutrition due to the increased metabolic demands and disease pathophysiology. Risk of malnutrition is further complicated by anosmia, swallowing difficulties, constipation, and drug-nutrient interactions. An emerging body of evidence suggests that the intestinal tract is affected early in the disease, creating therapeutic opportunities for early intervention. Dietary modification and nutritional supplementation may improve symptoms of constipation, depression, insomnia, dystonia, and help prevent cognitive dysfunction. This review summarizes the state of the science related to nutrition and nonmotor symptoms of PD.
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PMID:Nutrition and Nonmotor Symptoms of Parkinson's Disease. 2880 67

Anosmia, stroke, paralysis, cranial nerve deficits, encephalopathy, delirium, meningitis, and seizures are some of the neurological complications in patients with coronavirus disease-19 (COVID-19) which is caused by acute respiratory syndrome coronavirus 2 (SARS-Cov2). There remains a challenge to determine the extent to which neurological abnormalities in COVID-19 are caused by SARS-Cov2 itself, the exaggerated cytokine response it triggers, and/or the resulting hypercoagulapathy and formation of blood clots in blood vessels throughout the body and the brain. In this article, we review the reports that address neurological manifestations in patients with COVID-19 who may present with acute neurological symptoms (e.g., stroke), even without typical respiratory symptoms such as fever, cough, or shortness of breath. Next, we discuss the different neurobiological processes and mechanisms that may underlie the link between SARS-Cov2 and COVID-19 in the brain, cranial nerves, peripheral nerves, and muscles. Finally, we propose a basic "NeuroCovid" classification scheme that integrates these concepts and highlights some of the short-term challenges for the practice of neurology today and the long-term sequalae of COVID-19 such as depression, OCD, insomnia, cognitive decline, accelerated aging, Parkinson's disease, or Alzheimer's disease in the future. In doing so, we intend to provide a basis from which to build on future hypotheses and investigations regarding SARS-Cov2 and the nervous system.
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PMID:Neurobiology of COVID-19. 3253 57