What Part Of The Brain Does Narcolepsy Affect – Lung ultrasound and neutrophil-lymphocyte ratio in early diagnosis and differentiation between viral and bacterial pneumonia in young children
A neural marker of habituation at 5 months correlates with delayed imitative performance at 12 months: a longitudinal study in the UK and The Gambia.
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What Part Of The Brain Does Narcolepsy Affect
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My Scary Narcolepsy Symptoms Finally Led Me To A Diagnosis
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Structural Brain Alterations Associated With Rapid Eye Movement Sleep Behavior Disorder In Parkinson’s Disease
Beatrice Laus Beatrice Laus Scilit Preprints.org Google Scholar 1, Anna Maria Carolio Anna Maria Carolio Scilit Preprints.org Google Scholar 2, Giovanna Stefania Colfati Scilit Preprints.org Google Scholar Google Scholar and 3 Preprint Scholar Moprint Morosro, Rocim Rocim Rocim .org Google Scholar 5, 6, Michela Ada Norris Ferrilli Michela Ada Norris Ferrilli Scilit Preprints.org Google Scholar 6, Massimiliano Valeriani Massimiliano Valeriani Scilit Preprints. Mastronuzzi Scilit Preprints.org Google Scholar 2, * and Antonella Cacchione Antonella Cacchione Scilit Preprints.org Google Scholar 2
Department of Onco-Hematology, Cell Therapy, Gene Therapy, Haemopoietic Transplantation, Bambino Gesu Children’s Hospital (IRCCS), Piazza Sant’Onofrio 4, 00165 Rome, Italy
Received: 6 August 2022 / Revised: 15 September 2022 / Accepted: 20 September 2022 / Published: 23 September 2022
Narcolepsy, a neurological disorder causing excessive daytime sleepiness, represents a rare consequence of neoplastic lesions involving the ventral/parasellar and hypothalamic anatomical regions responsible for wakefulness. Optic pathway gliomas represent the most common neoplasm in these regions and are the main causes of poor overall survival and long-term neurological complications such as vision loss, endocrinopathy or sleep disorders. In this case report, we describe a non-NF1 patient with a highly advanced optic tract glioma with radiographic status of stable disease years after diagnosis, a rare complication of severe drug-induced death. the patient
Narcolepsy: Symptoms, Causes, Diagnosis, Treatment
Narcolepsy is a neurological disorder characterized by excessive daytime sleepiness and sudden sleep attacks associated with cataplexy and rapid eye movement (REM) sleep-related phenomena. It is a rare pediatric condition that is predominantly idiopathic and in its secondary form can sometimes be associated with central nervous system (CNS) tumors. Although this phenomenon is rare, it is difficult to estimate the exact prevalence of excessive daytime sleepiness in pediatric neuro-oncology patients; While many cases of secondary narcolepsy in adults have been published, there are a few concepts in children [1, 2, 3, 4, 5, 6, 7, 8]. Orexin deficiency is the main cause of this disorder, and in CNS tumors, direct damage (by surgery, radiation, or tumor invasion itself) to the hypothalamic neurons that produce this excitatory neurotransmitter can occur. Narcolepsy treatment is based on the use of pharmacotherapy targeting dopaminergic, noradrenergic or histaminergic pathways [10]. These treatments are generally well tolerated and improve symptoms.
Cancers of the hypothalamic/pituitary region have been associated with the development of childhood narcolepsy, and craniopharyngioma, pituitary adenoma, and low-grade gliomas (LGG) are common [9, 11, 12].
Optic pathway gliomas (OPGs) represent LGGs that can develop anywhere along the optic pathway, including one or both optic nerves, but can also spread and invade adjacent brain structures [ 13 , 14 , 15 , 16 ]. OPG presents an excellent prognosis with an overall survival (OS) approaching 100% in the optic nerve alone. However, when this location is very close to the hypothalamus and pituitary gland, surgical treatment is challenging, and the tumor and its treatment can lead to long-term neurological disorders, for example, vision loss, endocrine diseases or sleep disorders [17, 18, 19, 20, 21].
We describe a 3-year-old patient with OPG, who had never been treated with radiotherapy, suddenly developed narcolepsy in an inebriated state. Rapid clinical deterioration occurred several years after diagnosis and at any stage of radiological stability of the cancer.
Spinocerebellar Ataxia 40: Another Etiology Underlying Essential Tremor Syndrome
A 3-year-old boy was brought to our attention for evidence of visual impairment, convergent strabismus in the left eye, and hypotrophy of the optic disc at the fundus. He had a history of seizures within 18 months of treatment with sodium valproate.
On physical examination, the patient has adequate general condition and neurocognitive development, revealing severe bilateral hypovision (bilateral optical hypotrophy, OCT (optical correlation tomography), retinal nerve fiber layer thickness (RNFL) 2/10 in the left eye and 4/ in the right 10 of the eye). Transverse nystagmus, divergent strabismus of the left eye and pupillary response to photostimulation.
A single café au lait locus was detected, but neurofibromatosis type 1 (NF1) had previously been excluded by genetic analysis.
Magnetic resonance imaging (MRI) of the brain and spine documented a space-occupying lesion involving the optic-chiasmatic region (Figure 1).
The Struggle To Remember: Can Narcolepsy Affect Memory?
According to the latest version of the World Health Organization (WHO) central nervous system classification, the patient underwent biopsy (stereotactic robot-assed needle biopsy. : positive for CD34+, GFAP, OLIG2; p53 negative, BRAFV600 negative in immunohistochemistry and molecular analysis) system (immunohistochemistry).
Chemotherapy treatment was initiated according to the International Society of Pediatric Oncology-Low-Grade Glioma (SIOP LGG) protocol [ 22 ].
About a year after starting the therapy, the patient started to show a clinical picture of cachexia, and brain MRI showed the progression of the disease (Figure 2). A new ophthalmologic evaluation confirmed further loss of visual acuity with complete bilateral hypovision. Therefore, second-line chemotherapy is initiated first and targeted therapy second. Five years later (at 8 years of age) the patient presented to the emergency department sedated but arousal by verbal or tactile stimuli and well focused when awake. A computed tomography (CT) scan of the brain and a new MRI were performed, showing stable disease compared to the latest MRI.
Although hydrocephalus was considered the cause of the clinical deterioration, MRI showed no signs of increased intracranial pressure. Other systemic causes of sedation such as electrolyte imbalance or anemia were excluded.
Enhanced Food Related Responses In The Ventral Medial Prefrontal Cortex In Narcolepsy Type 1
The possibility of surgery was discussed at the oncology panel and was deemed futile as the tumor had invasive growth and imaging showed no signs of intracranial hypertension.
Excessive daytime sleepiness (EDS) associated with sleep paralysis and hypnotic hallucinations raised the suspicion of secondary narcotics in the differential diagnosis with autoimmune encephalitis.
Autoimmune antibodies (anti-GAD, anti-Hu, anti-U, anti-NMDA, and voltage-gated K channel antibodies) were negative. A multi-sleep latency test (MSLT) performed after video-polysomnography of more than 6 h of nocturnal sleep showed excessive daytime sleepiness and very short sleep onset latency (<2 min) with SOREM 2 (sleep onset REM). , thus resembling a pattern of narcolepsy. Narcolepsy treatment was initiated with modafinil, which was only partially effective in reducing daytime sleepiness and caused side effects such as tachycardia and psychomotor agitation.
Pitolisant was later tested as an adjunct, but was associated with severe anxiety symptoms without hypersomnia benefit; So it was withdrawn.
The Neurobiological Basis Of Narcolepsy
Over the following months, the child developed progressive and significant neurologic deterioration with persistent dyskinesias, psychosis, distortions, encopresis, enuresis, and secondary autism spectrum disorders. The nervous breakdown led to the child’s death within a few months.
Narcolepsy is defined as a debilitating condition characterized by excessive daytime sleepiness and sudden sleep attacks, which may include cataplexy, sleep paralysis, hallucinations, and nocturnal sleep disturbances [ 8 , 12 , 23 , 24 , 25 , 26 , 27 ]. However, in juvenile patients, narcolepsy may present with hyperactivity, aggression, and irritability [11]. The prevalence of narcolepsy in childhood is estimated to be approximately 0.02–0.05% [12]. In most cases, narcolepsy is a primary disease that causes the loss of hypocretin neurons in the posterolateral hypothalamus. Recently,
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