Autonomic Nervous System Dysfunctions as a Basis for a Predictive Model of Risk of Neurological Disorders in Subjects with Prior History of Traumatic Brain Injury: Implications in Alzheimer’s Disease

O artigo discute dados de escrita de um homem de 27 anos (AL) que foi diagnosticado como disléxico na 7ª série do ensino fundamental – razão pela qual abandonou os estudos – e que sofreu, aos 23 anos, um traumatismo crânio-encefálico devido a um acidente automobilístico, o que ocasionou um quadro de Síndrome Frontal. O acompanhamento longitudinal, baseado nos pressupostos teórico-metodológicos da Neurolingüística Discursiva, mostra que: (1) ALnunca foi disléxico, (2) mesmo apresentando dificuldades decorrentes do quadro neurológico, ALé capaz de reconstruir a sua relação com a escrita.PALAVRAS-CHAVE: Neurolingüística. Síndrome Frontal. Escrita. Dislexia.ABSTRACT The article discusses writing datas of a 27 year-old-man (AL) who was diagnosed as dyslexic on the seventh grade of junior-high school – the reason he left his studies - and suffered a traumatic brain injury, when he was 23, due to a car accident, which led a Frontal Syndrome picture. The longitudinal follow-up - based on the theoretic referential theoretical of Discursive Neurolinguistics - shows that: (1) AL was never dyslexic, (2) AL is able to rebuild his relationship with the writing ability despite his neurological disorders. KEYWORDS: Neurolinguistic. Frontal Syndrome. Writing, Dyslexia.

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A-010 Traumatic Brain Injury, APOE, and Age at Diagnosis of Alzheimer’s Disease

Archives of Clinical Neuropsychology ◽

10.1093/arclin/acaa068.010 ◽

2020 ◽

Vol 35 (6) ◽

pp. 800-800

Author(s):

Alexander C ◽

Suhr J

Keyword(s):

Alzheimer’S Disease ◽

Alzheimer's Disease ◽

Traumatic Brain Injury ◽

Brain Injury ◽

Age Of Onset ◽

Inclusion Criteria ◽

Health History ◽

Health Factors ◽

Age Of Diagnosis ◽

History Of

Abstract Objective Traumatic brain injury (TBI) is potentially a risk factor for Alzheimer’s disease (AD). This relationship may depend on the severity of TBI as well as other risk factors including APOE. We examined whether TBI status affects age of onset of AD, while improving on prior literature’s methodological issues. Method Data from the National Alzheimer’s Coordinating Centers were used. Inclusion criteria included: normal cognition at baseline; eventual diagnosis of AD; adults aged 50 and older; at least 3 years of follow-up data. Covariates included age at baseline and history of TIA, stroke, or hypertension. The resulting sample (N = 485) was 65.2% female; 89.1% White, 9.1% Black; and 4.5% Hispanic; 8% with TBI; and 42% with APOE4. Average age at baseline was 79.2 (SD = 7.6). ANCOVAs were used to determine whether TBI status (no TBI; TBI with brief LOC; TBI with extended LOC) was associated with earlier age of diagnosis for AD, controlling for age at baseline and health factors. APOE status was added to a second ANCOVA. Results Age at baseline (p < .001), but not health history (p = .777), was related to age of AD diagnosis. TBI status was not associated with age of AD diagnosis (p = .737). When APOE and the interaction between APOE and TBI status were added to the model, neither was significant (p’s = .150, .647). Conclusions When controlling for baseline cognition, age at baseline, and health factors, there was no relationship between TBI status and age of diagnosis of AD. However, use of more stringent inclusion criteria as compared to previous studies may have reduced power significantly.

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820 An Unusual Case of Post-Traumatic Brain Injury Kleine-Levin Syndrome with Anti-GAD-65 Autoantibodies

SLEEP ◽

10.1093/sleep/zsab072.817 ◽

2021 ◽

Vol 44 (Supplement_2) ◽

pp. A320-A320

Author(s):

Caroline Tse ◽

Emmanuel Mignot ◽

Miranda Lim

Keyword(s):

Traumatic Brain Injury ◽

Brain Injury ◽

Autoimmune Diabetes ◽

Autoimmune Encephalitis ◽

The United States ◽

United States Government ◽

Prior History ◽

Thalassemia Minor ◽

History Of ◽

Gad 65

Abstract Introduction Kleine-Levin Syndrome (KLS) is a rare clinical syndrome, and is precipitated by traumatic brain injury (TBI) in 9% of cases. An autoimmune component to KLS has previously been suggested. Autoantibody profiles in KLS are diverse and its overlap with autoimmune encephalitis is still not well described or understood. Here, a case of KLS in a patient with autoimmune diabetes with very high levels of serum autoimmune GAD-65 antibodies is presented. Report of case(s) A 36-year-old male Veteran with a history of alpha-thalassemia minor, prior history of insomnia with nightly sleep of 6 hours, prior history of mild OSA with AHI of 5.8 on PSG in 2018, sustained a mild TBI on 11/13/2019 after a 50-pound box fell on his head. CT head and cervical spine were normal. One week later, he developed recurrent episodes of hypersomnia, sleeping up to 80 hours continuously, waking briefly only to urinate or eat, with hyperphagia, irritability, and derealization present during episodes. One month after the TBI, he was diagnosed with Latent Autoimmune Diabetes in Adults (LADA) after blood glucose was found to be elevated at 566. Serum GAD-65 antibody level was very elevated at 10,594 U/mL (ref range: 0–5 U/mL), hemoglobin a1c was 7.7%, and insulin was started. Six months later, he was evaluated in the VA Sleep Clinic for continued hypersomnia, despite controlled diabetes. Neurological examination, MRI brain, and sleep-deprived EEG were normal. Cerebrospinal fluid testing was normal, with the exception of a CSF autoimmune encephalitis panel with a positive GAD-65 titer of 0.24 nmol/L (range <0.02 nmol/L) – non-diagnostic for autoimmune encephalitis. HLA-DQ1B status is pending. Conclusion Autoimmunity is an emerging topic of clinical significance in KLS. GAD-65 serum antibodies have both endocrine and neurologic significance, with high levels seen in autoimmune diabetes, encephalitis, stiff-person syndrome, and cerebellar ataxia. An autoantibody panel can be considered in patients with KLS, as the presence of autoimmune encephalitis may support the use of immunotherapy. Support (if any) Portland VA Research Foundation to Dr. Lim. The contents do not represent the views of the United States Government.

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