Our objective was to examine whether severe head injury, subtypes of head injury, or repeated head injuries are associated with ALS risk based on the Swedish population and health registers. We conducted a case-control study, nested within a cohort of 5,764,522 individuals who were born in Sweden during 1901-1970 and followed between 1991 and 2007. The study included 4004 ALS patients identified from the Swedish Patient Register during follow-up and 20,020 randomly selected controls matched by gender and birth year. We evaluated hospitalization for severe head injury that was recorded in the inpatient register before ALS diagnosis. Conditional logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (CIs). Results showed that there was an association of ALS risk with severe head injury ≤ 1 year before diagnosis (OR: 3.9, 95% CI 2.6-6.1). No association was observed for severe head injury > 3 years before ALS diagnosis, nor was ALS associated with subtypes of head injury or repeated injuries occurring > 3 years before diagnosis. In conclusion, our findings from the Swedish registers provide no strong support for an etiological relationship between severe head injury in adulthood and ALS risk.
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http://dx.doi.org/10.3109/21678421.2012.754043 | DOI Listing |
Endocrine
January 2025
Centro di Ricerca e Innovazione sulle Patologie Surrenaliche, AOU Careggi, Florence, Italy.
Purpose: To compare functional deficits associated to surgery with those caused by the growth of the head and neck paragangliomas (HNPGLs).
Methods: 72 patients with HNPGLs were included. Patients were divided in group A (49 patients undergoing surgery) and group B (23 patients following a wait and see approach).
Transl Psychiatry
January 2025
Department of Neurosurgery, General Hospital of Northern Theater Command, Postgraduate Training Base of General Hospital of Northern Theater Command of Jinzhou Medical University, Shenyang, Liaoning, China.
Traumatic brain injury (TBI) is identified as a risk factor for Parkinson's disease (PD), which is a neurodegenerative disease characterized by the loss of dopaminergic neurons in the substantia nigra (SN). However, the precise mechanism by which chronic TBI initiates PD pathogenesis is not yet fully understood. In our present study, we assessed the chronic progression and pathogenesis of PD-like behavior at different intervals in TBI mice.
View Article and Find Full Text PDFLancet Neurol
February 2025
Department of Neurology AB51, University of Groningen, University Medical Center Groningen, Groningen, Netherlands.
The age-specific incidence of traumatic brain injury in older adults is rising in high-income countries, mainly due to an increase in the incidence of falls. The severity of traumatic brain injury in older adults can be underestimated because of a delay in the development of mass effect and symptoms of intracranial haemorrhage. Management and rehabilitation in older adults must consider comorbidities and frailty, the treatment of pre-existing disorders, the reduced potential for recovery, the likelihood of cognitive decline, and the avoidance of future falls.
View Article and Find Full Text PDFInjury
January 2025
Department of Otolaryngology-Head and Neck Surgery, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Objective: Our primary objective was to identify and describe demographic trends in head and neck injuries incurred while participating in horseback riding.
Study Design: Cross-sectional analysis.
Setting: National Database.
Inflamm Res
January 2025
Department of Ultrasound, The Second Xiangya Hospital of Central South University, Changsha, 410011, China.
Background: Hyperoxia-induced brain injury is a severe neurological complication that is often accompanied by adverse long-term prognosis. The pathogenesis of hyperoxia-induced brain injury is highly complex, with neuroinflammation playing a crucial role. The activation of the nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3) inflammasome, which plays a pivotal role in regulating and amplifying the inflammatory response, is the pathological core of hyperoxia-induced brain injury.
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