Fame and Mortality: Evidence from a Retrospective Analysis of Singers
November 26, 2025
Background
Traumatic brain injury (TBI) disrupts normal brain function due to trauma. It refers to brain dysfunction caused due to an external mechanical force.
Primary injury results from mechanical force through contact or acceleration-deceleration at injury occurrence.
Secondary injury is non-mechanical, may be delayed, and can exacerbate existing brain injuries from impact.
Classification as follows:
Primary injuries
Secondary injuries
A sudden trauma to the head disrupts normal brain function through blows or penetrative injuries.
TBI varies from mild concussion to severe cognitive impairment.
Biphasic injury complexity requires interventions for immediate trauma and long-term neuroprotection.
Glasgow Coma Scale (GCS) measures consciousness and neurologic function from 3 to 15 points through motor, verbal, and eye responses.
Loss of consciousness is classified as mild, moderate, or severe based on duration and symptoms.
Posttraumatic amnesia is the duration until patients can show continuous memory post-injury.
Epidemiology
Males have nearly double the hospitalization risk for TBI than females and almost three times the TBI-related death risk.
Sources indicated that individuals aged 75 or older accounted for 32% of TBI-related hospitalizations and 28% of related deaths observed.
Mortality rates post-severe TBI are notably high, with survivors more prone to death from seizures, pneumonia, digestive issues, and various external injuries compared to similarly aged individuals.
TBI is a significant global health concern to cause high mortality and disability rates. WHO predicts it will become a leading cause of death by 2030.
Anatomy
Pathophysiology
Primary injury occurs immediately due to mechanical force, while secondary injury develops later and can exacerbate existing damage to the brain from the initial injury.
They are located on the poles and inferior aspects of the frontal lobes, cortex near the operculum, and lateral temporal lobes.
Epidural hematomas involve rapid blood clots between bone and dura, as arterial bleeding increases pressure on brain tissue.
Secondary injury from TBI can arise hours or days later due to impaired cerebral blood flow.
It decreased cerebral blood flow from edema, hemorrhage, or increased ICP leads to failed ion pumps and calcium-sodium imbalance.
Etiology
The causes of TBI are as follows:
Falls
Motor Vehicle Accidents
Sports and Recreational Injuries
Assaults and Violence
Blast Injuries
Workplace and Industrial Accidents
Penetrating Injuries
Recreational and Domestic Incidents
Genetics
Prognostic Factors
Determining TBI prognosis is complex due to varied patient health statuses, injury types, severities, and treatment timings.
Retrospective cohort study showed that patients aged 45-64 years had twice the likelihood of poor outcomes and patients over 80 years had five times the likelihood compared to ages 18-44.
Patients with moderate to severe TBI experienced high long-term unemployment risk due to comorbid psychiatric symptoms and cognitive impairment.
Davis’s study found that increased GCS scores predict survival from field to emergency department.
Clinical History
Collect details including the mechanism of injury, timeline and events after injury, medical and family history to understand clinical history of patients.
Physical Examination
Head and Scalp Examination
Neurological Examination
Spine Examination
Age group
Associated comorbidity
Associated activity
Acuity of presentation
Immediate symptoms are:
Loss of consciousness, post-traumatic seizures, vomiting, severe headache, visible trauma
Delayed symptoms are:
Subtle cognitive impairment, sleep disturbances, persistent headache, mood changes
Differential Diagnoses
Subdural hematoma
Cerebral contusion
Delirium
Syncope
Psychogenic non-epileptic seizures
Laboratory Studies
Imaging Studies
Procedures
Histologic Findings
Staging
Treatment Paradigm
3% saline bolus hyperosmolar therapy is recommended for ICP, with doses of 2-5 mL/kg.
Avoid midazolam and fentanyl bolus to prevent cerebral hypoperfusion risks.
Moderate hypothermia helps control ICP but not overall outcomes improvement.
Early enteral nutrition supports reduced mortality and better outcomes.
First-line imaging for suspected moderate to severe TBI or high-risk mild TBI.
by Stage
by Modality
Chemotherapy
Radiation Therapy
Surgical Interventions
Hormone Therapy
Immunotherapy
Hyperthermia
Photodynamic Therapy
Stem Cell Transplant
Targeted Therapy
Palliative Care
use-of-non-pharmacological-approach-for-traumatic-brain-injury
Perform soft restraints if necessary to prevent self-harm or tube dislodgement.
Remove unnecessary equipment that causes injury during seizures.
Use shower chairs for those with impaired balance.
Home safety evaluation includes remove clutter, improve lighting, and remove throw rugs.
Proper awareness about TBI should be provided and its related causes with management strategies.
Appointments with neurologist and preventing recurrence of disorder is an ongoing life-long effort.
Use of Osmotic Agents
Mannitol:
It increases glomerular filtrate osmolarity to reduce water reabsorption.
Use of Antiepileptics
Levetiracetam:
It has antiepileptic effects that involve calcium channels and neurotransmitter release modulation.
Use of Vasopressors
Norepinephrine:
It increases cardiac output and heart rate to decrease renal perfusion.
use-of-intervention-with-a-procedure-in-treating-traumatic-brain-injury
The procedural interventions for airway and ventilation procedures include endotracheal intubation and mechanical ventilation.
Surgical interventions include craniotomy and decompressive craniectomy.
use-of-phases-in-managing-traumatic-brain-injury
In the immediate assessment and stabilization phase, the goal is to prevent secondary injury and rapid transport.
Pharmacologic therapy is effective in the treatment phase as it includes the use of osmotic agents, antiepileptics, and vasopressors.
In supportive care and management phase, patients should receive required attention such as lifestyle modification and surgical interventional procedures.
The regular follow-up visits with the neurologist are scheduled to check the improvement of patients along with treatment response.
Medication
Future Trends
Traumatic brain injury (TBI) disrupts normal brain function due to trauma. It refers to brain dysfunction caused due to an external mechanical force.
Primary injury results from mechanical force through contact or acceleration-deceleration at injury occurrence.
Secondary injury is non-mechanical, may be delayed, and can exacerbate existing brain injuries from impact.
Classification as follows:
Primary injuries
Secondary injuries
A sudden trauma to the head disrupts normal brain function through blows or penetrative injuries.
TBI varies from mild concussion to severe cognitive impairment.
Biphasic injury complexity requires interventions for immediate trauma and long-term neuroprotection.
Glasgow Coma Scale (GCS) measures consciousness and neurologic function from 3 to 15 points through motor, verbal, and eye responses.
Loss of consciousness is classified as mild, moderate, or severe based on duration and symptoms.
Posttraumatic amnesia is the duration until patients can show continuous memory post-injury.
Males have nearly double the hospitalization risk for TBI than females and almost three times the TBI-related death risk.
Sources indicated that individuals aged 75 or older accounted for 32% of TBI-related hospitalizations and 28% of related deaths observed.
Mortality rates post-severe TBI are notably high, with survivors more prone to death from seizures, pneumonia, digestive issues, and various external injuries compared to similarly aged individuals.
TBI is a significant global health concern to cause high mortality and disability rates. WHO predicts it will become a leading cause of death by 2030.
Primary injury occurs immediately due to mechanical force, while secondary injury develops later and can exacerbate existing damage to the brain from the initial injury.
They are located on the poles and inferior aspects of the frontal lobes, cortex near the operculum, and lateral temporal lobes.
Epidural hematomas involve rapid blood clots between bone and dura, as arterial bleeding increases pressure on brain tissue.
Secondary injury from TBI can arise hours or days later due to impaired cerebral blood flow.
It decreased cerebral blood flow from edema, hemorrhage, or increased ICP leads to failed ion pumps and calcium-sodium imbalance.
The causes of TBI are as follows:
Falls
Motor Vehicle Accidents
Sports and Recreational Injuries
Assaults and Violence
Blast Injuries
Workplace and Industrial Accidents
Penetrating Injuries
Recreational and Domestic Incidents
Determining TBI prognosis is complex due to varied patient health statuses, injury types, severities, and treatment timings.
Retrospective cohort study showed that patients aged 45-64 years had twice the likelihood of poor outcomes and patients over 80 years had five times the likelihood compared to ages 18-44.
Patients with moderate to severe TBI experienced high long-term unemployment risk due to comorbid psychiatric symptoms and cognitive impairment.
Davis’s study found that increased GCS scores predict survival from field to emergency department.
Collect details including the mechanism of injury, timeline and events after injury, medical and family history to understand clinical history of patients.
Head and Scalp Examination
Neurological Examination
Spine Examination
Immediate symptoms are:
Loss of consciousness, post-traumatic seizures, vomiting, severe headache, visible trauma
Delayed symptoms are:
Subtle cognitive impairment, sleep disturbances, persistent headache, mood changes
Subdural hematoma
Cerebral contusion
Delirium
Syncope
Psychogenic non-epileptic seizures
3% saline bolus hyperosmolar therapy is recommended for ICP, with doses of 2-5 mL/kg.
Avoid midazolam and fentanyl bolus to prevent cerebral hypoperfusion risks.
Moderate hypothermia helps control ICP but not overall outcomes improvement.
Early enteral nutrition supports reduced mortality and better outcomes.
First-line imaging for suspected moderate to severe TBI or high-risk mild TBI.
Physical Medicine and Rehabilitation
Perform soft restraints if necessary to prevent self-harm or tube dislodgement.
Remove unnecessary equipment that causes injury during seizures.
Use shower chairs for those with impaired balance.
Home safety evaluation includes remove clutter, improve lighting, and remove throw rugs.
Proper awareness about TBI should be provided and its related causes with management strategies.
Appointments with neurologist and preventing recurrence of disorder is an ongoing life-long effort.
Physical Medicine and Rehabilitation
Mannitol:
It increases glomerular filtrate osmolarity to reduce water reabsorption.
Physical Medicine and Rehabilitation
Levetiracetam:
It has antiepileptic effects that involve calcium channels and neurotransmitter release modulation.
Physical Medicine and Rehabilitation
Norepinephrine:
It increases cardiac output and heart rate to decrease renal perfusion.
Physical Medicine and Rehabilitation
The procedural interventions for airway and ventilation procedures include endotracheal intubation and mechanical ventilation.
Surgical interventions include craniotomy and decompressive craniectomy.
Physical Medicine and Rehabilitation
In the immediate assessment and stabilization phase, the goal is to prevent secondary injury and rapid transport.
Pharmacologic therapy is effective in the treatment phase as it includes the use of osmotic agents, antiepileptics, and vasopressors.
In supportive care and management phase, patients should receive required attention such as lifestyle modification and surgical interventional procedures.
The regular follow-up visits with the neurologist are scheduled to check the improvement of patients along with treatment response.
Traumatic brain injury (TBI) disrupts normal brain function due to trauma. It refers to brain dysfunction caused due to an external mechanical force.
Primary injury results from mechanical force through contact or acceleration-deceleration at injury occurrence.
Secondary injury is non-mechanical, may be delayed, and can exacerbate existing brain injuries from impact.
Classification as follows:
Primary injuries
Secondary injuries
A sudden trauma to the head disrupts normal brain function through blows or penetrative injuries.
TBI varies from mild concussion to severe cognitive impairment.
Biphasic injury complexity requires interventions for immediate trauma and long-term neuroprotection.
Glasgow Coma Scale (GCS) measures consciousness and neurologic function from 3 to 15 points through motor, verbal, and eye responses.
Loss of consciousness is classified as mild, moderate, or severe based on duration and symptoms.
Posttraumatic amnesia is the duration until patients can show continuous memory post-injury.
Males have nearly double the hospitalization risk for TBI than females and almost three times the TBI-related death risk.
Sources indicated that individuals aged 75 or older accounted for 32% of TBI-related hospitalizations and 28% of related deaths observed.
Mortality rates post-severe TBI are notably high, with survivors more prone to death from seizures, pneumonia, digestive issues, and various external injuries compared to similarly aged individuals.
TBI is a significant global health concern to cause high mortality and disability rates. WHO predicts it will become a leading cause of death by 2030.
Primary injury occurs immediately due to mechanical force, while secondary injury develops later and can exacerbate existing damage to the brain from the initial injury.
They are located on the poles and inferior aspects of the frontal lobes, cortex near the operculum, and lateral temporal lobes.
Epidural hematomas involve rapid blood clots between bone and dura, as arterial bleeding increases pressure on brain tissue.
Secondary injury from TBI can arise hours or days later due to impaired cerebral blood flow.
It decreased cerebral blood flow from edema, hemorrhage, or increased ICP leads to failed ion pumps and calcium-sodium imbalance.
The causes of TBI are as follows:
Falls
Motor Vehicle Accidents
Sports and Recreational Injuries
Assaults and Violence
Blast Injuries
Workplace and Industrial Accidents
Penetrating Injuries
Recreational and Domestic Incidents
Determining TBI prognosis is complex due to varied patient health statuses, injury types, severities, and treatment timings.
Retrospective cohort study showed that patients aged 45-64 years had twice the likelihood of poor outcomes and patients over 80 years had five times the likelihood compared to ages 18-44.
Patients with moderate to severe TBI experienced high long-term unemployment risk due to comorbid psychiatric symptoms and cognitive impairment.
Davis’s study found that increased GCS scores predict survival from field to emergency department.
Collect details including the mechanism of injury, timeline and events after injury, medical and family history to understand clinical history of patients.
Head and Scalp Examination
Neurological Examination
Spine Examination
Immediate symptoms are:
Loss of consciousness, post-traumatic seizures, vomiting, severe headache, visible trauma
Delayed symptoms are:
Subtle cognitive impairment, sleep disturbances, persistent headache, mood changes
Subdural hematoma
Cerebral contusion
Delirium
Syncope
Psychogenic non-epileptic seizures
3% saline bolus hyperosmolar therapy is recommended for ICP, with doses of 2-5 mL/kg.
Avoid midazolam and fentanyl bolus to prevent cerebral hypoperfusion risks.
Moderate hypothermia helps control ICP but not overall outcomes improvement.
Early enteral nutrition supports reduced mortality and better outcomes.
First-line imaging for suspected moderate to severe TBI or high-risk mild TBI.
Physical Medicine and Rehabilitation
Perform soft restraints if necessary to prevent self-harm or tube dislodgement.
Remove unnecessary equipment that causes injury during seizures.
Use shower chairs for those with impaired balance.
Home safety evaluation includes remove clutter, improve lighting, and remove throw rugs.
Proper awareness about TBI should be provided and its related causes with management strategies.
Appointments with neurologist and preventing recurrence of disorder is an ongoing life-long effort.
Physical Medicine and Rehabilitation
Mannitol:
It increases glomerular filtrate osmolarity to reduce water reabsorption.
Physical Medicine and Rehabilitation
Levetiracetam:
It has antiepileptic effects that involve calcium channels and neurotransmitter release modulation.
Physical Medicine and Rehabilitation
Norepinephrine:
It increases cardiac output and heart rate to decrease renal perfusion.
Physical Medicine and Rehabilitation
The procedural interventions for airway and ventilation procedures include endotracheal intubation and mechanical ventilation.
Surgical interventions include craniotomy and decompressive craniectomy.
Physical Medicine and Rehabilitation
In the immediate assessment and stabilization phase, the goal is to prevent secondary injury and rapid transport.
Pharmacologic therapy is effective in the treatment phase as it includes the use of osmotic agents, antiepileptics, and vasopressors.
In supportive care and management phase, patients should receive required attention such as lifestyle modification and surgical interventional procedures.
The regular follow-up visits with the neurologist are scheduled to check the improvement of patients along with treatment response.

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