Tag Archives: Death

THE TRAGIC DEATHS OF GENE HACKMAN AND BETSY ARAKAWA

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On February 26, 2025, the decomposing bodies of legendary Hollywood actor Gene Hackman and his wife Betsy Arakawa were found inside their cloistered estate at Santa Fe, New Mexico. The medical investigator ruled both died of natural causes approximately five days apart—Arakawa passing on February 12, and Hackman being deceased on February 17. There was no evidence of foul play or accident, but there is a sad and compelling story behind the tragic deaths of Gene Hackman and Betsy Arakawa.

The bodies were discovered by maintenance workers who became suspicious as neither Arakawa nor Hackman had been seen in some time. They peered through a window and saw a body on the floor. Police immediately attended as did death scene examiners from the New Mexico Office of the Medical Investigator.

Autopsy and investigation information was released to the public on March 7. “It is unprecedented for the Office of the Medical Investigator to make public statements about sudden death investigations so soon in the process. However, the circumstances surrounding these two deaths require accurate dissemination of important information,” the New Mexico Chief Medical Investigator Dr. Heather Jarrell said at a press conference.

This was a prudent move given the high-profile nature of the Hackman-Arakawa case. In the nine days between the body discoveries and the conference, the media—especially social media—was alive with rumours and false assumptions. It’s to be expected with someone as well known as Gene Hackman and the strange circumstances of this death case.

Although the autopsy reports and scene imagery were quickly sealed by a judge acting on a petition from the Hackman-Arakawa estates, the medical investigator did offer a clear account of the death causes and the circumstances leading up to their tragic demise. Here’s what’s publicly known.

Betsy Arakawa, age 64, was last seen alive between 3:30 and 5:00 pm on February 11. She was filmed on surveillance cameras at Sprouts Farmers Market, CVS Pharmacy, and a pet food store in downtown Santa Fe. Her car entered the couple’s gated community at 5:15 pm using the remote control assigned to her. Cell phone records and inquiries established she’d called a private medical clinic on the morning of February 12 and made an afternoon appointment with a doctor. She never showed up.

Arakawa’s body was positioned on the floor of one of their home’s bathrooms. An open vial and scattered pills were near her, but the medical examiner determined they were a routine prescription for a thyroid condition and had nothing to do with her death. It seemed she’d suddenly collapsed, became unconscious, and shortly died.

Her autopsy showed a serious lung condition, and she suffered from an escalating case of hantavirus infection. Without question, this proved fatal and Hantavirus Pulmonary Syndrome (HPS) clearly was the cause of her death. Hantavirus primarily infects rodents and is highly transferable to humans. The death scene property outbuildings showed evidence of deer mouse infestation which results in airborne particles from droppings or discharges being human-inhaled. HPS can manifest in the body for weeks before sharply increasing in respiratory difficulties and then sudden death.

Hantavirus Pulmonary Syndrome is rare, but the State of New Mexico Health Department recorded 136 infections over the last 50 years. Nearly half of the cases were fatal. HPS is treatable if caught in the early stages, but the autopsy conclusions found Betsy Arakawa was in an advanced, chronic condition. Likely, the rapidly escalating symptoms is why she made the doctor appointment and why she expired so quickly.

Gene Hackman was already aged and frail. He was 95 when he died, and his autopsy showed he was in an advanced stage of dementia—confirmed in the brain dissection and MRIs as Alzheimer’s Disease. Hackman also suffered from significant atherosclerotic cardiovascular disease (plaque-clogged heart arteries) as well as renal disease (failing kidneys).

The medical investigator ruled Gene Hackman’s cause of death was due to complications from heart failure, dementia, and his kidneys shutting down. This is also known as Multiple Organ Dysfunction Syndrome (MODS) and is a common end-of-life condition for the very elderly. Basically, the body progressively quits.

There was strong evidence for Hackman’s death date of February 17. That was the day his pacemaker stopped which is proof of death. Although there’s no doubt about where, when, and how Hackman died, the disturbing and unanswered question is what he knew—what he was aware of—while his wife—his sole caregiver and life support system—lay deceased and decomposing on the bathroom floor. This is truly tragic. Just awful to think of that helpless and alone old man.

Additionally tragic is that one of the couple’s dogs also died during the time Hackman and Arakawa went undiscovered. The animal was recovering from a veterinary procedure and was kept caged. The poor pet probably succumbed to dehydration.

In the time after the body discoveries on February 26 and the official information release on March 7, a lot of media speculation went on about the states of the Arakawa and Hackman corpses, specifically around the reports/rumors of mummification. This has been clearly addressed by forensic pathologist Dr. Judy Melinek in her article on MedPageToday.

Long-term followers of DyingWords.net may remember Judy when she guest posted on this site corresponding to the release of her first book Working Stiff: Two Years, 262 Bodies, and the Making of a Medical Examiner which documented her World Trade Center bombing experience.

Here’s Dr. Melinek’s piece titled Gene Hackman’s Death: How the Mystery Unfolded — Determining time of death can help inform the cause of death.

When actor Gene Hackman and his wife, pianist Betsy Arakawa, were found dead and decomposed in their Santa Fe, New Mexico home on February 26, much of the media fixated on a phrase in the police report describing “mummification” of their hands and feet. People who hear that phrase tend to immediately think of embalmed cadavers from ancient Egypt, as seen in bad movies.

The medical term, however, describes a natural process of postmortem change. Mummification of the extremities occurs as a process of desiccation: the skin dries out, turns brown, wrinkles up. We usually find it in a warm, dry environment, and though it can happen over the course of weeks, it might also set in as quickly as a matter of days.

Given that these two decedents were found indoors in arid Santa Fe, and that there was a space heater in the bathroom near Arakawa’s body, the finding of mummification is not surprising. Subsequent interrogation of Hackman’s pacemaker indicated that the last cardiac activity was on February 17 — 9 days before the bodies were found — and that workers had last been to the residence approximately 2 weeks prior. Meanwhile, Arakawa was last seen on the gated community CCTV and was communicating via e-mail on February 11.

It’s these circumstantial bits of information from the scene that are often the most helpful clues in narrowing down the time of death in the early phases of a death investigation. Let’s dive deeper into the role of a forensic pathologist and other key players in a mysterious case like Hackman and Arakawa’s.

Narrowing Down Time of Death

Time of death estimation is a complex process that depends on multiple factors both intrinsic to the body and found in the immediate environment around it. These variables can include the body’s weight and clothing, the ambient temperature, whether the death occurred indoors in a controlled environment or outdoors where temperatures fluctuate, the health status of the individual just prior to death, and the presence or absence of animals (including insects) that can feed on the body.

Experienced forensic pathologists carry around a mental library of cases that inform us over the course of a career of what a decomposing human body will look like after 24 hours, 48 hours, weeks, and months — and in all different ambient conditions. Death scene investigators can also take a measurement of the core body temperature at the scene that we can compare to published data to help narrow down a tighter death interval using nomograms opens in a new tab or window.

Post-mortem interval estimation isn’t perfectly empirical, but its reliability increases with each bit of information gleaned about a case, the forensic expertise of the person doing the assessment, and the thoroughness of the police investigation. It’s often our role early on to help the police focus their investigation on a reasonable time frame by providing a ballpark estimate of when the person died, and to help them dismiss incompatible testimony or unlikely suspects.

The Cause of Death

What about the cause of death? You have to be concerned about an environmental toxin like carbon monoxide or natural gas when two people and a pet are dead in the same enclosed residence. So, hazardous-materials crews would need to assess such a scene prior to arrival of medical first responders, who might otherwise be putting their own lives at risk. Environmental testing was performed at the residence of Hackman and Arakawa, and additional carbon monoxide testing was also performed on the human remains. All these tests were negative.

The deaths remained a mystery until Friday, March 7, when the medical examiner held a news conference to report that Arakawa had died from hantavirus, a rare pathogen that can be transmitted from rodent droppings, and that Hackman, who had been suffering from Alzheimer’s and cardiovascular disease and had relied on his wife’s care, likely died of heart disease opens in a new tab or window in the same house a week later. It’s not clear if Hackman knew his wife was dead.

This is a heartbreaking conclusion. It came after extraordinarily intensive and quick work by New Mexico’s state Office of the Medical Investigator (OMI) and underscores their dedication and professionalism. The New Mexico OMI has extensive experience with infectious diseases and is one of the select death-investigation facilities in the U.S. with a BSL-3 biosafety level morgue where they can handle infectious agents that spread through airborne transmission.

I suspect that there might have been signs at autopsy that pointed to a lung infection, and that hantavirus was then detected by identifying its genetic signature through polymerase chain reaction (PCR) testing of a nasopharyngeal or lung tissue swab. The Hackman-Arakawa property was in a remote area of Santa Fe, and there was evidence of rodent activity there. The couple had three dogs, and sometimes pets can come in contact with wild rodents and bring them into the house. The necropsy on the dead dog is still pending and may answer more questions about the source of viral exposure.

The Risk of Isolation

I know a lot of gut-wrenching death stories, and the worst ones always involve either the feeling that death may have been preventable, or that the decedent suffered. Everyone who’s been following this shocking and complex public mystery should be grateful to the New Mexico OMI for giving us — and the Hackman-Arakawa family — a speedy and decisive resolution.

If you have people in your lives who are the sole caregivers to a medically fragile patient, please reach out frequently to give them as much help and support as you can. Balancing their need for privacy with your own concerns for their wellbeing is never simple, but maybe these public deaths will open conversations with them about a less isolated environment for their end-of-life care.

Judy Melinek, MD, is an American forensic pathologist currently working as a contract forensic pathologist in Wellington, New Zealand. She is the co-author with her husband, writer T.J. Mitchell, of the memoir Working Stiff: Two Years, 262 Bodies, and the Making of a Medical Examiner, and the forensic-detective novels First Cut and Aftershock. You can follow her on BlueSky @drjudymelinek and Facebook/DrJudyMelinekMD.

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Tragic is an appropriate word to describe the Hackman/Arakawa death case. Here was once an A-List, Oscar-winning movie star and now a very wealthy man living a recluse life with his also-accomplished wife of 30 years. They have no contact with the outside for two weeks, and no one in the family or friend sphere thinks to check on them. An old, frail, and demented man and his increasingly ill younger wife die alone, days apart, and rot on the floor of their multi million-dollar mansion.

The magazine Architectural Digest once ran a feature on the Hackman/Arakawa Santa Fe home. Here’s some pictures of it. It makes one think.

WHAT REALLY KILLED ROBIN WILLIAMS

On August 11, 2014, entertainment genius Robin Williams took his own life inside his Paradise Cay, California home near San Francisco. The coroner initially ruled that Williams, age 63, died by suicide—asphyxia by hanging antecedent to, or caused by, clinical depression. However, when the final autopsy results were in, an entirely different picture played out. Robin Williams was in the advanced stage of a somewhat common, but almost always undiagnosed, brain disease called Lewy Body Dementia or LBD.

As Williams’ window, Susan Schneider Williams who now represents the Lewy Body Dementia Association, stated, “The disease was a terrorist in my husband’s head. Any way you look at it, the presence of Lewy bodies in his brain took his life. Depression was only a symptom. Unfortunately, we as a culture don’t have the vocabulary to discuss brain disease in the way we do about depression. Depression is only a side effect of LBD—it’s rooted in neurology. His brain was literally falling apart, and not one thing could be done about it.”

Lewy Body is a strange term. We’ll examine where that name came from, what exactly LBD is, what causes it, and how this always-fatal disease can be managed in its three progressive stages: early, mid, and late. But first, let’s have a brief look at this remarkable man’s achievements. Perhaps “remarkable” isn’t a powerful enough word for Robin Williams.

Robin McLaurin Williams was born on July 21, 1951, into an average American family. But from an early age, there was nothing average about him. He showed a God-given gift for improvision comedy and acting. By the early 1970s, Williams was in high demand as a San Francisco-based stand-up comedian, and he went on to be one of the funniest funnies of all time.

Few can forget many of Robin Williams’ outstanding character roles. He got his television start in Mork & Mindy and went on to film. Popeye. Hook. Good Will Hunting. Dead Poets Society. Good Morning Vietnam. The World According to Garp. World’s Greatest Dad. Night at the Museum. The Birdcage. Moscow on the Hudson. Jumanji. And, of course, Mrs. Doubtfire.

Williams also did voice-overs in Aladdin, Robots, and Happy Feet. He won numerous awards—six Golden Globes, five Grammys, two Primetime Emmys, two Screen Actors Guilds, and an Oscar for Best Supporting Actor. As well, Williams won the Cecille B. DeMille award in 2005.

Robin Williams had his struggles through life, though. He was addicted to cocaine and alcohol which set him into fitful mood swings. He was in and out of rehab for years. However, by 2010 he was stable and substance free, except for therapeutic prescriptions issues to combat what was thought to be clinical depression.

It was not. Robin Williams had an undiagnosed brain disorder. A disease that was only discovered after his death and was verified by brain sectioning at his autopsy. What was suspected to be Alzheimer’s or Parkinson’s in the last year of his life turned out to be Lewy’s Body Dementia—a condition under the general dementia umbrella and an extremely deadly disease.

You’re likely wondering what this weird name is and what it entails. Rather than me paraphrasing the information, let’s go to the best source available. No, not Wikipedia or ChatGPT.  It’s the website of the Lewy Body Dementia Association, and here’s what it says:

Lewy body dementia (LBD) is the 2nd most common type of progressive dementia after Alzheimer’s disease. The name comes from a discovery by Dr. Friedrich Lewy in the early 1900s of abnormal bodies or deposits of alpha-synuclein proteins in areas of the brain that can only be verified through an autopsy. These bodies alter the production of dopamine and acetylcholine that are vital neural transmitters.

LBD is not a rare disease. It affects more than a million people in the United States alone. Because LBD symptoms may closely resemble other, more commonly known disorders like Alzheimer’s and Parkinson’s disease, it is widely under-diagnosed.

LBD is an umbrella term for two related diagnoses:

  • A person with dementia with Lewy bodies will develop dementia and other LBD symptoms, one of which may be changes in movement, like a tremor (parkinsonism).
  • With the other form of LBD, people will present first with changes in movement, leading to a Parkinson’s disease diagnosis; over time many will develop dementia years later. This is diagnosed as Parkinson’s disease dementia.

As time passes, people with both diagnoses will develop very similar cognitive, physical, sleep, and behavioral symptoms. The earliest symptoms of dementia with Lewy bodies and Parkinson’s disease dementia are different, but both are due to the same underlying biological changes in the brain.

LBD is a multi-system disease and usually requires a comprehensive treatment approach with a collaborative team of physicians and other health care professionals like occupational, physical, or speech therapists. Early diagnosis and treatment may extend your quality of life and independence. Many people with LBD enjoy significant lifestyle improvement with a comprehensive treatment approach, and some may even experience little change from year to year.

For a more in-depth explanation of Lewy Body Dementia disease, here’s a trip to the medical research department at Johns Hopkins University:

Lewy Body Disease (LBD) is a complex and often misunderstood neurodegenerative disorder that affects millions of individuals worldwide. Characterized by the accumulation of abnormal protein deposits called Lewy bodies in the brain, LBD poses significant challenges to both patients and caregivers. In this article, we delve into the neurological aspects of LBD, exploring its development, detection, effects on the human body, and its associated symptoms.

Development of Lewy Body Disease

Lewy Body Disease primarily affects older adults, typically manifesting after the age of 50. While the exact cause of LBD remains unknown, researchers believe that a combination of genetic, environmental, and lifestyle factors may contribute to its development. Genetic mutations, particularly in genes associated with the production and clearance of alpha-synuclein protein, have been implicated in some cases of familial LBD. However, most cases of LBD occur sporadically without a clear genetic link.

Neurological Pathology

At the core of LBD pathology is the abnormal accumulation of alpha-synuclein protein, forming Lewy bodies within neurons. These protein aggregates disrupt normal cellular function and communication within the brain, leading to widespread neurodegeneration. Areas of the brain particularly affected by Lewy bodies include the substantia nigra, which plays a crucial role in movement control, and the cerebral cortex, responsible for cognitive functions.

Detection and Diagnosis

Diagnosing LBD can be challenging due to its overlapping symptoms with other neurodegenerative disorders such as Parkinson’s disease and Alzheimer’s disease. A comprehensive medical history, neurological examination, and a battery of neuropsychological tests are often employed to assess cognitive function, motor abilities, and psychiatric symptoms.

Brain imaging techniques, such as MRI and PET scans, may reveal characteristic patterns of brain atrophy and dysfunction associated with LBD. Additionally, a definitive diagnosis of LBD can only be made post-mortem through the examination of brain tissue for the presence of Lewy bodies.

Effects on the Human Body

Lewy Body Disease has profound effects on both motor and non-motor functions, significantly impacting quality of life. Motor symptoms include bradykinesia (slowed movements), rigidity, tremors, and gait disturbances resembling those seen in Parkinson’s disease. Non-motor symptoms encompass cognitive impairment, hallucinations, fluctuations in attention and alertness, sleep disturbances, autonomic dysfunction (such as orthostatic hypotension and urinary incontinence), and psychiatric manifestations like depression and anxiety.

Treatment and Management

While there is no cure for Lewy Body Disease, various treatment strategies aim to alleviate symptoms and improve patients’ quality of life. Medications targeting dopamine levels in the brain, such as levodopa, may help alleviate motor symptoms. Cholinesterase inhibitors, commonly used in Alzheimer’s disease, may improve cognitive function and psychiatric symptoms in some LBD patients. Multidisciplinary approaches involving physical therapy, occupational therapy, speech therapy, and psychological support are essential for managing the diverse array of symptoms associated with LBD.

Takeaway

Lewy Body Disease presents a complex clinical picture characterized by the interplay of motor, cognitive, and psychiatric symptoms. Understanding its neurological underpinnings is crucial for early detection, accurate diagnosis, and effective management of the disease. Ongoing research efforts aimed at unraveling the molecular mechanisms underlying LBD pathogenesis hold promise for the development of targeted therapies that can ultimately improve outcomes for individuals living with this challenging condition.

I’ll jump back to the Lewy Body Dementia Association for the diagnostic symptoms of the disease.

Motor Symptoms

  • Bradykinesia (slowed movements)
  • Rigidity (stiffness)
  • Tremors (usually less prominent than in Parkinson’s disease)
  • Gait disturbances (shuffling gait, balance problems)

Cognitive Symptoms

  • Fluctuating attention and alertness
  • Memory loss
  • Executive dysfunction (problems with planning, organizing, and problem-solving)
  • Visuospatial difficulties (problems with spatial awareness and perception)

Psychiatric Symptoms

  • Hallucinations (visual hallucinations are particularly common)
  • Delusions (often related to the hallucinations)
  • Depression
  • Anxiety
  • Apathy
  • Irritability or aggression
  • Sleep disturbances (REM sleep behavior disorder, vivid dreams, acting out dreams)

Autonomic Dysfunction

  • Orthostatic hypotension (drop in blood pressure upon standing)
  • Urinary incontinence or urgency
  • Constipation
  • Erectile dysfunction (in men)

Other Symptoms

  • REM sleep behavior disorder (acting out dreams physically)
  • Sensitivity to neuroleptic medications (may worsen symptoms)
  • Changes in sense of smell
  • Difficulty swallowing (dysphagia)

Note that not all individuals with LBD will experience all of these symptoms, and the severity and combination of symptoms can vary widely from person to person. Additionally, symptoms may fluctuate over time, with periods of relative stability interspersed with episodes of worsening symptoms. Early recognition and management of these symptoms are crucial for improving the quality of life for individuals living with LBD.

Detecting and verifying Lewy Body Disease (LBD) involves a comprehensive approach that combines clinical evaluation, neurological assessments, and diagnostic tests. Here’s a breakdown of the steps involved in the detection and verification process.

Clinical Evaluation

  • A thorough medical history is obtained from the patient and their caregivers, focusing on the onset and progression of symptoms.
  • A neurological examination is conducted to assess motor function, cognitive abilities, and psychiatric symptoms. This may include assessing gait, muscle tone, reflexes, coordination, memory, attention, and mood.
  • Careful observation of symptom patterns, including fluctuations in cognition and alertness, visual hallucinations, and motor symptoms resembling Parkinson’s disease.

Diagnostic Criteria

  • LBD is diagnosed based on established clinical criteria, such as the consensus criteria proposed by the DLB Consortium or the McKeith criteria.
  • These criteria outline the characteristic features and diagnostic markers of LBD, including cognitive fluctuations, visual hallucinations, Parkinsonism, and rapid eye movement (REM) sleep behavior disorder.
  • Criteria may also specify supportive features, such as neuroimaging findings and autonomic dysfunction, which further support the diagnosis of LBD.

Neuropsychological Assessment

  • Neuropsychological tests are administered to evaluate cognitive function, including memory, attention, executive function, and visuospatial abilities.
  • These tests help quantify cognitive impairment and track changes over time.

Neuroimaging Studies

  • Magnetic resonance imaging (MRI) and positron emission tomography (PET) scans may be performed to assess brain structure and function.
  • MRI may reveal patterns of cortical atrophy and changes in brain volume associated with LBD.
  • PET imaging with radiotracers targeting dopamine transporters or amyloid plaques can provide additional evidence supporting the diagnosis and differentiate LBD from other neurodegenerative disorders like Alzheimer’s disease.

Cerebrospinal Fluid Analysis

  • Lumbar puncture may be performed to analyze cerebrospinal fluid (CSF) biomarkers associated with LBD, such as levels of alpha-synuclein protein and markers of neuroinflammation.
  • While not routinely performed, CSF analysis can provide supplementary information to support the diagnosis of LBD in some cases.

Genetic Testing

  • Genetic testing may be considered in cases of familial LBD or when there is a strong family history of neurodegenerative diseases.
  • However, genetic testing is not typically performed as part of routine diagnostic evaluation for sporadic LBD.

Multidisciplinary Evaluation

  • A multidisciplinary team approach involving neurologists, neuropsychologists, geriatricians, psychiatrists, and other healthcare professionals is often utilized to ensure a comprehensive assessment and accurate diagnosis of LBD.
  • Verification of LBD relies on the integration of clinical findings, diagnostic tests, and adherence to established diagnostic criteria.
  • Given the complexity and variability of LBD presentation, accurate diagnosis and ongoing monitoring are essential for effective management and supportive care.

Treatment Options

  • LBD is a multi-system disease and typically requires a comprehensive treatment approach, meaning a team of physicians from different specialties, who collaborate to provide optimum treatment of each symptom without worsening other LBD symptoms.  ​
  • A comprehensive treatment plan may involve medications, physical, occupational, speech or other types of therapy, and counseling.

Medications

  • There are many treatments that can help with the symptoms; all medications prescribed for LBD are approved by the Food and Drug Administration to treat symptoms in other diseases, like Alzheimer’s disease and Parkinson’s disease.
  • These medications can offer symptomatic benefits for cognitive, movement, sleep, mood and behavioral changes in LBD.
  • There are not yet any medications that slow or stop the progression of LBD.

Cognitive Symptoms

  • Medications called cholinesterase inhibitors are considered the standard treatment for cognitive symptoms in LBD.
  • These medications were developed to treat Alzheimer’s disease. However, some researchers believe that people with LBD may be even more responsive to these types of medications than those with Alzheimer’s.
  • These drugs sometimes help control behavior problems and hallucinations as well.
  • Another medication that may be helpful is memantine (Namenda).

Movement Symptoms

  • Movement symptoms may be treated with a Parkinson’s medication called carbidopa/levodopa (Sinemet), but if the symptoms are mild, it may be best to not treat them in order to avoid potential medication side effects.

Visual Hallucinations

  • If the hallucinations are not disruptive, they may not need to be treated. However, if they are frightening or create challenging behavioral changes, a physician may recommend treatment.
  • Cholinesterase inhibitors are sometimes effective in treating hallucinations and other psychiatric symptoms of LBD. In addition, newer ‘atypical’ antipsychotic medications may be tried.
  • Most LBD experts prefer quetiapine or clozapine when treatment is necessary for safety or quality of life concerns.
  • Caution is required to find the lowest effective dose in this situation.
  • A newer medication, pimavanserin, was approved to treat psychosis in Parkinson’s disease; results from another clinical trial of this medication in people with dementia and psychosis are pending.
  • While older ‘traditional’ antipsychotic medications such as thorazine and haloperidol are commonly prescribed for Alzheimer’s patients with disruptive behavior, these medications may cause severe side effects in those with LBD.
  • For this reason, older traditional antipsychotic medications like haloperidol should be avoided.

WARNING: Up to 50% of LBD patients treated with any antipsychotic medication may have a severe reaction, such as worsening confusion, heavy sedation, and increased or possibly irreversible parkinsonism. If severe fever or muscle rigidity occurs, contact your doctor immediately; you may have a potentially life-threatening condition that is treated by stopping the medication.

REM Sleep Behavior Disorder (RBD)

  • RBD can be quite responsive to treatment, so your physician may recommend a medication like melatonin and/or clonazepam.

Medication Side Effects

  • Speak with your doctor about possible side effects.
  • The following drugs may cause sedation, motor impairment, or confusion:
  • Benzodiazepines, tranquilizers like diazepam and lorazepam
  • Anticholinergics (antispasmodics), such as oxybutynin and glycopyrrolate
  • Older antidepressants
  • Certain over-the-counter medications, including diphenhydramine and dimenhydrinate.
  • Some medications, like anticholinergics, amantadine, and dopamine agonists, which help relieve parkinsonian symptoms, might increase confusion, delusions, or hallucinations.

Surgery and Anesthesia

  • Be sure to meet with your anesthesiologist in advance of any surgery to discuss medication sensitivities and risks unique to LBD.
  • People with LBD often respond to certain anesthetics and surgery with acute states of confusion or delirium and may have a sudden significant drop in functional abilities, which may or may not be permanent.
  • Possible alternatives to general anesthesia include a spinal or regional block. These methods are less likely to result in postoperative confusion.
  • If you are told to stop taking all medications prior to surgery, consult with your doctor to develop a plan for careful withdrawal.

Other Types of Treatments

  • Lifestyle interventions include eating a healthy diet, exercising, and remaining socially active.
  • Physical therapy includes cardiovascular, strengthening and flexibility exercises, as well as gait training.
  • Speech therapy may improve low voice volume, poor enunciation, muscular strength, and swallowing difficulties.
  • Occupational therapy helps maintain skills and promotes functional ability and independence.
  • Music and aromatherapy may reduce anxiety and improve mood.
  • Individual and family psychotherapy may be useful for learning strategies to manage emotional and behavioral symptoms and to help make plans that address individual and family concerns about the future.
  • Support groups may be helpful for caregivers and persons with LBD to identify practical solutions to day-to-day frustrations and to obtain emotional support from others.

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This might be a lot of cut & pasted material—some maybe repetitive—however I think it’s important to be aware of Lewy Body Dementia.

So far, LBD is incurable but somewhat manageable if detected early-on. Our population is aging. Today’s demographics represent an ever-increasing older population, and the numbers are that many of our folks and friends around us, including ourselves, will develop some form of a degenerative brain disorder like LBD which is what really killed Robin Williams.

IT’S TIME FOR A NEW SCIENCE OF DEATH

Is there life after death? That’s a question folks have asked since the dawn of humanity. Historically, the answer has been faith-based. But today, modern science is closer to the truth following a major medical discovery at the University of Michigan. However, it depends on what your definition of life is. And your definition of death.

In 2014, a 24-year-old woman collapsed at home. She was taken to Emergency at U of M medical center where staff were unable to regain her consciousness. They moved her to the Intensive Care Unit (ICU), and she remained in ICU for four days while hooked to an electroencephalograph (EEG) to monitor her brain function. It showed she was in “brain death”.

Despite being on organic life support, (heart-lung machine) she flatlined on the electrocardiogram (ECG) monitor and went into cardiac arrest with her respiration ceasing — “clinical death” as it’s commonly called. Because her physical death seemed inevitable during the four days, her family had signed a Do Not Resuscitate (DNR) order. The woman remained in her bed, not breathing nor beating, and was still connected to the EEG for some time before she was removed to the morgue.

That was the end of this woman’s bodily life. Her physical life. But it wasn’t the end of her conscious life. In 2022, a researcher at the U of M reviewed the woman’s EEG charts and found that, astonishingly, at the moment of clinical death the woman’s brain came back to life—in fact into a hyperdrive in activity in the regions associated with consciousness. According to the researcher, “Something happened in that brain that makes no sense at all.”

We’ll closely examine what took place in that ward where Patient One, as she’s now known in the medical research community, physically passed away. And we’ll look at what consciousness, as that term applies to living human beings, might be. First, let’s review the definitions of death as they apply to clinical death and brain death, which are two separate deals. And see if it’s time for a new science of death.

I found a great death explanation resource at the United States National Library of Medicine. At their National Center for Biotechnology Information (NCBI) section there’s a multi-part series, one of which is titled Definitions of Death: What and When is Death? Interestingly, they divide it into two aspects. One is biological death. The other is social death.

To quote them. “The commonplace notion of death is to characterize it as an end state: being dead. Nevertheless, being dead is not the same as the event of death or the dying process.

Biological death can be understood as:

  1. A final event.
  2. An absolute state: being dead.
  3. Part of the dying process.

The absolute state of being dead is synonymous with the idea of medical or clinical death—where an individual has sustained irreversible cessation of circulatory and respiratory functions or irreversible cessation of all functions of the entire brain, including the brain stem.

Social death is a relational change in the meaning of a human life. It involves a change in the narrative identity of persons that either still biologically exist or have once existed.”

Biological death and social death, as set out in the NCBI paper, is broader coverage than what’s usually weighed in the mainstream medical community, such as physicians and coroners would use. From my experience in the death investigation business, we almost always relied on the clinical death measurement rather than the brain death evaluation. That’s because very few deaths are recorded on EEGs, and there is no brain activity to monitor. Therefore, the declaration of death usually refers to the standard definition of clinical death which is:

The cessation of blood circulation and breathing; the two criteria necessary to sustain human life.

Brain death is a different matter—the classic definition being:

The complete and irreversible loss of brain function to the point where there is no return.

So, is it possible to be dead and alive at the same time? Apparently, yes, as in the case of Patient One whose circumstances we’ll examine shortly. Before that, let’s look at the Florida Boy case as reported in the NCBI literature.

Florida Boy is a legal precedent of a boy who spent 14 years in an ICU connected to a heart-lung machine after an initial diagnosis of complete and total brain failure. He showed no EEG activity at all during that time. His parents demanded that he be artificially ventilated, fed, and hydrated in the hospital.

Over the 14 years, the boy biologically grew into a man as if he were normal—except in total death as in any form of consciousness. Interestingly, as his thorax and abdomen organ cellular activity functioned normally, his brain cells gradually replaced themselves and became a “grey goo of ghost-like tissues”. Apparently, without brain activity, the entire cerebral system decomposes. Not so with the neck-down region. The boy-turned-man was eventually disconnected via a court order, and he completed his clinical death cycle.

Let’s return to Patient One. Dr. Jimo Borjigin is a professor of neurology at the University of Michigan. As a project of interest, she investigated reports of Near Death Experiences (NDE) reported by resuscitated patients. Her studies expanded into those who were officially ‘brain dead” as in EEG monitored while still clinically alive. She stumbled upon the Patient One records and found an anomaly never before seen in medical experience.

Here’s Dr. Borjigin’s account:

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In the moments after Patient One was taken off oxygen, there was a surge of activity in her dying brain. Areas that had been nearly silent while she was on life support suddenly thrummed with high-frequency electrical signals called gamma waves. In particular, the parts of the brain that scientists consider a “hot zone” for consciousness became dramatically alive. In one section, the signals remained detectable for more than six minutes. In another, they were 11 to 12 times higher than they had been before Patient One’s ventilator was removed.

As she clinically died, Patient One’s brain was functioning in a kind of hyperdrive. For about two minutes after her oxygen was cut off, there was an intense synchronization of her brain waves, a state associated with many cognitive functions, including heightened attention and memory. The synchronization dampened for about 18 seconds, then intensified again for more than four minutes. It faded for a minute, then came back for a third time.

In those same periods of dying, different parts of Patient One’s brain were suddenly in close communication with each other. The most intense connections started immediately after her oxygen stopped and lasted for nearly four minutes. There was another burst of connectivity more than five minutes and 20 seconds after she was taken off life support.

In particular, areas of her brain associated with processing conscious experience—areas that are active when we move through the waking world, and when we have vivid dreams—were communicating with those involved in memory formation. So were parts of the brain associated with empathy. Even as she slipped irrevocably deeper into death, something that looked astonishingly like life was taking place over many minutes in Patient One’s brain.

Those glimmers and flashes of something like life contradict the expectations of almost everyone working in the field of resuscitation science and near-death studies. The predominant belief—expressed by Greyson, the psychiatrist and co-founder of the International Association of Near Death Studies, in the Netflix series Surviving Death—was that as soon as oxygen stops going to the brain, neurological activity falls precipitously. Although a few earlier instances of slight and fading brain waves had been reported in dying human brains, nothing as detailed and complex as what occurred in Patient One had ever been detected.

Given the levels of activity and connectivity in particular regions of her dying brain, I believe it’s likely that Patient One had a profound near-death experience with many of its major features: out-of-body sensations, visions of light, feelings of joy or serenity, and moral re-evaluations of one’s life. Of course, Patient One did not recover, so no one can prove that the extraordinary happenings in her dying brain had experiential counterparts.

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Near Death Experiences. NDEs. Are these events of total imagination? Or are they completely real?

We’ve all heard the stories—the familiar kitsches of NDEs. Being elevated from the operating table. Floating toward an immense light. Traveling down a tunnel. Complete bliss and harmony. Being beckoned by an infinite intelligence. Meeting dead relatives. And not wanting to return to normal life.

While these NDE experiences can be simulated by taking a hero’s worth of ketamine, almost all reports come from rational and sober people who clearly felt they went through something extraordinary. Some say paranormal. Others say supernatural.

This brings us to that mysterious and mostly unknown subject of consciousness. Almost nothing is solidly understood about what consciousness really is. Partly, that’s because no one has found a way to isolate and measure consciousness—it’s very difficult (almost impossible) to fund studies that can’t be isolated and measured.

Dr. David Chalmers is a world-leading consciousness researcher. (I wrote a blog post on Chalmers and his consciousness theories a few years ago. You can read it here.) Dr. Chalmers posits that consciousness may be a fundamental property of the human brain and that consciousness may be a universal entity of the cosmos that sends signals to us. Chalmers breaks consciousness into two arenas—the easy problem of recognizing that it exists and the hard problem of explaining how it operates. Or what it is.

All of us experience at least two consciousness forms. One is our awake state, which you’re in at the present. The other is our asleep state, also known as the subconscious. As long as we’re “alive”, both states exist and are vital to our function and survival.

So, what gives with someone like Patient One? Why was she clinically dead—according to the standard description—after she flatlined in the ICU—yet came fully alive in her once-thought-dead brain? The answer seems to be that death, clinical and brain, is not a precise time point. Rather, both are processes that can take extensive linear time to complete.

There are countless stories of people being resuscitated minutes and even hours after their hearts stopped beating and their lungs stopped breathing. Many events occurred in hypothermic conditions; temperature being a huge life-preservation factor. But bringing someone back from brain death? It’s never been recorded before Dr. Borjigin stumbled upon Patient One’s charts.

This seems to be because no one has looked at this angle before. Once a patient flatlines in a medical environment and there’s no resuscitation made, there’s no reason to review the EEG charts—if there even are recordings. It’s just shut things down, shroud them, send them downstairs, and move on to the next.

Makes me wonder how many people are written off for dead when they’re still very much alive.

Maybe it’s time for a new science of death.