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IS AMANDA KNOX REALLY INNOCENT OF MURDERING MEREDITH KERCHER?

The Amanda Knox story captured worldwide attention during the years she passed through the Italian legal system and was convicted—twice—of complicity in murdering her college roommate, Meredith Kercher. Ultimately, Knox was exonerated of the murder charges but convicted of criminal slander based on coerced statements she made while under initial and unlawful police interrogation. Now, the international spotlight is again upon Knox with a retrial underway after her slander charge was overthrown by Italy’s highest court. All this circles back to many still questioning if Amanda Knox really is innocent of murdering Meredith Kercher.

There’s a lot of internet information on the Amanda Knox murder case. Some of it’s factual. Much is sensational tabloid junk about “Foxy Knoxy”—the “Ice Lady”—disseminated by socially dysfunctional trolls operating from surplus metal sea-cans converted into dwellings via an extension cord hooked to one bare light bulb. To find out the truth, it’s necessary to first look at the overall facts and then examine how the Italian legal system handled the case through a dragged-out, eight-year-long process.

Meredith Kercher

In 2007, Amanda Knox was a 20-year-old student from Seattle, Washington. She moved to Perugia in central Italy (slightly north of Rome) to further her journalism studies as Perugia was well-known for outstanding universities and educational opportunities—a popular place for foreign students. Here, Knox met a British exchange student, 21-year-old Meredith Kercher, and they shared a ground-floor, four-bedroom apartment with two other young ladies.

Quickly, Knox became romantically involved with a young Italian man, Raffaele Sollecito, and Kercher did the same with Giacomo Silenzi. At the time, Knox also worked part-time in a nightclub run by Patrick Lumumba. It was this pentagon of five that the Italian prosecutors would present as a sex game gone wrong that resulted in Meredith Kercher’s death.

On the evening of November 1, 2007, Knox, Sollecito, Silenzi, and Kercher socialized with others at Sollecito’s apartment near to where the ladies roomed. Present was a man named Rudy Guede who was invited by one of the group members but who was unknown to Knox and Kercher. Around 9 pm, Kercher excused herself from the gathering and walked back to her residence alone. Bit by bit, the gathering broke up leaving Knox and Sollecito to overnight there together.

At midday on November 2, Knox repeatedly tried to phone Meredith Kercher. She got no answer and became concerned, so Knox and Sollecito went to the co-habitation and found Kercher’s bedroom door locked. Knox tapped on the door and called out, but Kercher didn’t answer. Then Knox and Sollecito noticed some bloodstains, including a bloody footprint, in the bathroom.

Being alarmed, Knox called her mother in America who directed Knox to call the Italian police. She did so. However, there was a significant delay which was advanced as part of the prosecution’s later case against Knox and was supported by a timeline presented through cell phone records.

The first attending police officers were not homicide detectives. They were an Italian version of postal inspectors crossed with communication fraud investigators. There hadn’t been a murder in Perugia in over twenty years, so it was a considerable time before “competent” scene processors and trained murder cops arrived. Naturally, the scene was contaminated, and the ensuing DNA evidence used in convicting Amanda Knox of murdering Meredith Kercher was compromised.

What the scene processing showed was Kercher had been attacked, raped, and had her throat cut in her bedroom. Her official cause of death was exsanguination (bleeding out) after being injured with a sharp-edged weapon. Kercher’s bedroom window was open, and the investigators deduced that to mean that a break-in had been staged with the real killer setting the crime up to appear that a stranger was involved.

Police initially treated Amanda Knox as a witness. She was questioned on different occasions, but the homicide investigators slowly formulated a theory that Knox was lying to protect the actual murderer. They also developed a motive theory that Kercher was killed because she refused to take part in a multi-person sexual trist. An orgy.

On November 6, the Italian homicide detectives again brought Knox in for questioning. This time it turned into a full-on, hard-core interrogation that lasted hours. This is a complex and controversial part of the Amanda Knox story and precise details—at least as precise as possible because the authorities did not audio or video record it (rather they elicited a written confession from Knox)—can be read on the website amandaknoxcase.com under The Interrogation of Amanda Knox.

In Amanda Knox’s written confession, she states to have been present while her nightclub boss, Patrick Lumbumba, raped and murdered Meredith Kercher. Knox did not supply any motive or any details which only an involved person would know. Lumbuba was arrested on the strength of Knox’s statement and it was shortly proven, beyond all doubt, that Lumbumba had an air-tight alibi and he was flat-out innocent. (This “accusation’ against Lumbumba is what led to her criminal slander conviction which is once again, in 2024, before the Italian courts. A verdict in set for June 5th.)

Rudy Guede

Amanda Knox was held in custody while the prosecution put an indictable case together. Meanwhile, the scene forensic evidence identified a DNA profile from semen on Kercher’s body. They conclusively linked it to Rudy Guede who had been at the social gathering on the evening when Kercher was last seen alive. Guede was arrested in Germany where he confessed and indicated that Amanda Knox had nothing to do with Kercher’s murder.

By now, the Italian legal system had a freight train rolling along the justice track. Instead of applying the brakes, the police, prosecutors, and judges threw more coal on the fire and kept on persecuting Amanda Knox. This was due to the archaic inquisitional system Italy was trying to gentrify into a western adversarial legal framework.

The common US-style evidence rules didn’t apply in the Italian arena. Despite Amanda Knox being hardline interrogated for hours without legal representation, being informed of her rights, denied food, water, and toilet facilities, slapped around, and breaking down in the middle of the night, the Italian court accepted Knox’s coerced confession as solid evidence that had to be admitted under their law structure. It didn’t matter that the prosecution’s perceived motive—some kinky sex game—had no factual basis, and it didn’t matter that Knox’s boyfriend, Raffaele Sollecito, provided Knox with her air-tight alibi. No, the Italian legal machine went right on persecuting Amanda Knox.

Knox stood trial through the summer and fall of 2009. Her case received massive public attention and the British tabloids sensationalized it like nothing ever seen. This was now the day of the emerging internet where chatrooms and social media made a spectacle of the trial and a massive mess of Amanda Knox’s life.

Amanda Knox was convicted of Meredith Kercher’s murder on December 4, 2009. She was sentenced to 26 years in jail. She appealed and had her murder conviction overturned on October 3, 2011, now having served nearly two years in an Italian prison.

In March of 2013, Italy’s Court of Cassation ordered a new trial and on January 30, 2014, she was once again convicted for killing Meredith Kercher. By now, Amanda Knox was back in America and was not returned to Italy during her new appeal. On March 27, 2015, Italy’s highest court again overturned her conviction, and her legal persecution was over.

Any rational person asks, “How could this miscarriage of justice possibly happen?” The answer is as complicated as the Amanda Knox story, if that’s possible to fully tell. It’s a murky mix of systematic incompetence and utter lack of regard for the truth. In the high court’s final ruling, the judge cited “sensational failures”, “glaring errors”, “investigative amnesia”, “guilty and culpable omissions”, “ignorance of expert forensic testimony that demonstrated contamination of evidence”, “outright falsification of forensic evidence”, and “a case without any foundation”.

The horrific Amanda Knox wrongful conviction story is best told by Amanda, herself. In a past interview with The Atlantic titled Who Owns Amanda Knox? , Amanda says:

Does my name belong to me? Does my face? What about my life? My story? Why is my name used to refer to events I had no hand in? I return to these questions again and again because others continue to profit off my identity, and my trauma, without my consent. Most recently, there is the film Stillwater, directed by Tom McCarthy and starring Matt Damon and Abigail Breslin, which was, in McCarthy’s words, “directly inspired by the Amanda Knox saga.” How did we get here?

In the fall of 2007, a British student named Meredith Kercher was studying abroad in Perugia, Italy. She moved into a little cottage with three roommates—two Italian law interns, and an American girl. Less than two months into her stay, a young man named Rudy Guede, an immigrant from the Ivory Coast, broke into the apartment and found Meredith alone. Guede had a history of breaking and entering. A week prior, he had been arrested in Milan while burglarizing a nursery school, and was found carrying a 16-inch knife. He was released.

A week later, he raped Meredith and stabbed her in the throat, killing her. In the process, he left his DNA in Meredith’s body and throughout the crime scene. He left his fingerprints and footprints in her blood. He fled to Germany immediately afterward, and later admitted to being at the scene.

I am the American girl in that story, and if the Italian authorities had been more competent, I would have been nothing more than a footnote in a tragic story. But as in many wrongful convictions, the authorities formed a theory before the forensic evidence came in, and when that evidence indicated a sole perpetrator, Guede, ego and reputation led them to contort their theory to maintain that I was still somehow involved. Guede was quietly convicted for participating in the murder in a separate fast-track trial, and then I became the main event for eight long years.

While I was on trial for the murder of Meredith Kercher, from 2007 to 2015, the prosecution and the media crafted a story, and a doppelgänger version of me, onto which people could affix all their uncertainties, fears, and moral judgments. People liked that story: the psychotic man-eater, the dirty ice queen, Foxy Knoxy. A jury convicted my doppelgänger and sentenced her to 26 years in prison.

But the guards couldn’t handcuff that invented person. They couldn’t escort that fiction into a cell. That was me, the real me, who returned to that windowless prison van, to those high cement walls topped with barbed wire, to those cold, echoing hallways and barred windows, to that all-consuming loneliness.

Ten years ago, at the age of 24, I was acquitted, and I tumbled into a kind of purgatory. I left one cell and immediately entered another: the quiet of my childhood bedroom. Outside, the telephoto lenses were fixed on my closed blinds. Prison had given me an appreciation for all the freedoms I’d taken for granted. Freedom showed me how many I still lacked.

As I walked back into the free world, I knew that my doppelgänger was there alongside me. I knew that everyone I would ever meet from then on would have already met, and judged, her. I had been acquitted in a court of law, but sentenced to life by the court of public opinion as, if not a killer, then at least a slut, or a nutcase, or a tabloid celebrity. Why doesn’t she just go away already? Her 15 minutes are over.

In freedom, I had become a pariah. Looking for work, going back to school, buying tampons at the pharmacy, everywhere I went I met people who already thought they knew who I was, what I’d done or not done, and what I deserved. I was threatened with abduction and torture in broad daylight; I was threatened with having Meredith’s name carved into my body. Strangers sent me lingerie and bizarre love letters.

All over the world, people believed they knew me, a warped assumption that turned me into a monster to some and a saint to others. I felt like I was always standing behind that cardboard cutout, Foxy Knoxy, saying, Hey, back here, the real me! Even most of the strangers who offered kindness and support didn’t truly see me. They loved her.

It’s hard to make friends, to date, to be a regular person when everyone you meet has a preconceived notion of who you really are, whether positive or negative. I could have chosen to hide out, to change my name, to dye my hair, and hope no one recognized me ever again. Instead, I decided to embrace the world that had dehumanized me, and all those who turned me into a product.

From the moment I was arrested, my name and face and trauma became a source of profit for news organizations, filmmakers, and other artists, scrupulous and unscrupulous. The most intimate details of my life, from my sexual history to my thoughts of death and suicide in prison, were taken from my private diary and leaked to journalists. Those journalists turned my darkest fears into fodder for hundreds of articles, thousands of blog posts, and millions of hot takes.

People speculated about my mental state and sexuality, they diagnosed me from afar, they used my predicament as a metaphor, they made TV movies about me, based characters in legal shows on me, and the worst of them took every opportunity they could, while I was in prison and while I’ve been out, to shame me for something I didn’t do, to shame me for living while Meredith is dead, to shame me for being in the very headlines they write, for being in the photographs they take without my consent.

The hypocrisy and the cruelty are maddening. And yet, being under that microscope has given me insight into how wrong a media narrative can be, how easy it is for all of us to consume other people’s lives as if they were mere content to fill up our Twitter feeds.

This focus on me led many to complain that Meredith Kercher had been forgotten. But whom did they blame for that? Not the Italian authorities. Not the press. Somehow it was my fault that the police and media focused on me at Meredith’s expense. The result of this is that 14 years later, my name is the name associated with this tragic series of events I had no control over.

Meredith’s name is often left out, as is Rudy Guede’s. When he was released from prison in late 2020, the New York Post headline read: “Man Who Killed Amanda Knox’s Roommate Freed on Community Service.” My name is the only name that shouldn’t be in that headline.

I never asked to become a public person. The Italian authorities and global media made that choice for me. And when I was acquitted and freed, the media and the public wouldn’t allow me to become a private citizen again.

I have not been allowed to return to the relative anonymity I had before Perugia. I have no choice but to accept the fact that I live in a world where my life, and my reputation, are freely available for distortion by a voracious content mill.

———

There is no doubt—no doubt whatsoever—that Amanda Knox really is innocent of murdering Meredith Kercher. She’s a true victim. A victim of a horrific crime. A victim of an abominable justice system. A victim of disgusting tabloids. And a victim of soulless trolls.

Footnote: Today, Amanda Knox is 36 years old and a mother of two. She hosts a successful podcast titled Labyrinths: Getting Lost with Amanda Knox with the themes of injustice and wrongful conviction. Amanda is a professional journalist, author, and activist. She recently signed with Hulu for a 12-part series based on her life story. One of the film’s co-producers is Monica Lewinsky.

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.

—   —   —

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.