Author: rgbrill

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Warning: This post contains discussion of murder and sexual abuse.

Vince Gilmer was a kind, well-liked doctor in his small town of Cane Creek, North Carolina – that is, until July 2004, when he was arrested for the vicious murder of his father. How could this beloved man turn into a violent criminal?

In court, Vince defended his actions by explaining that he had been a victim of his father’s sexual abuse since childhood and that his father had assaulted him on the day of the murder. Despite these claims, Vince was found guilty of the murder.

Five years later, another Dr. Gilmer arrived in Cane Creek. Benjamin Gilmer was not related to Vince, but because of the similarities between the two men (surname, profession, age), the case grabbed Benjamin’s interest. Sarah Koenig, a reporter with the program This American Life, got in contact with Benjamin and they decided to investigate Vince’s story together.

People described Vince’s behavior in the months leading up to the murder as unstable. He had gotten into a serious car accident (possibly intentionally) in which he hit his head; had started drinking heavily following his divorce; and had stopped taking his prescribed antidepressant (Lexapro, an SSRI). When Benjamin and Koenig visited Vince in prison, he told them that he had heard voices on the day he committed the murder. Vince theorized that he might have been suffering from SSRI withdrawal.

Benjamin thought SSRI withdrawal was a plausible diagnosis, and he also wondered if perhaps Vince had gotten a traumatic brain injury from his car accident. To get a psychiatrist’s perspective, Benjamin invited a friend of his to meet Vince. Noticing Vince’s odd gait and wide gesticulations, the psychiatrist had a different suggestion: Vince might have Huntington’s disease. 

Huntington’s is a neurodegenerative disease that can cause motor impairment as well as cognitive/emotional issues like confusion, anxiety, and impulsivity (Novak & Tabrizi, 2010). Koenig describes it as “a cruel trifecta of Alzheimer’s, Parkinson’s, and Lou Gehrig’s disease, rolled into one.” The average age of onset is 40 years, and life expectancy after diagnosis is only 10-25 years. Huntington’s is a genetic disease – offspring of affected parents have a 50% chance of getting it too (Novak & Tabrizi, 2010). It’s possible Vince’s father had it, as he had exhibited some symptoms but was never diagnosed. There is no cure for Huntington’s and no way to halt the progression of the disease, although some drugs such as Tetrabenazine have been shown to reduce symptoms of chorea (the sudden jerking movements characteristic of the disease) (Novak & Tabrizi, 2010). 

Symptoms of Huntington’s include hallucinations, irritability, moodiness, paranoia, hyperkinesia, confusion, memory loss, and anxiety. Vince basically checked every box. To diagnose Huntington’s, a DNA test is required to detect CAG trinucleotide expansion in the HTT gene (DynaMed). A normal HTT gene will have fewer than 36 CAG repeats, while a gene with 40+ repeats is strongly indicative of Huntington’s. Imaging can also be useful for diagnosis, as Huntington’s is characterized by cerebral atrophy (Novak & Tabrizi, 2010). Vince’s DNA test confirmed that he had Huntington’s. 

But does Huntington’s create murderers? People with Huntington’s are actually much more likely to be the victims of violence than to commit violence (Finan, 2022). But perhaps the combination of Huntington’s, antidepressant withdrawal, stress, and years of abuse could cause somebody to “snap”. That’s what Dr. Mary Edmonson suggests happened in Vince’s case (Finan, 2022). What do you think?

After many years, Benjamin succeeded in his mission to get Vince’s conviction overturned. In January 2022, the Virginia governor granted Vince a pardon. Vince is now in late-stage Huntington’s and has become more physically disabled; he has extreme difficulty with talking and swallowing, and though he can still walk, he falls often. As of March of this year, Benjamin was in the process of becoming Vince’s legal guardian and was making plans for Vince to go to a medical care facility where he will receive appropriate treatment. 

Do you know of another interesting true crime case with medical connections? Email Rachel Brill at rgbrill@gwu.edu.

References and Further Reading:

DynaMed. Huntington Disease. EBSCO Information Services. Accessed August 11, 2022.  https://proxygw.wrlc.org/login?url=https://www.dynamed.com/condition/huntington-disease 

Finan E. After a Beloved Small-Town Doctor Murdered His Own Father, the Clinic's New Doc Solved the Mystery of Why. People. March 3, 2022. https://people.com/crime/after-a-beloved-small-town-doctor-murdered-his-own-father-the-clinics-new-doc-solved-the-mystery-of-why/

Gilmer, Benjamin. The Other Dr. Gilmer. Ballantine Books; 2022.

Koenig, S. Dr. Gilmer and Mr. Hyde. This American Life. April 12, 2013. https://www.thisamericanlife.org/492/dr-gilmer-and-mr-hyde  

Novak MJ, Tabrizi SJ. Huntington's disease. BMJ. 2010 Jun 30;340:c3109. doi: 10.1136/bmj.c3109. PMID: 20591965. https://proxygw.wrlc.org/login?url=https://www.bmj.com/content/340/bmj.c3109.long 

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Warning: This post contains discussion of murder.

June 2013: Odin Lloyd is found dead, and professional football player Aaron Hernandez is charged with first-degree murder. But could brain damage have influenced Hernandez’s actions?

Hernandez, who was a tight end for the New England Patriots, already had a long history of violent and criminal behavior. In 2015, he was found guilty of Lloyd’s murder and received a life sentence.

Two years later, while in the process of filing an appeal for the murder conviction, Hernandez, 27 years old, committed suicide. Hernandez was posthumously diagnosed with chronic traumatic encephalopathy (CTE) at the Boston University CTE Center, which has studied the brains of over 300 deceased football players (Pfeiffer, 2018). This diagnosis led to speculation that Hernandez’s deadly behavior might have been influenced or caused by intense traumatic injury to his brain.

CTE is a neurodegenerative disorder that develops because of repeated trauma to the head. Over time, repetitive head impacts, including both concussive and subconcussive blows, lead to CTE, but the exact amount of trauma required is unknown. CTE is a progressive disease that occurs in a number of stages (either three or four depending on how you divide it up) linked to changes in neuropathology (McKee et al., 2013). The first stage can include confusion, dizziness, and headache. The second stage can include memory loss and impulsivity. The third and fourth stages can include dementia, speech impediments, sensory processing disorders, tremors, depression, and suicidal behavior.

The majority of documented CTE cases have occurred in athletes in contact sports like football, wrestling, and boxing. CTE is common among this population: for example, a recent cohort study found that in a sample of 202 deceased football players, 87% were diagnosed postmortem with CTE – including 110 of the 111 NFL players in the sample (Mez et al, 2017).

CTE is a tauopathy, like Alzheimer’s, described as “a progressive neurodegeneration characterized by the widespread deposition of hyperphosphorylated tau (p-tau) as neurofibrillary tangles” (McKee et al., 2013). As of now, there is no test that can definitively determine the existence of CTE in a living person. The diagnosis can only occur during an autopsy because it requires the removal of the brain in order to analyze the tissue (Pfeiffer, 2018). Although CTE can only be diagnosed posthumously, it should be considered likely in patients with Traumatic Encephalopathy Syndrome (TES) and one or more CTE biomarkers (DynaMed). There is no known cure for CTE, but some symptoms can be managed with medications and behavioral therapies.

At his autopsy, Hernandez was determined to have stage-3 CTE, never before seen in a person as young as him (Pfeiffer, 2018). Did CTE cause Hernandez to kill Lloyd? And if so, is that a viable defense against a murder charge? What do you think?

Do you know of another interesting true crime case with medical connections? Email Rachel Brill at rgbrill@gwu.edu.

References and Further Resources

Bryant C & Clark J. What’s the Deal with Chronic Traumatic Encephalopathy? [Podcast episode]. Stuff You Should Know. November 2016.

Dillard, J. Amy and Tucker, Lisa A. “Is C.T.E. a Defense for Murder?” September 2017. The New York Times.

DynaMed. Concussion and Mild Traumatic Brain Injury. EBSCO Information Services. Accessed July 12, 2022. https://proxygw.wrlc.org/login?url=https://www.dynamed.com/condition/concussion-and-mild-traumatic-brain-injury

McKee AC, Abdolmohammadi B, Stein TD. The neuropathology of chronic traumatic encephalopathy. Handb Clin Neurol. 2018;158:297-307. doi: 10.1016/B978-0-444-63954-7.00028-8. https://pubmed-ncbi-nlm-nih-gov.proxygw.wrlc.org/30482357/

McKee AC, Stern RA, Nowinski CJ, Stein TD, Alvarez VE, Daneshvar DH, Lee HS, Wojtowicz SM, Hall G, Baugh CM, Riley DO, Kubilus CA, Cormier KA, Jacobs MA, Martin BR, Abraham CR, Ikezu T, Reichard RR, Wolozin BL, Budson AE, Goldstein LE, Kowall NW, Cantu RC. The spectrum of disease in chronic traumatic encephalopathy. Brain. 2013 Jan;136(Pt 1):43-64. doi: 10.1093/brain/aws307. Epub 2012 Dec 2. Erratum in: Brain. 2013 Oct;136(Pt 10):e255. https://www-ncbi-nlm-nih-gov.proxygw.wrlc.org/pmc/articles/PMC3624697/

Mez J, Daneshvar DH, Kiernan PT, Abdolmohammadi B, Alvarez VE, Huber BR, Alosco ML, Solomon TM, Nowinski CJ, McHale L, Cormier KA, Kubilus CA, Martin BM, Murphy L, Baugh CM, Montenigro PH, Chaisson CE, Tripodis Y, Kowall NW, Weuve J, McClean MD, Cantu RC, Goldstein LE, Katz DI, Stern RA, Stein TD, McKee AC. Clinicopathological Evaluation of Chronic Traumatic Encephalopathy in Players of American Football. JAMA. 2017 Jul 25;318(4):360-370. doi: 10.1001/jama.2017.8334. https://jamanetwork-com.proxygw.wrlc.org/journals/jama/fullarticle/2645104

Pfeiffer, Sacha. “A Terrible Thing to Waste.” October 2018. The Boston Globe.

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WARNING: This post contains discussion of murder.

On the night of February 2, 1933, in Le Mans, France, René Lancelin headed home from a dinner party. René was upset because his wife Léonie and daughter Genevieve were supposed to have joined him at the party, but they had never shown up. He grew suspicious when he found the front door of his house bolted shut, which was unusual, and he went to the police. When the police broke into the house, they discovered the bodies of Léonie and Genevieve. Both women had been horrendously bludgeoned and stabbed to death.

The police then went to the bedroom of the Lancelin family’s maids, sisters Christine and Léa Papin, fearing that the two of them had also been murdered. But inside their room, the sisters were alive, and they were sitting together on their bed, naked and bloody. The sisters immediately confessed to the murders.

27-year-old Christine and 21-year-old Léa were placed in prison, in separate cells. Christine, in particular, grew extremely distressed due to this separation. At trial, their lawyer pleaded on their behalf not guilty by reason of insanity. Although the consulted doctors initially determined that the girls showed no signs of insanity, they reconsidered when it was revealed that the Papin family had a history of mental illness.

The doctors in this case then concluded that the Papin sisters suffered from folie à deux, which in French means “madness between two people.” The condition is also known as shared paranoid disorder, shared or induced delusional disorder, or shared psychosis. This is a psychological syndrome in which delusions and sometimes hallucinations are transmitted from one person (the ‘inducer,’ who already has a psychotic disorder) to another. (In less common cases with more than two people involved, the condition can be called folie à trois, folie à quatre, and so on.) While the exact etiology of the disorder is unknown, two main factors are believed to be stress and social isolation, and the majority of cases involve women.

In order to be diagnosed with folie à deux, the following criteria must be met (Sadock & Sadock, 2007, table 14.3-5):

The individual(s) must develop a delusion or delusional system originally held by someone else with a disorder classified in schizophrenia, schizotypal disorder, persistent delusional disorder, or acute and transient psychotic disorders.
The people concerned must have an unusually close relationship with one another, and be relatively isolated from other people.
The individual(s) must not have held the belief in question before contact with the other person, and must not have suffered from any other disorder classified in schizophrenia, schizotypal disorder, persistent delusional disorder, or acute and transient psychotic disorders in the past.

Under certain classification systems, only the secondary case (i.e. the ‘induced’ person) can receive a diagnosis of folie à deux (Menculini et al., 2020).

It was believed that the Papin sisters had suffered from shared paranoid disorder, which caused them to commit the heinous crime. Despite this diagnosis, the Papin sisters were convicted of the murders of Léonie and Genevieve. Léa, who was believed to have been heavily influenced by her sister, received a ten-year sentence, while Christine, the ‘inducer,’ received a life sentence. Separated from Léa, Christine grew depressed and died in 1937, having starved herself to death. What happened to Léa is less sure: after leaving prison she assumed a new identity, and she either died in 1982 or 2001. Due to its bizarre and grisly nature, this murder case has inspired a number of books, movies, and plays. Bong Joon-ho even cited it as an inspiration for his recent Oscar-winning film “Parasite” (Jung, 2020).

Do you want to learn more about this poorly understood condition? The MeSH term (medical subject heading) is “Shared Paranoid Disorder”. In the DSM-5, the condition is not listed as a separate disorder but is instead classified under “Other Specified Schizophrenia Spectrum and Other Psychotic Disorder” and is described as “delusional symptoms in [the] partner of [an] individual with delusional disorder.” In the International Classification of Diseases (ICD), the condition is referred to as “shared psychotic disorder” and has code F24.

Do you know of another interesting true crime case with medical connections? Email Rachel Brill at rgbrill@gwu.edu.

Works Cited

Diagnostic and statistical manual of mental disorders. 5th ed. American Psychiatric Association; 2013. https://doi.org/10.1176/appi.books.9780890425596

Jung, E. A. Bong Joon Ho on Why He Wanted Parasite to End With a ‘Surefire Kill’. Vulture. January 14, 2020. https://www.vulture.com/article/parasite-ending-explained-by-bong-joon-ho.html

Menculini G, Balducci PM, Moretti P, Tortorella A. “‘Come share my world’ of ‘madness’: a systematic review of clinical, diagnostic and therapeutic aspects of folie à deux.” International Review of Psychiatry. 2020;32(5-6):412-423. doi: 10.1080/09540261.2020.1756754. https://proxygw.wrlc.org/login?url=https://www.tandfonline.com/doi/full/10.1080/09540261.2020.1756754

Sadock BJ, Sadock VA. Kaplan and Sadock’s Synopsis of Psychiatry: Behavioral Sciences, Clinical Psychiatry. 10th ed. Lippincott Williams & Wilkins; 2007.

Shared Psychotic Disorder. ICD 10 Data. Accessed June 30, 2022. https://www.icd10data.com/ICD10CM/Codes/F01-F99/F20-F29/F24-

This is the first post in Himmelfarb’s new series “Disorder in the Court,” which will examine true crime stories with medical connections. Know of a great story to feature? Email Rachel Brill at rgbrill@gwu.edu.

Warning: This post contains discussion of a child’s death.

In July 1989, Patricia Stallings took her 3-month-old son Ryan to a children’s hospital. He was presenting with lethargy, emesis, and tachypnea (rapid breathing). A gas chromatography test revealed an elevated level of ethylene glycol in Ryan’s blood (Shoemaker et al., 1992). This is a compound found in antifreeze. Authorities believed that Stallings had intentionally poisoned her son with antifreeze.

After medical treatment, Ryan was placed in protective custody. The next month, Stallings was granted a short visit with her son. Only a few days after that visit, Ryan’s medical issues resurfaced. He received treatment for ethylene glycol poisoning, but sadly, he died.

Stallings was charged with first-degree murder. In 1991, she was convicted of Ryan’s murder and sentenced to life in prison. But only a few months later, Stallings was acquitted. Medical evidence proved that she had not killed her son.

While awaiting trial, Stallings had given birth to another son, D.J. He was placed in foster care. At only one month old, D.J. began displaying symptoms similar to the ones Ryan had. Doctors diagnosed D.J. with a genetic disorder called methylmalonic acidemia (MMA), a type of organic acidemia (DynaMed). This disorder disrupts normal amino acid metabolism, resulting in the inability to digest certain fats and proteins. This causes an often-fatal buildup of methylmalonic acid in the blood. MMA is rare, occurring in about 1 of 50,000 births (Baumgartner et al., 2014). One fact critical to this story is that methylmalonic acidemia causes the production of propionic acid, which is almost indistinguishable from ethylene glycol.

D.J. was treated for MMA and recovered. At first, Stallings and her lawyer were unable to prove that Ryan also had had MMA. Without strong evidence, the judge dismissed the theory. But after Stallings’ conviction, her case was featured on Unsolved Mysteries. Dr. William Sly and Dr. James Shoemaker of St. Louis University saw the episode and offered to test a blood sample from Ryan. Shoemaker knew that in order to identify propionic acid correctly, a gas chromatography - mass spectrometry test is required, rather than gas chromatography alone (Shoemaker et al., 1992). This test determined that Ryan had in fact died from MMA.

Stallings was released from prison in July 1991 pending a new trial, and the case against her was dropped entirely in September 1991. She later reached an out-of-court settlement with the hospitals and laboratories involved in the case.

References

Baumgartner MR, Hörster F, Dionisi-Vici C, Haliloglu G, Karall D, Chapman KA, Huemer M, Hochuli M, Assoun M, Ballhausen D, Burlina A, Fowler B, Grünert SC, Grünewald S, Honzik T, Merinero B, Pérez-Cerdá C, Scholl-Bürgi S, Skovby F, Wijburg F, MacDonald A, Martinelli D, Sass JO, Valayannopoulos V, Chakrapani A. Proposed guidelines for the diagnosis and management of methylmalonic and propionic acidemia. Orphanet Journal of Rare Diseases. 2014;9:130. doi: 10.1186/s13023-014-0130-8. https://wrlc-gwahlth.primo.exlibrisgroup.com/permalink/01WRLC_GWAHLTH/gr7gmc/cdi_gale_incontextgauss_ISR_A540650471

DynaMed. Organic Acidemias. EBSCO Information Services. Accessed April 27, 2022. https://www.dynamed.com/condition/organic-acidemias-23

Shoemaker JD, Lynch RE, Hoffmann JW, Sly WS. Misidentification of propionic acid as ethylene glycol in a patient with methylmalonic acidemia. The Journal of Pediatrics. 1992;120(3):417-21. doi: 10.1016/s0022-3476(05)80909-6. https://wrlc-gwahlth.primo.exlibrisgroup.com/permalink/01WRLC_GWAHLTH/gr7gmc/cdi_webofscience_primary_A1992HG94000013CitationCount