TEXAS SHOOTER Charles Whitman: The Amygdala & Mass Murder

Charles Whitman:The Amygdala & Mass Murder


Rhawn Gabriel Joseph, Ph.D.

FEAR, RAGE & AGGRESSION

Initially, electrical stimulation of the amygdala produces sustained attention and orienting reactions. If the stimulation continues the subject may begin to experience, wariness, fear and/or rage (Cendes et al. 1994; Davis et al., 1997; Gloor 1992; Halgren 1992; LeDoux, 1996; Rosen & Schulkin, 1998; Ursin & Kaada, 1960). When fear follows the attention response, the pupils dilate and the subject will cringe, withdraw, and cower. This cowering reaction in turn may give way to extreme fear and/or panic such that the animal will attempt to take flight.

Among humans, the fear response is one of the most common manifestations of amygdaloid electrical stimulation and abnormal activation (Davis et al., 1997; Gloor, 1992, Halgren, 1992; LeDoux, 1996; Rosen & Schulkin, 1998). Moreover, unlike hypothalamic on/off emotional reactions, attention and fear reactions can last up to several minutes after the stimulation is withdrawn.

In addition to behavioral manifestations of heightened emotionality, amygdaloid stimulation can result in intense changes in emotional facial expression. This includes crying and facial contortions such as baring of the teeth, dilation of the pupils, widening or narrowing of the eye-lids, flaring of the nostrils, as well as sniffing, licking, and chewing (Anand & Dua, 1955; Ursin & Kaada, 1960). Indeed, some of the behavioral manifestations of a seizure in this vicinity (i.e. temporal lobe epilepsy) typically include throat and mouth movements, including chewing, smacking of the lips, licking, and swallowing–a consequence, perhaps of amygdala activation of the brainstem periaqueductal gray and nuclei subserving mastication.

 

In many instances patients or animals will react defensively and with anger, irritation, and rage which seems to gradually build up until finally the animal or human will attack (Egger & Flynn, 1963; Gunne & Lewander, 1966; Mark et al., 1972 Ursin & Kaada, 1960; Zbrozyna, 1963). Unlike hypothalamic “sham rage”, amygdaloid activation results in attacks directed at something real, or, in the absence of an actual stimulus, at something imaginary. There have been reported instances of patient’s suddenly lashing out and even attempting to attack those close by, while in the midst of a temporal lobe seizure (Saint-Hilaire et al., 1980), and/or attacking, kicking, and destroying furniture and other objects (Ashford et al., 1980).

Moreover, rage and attack will persist well beyond the termination of the electrical stimulation of the amygdala. In fact, the amygdala remains electrophysiologically active for long time periods even after a stimulus has been removed (be it external-perceptual, or internal-electrical) such that is appears to continue to process–in the abstract–information even when that information is no longer observable (O’Keefe & Bouma, 1969).

http://brainmind.com/Case5.html

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TEXAS SHOOTER

The Mind Of A Mass Murderer: Charles Whitman, Brain Damage, And Violence (VIDEO)

By Cara Santa Maria

On August 1, 1966, Charles Whitman murdered his mother and his wife before traveling to the campus of the University of Texas, climbing inside the tower, and killing fourteen others. He was dubbed the infamous UT sniper, but his story involves much more than Marine Corps training and a proclivity for violence. In fact, Whitman complained of headaches and an altered mental state in the days and weeks leading up to the killings. His own suicide note read that “I do not really understand myself these days. I am supposed to be an average reasonable and intelligent young man. However, lately (I cannot recall when it started) I have been a victim of many unusual and irrational thoughts.”

Whitman knew that something was wrong. His note further reads, “After my death I wish that an autopsy would be performed on me to see if there is any visible physical disorder.” And indeed there was. Whitman was found to have a glioblastoma, a type of brain tumor, pressing against regions of the brain thought to be responsible for the regulation of strong emotions.

To learn more about the link between brain damage and violence, I reached out to Dr. Michael Koenigs of the University of Wisconsin-Madison Neuroscience Training Program, a researcher specializing in emotional, social, and personality changes following focal brain lesions. Please see the video above and/or the transcript below. And don’t forget to weigh in by leaving a comment at the bottom of this page.

https://www.huffingtonpost.com/2012/03/27/mind-murderer_n_1384102.html

Psychosis With Pancreatitis A Frequent Occurrence Infrequently Recognized

Abstract

HALLUCINATIONS are rarely reported in association with chronic relapsing pancreatitis, although diabetes, steatorrhea, and pancreatic calcification are commonly recognized complications of this disorder. Clinical observation led us to suspect that hallucinations often accompany pancreatitis, and a survey of the medical records at the Johns Hopkins Hospital of patients with pancreatitis confirmed the frequent association of these two conditions. The present report is based on a prospective medical and psychiatric evaluation of 30 patients with pancreatitis and a similar number of alcoholics with pneumonia. The incidence of hallucinations in each of the two groups is compared in order to evaluate the significance of associated psychosis. In addition, the incidence of hallucinations in patients with pancreatitis is compared with the incidence of diabetes, steatorrhea, and pancreatic calcification as a means of determining the relative importance of psychosis as a complication of pancreatitis.

Materials and Methods  Thirty consecutive patients admitted to the

read more here:

https://jamanetwork.com/journals/jamainternalmedicine/article-abstract/571770

Neuroendocrine Carcinoid Cancer Associated with Psychosis

Neuroendocrine Carcinoid Cancer Associated with Psychosis

Dear Editor

We report a case of an episode of psychosis in a patient with no known psychiatric history who was diagnosed with neuroendocrine carcinoid cancer. The case raises the possibility of a link between carcinoid cancer and psychotic symptoms. The case also discusses the treatment options of psychosis in a patient with carcinoid cancer.

Case report

A 62-year-old man with no known psychiatric history was admitted to an inpatient psychiatric unit for symptoms of paranoia and agitation that appeared one month earlier. He was diagnosed with neuroendocrine carcinoid cancer three months prior to admission after having complaints of persistent nausea. On admission, the cancer also spread to his liver and spine.

He presented for admission to the psychiatric inpatient unit for worsening psychotic symptoms, which included feelings that his family and neighbors were trying to hurt him and that people in the neighborhood were talking about him behind his back. The psychotic symptoms started two weeks before his admission. His symptoms also included anxiety with decreased sleep, psychomotor agitation, and irritability. He denied any hallucinations or perceptual disturbances. There was no prior psychiatric history of psychosis. The patient did not receive any psychiatric medications and was not on any psychotropic medications prior to admission. His admission labs were within normal limits. He was receiving weekly octreotide acetate injections that he had been receiving for two months.

On admission, the patient was started on quetiapine that was titrated to a dose of 100mg per day. The patient improved over the course of a week as he slept better, denied paranoid delusions or ideas of reference, and was less anxious. He was discharged home on quetiapine 100mg at bedtime.

Discussion

The overall incidence of carcinoid cancer in the United States is estimated to be 1 to 2 per 100,000 people a year.1 The tumors are typically diagnosed in the fifth or sixth decade of life, and many patients are asymptomatic at presentation. In the patient with carcinoid tumor, tumor cells manufacture serotonin. Carcinoid syndrome is characterized by flushing, diarrhea, and abdominal cramping and occasionally by wheezing, heart-valve dysfunction, and pellagra. The incidence of the syndrome is higher with metastatic disease.2

Psychiatric symptoms have been reported in patients with metastatic carcinoid disease.3 The reported frequency of depression in carcinoid patients varies widely from 50 percent to less than one percent among all patients in two different studies.4,5 Carcinoid syndrome has been associated with psychosis in two case reports in the literature.6,7

 

read more here:  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2695745/

Recurrent Psychosis Associated with Liver Disease and Elevated Blood Ammonia

Recurrent Psychosis Associated with Liver Disease and Elevated Blood Ammonia

Leston L. Havens, M.D., and Charles G. Child, III, M.D.

N Engl J Med 1955; 252:756-759May 5, 1955DOI: 10.1056/NEJM195505052521804

AN increasing body of evidence suggests that ingestion of dietary protein or some other nitrogenous substances may, under certain conditions, precipitate hepatic coma or impending hepatic coma.1 2 3Adams and Foley4 and Foley et al.5 have detailed the clinical and laboratory signs of impending hepatic coma. These include a “flapping tremor,” electroencephalographic abnormalities and changes in mental status, chiefly “reduction of awareness, followed by a brief period of quiet delirium” progressing to stupor.5 The blood ammonia nitrogen level may be elevated.1 2 3 The changes in mental function reported after protein administration have usually been transient and reversible. In the case reported below . . .

 

read more here: http://www.nejm.org/doi/full/10.1056/NEJM195505052521804

Supersensitivity psychosis in a case with clozapine tolerance.

Eur Rev Med Pharmacol Sci. 2012 Oct;16 Suppl 4:70-3.

Abstract

Despite its serious side effects, clozapine is still the golden standard in treatment of schizophrenia due to its effectiveness and lack of extrapyramidal side effects. Some studies have mentioned withdrawal symptoms, including withdrawal psychosis after stopping clozapine, and have tried to explain this severe symptom through dopamine receptor supersensitivity. This phenomenon, called supersensitivity psychosis, can be explained by the development of tolerance towards the effect of the medication. In literature, there are several cases of supersensitivity psychosis while using other neuroleptics. However, to our knowledge, there are no published cases reporting an association between clozapine and supersensitivity psychosis. The current patient, who has been diagnosed as resistant schizophrenia, responded well to the clozapine in the beginning of treatment. Due to an effective dose of clozapine, he had psychotic exacerbation with significant positive symptoms. We discuss the probable reasons causing this situation and the relationship between tolerance to the treatment effect and the dopamine supersensitivity.<br />

Clozapine withdrawal resulting in delirium with psychosis: a report of three cases.

Abstract

BACKGROUND:

Withdrawal symptoms for typical antipsychotics are generally mild, self-limited and do not include development of psychotic symptoms. In contrast, withdrawal symptoms for clozapine can be severe with rapid onset of agitation, abnormal movements, and psychotic symptoms. Different pathophysiologic etiologies have been suggested for these severe symptoms, including dopaminergic supersensitivity and rebound.

METHOD:

Three case reports of clozapine withdrawal symptoms are presented. A review of previous case reports and discussion of the etiology of withdrawal symptoms of typical antipsychotics and clozapine are provided.

RESULTS:

These three patients developed delirium with psychotic symptoms that resolved rapidly and completely upon resumption of low doses of clozapine.

CONCLUSION:

The severe agitation and psychotic symptoms after clozapine withdrawal in these three patients were due to delirium, perhaps the result of central cholinergic rebound. The withdrawal symptoms and delirium resolved rapidly with resumption of low doses of clozapine. Severe withdrawal symptoms can probably be avoided by slowly tapering clozapine and/or simultaneously substituting another psychotropic with high anticholinergic activity, such as thioridazine,

How to Identify Substance-Induced Psychosis

According to the National Alliance on Mental Illness, psychosis refers to an episode in which an individual has a break from reality. This often includes but doesn’t require delusions, or false beliefs that are firmly held despite clear evidence to the contrary, and hallucinations. About 3 in every 100 people will experience at least one episode of psychosis in their lifetimes.

Drug-induced psychosis, also known as substance-induced psychotic disorder, is simply any psychotic episode that is related to the abuse of an intoxicant. This can occur from taking too much of a certain drug, having an adverse reaction after mixing substances, during withdrawal from a drug, or if the individual has underlying mental health issues. Though it’s not actually true that taking a certain kind of drug can suddenly trigger a severe mental illness where none had existed, mental illness is a predictor of substance abuse, and someone prone to psychosis can be triggered by becoming overly intoxicated.

read more here

Association between psychiatric disorders and iron deficiency anemia among children and adolescents: a nationwide population-based study

  • Mu-Hong Chen,
  • Tung-Ping Su,
  • Ying-Sheue Chen,
  • Ju-Wei Hsu,
  • Kai-Lin Huang,
  • Wen-Han Chang,
  • Tzeng-Ji Chen and
  • Ya-Mei BaiEmail author
BMC Psychiatry201313:161

https://doi.org/10.1186/1471-244X-13-161

Received: 11 May 2012

Accepted: 28 May 2013

Published: 4 June 2013

Abstract

Background

A great deal of evidence has shown that iron is an important component in cognitive, sensorimotor, and social-emotional development and functioning, because the development of central nervous system processes is highly dependent on iron-containing enzymes and proteins. Deficiency of iron in early life may increase the risk of psychiatric morbidity.

Methods

Utilizing the National Health Insurance Database from 1996 to 2008, children and adolescents with a diagnosis of IDA were identified and compared with age and gender-matched controls (1:4) in an investigation of the increased risk of psychiatric disorders.

Results

A total of 2957 patients with IDA, with an increased risk of unipolar depressive disorder (OR = 2.34, 95% CI = 1.58 ~ 3.46), bipolar disorder (OR = 5.78, 95% CI = 2.23 ~ 15.05), anxiety disorder (OR = 2.17, 95% CI = 1.49 ~ 3.16), autism spectrum disorder (OR = 3.08, 95% CI = 1.79 ~ 5.28), attention deficit hyperactivity disorder (OR = 1.67, 95% CI = 1.29 ~ 2.17), tic disorder (OR = 1.70, 95% CI = 1.03 ~ 2.78), developmental delay (OR = 2.45, 95% CI = 2.00 ~ 3.00), and mental retardation (OR = 2.70, 95% CI = 2.00 ~ 3.65), were identified. A gender effect was noted, in that only female patients with IDA had an increased OR of bipolar disorder (OR = 5.56, 95% CI = 1.98 ~ 15.70) and tic disorder (OR = 2.95, 95% CI = 1.27 ~ 6.86).

Conclusion

Iron deficiency increased the risk of psychiatric disorders, including mood disorders, autism spectrum disorder, attention deficit hyperactivity disorder, and developmental disorders. Further study is required to clarify the mechanism in the association between IDA and psychiatric disorder.

Keywords

Iron deficiency anemia Psychiatric disorders Comorbidity

Background

According to the World Health Organization, iron deficiency (ID) is the most prevalent nutritional deficiency. A 30% prevalence of iron deficiency anemia (IDA), at a minimum, has been noted among children, adolescents, and women in non-industrialized countries, and ID is also the most prevalent nutritional deficiency in industrialized countries [1234]. ID, defined by two or more abnormal measurements (serum ferritin, transferrin saturation, erythrocyte protoporphyrin), is insidious and uneasily detected by patients themselves and may not develop significant clinical symptoms [1234]. IDA is characterized by a defect in hemoglobin synthesis owing to significant ID, resulting in the reduced capacity of the red blood cells to deliver oxygen to body cells and tissues, and many clinical symptoms, such as pale conjunctiva, shortness of breath, dizziness, and lethargy [1234]. The main risk factors for IDA and ID include a low intake of iron, poor absorption of iron from diets, chronic loss of iron (i.e., ulcer, metrorrhagia), and some specific periods of life when iron requirements are especially high, such as growth and pregnancy [1234].

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