The Lived Experience of Anemia Without a Cause.

This article explores anemia without an obvious cause from two perspectives: a patient and the evidence. Although evidence is required to drive favorable patient outcomes, the focus on evidence often hides the patient experience during diagnosis and treatment. Knowledge of experience with evidence can provide a deeper perspective for clinical decision making and meet nursing's ethical mandate to relieve suffering. Although one patient experience does not reflect every patient experience, this patient's experience demonstrates how difficult and dark anemia can be.

[Neuropsychiatric manifestations ushering pernicious anemia]. / Manifestations neuropsychiatriques inaugurant une maladie de Biermer.

Biermer disease or pernicious anemia is an autoimmune atrophic gastritis characterized by the lack of secretion of gastric intrinsic factor. This leads to an insufficient absorption of vitamin B12 in the ileum. Clinical manifestations are mainly hematologic. Neuropsychiatric manifestations are known but are less frequent especially early in the disease. Inaugural neuropsychiatric arrays are rare and various thus making diagnosis difficult. In this article, we report through two clinical cases different neuropsychiatric manifestations revealing pernicious anemia. Mrs. C.O., aged 56, presented after surgery for gallstones, an acute psychiatric array associated with gait disorders. She had no history of neurological or psychiatric problems. The psychiatric interview revealed delirious syndrome, depressive symptoms and anxiety. Neurological examination noted a flaccid paraplegia with peripheral neuropathic syndrome and myoclonus in the upper limbs. At the full blood count, a macrocytosis (VGM: 112.2fl) without anemia was found. The level of vitamin B12 in the blood was low. Cerebro-spinal MRI was suggestive of a neuro-Biermer and showed hyper signal in the cervical cord on T2-weighted sagittal section. In axial section, hyper signal appears at the posterior columns in the form of V. There were no brain abnormalities. A sensorimotor axonal polyneuropathy was diagnosed. The patient received vitamin B12 intramuscularly for ten days associated with neuroleptic treatment. Mrs. R.M., aged 40, was brought to the psychiatry consultation for acute behavioral disorders progressively worsening over a month. An anxiety syndrome, depressive syndrome and delirious syndrome were identified. Neurological examination showed a posterior cordonal syndrome with quadripyramidal syndrome. Full blood count showed a macrocytic anemia. Serum B12 level was collapsed. Cerebro-spinal MRI was normal. She received vitamin B12 with clinical and biological improvement. Features of pernicious anemia vary according to studies and age range. Digestive and hematological manifestations are well known. Neurological and psychiatric manifestations of pernicious anemia were also described in the early literature. They can be the initial symptoms or the only ones. However, inaugural neuropsychiatric features are often unrecognized. The most common psychiatric symptoms were depression, mania, psychotic symptoms, cognitive impairment and obsessive compulsive disorder. Neurological involvement includes mainly combined spinal sclerosis, peripheral neuropathy and dementia. Cerebellar ataxia and movement disorders are reported less often. Severity of neuropsychiatric features and therapeutic efficacy depends on the duration of signs and level of B12 deficiency. Macrocytic anemia may lack. Neuropsychiatric manifestations could be isolated or be the first manifestation of vitamin deficiency and occur without any hematological or gastrointestinal context. Pernicious anemia and serum B12 assay should be discussed in all patients with organic mental disorders, atypical psychiatric symptoms and fluctuation of symptomatology. Nevertheless, B12 level could be normal in genuine pernicious anemia diseases and macrocytic anemia may lack. Substitutive vitaminotherapy is required when diagnosis is strongly suspected and etiologic assessment is negative.

La voluntad de morir / The death wish

En la carta del 19 de febrero de 1923, Ferenczi da cuenta a Groddeck de la muerte de una paciente suya por anemia perniciosa. De esa misma enfermedad moriría 10 años después el mismo Ferenczi. En esos 10 años su contribución teórico clínica fue extraordinaria y atravesó momentos cruciales del desarrollo de la teoría psicoanalítica como la conceptualización de Freud sobre la pulsión de muerte, la configuración de la segunda tópica, la publicación de Thalassa y "el principio de afirmación del displacer", la segunda teoría de Freud sobre la angustia y un intercambio epistolar con Groddeck que permite percibir los primeros esbozos de una teoría sobre la sintomatología psicosomática que sería posteriormente desarrollada. El autor intenta establecer las conexiones teóricas entre todos estos argumentos, destacando la aportación genial de Ferenczi que se nutría en muchos momentos de su propia experiencia patológica y de su propio sufrimiento interno. Una de las obras en las que con mayor claridad se refleja esta cuestión, es en su trabajo sobre "El niño mal recibido y la pulsión de muerte", donde aparece claramente conceptualizada la voluntad de morir, a la que se refiere todo este trabajo (AU)

In a letter of the 19th of February, 1923, Ferenczi tells Groddeck about the death of a patient of his by progressive pernicious anaemia. Ferenczi would die of that same illness ten years later. In those ten years his theoretical-clinical contribution was extraordinary, and went through crucial moments of the development of psychoanalytical theory such as Freud´s death drive, the configuration of the second topic, the publication of Thalassa and the problem of the acceptance of unpleasant ideas, Freud´s second theory of anxiety, and a correspondence with Groddeck that allows us to perceive the first outline of a theory on psycosomatic symptomatolgy that would be developed later. The author endeavours to establish some theoretical connections between these two arguments, highlighting Ferenczi´s brilliant contribution, which was often fueled by his own pathological experience and inner suffering. One of the works in which this matter is treated with great clarity is The Unwelcome Child and his Death Drive, in which the death wish, to which I will refer to throghout this work, is clearly conceptualized (AU)

Ferenczi's fatal illness in historical context.

In August 1932, Ferenczi was already manifesting symptoms of his fatal illness, pernicious anemia. This was diagnosed between September 20 and October 2 of that year, less than a month after the Twelfth International Psychoanalytic Congress in Wiesbaden. Despite seemingly successful treatment with injectable liver extract, he underwent an acute psychotic episode in March 1933, triggered by the neurological symptoms of his illness. These facts substantiate the subsequent claim of Freud and Jones that Ferenczi suffered from paranoia near the end of his life, but they do not support the commonly-held view that the writings and experiments in psychoanalytic technique of his last five years were symptomatic of a progressive mental illness.

An association between subcortical dementia and pernicious anemia--a psychiatric mask.

A case report from our psychiatric ward demonstrates the emergence of two different organic pathologies, a subcortical dementia and a pernicious anemia, preceded by a psychiatric presentation mimicking a dementia of depression. We emphasize that the psychiatric mask and the lack of other clinical and paraclinical cobalamin deficiency signs were the chief obstacles to early diagnosis. Only a complete and thorough assessment allowed the real diagnosis. We describe a subcortical dementia, and after a review of the literature, we support the causalty of B12 hypovitaminosis (pernicious anemia) in the genesis of this dementia, in the absence of other organic causes of mental syndromes and in the presence of a positive and well-maintained response to vitamin B12 administration.

Psychiatric syndromes in pernicious anaemia--a case report.

Surveys of psychiatric population had previously shown a high incidence of patients with low serum vitamin B12. A variety of psychiatric syndromes have been described, ranging from mild disturbance in mood state like depression to maniacal excitement; psychotic conditions like paranoid states and schizophrenia; and cognitive dysfunctions such as memory defect, delirium and dementia. A case of a 67-year-old Chinese lady suffering from pernicious anaemia, but presenting with prominent paranoid delusions is reported. Treatment with cyanocobalamine and anti-psychotic medication led to prompt resolution of her psychotic experience. Subsequently she developed a transient depressive syndrome which also responded well to a short course of antidepressant.

What are the psychiatric manifestations of vitamin B12 deficiency?

Psychiatric symptoms attributable to vitamin B12 deficiency have been described for decades. The earlier reports are for the most part in accord with more recent ones, despite being diagnostically less specific in psychiatric and hematologic terms. These symptoms seem to fall into several clinically separate categories: slow cerebration; confusion; memory changes; delirium, with or without hallucinations and/or delusions; depression; acute psychotic states; and (more rarely) reversible manic and schizophreniform states. While there still remain abundant hematologic, psychiatric, neurologic, or nutritional reasons for obtaining a serum vitamin B12 level, its use in the investigation of the etiology of a patient's dementia seems unjustified. However, acute or subacute changes in a demented patient's mental status, specifically a clouding of their consciousness, may make such testing advisable as part of the complete workup of their delirium regardless of a normal hematologic picture.

Vitamin B-12, megaloblastic madness, and the founding of Duke University.

When James D. Duke died in 1925, he had left $19 million to build Duke University. He died from pernicious anemia, a vitamin B-12 deficiency. The author gives evidence that Duke made his gift when he was brain damaged and depressed from a vitamin B-12 deficiency, that he donated the money in an attempt to relieve guilt feelings.

Precursor lesions of the GI tract and psychosocial risk factors for prediction and prevention of gastric cancer.

In two prospective studies, including a total of 1,353 and 1,914 male and female participants, a variety of medical and psychosocial risk factors were assessed by means of personal interviews and observational categories. The incidence of gastric cancer was determined for the following study groups: 1) all persons with chronic atrophic gastritis and pernicious anemia who had one to three relatives with a history of gastric cancer, 2) persons with a previous operation for gastric ulcer (partial resection) and one to three relatives with gastric cancer, and 3) a comparable group without any of these characteristics, serving as a reference. The hypothesis was that significantly more gastric cancer was to be expected in groups 1 and 2. A second hypothesis was that interaction between the specific precursors and psychosocial risk factors (chronic hopelessness due to withdrawing objects) was useful for the prediction of gastric cancer. The results may open new avenues for the prevention of gastric cancer via preventive psychotherapy in identified risk groups.

Cognitive effects of nutritional deficiency.

Deficiencies of various nutrients, primarily vitamins, impair cognition. The link is strongest for vitamin B12, thiamine, and niacin. Yet even for these, the role of mild "subclinical" or multiple deficiencies in the genesis of mental dysfunction is unclear. Most information in this field is based on animal studies often poorly applicable to the human condition or on clinical pathology complicated by advanced age, alcoholism, and intercurrent disease. There is a need for well controlled, double-blind, prospective trials to elucidate the cognitive effects of malnutrition.