Neurologic Associations With Cardiac, Pulmonary, Renal, Hepatobiliary, and Hematologic Disease

2021 ◽  
pp. 1160-1169
Author(s):  
Shivram Kumar ◽  
Kelly D. Flemming

The brain has a higher demand for cardiac output than any other organ, and it strictly relies on oxygen and glucose metabolism. Consequently, the brain is exquisitely sensitive to homeostatic disturbances and extraneural organ dysfunction leading to cardiac, pulmonary, renal, hepatobiliary, and hematologic diseases. The primary neurologic manifestation of extraneural organic dysfunction is diffuse bihemispheric dysfunction or encephalopathy, which often lacks lateralizing or localizing signs. Common clinical findings are lethargy, difficulty with attention and orientation, sleep-wake disturbance, and psychomotor slowing. As organic dysfunction progresses, a moderate encephalopathy ensues, with worsening cognitive function, gross disorientation, hypoactive or hyperactive psychomotor state, frontal release signs, asterixis, and myoclonus. If organ failure (eg, hepatic or renal) progresses further, stupor and coma may result unless organ function improves. Patients with underlying organic brain disease from degenerative dementia can decompensate out of proportion to neurologically normal counterparts, resulting in encephalopathy even from minor organ dysfunction or infection.

1972 ◽  
Vol 121 (562) ◽  
pp. 259-264 ◽  
Author(s):  
Randall Rosenthal ◽  
Llewellyn B. Bigelow

Despite extensive gross and microscopic scrutiny, no consistent pathological findings have emerged from studies of autopsy material from schizophrenic patients. Dunlap (1924) carried out the first controlled study involving schizophrenic and control brains and concluded that ‘there was not even a suspicion of consistent organic brain disease as a basis for the psychosis of schizophrenia’. More recently both Wolf and Cowen (1952), and Weinstein (1954), reviewed the neuropathological literature and concluded that there were no consistent findings at autopsy that could be construed as characteristic of schizophrenia. These authors felt that earlier claims were based on failure to appreciate the range of normal variation in the brain as well as a failure to include an adequate control population in the study.


1935 ◽  
Vol 81 (332) ◽  
pp. 173-183
Author(s):  
T. J. Hennelly ◽  
E. D. Yates

Early investigators differed widely in their estimations of the bromine content of normal blood (1, 2), and it was not until the development of a refined technique by Bernhardt and Ucko (3) that it was generally recognized that blood bromine varied around 1 mgrm. %. These authors gave a range of 1.0 to 1.6 mgrm. %. Their studies, however, were not extensive. During 1931–3 Zondek and Bier (4, 5, 6) published the results of a series of investigations into the bromine content of the blood of normal and psychotic patients. From a study of 150 mentally normal patients they considered that blood bromine usually varied between 0.8 and 1.0 mgrm. %, a range later extended to 0.731.10 mgrm. % as a result of further study. In a large number of psychotics examined by them, values lying within these limits were found with the notable exception that 85%-90% of 60 cases of endogenous manic-depressive psychoses gave figures 40% to 60% below their normal levels (Zondek, 1933) (6). These low figures appeared only to be associated with this psychosis, although of the 16 cases of schizophrenia examined by them, 5 gave figures lower than the normal. They stated that in these 5 cases the mental picture was characterized by more or less marked depression, and they considered the possibility of their ultimately turning out to be manic-depressive in character. In a later paper, three examples are cited of low blood bromine associated with organic brain disease, and thought to be due to interference with a bromine-regulating centre in the brain. The low values found in manic-depressive psychoses were shown to be independent of the phase, and it was stated that values in general were not subject to seasonal variations, to menstrual fluctuations, or to alterations due to variable salt intake.


2018 ◽  
Vol 59 (5) ◽  
pp. 686-696 ◽  
Author(s):  
Peter R. Breggin

Extreme states can be psychospiritual and “functional” in origin or they can be “organic” and driven by biological dysfunction. Contemporary psychiatry largely rejects this distinction, preferring to insist that everything “extreme” is biological in origin; but the distinction is important for understanding and helping people. Psychospiritual crises, including those labeled bipolar or schizophrenic, are “functional” and express meaning. As “bizarre” as the language or the symbols may seem, meanings that often reflect childhood abuse can be explored in a trusting, kind, and caring therapeutic relationship. The more that a real biological or organic dysfunction, such as traumatic head injury or neurotoxic exposure, is the root cause of the extreme state, the less sense its manifestations will make. Nonetheless, drug-induced extreme states, even when caused by hallucinogens or by psychiatric “medicines,” often leave sufficient brain function operational to reveal important meanings about the person’s experience, along with the otherwise senseless intoxication. With so many people prescribed psychiatric drugs, these neurotoxic chemicals are now the most common cause of extreme states in clinical practice, and withdrawal from these offending agents is critical to recovery (Breggin, 2013). However, even when the extreme state is driven by neurological dysfunction, a safe space and skilled therapists can help relieve the individual’s otherwise overwhelming feelings of anxiety or terror.


Author(s):  
Armin Schnider

What diseases cause confabulations and which are the brain areas whose damage is responsible? This chapter reviews the causes, both historic and present, of confabulations and deduces the anatomo-clinical relationships for the four forms of confabulation in the following disorders: alcoholic Korsakoff syndrome, traumatic brain injury, rupture of an anterior communicating artery aneurysm, posterior circulation stroke, herpes and limbic encephalitis, hypoxic brain damage, degenerative dementia, tumours, schizophrenia, and syphilis. Overall, clinically relevant confabulation is rare. Some aetiologies have become more important over time, others have virtually disappeared. While confabulations seem to be more frequent after anterior brain damage, only one form has a distinct anatomical basis.


2018 ◽  
Vol 39 (5) ◽  
pp. 719-738 ◽  
Author(s):  
Megan E Capozzi ◽  
Richard D DiMarchi ◽  
Matthias H Tschöp ◽  
Brian Finan ◽  
Jonathan E Campbell

Abstract Glucagonlike peptide 1 (GLP-1) receptor agonists have been efficacious for the treatment of type 2 diabetes due to their ability to reduce weight and attenuate hyperglycemia. However, the activity of glucagonlike peptide 1 receptor–directed strategies is submaximal, and the only potent, sustainable treatment of metabolic dysfunction is bariatric surgery, necessitating the development of unique therapeutics. GLP-1 is structurally related to glucagon and glucose-dependent insulinotropic peptide (GIP), allowing for the development of intermixed, unimolecular peptides with activity at each of their respective receptors. In this review, we discuss the range of tissue targets and added benefits afforded by the inclusion of each of GIP and glucagon. We discuss considerations for the development of sequence-intermixed dual agonists and triagonists, highlighting the importance of evaluating balanced signaling at the targeted receptors. Several multireceptor agonist peptides have been developed and evaluated, and the key preclinical and clinical findings are reviewed in detail. The biological activity of these multireceptor agonists are founded in the success of GLP-1-directed strategies; by including GIP and glucagon components, these multireceptor agonists are thought to enhance GLP-1’s activities by broadening the tissue targets and synergizing at tissues that express multiple receptors, such at the brain and pancreatic isletβ cells. The development and utility of balanced, unimolecular multireceptor agonists provide both a useful tool for querying the actions of incretins and glucagon during metabolic disease and a unique drug class to treat type 2 diabetes with unprecedented efficacy.


2003 ◽  
Vol 40 (1) ◽  
pp. 97-102 ◽  
Author(s):  
B. Porter ◽  
A. DeLahunta ◽  
B. Summers

Gliomatosis cerebri is a well-recognized entity in human medicine characterized by unusually widespread infiltration of the neuraxis by neoplastic glial cells with relative preservation of brain architecture. This report describes the pathologic features of the disease in six dogs. The dogs ranged from 3 to 9 years of age (mean 6.1 years) without evidence of breed predilection; five of the six dogs were neutered or intact males. The clinical findings were mixed (including depression, circling, cranial nerve deficits), reflecting the diffuse nature of the disease. Histologically, there was remarkably diffuse infiltration of the white and gray matter of the brain by small numbers of elongated neoplastic cells. Areas of greater cellularity formed grossly visible lesions in four cases. Anisocytosis and pleomorphism were greater in areas of higher cellularity. Other features of tumor growth included subpial accumulation, neuronal satellitosis, perivascular cuffing, and tropism for cranial nerve and brain stem nuclei. Neoplastic cells were negative on immunohistochemical stains for glial fibrillary acid protein (GFAP) and leukocyte markers, reflecting the uncertain histogenesis of these unusual neoplasms.


1981 ◽  
Vol 14 (2) ◽  
pp. 105-111
Author(s):  
G. Ladurner ◽  
W. Pieringer ◽  
W.D. Sager

1983 ◽  
Vol 13 (2) ◽  
pp. 155-159 ◽  
Author(s):  
Robert W. Butler ◽  
William A. Dickinson ◽  
Charles Katholi ◽  
James H. Halsey

1997 ◽  
Vol 3 (4) ◽  
pp. 211-218 ◽  
Author(s):  
David Jolley ◽  
David Baxter

The purpose of this review is to outline current knowledge on the life expectation of people suffering from organic brain disease, the techniques available for describing and comparing life expectation in populations, factors which are associated with longer and shorter life expectation, and the causes of death among patients with this condition.


1970 ◽  
Vol 26 (1) ◽  
pp. 123-142
Author(s):  
Jean Gové

This paper investigates the notion of ‘distributed cognition’ – the idea that entities external to one’s organic brain participate in one’s overall cognitive functioning – and the challenges it poses. Related to this is also a consideration of the ever-increasing ways in which neuroprostheses replace and functionally replicate organic parts of the brain. However, the literature surrounding such issues has tended to take an almost exclusively physicalist approach. The common assumption is that, given that non- physicalist theories (dualism, hylomorphism) postulate some form of immaterial ‘soul’, then they are immune from the challenges that these advances in cognitive science pose. The first aim of this paper, therefore, is to argue that this is not the case. The second aim of this paper is to attempt to elucidate a route available for the non- physicalist that will allow them to accept the notion of distributed cognition. By appealing to an Aristotelian framework, I propose that the non-physicalist can accept the notion of distributed cognition by appeal to the notion of ‘unitary life’ which I introduce as well as Aristotle’s dichotomy between active and passive mind.


Sign in / Sign up

Export Citation Format

Share Document