When Paula suddenly became mostly silent, this was certainly interpreted as new and strange behaviour. New and strange, because she did not respond normally in conversations with friends and family. She was quiet, more so than usual. She suddenly had no idea what to say…. for months…
The most common interpretation for this was that Paula had suddenly become silent and moody. She was not her usual helpful and smiling self. Something was clearly wrong. And that something was assumed to be psychological. People thought she was preoccupied due to some conflict at work or at home. This is a perfectly normal interpretation.
No one could have interpreted her moody looking silence and one word answers as amnesia with psychomotor slowing. And her own experience of what was happening to her felt like anguish, distress and fear with fleeting disappearing thoughts that she could not keep in her mind. It did not seem like amnesia to her because she knew who she was and recognized others. She just had nothing to say. Because her mind was strangely blank. She could not remember any of her thoughts, opinions, facts, and could no longer function normally. She had no idea suddenly of how to do her job even though she’d been doing it a long time and was perfectly fine the day before. She seemed superficially like herself; she could still punctuate conversations with stereotypic phrases but not much else.
How could anyone have guessed that she was amnesic, especially as she did not know herself.
One way is to ask patients [who suddenly look depressed and who’s coworkers, friends and families report changes in behavior [resulting in especially quiet behavior with few words] , if they are having difficulty wth their memory. If the patient is very confused they may answer “I don’t know”, a frequent response which indicates that they are too confused to be sure which tells you right away that you must give them a basic memory test to see. Paula might have answered “I don’t know” or maybe she would have said yes. Especially early on.
Paula also did not recognize that she was in respiratory distress. She was very aware of the sense of dyspnea or anguish, and was briefly aware of shortness of breath when she did speak; she was unable to say more than 2 or 3 words, and only with great effort.
I am still working on this post…..editing and adding ….it is not easy to explain the unimaginable…
Could this sudden memory impairment and cognitive impairment and speech limitations be due to weakness of the respiratory muscles in a person in their early or mid twenties?. Yes. Especially if they have had a spell of illnesses recently, loss of weight, nausea, vomiting, diarrhoea etc…or a recent head injury or recent blood loss [including heavy menstruation or major loss of blood during childbirth. And even more so if muscle weakness ran in her parents and her parents siblings. , Also being born in distress, needing to be suctioned and resuscitated and transfused….this takes it toll as well. It might even point to some sort of mitochondrial myopathy. The respiratory muscles can be weakened in mitochondrial myopathies. Or it could simply be sarcopenia of the respiratory muscles.
How early can sarcopenia in the respiratory muscles start?
~30 years of age.
In humans, the progressive aging-related decline in skeletal muscle mass and strength (sarcopenia) begins at ~30 years of age (similar to other physiologic systems; (Sehl and Yates, 2001)), progressing thereafter at a rate of 0.5–1% of muscle mass lost per year with a more rapid decline in humans >65 years of age ( …Oct. 20, 2015
Functional impact of sarcopenia in respiratory muscles – NCBIhttps://www.ncbi.nlm.nih.gov › articles › PMC4838572
The act of breathing depends on coordinated activity of the respiratory muscles to generate subatmospheric pressure. This action is compromised by disease states affecting anatomical sites ranging from the cerebral cortex to the alveolar sac. Weakness of the respiratory muscles can dominate the clinical manifestations in the later stages of several primary neurologic and neuromuscular disorders in a manner unique to each disease state. Structural abnormalities of the thoracic cage, such as scoliosis or flail chest, interfere with the action of the respiratory muscles—again in a manner unique to each disease state. The hyperinflation that accompanies diseases of the airways interferes with the ability of the respiratory muscles to generate subatmospheric pressure and it increases the load on the respiratory muscles. Impaired respiratory muscle function is the most severe consequence of several newly described syndromes affecting critically ill patients. Research on the respiratory muscles embraces techniques of molecular biology, integrative physiology, and controlled clinical trials. A detailed understanding of disease states affecting the respiratory muscles is necessary for every physician who practices pulmonary medicine or critical care medicine.Keywords: respiratory insufficiency; heart failure; nervous system diseases; neuromuscular diseases; sepsis Disorders of the Respiratory Muscles Franco Laghi , and Martin J. Tobin American Journal of Respiratory and Critical Care Medicine Volume 168, Issue 1
Cognitive impairment in survivors of acute respiratory distress syndrome: clinical burden and long-term sequelae
Acute Respiratory Distress [ARDS ] survivors experience a high prevalence of cognitive impairment: 70–100% at hospital discharge, 46–80% at 1 year, and 20% at 5 years [3, 4]. ARDS survivors score significantly lower on standardized quality of life assessments compared to severity-matched controls at 6- and 12-month follow-up [5, 6]. ARDS survivors also experience higher overall healthcare costs, exercise limitations, and persistent psychological and physical disability despite lung function recovery at 5-year follow-up . Upon 1-year follow-up, survivors demonstrate impaired executive function and short-term memory and increased rates of anxiety and depression [1, 8], in addition to post-traumatic stress disorder . Neurocognitive testing of ARDS survivors at 2-year follow-up reveals residual emotional and cognitive sequelae in nearly half of patients . In addition to depression and anxiety, testing shows impairments in executive function, learning, and memory, with 50% of those affected performing below the 6th percentile on multiple instruments  . published: Long-term cognitive impairment after acute respiratory distress syndrome: a review of clinical impact and pathophysiological mechanisms Cina Sasannejad, E. Wesley Ely & Shouri Lahiri
Brain CT scans from 15 survivors of ARDS were compared to age- and sex-matched normal controls. Clinical radiological findings and ventricular volumes, brain volume and generalized brain atrophy. The patients with ARDS and brain imaging had cognitive impairments, significant brain atrophy, ventricular enlargement and 53% had atrophy or lesions by radiological report. Clinicians need to be aware that ARDS can cause significant long-term brain-related morbidity manifest by brain atrophy, lesions and neurocognitive impairments. Brain atrophy and cognitive impairment in survivors of Acute Respiratory Distress Syndrome April 2006 Brain Injury 20(3):263 DOI:10.1080/02699050500488199
People with bipolar disorder suffer from accelerated brain tissue loss, which is associated with progressive decline in some areas of mental ability. This discovery has implications not only for the way we research the disease, but may also impact the way this condition is treated.Jul. 21, 2007
Manic Depression Linked With Brain Tissue Loss – ScienceDaily
The science daily update shown above came from this following study:
Conclusions: Patients with BPD lose hippocampal, fusiform and cerebellar gray matter at an accelerated rate compared with healthy control subjects. This tissue loss is associated with deterioration in cognitive function and illness course. Psychiatry 2007 Oct 15;62(8):894-900. doi: 10.1016/j.biopsych.2007.03.005.Epub 2007 Jul 9. Progressive gray matter loss in patients with bipolar disorder T William J Moorhead 1, James McKirdy, Jessika E D Sussmann, Jeremy Hall, Stephen M Lawrie, Eve C Johnstone, Andrew M McIntosh
Complaints of impaired memory are amongst the most common symptoms voiced by patients to physicians in the fields of neurology, psychiatry, medicine, and surgery. Impairment of memory is one of the most disabling aspects of many neurological disorders, including neurodegenerative diseases, strokes, tumors, head trauma, hypoxia (reduced exposure of tissue to oxygen), cardiac surgery, malnutrition, attention deficit disorder, depression, anxiety, medication side-effects, and normal aging. This memory loss often impairs the patient’s normal daily activities, profoundly affecting both the patients and their families. Research in memory began with neuropsychological studies of patients with focal brain lesions and now includes new methods such as PET (positron emission tomography, where the decay of an injected radioactive element or drug creates an image) and functional MRI (magnetic resonance imaging, where hydrogen atoms are polarized by a magnet and the summation of their spinning energy creates an image). Event-related methodologies have provided us with more refined and improved classification systems. Rather than conceptualizing memory as “short-term” and “long-term,” we now think of memory as a collection of mental abilities that use different systems within the brain. In the present article we will summarize the four memory systems that are of clinical relevance: episodic memory, semantic memory, procedural memory, and working memory. Discov Med. 2005 Apr;5(26):135-41. Memory dysfunction in clinical practice Andrew E Budson 1, Bruce H Price PMID: 20704899
Note the possibility that the cognitive and memory dysfunction and atrophy of the “hippocampal, fusiform and cerebellar gray matter ” can certainly be due to periods of unknown acute respiratory distress syndrome. ARDS also results in brain atrophy and ventricle enlargement.
Measurements of vital signs, including respiratory rates would be one basic way to determine if bipolar patients [unmedicated] have baseline resting respiratory rates that are abnormal during depressive and manic attacks, both causing cognitive and memory impairment.
to be continued.