Well now, that is a very important question. It would certainly explain a lot. It would explain the very recognizable psychomotor retardation, a feature of depression mentioned by observers since antiquity. Psychomotor retardation is a motor sign which is visible to others and the mental slowing is also visible with basic cognitive testing.
….…..”Psychomotor retardation has been characterized as a major feature of depression since antiquity. Hippocrates and Aretaeus of Cappadocia both described psychomotor retardation as a characteristic of depression (Sobin and Sackeim, 1997; Whitwell, 1936; Zilboorg, 1944). Darwin also discussed visible psychomotor symptoms and depressed patients who “no longer wish for action but remain motionless and passive, or may occasionally rock themselves to and fro” (Dantchev and Widlocher, 1998; Greden and Carroll, 1981). In the proceeding decades, authors such as Kraepelin expanded on psycho-motor retardation, building upon the knowledge of this noteworthy phenomenon by describing how it was more prominent than depressed mood and involved constrained speech, thought, and behavior (Greden and Carroll, 1981; Sobin and Sackeim, 1997).” Buyukdura JS, McClintock SM, Croarkin PE. Psychomotor retardation in depression: biological underpinnings, measurement, and treatment. Prog Neuropsychopharmacol Biol Psychiatry. 2011 Mar 30;35(2):395-409. doi: 10.1016/j.pnpbp.2010.10.019. Epub 2010 Oct 31. PMID: 21044654; PMCID: PMC3646325.
Paula had slowed speech, decreased movement and impaired cognitive function. And exactly like Kraepelin observed her condition involved “constrained speech, thought, and behavior “. Speech especially was constrained by a rigidity of her facial muscles and by shortness of breath [being unable to say more than 2-3 words in a single breath] . Her thoughts were constrained by instant loss of memory for whatever she was thinking. Her behaviour was constrained by her inability to start because of all three factors mentioned ; rigidity of muscles, shortness of breath, loss of memory for what she wished to do. Paula can tell us this now. Paula could not tell us while it was happening to her.
” Manifestations of psychomotor retardation include slowed speech, decreased movement, and impaired cognitive function. It is common in patients with melancholic depression and those with psychotic features. Biological correlates may include abnormalities in the basal ganglia and dopaminergic pathways………
……..Despite its long observed prevalence in MDD, [manor depressive disorder] the characterization and clinical significance of psychomotor retardation are poorly understood………………...Psychomotor retardation is unique in regards to depressive symptomatology as it is assessed through direct behavioral observations of speech, facial expression, eye movements, self-touching, posture, and speed and degree of movements (Jones and Pansa, 1979; Parker and Hadzi-Pavlovic, 1996; Sobin and Sackeim, 1997; Widlocher, 1983). Speech has been extensively studied in the context of depression and psychomotor retardation (Greden et al., 1981; Hardy et al., 1984; Sobin and Sackeim, 1997; Szabadi et al., 1976). Specifically, investigations have involved observations of pause and speech times, volume, tone, infection, articulation, and response length (Greden et al., 1981; Greden and Carroll, 1981; Hardy et al., 1984; Sobin and Sackeim, 1997; Szabadi et al., 1976). Clinicians can easily assess marked speech abnormalities such as gross changes in volume and prosody (Greden, 1993). Characteristic eye movements of patients with psychomotor retardation are fixed gaze and poor maintenance of eye contact (Sobin et al., 1998; Widlocher, 1983). Another characteristic symptom is gross psychomotor slowing, including movement of the hands, legs, torso, and head (Parker and Hadzi-Pavlovic, 1996; Sobin et al., 1998; Widlocher, 1983). Slumped posture is also a manifestation of psychomotor retardation (Parker and Hadzi-Pavlovic, 1996; Sobin et al., 1998; Widlocher, 1983). In addition, patients with psychomotor retardation have been found to engage in increased self-touching, especially of the face (Sobin and Sackeim, 1997). (Greden and Carroll, 1981; Sobin and Sackeim, 1997). Buyukdura JS, McClintock SM, Croarkin PE. Psychomotor retardation in depression: biological underpinnings, measurement, and treatment. Prog Neuropsychopharmacol Biol Psychiatry. 2011 Mar 30;35(2):395-409. doi: 10.1016/j.pnpbp.2010.10.019. Epub 2010 Oct 31. PMID: 21044654; PMCID: PMC3646325.
It seems clear to me that what is described under the concept of psychomotor retardation, a psychiatric term, is the same as neurological motor and systemic reflex disturbances. Psychiatrists simply do not understand the neuromuscular disorders of neurological syndromes. The reason for this is the mistaken belief of psychiatry that these syndromes are “mental” rather neurological in nature.
These neurological variables need to be observed and elicited. This can only be done by a doctor who is familiar with the neurological disease process.
“To paraphrase John Hughlings Jackson (1835–1911), clinical phenomena are experiments on the nervous system made by disease. Neurological signs might therefore be (loosely) characterized as the ‘dependent variables’ of the experi- ments wrought by neurological disease. Observing or eliciting these signs may therefore give insight into neurological disease processes.” from A DICTIONARY
OF NEUROLOGICAL SIGNS. THIRD EDITION. A.J. LARNER. MA, MD, MRCP (UK), DHMSA Consultant Neurologist Walton Centre for Neurology and Neurosurgery, Liverpool Honorary Lecturer in Neuroscience, University of Liverpool Society of Apothecaries’ Honorary Lecturer in the History of Medicine, University of Liverpool Liverpool, U.K. ISBN 978-1-4419-7094-7. DOI 10.1007/978-1-4419-7095-4
Springer New York Dordrecht Heidelberg London. Library of Congress Control Number: 2010937226 © Springer Science+Business Media, LLC 2001, 2006, 2011
Instead of using psychiatric terms like psychomotor retardation, , Paula and I find that it is much clearer to use the neurological terms that apply. Manic depressive is a type of movement disorder.
Paula was never examined by a neurologist. Her psychiatrist noted but did not understand the neurological implications of the physical signs that Paula was exhibiting. The physical signs were obvious. Everyone could see them. They are neurological in nature. And this matters to how this disease should be viewed. And it will matter to the treatments needed to help the patient.
Paula and I will be using the neurological terms from the book A DICTIONARY
OF NEUROLOGICAL SIGNS to illustrate Paula’s current understanding of her signs and symptoms.
Abulia
A neurologist examining Paula would note that she was exhibiting abulia; this is what psychomotor retardation is. This is what the psychiatrists are noticing, but they do not know that it is a neurological sign. It suggests dysfunction of the frontal lobes.
Abulia
Abulia (aboulia) is a ‘syndrome of hypofunction’, characterized by a lack of initiative, spontaneity and drive (aspontaneity), apathy, slowness of thought (bradyphrenia), and blunting of emotional responses and response to external stimuli. It may be confused with the psychomotor retardation of depression and is sometimes labelled as ‘pseudodepression’. More plausibly, abulia has been thought of as a minor or partial form of akinetic mutism. A distinction may be drawn between abulia major (= akinetic mutism) and abulia minor, a lesser degree of abulia associated particularly with bilateral caudate stroke and thala- mic infarcts in the territory of the polar artery and infratentorial stroke. There may also be some clinical overlap with catatonia.
Abulia may result from frontal lobe damage, most particularly that involving the frontal convexity, and has also been reported with focal lesions of the caudate nucleus, thalamus, and midbrain. As with akinetic mutism, it is likely that lesions anywhere in the ‘centromedial core’ of the brain, from frontal lobes to brainstem, may produce this picture.
Pathologically, abulia may be observed in:
- Infarcts in anterior cerebral artery territory and ruptured anterior commu- nicating artery aneurysms, causing basal forebrain damage;
- Closed head injury;
- Parkinson’s disease; sometimes as a forerunner of a frontal lobe dementia;
- Other causes of frontal lobe disease: tumour, abscess;
- Metabolic, electrolyte disorders: hypoxia, hypoglycaemia, hepaticencephalopathy. Treatment is of the underlying cause where possible.
Secondary Acalculia.
Paula exhibited secondary acalculia. Paula was working overtime at work when she became ill. Try as she might, she was completely incapable of adding up her overtime hours, on paper or in her head. She found this very distressing, as it should have been a simple task.
Acalculia
Acalculia, or dyscalculia, is difficulty or inability in performing simple mental arithmetic. This depends on two processes, number processing and calculation; a deficit confined to the latter process is termed anarithmetia. Acalculia may be classified as:
Primary:
A specific deficit in arithmetical tasks, more severe than any other coexisting cognitive dysfunction.
Secondary:
In the context of other cognitive impairments, for example of lan- guage (aphasia, alexia, or agraphia for numbers), attention, memory, or space perception (e.g. neglect). Acalculia may occur in association with alexia, agraphia, finger agnosia, right–left disorientation, and dif- ficulty spelling words as part of the Gerstmann syndrome with lesions of the dominant parietal lobe.
Secondary acalculia is the more common variety.
Agnosia
Paula had impaired recognition or Agnosia;; she said hello to people she did not know but thought she knew, because they had physical characteristics similar to those she knew. So for example, bald men of a certain height, women with red hair and a certain body type, she would confuse these category of strangers with people she knew who had similar physical traits. She would realize that she’d made a mistake, due to people’s reactions and immediately recognized her error and felt really stupid.
Agnosia
Agnosia is a deficit of higher sensory (most often visual) processing causing impaired recognition….…With the passage of time, agnosic defects merge into anterograde amnesia (failure to learn new information).
Anatomically, agnosias generally reflect dysfunction at the level of the association cortex, although they can on occasion result from thalamic pathol- ogy. Some may be of localizing value. The neuropsychological mechanisms underpinning these phenomena are often ill understood.
Agraphia
All of a sudden, Paula could not spell words properly. She forgot the proper spellings and could no longer recognize a correct from an incorrect spelling. This is called Agraphia.
Agraphia
Agraphia or dysgraphia is a loss or disturbance of the ability to write or spell. Since writing depends not only on language function but also on motor, visuospatial, and kinaesthetic function, many factors may lead to dysfunction. Agraphias may be classified as follows:
- Central, aphasic, or linguistic dysgraphias:
These are usually associated with aphasia and alexia, and the deficits mirror those seen in the Broca/anterior/motor and Wernicke/posterior/sensory types of aphasia. Oral spelling is impaired.
Alexia
Paula also experienced Alexia; she could no longer read at her normal grade level. She could not remember the words long enough to make sense of a sentence. This seemed to be part of her cognitive impairment.
Alexia
Alexia with aphasia:
Patients with aphasia often have coexistent difficulties with reading (reading aloud and/or comprehending written text) and writing (alexia with agraphia.
Amnesia
Paula lost most of her autobiographical memory, including loss of her address and phone number. She lost her memory for how to do her job overnight, but did not know she lost this ability till she went to work. [She remembered to go to work and remembered how to get there. She recognized her coworkers but forgot how to converse with them, she lost her social skills.] In addition to having retrograde memory loss, she also had anterograde memory loss. As soon as she realized that she no longer remembered what to do at work, she soon forgot this and tried again and again, realizing she’d forgotten, then losing that insight immediately. The amnesia was one feature of a more widespread impairment of cognition.
Amnesia
Amnesia is an impairment of episodic memory or memory for personally experi- enced events (autobiographical memory). This is a component of long-term (as opposed to working) memory which is distinct from memory for facts (semantic memory), in that episodic memory is unique to the individual whereas semantic memory encompasses knowledge held in common by members of a cultural or linguistic group. Episodic memory generally accords with the lay perception of memory, although many complaints of ‘poor memory’ represent faulty atten- tional mechanisms rather than true amnesia. A precise clinical definition for amnesia has not been demarcated, perhaps reflecting the heterogeneity of the syndrome.
Amnesia may be retrograde (for events already experienced) or anterograde (for newly experienced events). …….Amnesia may occur as one feature of more widespread cognitive impairments.
Motor system: usually part of aging, seen in elderly.
Appearance: loss of muscle bulk; ‘senile’ tremor;
Tone: rigidity; gegenhalten/paratonia;
Power: decline in muscle strength;
Coordination: impaired speed of movement (bradykinesia).
Reflexes
Achilles Reflex
still editing…to be continued…
Of Sound Mind 