Table of contents:
- Neuromotor bases of the automaticity of writing
- The prefrontal cortex and its relationship with the signature
- Alzheimer's and signature decline
- The dysgraphic features scale
- The dysgraphic features of impairment scale
- Factors and variables to take into account about the signature during Alzheimer's
- Age
- Differential diagnosis
- Characteristics of structural tests
- Control of learning acquired before the disease
- Drugs administered to the elderly with Alzheimer's
- Sex
- Other variables that can be considered
- Practical case of alterations and perseverance of the firm in Alzheimer's
- Continuation of the case study
- Results of the case study
- Conclusions of the case study
By Alberto Angoso García. February 12, 2018
In PsicologíaOnline we present the results of the work on the deterioration of writing in people affected by Alzheimer's, a work carried out in the Department of Neurophysiology of the Faculty of Medicine of Salamanca, directed by Doctor Javier Yajeya Pérez and with the collaboration of all the members of the Department. This work in its original sense presents a very extensive section dedicated to the Neurophysiology of writing and its mechanisms. This section is not included due to the shortness of time, and considering that the explanation of the method developed, the data of interest and results, can be very beneficial to help the specialist in the neuropsychological evaluation of the elderly through their graphic products.
Writing is common in our daily lives, but if we analyze such activity from the point of view of its neuromotor performance, we find a complex system that requires perfect synchronization of all the muscles located in the different joints of the hand, forearm, arm., shoulder, maintenance of posture, balance, and a very fine muscle control to maintain visual-spatial control. The motor regulation required for learning to write takes years to acquire and is subject to many variables; In image 1 we see the tracing of a four-year-old boy learning to write, it is easy to observe the clumsiness of movements, the lack of firmness, the polygonal ovals, the incorrect morphology and other features. Beside him we see the signature of a mature person, a spontaneous, agile and automated line.Keep reading this article to find out all aboutsignature alterations and perseverance in Alzheimer's.
You may also be interested in: Differences between Alzheimer's and vascular dementia Index- Neuromotor bases of the automaticity of writing
- The prefrontal cortex and its relationship with the signature
- Alzheimer's and signature decline
- The dysgraphic features scale
- The dysgraphic features of impairment scale
- Factors and variables to take into account about the signature during Alzheimer's
- Practical case of alterations and perseverance of the firm in Alzheimer's
- Continuation of the case study
- Results of the case study
- Conclusions of the case study
Neuromotor bases of the automaticity of writing
The facility we have to make our signature in a quick and spontaneous gesture derives from a continuous exercise that promotes a corrective modulation by our nervous system until we obtain the desired result. The signature is a graphic conduct that we design on numerous occasions throughout our lives. The neurophysiological basis for the automation of the signature (as well as other activities) lies in a substantial increase in interneural communicationpromoted by continuous exercise. By performing a certain sequence of motor acts over and over again, these tend to be facilitated because the effector neurons establish stronger synaptic links and new intercellular junctions, so that the activity is facilitated and improved both from the point of view of their duration and its results (Hebb DO 1949. Kandel E. and Schwartz, 1982. Bliss T. and Lomo T. 1973). This process of synaptic plasticity, which materially constitutes the basis of learning, is called Activity-dependent Synaptic Facilitation.
From a more neuroanatomical perspective, another very important mechanism is a process of undercorticalization of graphic behavior.. Certain subcortical structures are responsible for modulating certain automatic movements performed without the contribution of conscious cortical areas. A fundamental center in scriptural automatism is the cerebellum. This structure receives instantaneous proprioceptive inputs from the muscles and inputs from the premotor cortex that indicate the movement required at this precise moment. In a sequence of precise movements, he continuously performs a corrective activity adjusting the duration and intensity of contraction of the required muscle, and planning a priori (Serratrice, Habbib, 1993) the successive rapid movements so that they are basted in a coherent sequence in their execution motor and its concrete results.
In close association with the cerebellum, and in practice receiving signals from all the areas that regulate the motor system, are the basal ganglia (image 2), located on the external part of the thalamus and occupying a large portion of the deeper structures of the cerebral hemispheres. The basal ganglia play a major role in the execution of capacities that involve many different muscles in intricate activities, planning multiple parallel and sequential patterns of movement that the mind must associate to achieve a task with a purpose. It has been shown that when there is severe damage to the basal ganglia, writing becomes rough and rudimentary, as if we were learning to write again. (Guyton, 1997)
It can be said, in an easy to understand expression, that the basal ganglia, together with the cerebellum, are the most responsible for the speed and agility in the execution of writing and signing, which is considered as a pattern of motor activity that unifies a sequence of very diverse movements, of the intrinsic characteristics of the same signature for each one of the clerks, and of its correct execution as we can visualize it in most of the people in school.
The prefrontal cortex and its relationship with the signature
A very important brain area for our work would be the area of the prefrontal cortex located in the anterior half of the frontal lobe (image 3), this constitutes the maximum expression of brain development of the human species and is the area most directly related to the processes of cognition. The decision to sign a Document with discernment rests largely in the prefrontal cortex. Once the mental analytical processes determine the convenience of signing, this center triggers the entire sequence that leads to the execution of the graphic movement of the signature.. However, by itself, and despite being directly responsible for originating volitional motor activities, the prefrontal area does not participate directly in their performance. Even receiving various projections from the thalamic nuclei, it does not have direct communication with the brain stem or spinal cord. Therefore, he decides when to make the move, but has no immediate influence on it (Portellano, 2205).
The problem that arises, therefore, is that the alteration of a motor behavior does not imply a dysfunction of the "higher" psychic capacities, such as the rational discursive mental course and critical judgment. The nervous system involves numerous areas of neuromotor integration that can malfunction and manifest executive dysgraphia unrelated to the cognitive state of the subject. And vice versa, a person can suffer from a significant degree of dementia and at the same time make his signature perfectly or quite acceptable.
Alzheimer's and signature decline
As experts, the question we are interested in answering is the following: What extent of impairment, neuromotor and cognitiveCan we infer through the writings of a sick person? A pertinent question if we look at the increase in life expectancy in "developed" societies that provide non-existent medical care at the beginning of the 20th century. This favors the presence of a large number of elderly people whose medical-clinical care requires constant effort. Image 4 shows three moments of the population pyramid of Spain during the 20th century, note that while in 1900 the percentage of people with a higher age did not exceed 1%, today it almost reaches 5%, with clear indications of being surpassed in the future due to advances in medicine and social services. This percentage of senility is higher in countries that began industrial development before Spain.
A typical symptom of Alzheimer's is brain damagediffuse in its advanced stages (image 5). Correlatively to this cell destruction, there is a substantial increase in the brain tissue of neuritic plaques (degenerated nerve fibers interspersed with aggregates of abnormal amyloid proteins) and neurofibrillary tangles (image 6). These neurofibrillary tangles are large accumulations of neurofilaments that constitute the supporting cytoskeleton of neurons in the nervous system; In the autopsy of Alzheimer's patients, numerous abnormal accumulations of this material are detected in neurons, contributing decisively to the death of the cell. At present, these phenomena are considered as demonstrative physiological symptoms of Alzheimer's. They are also found in the brain of the non-demented elderly (although in much less abundance),so it can be said that they are inherent to old age.
Another more practical and clinical perspective considers an Alzheimer patient to be an elderly person who, without signs of other etiological pathologies, presents a specific dementia picture that prevents him from performing basic operations such as dressing, eating, taking care of himself, confusion of people and objects, significant memory problems, and lack of the intellectual abilities that he enjoyed before presenting this symptomatology. In essence, presenting an insane picture that prevents him from leading an adequate existence to his environment, adequately discriminating stimuli, and which can endanger his own life if left alone.
The expert in writing, who can often lack the adequate background of neuropsychological or neurological knowledge, and above all, the direct evaluation of the patient, must be very cautious when extrapolating brain or cognitive alterations from graphic-constructive apraxia especially if we only have a few signatures.
It must be said clearly that sometimes we will not be able to infer the existence of Alzheimer's dementia through one or more signatures. The graphic execution of the signature, acquired in years prior to the pathology, supposes an implicit learning of an automatic or reflex nature, and its formation and evocation do not depend entirely on consciousness or cognitive processes. This type of memory accumulates slowly through repetition over many trials, basically manifested by an increase in performance or ease of execution. Examples of implicit learning can be considered learning to drive the car properly, learning a new language or one's own native language during childhood.Such learnings are automatically evoked without deliberate effort and can be preserved for a long time (Kandel E. & Hawkins D., 1996).
A fundamental symptom of Alzheimer's in its initial stages is the difficulty of acquiring new memories and learning new things, however, patients, despite coping with a significant dementia, can preserve many skills and knowledge learned in years before the onset of the disease. disease, in short: a memory or preservation of retrograde learning, in the presence of anterograde amnesia after the disorder. As the disease progresses, such skills and knowledge will certainly be lost, but they can last for a while and gradually deteriorate over many years. Such is often the case with personal signature.
At present, a hypothesis originating from many investigations assumes that the cause of Alzheimer's lies in the deficiency of the neurotransmitter acetylcholine in the hippocampus and associated areas. AC is the neurotransmitter of the neuromuscular junction as well as other interneural junctions within the central nervous system. The hippocampus is a deep structure of the temporal lobe that plays a fundamental role in the formation of memory networks in the associative cortex (image 7). Patients with lesions in the hippocampus suffer from anterograde amnesia and have serious difficulties in consolidating new memories and memorizing new things, but they can perform memorized learning in other parts of the brain (Milner B., 1985). The cholinergic terminals of the hippocampus are crucial for the formation of these processes, therefore,it is more than likely that some cognitive defects in Alzheimer's disease are a direct result of a deficit in cholinergic neurotransmission (Wurtman, 1985).
The dysgraphic features scale
Through the bibliographic review on dysgraphic alterations and the detailed study of specific cases, we have drawn up a list of the graphic-scriptural alterations typical of Alzheimer's, although it is applicable to many other demential processes. More than an Alzheimer's diagnostic tool, it serves to assess the presence of dementia states in the clerk or the patient.
The scale consists of 70 symptomatic items of motor disturbances and mental-cognitive impairment. The items are divided into two sections: one for motor dysgraphia (dyssynergia, dyskinesias, and dysmetria), and another for features that mainly indicate language disorders and mental-cognitive disorders. It can be objected that a language alteration does not imply a cognitive deficit, which is true, however, in the final stages of Alzheimer's, language and communication can be drastically altered. In the specific case of this pathology, it is admitted that a significant element that confirms an important mental-cognitive deterioration is the loss of graphic-linguistic communication skills (Junqué C. and Jurado MA 1994).
The scale is divided into the following sections and sub-sections:
A) GRAPHOMOTIVE SUBSCALE:
A.1) Graphic dyssynergy.
A.2) Dysmetria.
A.3) Dyskinesias.
B) COGNITIVE SUBSCALE:
B.1) Morphological alterations.
B.2) Omission of scriptural sections.
B.3) Undue inclusion of scriptural sections.
B.4) Undue reiteration of scriptural sections.
B.5) Confusion of scriptural sections (paragraphs).
C) ITEMS COMMON TO THE TWO SUBSCALES:
C.1) Drawn writing.
The ideal application requires signatures or writings prior to the pathological process in order to control the variables that are detailed later.
The dysgraphic features of impairment scale
A) GRAPHOMOTIVE SUBSCALE:
A.1) GRAPHIC DYSYNERGY: SEQUENTIAL WRITING:
1. Difficulty drawing curves and plenty of angles.
2. Ovals and polygonal letters.
3. Fragmentation of the internal structure of the letters.
4. Letters detached in writing.
5. Abundance of rectilinear lines.
6. Arrests located at address changes.
A.2) DISMETRIES AND ALTERATIONS OF THE SPACE ORDER:
TRAIL DYSMETRY:
7. Arbitrarily placed initial and final strokes of letters and rubrics:
8. Non-calligraphic driven strokes.
9. Excessively long lines (hypermetry).
10. Excessively short strokes.
INTERPALABRA DYSMETRY:
11. Very irregular distance between letters: very close together or very far apart.
12. Outstanding disproportion in the inter-letter size ratio.
13. Lack of baseline in the progression of letters.
INTRALINE DYSMETRY:
14. Very irregular distance between words: very close together or very far apart.
15. Outstanding disproportion in interword size ratio.
16. Lack of baseline in the progression of words within the line.
17. Ostensible inclination inequalities not due to scriptural tonic.
INTRA-WRITTEN DYSMETRY:
18. Confusion or mixing of some lines with others.
19. Very irregular distance between lines.
EXTRA WRITTEN DYSMETRY:
20. Orientation of the anarchic and irregular lines with respect to the axes of the folio.
21. Disproportionate top margin due to excess or default.
22. Disproportionate lower margin due to excess or default.
23. Very irregular right margin.
24. Disproportionate right margin due to excess or defect.
25. Very uneven left margin.
26. Left margin disproportionate due to excess or defect.
27. Lack of spatial adaptation to the Lockers.
28. Lack of spatial adaptation to the baseline points or lines.
29. Lack of spatial adaptation to other writings, signatures or sections of the text.
A.3) DYSCINESIAS:
30. Broken or interrupted lines.
31. Heavy writing, either continuously or discontinuously.
32. Pastures or ink residues not due to the writing tool.
33. Absence of saturation due to lack of pressure when gripping the tool.
34. Superficial writing.
35. High amplitude tremors (essential) in vertical crossbars.
36. Low amplitude tremors (physiological) in vertical struts.
37. High amplitude tremors (essential) in horizontal beams.
38. Low amplitude tremors (physiological) in horizontal beams.
39. Torsions in vertical cross members.
40. Torsions in horizontal cross members.
41. Hypokinesia in vertical lines.
42. Hypokinesia in horizontal lines.
43. Micrograph.
B) COGNITIVE SUBSCALE:
B.1) MORPHOLOGICAL ALTERATIONS:
44. Amorphologies: Letters or calligraphy without a determined form (illegible).
45. Clumsy and very precarious execution lyrics.
46. Warps: Letters with incorrect structure.
47. Irregularity or regularity in the structure of the letters.
48. Presence of erasures or corrections.
49. Fusion of two or more letters in a single structure.
B.2) OMISSION OF SCRIPTURAL SECTIONS:
50. Omission of complete letters.
51. Omission of structural parts of the letters.
52. Omission of sections of the word.
53. Omission of whole words.
54. Omission of other scriptural sections (rubric, ornaments, lines…).
B.3) UNDUE INCLUSION OF SCRIPTURAL SECTIONS:
55. Inclusion of complete letters.
56. Inclusion of structural parts of the letters.
57. Inclusion of sections of the word
58. Inclusion of whole words.
59. Accessory lines without meaning.
B.4) UNDUE REITERATION OF SCRIPTURAL SECTIONS:
60. Reiteration of structural parts of the letters.
61. Reiteration of full letters.
62. Reiteration of sections of the word.
63. Reiteration of whole words.
B.5) CONFUSION OF SCRIPTURAL SECTIONS (PARAGRAPHS):
64. Undue substitution of some letters for others.
65. Undue substitution of letters or graphemes for other graphic elements.
66. Wrong placement of graphic signs: points "i", accents, commas, etc.
C) ITEMS COMMON TO THE TWO SUBSCALES:
C.1) WRITING DRAWN:
67. Graphic bradykinesia (bradygraphy).
68. Increase in size.
69. Lack of scriptural rhythm.
70. Loose writing or without tension (Hypotonia or Atony).
These last 4 items are included in the two subscales, in the graphomotor subscale the items function like any of the others, since they refer to movement disorders (dyskinesias). In the cognitive subscale they are only added when they appear all together: the subject is drawing and not writing. When these four points appear together in a signature there is a high probability of cognitive impairment in the elderly.
C.2) SERIOUS IMPAIRMENT FEATURES:
71) Dyskinesia or dyssynergia in very wide movements (rubric).
72) General deterioration in all sections of the firm.
All the points of the previous scale are quantified in the following way:
SCORE 0. THE TRAIT DOES NOT EXIST.
SCORE 1. SLIGHT PRESENCE OF THE TRAIT.
Although the trait is found in some strokes or graphic elements, it appears incidentally or sporadically.
SCORE 2. AVERAGE PRESENCE OF THE TRAIT.
The trait is seen in a general way but not excessively.
SCORE 3. HIGH PRESENCE OF THE TRAIT.
The trait is observed in a recurring and constant way throughout the entire writing or a good part of it.
The writing above belongs to a healthy woman (case 2) who performed the word with agility and a correct kinetic melody, something that is verified when analyzing the pressure in the absence of the pigment (right image). In the image below, he suffered a neurodegenerative process, among whose manifestations we find the presence of a melokinetic apraxia that imposes a very poor and rudimentary sequential writing.
Factors and variables to take into account about the signature during Alzheimer's
Age
The probability of suffering from Alzheimer's increases with age. Although there are some quantitative differences between one and the other studies, it can be affirmed that from the age of 85 the possibility of suffering a dementia process due to Alzheimer's is 50%. On the other hand, Alzheimer's-type dementias, whether in its simple form or mixed with some type of vascular disorder, account for approximately 75% of all dementias (image 11).
Differential diagnosis
Differential diagnosis can be very complicated. Often the elderly will be affected by a myriad of pathologies that affect writing and that may seem like symptoms of cognitive dysfunction: osteoarthritis in the upper extremities or disorders in the peripheral nervous system that generate a very important graphic dysfunction, myopia, astigmatism, tremors or bradykinesia from other causes, etc. On the other hand, the causes responsible for the appearance of a demented condition are very numerous.
It is especially in the alterations that occur with specific language disorders where the diagnosis can be more complex, such as Broca, Wernicke, or conduction aphasia, resulting in significant apraxia and even complete agraphia. In this sense, having medical-clinical reports is almost essential and they will help us a lot, especially if we only have a few signatures. In many cases the differential diagnosis through writing or signing can be quite difficult if not impossible. It is always convenient to analyze which scriptural dimensions are deteriorated to a greater degree, since this specificity can often indicate some data of interest.
Characteristics of structural tests
The graphics of the signature is the last thing that deteriorates because its continuous testing promotes a greater degree of undercorticalization with respect to texts written according to different modalities. If we have a choice, what is relevant is that we have several signatures and some written text, and make an assessment of the following capabilities:
A. Write a text freely without model, free writing.
B. Write a text to dictation.
C. Copy a written text.
D. Sign multiple times.
Especially in the initial stages of senile deterioration it is very difficult to evaluate cognitive deterioration with the mere presence of a signature and without the aid of other writings. As an important indication, and according to our professional experience as well as the bibliographic review, in a typical case of Alzheimer's the first skill to be lost is A, the last D, passing through successive phases of loss of skills that more or less follow the previous progression. In many cases the subjects are capable of signing but almost totally incapable for a free-form text, a dictation, or to write familiar and common names, etc (Horner et al., 1986).
In the signature, the separate verification of each element according to the order of appearance in the graphic is pertinent. As a general rule, the proper name is better designed than the first surname, and this in turn better than the second surname. The proper name is heard more times, it is written more often in intimate letters, and this greater familiarity generates a greater preservation of the name to the detriment of the first surname, and this with respect to the second. This rule does not have to be necessary, you have to see each individual case, but it is the most common.
Control of learning acquired before the disease
The determination of the schooling, academic degree and profession of the signature writer.
The writings of unschooled subjects can maintain characteristics very similar to those of old age and those of Alzheimer's dementia (image-12), extremely precarious, full of corrections, misspellings, slow strokes, increased size, paragraphies and confusion, as well as other typical features. It is necessary that before deciding a deterioration through writing, the academic training and the possibility that the subject has had to facilitate the automatism in their professional and existential performance is known.
On the opposite line, in certain offices, notaries, magistrates, secretaries, it is required to be continuously signing to legally validate the documents. These subjects, as is evident, will have a better chance of preserving the intrinsic qualities of graphics for many more years due to increased exercise.
In our assessment of the general state of the patient affected by Alzheimer's it is necessary that we have signatures or other writings prior to the pathological process, we will not be able to properly analyze the state of a patient if we do not first have proof of how he signed and wrote, what has been altered and what has been the evolution of dysgraphia since its non-pathological state. However, in the absence of other data, on the scale we indicated certain dysgraphic features typical of Alzheimer's.
Drugs administered to the elderly with Alzheimer's
It is difficult to verify its effects in most cases, due to:
A) Diffusion of the affected brain area in the disease.
B) Large amount of drugs administered (other diseases concomitant with old age), and their possible interactions.
C) Elimination and absorption difficulties suffered by the elderly due to their physical condition.
Sex
According to numerous studies, and confirmed by our professional experience, women are more likely to suffer from Alzheimer's, however these results must be evaluated with caution due to the longer life expectancy of women.
Other variables that can be considered
- Locality, country: Rural or urban environment. Degree of industrialization or development of the country.
- Family history.: Level of academic training of parents, other cases in the family.
- Personality: There is a hypothesis that people who have exercised more memory and intellectual functions during their lives are less likely to suffer from Alzheimer's. At present these studies are premature and more data is lacking.
- Genetic inheritance: Numerous studies are carried out in this field but are still insufficient to establish reliable conclusions.
- Posture, support, scriptural tool, etc. The elderly often have to write with a thick black marker because they are unable to visualize the lines of the pens.
Practical case of alterations and perseverance of the firm in Alzheimer's
It belongs to a woman who left a series of signatures distributed over a period of 40 years, from 52 to 91 years old, the age at which she died from a cardio-respiratory arrest and with an Alzheimer's diagnosis on the certificate death physician. The first signature corresponds to the 52 years. We see in it the agility and ease with which the different curvilinear ellipses that adorn the writing succeed one another, the adequate proportionality of its components and the sustained rhythm that shows us the good neuromotor disposition of the author (image 14). There are, however, certain features that may seem indicative of a certain pathological process, but in essence this signature does not present any significant dysgraphia.
Applying the scale to the successive signatures (Im. 15) we see that the evolution of dysgraphia adjusts to the phenomenology described, a gradual deterioration over the years until reaching a general crisis in the last year of life, where neuromotor functions are severely impaired. This is the type of evolutionary pattern that we can find in the signatures of Alzheimer's patients. Note that the progression breaks his trajectory over 85 years, remaining stable in the preceding years. It is not necessary to explain the influence that trauma or specific injuries of a certain intensity (ischemia, hemorrhage, head trauma, etc.) could have on abrupt ascents.
The second signature that we present is at 86 years of age (image 16). The most indicative feature is the difficulty in designing ellipses and curvilinear gestures, a kinetic dyssynergy that affects the correct structure of the letters. Neuromotor dyssynergia is the breakdown of a complex movement in which different muscles and joints contribute. The execution of the letters requires a very fine adjustment of the muscle contractions of the distal limb to obtain a good result. In dysnergic disorders, movements become uncoordinated and imprecise, the patient cannot unitaryly execute an action that requires the consecutive action of a series of distal and proximal muscles, instead moving each joint sequentially,acting in a univocal way on the synergistic muscles and their antagonists but without keeping a sequence of continuity with the previous muscular activations. The consequence of such a decomposition of complex movement when making ovals, ellipses, and other graphic structures, is that the designs do not come out curved, but polygonal.
In reality, and as readers will have easily verified, we are clearly facing a pekinetic apraxia that divides and separates the graphic sequence into its units of movement, as perceived in the image. The volume "Neuropsychology" by Peña Casanova and Barraquer (1983) makes a complete review of this type of disorders:
(…) "A well-chosen, well-placed cinema imposes a perfect synergy of the agonist and antagonist muscles, an eventual kinesthetic and visual control, and furthermore, its execution is not isolated, inscribing itself in a chain that constitutes the kinetic melody. Disturbance at this level constitutes motor (pekinetic) apraxia. " (…)
(Peña C. J, Barraquer B. LL. Neuropsychology. Ed. Toray, 1983)
The "cinema" is the elementary unit of simple movement, and is understood by the unit of muscular contraction and its corresponding antagonistic disinhibition. The following text, by the same authors, is very interesting:
(…) "The skilled worker - Luria comments - loses the ability to carry out the successive system of movements that he normally executed. The musician is disoriented before his instrument, losing the ability to carry out the successive system of automatisms previously acquired. An amusia appears instrumental The writing is altered and each feature of the graphemes requires a special effort The typographer loses speed and his work is increasingly clumsy.
"The patient behaves as if he were performing the movements that are part of his habitual repertoire for the first time, as if he had never performed the acquired dynamic stereotypes." (…)
Finally, we present the brilliant description of Serratrice-Habib, which does not require special comment:
(…) "Finally, motor apraxia, traditionally called melokinetic, that is to say, affecting the performance of the gesture by the extremity of the limb, is a disorder of the synergy of the agonist and antagonist muscles, and of the kinetic melody of the movement, according to Luria's expression, that is, the harmonious succession of the different movements that make up the gesture. The speed, finesse and dexterity of the movement are affected. Its expression is unilateral. Its exact place in pathology has been discussed often and in It is sometimes considered an intermediate disorder between apraxia and paralysis. On the other hand, it is sometimes called innervation. It is contralateral to the causal lesion that affects the premotor frontal area and the anterior parietal region. " (…) (G. Serratrice, M Habib. Writing and Brain, Ed. Masson, 1997).
Continuation of the case study
The following signature was made when she was 91 years old (image 17), the age at which the patient died. It is evident that the automatism has degraded substantially. Apart from the various types of tremor, there are other typical scriptural features of old age that do not by themselves indicate a cognitive deterioration, they are those that affect the speed, rhythm and pressure of writing (see scale), and that we have included as Dyskinesias. Which, although they are fundamental for the calligraphic comparison and identification of signatures, they are not so fundamental to draw inferences about the psychic functionality of the elderly because their etiology may be more related to the nervous and spinal periphery than to the encephalic one. We are now, therefore, with an ideomotor apraxia.
Peña Casanova's book introduces this section with a text by Ajuriaguerra (1975):
(…) "It is the apraxia of the simple gesture; the ideational plan of complex activities is preserved; such activities are only altered at the level of their fragments and not in the harmony of their totality (De Ajuriaguerra, Hecaen and Angelergues, 1960)" (…)
In another section they describe the vision of Signoret and North (1979):
(…) "Ideomotor apraxia is, for Signoret and North, a disturbance that affects the selection and combination of cinemas. Gestural performance offers a global impression of clumsiness; the well-chosen gesture can be identified, but some of its components, cinemas, are erroneous, displaced. For example, in the military salute, the hand is placed wrong and in an inappropriate place on the head. (…)
We present the Serratrice-Habib perspective:
(…) "Ideomotor apraxia is an alteration of the elemental motor act. The concept of movement is correct, the gesture is chosen well, but it is full of spatial and temporal errors that produce the impression of clumsiness, of which the patient is aware Words are slowly and laboriously arranged in an irregular way, and displaced, with a distortion of graphemes, which are disorganized or with a kind of literal paragraphy. In these cases, anomalies are observed both in the copy and in the dictation. it is a deficient execution of the symbolic gesture of writing, which Morlaas once interpreted as spatial dyskinesia, an exaggerated interpretation because it does not constitute a primary anomaly of the representation of space. " (…)
The authors define this type of apraxia in other ways such as graphic-constructive or merely constructive apraxia. The essential is exposed: "an alteration of the elemental motor act" (Serratrice, 1993), with a preservation of the "ideational plan" of the activity (Ajuriaguerra, 1960). And these are the two main ideas in our opinion. The cognitive functions of linguistic communication, the graphemic or lexical-semantic selection are preserved, but there is a motor dysfunction that alters the entire sequence of activity in a substantial and relevant way, the graphic-scriptural distortions of this type of apraxia can be very varied depending on the area or section affected (image 17).
Image 17. Graphic idemotor apraxia. The lack of pressure and firmness is evident, the gestures are thrown but without force, the outlined shapes without success, some lines are unsaturated, with numerous pastosities due to an incorrect inclination of the tool on the surface of the blade.
The last signature is also at the age of 91 (image 18) and is the closest to the date of death. This writing is much more deficient in terms of morphology, inequalities and general appearance.
This signature is not properly writing, but rather a highly deficient drawing that we can include within the so-called Scriptural Ideatoria Apraxia. Serratrice-Habib's review is very clear:
(…) "The ideational apraxia, sometimes described as an alteration of the gestation is an alteration of the idea of the complex gesture, whose internal model is no longer evoked. The plan of the sequence of the action to be executed is no longer conceived. There is a disorder of the knowledge of the use of objects, which led Morlaas to interpret ideational apraxia as an agnosia of use. Loss of the gestate alters the set of the gesture, both symbolic - mimicking the writing - and concrete - manipulating the pencil or the pen.. However, the degree of alteration is inversely proportional to the degree of automation. A simple gesture, often repeated, such as removing the cap from the pen, does not require recourse to gestation. It is carried out automatically. Parapraxias, that is to say, one gesture for another,the most common example being that of a patient who writes with keys or scissors. Baxter and Warrington described an exemplary case of ideational agraphy that "(…)" was not related to manipulation, but to the symbol of writing. These researchers interpret it as a defect of access to the storage of the graphomotor engrams and the pattern of the motor sequences. In reality, the alteration of the writing was isolated and independent of any other apraxic manifestation. The patient, protruding from a left parieto-occipital glial tumor, was unable to write letters or words when dictated, but was able to copy them again. It also recognized and spelled letters and words. In this way, when a model was presented to him, he could execute the graphic movement. However,in the absence of an external model, it did not use the internal model. This could correspond "(…)" to a defect of access to the sequences of the program of the graphomotor standards. "(…)
Regardless of the cognitive function or mechanism that is "altered", the fundamental thing is that "the internal model stops being evoked". The symbolic-scriptural gestemas, the sequential motor patterns of writing, the kinetic melody, the motor engrams of the letters, the graphic-motor praxia (whatever you want to call it), we no longer find it in the internal space of our mind. It may be because it is no longer recognized (functional agnosia), or because it no longer exists because of deterioration or disease. The subject can copy the letters using mechanisms similar to those of the child who is learning to write, but cannot write by dictation or make a sentence freely.
The sequential pattern of scriptural movements has an execution plan, this plan supposes an anticipation of the graphic-motor activity, in a certain way it can be said that it is done before being carried out. This previous plan has disappeared. The writing would no longer be properly so, but rather a drawing. The last phases of the deterioration of the elderly are characterized by a global destruction of writing ability, all the dynamic play of tensions, pressures, different speeds and rhythms (all the harmony of the kinetic melody) with which writing is designed has disappeared, in instead we see a very slow layout, a slowness that is necessary so as not to err in the structural form that it is intended to imitate. The pressure of the line can now be light or heavy, as if the tool had an excessive weight,or as if the hand did not have enough force to press on the paper and saturate it with ink. It also increases the size, since the elderly need visual-motor feedback to see what he is really writing. The ability to write with closed eyes is forbidden in the elderly as in the child, they need to visually follow the result of their graphic movements step by step.
Apart from the features that concern language or written expression (ultimately essential), there are certain motor features that may not be indicative of Apraxia Ideatoria in Alzheimer's.
- Graphic bradykinesia (bradygraphy).
- Increase in size.
- Lack of scriptural rhythm.
- Loose or tensionless writing (Dystonia or Atonia).
There are other concomitant features, but the previous four seem to us the most demonstrative and revealing.
Results of the case study
The results show well-defined stages in the writing impairment of Alzheimer's, at least in this case. In image 20 we see the different evolution of the graphomotor subscales: motor dyssynergia, dyskinesia and graphic drawing. Three phases or defined graphical states that are summarized below:
1) Dysynergic Phase: Predominance of dyssynergia, with abundant rectilinear lines, angular and polygonal writing, while dyskinetic features remain contained. The period covers firms between 73 and 86 years old.
2) Dyskinetic Phase: A second period corresponds to two of the last firms located in the 91 years; tremor predominates in all its modalities, torsions, alterations in pressure and lack of muscle tone. They involve movement disorders unrelated to dyssynergic processes. Which ostensibly descend.
3) Phase of the Graphic Drawing: The third period corresponds to the last signature or Terminal phase of the patient. We call it "Graphic Drawing", and it shows abundant dyskinetic features apart from those of drawn writing, as we saw in a previous section.
Image 21 also shows the progressive evolution of motor dysgraphia in the face of stagnation of cognitive traits in a wide range that covers from 50 to 85 years. Then, from the 90s, cognitive increases substantially in a strong trend of global deterioration. The assessment that we can make is that the writing automatism is preserved in parallel with the increase in dysgraphic processes of neuromotor etiology. We see in the last three signatures, corresponding to 91 years, a characteristic reflection of the generalized Alzheimer's crisis.
The scale has also been applied separately to the first and last names to analyze the variable called Reinforced Learning by Family Graphics test. The results confirm its full influence. Image 22 shows how the surname suffers more directly from the deterioration progress than the signatory's own name (20.8% less on average). Note, however, how both graphics maintain a similar trend of evolution until practically the last months of the patient's life, where the degradation of the writing affects all the components of the signature equally without distinction, however, it is the name's resistance to graphic degradation is striking.
To finish we will say that we have verified the evolution exposed in many other cases, without this meaning that it is a fixed nor axiomatic tonic. It is convenient not to lose sight of the variables exposed in the previous section.
Conclusions of the case study
1. The signature is a bad indicator of the degree of deterioration in its initial and intermediate stages due to the influence of the Reinforced Learning Variable per trial. That promotes the continued performance of an acceptable signature that does not reflect neuromotor impairment. The best indicator of the deterioration of the patient is in direct relation with the non-dependent functions of the aforementioned variable, in this sense, a handwritten text either dictated, copied or freely written.
2. The name is more resistant to graphic degradation than the surnames. The influence Variable Learning Reinforced by essays is directly proportional to the ordinal place that the elements occupy within the signature, in this sense: 1st) Name, 2nd) First Surname, 3rd) Second surname.
3. The neurographic deterioration of the signature is concomitant with the critical deterioration of patients in their final stages. It is possible to understand that at this stage there is a serious alteration of the somatic seating (subcortical, cerebellar, cortico-spinal, etc.) of the Reinforced Learning Variable per trial.
4. Three main stages of senile graph deterioration or Alzheimer's are detected, without this meaning that they are the only typologies (there are others), necessary or generalized. These phases are: 1st) Dysynergic (peachine apraxia), 2nd) Dyskinetic (ideomotor apraxia), and 3rd) Graphic Drawing (ideational apraxia). The prevalence of one of the phases in the evolution of the deterioration is verified in all cases. The first being dyssynergic and the last being the graphic drawing.
5. In the dyssynergic and dyskinetic neurographic stages, both scales are inversely proportional. Dysynergia predominates in the early stages (approx. 70 to 80 years), and is displaced by dyskinetic factors as age and deterioration progress. In the final stages, dyskinetic dysgraphic features predominate without excluding the former.
6. The significant general impairment (motor and cognitive) coincides with the last and most dysgraphic stage: drawn writing. This stage includes a very intense ideational apraxia and drawn morphological creation. It is inferred that the graphic drawing stage is concomitant to the cessation of the influence of the Variable "Reinforced Learning by trial". In the graphic drawing stage, all the elements of the signature deteriorate regardless of their location within the signature and their greater or lesser familiarity.
7. The Graphic drawing stage is concomitant with a decrease in dyskinetic traits and a significant increase in Cognitive dysgraphic Traits, as well as the following Traits: Large size, Hypotonia, Arrhythmia and Bradygraphy. Likewise, it coincides with important malformations in the rubric.
The above conclusions do not affect people with a poor level of education.
This article is merely informative, in Psychology-Online we do not have the power to make a diagnosis or recommend a treatment. We invite you to go to a psychologist to treat your particular case.
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