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Revista Mexicana de

NeurocienciaPublicación oficial de la Academia Mexicana de Neurología A.C.

Órgano Oficial de Difusión de la AMN

AcademiaMexicana deNeurología, A.C.

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ONAC

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Vol. 18, núm. 6 (noviembre-diciembre de 2017)

Editorial committee 2017Chief editor: Dr. en C. Ildefonso Rodríguez Leyva [email protected]: M.C. Carolina León Jimenez Dr. en C. Antonio Arauz Góngora [email protected] editor: Dra. Lilia Núñez OrozcoEmeritus editor: Dr. en C. Carlos Cantú Brito

International editorial comitee

National editorial comitee

Dr. Anthony Amato Dr. José BillerDr. Andre KannerDra. Farrah MateenDr. José Merino

Dr. Sergio de Jesús Aguilar Castillo Dr. Marco Antonio Alegría LoyolaDra. Alma Yolanda Alvarado GutierrezDr. Carlos Gabriel Ascanio RodríguezDra. Catherine Boll WoehrlenDr. Antonio Bravo OroDr. Jorge Burgos CentenoDra. Graciela Cárdenas HernándezDr. Paul Carrillo MoraDra. Teresa Corona VázquezDra. Beatriz ChavezDr. Bruno Estañol VidalDra. Agnes FleuryDr. José Flores RiveraDra. Silvia GarcíaDr. Fernando Góngora RiveraDra. Margarita González CruzDra. Alejandra González-DuarteDr. Oscar González-Vargas

Dr. Rubén Haro Silva Dr. Juan Calixto Hernández AguilarDr. Héctor Gerardo Hernández RodríguezDr. Jesús Higuera CallejaDr. Javier Jaramillo de la TorreDr. Humberto Juárez JiménezDr. Rubén Martínez HernándezDra. Iris E. Martínez JuárezDra. Adriana Martínez MayorgaDr. Francisco Mena-BarrancoDra. Roxana Millán CepedaDra. Rebeca Millán GuerreroDr. Alberto Mimenza AlvaradoDra. Leticia Munive BaezDr. Luis Manuel Murillo BonillaDr. Alfredo Ponce de LeónDr. Guillermo Punzo BravoDra. Sandra Quiñones AguilarDra. María Teresa Reyes

Héctor Gerardo Hernández RodríguezMaestro Alejandro GarcíaRebeca BarrosoDesign Cortex

Statistical AdvisorStyle corrector

TranslatorDesign

Dra. Mayela Rodríguez ViolanteDr. Leopoldo Rivera CastañoDr. Ulises Rodríguez OrtizDr. Francisco Rogel OrtizDr. Luis Ángel Ruano Calderón Dra. Angélica Ruiz-FrancoDr. José Luis Ruiz-SandovalDr. José Manuel Sandoval RiveraDr. Daniel San JuanDr. Horacio Sentíes MadridDra. Mónica Sierra del RioDra. Ana Luisa Sosa Ortiz Dr. José Luis Soto-HernándezDr. Gersain Trujillo AlonsoDr. Steven Vargas CañasDr. Rubén Darío Vargas GarcíaDra. Karina Vélez JiménezDr. Marco Zenteno Castellanos

Dr. José Obeso Dr. Julio PascualDr. Marc Patterson Dr. Eduardo TolosaDr. Samuel Wiebe

Contenidos ContentsGUÍAS DE PRÁCTICA CLÍNICA• Recomendaciones sobre el diagnóstico

y tratamiento de la polineuropatía desmielinizante inflamatoria crónica

CONTRIBUCIONES ORIGINALES• Quejas subjetivas de memoria en población

geriátrica y sus factores asociados: estudio piloto en población mexicana

• Funciones ejecutivas y conducta de estudiantes secundarios ecuatorianos

• Desarrollo y salud en el diagnóstico en trastorno por déficit de atención / hiperactividad

REVISIONES • Cefaleas por esfuerzo• Ganglios Basales y Conducta• Infecciones del Sistema Nervioso Central,

parte 2: neuroinfecciones en pacientes con Infección por Virus de Inmunodeficiencia Humana

REPORTES DE CASO• Marchiafava bignami: reporte de un caso y

revisión de la literatura

EDITORIAL• Carta Editorial por Ildefonso Rodríguez Leyva

CLINICAL PRACTICE GUIDELINES• Recommendations on the diagnosis

and treatment of chronic inflammatory demyelinating polyneuropathy

ORIGINAL CONTRIBUTIONS• Memory subjective complaints in geriatric

population and its related factors: a pilot study in Mexican population

• Executive functions and behavior of ecuadorian high school students

• Development and health in the diagnosis in attention-deficit / hyperactivity disorde

REVIEWS• Falta título• Basal Ganglia and Behavior• Infectios of the Central Nervous System, part

2: neuroinfections in patients with Infection by Human Immunodeficiency Virus

CASE REPORTS• Marchiafava-Bignami: case report

EDITORIAL• Editorial Letter by Ildefonso Rodríguez Leyva

Revista Mexicana de Neurociencia November-December, 2017; 18(6):1-18

Systemic review Clinical practice guideManagement of chronic inflammatory demyelinating polyneuropathy

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Recommendations for the diagnosis and treatment of chronic inflammatory demyelinating polyneuropathy

Recomendaciones sobre el diagnóstico y tratamiento de la polineuropatía desmielinizante inflamatoria crónica

Clinical practice guide

Edwin Steven Vargas-Cañas,1 Erwin Chiquete,2 Luis A. Ruano-Calderón,3 Elizabeth León-Manríquez,1 Mónica Edith Salmerón-Mercado,1 Noel Isaías Plascencia-Álvarez,4 Gabriela Madrigal-Salas,2 David Gilberto Zúñiga-García,1 Humberto Juárez-Jiménez,5 Raúl Carrera-Pineda6

1 Neuromuscular Diseases Clinic, National Institute of Neurology and Neurosurgery “Manuel Velasco Suárez,” Mexico City, Mexico. 2Neuromuscular Diseases Clinic, Department of Neurology and Psychiatry, National Institute of Medical Science and Nutrition “Salvador Zubiran,” Mexico City, Mexico. 3Department of Neurology, Durango General Hospital, Durango, Mexico. 4Department of Neurology, ISSSTE National Medical Center “20 de Noviembre,” Mexico City, Mexico .5Department of Neurology, General Hospital “Doctor Gaudencio González Garza” at the IMSS National Medical Center “La Raza,” Mexico City, Mexico. 6Department of Neurology, IMSS National Medical Center “Siglo XXI,” Mexico City, Mexico.

Abstract

Introduction. Chronic inflammatory demyelinating polyneuropathy (or polyradiculoneuropathy, CIDP) is an uncommon entity of very heterogeneous clinical behavior, but susceptible to treatment. Several proposals on electrophysiological diagnostic criteria exist as well as numerous studies on the response to immunomodulatory treatments. The general consensus about its diagnosis and management, however, has not been reached in Mexico through its major health institutions.

Objective. To develop a guideline on definition, diagnosis and treatment of the CIDP by using the best existing scientific evidence and when not available, the consensus of experts.

Methods. A group of neurologists of Mexican institutions pertaining to the Study Group of Neuromuscular Diseases of the Mexican Academy of Neurology carried out a MEDLINE and Cochrane systematic reviews search, selecting the best available evidence and qualifying the recommendations according to the GRADE (Grading of Recommendations Assessment, Development and Evaluation) system. The recommendations are organized into short statements that are supported by a brief dissertation on the scientific evidence of which the statements derived.

Recommendations. This panel recommends testing and diagnostic criteria proposed by the EFNS/PNS (European Federation of Neurological Societies / Peripheral Nerve Society) that are described in the present document. For treatment aspects, this panel recommends intravenous immunoglobulin or steroids as first line treatment for the classical sensorimotor forms of CIDP, immunoglobulin exclusively for pure motor forms and plasma exchange in case of treatment failure



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Resumen

Introducción. La polineuropatía (o también polirradiculoneuropatía) desmielinizante inflamatoria crónica (PDIC) es una entidad infrecuente, de comportamiento clínico muy heterogéneo, pero susceptible de tratamiento. Existen varias propuestas sobre los criterios de diagnóstico electrofisiológico, así como numerosos estudios sobre la respuesta a tratamientos inmunomoduladores. El consenso general sobre su diagnóstico y manejo, sin embargo, no se ha alcanzado en México a través de sus principales instituciones sanitarias.

Objetivo. Elaborar una guía sobre definición, diagnóstico y tratamiento de la PDIC utilizando la mejor evidencia científica existente y cuando no esté disponible, el consenso de expertos.

Métodos. Un grupo de neurólogos de instituciones mexicanas y pertenecientes al grupo de estudio de Enfermedades Neuromusculares de la Academia Mexicana de Neurología realizó una búsqueda en MEDLINE y revisiones sistemáticas Cochrane, seleccionando la mejor evidencia disponible clasificando la recomendación de acuerdo al sistema GRADE (Grading of Recommendations Assessment, Development and

Palabras claveDefinición, diagnóstico, guía de práctica clínica, tratamiento, polineuropatía desmielinizante inflamatoria crónica.

Corresponding Author:≠Dr. Edwin Steven Vargas-Cañas. Clínica de Enfermedades Neuromusculares. Instituto Nacional de Neurología y Neurocirugía “Manuel Velasco Suárez”. Insurgentes Sur, 3877. Col. La Fama. CP 14269. Tlalpan, México DF, México. Fax: +52-51710890. E-mail: [email protected]

KeywordsClinical practice guideline, chronic inflammatory demyelinating polyradiculoneuropathy, definition, diagnosis, management, treatment.

or incomplete response to immunoglobulin or steroids. In case of inappropriate response or required high doses or long periods of first-line drugs, immunomodulatory adjuvant therapy should be considered alone or in combination.

Evaluation). Las recomendaciones se organizan en enunciados breves que son sustentados por una breve disertación sobre la evidencia científica de la que derivaron.

Recomendaciones. Este panel recomienda utilizar las pruebas y criterios diagnósticos propuestos por la EFNS/PNS (European Federation of Neurological Societies/ Peripheral Nerve Society), mismos que son expuestos en este documento. El panel recomienda la inmunoglobulina humana o esteroides como primera línea de tratamiento para las formas sensitivo-motoras clásicas de la PIDC, exclusivamente inmunoglobulina para la PDIC motora pura y en caso de falla a inmunoglobulina o esteroide debe ser considerado el recambio plasmático. Si la respuesta es inapropiada o se requieren dosis altas o largos periodos con los medicamentos de primera línea, debe ser considerada la terapia coadyuvante sola o combinada con inmunomoduladores.



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IntroductionChronic inflammatory demyelinating polyneuropathy (CIDP—also known as chronic inflammatory demyelinating polyradiculoneuropathy) is the most common of chronic autoimmune neuropathies.1 It is a group of acquired disorders of the peripheral nerves and nerve roots that converge in a pathogenesis common to all of them: the immune-mediated demyelination of the peripheral nerve.1,2 For many decades there have been descriptions of patients with disorders that would today be considered CIDP. The reader should be aware, however, that clinical descriptors are evolving as new scientific evidence accumulates, so the CIDP concept is now considered an “umbrella” descriptor that groups conditions with shared pathogenesis, but whose clinical presentation, subtype of immunopathogenesis, prognosis, and response to treatments is actually very heterogeneous.1-3

The estimated prevalence of CIDP in the different populations of the world is as wide as 0.8 to 8.9 per 100,000 inhabitants.1 These estimates are derived from developed countries and, notably, in Mexico, there are no estimates or direct measurements of the health burden of this entity. CIDP can affect all ages but is more common in men over 40 years old. It is believed that progressive forms are more common in older subjects, while recurrent forms are seen more in younger patients.3 The classic, pure course with relapses and remissions occurs in a third of patients and the rest is thought to have a single-phase progressive course. However, it is possible that this classification might be reductionist and does not capture the essence of the temporary clinical behavior of CIDP, since perhaps the majority of patients considered with “pure” progressive forms have a superimposed course of relapses over a behavior of progression (mixed or recurrent-progressive forms).2,3

No specific predisposing factors for CIDP have been identified, although about 50% of patients have diabetes mellitus or carbohydrate intolerance (prediabetes states), but this, of course, is not specific to CIDP and the diagnosis of this entity

in subjects with diabetes mellitus can often go unnoticed because it is thought to be a diabetic neuropathy, whose pathogenic base is essentially toxic-metabolic.4 It is possible that in certain populations, like in Mexico, many patients with CIDP are misdiagnosed with diabetic neuropathy. However, this has not been adequately addressed in quality observational studies.

Whether CIDP is a disease or a syndrome continues to be controversial. Independently of this, currently we recognize clinical variants of CIDP that have chronicity, demyelination, inflammation, or immune mediation in common:1-4 Lewis-Sumner syndrome or multifocal acquired demyelinating sensory and motor neuropathy (MADSAM), pure motor CIDP, sensory-predominant CIDP, focal CIDP, acute-onset CIDP, chronic autoimmune sensory polyneuropathy, distal acquired demyelinating symmetric neuropathy (DADS), and demyelinating neuropathy associated with demyelination of the central nervous system. In contrast, most authors currently consider the following as separate syndromes (non-variants of CIDP) of chronic demyelination of the peripheral nervous system (PNS): multifocal motor neuropathy, distal demyelinating neuropathy with paraprotein IgM with or without anti-MAG (myelin-associated glycoprotein), demyelinating neuropathy with paraprotein IgG or IgA (monoclonal gammopathy of undetermined significance or MGUS), POEMS syndrome (Polyneuropathy, Organomegaly, Endocrinopathy, Monoclonal protein, Skin changes) and demyelinating neuropathies associated with systemic diseases (e.g. hepatitis B or C, HIV, lymphoma, diabetes mellitus, systemic lupus erythematosus and other collagenopathies, dysthyroidism, bone marrow transplant, nephrotic syndrome, and inflammatory bowel disease). The classification of inflammatory demyelinating neuropathies will continue to evolve as specific immune mechanisms are clarified.

This document aims to describe the results of a systematic review of diagnosis and management of CIDP, to serve as the scientific basis for the shaping of recommendations on these topics.



5

MethodsA working group formed by clinical neurologists with knowledge and interest in neuromuscular diseases was convened. Questions and topics about the diagnosis and treatment of CIDP were posited and an agreement was reached. This produced an agenda for a 12-hour face-to-face session distributed over a day and a half. Prior to the meeting, the topics and clinical questions were distributed among the participating clinicians for response and development in two groups of panelists. The members of the working group systematically formulated the pertinent answers to the questions posed according to the recommendations of the GRADE system (Grading of Recommendations Assessment, Development and Evaluation)(Table 1).5,6 Briefly, this system is mainly a series of steps to organize the systematized answer of clinical questions of interest, particularly with respect to diagnosis and treatment. It focuses mainly (but not exclusively) on qualifying the quality of the evidence and thus formulating a recommendation structured in a concise statement, which is properly the answer to the clinical question posed.

The workgroup agreed to use the GRADE system in order to systematize the development of the document and to evaluate the evidence, in order to offer the user of the guide certainty about the knowledge that supports each recommendation. The workgroup, however, is aware that there is no system for classifying the evidence that is perfect and that none of them have been scientifically proven in a proper way to support its use over the other systems. That is to say, so far we cannot know which system is the best; nevertheless, this method was chosen because it is widely used today and because it has the strength to provide texts that are easy to understand without excessive use of technicalities. The working group formulated recommendations for clinical practice based on evidence that provides a systematic review, with which semi-axiomatic principles on health care were formulated, considering equally the judgments about the perceived risk-benefit ratio

and costs of interventions, as well as the values and preferences of patients.

MEDLINE and PubMed were searched for articles on CIDP with specific keywords and MeSH terms in English related to the design of the study, treatment, and disease, as follows:

#1. Chronic inflammatory demyelinating polyneuropathy#2. CIDP#3. Long-term#4. Diagnosis#5. Treatment#6. Therapy#7. Trial#8. Clinical trial#9. Controlled trial#10. Randomized clinical trial#11. Guideline#12. Open-label study#13. Observational study#14. #1 AND #2#15. #2 AND #3#16. #1 AND #4#17. #3 AND #4#18. #1 OR #2 OR #3 OR #4 OR #5 OR #6 OR #7#19. #8 OR #9 OR #10 OR #11 OR #12#20. #13 OR #14 OR #15#21. #16 AND #17 AND #18

No date restrictions were applied to the searches. Additionally, reference lists of the selected relevant articles were searched manually. The evidence and recommendations were classified according to the GRADE system (Table 1).5 When only very low quality evidence was found (opinions of other expert panels, clinical anecdotes, or the working group’s own experience), the team made an attempt to reach a consensus and the recommendations were classified as “good practice points.”

The statements were reviewed one by one by all the members of the working group and were



8

Are there other useful neurophysiological tests to establish the diagnosis of CIDP?This panel suggests performing somatosensory evoked potentials (SEPs) especially in patients with the variant of sensory CIDP or atypical clinical presentations. (Good practice point)Somatosensory evoked potentials may be useful to demonstrate alteration of proximal sensory conduction, particularly in sensory CIDP18,19 and may contribute to the diagnosis of CIDP when neuroconduction studies result insufficient to detect peripheral demyelination.20

Clinical phenotypeSensorimotor, distal and proximal, symmetric,

evolution >8 weeks.

Sensory predominant, it can develop minor

motor symptoms, distal and proximal,

symmetrical, evolution >8 weeks.


motor symptoms, distal, symmetrical, evolution

>8 weeks.

Sensorimotor, distal and proximal, symmetrical,

evolution 8 weeks.

Sensory ataxia, distal and proximal, symmetrical,

evolution >8 weeks.

Predominantly motor, distal and proximal,


Sensorimotor, focal, can progress to diffuse form

with time, asymmetrical, evolution >8 weeks.

Clinical variantTypical CIDP

Sensory CIDP

DADS

Acute-onset CIDP

Lewis-Sumner syndrome (MADSAM)

Chronic autoimmune sensitive polyneuropathy

Motor CIDP

Focal CIDP

Frecuency (%)40–01

4–35

2–17

2–16

6–15

5–12

4–10

0-5–1

The percentages do not necessarily add up to 100% due to the variability of the distribution of the variants among the different populations.DADS: distal acquired demyelinating symmetric neuropathy.MADSAM: multifocal acquired demyelinating sensory and motor neuropathy.

Table 2. Currently recognized clinical variants of chronic inflammatory demyelinating polyradiculopathy (CIDP).

Is the repetition of the neurophysiological protocol valid when there is a high clinical suspicion which did not meet the criteria proposed by the EFNS/PNS for CIDP in the initial evaluation?This panel suggests repeating the neurophysiological evaluation proposed by the EFNS/EPN, in case of not meeting the criteria for definitive CIDP in the initial evaluation. (Weak recommendation, low quality of evidence: 2C)If the electrodiagnostic criteria are not initially met for definitive CIDP, repetition of the study at a later date should be considered. This can avoid false negatives and could narrow the differential diagnosis.10



7

motor nerves in suspicion of CIDPThis panel recommends performing neuroconduction tests to explore at least four motor nerves, using the demyelination diagnostic criteria proposed by the EFNS/PNS. (Strong recommendation, high quality of evidence: 1A)The criteria of the European Federation of Neurological Societies and Peripheral Nerve Society (EFNS/PNS)3 have a sensitivity of 81% and specificity of 96% to establish the diagnosis of CIDP, compared to the original criteria proposed by the American Academy of Neurology (AAN) (100% specificity and 45% sensitivity).7-12 According to the criteria met, the diagnosis of definitive, probable, or possible CIDP can be established (Table 3). The sensitivity of electrodiagnostic criteria for motor nerves can be improved by examining more than four nerves, including proximal stimulation in the upper limb13,14 and examining sensory nerves.15,16

To apply these criteria, evaluate the nerves median, ulnar (stimulus below the elbow), peroneal (stimulus under the fibular head), and tibial on just one side. If the criteria are not met, the same nerves are evaluated contralaterally and/or the median and ulnar nerves are stimulated bilaterally in the armpit and Erb’s point. The blockage of the motor conduction is not considered in the ulnar nerve in its passage through the elbow and there must be at least 50% reduction in the amplitude between Erb’s point and the wrist to consider a probable conduction block. The temperature should be maintained at least 33°C in the palm and 30°C in the external malleolus.3

Usefulness of neurophysiological evaluation of sensory nerves in suspicion of CIDPThis panel recommends conducting sensory neuroconduction to patients with clinical suspicion of typical or atypical CIDP. (Weak recommendation, low quality of evidence: 2C)The sensitivity of the electrodiagnostic criteria for motor nerves can be improved by examining more than four nerves, including proximal stimulation in the upper limb,13,14 and there are reports of cases where atypical CIDP was suspected where the examination of sensory nerves increased the diagnostic certainty.15,16

onset forms. The latter ones are challenging to distinguish from Guillain-Barré syndrome (GBS).1

The mechanism of injury is undoubtedly immune-mediated. The experimental models of allergic neuritis and the histopathological similarities with GBS support this premise; however, the immunopathogenesis remains imprecise. To date, no triggering event has been identified, the exposure of individuals genetically susceptible to various environmental or infectious agents has been proposed on multiple occasions without being able to firmly establish the association.1 Recently, autoantibodies against the paranodal proteins contactin-1 (CNTN1) and NF155 have been described in a small subgroup of patients with CIDP with a homogeneous clinical pattern. Outside of these associations, pathogenic autoantibodies or specific antigens are unknown in the PNS.4 Isolated reports of CIDP associated with tumors (melanoma) or post-vaccination suggest that molecular mimicry could be involved in the pathogenesis.1-3

The diagnostic suspicion is established based on suggestive clinical manifestations. The typical CIDP (which is not precisely the most common) presents with at least eight weeks of evolution of distal paresthesias with stocking/glove distribution, symmetric, with progressive distal paresis and eventual involvement of shoulder girdle and pelvic girdle, which can progress to loss of autonomic ambulation and the appearance of atrophy. Still, this is not the only clinical presentation of CIDP, which has led to the recognition of clinical variants (Table 2).

Diagnostic criteria Given the wide phenotypic variability (50% of cases), the protocol of diagnostic auxiliaries becomes relevant to confirm the diagnostic certainty and reasonably exclude differential diagnoses. In this vein, the pertinence of lumbar punctures, electrophysiology studies, magnetic resonances, and peripheral nerve biopsies will be weighted according to the best evidence available in the body of this document.Electrophysiological criteriaUsefulness of neurophysiological evaluation of



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Are there other useful neurophysiological tests to establish the diagnosis of CIDP?This panel suggests performing somatosensory evoked potentials (SEPs) especially in patients with the variant of sensory CIDP or atypical clinical presentations. (Good practice point)Somatosensory evoked potentials may be useful to demonstrate alteration of proximal sensory conduction, particularly in sensory CIDP18,19 and may contribute to the diagnosis of CIDP when neuroconduction studies result insufficient to detect peripheral demyelination.20

Fenotipo clínicoSensorimotor, distal and proximal, symmetric,

evolution >8 weeks.


motor symptoms, distal and proximal,



motor symptoms, distal, symmetrical, evolution

>8 weeks.

Sensorimotor, distal and proximal, symmetrical,

evolution 8 weeks.

Sensory ataxia, distal and proximal, symmetrical,

evolution >8 weeks.

Predominantly motor, distal and proximal,


Sensorimotor, focal, can progress to diffuse form

with time, asymmetrical, evolution >8 weeks.

Clinical variantTypical CIDP

Sensory CIDP

DADS

Acute-onset CIDP

Lewis-Sumner syndrome (MADSAM)

Chronic autoimmune sensitive polyneuropathy

Motor CIDP

Focal CIDP

Frecuencia (%)40–01

4–35

2–17

2–16

6–15

5–12

4–10

0-5–1

The percentages do not necessarily add up to 100% due to the variability of the distribution of the variants among the different populations.DADS: distal acquired demyelinating symmetric neuropathy.MADSAM: multifocal acquired demyelinating sensory and motor neuropathy.

Table 2. Currently recognized clinical variants of chronic inflammatory demyelinating polyradiculopathy (CIDP).

Is the repetition of the neurophysiological protocol valid when there is a high clinical suspicion which did not meet the criteria proposed by the EFNS/PNS for CIDP in the initial evaluation?This panel suggests repeating the neurophysiological evaluation proposed by the EFNS/EPN, in case of not meeting the criteria for definitive CIDP in the initial evaluation. (Weak recommendation, low quality of evidence: 2C)If the electrodiagnostic criteria are not initially met for definitive CIDP, repetition of the study at a later date should be considered. This can avoid false negatives and could narrow the differential diagnosis.10



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1. Definitive CIDP: at least one of the followingA. Prolonged distal motor latency ≥50% above the ULN in two nerves (excluding carpal tunnel syndrome), or

B. Reduction of the CV ≥30% under the LLN in two nerves, or

C. F waves with prolonged latency ≥30% of the ULN in two nerves (≥50% if the amplitude of the negative peak

CMAP is 30% increase in duration between proximal and distal negative peak

CMAP) in at least two nerves, or

G. Duration of distal CMAP (interval between the beginning of the first negative peak and the return to

baseline of the last negative peak) increased in at least one nerve (median 6.6 ms, ulnar 6.7 ms, peroneal 7.6 ms,

tibial 8.8 ms) (b) + at least some other demyelination parameter in at least some other nerve (a)

2. Probable CIDP≥30% reduction of the amplitude of the proximal negative peak CMAP in relation to the distal, excluding the

posterior tibial nerve, if the distal negative peak is ≥20% of the LLN in two nerves, or in one nerve + at least

some other parameter of demyelination in at least some other nerve.

3. Possible CIDPLike "1" but in just one nerve

CV: Conduction VelocityCMAP: Compound Muscle Action PotentialULN: Upper Limits NormalLLN: Lower Limits Normal

(a) Any other nerve that meets any of the A-G criteria(b) Isose S. et al.15

Table 3. Electrodiagnostic criteria for chronic inflammatory demyelinating polyradiculopathy (CIDP).

Lumbar puncture practice for patients with clinical suspicion of CIDPThis panel recommends that in the event of clinical suspicion of CIDP, a lumbar puncture be performed for routine cytological and cytochemical analysis. (Strong recommendation, high quality of evidence: 1A)The presence of hyperproteinorrachia in patients with CIDP occurs between 76 and 90% of patients, where a protein level is demonstrated >45 mg/dL.9,21-22 Normally no pleocytosis should be observed in the CSF; if observed, it usually suggests coexisting infection, for example by HIV.23 Cyto-protein dissociation is the most

important piece of information in the CSF analysis. Although its usefulness is reported in some studies, the determination of oligoclonal bands for cases without demyelination of the CNS is, in fact, debatable and of limited utility.23

Nerve biopsy practice in patients with suspicion of CIDPThis panel suggests performing a sural nerve biopsy when the clinical, neurophysiological, and CSF elements are insufficient to support the diagnosis of CIDP or in selected cases of atypical clinical presentations. (Weak recommendation, low quality of evidence: 2C)



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The nerve biopsy can provide evidence to support the diagnosis of CIDP when the results of other diagnostic tests are inconclusive.22 However, the histopathological findings are not specific and their absence does not exclude the diagnosis. The biopsy of the sural nerve is preferred because of its easy access and fewer adverse events. The one that is clinically and/or electrophysiologically most affected should be chosen. Other options are the superficial peroneal or superficial radial nerves. Histopathological findings of CIDP include the inflammatory reaction associated with macrophages, onion bulb formations (demyelination-remyelination), endoneurial edema, mononuclear infiltration in endoneurium and variations between the fascicles.12,25

Nuclear magnetic resonance (NMR) study of plexuses and spinal roots in the diagnosis of CIDP and its variantsThis group suggests conducting NMR imaging of roots and spinal plexuses as a diagnostic aid for CIDP of initial atypical presentation and in which the neurophysiological and CSF evaluation has not allowed to establish a definitive diagnosis. (Good practice point) In some patients with atypical CIDP, alterations in NMR have been demonstrated, such as hypertrophy of the brachial or lumbar plexus and/or extraforaminal roots with gadolinium uptake, which denotes inflammation with vascular leakage. These alterations are mostly asymmetrical and are more frequently observed in the brachial plexus than in the lumbar.12,24

NMR of the spinal cord and/or brain in the diagnosis of CIDP and its variantsThis panel does not suggest carrying out routine NMR imaging studies of the spinal cord and/or brain in patients with suspected CIDP, except in cases in which the physical examination indicates involvement of the CNS. (Weak recommendation, low quality of evidence: 2C)Some studies have looked for the presence of concomitant alterations in the CNS in patients with CIDP. There are only small series of patients subjected to this type of research and the number of patients in whom this type of alterations have been corroborated has been a minority.26 White matter hyperintensities in T2 sequences and atrophy of

cervical cord have been described in isolation, but the clinical and prognostic significance of these findings is still controversial.27-31

Chemical and/or immunological analysis in the patient diagnosed with CIDPThis panel suggests carrying out the necessary investigations to search for other concomitant diseases in the patient diagnosed with possible, probable, or definite CIDP, based on a detailed clinical history. (Good practice point)Mainly based on case reports, numerous diseases have been associated with CIDP.12 These include diabetes mellitus, monoclonal gammopathies IgG or IgA, monoclonal gammopathy by IgM without antibodies against myelin-associated glycoprotein, HIV infection, chronic active hepatitis, systemic lupus erythematosus or other connective tissue diseases, sarcoidosis, thyroid disease, inflammatory bowel disease,32 membranous glomerulonephritis,33 and transplantation of bone marrow or solid organs.34 There is insufficient evidence to consider a direct association between CIDP and these diseases, however, consider the necessary investigations to rule out concomitant diseases. Perhaps, over time, some of these systemic diseases causing demyelinating neuropathies may be considered forms of CIDP of determinate cause.

TreatmentOral steroids for the treatment of CIDPThis panel recommends prednisone as a first-line treatment for patients with sensory-motor CIDP. (Strong recommendation, high quality of evidence: 1A) There is only one multicenter, randomized, and controlled study with prednisone at a dose of 60 mg daily that proved superior against not receiving treatment.33 However, there are many observational studies that indicate the efficacy of prednisone in CIDP, except for pure motor CIDP, whose use could even lead to clinical deterioration.12 There is no consensus on which is the best prednisone administration scheme considering daily regimens, on alternate days, or intermittent monthly.12 This panel suggests prednisone 60 mg daily or on alternate days for at least a month or until reaching a symptoms



11

stabilization phase, then start a gradual reduction scheme of 10 mg per month until reaching 5 mg daily or every other day and complete two years of treatment at this dosage, at the end of which, if the patient is asymptomatic or only minor sensory symptoms persist, prednisone may be discontinued and the patient kept under medical observation 1 to 2 times per year for 3 years.35-38

(Good practice point.)

Intravenous steroids for the treatment of CIDPThis panel recommends methylprednisolone as a first-line treatment for patients with sensory-motor CIDP. (Strong recommendation, low quality of evidence: 1C)In some observational studies and clinical trials, intravenous methylprednisolone 1 g has been evaluated for 3 to 5 days, followed by 1 g monthly for 6 months, which has been shown to be as effective as oral steroids at 6 months of follow-up, however, it requires more long-term studies.39,40

Polyvalent human immunoglobulin for the treatment of CIDPThis panel recommends the use of human immunoglobulin as the first line of treatment for adult patients with CIDP. (Strong recommendation, high quality of evidence: 1A)A meta-analysis that included four randomized, double-blind studies, two of them controlled by placebo, demonstrated the efficacy and safety of intravenous immunoglobulin (IVIG) in patients with CIDP and its clinical variants.41-44 Given the short half-life of IVIG, it should be administered at regular intervals and at individualized frequency. Crossover studies have shown no difference in efficacy when comparing IVIG against plasma exchange, nor IVIG against prednisolone. A total induction dose of 2 g/kg fractionated in 2 to 5 days is recommended, followed by a maintenance dose of 1 to 2 g/kg fractionated in 2 to 5 days every 2 to 6 weeks.41-44

The scheme should be sustained until a symptom stabilization phase is observed, then it is recommended to reduce the dose of IVIG (10 to 15%) before extending the administration intervals. (Good practice point)

In the case that the patient requires sustained full doses of IVIG to maintain stability, it is suggested to add oral steroids or immunomodulatory drugs. (Good practice point)

Plasmatic exchange for the treatment of CIDPThis panel recommends the use of plasma exchange in patients with CIDP refractory to steroids and IVIG in the induction phase. (Strong recommendation, high quality of evidence: 1A)In randomized, controlled, and double-blind studies, the manifestations of CIDP have shown short-term benefits with plasma exchange. It is suggested to be administered 2 to 3 times a week. However, a rapid deterioration after the procedure is reported, so the use of other treatment measures is recommended for stabilization in the medium and long term.45,46

General therapeutic recommendations

Induction treatment1. IVIG and steroids are considered first-line treatments in patients with CIDP, except for pure motor CIDP, where steroids could cause clinical deterioration and IVIG should be considered as the first-choice treatment. (Good practice point)

2. The presence of relative contraindications for each of the drugs can influence the therapy decision-making. In either case, the advantages and disadvantages of both options should be discussed with the patients to involve them in making the decision. (Good practice point)

3. For refractory forms of CIDP that do not respond to steroids or IVIG, plasma exchange should be considered as the second line of treatment. (Good practice point)

Maintenance treatment1. In case of effectiveness during the induction phase, the treatment must be maintained until clinical stability is reached and then gradually reduce the dose. (Good practice point)2. For patients under treatment with IVIG at high doses and short intervals, steroids or



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immunosuppressive drugs should be considered as adjuvant therapy. (Good clinical practice point)

Immunomodulatory drugs

No randomized, controlled study has been conducted to demonstrate the efficacy and tolerance of any immunomodulatory drug in the treatment of CIDP other than azathioprine. Its use is reserved only during the maintenance phase or in cases refractory to conventional treatment.

AzathioprineThis panel suggests the use of azathioprine at doses of 100 to 200 mg/day as treatment for sensorimotor CIDP. The use of this immunomodulator is as a steroid-sparing agent and usually in concomitance with prednisone. (Weak recommendation, low quality of evidence: 2C)There is only one randomized study with azathioprine in patients with CIDP that did not demonstrate efficacy when used concomitantly with prednisone; however, the study included a small number of patients, the follow-up was short, and the dose used was suboptimal.47

MethotrexateThis panel suggests the use of methotrexate at a dose of 15 mg/week for the treatment of CIDP. The use of this immunomodulator is as a steroid-sparing agent and usually in concomitance with prednisone. (Weak recommendation, low quality of evidence: 2C)There is only one randomized, double-blind, placebo-controlled study that used methotrexate at a dose of 15 mg/week in patients with CIDP but showed no benefit over placebo. However, the study suffered from severe limitations in its design, so its benefit for patients with CIDP remains uncertain.48

CyclophosphamideThis panel suggests the use of intravenous cyclophosphamide at a dose of 1 g/m2 monthly for 6 to 12 months to treat for CIDP. (Weak recommendation, low quality of evidence: 2C)An open non-controlled study with cyclophosphamide at a dose of 1 g/m2 per month

for 6 months was effective in the treatment of CIDP cases that did not respond to steroids, human immunoglobulin, or plasma exchange.49

Mycophenolate mofetilThis panel suggests the use of mycophenolate mofetil at a dose of 2 g/day for the treatment of sensorimotor CIDP. (Weak recommendation, moderate quality of evidence: 2B)One retrospective study evaluated the efficacy of mycophenolate mofetil at a dose of 2 g/day in patients with CIDP, without demonstrating a difference in strength, sensitivity, or modified Rankin scale before and after treatment. A second study, also retrospective, suggested efficacy in the treatment of this condition.50,51

Interferon betaThis panel does not recommend the use of interferon beta in patients with CIDP. (Strong recommendation, high quality of evidence: 1B)A prospective, randomized, double-blind, placebo-controlled study that used interferon beta 1a at a dose of 30 or 60µg twice a week for 4 months showed no benefit in symptom control or reduced IVIG dosage compared against placebo. In this case, the evidence, although not completely conclusive, is considered of sufficient quality to recommend against the use of interferon beta in cases with CIDP.52

Monoclonal antibodies

RituximabThis panel suggests the use of rituximab at a dose of 375 mg/m2, one cycle every week for four weeks in adult patients with CIDP with IgG4 anti-CNTN1/NF155 or hematological diseases antibodies. (Weak recommendation, low quality of evidence: 2C).A report of two cases of CIDP associated with IgG4 anti-CNTN1/NF155 antibodies resistant to conventional therapy showed a significant improvement or CIDP associated with hematological pathology or coexisting with another autoimmune disease.53

AlemtuzumabThis panel suggests the use of alemtuzumab in



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selected patients with CIDP resistant to conventional treatment. (Weak recommendation, low quality of evidence: 2C)A case report that included seven patients with CIDP resistant to conventional therapy treated with alemtuzumab showed prolonged remission in two of them, partial improvement in two, and three had no benefit.54

NatalizumabThis panel suggests the use of natalizumab in selected patients with CIDP resistant to conventional therapy. (Weak recommendation, low quality of evidence: 2C)A report of three cases of patients with CIDP resistant to conventional therapy who were treated with natalizumab reported sustained improvement in one, dramatic improvement in another, and stabilization in the third. Other studies have not been consistent in their results.55

Physical therapy and rehabilitation

This panel suggests counseling patients regarding lifestyle changes including a balanced diet, regular physical activity, special dedication to foot care, physical rehabilitation (stretching exercises, strengthening, and occupational therapy) and, depending on the needs of the patients, psychological support. (Good practice point)

There are no observational or intervention studies that show, with traditional objective outcomes, the effectiveness of different physical therapy schemes. This is an area of opportunity for research. In our experience, almost any regime that provides regular use of facilities and therapist services is associated with greater patient satisfaction, but with minimal effects in the improvement of independence, autonomous ambulation, or reversal of the physical limitations imposed by the disease. Nevertheless, this must be demonstrated with scientific rigor in the future.

This guide in perspective

Research recommendations

This is, to the best of our knowledge, the first clinical practice guide on diagnosis and treatment of CIDP using a system of evaluation for the quality of evidence and grading the strength of the recommendations with the participation of members of diverse Mexican institutions. Its text gathers, orders, summarizes, and combines the best available evidence in a clear and simple format in order to reduce the variability of clinical practices in the management of CIDP. Its original design weighs equally the diagnosis and treatment, fostering, on one hand, the encounter between research and clinical practice by reporting the quality of the available evidence in the statements, and, on the other hand, improving the quality of health service management.

The high variability of treatments, doses, schedules, and routes of administration makes standardization and comparison with different therapeutic maneuvers complex and laborious, partly explained by the heterogeneous nature of the disease discussed. This opens areas of opportunity to design multicenter studies that provide the best level of evidence in terms of diagnosis and treatment as well as explore new diagnostic tools for atypical forms. There should be an evaluation of the role of rescue therapies and second-line therapies, as well as different physical therapy techniques and multimodal treatments with different traditional objective outcomes (or added) to the overall satisfaction of the patient.



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Guide synopsis

1. This panel recommends performing neuroconduction tests by exploring at least four motor nerves using the diagnostic demyelination criteria proposed by EFNS/PNS. (Strong recommendation, high quality of evidence: 1A)

2. This panel suggests performing sensory neuroconduction in patients with clinical suspicion of typical or atypical CIDP. (Weak recommendation, low quality of evidence: 2C)

3. This panel suggests performing somatosensory evoked potentials (SEPs) in patients with sensory variant CIDP or atypical clinical presentation. (Good practice point)

4. This panel suggests repeating the neurophysiological evaluation proposed by EFNS/EPN in case of not meeting the criteria for definitive CIDP in the initial evaluation. (Weak recommendation, low quality of evidence: 2C)

5. Recommendation: This panel recommends, in the event of clinical suspicion of CIDP, lumbar puncture. (Strong recommendation, high quality of evidence: 1A)

6. This panel suggests performing a sural nerve biopsy when the clinical, neurophysiological, and CSF elements are insufficient to support the diagnosis of CIDP, or when faced with atypical clinical presentations. (Weak recommendation, low quality of evidence: 2C)

7. This group suggests carrying out NMR imaging of spinal roots and plexuses as a diagnostic aid for CIDP of initial atypical presentation and when the neurophysiological and CSF evaluation have not allowed establishing a definitive diagnosis. (Good practice point)

8. This panel does not suggest performing spinal and/or brain NMR imaging studies in patients with suspected CIDP. (Weak recommendation, low quality of evidence: 2C)

9. This panel suggests conducting the necessary investigations to search for other concomitant diseases in the patient with a diagnosis of

possible, probable, or definite CIDP, based on a detailed clinical history. (Good practice point)

Treatment

1. This panel recommends prednisone as first-line treatment for patients with sensorimotor CIDP. (Strong recommendation, high quality of evidence: 1A)

2. This panel recommends methylprednisolone as first-line treatment for patients with sensorimotor CIDP. (Strong recommendation, high quality of evidence: 1C)

3. This panel recommends the use of human immunoglobulin as first-line treatment for adult patients with CIDP. (Strong recommendation, high quality of evidence: 1A)

4. This panel recommends the use of plasma exchange in patients with steroid-refractory CIDP and IVIG in the induction phase. (Strong recommendation, high quality of evidence: 1A)

5. This panel suggests the use of azathioprine at doses of 100 to 200 mg/day as treatment for sensorimotor CIDP. (Weak recommendation, low quality of evidence: 2C)

6. This panel suggests the use of methotrexate at a dose of 15 mg/week for the treatment of CIDP. (Weak recommendation, low quality of evidence: 2C)

7. This panel suggests the use of intravenous cyclophosphamide at a dose of 1 g/m2 monthly for 6 to 12 months for the treatment of CIDP. (Weak recommendation, low quality of evidence: 2C)

8. This panel suggests the use of mycophenolate mofetil at a dose of 2 gr/day for the treatment of sensorimotor CIDP. (Weak recommendation, low quality of evidence: 2B)

9. This panel does not recommend the use of interferon B1 in patients with CIDP. (Strong recommendation, high quality of evidence: 1B)

10. This panel suggests the use of rituximab at a dose of 375 mg/m2, one cycle every week for four weeks in adult patients with CIDP associated with IgG4 anti-CNTN1/NF155 or hematological diseases antibodies. (Weak recommendation, low quality of evidence: 2C)

Diagnosis



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11. This panel suggests the use of alemtuzumab in patients with CIDP resistant to conventional treatment. (Weak recommendation, low quality of evidence: 2C)

12. Recommendation: This panel suggests the use of natalizumab in patients with CIDP resistant to conventional therapy. (Weak recommendation, low quality of evidence: 2C)

13. This panel suggests advising patients on lifestyle changes that include a balanced diet, regular physical activity, extreme foot care, physical rehabilitation (stretching exercises, strengthening, and occupationa occupational therapy), and, depending on the patient’s need, psychological support. (Good practice point)

Acknowledgments

The authors express their gratitude to Innovare S.A. de C.V. and LFB France for the support received for the meeting of experts to take place in an academic environment and without pressure or coercion of any kind.

Conflicts of interestThere are no potential conflicts of interest for any of the authors in this scientific report.

Funding sourcesThis work received logistic support partially funded by Innovare S.A. de C.V. and LFB France. The pharmaceutical companies did not participate, directly or indirectly, in the design of the project, selection of the information, analysis, synthesis of the data, in the elaboration of this article, nor in its publishing.



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Original contributionSubjective memory complaints in Mexico

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Subjective memory complaints in the geriatric population and related factors: a pilot study in Mexican population

Quejas subjetivas de memoria en población geriátrica y sus factores asociados: Estudio piloto en población mexicana

Original contribution

Paul Carrillo-Mora,1 Brenda García-Juárez,2 Yesenia Lugo-Rodríguez,2 Elena del Pilar Moreno-Méndez,2 Leonardo Cruz-Alcalá 3

1 Department of Neurosciences/Neurobiology Subdivision.National Institute of Rehabilitation “Luis Guillermo Ibarra Ibarra.”Coordinator of the Dementia Study Group, AMN.2 Faculty of Psychology, UNAM3 Department of Clinics, University Center at Los Altos, University of Guadalajara.

Abstract

Introduction. Subjective Memory Complaints (SMC) represent the individual’s perception of a change in their memory. In the elderly population, a variable frequency of 10 to 90% has been reported. The significance of SMC is still controversial in the geriatric population and there are no studies that have explored the frequency of SMC and their associated factors in Mexico.

Objective. To identify the frequency of SMC using a structured questionnaire, as well as to identify the associated factors in the elderly population.

Methods. A clinical pilot, observational, cross-sectional study of individuals over 60 years old of both sexes. Exclusion criteria: diagnosis of cognitive impairment, dementia or delirium, other neurodegenerative or psychiatric diseases, history of traumatic brain injury, or stroke in the previous six months. Instruments: the Spanish version of the Subjective Memory Complaints Questionnaire (SMCQ), the Folstein Mini-Mental State Examination (MMSE), the Hospital Anxiety and Depression Scale (HADS), and a questionnaire of interest variables were applied.

Results. A total of 100 patients were included: 77 women and 23 men with a mean age of 72.8 years; 96% of the individuals reported at least one SMC, and 53% had significant SMC (>5). There was no observed association between SMC and the MMSE, only a significant correlation with the anxiety and depression scores (HADS) was shown. In addition, elevated education levels, reading habits, and exercise were associated with a lower number of SMC.



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Resumen

Introducción. Las Quejas Subjetivas de Memoria (QSM) representan la percepción del individuo a cerca de un cambio en su memoria. En población adulta mayor se ha reportado una frecuencia variable de entre 10 al 90%. El significado de las QSM aún resulta controversial en la población geriátrica y en nuestro país no existen estudios previos que hayan explorado la frecuencia de QSM y sus factores asociados.

Objetivo. Conocer la frecuencia de QSM usando un cuestionario estructurado, así como conocer cuáles son sus factores asociados en población adulta mayor.

Métodos. Se realizó un estudio clínico piloto, observacional, transversal. Se incluyó a individuos > 60 años de ambos sexos. Criterios de exclusión: diagnostico de deterioro cognitivo, demencia o delirium, otras enfermedades neurodegenerativas o psiquiátricas, antecedente de trauma craneal o enfermedad vascular cerebral en los 6 meses previos. Se aplicó la versión en español del Subjective Memory Complaints Questionnaire, el Mini mental de Folstein (MMSE), la Escala de Ansiedad y Depresión Hospitalaria (HADS) y un cuestionario de variables de interés.

Palabras claveQuejas subjetivas de memoria, deterioro cognitivo, depresión, ansiedad, México.

Correspondence: Dr. en C. Paul Carrillo-Mora. Instituto Nacional de Rehabilitación.Calz. México-Xochimilco No. 289 Col. Arenal de Guadalupe, México D.F.,14389, México.Tel.(+52-55) 5999-1000 Ext. 19204. Fax.(+52-55) 5603-9138.Correo electrónico: [email protected]

KeywordsSubjective memory complaints, cognitive impairment, depression, anxiety, México.

Resultados. Se incluyó un total de 100 pacientes: 77 mujeres y 23 hombres con un promedio de edad de 72.8 años. Se encontró que el 96% de los individuos referían al menos una QSM, y el 53% presentaban QSM significativas (>5). No se observó asociación entre QSM y el MMSE, y solo se demostró una correlación significativa con las puntuaciones de la escala de ansiedad y depresión (HADS). Además, la escolaridad elevada, el hábito de lectura y el ejercicio se asociaron con un menor número de QSM.

Conclusiones: Se encontró una elevada frecuencia de QSM (>90%), y éstas se relacionaron con los síntomas de ansiedad y depresión. No se observó asociación con el rendimiento cognitivo y se evidenció que la escolaridad, el hábito de lectura y el ejercicio regular modulan positivamente el número de QSM.

Conclusions: A high frequency of SMC (>90%) was found, and these were related to the symptoms of anxiety and depression. There was no association with cognitive performance and it was evidenced that education, reading habits, and regular exercise positively modulate the number of SMC.



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Introduction

Subjective Memory Complaints (SMC) represent an individual’s perceived change in the state that maintains their mnesic abilities (with respect to a previous state). Even though SMC can present at any age, those occurring in individuals over 60 years old have recently become relevant.1

SMC are one of the main reasons for consultation in the elderly population; however, in clinical studies, the prevalence varies from 12% to 90% of cases.2,3 This variance can be related to issues such as study design, type of population studied, age groups, etc., but one of the most important factors is that there is still no universally accepted and validated questionnaire to measure SMC.4

The relevance of SMC lies not only in their frequency but also in their meaning. There are two positions in the literature with regards to this. On one hand, some studies suggest that such complaints are associated with a lower cognitive performance and indicate an increased risk of developing mild cognitive impairment or dementia in the future.5,6 On the other hand, there is the suggestion that SMC are the manifestation of an altered mood, since in some studies they are only related to the presence and severity of anxiety and depression symptoms.7,8 For this reason, the meaning of SMC is still controversial, which is why it is important to carry out more studies to try to understand their significance and causal factors. To date, there are very few studies conducted in Latin America, and to our knowledge, there are no previous studies on SMC performed in the Mexican population; therefore, this study aims to learn the frequency of SMC and its associated factors in a sample of older adults in Mexico.

Methods

A clinical, observational, cross-sectional, descriptive and analytical study was designed and participants were selected from the different external consultation areas of the National Institute of Rehabilitation “Luis Guillermo Ibarra Ibarra” (INR-LGII). A sample size calculation was not performed since it was an exploratory study, so it was done for convenience. It included all patients over 60 years old, of both sexes, who agreed to participate through informed consent. The following were considered exclusion criteria: previous or current diagnosis of cognitive impairment, dementia or delirium, other neurodegenerative or psychiatric diseases, history of cranial trauma or cerebrovascular disease in the past 6 months, and current consumption of drugs affecting cognitive performance (anticholinergics, benzodiazepines, neuroleptics, etc.). Patients who did not adequately complete all of their evaluations were removed from the study. The Spanish version of the Subjective Memory Complaints Questionnaire (SMCQ) was applied to assess SMC.9 It is a short questionnaire (15 items) which in previous studies has demonstrated adequate reliability (α Cronbach: 0.86) and a good correlation with the neuropsychological evaluations, plus it can be self-applied when a reliable informant does not exist (Appendix 1). In addition, a cognitive screening was applied through Folstein’s Mini-Mental State Examination (MMSE), the Hospital Anxiety and Depression Scale (HADS),10 and a survey of sociodemographic variables of interest: age, schooling, comorbidities, body mass index (BMI), sleep quality, drug use, etc. Statistical analysis was performed using the statistical program GraphPad Prism version 5.0 using measures of central tendency and dispersion, associations between variables were performed with a Spearman correlation, and categorical variables were analyzed using an X2 or Fisher’s exact test.



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ResultsA total of 100 patients participated in the study: 77 women and 23 men, with an average age of 72.8 years (SD: 6.3, range 60-89 years) and an average schooling of 9.08 years (SD: 5.5, range 0-20 years). The average BMI was 26.28 (SD: 4.2, range 17-38). Considering this BMI, only 36% of the subjects had a normal weight, whereas 64% had some degree of overweight or obesity. In terms of marital status, 46% of the subjects were married and the other 54% had no partner for various reasons (widowed, separated, divorced, or single). Regarding current work, only 37% had some paid activity. As for other activities, 41% exercised regularly (at least three times a week) and 63% had a regular reading habit. Concerning the subjective quality of sleep, an average score of 7.2 was reported (SD: 2), a score of 4.4 in presence of daytime hypersomnia (maximum 10), and an average of 5.7 hours (SD: 1.9) of nocturnal sleep. Regarding the presence of comorbidities (hypertension, diabetes, dyslipidemia, cancer, heart disease, etc.), only nine patients had none while the average was 2.5 comorbidities per individual (range 0-7). As for SMC, only 4% did not report any, while 96% reported at least one, and the average was 5.2 SMC per individual (SD: 3.4). Figure 1 shows the distribution of cases

in relation to the number of SMC. Taking into consideration the cut-off point suggested by the authors of the SMCQ (5 points), we found that 53% of the cases had significant SMC. In regards to cognitive evaluation, the average obtained in the MMSE was 18.5 points (SD: 9.3). Considering the cut-off point of 23 points, it was observed that 15% of the cases presented a score that suggests some degree of cognitive deterioration. The average in the total HADS score was 5.3 points (SD: 3.4) and considering the cutoff point of >15 points for the total HADS, a frequency of 21% of significant anxiety and depression was attained. It is important to note that patients who scored high on the HADS scale or low on the MMSE were channeled for psychiatric or neurological assessments, respectively.

When trying to relate the number of SMC to different variables, we found the following: First, a correlation analysis was performed between the total number of SMC and the variables (age, schooling, BMI, weight, number of comorbidities, subjective sleep quality, hours of nocturnal sleep, daytime sleepiness, MMSE score, and HADS scores) and only a significant correlation was obtained with the different HADS scores. See

100

10

20

30

40

50

SMC

No.

Cas

es

4741

12

Figure 1. Frequency of cases in relation to the number of SMC.



23

VariableHADS THADS AHADS D

Value de P



24

Figure 3. Number of SMC in relation to regular exercise. The bars represent the average SME * p=0.0315, Mann-Whitney U.

Figure 4. Number of SMC in relation to reading habits. The bars represent the average SME * p=0.0230, Mann-Whitney U

Figure 5. Number of SMC in relation to low/high schooling. The bars represent the average SME * p=0.0471, Mann-Whitney U.

With E Without E0

2

4

6

8

*

SMC

NO YES0

2

4

6

8

*

SMC

Low (9a)0

2

4

6

8

SMC



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The clinical significance of SMC in the elderly is still a matter of debate. As previously mentioned, there is as much evidence suggesting it may be an indicator of cognitive decline11 or a risk factor for the development of cognitive impairment,12 as there is proposing that it is only an alteration of self-perception of the cognitive state caused by mood disorders (anxiety and depression).13

To our knowledge, the present pilot study represents the first research of this type in the Mexican population. We consider that some of the main characteristics of the population included in this study are representative of the Mexican population in this age stratum: a female predominance (77%), a low schooling average (9 years), a high incidence of overweight and obesity (64%), high number of comorbidities (91%, average: 2.5), and a low frequency of paid work (37%).14 Regarding their exercise habits, the proportion of regular exercise was found at 41%, which we considered to be high; a previous study carried out in Mexico, however, reports a frequency of regular exercise in this age group of up to 70%,15 though this divergence may be due to the definition of regular exercise used in each study. Regarding reading habits, which were reported in 63% of the cases, we did not find figures in the national literature with which to compare it, although we estimate that it is perhaps a high figure notwithstanding the low level of schooling of the sample. It is important to note that our sample of patients was obtained from an outpatient hospital population (external consultation) which may affect the frequency of comorbidities and pharmacological treatment, as well as other factors which may not be fully representative of the general population.

Another important data to consider is that in our sample the average obtained in the cognitive screening performed with the MMSE was 18.5 points, in addition to the 15% of the individuals who obtained a score suggestive of some degree of cognitive impairment (5 SMC). These figures are similar to those obtained by Slavin et al. in 2010, who found that 95.5% of their sample of 1,037 individuals reported some cognitive problem; in that study, however, a different questionnaire was used to search for cognitive complaints, and the age group was older (>70 years).18 The frequency of SMC reported in the literature varies greatly from less than 10% to more than 90% of cases; the are various reasons for this wide variability, perhaps related to the methodological differences of the studies and their populations: population surveys, memory clinics, hospital population, retirement homes, nursing homes, women-only samples, and even telephone interviews.19 Another important source of discrepancy is the instrument used to search for cognitive complaints. Since there is no universally accepted or standardized questionnaire, some studies are based only on one or two non-specific questions about the opinion of the state of their memory, and others use structured questionnaires with dichotomous (yes/no) responses, or even Likert-like scores4,18,19

which undoubtedly greatly affects the frequency



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of SMC reported in each study. Furthermore, although some questionnaires explore several cognitive domains, most focus on aspects related to memory, so it is debatable to say we’re talking about cognitive complaints when in reality it is only memory complaints. In this study, we used the Spanish version of the SMCQ (Appendix 1), which is a brief self-application tool that has demonstrated adequate internal consistency and a significant correlation with neuropsychological performance in patients with cognitive impairment. Additionally, this instrument contains questions that, in addition to exploring possible flaws in different aspects of memory in the daily environment, also allows us to estimate the degree of functional impact that these complaints have on the patient’s life.9 However, we must consider that when applying an instrument that intentionally interrogates the state of memory of individuals, this can increase the frequency of reports of complaints when compared with spontaneous complaints that the patient could offer—something which has, incidentally, already been investigated and demonstrated in recent studies.20

Another of the main objectives of this study was to try to identify the factors associated with the presence and the number of SMC. In the correlation analysis, a significant association of the number of SMC was observed only with the severity of the symptoms of anxiety and depression that the HADS scale measures. This association was most significant in the test’s total score, followed by the anxiety score, and finally in the depression score. These findings coincide with those extensively described in other literature on cognitive complaints, especially in cross-sectional studies.13,18,21 It is important to note here that the frequency of anxiety-depressive symptoms observed in this study (21%) coincides with that reported in the international literature22,23 although there is also great variability in these figures—for instance, a study in the Mexican geriatric population observed the incidence of depression was over 41%,24 which suggests that it is a prevalent disorder in this age group.

In order to explain this association between SMC

and symptoms of anxiety and depression, different hypotheses have been proposed. The most common is that SMC is actually an altered perception of the cognitive state caused by the coexisting symptoms of anxiety and depression—that is, that the older adult patient with anxiety and depression may pay more attention or magnify some cognitive errors that are not really significant.4 This might lead us to assume that depressive symptoms should also affect the performance of individuals in cognitive assessments; however, at least in our study, there was no significant correlation between the HADS scale score and the score obtained by the MMSE (p=0.1942), even when only patients with more severity in their emotional symptoms were considered (HADS >15) this association was not observed (p=0.1421). In other words, anxiety and depression appear to have no significant influence on cognitive performance.

It is important to note that in our study there was no association between the current cognitive performance and the number of SMC. A relationship was found only between the level of schooling and the number of SMC, with a greater number of complaints in the low schooling group (



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it is interesting to remark that some studies, especially longitudinal studies and studies in which some biomarkers (amyloid beta) have been measured, do suggest that SMC appear to raise the risk of cognitive impairment.28,29 Recent studies show that cognitive complaints reported by an informant seem to be more closely related to cognitive performance and to the risk of future cognitive impairment.30 This difference between the cross-sectional and longitudinal studies suggests that perhaps the cognitive changes that occur in patients with SMC are actually very dynamic and highly dependent on each individual, so that only the long-term and serial evaluations allow us to notice changes in the cognitive status that cross-sectional studies cannot demonstrate.

Finally, it should be pointed out that due to the limitations of our study, because it was a pilot study, the sample was very small, and a broader neuropsychological evaluation was not performed, nor were functional scales used to distinguish patients with functional impairment associated with cognitive impairment. Therefore, more studies will be required in the future—especially longitudinal studies using broad and standardized neuropsychological batteries that consider both spontaneous complaints as well as complaints recalled by memory, and take the point of view of an external informant to improve the methodological quality of the studies and to be able to know with greater certainty the implications of SMC in this age group.

1. Do you think you have a problem with your memory?

2. Do you think that your memory is worse now than it was 10 years ago?

3. Do you think that your memory is worse than that of other people your same age?

4. Do you feel that your daily life is more complicated now because your memory has diminished?

5. Have you had difficulties remembering a recent event?

6. Have you had difficulties remembering a conversation you had a few days ago?

7. Have you had difficulties remembering a commitment you made a few days ago?

8. Are you experiencing difficulty recognizing the faces of people close to you?

9. Are you having difficulty remembering where you have left things?

10. Have you lost things more frequently now?

11. Have you got lost or gone astray somewhere outside your home?

12. Have you had trouble remembering to get two or three articles when you go shopping for groceries?

13. Do you have trouble remembering to turn off the stove or the lights in your house?

14. Do you have trouble remembering the phone numbers of your children?

15. Do you think these memory problems have interfered significantly in your daily life?

Question Yes No

Appendix 1.Spanish Version of the Subjective Memory Complaints Questionnaire.9

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