This document provides an overview of approach to myopathy. It discusses types of muscle fibers, symptoms associated with myopathies including myalgia, fatigue, stiffness and others. It describes etiology such as acquired, hereditary and associated with systemic illness. Temporal evolution from onset in birth, childhood and adulthood is explained. Pattern of weakness like proximal, distal, axial and others and associated systemic symptoms are covered. Investigation approach including CK, EMG, muscle biopsy and genetic testing is summarized. Specific myopathies and their features are highlighted.
MYOPATHIES A SPECIAL AND SEPERATE ENTITY WITH SPECIFIC FEATURES IN EACH DISORDER MAKING US EASY FOR DIAGNOSIS,CONFIRMATION BY MUSCLE BIOPSY.THE SEMINAR WAS PRSENTED ON 06/07/2011...AT 09.00AM
HAVE A LOOK ..AND COMMENT..WITHOUT BIAS..
This presentation is about different diseases which presents or are associated with myotonia. Referrences were taken from Bashir Katirji Neuromuscular textbook, continuum, and seminar of neurology journal.
MYOPATHIES A SPECIAL AND SEPERATE ENTITY WITH SPECIFIC FEATURES IN EACH DISORDER MAKING US EASY FOR DIAGNOSIS,CONFIRMATION BY MUSCLE BIOPSY.THE SEMINAR WAS PRSENTED ON 06/07/2011...AT 09.00AM
HAVE A LOOK ..AND COMMENT..WITHOUT BIAS..
This presentation is about different diseases which presents or are associated with myotonia. Referrences were taken from Bashir Katirji Neuromuscular textbook, continuum, and seminar of neurology journal.
Myopathies - In detail (Classification and images) Dr. Tushar Kariya
In this presentation I've tried to cover myopathies, its classification and related images with H&E and special stain wherever its possible. Hope it helps you guys to understand the entity better.
Myopathies - In detail (Classification and images) Dr. Tushar Kariya
In this presentation I've tried to cover myopathies, its classification and related images with H&E and special stain wherever its possible. Hope it helps you guys to understand the entity better.
CONCEPT OF NODOPATHIES AND PARANODOPATHIES.pptxNeurologyKota
emergence of autoimmune neuropathies and role of nodal and paranodal regions in their pathophysiology.
Peripheral neuropathies are traditionally categorized into demyelinating or axonal.
dysfunction at nodal/paranodal region key for better understanding of patients with immune mediated neuropathies.
antibodies targeting node and paranode of myelinated nerves have been increasingly detected in patients with immune mediated neuropathies.
have clinical phenotype similar common inflammatory neuropathies like Guillain Barre syndrome and chronic inflammatory demyelinating polyradiculoneuropathy
they respond poorly to conventional first line immunotherapies like IVIG
This presentation briefs out the approach of dementia assessment in line with consideration of recent advances. Now the pattern of assessment has evolved towards examining each individual domain rather than lobar assessment.
This presentation contains information about Dementia in Young onset. Also it describes the etiologies, clinical feature of common YOD & their management.
Entrapment Syndromes of Lower Limb.pptxNeurologyKota
This presentation contains information about the various Entrapment syndromes of Lower limb in descending order of topography. It also contains information about etiology, clinical features and management of each of these entrapment syndromes with special emphasis on electrodiagnostic confirmation.
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
New Drug Discovery and Development .....NEHA GUPTA
The "New Drug Discovery and Development" process involves the identification, design, testing, and manufacturing of novel pharmaceutical compounds with the aim of introducing new and improved treatments for various medical conditions. This comprehensive endeavor encompasses various stages, including target identification, preclinical studies, clinical trials, regulatory approval, and post-market surveillance. It involves multidisciplinary collaboration among scientists, researchers, clinicians, regulatory experts, and pharmaceutical companies to bring innovative therapies to market and address unmet medical needs.
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
The Gram stain is a fundamental technique in microbiology used to classify bacteria based on their cell wall structure. It provides a quick and simple method to distinguish between Gram-positive and Gram-negative bacteria, which have different susceptibilities to antibiotics
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
Follow us on: Pinterest
Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
Basavarajeeyam is a Sreshta Sangraha grantha (Compiled book ), written by Neelkanta kotturu Basavaraja Virachita. It contains 25 Prakaranas, First 24 Chapters related to Rogas& 25th to Rasadravyas.
4. History
Which negative and/or positive
symptoms and signs does the
patient demonstrate?
What is the distribution of
weakness?
Family history What is the temporal
evolution?
Are there precipitating
factors that trigger episodic
weakness or myotonia?
Are associated systemic
symptoms or signs present?
8. Stiffness: decrease ability to relax
Improve with exercise
Myotonia: Na or Ca channelopathy
Worsen with exercise/ cold
Paramyotonia
Brody disease
With fixed weakness
Myotonic dystrophy
Becker disease (AR Cl channelopathy
Other
Malignant hyperthermia
Neuromyotonia
Stiffperson syndrome
14. Temporal evolution: episodic or constant weakness?
Causes of episodic weakness:-
Hypo and hyper kalemic periodic paralysis
Anderson- tawil syndrome
Secondary PP
Metabolic myopathy (glycolytic enzyme defect)
15. Constant weakness
• acute or subacute progression
– inflammatory myopathies (dermatomyositis and polymyositis);
• chronic slow progression over years
– most muscular dystrophies
– IBM
• nonprogressive weakness with little change over decades
– congenital myopathies
16. Precipitating factors
• illegal drug or prescription medication use that might produce a myopathy.
• weakness, pain, and/or myoglobinuria provoked by exercise
– a glycolytic pathway defect.
• Episodes of weakness with a fever
– carnitine palmityl transferase deficiency.
• Periodic paralysis -provoked by exercise or ingestion of a carbohydrate meal followed
by a period of rest.
• paramyotonia congenita -cold exposure
27. Hepatomegaly
• may be seen in acid maltase, debranching enzyme deficiency
• mitochondrial disorder.
28.
29. DMD sarconoglycanopathy
inheritance X- linked recessive Autosomal recessive
Female sex Less likely May be affected
Calf hypertrophy present May be present
Muscle knee extensors
and hip abductors more
commonly involved than knee
flexors and hip adductors
Deltoid and infraspinatus
preserved
Hamstring>quadriceps
Biceps and deltoid
involved
Triceps preserved
intelligence May be subnormal normal
cardiac involved Less likely
Scapular winging Not usually May be present
31. Approach to metabolic myopathy
Darras BT, Friedman NR. Metabolic myopathies: A clinical approach; Part I. Pediatr Neurol 2015;22:87-97.
When to suspect
• Cramps, myalgias and exercise intolerance
• Rhabdomyolysis
How to investigate
• Ischemic exercise test
• Muscle biopsy
• Genetic tests
32. Examination
Muscle appearance – wasting ,atrophy (neurogenic)
ABSENT fasciculations (+Denervation)
Tenderness on palpation
Tone –normal ,decreased in advanced cases.
Distribution of weakness –proximal,distal (distal myopathies)
Tendon reflexes – normal /hypoactive in adv.cases
Babinski sign negative
SENSORYsystem is normal.
GAIT – lordosis on stance,increased on toe walking
Waddling gait – b/l pelvic girdle weakness
Genu recurvatum –quadriceps weakness
33. Creatininekinase
• CK is elevated in the majority of myopathies but may be normal in slowly
progressive myopathies.
• CK level may not be elevated in
corticosteroid administration,
collagen diseases,
Alcoholism
hyperthyroid
profound muscle wasting
Metabolic myopathies
34. Differential Diagnosis of Creatine Kinase Elevation
• Myopathies
– Muscular dystrophies
– Congenital myopathies
– Metabolic myopathies( macrdle disease)
– Inflammatory myopathies
– Drug/toxin-induced
– Carrier state (dystrophinopathies)
• Channelopathies
• Motor Neuron Diseases
– ALS
– SMA
– Postpolio syndrome
• Neuropathies
– GBS
– CIDP
• Viral Illness
• Medications
• Hypothyroidism/ Hypoparathyroidism
• Surgery/Trauma (electromyography studies,
intramuscular or subcutaneous injections)
• Strenuous Exercise
• Increased Muscle Mass
• Race
• Sex
• ‘‘Idiopathic HyperCKemia’’
36. EMG
Indication:-
To confirm muscle localization and rule outAHC, neuropathy
Guide for muscle biopsy
Common pattern:-
Brief duration small amplitude MUAP with early recruitment
37. Muscle biopsy
Should not be taken from muscle with grade 3 or less power
Avoid biopsy from EMG needle site insertion
Punch biopsy is preferred over open biopsy
Common site:- biceps, deltoid, vastus lateralis
Emergence of genetics has reduce need of biopsy
38. Muscle biopsy
Common pattern:-
Central nuclei, both small and large hypertrophic round fibers, split fibers, and
degenerating and regenerating fibers
Inflammatory myopathy:-
Presence of mononuclear inflammatory cells in the endomysial and perimysial
connective tissue between fibers and occasionally around blood vessels
Dermatomyositis, atrophy of fibers located on the periphery of a muscle fascicle,
perifascicular atrophy, is a common finding
Chronic myopathies frequently show evidence of increased connective tissue and
fat.
42. Valley sign :-DMD
Pradhan S. Valley sign in duchenne muscular dystrophy : importance in patients with inconspicuous calves. Neurol
India [serial online] 2002 [cited 2021 Jul 16];50:184
valley sign- simultaneous hypertrophy
of deltoid superolaterally, infraspinatus
inferomedially and wasting of posterior
axillary fold
48. Clinical features frequently observed in patients with LGMD: Gower’s manoeuvre in LGMD2A (a), atrophy of gastrocnemius
muscle in distal Miyoshi myopathy (b), Achilles tendon retraction in LGMD2A (c), scapular winging and atrophy of scapular
girdle muscles in LGMD2A (d), scoliosis in LGMD1F (e), severe hip and knee contractures in LGMD2C (f), tongue muscle
hypertrophy or macroglossia in LGMD2E (g).
49. Calpainopathy. (a) Scapular winging. (b) Abdominal hernia
due to weakness of external oblique muscle
GNE myopathy. (a) Wasting of tibialis anterior muscle
resulting in prominence of shin of tibia. (b) Wasting of first
dorsal interosseous muscle (distal myopathy) quadriceps
sparing myopathy.
50. Swan neck in myotonic dystrophy.
The hip abduction sign- LGMD (sarcoglycanopa
Khadilkar SV, Singh RK. Hip abduction sign: A new clinical sign in sarcoglycanopathies. J Clin Neuromusc Dis
2001;3:13-5
Mild ptosis, hatchet face and
thin neck in a patient with DM1
51. Rigid spine syndrome
Emery–Dreifuss muscular dystrophy
Nemaline myopathy,
multiminicore disease,
Bethlem myopathy,
and rigid spine muscular dystrophy
Contractures of the spine: As this patient tries to
bend forward, the lower and mid spine remain in the
extended
position.
Herculean appearance in two brothers with MC
a) Asymmetrical left > right foot drop and (b) asymmetrical calf atrophy (left >
right) in brothers with anoctaminopathy
52. Pradhan S. Shank sign in myotonic dystrophy type-I (DM-I): Utility in differentiation from DM-II and
some other common muscular dystrophies. J Clin Neurosci 2007;14:27-32
53.
54.
55.
56. References
• Jackson et al A Pattern Recognition Approach to Myopathy Continuum (Minneap
Minn) 2013;19(6):1674–1697
• Khadilkar SV, Singh RK. Limb girdle muscular dystrophies in India. Neurol India
[serial online] 2008 [cited 2021 Jul 16];56:281-8
• Bradely’s Neurology In Clinical Practise, 8th Edition
• Pradhan S. Clinical and magnetic resonance imaging features of 'diamond on
quadriceps' sign in dysferlinopathy. Neurol India 2009;57:172-5
• Pradhan S. Shank sign in myotonic dystrophy type-I (DM-I): Utility in
differentiation from DM-II and some other common muscular dystrophies. J Clin
Neurosci 2007;14:27-32
• Up to date.com
57. Case
• A 55-year-old man noticed gradually progressive weakness of both lower limbs since age of 25 years. Initially, he noticed
weakness of the left calf and soon within months the right calf weakened. In the ensuing 3 years, he developed bilateral
progressive foot drop. Over the next few years, he developed wasting of calves and then anterior leg muscles, which was
much more prominent on the left calf. Since 10–11 years, he noticed gradually progressive weakness of both lower limbs
and had developed difficulty in getting up from chair. Since 5–6 years, he has noticed mild weakness of arms associated
with wasting, more noticeable on the left side. On examination, there was evidence of asymmetric (left > right), bilateral
distal > proximal lower limb weakness affecting plantar flexors > dorsiflexors, quadriceps, hamstrings and hip adductors.
Deep tendon reflexes were present. Sensory examination was normal. His brother was also affected with similar
phenotype. Investigations revealed CK value of 3430 U/L. NEE showed myopathic potentials
• Summary: Familial, slowly progressive, asymmetric distal (calves > anterior leg muscles) > proximal lower limb weakness
followed by wasting, mild affection of upper limb proximal muscles and much elevation of serum CK.
• Discussion: Since calves were affected at the onset of illness, possibilities of dysferlinopathy and anoctaminopathy were
considered. The asymmetry of weakness, very gradual course of the illness and involvement of upper limbs starting after
almost 30 years of illness favoured anoctaminopathy. On genetic testing, no mutation was detected in dysferlin gene.
There was homozygous mutation in ANO5 gene which suggested diagnosis of anoctaminopathy.