This document provides information about myoclonus, which are sudden, shock-like contractions of muscles. It describes different types of myoclonus including focal, cortical, brainstem, spinal, peripheral, multifocal, generalized, essential, and childhood myoclonic epilepsies. Diagnostic tests like EMG and EEG are discussed. Various causes and treatment options are also mentioned.
FA is a very rare, genetic, recessive disease, affecting 1/50,000 people.
Originates from mutations in the “coding” of the mitochondria.
Discovered by Nicholaus Friedreich in the early 1860’s.
Both parents must have the dominant trait for a 25% chance of an offspring possessing the disease.
Not necessarily a disease that kills you, but eventually a wheelchair and regular assistance will be required.
Onset before age 20-25 year.
FA is a very rare, genetic, recessive disease, affecting 1/50,000 people.
Originates from mutations in the “coding” of the mitochondria.
Discovered by Nicholaus Friedreich in the early 1860’s.
Both parents must have the dominant trait for a 25% chance of an offspring possessing the disease.
Not necessarily a disease that kills you, but eventually a wheelchair and regular assistance will be required.
Onset before age 20-25 year.
Epilepsy is a group of disorders of the CNS characterized by paroxysmal cerebra dysrhythmia, manifesting as brief episode (seizures) of loss or disturbance of consciousness, with or without characteristic body movements (convulsions), sensory or psychiatric phenomenon.
Seizure – refers to abnormal firing of neurons
Convulsions – refers to motor incoordination
Chronic progressive external ophthalmoplegiaPS Deb
Chronic progressive external ophthalmoplegia (CPEO) is a descriptive term for a heterogeneous group of disorders characterized by chronic, progressive, bilateral, and usually symmetric ocular motility deficit and ptosis, without pain, proptosis and pupil involvement. Commonly a syndrome of Mitochondrial Cytopathy.
This is a short presentation at Down Town Hospital clinical meeting for DNB Medicine students. It dose not cover the all aspects of stroke care especially Thrombolysis, since it is difficult to practice for Medical specialist, and ischemic stroke is not common in North East India
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.
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.
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.
Basavarajeeyam is an important text for ayurvedic physician belonging to andhra pradehs. It is a popular compendium in various parts of our country as well as in andhra pradesh. The content of the text was presented in sanskrit and telugu language (Bilingual). One of the most famous book in ayurvedic pharmaceutics and therapeutics. This book contains 25 chapters called as prakaranas. Many rasaoushadis were explained, pioneer of dhatu druti, nadi pareeksha, mutra pareeksha etc. Belongs to the period of 15-16 century. New diseases like upadamsha, phiranga rogas are explained.
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
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
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
Adv. biopharm. APPLICATION OF PHARMACOKINETICS : TARGETED DRUG DELIVERY SYSTEMSAkankshaAshtankar
MIP 201T & MPH 202T
ADVANCED BIOPHARMACEUTICS & PHARMACOKINETICS : UNIT 5
APPLICATION OF PHARMACOKINETICS : TARGETED DRUG DELIVERY SYSTEMS By - AKANKSHA ASHTANKAR
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.
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...
Myoclonus
1. MYOCLONUS
Dr PS Deb MD, DM
Director Neurology
GNRC Hospitals ,
Guwahati,
Assam, India
2. MYOCLONUS
Definition
Sudden shock like contraction of muscle.
Flexor of upper limb and extensor of lower limb
Varying in severity from insufficient to move the joints to fall in
ground
Sensory stimulation aggravate attack.
EMG
Burst of 30-60 ms synchronous
Burst of 75-125 ms asynchronous
Burst of >150 ms synchronous
C-reflex – Stimulation of nerve → time locked response.
EEG
Variable pattern
Time lag with EMG activity before or after
Back averaging required
3. FOCAL MYOCLONUS
Rhythmic, unchanged by rest, action, sleep,
walking due to generation of discharge from
discrete segment of neuraxis.
Segmental myoclonus when segment of neuraxis
involved. Arrhythmic.
Spontaneous / Action / intentional / reflex
Cortical
Usually multifocal
Distal > proximal, flexor > extensor
Intentional or reflex , may be modality specific
4. EPILEPSIA PARTIALIS CONTINUA
Rhythmic form, Group of muscles – face, arm or leg,
persist for months
Etiology – vascular, trauma, infection, MS, tumor
EMG: Burst of agonist muscles, synchronous with
antagonistic muscle
EEG – Focal positive negative transient over sensory-
motor cortex contralateral to the jerk, time locked 20sec.
C-Reflex – correlated with giant somato-sensory evoked
potential
Evoked potential – large component of P1N2 has some
relation to C-reflex as the positive negative transient to
the spontaneous jerk
Cranial nerve involvement cephalocaudal
5. CORTICAL MYOCLONUS
Mechanism
Hyper excitability of the sensory-motor cortex → large
synchronous discharge → muscle jerk
Paroxysmal depolarization shift (fragment of epilepsy)
Cause
Any focal cortical damage
Tumor,
Angioma
Encephalitis
Idiopathic
Treatment
Surgical removal of the cause
Anticonvulsant
6. BRAINSTEM MYOCLONUS: PALATAL
MYOCLONUS
Clinical
Rhythmic oscillation of palate sometime other part
(ocular, tongue, larynx, pharynx, diaphragm)
Brachial muscles are affected related to rhythmicity of
respiration/gill movement
Persist during sleep -1.5-3Hz
Mechanism:
Tegmental tract lesion → Inf. Olive oscillate → Purkunji
cell → Reticulospinal tract / vestibulospinal tract
Any lesion of Gullain Mollaret Triangle – Dentate – Red
nucleus – Inf. Olive
Pathology
Hypertrophic degeneration of inf. Olive.
7. PALATAL MYOCLONUS CONT…
Cause
Idiopathic
Stroke
Trauma
Tumor → 10months later
Metabolic encephalopathy
Prognosis: Resistant
Treatment
Tetrabenazine
Halloparidol
5-Hydroxytryptophan
Carbamazipine
Bulbar myoclonus: Tongue and neck movement
8. SPINAL MYOCLONUS
Clinical
Rhythmic > arrhythmic
Spontaneous, persist in sleep
One limb, adjacent trunk or both legs
Cause
Degenerative
Demylination
C. myelopathy
Tumor,
Following spinal anesthesia
Contrast injection
Rarely idiopathic
Ischemic myelopathy : stimulus sensitive myoclonus
Rx: Clonazepam
9. PERIPHERAL MYOCLONUS
Rarely true myoclonus is seen with acute or chronic
denervation in involved muscle
Lesion:
Nerve
Brachial plexus
Nerve root
Essential – rarely focal
Treatment: Clonazepam
10. MULTIFOCAL OR GENERALIZED (EPILEPTIC
MYOCLONUS)
Types
Multifocal : focal jerks at different part of body
Generalized: Large part of body affected
Etiology may be same
Cortical:
Increased excitability of brain due to paroxysmal
depolarization shift involving group of neuron in different
part of brain – Fragment of epilepsy
EEG shows typical multifocal discharge and cortical
correlation
SSEP - ↑
11. RETICULAR – GENERALIZED
Clinical
Proximal more than distal
Flexor more than extensor
Sometime segment of body all muscle
Spontaneous or reflex or action
Cranial muscle → caudo-cephalic involvement
Mechanism
Hyper-excitability of a portion of the caudal brain stem reticular
formation – the nucleus reticularis gigentocellularis
EEG:
Spike, generalized highest amplitude vertex
Follow the EMG burst of myoclonus
Spike is not time locked to the myoclonus, spike is projected and
not directly responsible for myoclonus
SEP is not enhance (no cortical hyperactivity)
Combined Reticular and Cortical myoclonus due to combined
lesion
12. PRIMARY GENERALIZED EPILEPTIC
MYOCLONUS
Focal
Commonly small focal movement with finger movement
(minipolymyoclonus also seen with peripheral denervation)
Generalized
Synchronized whole body jerk (fragment of gen. epilepsy)
Cranial muscle activation down the brain stem
Mechanism
Whole cortex is hyper excitable and is driven to a paroxysm
by normal ascending impulse from the brain stem reticular
formation and non specific thalamic nuclei.
Ascending impulse could be paroxysmal
EEG:
Generalized fronto central predominance, slow negativity
which precedes the myoclonus
For small jerk this event last 100-250 ms and jitter in time with
respect to jerk
13. PROGRESSIVE MYOCLONIC EPILEPSY
Nonspecific, various condition with progressive multifocal or
generalized epilepsy ± dementia
1. Spinocerebellar Degeneration
Clinical
Heterogenous syndrome (Prototype : Mitochondrial myopathy,
Hexose aminidase A deficiency)
Progressive myoclonus Reflex + action
Generalized epilepsy
Cerebellar ataxia
Sporadic or AR
Onset 5-15 years
Occasional associated
Dementia
Spasticity
Myopathy
Neuropathy
Deafness
19. ESSENTIAL MYOCLONUS -
Friedrich – Paramyoclonus multiplex
Myoclonus without seizure, dementia, ataxia
Multifocal or generalized variable magnitude
May present at rest movement or action
No reflex myoclonus
EEG and other lab test should be normal
Familial or sporadic AD, M:F equal
Onset – 1st to 2nd decade
Korten 1974 in a family
Essential myoclonus + tremor
Other member tremor
Both relieved by alcohol
Some cases have dystonia
Balastic movement overflow myoclonus
Treatement: 5HT, VAL, CLZ, Alcohol
20. CHILDHOOD MYOCLONIC EPILEPSIES
Infantile Myoclonus: West syndrome
Benign myoclonic epilepsy of infancy
3-8 months onset
Repetitive flexor spasm
No mental disturbance
Self limiting
Lanox Gastaut syndrome
True myoclonic epilepsy – symptomatic /
cryptogenic
Late Childhood / adolescent –
Myoclonic with absence
Myoclonic epilepsy of adolescent
21. OSCILLATORY MYOCLONUS
Burst of myoclonic jerk which tend to wane in
amplitude
Once started in part of the body the movement may
spread to other part and gradually wane
No other abnormality
Obeso described anoxic injury
22. STARTLE SYNDROME
Clinical
Sudden muscular contraction to surprise stimuli
Onset when start walking
Exaggerated startle → stiffness of body may → fall ± shout
Prominent hypnogogic ± diurnal generalized myoclonic jerks
Hesitant broad based gait
May improve or persist in later life
EMG
response are shorter than normal latency
EEG –
Abrupt onset of spike and slow wave complex maximum from
centrally → background dysynchronization → normal
SSEP –
significant increased amplitude
Hyperactive long latency reflex due to dys-inhibition of certain
brainstem center
May be stimulus sensitive myoclonic disorder
23. STARTLE EPILEPSY
Non habituating startle → tonic extensor spasm →
epilepsy ±
EEG – Desynchornization → frank epileptiform
discharge bilaterally symmetrical or even focal
Jumping/ Latah/ Myriachit – Initial violent startle in
response to sudden unexpected sensory
stimulation → echolalia, echopraxia, coprolalia or
the assumption of defensive posture
24. NOCTURNAL MYOCLONUS
Physiological
Familial nocturnal start
Occur at sleep onset
Gross, generalized body jerk → arousal
Physiological fragmentary myoclonus
Small fragmentary jerk of head face or diffuse
REM sleep or drowsiness
Benign neonatal sleep myoclonus
During all stages of sleep
Lack EEG correlation
No neurological abnormality
25. NOCTURNAL MYOCLONUS
Pathological
Periodic movement in sleep
EEG burst of 200-500ms more than myoclonus
Common in flexor muscle
Periodic 20-30 sec
Two side of the body can be activated independently
Simultaneously or alternating during
NREM sleep or drowsiness
Normally asymptomatic
Baclofen reduces amplitude
26. SLEEP RELATED MOVEMENT DISORDER
Restless leg syndrome
Intense feeling of paresthesia or funny feeling in leg →
desire to move → improve
May be associated with peripheral neuropathy or familial
May be associated with myoclonus or PMS
Clonazepam
Excessive fragmentary myoclonus in NREM sleep
> 50 jerks/ min for 20 consecutive NREM
Associated with other disorder and PMS