Migraine is a common type of primary headache characterized by recurrent attacks of moderate to severe pulsating headache accompanied by nausea, vomiting, and sensitivity to light and sound. It is classified into migraine with aura and migraine without aura, and treatment involves both acute abortive medications as well as preventive medications and lifestyle modifications to reduce triggers and attack frequency. Diagnosis is based on clinical history and examination along with diagnostic criteria, while management involves a multifaceted approach including both pharmacological and non-pharmacological options.
Epilepsy
Epilepsy is a group is neurological disorder. An epileptic seizure is a paroxysm(sudden) of uncontrolled discharges of neurons causing an event that is discernible(visible) by the person experiencing the seizures or by the observer. The tendency to have recurrent attacks is known as epilepsy.
phenytoin,phenobarbital,sodium valporate ,carbamazepine,clonazepam and diazepam, lamotrigine,pregabalin,felbamate,zonisamide, ETHOSUXIMIDE, LEVETIRACETAM, OXACARBAZEPINE, PRIMIDONE
Epilepsy
Epilepsy is a group is neurological disorder. An epileptic seizure is a paroxysm(sudden) of uncontrolled discharges of neurons causing an event that is discernible(visible) by the person experiencing the seizures or by the observer. The tendency to have recurrent attacks is known as epilepsy.
phenytoin,phenobarbital,sodium valporate ,carbamazepine,clonazepam and diazepam, lamotrigine,pregabalin,felbamate,zonisamide, ETHOSUXIMIDE, LEVETIRACETAM, OXACARBAZEPINE, PRIMIDONE
learning objective includes : pathogenesis,clinical features, classification of migraine, pharmacology about specific antimigraine drugs, coverage to newer triptan- Lasmiditan and newer prophylactic drug Erenumab a CGRP receptor antagonist.
This PPT focuses on the diagnosis and treatment of the primary headache disorders, with special emphasis on migraine, the headache most likely to bring patients to physicians and pharmacists. warning signs of the ominous headache, which, although rare, can herald a life-threatening condition. Clinical characteristics of the primary headache types, migraine, tension-type headache, and cluster headache, are described
Fluoroscopy ,Radiation safety and contrast agents including adverse effect an...Dr Ravi Shankar Sharma
IT includes everything related to fluoroscopy, radiation exposure, it,s effects, contrast agents , and it,s newer variants including gadolinium, anaphylaxis reactions and it,s management, images for epidural,intrathecal,subdural, intrarterial and intravenous contrast picture.
comparative evaluation of effects of different doses of intrathecal clonidine...Dr Ravi Shankar Sharma
this was the winning paper as best free paper in MPISACON14 GWAlOR,which demonstrates comparative evaluation of effects of different doses of intrathecal clonidine with bupivacaine on post operative pain releif
Title: Sense of Smell
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 primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
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.
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
CDSCO and Phamacovigilance {Regulatory body in India}NEHA GUPTA
The Central Drugs Standard Control Organization (CDSCO) is India's national regulatory body for pharmaceuticals and medical devices. Operating under the Directorate General of Health Services, Ministry of Health & Family Welfare, Government of India, the CDSCO is responsible for approving new drugs, conducting clinical trials, setting standards for drugs, controlling the quality of imported drugs, and coordinating the activities of State Drug Control Organizations by providing expert advice.
Pharmacovigilance, on the other hand, is the science and activities related to the detection, assessment, understanding, and prevention of adverse effects or any other drug-related problems. The primary aim of pharmacovigilance is to ensure the safety and efficacy of medicines, thereby protecting public health.
In India, pharmacovigilance activities are monitored by the Pharmacovigilance Programme of India (PvPI), which works closely with CDSCO to collect, analyze, and act upon data regarding adverse drug reactions (ADRs). Together, they play a critical role in ensuring that the benefits of drugs outweigh their risks, maintaining high standards of patient safety, and promoting the rational use of medicines.
- 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
Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...Oleg Kshivets
Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
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
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
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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.
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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
2. DEFINITION
“Migraine is a familial disorder characterized by
recurrent attacks of headache widely variable in
intensity, frequency and duration. Attacks are
commonly unilateral and are usually associated
with anorexia, nausea and vomiting”
-World Federation of Neurology
2
3. EPIDEMIOLOGY
Migraine is (16%) of PRIMARY headaches, 10-20% of the general
population
Initial attack start mostly in adolescents
less frequent in old age group.
predominance in female 2:1
Evidence of positive family history is present in >90% cases.
NEJM 2002; 346(4): 257-269; XI Congress of the IHS, 2004
3
5. CLASSIFICATION ICHD-3rd ed (Beta version)
1. Migraine
1.1 Migraine without aura
1.2 Migraine with aura
1.2.1 Migraine with typical aura
1.2.1.1 Typical aura with
headache
1.2.1.2 Typical aura without
headache
1.2.2 Migraine with brainstem
aura
1.2.3 Hemiplegic migraine
1.2.3.1 Familial hemiplegic
migraine (FHM)
1.2.3.1.1 Familial
hemiplegic migraine type 1
(FHM1)
1.2.3.1.2 Familial
hemiplegic migraine type 2
(FHM2)
1.2.3.1.3 Familial
hemiplegic migraine type 3
(FHM3)
1.2.3.1.4 Familial
hemiplegic migraine, other
loci
1.2.3.2 Sporadic hemiplegic
migraine
1.2.4 Retinal migraine
1.3 Chronic migraine
1.4 Complications of migraine
1.4.1 Status migrainosus
1.4.2 Persistent aura without
infarction
1.4.3 Migrainous infarction
1.4.4 Migraine aura-triggered
seizure
1.5 Probable migraine
1.5.1 Probable migraine without
aura
1.5.2 Probable migraine with
aura
1.6 Episodic syndromes that may
be associated with migraine
1.6.1 Recurrent gastrointestinal
disturbance
1.6.1.1 Cyclical vomiting
syndrome
1.6.1.2 Abdominal migraine
1.6.2 Benign paroxysmal vertigo
1.6.3 Benign paroxysmal
torticollis
5
6.
7. MIGRAINE
Migraine Without Aura Migraine With Aura
No aura or Prodrome Aura or prodrome is present
Unilateral throbbing headache
may be accompanied by nausea
and vomiting
Unilateral throbbing headache
and later becomes generalised
During headache, patient
complains of phonophobia and
photophobia
Patient complains of visual
disturbances and may have
mood variations
7
10. PHASES OF ACUTE MIGRAINE
Prodrome
Aura
Headache
Postdrome
10
11. 1- PRODROME
Vague premonitory (early) symptoms that begin from 12 to 36 hours
before attack in 25% of patients and last for 15 to 20 min
11
Prodromal
symptoms include
Lethargy
Craving for food
Distaste for foods
12. 2- AURA
Aura is a warning or signal before onset of headache
last for 15-30 min
1. Visual aura: is the most common symptoms and occurs as
visual disturbance known as Flashing of lights, Zig-zag lines or
difficulty in focusing
2. Sensoriel aura is the second most common and occurs as
paraesthesia followed by numbness.
3. Lagunage aura is a mild confusion and difficulty in
concentrating or may be sever like alexia or agraphia.
12
14. 3- HEADACHE
• Headache is generally unilateral and is associated
with:
Anorexia
Nausea
Vomiting
Photophobia
Phonophobia
Tinnitus
• Duration is 4-72 hrs
14
15. 4- POSTDROME (Resolution phase)
Duration: Few hours - 2 days
Complains of:
• Fatigue
• Depression
• Severe exhaustion
• Some patients feel unusually fresh
15
21. The pathophysiology of migraine is very complicated and
has many mechanisms, so to understand it we have to
consider the following essential roles of factors:
1. Serotonin role:
2. Calcitonin gene-related peptide (CGRP) role:
3. Genetic role:
4. Vascular role
5. Cortical spreading depression (CSD) of Leão.
6. Trigeminovascular system activation.
Pathophysiology
22. Serotonin ( 5- hydroxytryptamine), may be an important mediator of
migraine by the following observations:
Serotonin role:
Serotonin causes:
• vasodilation in large artery
• vasoconstriction in small artery and capillary
23. a potent vasodilater of cerebral and dural vessels.
It may mediate trigeminovascular pain transmission and the
vasodilatory component of neurogenic inflammation.
Calcitonin gene-related peptide
(CGRP) role:
24. The genetic basis of migraine is likely to be
complex-familial hemiplegic migraine
FHM1,2 gene
Genetic role:
25. Vascular theory
Intracerebral blood vessel vasoconstriction – aura
Intracranial/Extracranial blood vessel vasodilation – headache
25
SUPPORT- Vascular theory
Radioactive xenon cerebral blood flow studies show
significantly reduced regional blood flow through
cortex during aura stage of migraine.
28. MIDAS headache score
Migraine disability assessment(questionnaire)
Some doctors like to
estimate how much
migraines disrupt normal
activities before treatment
begins.
A questionnaire is given to the
patient to estimate how often
they miss various functions
(school, work, family activities)
because of migraines.
28
32. MEDICAL IMAGING
(ONLY TO EXCLUDE SECONDARY CAUSES)
• Neuroimaging used in some cases to exclude secondary causes
of headache or ischemic complications.
• CT SCAN is of extremely low yield
• CT Perfusion may be very useful to analyze acute attacks
perfusion regional changes.
• MRI: It is more sensitive than CT in the detection of an
intracranial abnormality
32
33. DIFFERENTIAL DIAGNOSIS
Mild to moderate
headache
associated with muscle
contraction leads to
headache.
Headache quality is of a
tightening (non-pulsating)
Severe headache
associated with lacrimation,
nasal congestion, rhinorrhea,
facial sweating or eyelid
edema.
Pain lasts for 15 to 180
minutes.
More common in male33
Moderate to Severe
headache
associated nausea,
vomiting, photophobia,
phono phobia
More common in female
36. Non pharmachological treatment
Reducing the attack frequency and severity by avoiding triggers
Lifestyle modifications
Diet therapy:
Exercise therapy:
Meditation
Relaxation therapy (yoga):
Alternative Therapy: Acupuncture:
Psychotherapy
Biofeedback techniques:
36
to reduce migraine triggers like stress and
early symptoms such as muscle tension
38. TRIPTANS
Mechanism of action:
selective agonistic activity on 5-TH-Receptors.
5-HT1B-Receptor agonist causes vasoconstriction,
5 HT1D-Receptor agonist inhibits sensory neuropeptide release from perivascular trigeminal afferents.
It act at central and peripheral components of the trigeminal vascular system by activation of both types
of serotonin Receptors there so it attenuate the excitability of cells in the TNC (Trigeminal Nucleus Caudalis),
38
Side effects:
1. Nausea and dizziness,
2. Paresthesia: (tingling or flushed sensation).
3. chest pain or unpleasant heaviness
4. minor coronary spasm
Contra indications:
1. hypertension,
2. heart disease
3. stroke
New class of antimigraine drugs are the most commonly prescribed
39. ERGOTAMINESDerivatives
Side effects:
nausea, dizziness, muscle pain,
or an unusual or bad taste in
the mouth
39
Mechanism of action: agonistic activity on 5 HT receptors
Have both vasodilator and vasoconstriction effects depending on
dose and resting tone of target vessels.
usually not as effective as triptans.
Mode of administration : oral, parenteral, nasal, rectal.
Dose: 2 mg s/l repeated in 30 minutes if needed.
If more than 6 mg of ergotamine is required per week, use an
alternative preparation.
Contraindication
1. Coronary artery disease, hypertension,pvd
2. pregnancy
3. Hemiplegic migraine, basilar-type migraine or prolonged aura
4. Neurologic deficit.
40. CGRP Antagonist
Calcitonin Gene-Related Polypeptide
Gepants
A novel CGRP antagonist is currently undergoing evaluation in human trials.
Actions: has little vasoconstrictive effect on vascular smooth muscle,
So it benefit patients in whom
•triptan and ergotamine use is CI or has a lot of SE
•comorbid coronary artery disease.
40
42. 1. Frequency of attack > 2 /week
2. Duration of attack > 2 days
3. severity is extreme
4. Presence of prolonged aura
5. If acute migraine treatment
1. Present unacceptable adverse effects
2. Contraindication to use
3. Not effective (patient can’t perform his daily routine)
6. Special circumstances such as
hemiplegic migraine or
attacks with a risk of permanent neurologic injury
7. Patient preference
Indications:-
42
43. 1- Β-Adrenergic blockers: Propranolol, Timolol
43
Propranolol is the ‘gold standard’ in migraine prophylaxis,
especially if patient has hypertension or anxiety co-exist.
Mechanism of action: Vasoconstriction, Anxiolytic action and Decreased
sympathetic activity
Limitations ; Short t½ of 3-5 hrs so patient will need multiple daily dosing
Propranolol long-acting preparations: Starting dose; 40-80 mg once daily
and max. (max 240 mg).
Side effects: Lethargy, depression, hypotension, bradycardia, impotence,
insomnia, and nightmares.
Contraindication: Asthma, severe depression and DM (it may mask the
adrenergic symptoms of hypoglycemia).
44. 2-Antidepressants
Amitriptyline Dosage : 10 to 50 mg at night
Mechanism of action:
1. Blockade of noradrenaline uptake at catecholamine terminals
2. Inhibition of serotonin reuptake may be related,
Side effects: (anticholinergic SE)
If tolerated, give the tricyclic agents a trial of at least 3 months after reaching a
therapeutic dose.
The optimal dose is determined by titration to the effective or maximum
tolerated dose within the therapeutic range (usually 40-320 mg qid) 44
Amitriptyline, Imipramine,
Desipramine, Nortriptyline,
45. 3-calcium channel blockers
Mechanism of action: Prevent vasoconstriction and platelet
aggregation and alterations in release and reuptake of serotonin.
Verapamil in doses of 80 to 160 mg 3 times, not as useful in
migraine without aura.
Flunarizine is weak drug as it reduce the frequency of attacks, but
the intensity and duration is less documented.
Side effect: sedation, constipation, dryness of mouth, hypotension,
flushing, weight gain, rarely extra-pyramidal symptoms.
45
Verapamil, Flunarizine,
Nimodipine
46. 4- Anticonvulsants
Mechanisms of action unknown.
Side effect:
Sedation, dizziness, increased appetite,
increased bleeding time, increased
fragility of hair, and an asymptomatic
increase in liver function test values.
Contraindication:
pregnancy.
46
Gabapentin: is effective in the
reduction of migraine incidence
The usual therapeutic dose range for
gabapentin is 900 to 3600 mg/day.
Valproic acid: given in the form
of divalproex sodium,
Dose range of 500 to 1750 mg/day
taken in divided doses.
47. 5- Serotonergic agents
Cyproheptadine is a peripheral serotonin antagonist.
It has weak anti-bradykinin activity and prevents platelet
aggregation.
it is more effective in children.
Side effect:-it causes drowsiness and significant weight gain.
47
48. 6- Other prophylactic agents
Riboflavin administered orally in a dose of 400 mg/day has
been shown to be effective in migraine prophylaxis in a
prospective randomized controlled study
48
49. 49
Topiramate
Mode of action: effects not only on γ-aminobutyric acid (GABA) but also on
non-NMDA glutamate and carbonic anhydrase activity.
Side effects :It may have prominent sedating and cognitive side effects.
paresthesia and weight loss, mildly increased risk for kidney stones.
Dosage: Slow gradual titration of the drug (15-25 mg/wk initially) to the
therapeutic range of 75 to 200 mg/day the most successful strategy.
50. BOTULINUM TOXIN FOR CHRONIC MIGRAINE
Two randomized, placebo-controlled studies
of onabotulinumtoxinA injections (12 weeks
apart) for the prevention of chronic migraine
headaches, with follow-up for 24 weeks (679
and 705 subjects),
revealed no change in frequency, but fewer headache days and migraine days com
pared to placebo,
Most common adverse effects with Botox injections were neck pain, muscle
weakness, eyelid ptosis, myalgia, and muscle stiffness, as well as, paradoxically,
worsening migraine.
50
52. NERVE BLOCKS FOR HEADACHE RELIEF
52
26-gauge, 1/2” needle introduced
medial to the external occipital
protuberance.
Needle advanced to periosteum,
then withdrawn 1-2 mm.
Mixture of bupivacaine (Marcaine)
0.5%, 1-2 ml, and triamcinolone
(Kenalog) 40 mg/ml, 0.5 ml,
injected slowly in 0.5 cc aliquots,
with aspiration prior to each
injection.
Occipital nerve block