bagaimana hubungan nyeri kepala dengan epilepsi? epilepsi menyebabkan nyeri kepala? nyeri kepala menyebabkan epilepsi? epilepsi yang manifestasinya nyeri kepala? kapan kita curiga suatu nyeri kepala merupakan bentuk kejang?
this presentation discusses pain pathways, definition and glossary of pain symptoms, classification of pain, pathogenesis, causes, diagnosis , types and treatment of neuropathic pain
illustrated with figures
this presentation discusses pain pathways, definition and glossary of pain symptoms, classification of pain, pathogenesis, causes, diagnosis , types and treatment of neuropathic pain
illustrated with figures
Pain is the production (out put ) of the brain.
Pain is invisible disease, we can’t see it like other disease, such as struma, fracture or blind.
What you have to do is to believe what ever the patient says.
Pain is what ever the patient says it is
Pain is invisible diseases, but is real for patient.
Pain Physicians should consider nerve blocks when systemic analgesics are failing. (Adjuvant therapy)
Careful selection of patients
Benefits should outweigh the risks
Thorough knowledge of the limitations and side effects
Need for randomized controlled clinical trials.
Effective pain management in terminally ill requires
Understanding of pain control strategies
Ongoing assessment
Diagnosis of pain
Breakthrough pain relief
Fine adjustment of medications
Opioid rotation
Unresolved psychosocial or spiritual issue can be great impact to pain management
Pain is the production (out put ) of the brain.
Pain is invisible disease, we can’t see it like other disease, such as struma, fracture or blind.
What you have to do is to believe what ever the patient says.
Pain is what ever the patient says it is
Pain is invisible diseases, but is real for patient.
Pain Physicians should consider nerve blocks when systemic analgesics are failing. (Adjuvant therapy)
Careful selection of patients
Benefits should outweigh the risks
Thorough knowledge of the limitations and side effects
Need for randomized controlled clinical trials.
Effective pain management in terminally ill requires
Understanding of pain control strategies
Ongoing assessment
Diagnosis of pain
Breakthrough pain relief
Fine adjustment of medications
Opioid rotation
Unresolved psychosocial or spiritual issue can be great impact to pain management
Recent Migraine Headache Approach and Treatment.pptxSURENDRAKHOSYA2
A migraine is a headache that can cause severe throbbing pain or a pulsing sensation, usually on one side of the head. It's often accompanied by nausea, vomiting, and extreme sensitivity to light and sound. Migraine attacks can last for hours to days, and the pain can be so bad that it interferes with your daily activities.
For some people, a warning symptom known as an aura occurs before or with the headache. An aura can include visual disturbances, such as flashes of light or blind spots, or other disturbances, such as tingling on one side of the face or in an arm or leg and difficulty speaking.
Medications can help prevent some migraines and make them less painful. The right medicines, combined with self-help remedies and lifestyle changes, might help.
Migraines are often undiagnosed and untreated. If you regularly have signs and symptoms of migraine, keep a record of your attacks and how you treated them. Then make an appointment with your health care provider to discuss your headaches.
Even if you have a history of headaches, see your health care provider if the pattern changes or your headaches suddenly feel different.
if you have any of the following signs and symptoms, which could indicate a more serious medical problem:
An abrupt, severe headache like a thunderclap.
Headache with fever, stiff neck, confusion, seizures, double vision, numbness or weakness in any part of the body, which could be a sign of a stroke.
Headache after a head injury.
A chronic headache that is worse after coughing, exertion, straining or a sudden movement.
New headache pain after age 50.
getting too much sleep can trigger migraines in some people.
Physical strain. Intense physical exertion, including sexual activity, might provoke migraines.
Weather changes. A change of weather or barometric pressure can prompt a migraine.
Medications. Oral contraceptives and vasodilators, such as nitroglycerin, can aggravate migraines.
Foods. Aged cheeses and salty and processed foods might trigger migraines. So might skipping meals.
Food additives. These include the sweetener aspartame and the preservative monosodium glutamate (MSG), found in many foods.
Diagnostic presentation HeadacheUnited States UniversitLinaCovington707
Diagnostic presentation
Headache
United States University
Introduction
Headache is the most common pain in the united states.
Headache means pain or discomfort in the head, face, or neck.
Headache can be caused by inflammation or spasm related to cranial vessels, nerves, or muscles Headache can be primary or secondary. (Dlugasch & Story, 2021)
Classification of headache
Primary headache
Most common, not a symptom of underlying an underlying disease
Benign
Can be recurrent
It mainly occurs early in an individual
Decrease after ages 40 to 50
Migraine
Tension-type headache
Trigeminal autonomic cephalgia
Other primary headache disorders (Rizzoli & Mullally, 2018).
Secondary headache
Caused by an underlying condition
Trauma or injury to the head or neck
Cranial or cervical vascular disease
Nonvascular intracranial disorder
A substance or its withdrawal
Infection
Affliction of homeostasis
Illness of the skull, neck, eyes, ears, nose, sinuses, teeth, mouth, or other facial or cervical structure
Psychiatric disorder (Rizzoli & Mullally, 2018).
The red flag of headache
If an older patient complaint of New headache
Abnormal neurologic examination such as mental status changes and papilledema
If there is any New change in the headache pattern
Intensifying headache
New headache if in case of HIV risk factors, cancer, or an immunocompromised status
Systemic illness signs (e.g., fever, stiff neck, rash)
If precipitate by cough, exertion, Valsalva maneuver
If the Headache in pregnancy or postpartum period
If a patient says it is the First or worst headache of my life (Rizzoli & Mullally, 2018).
Pathophysiology of headache
Stimulation of primary nociceptors
Lesions in the pain-producing pathway of PNS and CNS
Pain producing structure
Scalp
Middle meningeal artery
Dural sinuses
Flax cerebri
Proximal segment of the large pial arteries (Dlugasch & Story, 2020)
Pathophysiology of headache continue
There are no nociceptors in the brain parenchyma
So the pain originates from surrounding structures, such as blood vessels, meninges, muscle fibers, facial structures, and cranial or spinal nerves.
Any stretching, dilatation, constriction, or any nociceptor when they stimulate stimulation structures can cause the perception of headache.
The secondary headache depends on the cause and diseases
( Rosenthal & Burchum, 2021)
migraine headache
Migraine headache is a headache associated with systemic complaints. The person feels a severe throbbing pain or a pulsing sensation, usually on one side of the head, along with nausea, vomiting, and extreme sensitivity to light and sound. The attacks can last for hours to days, and the pain can be severe that it interferes with daily activities (Dlugasch & Story, 2020).
Triggers to migraine headache
Emotional stress
Hormonal change during menstruation
Alcohol intake
Change in weather
Odors
Disturbance in sleep or not getting enough sleep
migraine heada ...
This presentation describes the concept of temporal plus syndrome, pseudotemporal epilepsy and paradoxical temporal lobe epilepsy and how to differentiate them from temporal lobe epilepsy.
"..The proposed definition, therefore, is not intended to be prescriptive but represents a working framework. Clinicians and researchers should exercise their judgment in interpreting the principles described in this report when applying the definition to diverse settings.."
-- Kwan P, et al, 2017
Klasifikasi tipe kejang terbaru tahun 2017 oleh ILAE didasarkan pada "onset" kejangnya. Focal atau General. Kenapa kita harus tahu tipe kejang yang diderita ini focal atau general? Bagaimana kita tahu suatu kejang ini focal atau general? Apakah hanya berdasarkan "onset"-nya saja? Seberapa spesifik kah "focal" yang diperlukan untuk menentukan keputusan klinis kita? Apakah "focal" itu cukup sebatas mengetahui hemisfer kanan/kiri, atau sampai menentukan lobus yang terkait, atau gyrus, atau area yang lebih spesifik? Apa gold standar diagnosis topis sumber kejang? Apakah semiologi masih relevan dengan begitu berkembangnya teknologi imaging, EEG, genetika?
Sebenernya "filosofi" merupakan topik yang "ketinggian" buat si cip yang masih berada dalam stage mengasah "teknik" interpretasi. Dalam perjalanannya, sang guru sudah menanamkan filosofi ke dalam benak si cip, bahkan sejak hari pertama. "Bad EEG is worse than no EEG at all". Dan beliau tidak bosan-bosannya mengulang.
Mungkin, hikmah yang terpenting dari mempelajari "filosofi" interpretasi EEG sejak awal adalah membuat kita menyadari limitasi diri kita dan instrumen yang kita gunakan, menjadi pengingat agar tidak berhenti belajar, dan kemudian dengan cara yang terbaik mendayagunakan seluruh knowledge, skill & technique yang kita punya..
Stroke iskemik memiliki risiko kematian, disabilitas, dan serangan ulang yang berbeda-beda menurut subtipe yang didasarkan pada mekanisme penyebab stroke. Identifikasi penyebab stroke merupakan elemen penting dalam praktik klinis sehari-hari untuk memandu keputusan terapi, menentukan prognosis, dan mencegah kekambuhan stroke setiap pasien.
Kejadian stroke hemodinamik diperkirakan sekitar 10% dari seluruh infark otak. Pasien dengan stroke hemodinamik umumnya memiliki gejala ringan dibandingkan dengan subtipe stroke infark lainnya. Stroke hemodinamik jarang bersifat fatal sehingga kurang diperhitungkan. Padahal, pasien stroke hemodinamik sering disertai stenosis berat arteri mayor. Stroke hemodinamik berkaitan dengan peningkatan risiko perburukan neurologis, kekambuhan stroke, dan risiko kardiovaskular lainnya. Namun, stroke hemodinamik dapat dideteksi dengan gejala klinis tertentu & pemeriksaan radiologis. Pengenalan tentang adanya hipoperfusi sebagai faktor penyebab stroke iskemik akan membawa konsekuensi penting dalam perawatan dan manajemen pasien stroke..
Keunikan anatomi small vessel of the brain dan neurovascular unit, kontroversi peran stganasi vena dalam patofisiologi, klasifikasi small vessel disease, variasi kriteria diagnostik, pitfall dalam neuroimaging, pilihan antiplatelet untuk prevensi sekundar, dampaknya bagi outcome pasien, hubungannya dengan gangguan fungsi kognitif.
Hmm, apa lagi nih yang baru?
Blood-Pressure Management in Patients with Acute Cerebral Hemorrhage
Kontroversi hasil studi ATACH-2 dan dampaknya dalam manajemen hipertensi pada stroke perdarahan intraserebral akut.
Effect of Blood Pressure Lowering in Early Ischemic Stroke, Time to Change Pr...Ersifa Fatimah
Seorang rekan residen neuro sampai mengirim (via e-mail) sebuah jurnal yang baru ditelaahnya di larut malam. Kepada si cip, dia menyatakan bagaimana jurnal ini membuat pikirannya bergejolak, “Seperti dipaksa untuk menerima sebuah pemikiran baru yang melawan apa yang telah kita yakini bersama dalam proses belajar kita selama 5 tahun terakhir ini!”
Artikel itu berjudul Effect of Blood Pressure Lowering in Early Ischemic Stroke: Meta-Analysis oleh Lee et al., dan dipublikasi dalam jurnal Stroke Juli 2015.
Ischemic Stroke Subclassification, An Asian ViewpointErsifa Fatimah
Pada awalnya, sistem klasifikasi stroke diderivasi dari temuan autopsi yang dikaitkan dengan klinis pasien. Seiring dengan berkembangnya modalitas imaging & investigasi vaskular, klasifikasi stroke yang pada awalnya menitikberatkan pada sindroma klinis beralih menjadi suatu proses decision-making berdasarkan data klinis-radiologis-laboratoris.
Menariknya lagi, proporsi subtipe stroke ini pun berubah, sesuai sistem & kriteria yang digunakan...
Hmmm, bagaimana dengan klasifikasi dan proporsi tipe stroke di Asia?
Teruntuk Perempuan Indonesia,
Waspada risikonya dan cegah STROKE sejak dini.
*from NEUROLOGISTS, with LOVE.
Hari Stroke Dunia, 29 Oktober 2015 : Saya Perempuan.
Kapan aneurysma yang belum ruptur memerlukan intervensi?
"In the decision-making process, the PHASES score may be considered for predicting a patient’s risk of aneurysm rupture."
Terapi Endovaskuler, Standar Baru Manajemen Stroke Iskemik Akut? Ersifa Fatimah
Konon, plenary pertama International Stroke Conference (ISC) 2015 yang digelar di Nashville, Tennessee bulan Februari lalu merupakan sesi ISC terseru selama beberapa tahun terakhir. Sebagaimana diberitakan dalam Medscape (Hughes, 2015), para presenter terpaksa memberi jeda beberapa saat untuk menyambut applause dari audiens. Suatu kejadian langka dalam partemuan saintifik. Adalah MR CLEAN, ESCAPE, EXTEND-IA, dan SWIFT PRIME yang menjadi topik hangat lantaran keempat studi ini dirilis dengan hasil yang positif dramatis hingga diprediksi bakal menjadikan terapi endovascular sebagai standar baru dalam manajemen stroke iskemik akut. Sehebat apakah 4 studi yang “menyejarah” dalam tatalaksana stroke iskemik akut ini? Bagaimana bila studi-studi ini diadopsi dan diaplikasikan dalam praktik sehari-hari di sentra kita?
Note: Esai ini ditulis saat SWIFT PRIME fulltext belum published (akhir Maret-awal April 2015). Update & beberapa revisi dibuat menjelang presentasi tanggal 18 Mei 2015.
Parkinsonism Puzzle - Case
Saya banyak belajar dari kasus ini, bersyukur mendapat kesempatan belajar dari kasus ini.
Menanti advis dan kesempatan berdiskusi dengan rekan sejawat & pembaca.
*Semoga selalu yang terbaik untuk pasien kita!
note: cerita lengkapnya di [https://neurobsession.wordpress.com/2015/02/05/parkinsonian-dementia-chapter1-organic-vs-psychogenic-the-debate/]
Microsurgery for cerebral AVM, Theofanis et al, Neurosurg Focus, 2014Ersifa Fatimah
Microsurgery for cerebral AVM: postoperative outcomes & predictors of complications in 264 cases, by Theofanis et al, from Neurosurg Focus, 2014
--Topik journal reading-ku pas stase Neurosurgery..
Stroke prevention for nonvalvular AF, summary of evidence-based guidelinesErsifa Fatimah
Ternyata... guideline yang ngebahas prevensi stroke pada nonvalvular AF tu banyak banget! Yang dirilis komunitas Neuro maupun Cardio, yang internasional maupun yang lokal. Dan pertanyaan besarnya tetep: What's the best strategy?
*Bonus special issue: manajemen prevensi stroke infark dengan antikoagulan pasca brain hemorrhage.
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
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Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
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
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
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.
2. Introduction
• Abundant clinical and epidemiologic data
demonstrate that headache/migraine and
epilepsy are highly comorbid.
• The disorders share overlapping risk factors,
brain mechanisms, and treatments.
• The clinical presentation of migraine and
epilepsy may overlap, creating a challenge in
differential diagnosis.
Engel & pedley, Epilepsy, A Comprehensive Textbook, 2nd eds, 2008, p 5257 -5273
2
3. Introduction
• Periictal headache (PIH) displays a frequent
ancillary burden to seizures, but identification
of unequivocal predictors is still elusive. PIH is
frequent, severe and undertreated.
Duchaczeck B et al. Interictal and periictal headache in patients with epilepsy.
Eur J Neurol. 2012 Dec 25.
3
4. Introduction
• The relationship between headache and seizures is a
complicated one, since these two conditions are related in
numerous ways.
• In order to improve the care for patients with a clinical
connection between migraine and epilepsy, it is necessary to
try to understand more accurately the exact
pathophysiological point of connection between these two
conditions.
Papetti et al. “Headache and epilepsy”— How are they connected?
Epilepsy&Behavior26(2013)386–393
4
5. Introduction
• Major discrepancies and conflicting data about
comorbidity between headache and epilepsy due
to: [1]
– the confusion and mixture of epidemiological data
between adults and children across studies
– the significant underestimation of headache when it
is comorbid in populations with epilepsy.
• Due to the different methodologies and criteria
used, the studies are quite difficult to compare. [2]
5
7. Kasus
Px
LK
SR
PU
FM
SN
Jenis/ Usia
Karakteristik nyeri kepala
(thn)/ Status/
Pekerjaan
P/49/
“Kemeng”, unilateral (kiri)
Menikah/
sekitar mata & hidung,
Ibu rumah
tangga
Gejala
penyerta
Mata kiri
merah, kabur,
mual.
Variabel epilepsi & terapi
EEG
CT/MRI
(Riwayat syncope saat kanak Sharp wave & ISA
& pelo mendadak 5 tahun
temporal kiri
lalu)
Normal
P/29/ Belum
menikah/
Pembantu
rumah tangga
L/33/
Menikah/
“tukang
odongodong”
P/16/ Belum
menikah/
Pelajar
Berdenyut bilateral, 2-3
jam, muncul setelah kejang
Kejang fokal umum sekunder tonik klonik, aura: melihat
sawah
-
Berdenyut, unilateral (kiri),
muncul setelah kejang.
Mual
Automatisme sejak 10 tahun Sharp wave & ISA
lalu, kejang umum tonik
temporal D/S (Interklonik sejak 3 bulan lalu
ictal, 2013)
Toxo dd
Tuberculoma di
cerebellum
Berdenyut, unilateral
bilateral (mulai kanan), 1
jam, aura (-)
Mual, muntah,
fotofobia
Fokal kiri umum sekunder
tonik sejak usia 3 bulan
Normal (inter-ictal, 4
tahun lalu)
?
P/60/
Menikah/
Penjahit
Berat/ditekan bilateral
Rasa tidak
nyaman di
perut, depresi
Kejang parsial kompleks 7
tahun lalu, kejang umum
tonik-klonik sejak 1 tahun
lalu
Sharp wave di regio
temporal kiri (interictal?, 2012)
Normal
7
8. Kasus
Px
LK
SR
PU
FM
SN
Jenis/ Usia
Karakteristik nyeri kepala
(thn)/ Status/
Pekerjaan
P/49/
Kemeng, unilateral (kiri)
Menikah/
sekitar mata & hidung,
Ibu rumah
tangga
Gejala
penyerta
Mata kiri
merah, kabur,
mual.
P/29/ Belum
menikah/
Pembantu
rumah tangga
L/33/
Menikah/
“tukang
odongodong”
P/16/ Belum
menikah/
Pelajar
Berdenyut bilateral, 2-3
jam, muncul setelah kejang
P/60/
Menikah/
Penjahit
Berat/ditekan bilateral
•
•
•
Berdenyut, unilateral
•
bilateral (mulai kanan), 1
Berdenyut, unilateral (kiri),
muncul setelah kejang.
Variabel epilepsi & terapi
EEG
CT/MRI
(Riwayat syncope saat kanak Sharp wave & ISA
& pelo mendadak 5 tahun
temporal kiri
lalu)
Normal
Kejang fokal umum sekunder tonik klonik, aura: melihat
sawah
-
Perempuan >sejak 10 tahun Sharp wave & ISA
Laki
Automatisme
lalu, kejang
Usia muda >umum tonik temporal D/S (Interklonik sejak 3 bulan lalu
ictal, 2013)
Berdenyut > Nyeri kepala lain
Mual, muntah, Fokal kiri umum sekunder
(inter-ictal, 4
Lobus Temporal > Normallalu)
fotofobia
tonik sejak usia 3 bulan
tahun
Mual
Toxo dd
Tuberculoma di
cerebellum
?
jam, aura (-)
Rasa tidak
nyaman di
perut, depresi
Kejang parsial kompleks 7
tahun lalu, kejang umum
tonik-klonik sejak 1 tahun
lalu
Sharp wave di regio
temporal kiri (interictal?, 2012)
Normal
8
9. Kasus
Px
LK
SR
PU
FM
SN
Jenis/ Usia
Karakteristik nyeri kepala
(thn)/ Status/
Pekerjaan
P/49/
Kemeng, unilateral (kiri)
Menikah/
sekitar mata & hidung,
Ibu rumah
tangga
Gejala
penyerta
Mata kiri
merah, kabur,
mual.
P/29/ Belum
menikah/
Pembantu
rumah tangga
L/33/
Menikah/
“tukang
odongodong”
P/16/ Belum
menikah/
Pelajar
Berdenyut bilateral, 2-3
jam, muncul setelah kejang
P/60/
Menikah/
Penjahit
Berat/ditekan bilateral
•
•
•
Berdenyut, unilateral
•
bilateral (mulai kanan), 1
Berdenyut, unilateral (kiri),
muncul setelah kejang.
Variabel epilepsi & terapi
EEG
CT/MRI
(Riwayat syncope saat kanak Sharp wave & ISA
& pelo mendadak 5 tahun
temporal kiri (ictal,
lalu)
2013)
Normal
Kejang fokal umum sekunder tonik klonik, aura: melihat
sawah
-
Perempuan >sejak 10 tahun Sharp wave & ISA
Laki
Automatisme
lalu, kejang
Usia muda >umum tonik temporal D/S (Interklonik sejak 3 bulan lalu
ictal, 2013)
Berdenyut > Nyeri kepala lain
Mual, muntah, Fokal kiri umum sekunder
(inter-ictal, 4
Lobus Temporal > Normallalu)
fotofobia
tonik sejak usia 3 bulan
tahun
Mual
Toxo dd
Tuberculoma di
cerebellum
?
jam, aura (-)
Rasa tidak
nyaman di
perut, depresi
Kejang parsial kompleks 7
tahun lalu, kejang umum
tonik-klonik sejak 1 tahun
lalu
Sharp wave di regio
temporal kiri (interictal?, 2012)
Normal
9
10. Association between headache & epileptic seizure
according to their temporal occurrence
Pre-ictal headache
Ictal headache
Post-ictal headache
Inter-ictal headache
Cianchetti C, et al. Epileptic seizures and headache–migraine:
A review on types of association and terminology. Seizure: Eur J Epilepsy (2013)
10
11. Prevalence of headache and migraine in epilepsy
and its relationship with ictal and interictal period
Bianchin MM et al, Migraine and Epilepsy : A Focus on Overlapping Clinical, Pathophysiological, Molecular, and
11
Therapeutic Aspects. Curr Pain Headache Rep (2010)
12. Inter-ictal headache
prevalence
• Migraine in px wth epilepsy: 14-24%
• Epilepsy in px with migraine: 1.1-17%
Andermann et al, 1987, Tellez-Zenteno et al, 2005, Leinger et al, 2003
12
13. Inter-ictal headache
Tonini et al, 2012
• Research hypothesis:
comorbidity among patients with either disorder
would be expected to be higher than in the
general population
• Result:
prevalence of comorbidity in patients with
epilepsy and in those with headache roughly
overlaps that of the general population no
association between the two conditions.
13
14. Pre-ictal Headache/Migraine
Variants
• Migraine with aura followed by an
epileptic seizure
• ICHD-2: Migraine-triggered seizure
(Migralepsy) prevalence is
unknown, associated with basilar-type
migraine & menstrual migraines
• Migraine without
aura followed by an
epileptic seizure
• Headache followed
by an epileptic
seizure
• Pre-ictal headache
• Pre-ictal migraine, migraine-triggered seizure
– Migraine attack, fulfilling migraine criteria, +/- aura,
– Seizure fulfilling diagnostic criteria for 1 type of epileptic attack
– Seizure occurs during/within (conventionally) 1 hour after cessation of the
migraine attack
• Pre-ictal headache
– When criteria for migraine are not met
Bianchin, 2010; Cianchetti et al, 2013
19
15. Pre-ictal Headache/Migraine
• Migrainous aura is the clinical manifestation of
cortical spreading depression(CSD), a potent
excitatory electrical neuronal wave followed
by neuronal inhibition and glial activation
Neuronal activation generated by CSD
decreases the threshold in the epileptic focus
increasing the risk of seizures
Bianchin MM et al, Migraine and Epilepsy : A Focus on Overlapping Clinical, Pathophysiological, Molecular,
and Therapeutic Aspects. Curr Pain Headache Rep (2010)
20
16. Pre-ictal Headache/Migraine
Direct surgical observations & neuroimaging
findings:
• Increased blood flow that precedes epileptic
seizures may trigger trigeminovascular
activation & consequent headaches
Bianchin MM et al, Migraine and Epilepsy : A Focus on Overlapping Clinical, Pathophysiological, Molecular,
and Therapeutic Aspects. Curr Pain Headache Rep (2010)
21
17. Ictal headache
Epileptic headache / Ictal epileptic headache
• Headache (whether migraine or not)
• Onset, and cessation if isolated, coinciding with an EEG
pattern of epileptic seizure
(rarely EEG alterations may only be detectable using deep
electrodes)
Cianchetti et al, 2013
Variants
• Not followed by other epileptic • Followed by other epileptic
manifestations
manifestations
• Pure/isolated epileptic
• Epileptic seizure beginning
headache
with headache
• ICHD-2: Hemicrania epileptica
23
18. Ictal headache
Epileptic headache / Ictal epileptic headache
Relatively low prevalence of ictal headaches due
to:
• Cognitive / consciousness impairments
provoked by seizures.
• Seizures propagate to the thalamus
analgesic status may be rendered (evidence to
support this hypothesis is lacking)
Bianchin MM et al, Migraine and Epilepsy : A Focus on Overlapping Clinical, Pathophysiological, Molecular,
and Therapeutic Aspects. Curr Pain Headache Rep (2010)
24
19. Epileptic headache: Challenge
• Probably underdiagnosed
– Physician & patient tend to emphasize the other
epileptic manifestations
• Requiring a diagnostic differentiation from
other types of headache
– Particularly in pure epileptic headache & no
epileptic abnormalities are present in the
interictal EEG
Cianchetti C, et al. Epileptic seizures and headache–migraine:
A review on types of association and terminology. Seizure: Eur J Epilepsy (2013)
25
20. Migraine vs Epilepsy
• Share many features: chronic, episodic
manifestation, similarities of classification,
ictal progression, symptomology
• Differentiating is usually accomplished on
clinical ground
• EEG not routinely indicated in migraine, may
be useful
Haut S, Differentiating Migraine from Epilepsy. Adv Stud Med. 2005;5(6E):S658-S665
26
21. Migraine vs Epilepsy
Migraine
Epilepsy
Prevalence
Lower during earlier childhood,
decreasing again in older ages
Bimodal pattern, affecting
mostly children and the
Elderly
Sex
Female > Male
//
Consequences
Has not been associated with
reduced lifespan
Stigmatizing disease, being a
life-threatening condition
Bianchin MM et al, Migraine and Epilepsy : A Focus on Overlapping Clinical, Pathophysiological, Molecular,
and Therapeutic Aspects. Curr Pain Headache Rep (2010)
27
22. Migraine vs Epilepsy
Ictal Progression
Migraine
Preaura
prodrome/
Premonitory
phase
Aura
Epilepsy
Irritability, joy, or sadness
Talkactiveness or social withdrawal
Appetite change or anorexia
Water retention
Sleep diturbances
Heaviness, depression,
irritability
GI upset
(next table)
Ictus
Prolonged (4-72 hours) unilateral
Brief , self limited (1-2
throbbing headache with associated minute), exception:
features
status epilepticus
Automatism absent
Post-ictal
Impaired concentration, malaise, or
euphoria
Common post-ictal
state, marked after GTCS
Haut S, Differentiating Migraine from Epilepsy. Adv Stud Med. 2005;5(6E):S658-S665
28
23. Migraine vs Epilepsy
Aura
Migraine
Epilepsy
Definition
Complex of symtoms occuring
prior to, at onset, or during
migraine
Simple partial seizure, no
alteration on consciousness
Mechanism
Cortical spreading depression
Synchronous neuronal discharge,
limited distribution
Functional
imaging
Wave of decreased CBF
Increased cerebral blood flow &
metabolism
Duration
15-60 minutes, develops slowly
Brief (less than 1 minute)
Occur in
isolation
Yes. Acephalgic migraine, aura
without headache
Yes. Simple partial seizure
Common
symptoms
Visual: most common
Sensory: paresthesias
Motor: unilateral weakness
Limbic: abdominal sensation, fear,
deja vu
Sensory: paresthesias
Motor: twitching
Haut S, Differentiating Migraine from Epilepsy. Adv Stud Med. 2005;5(6E):S658-S665
29
24. Keywords
• Status migrainosus unresponsive to analgesic
therapy iv administration of lorazepam
induced the prompt resolution of the
symptoms.
Belcastro et al. Ictal epileptic headache mimicking status migrainosus: EEG and DWI-MRI
findings. Headache. 2011 Jan;51(1):160-2.
• Brief episodes (of a few minutes) of severe
frontal headache..
Chiancetti et al. Pure epileptic headache and related manifestations: a video-EEG report and
discussion of terminology. Epileptic Disord. 2013 Mar;15(1):84-92.
31
25. EEG in the evaluation of Headache
A new list from the American Academy of Neurology
(AAN) calls into question 5 clinical practices judged
to be of little or no benefit for patients.
• Don't perform electroencephalography (EEG) for
headaches.
– Recurrent headache is the most common pain
problem, affecting up to 20% of the general population.
– EEG has no advantage over clinical evaluation in
diagnosing headache, does not improve outcomes, and
increases costs.
Jeffrey S. AAN Points to 5 Questionable Practices in Neurology. Medscape,
Feb 22, 2013. http://www.medscape.com/viewarticle/779756
32
26. EEG in the evaluation of Headache
• A total of 50 patients yielded 50 routine EEGs
(headache NOS, n = 32; migraine n = 18).
• Overall, there were 37 (74%) normal EEGs and 13
(26%) abnormal.
• Routine EEGs are mostly normal in young patients
(18-40 years of age) who are referred to our
laboratory with a diagnosis of headache NOS or
migraine.
Senthi NK et al. Diagnostic utility of routine EEG study in identifying seizure as the
etiology of the index event in patients referred with a diagnosis of migraine and not
otherwise specified headache disorders. Clin EEG Neurosci. 2012 Oct;43(4):323-5.
33
27. EEG in the evaluation of Headache
• Contributed greatly to increasing understanding
of the pathogenesis of primary headache, but
little / no value in the clinical setting.
• Interictal EEG is not routinely indicated in the
diagnostic evaluation of patients with headache.
• Interictal EEG is, however, indicated if the clinical
history suggests a possible diagnosis of epilepsy
(differential diagnosis).
• Ictal EEG could be useful in certain patients
suffering from hemiplegic or basilar migraine.
Sandrini G et al, Neurophysiological tests and neuroimaging procedures in nonacute headache (2nd edition). Eur J Neurol. 2011 Mar;18(3):373-81.
34
28. EEG in the evaluation of Migraine
• Striking EEG patterns have been described in specific subtypes of
migraine.
• The brain regions most often involved in the published EEG samples
in basilar-type migraine include the posterior temporal, parietal,
and occipital regions. The posterior electrographic localization may
not pertain to other forms of migraine.
• Paroxysmal lateralizing epileptiform discharges (PLEDs) or PLED-like
activity has been associated with hemiplegic migraine, prolonged
migraine aura, or incipient migrainous infarction. Those patients
with PLED-like activity did not have any of the usual entities
associated with PLEDs, such as stroke, brain abscess, glioblastoma,
or viral encephalitis, and their PLEDs usually resolved within 24
hours. Certain migralepsy patients had clinical seizures when PLEDs
were present on their EEGs.
Schachter SC (ed). Differential diagnosis of migraine and epilepsy.
http://professionals.epilepsy.com/page/migraine_eeg.html
35
29. Post-ictal Headache
• Features of tension-type headache OR
migraine headache (in px with migraine)
• Develops within 3 hours after seizure
• Diseappears within 72 hours after the seizure
• Partial or generalized epileptic seizure
ICHD-2, International Headache Society, 2004
Ekstein D, Schachter SC. Postictal headache. Epilepsy & Behavior 19 (2010) 151–155
43
30. Post-ictal headache
Risk Factor
Age
Significantly higher in younger patient [1]
Sex
Significantly higher in female [2]
Male : Female = 1:1.8 (pediatric) [3]
Relationship to interictal
headache
Occurrence of IIH appears to increase the risk
of PIH [4], especially with migraine [5]
PIH shorter duration than IIH [6]
Relationship to family history
of headache
No association [7]
Ekstein & Schachter, 2010
Controversy.
Other studies: not statistically significant association
44
31. Post-ictal headache
Association with epilepsy-related variables
Duration
Younger age of onset epilepsy
(HELP study, 2010: 22.1 vs 28.8)
Longer duration of disease
(HELP study, 2010: 9.9 years vs 7.3 years)
Severity
PIH correlated with AED polytherapy [1]
Characteristic of seizure
PIH more frequent after GTCS & more severe after
prolonged/repetitive seizure [2]
Occurred in 96 & 28 % GTCS, 88-62& secondary GTCS, 43%
partial seizure, 70-22% CPS
GTCS ~ nonmigraineous/ steady
CPS ~ throbbing
Classification/location of
epilepsy
No clear association
PIH is more frequent in OLE (59-62%) > FLE (40-42%) > TLE
(23-41%) [3]
Ekstein & Schachter, 2010
45
32. Post-ictal headache
Pathophysiology
• Headaches may occur as following brainstem
activation, with consequent trigeminal
activation and vasodilation
(as for pre-ictal headaches)
Bianchin MM et al, Migraine and Epilepsy : A Focus on Overlapping Clinical, Pathophysiological, Molecular,
and Therapeutic Aspects. Curr Pain Headache Rep (2010)
46
33. Patofisiologi Kejang
Gangguan permeabilitas membran neuron
Ketidakseimbangan inhibisi dan eksitasi
Disfungsi sel glia
Kejang “Energy failure” Edema serebri Nyeri kepala
34. Pathophysiology of Primary Headache
Migraine [Suharjanti, 2009 & 2013; Sjahrir, 2008]
•
•
•
•
•
Hyperexcitability neuronal
Cortical spreading depression
Trigeminal activation: peripheral & central
PAG: progressive changes
Genetic
Tension-type Headache [Suharjanti, 2009; Machfoed, 2008; Basir, 2012]
•
•
•
•
Muscle contraction
Vascular theory
Humoral theory
Posture
Cluster Headache [Suharjanti, 2009; Blanda, 2012]
•
•
•
•
•
Periodicity ~hypothalamus, central disinhibition of nociceptive & autonomic pathways
Trigeminal-facial neuronal circuitry alteration due to central sensitization
Substance P neurons in V1&2
Vascular dilatation (neurogenic)
Histamine?
52
35. • The mechanisms underlying the association of
migraine and epilepsy are yet to be elucidated
• Several subtypes of migraine disorders & of
epilepsy mechanisms are likely to be
diverse
• Pathophysiological common aspects do exist
53
36. Migraine & Epilepsy
are characterized by
lower neuronal threshold
in the cortex
• Occipital cortex is particularly vulnerable to CSD
• Postictal headaches often having migraine-like
characteristics occur more in occipital epilepsy
• AEDs (eg, valproic acid, topiramate, gabapentin)
work for migraine prophylaxis
Bianchin et al, 2010
54
37. Migraine & Epilepsy
common genetic & molecular aspect
Gene/Locus
Migraine Epilepsy
CACNA1A (19p13)
pore-forming α1A-subunit of
voltage-dependent P/Q-type
calcium channels
FHM1
Different forms
of epilepsy
ATP1A2 (1q23)
poreforming α2 subunit of the
electrogenic Na+, K+-ATPase
FHM2
(occipitotempor
al epilepsy)
SCN1A
voltage-gated
Sodium (Na) channel α1-subunit
FHM3
Different forms
of epilepsy
SLC1A3
Excitatory aminoacid transporter1
POLG
mitochondrial DNA polymerase &
helicase
C10orF2
mitochondrial DNA polymerase &
helicase
Bianchin et al, 2010
55
38. Mutations
- Channelopathies ionic homeostasis
- GABAergic/Glutamatergic systems
- Mitochondrial functions
Spectrum of nervous system diseases
with frequent migraine/epilepsy
comorbidity
Bianchin MM et al, Migraine and Epilepsy : A Focus on Overlapping Clinical, Pathophysiological,
Molecular, and Therapeutic Aspects. Curr Pain Headache Rep (2010)
56
39. Therapeutic Aspects
• Migraine & epilepsy are associated clinicians
should be aware that individuals with one
disorder are more likely to have the other.
• Comorbidity should be considered when
developing treatment plan:
– TCA & neuroleptic drugs for migraine may lower
seizure thresholds
– Antimigraine anticonvulsants should be considered as
a simultaneous treatment for both disorders
Bianchin et al, 2010
57
41. ?
Jenis nyeri kepala yang mana?
Kaitan nyeri kepala dengan kejang?
Penyebab nyeri kepala?
Terapi?
59
42. Tn. PU/ L/33/ Menikah/ “tukang odong-odong”
• Kejang seluruh tubuh saat sedang tidur, sejak seminggu
sebelum berobat ke Poli, kedua lengan & tungkai kaku
menghentak-hentak selama 5 menit. Lidah tergigit +. Sebelum
kejang tidak ada gejala khusus. Setelah kejang pasien segera
sadar dan mengalami nyeri kepala berdenyut sebelah kiri, VAS
5-6, disertai mual, menghilang sendiri dalam beberapa jam
atau setelah minum obat dari toko. Kejang berulang 2-3x
seminggu, muncul sewaktu-waktu, dengan pola yang sama.
Pasien juga mengeluhkan nyeri kepala berdenyut & tegang di
bagian depan kepala kadang kumat saat kecapekan sejak 6
bulan ini. (Karakteristik nyeri kepala sama dengan yang setelah
kejang).
61
43. • Kejang sejak 10 tahun yang lalu (usia 23 thn),
gerakan seperti meniup & menepuk-nepuk tangan,
jalan mondar-mandir tanpa ingat arah, pasien tdk
ingat saat kejang.
• Tx: Valproat 2x250mg, Paracetamol prn
•
•
•
•
Pemeriksaan fisik: refleks palmomental +/+
EEG: Sharp wave & ISA temporal D/S
Lab: IgG Toxo (+), HIV (-)
MRI+K: infeksi di serebelum
62
47. Mrs. Lk/ F/49/ Married/ Housewife
• Headache, in left periorbital, dull, VAS 8-9, accompanied by
nausea, tearing & conjunctival injection of the left eye, begin
4 months ago, occur almost everyday and persist whole day
History of syncope in childhood and sudden slurred speech 5
years ago
66
48. • Physical examination: normal
• Blood work up: normal
• Brain imaging: normal
• EEG: Sharp wave & ISA in left temporal lobe
• Improved with valproate 250 mg bid
ictal cluster headache
???
67
Interictal headache (IIH), and in particular migraine, is considered a relevant co-morbidity in epilepsy; however, available data are ambiguous. Physicians should ask for PIH and offer specific analgesic treatment. To confirm these findings, future studies with a prospective approach implementing a headache and seizure diary should be performed.
Although the nature of this association is unclear, several plausible explanations exist: the two disorders coexist by chance; headache is part (or even the sole ictal phenomenon) of seizures or thepost-ictal state; both disorders share a common underlying etiology; and epilepsy mimics the symptoms of migraine.Seizures and headaches as well as their respective primary syndromes (epilepsy and headache/migraine) share several pathophysiological mechanisms. Papetti et al.“Headache and epilepsy”— How are they connected? Epilepsy&Behavior26(2013)386–393
[1]Parisi P, et al. The crossover between headache and epilepsy. Expert Rev. Neurother. 13(3), 231–233 (2013)[2]Striano p, et al. ‘‘Comorbidity’’ between epilepsy and headache/migraine: the other side of the same coin!. J Headache Pain (2011) 12:577–578
Perempuan > LakiUsiamudaBerdenyut > Nyerikepala lainLobus Temporal
Perempuan > LakiUsiamudaBerdenyut > Nyerikepala lainLobus Temporal
Perempuan > LakiUsiamudaBerdenyut > Nyerikepala lainLobus Temporal
The same patients mightpresent more than one subtype of peri-ictal headache andalso experience interictal headaches. More than a nuisance,they may have diagnostic importance. For example, intemporal lobe epilepsy, headache location is stronglycorrelated with the side of epileptogenic zone, being alateralization sign[13]. Bianchin 2010
thefrequencyofepilepsyamongpeoplewithmigraine(range1–17%)ishigherthaninthegeneralpopulation(0.5–1%),justastheprevalenceofmigraineamongpatientswithepilepsyisalsohigher(range8–15%) than that reported in healthyindividuals (Papetti, 2013(
thefrequencyofepilepsyamongpeoplewithmigraine(range1–17%)ishigherthaninthegeneralpopulation(0.5–1%),justastheprevalenceofmigraineamongpatientswithepilepsyisalsohigher(range8–15%) than that reported in healthyindividuals (Papetti, 2013(
Kenapamunculnya “dalam 1 jam”?
‘‘Ictal epileptic headache’’, used for the first time by Parisi, [1]appears repetitive,since per se ictal signifies ‘‘relating to a seizure’’ (Oxford dictionary), ‘‘relating to a seizure or convulsion ‘‘ (Farlex dictionary), ‘‘relating to or caused by a stroke or seizure’’ (The American Heritage W Medical Dictionary). Moreover, an ‘‘epileptic headache’’ is ‘‘per se’’ ictal.‘‘Ictal headache’’, first used by Piccioli et al., [14] could be confused with headachedue to an ‘‘ictus’’
FHM: familial hemiplegic migraine
[1] HELP, 2010; Syvertsen et al, 2007, Ito et al, 2004; [2] Wawrzyniak et al, 2009 ; [3] Toldo et al, 2010 ; [4] Ito et al, 2004; Ito & Schachter, 1996 ; [5] Ito et al, 2004; HELP,,2010: Schon & Blau,1987; [6] Leniger et al, 2001; [7] Toldo et al, 2010; Ito et al, 2000 & 2003
[1] Wawrzyniak et al, 2009 ; [2]Schon & Blau, 1987; [3] Ito et al, 1999, 2000, 2003, 2004
Nyerikepaladapatmunculbersamadengannyerikepala
Blanda M, Cluster Headache, Medscape, 18 Oct 2012. 21/9/13 13:11