management of common neuropsychiatri c problems
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Management of Common Neuropsychiatri c Problems. ศ.นพ.สุชาติ พหลภาคย์ ภาควิชาจิตเวชศาสตร์ รศ . นพ . สมศักดิ์ เทียมเก่า ภาควิชาอายุรศาสตร์ อ . นพ . สุรินทร์ แซ่ตัง รพ . ขอนแก่น. Management of Common Neuropsychiatri c Problems. Mild cognitive impairment - PowerPoint PPT PresentationTRANSCRIPT
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Management of Common Neuropsychiatric Problems
ศ.นพ. สุ�ชาติ พหลภาคย์� ภาควิชาจิติเวิชศาสุติร์� ร์ศ.นพ.สุมศ�กดิ์� เที�ย์มเก�า ภาควิชาอาย์�ร์ศาสุติร์� อ.นพ. สุ�ร์นทีร์� แซ่�ติ�ง ร์พ. ขอนแก�น
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Management of Common Neuropsychiatric Problemsศ.นพ. สุ�ชาติ พหลภาคย์�
ภาควิชาจิติเวิชศาสุติร์� คณะแพทีย์ศาสุติร์�
มหาวิทีย์าล�ย์ขอนแก�นMild cognitive impairment
Medication-induced movement disorder
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Management of Common
Neuropsychiatric Problemsร์ศ.นพ.สุมศ�กดิ์� เที�ย์มเก�า
ภาควิชาอาย์�ร์ศาสุติร์�
Headache
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Management of Common
Neuropsychiatric Problems ศ.นพ. สุ�ชาติ พหลภาคย์�
ภาควิชาจิติเวิชศาสุติร์� ร์ศ.นพ.สุมศ�กดิ์� เที�ย์มเก�า
ภาควิชาอาย์�ร์ศาสุติร์� อ.นพ. สุ�ร์นทีร์� แซ่�ติ�ง
ร์พ. ขอนแก�นCase discussion
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Management of Common
Neuropsychiatric Problemsศ.นพ. สุ�ชาติ พหลภาคย์�
ภาควิชาจิติเวิชศาสุติร์� คณะแพทีย์ศาสุติร์�
มหาวิทีย์าล�ย์ขอนแก�นMild cognitive impairment
Medication-induced movement disorder
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Neurops ychiatry
สุาขาหน$%งของการ์แพทีย์� เป็'นการ์เร์�ย์นร์()เก�%ย์วิก�บโร์คที�%ม�อาการ์ที�,งทีาง
จิติ cognition และป็ร์ะสุาทีวิทีย์า
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Mx of common neuropsychiatric problems 1. Mild cognitive impai
rment - 2. Medication induced
movement disorders
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Mild Cognitive Impai rment (MCI) defn
• Remains a research con struct•M emory loss in the transitional zone
between normal aging memory loss a nd very early Alzheimer’s disease
= D ementia prodrome, incipient dementia, isolated memory impairm
ent, cognitive impairment no dementia. = P athological, not a manifestation ofaging
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MCI its constr uct
MCI has been proposed to identify the individual at a
n earlier point in the cogni tive decline such that if th
erapeutic interventions be come available, clinician c
an intervene at this junctu re
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MCI types - 1. a MCI => memory impairme
() 2.md MCI=>multiple domain
eeeeeeeee => , eeeeeeee eee eeeeeeeeeeee eeeeee -21. md MCI+a - -22. md MCI a
3. Single nonmemory domaineee
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- a MCI :Diagnosis crit
eria 1. Memory complaint usuallyeeeeeeeeeeee ee ee eeeeee eee
2. Objective memory impairment - for age (test = 1.5 SD) 3. Essentially preserved general
cognitive function eeeeeee eeeeee eeeeeeeeee 4.
eeeeeeeeee eee eeeeeeee 5.
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- MCI : objective -memory test :
• Word list learning•P aragraph recall•N o generally accepted instrument for
this determination•N europsychological testing may be
useful
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1Table . The Short Test ofeeeeee eeeeee Subtests Testing score
Maximum Orientation Name; address; current location
8 (building); city; state; date (day); month; year Attention Digit span (present at 1 per second;) 7
acquisition (maximum of 4 trials)
rrrrrr rrrrrrr rrrrrrr rrrrr - - - -29683
- - - - -571946 - - - - - -2159362
immediate recall Mr Johnson, charity, tunnel. Learning and Learn our unrelated words:apple, 4 Record the number of trials for
rrrrrrrrrrr 5*13 = 4
weeks per year; define an island
- r 657
582/ = 29 11+ =
similarities dog/horse, table/bookcase.
Abstraction/ Similarities: orange/banana, 3 rrrrrr rrrrr rrrrrrrrrr rrrrr rrrrrrrrrr rrr rrr rr 4
Recall The 4 words apple, Mr Johnson, 4
Construction Copy the Necker cube. Draw a clock 4 1110face showing : .
charity, tunnel. *TotalScor e
38
- -* Total score = sum of the subtest scores (number of trials for acquisition rr r rrrrrrr rrrrrrr rrr r r rrrr rr rrr rrrrr rrrrr rrrrrrr rr r1 ). , 4
4ubtracted from the sum of the subtest scores. If a patient required trials to 4 , 3learn the words then was subtracted from the sum of the subtest score
r
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MCI : Biological abnormalities - 1. Over representation of the
4apolipoprotein E allele 2. Volumetric loss in entorhinal
cor t ex and hi ppocampus measured by MRI neuronal
counts in postmortem 3. Increased brain markers of
eeeeeeeee eeeeee 4. Abnormalities of the cholinergic
eeeeee -5. Depression or medical co
morbidity- So MCI i s het er ogeneous and not all MCI will progress to AD
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MCI :treatment- e e ee e eeeeeeee eeeicine eee ee ee ee eeeeeeeee eeee
t he at t endi ng MCI i s an incipient AD, then he may wish ee ee e eee eeeeeeeeeeeeee inhibitor or memantine
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MCI :treatment Donepesil risk of
developing A.D. during the firse eeee
but by the end of 3 year the risk was the same
as these taking Vit E or placebo Galantamine( Reminyl ) = no improvement
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Currently availab le treatment 1. Acetyl chol i neste rasei nhi bi tors =1
st choi ce donepe zi l , ri vasti gmi ne , gal antami ne
some researchs ai ddonepezi l l o wered the riskof developing AD on
l y duri ngthe fi rst year 2.Putative treatments
21. antiglutamatergic drugs = memanti ne
22. nootropics = piracetam - 23. antioxidants : ginko biloba,
Vee A,C,E,selegiline,MAOI, - 3. Anti inflammatory drugs
31. aspirin 32. NSAID
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Currently avail able treatment
4. ERT 5. Visionary interventions
51. targeting neureeeee olgical substrates
5 2. regulation of neur onal pl ast i ci t y
eeeeeeee ee6. - morbidity, controlling risk factors
7. Psychosocial intervention
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MCI Rx of the co- morbidity Vascular risk factors
- : high BP High serum choleste
rol High midlife diastolic
BP White matter hyperi
ntensity Presence of apolipop
rotein E4 genotype Low serum B
12 and f
olate
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P sychosocial intervention emotional and mental stimulat
ion
1. Extensive social network
2. Participating cognitiv ely stimulating activitie
s
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MCI : Rx wit h AChE• - Autopsy based study reported similar red
uctions in basal forebrain immunoreactiv e neurons = selective loss of cholinergic
neurons in MCI and AD => cholinergi ic differentiation of the cerebral cortex
•L ong term effects will be via modification of APP metabolism
•H owever a study observer ed specific upr egulation of choline acetyl transferase in
MCI subjects = compensatory process in preclinical phase and suggest limitation
of AChE inhibitor efficacy at this stage
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MCI : Rx with antiglut amatergic drugs•O veractivity of excitatory amino acid glu
tamate neurotoxcity•NMDA- mediated excitotoxicity tau p
hosphorylation NT = one of the major pathological subs
trates of AD•M - emantine = NMDA receptor antagonis
t
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MCI : Rx with nootropics
• Piracetam•E nhance memory function•N - onspecific action : energy metab
olism, cholinergic mechanism, exc - itatory amino acid receptor medi
ated function and steroid sensitivi ty
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MCI : Rx anti oxidants• Large amounts of unsaturated lipids
and catecholamines in the brain , β - protein precursor, Aβ , presenilins an
d APOE are link to reactive oxy gen s pecies (ROS) production apotosis
•O xidative stress atherogenesis•H igher ascorbic acid and β- carotene
plasma level better memory• Ginko biloba, Vit A, C, E = free radic
al scarvenger, MAOI = reduce free r adical formation
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MCI : Rx with an ti infl ammatory drugs
•eeeeee e eeeee eeeeeee eee eeeeeeee ee the pathogenesis of AD
•ee ee eee e pregulation of cytokines, acute phase proteins, activation of th
e complement regulatory proteins, ac cumulation of activated microglia
•R educed prevalence of AD in ptwith arthri t i s
• - Rxwithaspirin,NSAI D,COX2i nhi bi tors
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MCI : Rx wi th ERT•E strogen acts via ERα และ ERβ
activate nerve growth factors, synaptogene sis, modulate function of AC h,5 - HT, DA, NA, and cerebral blood flow
•E strogen has intrinsic antioxidant activi ty, neuroprotec tive effect by promoting
nonamyloi dgenic β- secretas e processi ng of APP
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Targeting neuropat hological substrate
s 1. R eduction of Aβ eeeeeeeeee 2. e nhibitors of Aβ eeeeeeeeeee
eeeeeee eee eeeeeeeeee eeee al s devel op behavi or al
abnormality before extensive eeeeeee eeeeeeeeee eeeeee
3. Neu rofibrillary changes be tter correlate with disease
eeeeeeee eeee eeeeeeeeeee 4. eeeeeeeeeeee ee eee
eeeeeeeesphoeeeeeeee
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Regulation of ne uronal plasticity
1. Nerve growth factor (NGF) =neurotropic factor for the
basal forebrain cholieeeeee eeeeee
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- Medication induced movement disorders
1. All first generation e:
eeeeeeeeeeeeee eeeeeeeeeeeeeeeeeeeeeeeeeeeeeeeeeee
2. Some second generation anti- psychotics; usueeee eeee eeeeeee
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- Medication induced movement disorders
3. Nonantipsychotic psychotripicseeeeeeeeeeeeeeeeeeeeee
Ant i depr essant s 4. Nonpsychotropics
Prochlorperazineeeeeeeeeeeeeee
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- Neuroleptic induced movement disorders
1. A cute dystonia 2. Akathisia
3. P - arkinsonian like
4. T ardive dyskinesia
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- Neuroleptic induced acute dystonia : Path
ophysiology = not known, may be
acute saturation of D2
receptors
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Neuroleptic induce d acute dystonia
•E - arly onset during the co urse of treatment with
neu roleptic• 30M > F, age < years >•R eceive high potency anti-
psychotic medication
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Neuroleptic induced acute dystonia :Dx
1A. (or more) of the followingeeeee ee eeeeeeee has developed in association wite eee eee of neureeeeeee e eeeeeeeee 1. e bn positioning of the he
ad and neck i n eeeeeeee ee body (retrocollis, ) 2. Spasms of the jaw muscle s(tri sm e e , , )
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Neuroleptic induced acute dystonia :Dx
3. I mpaired & wallowing (dyspepsia) speaking or
breathing 4 . T hickened or slurred s
peech due to hypertonic or enlarged tongue 5 . E ye deviated up, down , or sideward
(ocul ogyri c cri si s )
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Neuroleptic induced acute dystonia :Dx
6. T ongue protrusio
n or tongue dysfunction 7 . A bn positioning of
the distal limb or trunk
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Neuroleptic induced acute dystonia :Dx
B. Adeveloped within 7 days of starting or rapidly
raising the dose of neuroleptic medication or of reducing a medication to
or prevent acute EPS
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Treatment : 1. e nticholinergic or
anti hi stami nergi c drugs 2.If fails to respond to 3do
ses of these drug with in 2 hrs, then consider oth
er causes for the dystonia 3. e fter resolution of the
acute episode, give oral anticholinergic agents
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- Neuroleptic induced acute akathisia : Pat
hophysiology = DA neurons in the
ventral tegmental area
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- Neuroleptic induced tardive dyskinesia : P
athophysiology 1. S ustained D2
recept or blockade receptor
hypersensitivity 2. Blockade of presynap tic DA receptors
glutam atergic transmis sion oxidative
stress cell death
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- Neuroleptic induc ed acute akathisia
•R isk = middle aged women•O ccurs at some point in th
e course of medication (an tipsychotics, antidepressa
nts and sympathomimetic s)
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- Neuroleptic induced acute akathisia : Dx
A. subjective complaints of re stlessness after exposure t
e e eeeeeeeeeee eeeeeeeeee B. e - t least one of the following
1. fidgety movement or swi nging of the legs
2. rocking from foot to foot while standing
3. pacing to relieve restlessneee
4. e nability to sit or stand st ill for at least several minut
ee
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- Neuroleptic induced acute akathisia : Dx
C. onset of A and B occurs wi 4thin weeks of initiating
or increasing the dose of neuroleptic , or of reducing
e eeeeeeeee eeee ee Re ee eee vent acute EPS
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- Neuroleptic induced acute akathisia : R x
1. Reeeee eeeeeeeeeee eeeeeeeeee eeeeee
2. e ttempt to treat with B- eeeeeeeeee eeeeeeee eeeeee eeeeeeeeeeeeee , ,
3. Considering changing theeeeeeeeeeeeee
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Neurole ptic induc ed parkinsonism :
Pathophysiology = DA activity, this can be in duced by
1. Depletion of DA in presynapticstores(reserpi ne) 2. DA receptor blocking = aneeeeeeeeeee eee eeeeeeee calcium blocking agent (cie
)
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- Neuroleptic inducedparkinsonism;Dx
- A. One ( or moe e) of the follo wing signs or symptoms
eee eeeeeeeee ee association with use of
eeeeeeeeeee eeeeeeeeee 1. e ar ki nsoni an t r emor 2. Parkinsonian muscular rieeeeee 3. e ki nesi a
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-Neuroleptic induce
d parkinsonism;Dx B. A. developed with a fe w weeks of starting or
raising the dose of a neeeeeeeeee e eeeeeeeee ee of reducing ae eeeeeeeee eeee ee eeeee - ( or prevent) acute EPS(a
eeeeeee )
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Causes Blockade of > 80% of
D2 receptor in the
caudate at the termi nation of
the nigrostriatal dop amine neu rons
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Riske lderlyF emale > 50% of pt R x wi th longterm,hi ghpotency do
pamine receptor antag onists
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Treatment 1. R educe the dosage
of the neuroleptic 2. A nti EPSmedication
- for 1 4 2 1 days then attempt to reduce or st
op 3. P ossibly changing the
neurol e pti c
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- Medication induce d postural tremor
• Pathophysilolgy : based o n the class of drug implica
ted, eg, stimulant may cau se tremor due to the result ing hyperadrenergic state
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- Medication induce d postural tremor
• Causes : Li, valproic acid, β - adr energic blocker s stimulant, DA agonist, caffeine, theophy lline,
nureoleptic, antidepressant• - 8 12 Hz postural tremor affecti
ng limbs head, mouth, tongue
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1. Check for drug toxicity2. Check for emotional factors , alc withdrawal , hypoglycemia,
thyrotoxicosis3. Reduction of the dosage or switch to another agent in a
different class4. Use benzodiazepine or ß-blocker
- Medication induced postural tremor : Rx
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- Neuroleptic in duced tardive d
yskinesia : riskfactor• 25% of pts treated with dopamin
e eeeeeeee eee eeee e eeeee4• I ncreasing age•Feeeee•T he pr esence of a mood di sor der•T he presence of a cognitive disorde
e
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- Neuroleptic indu ced tardive dyskin esia : Diagnosis A. I nvoluntary movements of the ton
gue ja w, trunk or extremities have developed in association with the use of neuroleptic medication
B. A is present over a period of at leas t4 weeks and occur in any of the
following patterns 1. choreiform movements (rapid, j
erky, nonrepetitive ) 2. athetoid movement (slow, sinuo
us, continual) 3 . rhythmic movements (stereotypes)
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- Neuroleptic indu ced tardive dyskin esia : Diagnosis C. A and B develop during ex
eeeeee ee e eeeeeeeeeee 4medication or with in w
eeks of withdrawal from ee eeee ( 8or within wee
ks of withdrawal from a depot ) neuroleptic eeee
eeeeee D. Exposure to neuroleptic
medication for at least 3 months (1 month if age
60 years or older)
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- Neuroleptic ind uced tardive dys
kinesia :Rx 1. Rx for tardive dyskinesia have been unsuccessful but
the course is less relentless
2. Substitute the dopamine receptor antagonist with
SDA & which help limit the abn movement without
further worsening of the psychotic symptoms
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Common Problems in Neuropsychiatry
รศ.นพ.สมศกดิ์ � เที�ยมเก�าสาขาวิ ชาประสาทีวิ ทียาภาควิ ชาอาย�รศาสตร� คณะแพทียศาสตร�มหาวิ ทียาลัยขอนแก�น
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HeadacheHeadache
–Pain in various part of head
–Most common pain problem in practice
–12 months period
• occur 95% of young woman
• occur 91% of young man
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Outline 1.Migraine headache
2.Cluster headache 3.Trigeminal neuralgia 4.Tension type
headache5.Post traumatic
headache 6.Uncommon
headache7.Case demonstration
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Management of MigraineManagement of Migraine
• Diagnosis
• Treatment of acute attack
• Prevention of acute attack
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How Can We Best Treat Migraine?How Can We Best Treat Migraine?
• Nonpharmacologic intervention
• Pharmacologic intervention
–Acute therapy
–Chronic therapy
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Acute Therapies Acute Therapies for for
MigraineMigraine
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Goals of Acute TreatmentGoals of Acute Treatment• Abortive treatment is always indicated
• Treat attacks rapidly and consistency without recurrence
• Restore the patient’s ability to function
• Optimize self care and reduce subsequent use of resources
• Be cost effective for overall management
• Avoid or minimize adverse drug events
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Drug Efficacy AES Relative contraindication
Acetaminophen (paracetamol)
++ + Liver disease
Aspirin (ASA) ++ + Kidney disease, ulcer disease, PUD, gastritis, AGE<15yr
Barbital, caffeine and analgesics
++ +++ Use of other sedative; history of medication overuse
Caffeine adjuvant ++ + Sensitivity to caffeine
Isometheptens ++ + Uncontrolled HTN, CAD, PVD
Opioids +++ ++++ Drug or substance abused
NSIADs ++ + Kidney disease, PUD, gastritis
Dihydroergotamin
Injection
Intranasal
++++
+++
++
+
Uncontrolled HTN, CAD, PVD
Ergotamine
Tablet
Suppositories
++
+++
++
+++
Prominent nausea and vomiting Uncontrolled HTN, CAD, PVD
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Acute Medication OveruseAcute Medication Overuse
At least on of the following for at least one month1.Simple analgesics use
(>1000mg ASA/acetaminophen)
> 5days/week
2.Combination analgesics
(caffeine, barbiturate- containing medication)
> 3tablets/day > 3days/week
3.Opioids (>1tablet/day) > 2days/week
4. Ergotamine use (1mg PO or 0.5mg PR) > 2days/week
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Limitation of Acute TreatmentLimitation of Acute Treatment
• Side effects and intolerance • Contraindication• Habituation• Drug-induced headache • Interaction with prophylactic therapy• Non-responders
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Preventive Therapies Preventive Therapies for for
MigraineMigraine
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Goals of Preventive TreatmentGoals of Preventive Treatment Goals of Preventive TreatmentGoals of Preventive Treatment
Reduce attack frequency, severity, and durationReduce attack frequency, severity, and duration
Improve responsiveness to Rx of acute attacksImprove responsiveness to Rx of acute attacks
Improve function and reduce disabilityImprove function and reduce disability
Prevent disease progression?Prevent disease progression?
Reduce costsReduce costs
Reduce attack frequency, severity, and durationReduce attack frequency, severity, and duration
Improve responsiveness to Rx of acute attacksImprove responsiveness to Rx of acute attacks
Improve function and reduce disabilityImprove function and reduce disability
Prevent disease progression?Prevent disease progression?
Reduce costsReduce costs
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1.1. Migraine significantly interferes with patients' daily routine, despite acute Migraine significantly interferes with patients' daily routine, despite acute treatmenttreatment
2.2. Frequency of attacks Frequency of attacks ((≥≥3 / month)3 / month) with risk of acute medication overuse with risk of acute medication overuse
3.3. Acute medications ineffective, contraindicated, troublesome AEs, or Acute medications ineffective, contraindicated, troublesome AEs, or overusedoverused
4.4. Patient preferencePatient preference
5.5. Presence of uncommon migraine conditionsPresence of uncommon migraine conditions– Hemiplegic migraine Hemiplegic migraine – Basilar migraineBasilar migraine– Migraine with prolonged aura Migraine with prolonged aura – Migrainous infarctionMigrainous infarction
Consider Preventive Therapy If Consider Preventive Therapy If AnyAny of the of the Following Criteria Are Met:Following Criteria Are Met:
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Lipton RB et al. Headache. 2001;41:638-645; Lipton RB et al. Neurology. 2002;58:885-894.
Migraine Prevention UtilizationMigraine Prevention Utilization
53% of migraineursmeet disability and
frequency criteria for prevention
<5% of migraineurs are on preventive therapy
25% Frequency
28% Disability
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Preventive MedicationsPreventive MedicationsPreventive MedicationsPreventive Medications AnticonvulsantsAnticonvulsants
– Divalproex Divalproex
– TopiramateTopiramate
– Gabapentin, zonisamide, Gabapentin, zonisamide, levetiracetam levetiracetam
AntidepressantsAntidepressants– TCAsTCAs, SSRIs, MAOIs, SSRIs, MAOIs
-Blockers-Blockers– PropranololPropranolol
Ca channel blockersCa channel blockers– VerapamilVerapamil
NSAIDsNSAIDs
AnticonvulsantsAnticonvulsants– Divalproex Divalproex
– TopiramateTopiramate
– Gabapentin, zonisamide, Gabapentin, zonisamide, levetiracetam levetiracetam
AntidepressantsAntidepressants– TCAsTCAs, SSRIs, MAOIs, SSRIs, MAOIs
-Blockers-Blockers– PropranololPropranolol
Ca channel blockersCa channel blockers– VerapamilVerapamil
NSAIDsNSAIDs
5-HT antagonists5-HT antagonists– MethysergideMethysergide/methergine/methergine
NeurotoxinsNeurotoxins– BotulinumBotulinum
Angiotensin systemAngiotensin system– ACE inhibitorsACE inhibitors– AntagonistsAntagonists
OtherOther– Riboflavin, Feverfew, Riboflavin, Feverfew,
PetasitesPetasites
– Neuroleptics? Neuroleptics?
5-HT antagonists5-HT antagonists– MethysergideMethysergide/methergine/methergine
NeurotoxinsNeurotoxins– BotulinumBotulinum
Angiotensin systemAngiotensin system– ACE inhibitorsACE inhibitors– AntagonistsAntagonists
OtherOther– Riboflavin, Feverfew, Riboflavin, Feverfew,
PetasitesPetasites
– Neuroleptics? Neuroleptics?
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Setting Treatment PrioritiesSetting Treatment PrioritiesSetting Treatment PrioritiesSetting Treatment Priorities
Comorbid and coexistent diseaseComorbid and coexistent disease Therapeutic opportunity to Therapeutic opportunity to treat two disorders treat two disorders
with single drugwith single drug
• Hypertension or angina: Hypertension or angina: -blocker-blocker
• Depression: TCA or SSRIDepression: TCA or SSRI
• Epilepsy or mania: divalproex or topiramateEpilepsy or mania: divalproex or topiramate Therapeutic limitationsTherapeutic limitations
• Depression: avoidDepression: avoid -blocker-blocker
Comorbid and coexistent diseaseComorbid and coexistent disease Therapeutic opportunity to Therapeutic opportunity to treat two disorders treat two disorders
with single drugwith single drug
• Hypertension or angina: Hypertension or angina: -blocker-blocker
• Depression: TCA or SSRIDepression: TCA or SSRI
• Epilepsy or mania: divalproex or topiramateEpilepsy or mania: divalproex or topiramate Therapeutic limitationsTherapeutic limitations
• Depression: avoidDepression: avoid -blocker-blocker
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Use Drug Best for PatientUse Drug Best for PatientUse Drug Best for PatientUse Drug Best for Patient
Take advantage of drug’s side effects Take advantage of drug’s side effects Underweight patient:Underweight patient: Use flunarizine Use flunarizine Overweight:Overweight: Use topiramate Use topiramate Insomniac:Insomniac: Use TCAs Use TCAs Elderly or cardiac patient:Elderly or cardiac patient: Use Use
divalproex or topiramatedivalproex or topiramate Athlete:Athlete: Avoid Avoid -blockers-blockers
Take advantage of drug’s side effects Take advantage of drug’s side effects Underweight patient:Underweight patient: Use flunarizine Use flunarizine Overweight:Overweight: Use topiramate Use topiramate Insomniac:Insomniac: Use TCAs Use TCAs Elderly or cardiac patient:Elderly or cardiac patient: Use Use
divalproex or topiramatedivalproex or topiramate Athlete:Athlete: Avoid Avoid -blockers-blockers
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Cost of Medications Used for Migraine Prophylaxis Cost of Medications Used for Migraine Prophylaxis Trade Name Dose (mg) Baht (tablet) Unit (month) Baht Trade Name Dose (mg) Baht (tablet) Unit (month) Baht
(month)(month)
AmitriptylineAmitriptyline 10 10 0.500.50 30 15 30 15
2525 1 1 30 30 30 30
Flunarizine Flunarizine 1.501.50 30 45 30 45
1.501.50 60 90 60 90
PropranololPropranolol 10 10 0.500.50 60 30 60 30
4040 1.501.50 30 45 30 45
DepakineDepakine 200 200 7 7 90 630 90 630
500500 14 14 60 840 60 840
NeurontinNeurontin 300 300 33 33 90 2970 90 2970
Topamax Topamax 100 100 45 45 30 30 13501350
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Cluster Headache •Trigeminal autonomic
cephalagias •Severe head pain with cranial autonomic activation
•Described in 1745•A healthy middle aged man, pain which came on every day at the same hour, the same spot
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Clinical features
•Male : female = 4:1•Age 27-31 yr•60-90 min•Occur in series, last for weeks
•Remission, usually last for months or year
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Associated symptoms –Conjunctival injection –Lacrimation, nasal congestion
–Rhinorrhea, facial sweating
–Miosis, ptosis, eyelid edema
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ล�กษณะแติกติ�างร์ะหวิ�างโร์คป็วิดิ์ศ�ร์ษะ cluster และโร์คป็วิดิ์ศ�ร์ษะไมเกร์น
Cluster headache ไมเกร์นเพศ ชาย์ : หญิง4 -6: 1 หญิง
: ชาย์ -34 : 1ร์ะย์ะเวิลาที�%ม�อาการ์ ไม�เกนช�%วิโมง - 24 ช�%วิโมงอาย์� - 3040 ป็2 - 1525
ป็2อาการ์เติ3อน (aura) ไม�ม� ม�น4,าติาไหล ติาแดิ์ง ค�ดิ์จิม(ก พบไดิ์)บ�อย์ ไม�พบป็ร์ะวิ�ติ allergy ไม�ม� พบไดิ์)บ�อย์ป็ร์ะวิ�ติคร์อบคร์�วิ พบไดิ์)น)อย์มาก พบไดิ์)บ�อย์ช�วิงร์ะย์ะสุงบของโร์ค นานเป็'นป็2 วิ�น สุ�ป็ดิ์าห�
หร์3อเดิ์3อน
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Management of Acute Treatment •Oxygen •Triptans •Ergot derivative •Intranasal lidocaine
•Prednisolone?
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Oxygen •Standard acute treatment
•Mask 7-12 L/min, 15-20 min
•Effective 70%•Aborted of attack within 5-12 min
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Tension type headache
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Tension-typed headache
Diagnostic criteria A. Frequency > 15 days/month, > 6 months/year B. At least 2 of following
1. Pressing, tightening quality 2. Mild or moderately severity 3. Bilateral4. No aggravation by routine
activity C. No vomiting, no photophobia, phonophobia
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ป็5ญิหาการ์ดิ์(แลผู้()ป็7วิย์ TTH
1 .ป็ร์ะวิ�ติไม�สุมบ(ร์ณ�2. การ์ให)ค4าอธิบาย์ไม�เพ�ย์งพอ3. ติอบสุนองควิามติ)องการ์ผู้()ป็7วิย์ไม�ติร์ง
ป็ร์ะเดิ์:น4. ควิามอดิ์ทีนของแพทีย์�ไม�เพ�ย์งพอ5. ควิามสุ�มพ�นธิ�ร์ะหวิ�างแพทีย์�/ผู้()ป็7วิย์ไม�ดิ์�
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Acute medication for TTHDrugs Efficacy Side
effects ASA 2+ 2Paracetamol 2+ 1Indomethacin 3+ 2Ibuprofen 2+ 2Naproxen 3+ 2ASA + Para + Caffeine 3+ 2DZP ? 3
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Sinus headache : criteria
A.Headache location 1. Frontal, over the sinus, radiate to vertex,
behind eyes 2. Maxillary, over antral area, radiate to
upper teeth, forehead3. Ethmoiditis, behind eyes, radiate to
temporal area4. Sphenoiditis, occipital, vertex, frontal,
behind eyes
B. Clinical, laboratory, imaging C. Simultaneous onset D. Response to treatment
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Sinusitis headache
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Sphenoid sinusitis •3% of all sinusitis •Not adequate by routine x-ray,examination
•Headache or facial pain 55/56•Pain worse with head movement 26/26
•Nasal discharge 10/26 •Fever 15/26, N/V 8/14•Cavernous sinus syndrome
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•Diagnosis is frequently delayed •Periorbital pain is common, contrast to common teaching that vertex headache
•A severe, intractable, new-onset headache that interferes with sleep and is not relieved by simple analgesics should alert
•PE : not helpful, sinus tender : rare
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Trigeminal neuralgia •One or more distribution
of CN V, V2-V3•Trigger by sensory stimuli to skin, mucosa, teeth
•Electric shocklike, shooting, lancinating
•Last only seconds•Repetitive at short interval
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ผู้()ป็7วิย์หญิงอาย์� 34 ป็2 ที�%อย์(� อ4าเภอพ�งโคน จิ�งหวิ�ดิ์สุกลนคร์ HN: 0217GB
CC: ป็วิดิ์ศ�ร์ษะมา 1 ป็2PI : 1 ป็2 ม�อาการ์ป็วิดิ์ศ�ร์ษะที�%วิศ�ร์ษะ ป็วิดิ์มากบร์เวิณ
ที)าย์ทีอย์ ป็วิดิ์คร์�,งละไม�นาน ป็ร์ะมาณ 30 นาที� ม�อาการ์หล�งจิากไอ
จิาม หร์3อเบ�งถ่�าย์อ�จิจิาร์ะ ร์�กษาติามคลนกและโร์งพย์าบาลจิ�งหวิ�ดิ์ อาการ์ไม�ดิ์�ข$,น เคย์ติร์วิจิ - CT brain : ป็กติ อาการ์เป็'นมาก
ข$,นเร์3%อย์ๆ PH : ป็ฏิเสุธิโร์คป็ร์ะจิ4าติ�วิ ไม�ม�ย์าทีานป็ร์ะจิ4า
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อาการ์ป็วิดิ์ศ�ร์ษะที�%บ�งบอกวิ�าน�าจิะม�อาการ์ป็วิดิ์ศ�ร์ษะที�%บ�งบอกวิ�าน�าจิะม�โร์คภ�ย์ร์)าย์แร์งโร์คภ�ย์ร์)าย์แร์ง
1. อาการปวิดิ์ศ�รษะที�%แย�ที�%ส�ดิ์เที�าที�%เคยม�อาการ 2. อาการปวิดิ์ศ�รษะร�นแรงคร'งแรก3. อาการปวิดิ์ศ�รษะที�%เป(นมาก แลัะปวิดิ์มากข)'น
เร*%อยๆ ในเวิลัาเป(นวินหร*อสปดิ์าห�4. ม�การตรวิจพบอาการผิ ดิ์ปกต ทีางระบบ
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สาเหต�ไม�ไดิ์1
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อาการ์ป็วิดิ์ศ�ร์ษะที�%บ�งบอกวิ�าน�าจิะม�อาการ์ป็วิดิ์ศ�ร์ษะที�%บ�งบอกวิ�าน�าจิะม�โร์คภ�ย์ร์)าย์แร์งโร์คภ�ย์ร์)าย์แร์ง
6. อาการปวิดิ์ศ�รษะ ร�วิมกบ อาการอาเจ�ยน7. อาการเป(นมากข)'นเม*%อเอ�ยงตวิ ยกของ ไอ
หร*อ จาม8. อาการปวิดิ์ศ�รษะที�%ที3าให1ต*%นจากการนอนหลับ9. ม�ควิามผิ ดิ์ปกต ระบบอ*%น หร*อ ม�โรคประจ3า
ตวิอย5�ก�อน10. อาการปวิดิ์ที�%เป(น เม*%ออาย�มากกวิ�า 55 ป6
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Case demonstrationCase demonstrationNomenclatureNomenclature
Syndromic approachSyndromic approach
Common neuropsychiatric Common neuropsychiatric problemsproblems
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Common featureCommon feature
Psychic symptomsPsychic symptoms Organic pathology :Organic pathology :migraine, seizure , tumormigraine, seizure , tumor Cortical functionCortical function
Treatment :Treatment : Psychotropic drugPsychotropic drug Etiological treatmentEtiological treatment CounselingCounseling
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SymptomSymptom
Conscious : delirium ,apathyConscious : delirium ,apathy Movement : psychomotorMovement : psychomotor Special sensation : Special sensation : agnosia ,visuospatialagnosia ,visuospatial MemoryMemory PhasiaPhasia EmotionEmotion Behavior : executive functionBehavior : executive function
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Case discussionCase discussion
ชายไทียอาย� ชายไทียอาย� 74 74 ป6 อาช�พ รบจ1างป6 อาช�พ รบจ1าง CC : CC : ไม�ยอมนอนมา ไม�ยอมนอนมา 3 3 วิน วิน
PI : PI : 2 2 เดิ์*อนก�อนมา รพเดิ์*อนก�อนมา รพ . . ปวิดิ์ศ�รษะเวิ�ยนศ�รษะเป(นปวิดิ์ศ�รษะเวิ�ยนศ�รษะเป(นประจ3าตอนเย7นประจ3าตอนเย7น
มา รพมา รพ . . พบ พบ 212100BP / 212100BP / Dx HT Dx HT ให1ยาทีาน ให1ยาทีาน HCTZ ½ x 1 HCTZ ½ x 1 Dramamine 1 X 3 Dramamine 1 X 3 10Adalat mg stat 10Adalat mg stat Atenolol (50 mg) 1 X OD Atenolol (50 mg) 1 X OD
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ต�อมา มา ต�อมา มา 15080F/U BP / 15080F/U BP / Dx HT Dx HT withwith vertigo vertigo 1 1 เดิ์*อน ม�อาการเหม�อลัอย น%งน %ง เป(นพก ๆ บางเดิ์*อน ม�อาการเหม�อลัอย น%งน %ง เป(นพก ๆ บาง
คร'งที3าตาขวิาง ไม�พ5ดิ์ อารมณ�หง�ดิ์หง ดิ์ง�าย โมโหคร'งที3าตาขวิาง ไม�พ5ดิ์ อารมณ�หง�ดิ์หง ดิ์ง�าย โมโหง�าย แต�ไม�ยอมพ5ดิ์ เดิ์ นออกจากบ1านแลั1วิกลับบ1านไม�ง�าย แต�ไม�ยอมพ5ดิ์ เดิ์ นออกจากบ1านแลั1วิกลับบ1านไม�ถู5ก เดิ์ นวินไปมารอบบ1านถู5ก เดิ์ นวินไปมารอบบ1าน 3 3 วิน ป9สสาวิะไม�เป(นที�% ป9สสาวิะราดิ์ ไม�ยอมนอน วิน ป9สสาวิะไม�เป(นที�% ป9สสาวิะราดิ์ ไม�ยอมนอน
เดิ์ นออกนอกบ1านตอนกลัางค*นแลั1วิกลับบ1านไม�ถู5ก เดิ์ นออกนอกบ1านตอนกลัางค*นแลั1วิกลับบ1านไม�ถู5ก พลัเม*องดิ์�พากลับบ1าน พลัเม*องดิ์�พากลับบ1าน
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Physical examinationPhysical examination
Elderly man ,good looking ,not distress , mild agitationElderly man ,good looking ,not distress , mild agitation
BP BP 16364/ 16364/ Repeat Repeat 13060/13060/Heart lung abdomen- WNLHeart lung abdomen- WNLNeuro examinaitonNeuro examinaiton good consciousnessgood consciousness Motor - Grade V all ,DTR 2+Motor - Grade V all ,DTR 2+ Palmomental + bilat Palmomental + bilat Finger agnosia Finger agnosia -Lt-Lt RR t disorientation t disorientation No definite weakness No definite weakness Sensory Sensory - - intact intact Double simultaneous test – NA Double simultaneous test – NA
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DiscussionDiscussion
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• Deterioration of cognitive function
• Episodic alteration of consciousness
• Urinary incontinence
• HT
• Localization at fronto-parietal area
• Nature; tumor,chronic infection, NPH
DiscussionDiscussion
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DiscussionDiscussion
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InvestigationInvestigation
CBC Hct 34 NCNC, CBC Hct 34 NCNC, WBC 8400 ,PMN 70% EO 3%WBC 8400 ,PMN 70% EO 3% FBS 89 mg%FBS 89 mg% Na 140,K 3.8,HCO3 25,Cl 108Na 140,K 3.8,HCO3 25,Cl 108 Ca,PO4,Mg - WNLCa,PO4,Mg - WNL
CXR ---CXR --- EKG ---EKG ---
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Any investigationAny investigation
CT CT EEG – NoEEG – No X-rayX-ray
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DiagnosisDiagnosis
Cysticercosis with secondary epilepsyCysticercosis with secondary epilepsy
TreatmentTreatment Albendazole Albendazole DexamethazoneDexamethazone PhenytoinPhenytoin B1-2-12B1-2-12
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กรณ�ศ)กษาที�% กรณ�ศ)กษาที�% 22หญิ งไทียอาย� 37 ป6
CC: ชกมากข)'น 1 สปดิ์าห� PI :เป(นโรคลัมชกมา 30 ป6 รบประทีานยาไม�สม3%าเสมอต�อมา
6 7– ป6 รบประทีานยาสม3%าเสมอ แต�ยงม�อาการชกบ�อย ๆ บางเดิ์*อนไม�ม�ชก แต�บางวินชก 10 23– คร'ง/วิน อาการม� 2 แบบ
แบบที�% 1 ม�อาการที1องกระต�ก ไม�หมดิ์สต แบบที�% 2 ม�ชกเกร7งกระต�กที'งตวิ บางคร'งหมดิ์สต
1 สปดิ์าห� ม�อาการชกแบบที1องกระต�กบ�อยมาก ญิาต พามา รพ . ขณะรอแพทีย�ม�ชกเกร7งกระต�ก 1 คร'ง พยาบาลัจ)งให1ร�บเข1าห1องตรวิจ
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กรณ�ศ)กษาที�% กรณ�ศ)กษาที�% 22 PE:Obesity ,g um
hypertrophy ,hirsutism No skin stigmata Inducible – positive both
abdominal seizure ,GTC
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DiscussionDiscussion
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DiscussionDiscussion
Hiccup
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Non-epileptic seizure
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Complex partial seizure
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Patient with chronic and active epilepsy
1 .Revi ewdi agnosi s andeti ol ogy history EEG neuroimaging other investigation 2. Classify epilepsy 3 . Review compliance
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Discussion
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InvestigationInvestigation
CBC – WNLCBC – WNL DTX ,electrolyte , BUN,Cr,Mg,Ca,PO4DTX ,electrolyte , BUN,Cr,Mg,Ca,PO4 UAUA Thyroid functionThyroid function Psychological test : IQPsychological test : IQ
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Further investigationFurther investigation
CT – WNLCT – WNL EEG – normal tracingEEG – normal tracing MRI – not availableMRI – not available
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DiagnosisDiagnosis
EpilepsyEpilepsy Mental retardation ?Mental retardation ? Non epileptic seizureNon epileptic seizure
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TreatmentTreatment
Carbamazepine 1x 3Carbamazepine 1x 3 counselingcounseling
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Thank you for your interest