Management of Common Neuropsychiatri c Problems

Management of Common Neuropsychiatric Problems

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Management of Common Neuropsychiatric Problemsศ.นพ. สุ�ชาติ พหลภาคย์�

ภาควิชาจิติเวิชศาสุติร์� คณะแพทีย์ศาสุติร์�

มหาวิทีย์าล�ย์ขอนแก�นMild cognitive impairment

Medication-induced movement disorder

Management of Common

Neuropsychiatric Problemsร์ศ.นพ.สุมศ�กดิ์� เที�ย์มเก�า

ภาควิชาอาย์�ร์ศาสุติร์�

Headache


Neuropsychiatric Problems ศ.นพ. สุ�ชาติ พหลภาคย์�

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ภาควิชาอาย์�ร์ศาสุติร์� อ.นพ. สุ�ร์นทีร์� แซ่�ติ�ง

ร์พ. ขอนแก�นCase discussion


Neuropsychiatric Problemsศ.นพ. สุ�ชาติ พหลภาคย์�

ภาควิชาจิติเวิชศาสุติร์� คณะแพทีย์ศาสุติร์�

มหาวิทีย์าล�ย์ขอนแก�นMild cognitive impairment

Medication-induced movement disorder

Neurops ychiatry

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จิติ cognition และป็ร์ะสุาทีวิทีย์า

Mx of common neuropsychiatric problems 1. Mild cognitive impai

rment - 2. Medication induced

movement disorders

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

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

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

- 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.

- MCI : objective -memory test :

• Word list learning•P aragraph recall•N o generally accepted instrument for

this determination•N europsychological testing may be

useful

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

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

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

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

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

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

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

P sychosocial intervention emotional and mental stimulat

ion

1. Extensive social network

2. Participating cognitiv ely stimulating activitie

s

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

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

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

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

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

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

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

Regulation of ne uronal plasticity

1. Nerve growth factor (NGF) =neurotropic factor for the

basal forebrain cholieeeeee eeeeee

- Medication induced movement disorders

1. All first generation e:

eeeeeeeeeeeeee eeeeeeeeeeeeeeeeeeeeeeeeeeeeeeeeeee

2. Some second generation anti- psychotics; usueeee eeee eeeeeee

- Medication induced movement disorders

3. Nonantipsychotic psychotripicseeeeeeeeeeeeeeeeeeeeee

Ant i depr essant s 4. Nonpsychotropics

Prochlorperazineeeeeeeeeeeeeee

- Neuroleptic induced movement disorders

1. A cute dystonia 2. Akathisia

3. P - arkinsonian like

4. T ardive dyskinesia

- Neuroleptic induced acute dystonia : Path

ophysiology = not known, may be

acute saturation of D2

receptors

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

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 , , )


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 )


6. T ongue protrusio

n or tongue dysfunction 7 . A bn positioning of

the distal limb or trunk


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

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

- Neuroleptic induced acute akathisia : Pat

hophysiology = DA neurons in the

ventral tegmental area

- 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

- 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)

- 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

- 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

- 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

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

)

- 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

-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 )

Causes Blockade of > 80% of

D2 receptor in the

caudate at the termi nation of

the nigrostriatal dop amine neu rons

Riske lderlyF emale > 50% of pt R x wi th longterm,hi ghpotency do

pamine receptor antag onists

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

- 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

- 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

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

- 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

- 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)

- 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)

- 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

Common Problems in Neuropsychiatry

รศ.นพ.สมศกดิ์ � เที�ยมเก�าสาขาวิ ชาประสาทีวิ ทียาภาควิ ชาอาย�รศาสตร� คณะแพทียศาสตร�มหาวิ ทียาลัยขอนแก�น

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

Outline 1.Migraine headache

2.Cluster headache 3.Trigeminal neuralgia 4.Tension type

headache5.Post traumatic

headache 6.Uncommon

headache7.Case demonstration

Management of MigraineManagement of Migraine

• Diagnosis

• Treatment of acute attack

• Prevention of acute attack

How Can We Best Treat Migraine?How Can We Best Treat Migraine?

• Nonpharmacologic intervention

• Pharmacologic intervention

–Acute therapy

–Chronic therapy

Acute Therapies Acute Therapies for for

MigraineMigraine

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

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

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

Limitation of Acute TreatmentLimitation of Acute Treatment

• Side effects and intolerance • Contraindication• Habituation• Drug-induced headache • Interaction with prophylactic therapy• Non-responders

Preventive Therapies Preventive Therapies for for

MigraineMigraine

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

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:

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

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?

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

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

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

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

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

Associated symptoms –Conjunctival injection –Lacrimation, nasal congestion

–Rhinorrhea, facial sweating

–Miosis, ptosis, eyelid edema

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Cluster headache ไมเกร์นเพศ ชาย์ : หญิง4 -6: 1 หญิง

: ชาย์ -34 : 1ร์ะย์ะเวิลาที�%ม�อาการ์ ไม�เกนช�%วิโมง - 24 ช�%วิโมงอาย์� - 3040 ป็2 - 1525

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หร์3อเดิ์3อน

Management of Acute Treatment •Oxygen •Triptans •Ergot derivative •Intranasal lidocaine

•Prednisolone?

Oxygen •Standard acute treatment

•Mask 7-12 L/min, 15-20 min

•Effective 70%•Aborted of attack within 5-12 min

Tension type headache

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

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�

Acute medication for TTHDrugs Efficacy Side

effects ASA 2+ 2Paracetamol 2+ 1Indomethacin 3+ 2Ibuprofen 2+ 2Naproxen 3+ 2ASA + Para + Caffeine 3+ 2DZP ? 3

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

Sinusitis headache

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

•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

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

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

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

ประสาที5. พบร�วิมกบไข1หร*ออาการอ*%นที�%ยงอธิ บายหร*อหา

สาเหต�ไม�ไดิ์1

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

Case demonstrationCase demonstrationNomenclatureNomenclature

Syndromic approachSyndromic approach

Common neuropsychiatric Common neuropsychiatric problemsproblems

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

SymptomSymptom

Conscious : delirium ,apathyConscious : delirium ,apathy Movement : psychomotorMovement : psychomotor Special sensation : Special sensation : agnosia ,visuospatialagnosia ,visuospatial MemoryMemory PhasiaPhasia EmotionEmotion Behavior : executive functionBehavior : executive function

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

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

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

DiscussionDiscussion

• Deterioration of cognitive function

• Episodic alteration of consciousness

• Urinary incontinence

• HT

• Localization at fronto-parietal area

• Nature; tumor,chronic infection, NPH



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 ---

Any investigationAny investigation

CT CT EEG – NoEEG – No X-rayX-ray

DiagnosisDiagnosis

Cysticercosis with secondary epilepsyCysticercosis with secondary epilepsy

TreatmentTreatment Albendazole Albendazole DexamethazoneDexamethazone PhenytoinPhenytoin B1-2-12B1-2-12

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

กรณ�ศ)กษาที�% กรณ�ศ)กษาที�% 22 PE:Obesity ,g um

hypertrophy ,hirsutism No skin stigmata Inducible – positive both

abdominal seizure ,GTC



Hiccup

Non-epileptic seizure

Complex partial seizure

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

Discussion

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

Further investigationFurther investigation

CT – WNLCT – WNL EEG – normal tracingEEG – normal tracing MRI – not availableMRI – not available

DiagnosisDiagnosis

EpilepsyEpilepsy Mental retardation ?Mental retardation ? Non epileptic seizureNon epileptic seizure

TreatmentTreatment

Carbamazepine 1x 3Carbamazepine 1x 3 counselingcounseling

Thank you for your interest

Documents

Management of Common Neuropsychiatri c Problems