Management of Common Neuropsychiatric Problems

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Management of Common Neuropsychiatric Problems

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Management of Common Neuropsychiatric Problems

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Mild cognitive impairment Medication-induced
movement disorder
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Management of Common Neuropsychiatric Problems
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Headache
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Management of Common Neuropsychiatric Problems
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Case discussion
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Management of Common Neuropsychiatric Problems

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Mild cognitive impairment Medication-induced
movement disorder
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Neuropsychiatry

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  ?????????????????? cognition ??????????????

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Mx of common neuropsychiatric problems

• 1. Mild cognitive impairment
• 2. Medication - induced movement disorders

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Mild Cognitive Impairment (MCI) defn

• Remains a research construct
• Memory loss in the transitional zone between
  normal aging memory loss and very early
  Alzheimers disease
• Dementia prodrome, incipient dementia, isolated
  memory impairment, cognitive impairment no
  dementia.
• Pathological, not a manifestation of aging

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MCI its construct

• MCI has been proposed to identify the individual
  at an earlier point in the cognitive decline such
  that if therapeutic interventions become
  available, clinician can intervene at this
  juncture

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MCI types

• 1. a-MCI gt memory impairment (amnesia)
• 2. md MCIgtmultiple domain MCIgt language,
  executive
• function and visuospatial skills
• 2.1 md -MCIa
• 2.2 md -MCI-a
• 3. Single nonmemory domain MCI

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a-MCI Diagnosis criteria

• 1. Memory complaint usually corroborated by an
  informant
• 2. Objective memory impairment for age (test
  -1.5 SD)
• 3. Essentially preserved general cognitive
  function
• 4. Largely intact functional activities
• 5. Not demented

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MCI - objective memory test -

• Word list learning
• Paragraph recall
• No generally accepted instrument for this
  determination
• Neuropsychological testing may be useful

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Table 1. The Short Test of Mental Status
Maximum
Subtests
Testing

score
Orientation Name address
current location
8
(building) city state date (day)
month year
Attention Digit span (present at
1 per second)
7
record longest correct span)
2-9-6-8-3
5-7-1-9-4-6
2-1-5-9-3-6-2
Learning and Learn our unrelated
wordsapple,
4
immediate recall
Mr Johnson, charity, tunnel.
Record the number of trials for
acquisition (maximum of 4
trials)
Calculation 5 13
4
65-7
58/2
29 11
Abstraction/ Similarities
orange/banana,
3
similarities dog/horse,
table/bookcase.

Information President first
president number of
4

weeks per year define an
island
Construction Copy the Necker cube.
Draw a clock
4
face showing 1110.
Recall The 4
words apple, Mr Johnson,
4
charity, tunnel.
Total Score

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Total score sum of the subtest scores -
(number of trials for acquisition -1). For
example, if a patient learned all 4 words no the
first trial nothing is subtracted from the sum of
the subtest scores. If a patient required 4
trials to learn the 4 words, then 3 was
subtracted from the sum of the subtest score.
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MCI Biological abnormalities

• 1. Over - representation of the apolipoprotein E4
  allele
• 2. Volumetric loss in entorhinal cortex and
  hippocampus
• measured by MRI neuronal counts in postmortem
  
• 3. Increased brain markers of oxidative stress
• 4. Abnormalities of the cholinergic system
• 5. Depression or medical co-morbidity
• So-MCI is heterogeneous and not all MCI will
  progress to AD

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MCI treatment

• - No FDA approved medicine
• But if Dr is convinced that the attending MCI
  is an
• incipient AD, then he may wish to Rx with
  cholinesterase
• inhibitor or memantine

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MCI treatment

• Donepesil risk of developing A.D. during
  the first year
• 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 available treatment

• 1. Acetylcholinesterase inhibitors 1st choice
  donepezil ,
• rivastigmine ,galantamine some research
  said donepezil lowered the risk of developing AD
  only during the first year
• 2. Putative treatments
• 2.1 antiglutamatergic drugs memantine
• 2.2 nootropics piracetam
• 2.3 antioxidants - ginko biloba, Vit A, C,
  E, selegiline, MAOI,
• 3. Anti-inflammatory drugs
• 3.1 aspirin
• 3.2 NSAID

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Currently available treatment

• 4. ERT
• 5. Visionary interventions
• 5.1 targeting neuropatholgical substrates
• 5.2 regulation of neuronal plasticity
• 6. Treating co-morbidity, controlling risk
  factors
• 7. Psychosocial intervention

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MCI Rx of the co-morbidity

• Vascular risk factors - high BP
• High serum cholesterol
• High midlife diastolic BP
• White matter hyperintensity
• Presence of apolipoprotein E4 genotype
• Low serum B12 and folate

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Psychosocial intervention emotional and mental
stimulation

• 1. Extensive social network
• 2. Participating cognitively stimulating
  activities

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MCI Rx with AChE

• Autopsy-based study reported similar reductions
  in basal forebrain immunoreactive neurons
  selective loss of cholinergic neurons in MCI
  and AD gt cholinergiic differentiation of the
  cerebral cortex
• Long term effects will be via modification of APP
  metabolism
• However a study observered specific upregulation
  of choline acetyltransferase 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 antiglutamatergic drugs

• Overactivity of excitatory amino acid glutamate
  neurotoxcity
• NMDA- mediated excitotoxicity tau
  phosphorylation NT one of
  the major pathological substrates of AD
• Memantine NMDA - receptor antagonist
  

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MCI Rx with nootropics

• Piracetam
• Enhance memory function
• Nonspecific action - energy metabolism,
  cholinergic mechanism, excitatory amino acid
  receptor - mediated function and steroid
  sensitivity

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MCI Rx antioxidants

• Large amounts of unsaturated lipids and
  catecholamines in the brain , ß - protein
  precursor, Aß, presenilins and APOE are link to
  reactive oxygen species (ROS) production
  apotosis
• Oxidative stress atherogenesis
• Higher ascorbic acid and ß- carotene plasma level
  better memory
• Ginko biloba, Vit A, C, E free radical
  scarvenger, MAOI reduce free radical formation
  

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MCI Rx with anti inflammatory drugs

• Inflammatory process are involved in the
  pathogenesis of AD
• AD pt has upregulation of cytokines, acute phase
  proteins, activation of the complement regulatory
  proteins, accumulation of activated microglia
• Reduced prevalence of AD in pt with arthritis
• Rx with aspirin, NSAID, COX-2 inhibitors

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MCI Rx with ERT

• Estrogen acts via ERa ??? ERß activate
  nerve growth factors, synaptogenesis,
  modulate function of ACh,
• 5-HT, DA, NA, and cerebral blood flow
• Estrogen has intrinsic antioxidant activity,
  neuroprotective effect by promoting
  nonamyloidgenic ß- secretase processing of APP

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Targeting neuropathological substrates

• 1. Reduction of Aß production
• 2. Inhibitors of Aß aggregation
• However APP transgenic animals develop
  behavioral
• abnormality before extensive amyloid
  deposition occurs
• 3. Neurofibrillary changes better correlate with
  disease
• severity than amyloidosis
• 4. Intervention in tau hyperphosphorylation

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Regulation of neuronal plasticity

• 1. Nerve growth factor (NGF) neurotropic factor
  for the
• basal forebrain cholinergic neuron

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Medication - induced movement disorders

• 1. All first generation antipsychotics
• Chlorpromazine
• Thioridazine
• Perphenazine
• Haloperidol
• 2. Some second generation anti-psychotics
  usually dose related

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Medication - induced movement disorders

• 3. Nonantipsychotic psychotripics
• Lithium
• Anticonvulsants
• Antidepressants
• 4. Nonpsychotropics
• Prochlorperazine
• Metoclopramide

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Neuroleptic - induced movement disorders

• 1. Acute dystonia
• 2. Akathisia
• 3. Parkinsonian - like
• 4. Tardive dyskinesia

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Neuroleptic - induced acute dystonia
Pathophysiology

• not known, may be acute saturation of D2
• receptors

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Neuroleptic induced acute dystonia

• Early - onset during the course of treatment
  with neuroleptic
• M gt F, age lt 30 years gt
• Receive high potency anti-psychotic medication

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Neuroleptic induced acute dystonia Dx

• A. 1 (or more) of the following signs or
  symptoms
• has developed in association with the use
• of neuroleptic medication
• 1. Abn positioning of the head and neck in
  relation to
• body (retrocollis, tortiollis)
• 2. Spasms of the jaw muscles (trismus,
  gaping, grimacing )

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Neuroleptic induced acute dystonia Dx

• 3. Impaired wallowing (dyspepsia) speaking
  or
• breathing
• 4. Thickened or slurred speech due to
  hypertonic or
• enlarged tongue
• 5. Eye deviated up, down, or sideward
• (oculogyric crisis )

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Neuroleptic induced acute dystonia Dx

• 6. Tongue protrusion or tongue dysfunction
• 7. Abn positioning of the distal limb or
  trunk

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Neuroleptic induced acute dystonia Dx

• B. A developed 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. Anticholinergic or antihistaminergic drugs
• 2. If fails to respond to 3 doses of these drug
  with in
• 2 hrs, then consider other causes for the
  dystonia
• 3. After resolution of the acute episode, give
  oral
• anticholinergic agents

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Neuroleptic - induced acute akathisia
Pathophysiology

• DA neurons in the ventral tegmental area

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Neuroleptic - induced tardive dyskinesia
Pathophysiology

• 1. Sustained D2 receptor blockade receptor
  hypersensitivity
• 2. Blockade of presynaptic DA receptors
  glutamatergic transmission oxidative
  stress cell death

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Neuroleptic - induced acute akathisia

• Risk middle aged women
• Occurs at some point in the course of medication
  (antipsychotics, antidepressants and
  sympathomimetics)

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Neuroleptic - induced acute akathisia Dx

• A. subjective complaints of restlessness after
  exposure to a neuroleptic medication
• B. At least one-of the following
• 1. fidgety movement or swinging of the legs
• 2. rocking from foot to foot while standing
• 3. pacing to relieve restlessness
• 4. inability to sit or stand still for at
  least several minutes

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Neuroleptic - induced acute akathisia Dx

• C. onset of A and B occurs within 4 weeks of
  initiating
• or increasing the dose of neuroleptic , or
  of reducing
• medication used to Rx or prevent acute EPS
  

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Neuroleptic - induced acute akathisia Rx

• 1. Reduce neuroleptic medication dosage
• 2. Attempt to treat with B - adrenergic receptor
• antagonists, anticholinergic drugs,
  cyproheptadine
• 3. Considering changing the neueroleptics

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Neuroleptic induced parkinsonism
Pathophysiology

• DA activity, this can be induced by
• 1. Depletion of DA in presynaptic stores
  (reserpine)
• 2. DA receptor blocking antipsychotic and
  atypical
• calcium blocking agent (cinnarizine)

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Neuroleptic-induced parkinsonismDx

• A. One (-or more) of the following signs or
  symptoms
• has developed in association with use of
  
• neuroleptic medication
• 1. Parkinsonian tremor
• 2. Parkinsonian muscular rigidity
• 3. Akinesia

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Neuroleptic-induced parkinsonismDx

• B. A. developed with a few weeks of starting or
• raising the dose of a neuroleptic
  medication or
• of reducing a medication used to treat
• (-or prevent) acute EPS (anticholinergic
  agents)

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Causes

• Blockade of gt 80 of D2 receptor in the
• caudate at the termination of
• the nigrostriatal dopamine neurons

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Risk

• Elderly
• Female
• gt 50 of pt Rx with long term, high potency
  dopamine receptor antagonists

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Treatment

• 1. Reduce the dosage of the neuroleptic
• 2. Anti EPS medication for 14-21 days then
• attempt to reduce or stop
• 3. Possibly changing the neuroleptic

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Medication- induced postural tremor

• Pathophysilolgy based on the class of drug
  implicated, eg, stimulant may cause tremor due to
  the resulting hyperadrenergic state

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Medication- induced postural tremor

• Causes Li, valproic acid, ß - adrenergic
  blockers stimulant, DA agonist, caffeine,
  theophylline, nureoleptic, antidepressant
• 8-12 Hz postural tremor affecting limbs head,
  mouth, tongue

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Medication- induced postural tremor Rx

• 1. Check for drug toxicity
• 2. Check for emotional factors , alc withdrawal
  , hypoglycemia,
• thyrotoxicosis
• 3. Reduction of the dosage or switch to another
  agent in a
• different class
• 4. Use benzodiazepine or ß-blocker

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Neuroleptic - induced tardive dyskinesia risk
factor

• 25 of pts treated with dopamine receptor
  antagonists for over 4 years
• Increasing age
• Female
• The presence of a mood disorder
• The presence of a cognitive disorder

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Neuroleptic - induced tardive dyskinesia
Diagnosis

• A. Involuntary movements of the tongue jaw, trunk
  or
• extremities have developed in association
  with the use of neuroleptic
• medication
• B. A is present over a period of at least 4 weeks
  and occur in any of the
• following patterns
• 1. choreiform movements (rapid, jerky,
  nonrepetitive )
• 2. athetoid movement (slow, sinuous,
  continual)
• 3. rhythmic movements (stereotypes)

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Neuroleptic - induced tardive dyskinesia
Diagnosis

• C. A and B develop during exposure to a
  neuroleptic
• medication or with in 4 weeks of withdrawal
  from
• an oral ( or within 8 weeks of withdrawal
  from a
• depot ) neuroleptic medication
• D. Exposure to neuroleptic medication for at
  least 3
• months (1 month if age 60 years or older)

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Neuroleptic - induced tardive dyskinesia 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

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Headache

• 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 headache
5. Post traumatic headache
6. Uncommon headache
7. Case demonstration

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Management of Migraine

• Diagnosis
• Treatment of acute attack
• Prevention of acute attack

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How Can We Best Treat Migraine?

• Nonpharmacologic intervention
• Pharmacologic intervention
• Acute therapy
• Chronic therapy

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Acute Therapies for Migraine
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Goals of Acute Treatment

• Abortive treatment is always indicated
• Treat attacks rapidly and consistency without
  recurrence
• Restore the patients 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, AGElt15yr
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 Overuse
At least on of the following for at least one month At least on of the following for at least one month
1.Simple analgesics use (gt1000mg ASA/acetaminophen) gt 5days/week
2.Combination analgesics (caffeine, barbiturate- containing medication) gt 3tablets/day gt 3days/week
3.Opioids (gt1tablet/day) gt 2days/week
4. Ergotamine use (1mg PO or 0.5mg PR) gt 2days/week
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Limitation of Acute Treatment

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

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Preventive Therapies for Migraine
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Goals of Preventive Treatment

• Reduce attack frequency, severity, and duration
• Improve responsiveness to Rx of acute attacks
• Improve function and reduce disability
• Prevent disease progression?
• Reduce costs

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Consider Preventive Therapy If Any of the
Following Criteria Are Met

• Migraine significantly interferes with patients'
  daily routine, despite acute treatment
• Frequency of attacks (3 / month) with risk of
  acute medication overuse
• Acute medications ineffective, contraindicated,
  troublesome AEs, or overused
• Patient preference
• Presence of uncommon migraine conditions
• Hemiplegic migraine
• Basilar migraine
• Migraine with prolonged aura
• Migrainous infarction

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Migraine Prevention Utilization
lt5 of migraineurs are on preventive therapy
53 of migraineursmeet disability and frequency
criteria for prevention
25 Frequency
28 Disability
Lipton RB et al. Headache. 200141638-645
Lipton RB et al. Neurology. 200258885-894.
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Preventive Medications

• Anticonvulsants
• Divalproex
• Topiramate
• Gabapentin, zonisamide, levetiracetam
• Antidepressants
• TCAs, SSRIs, MAOIs
• ?-Blockers
• Propranolol
• Ca channel blockers
• Verapamil
• NSAIDs

• 5-HT antagonists
• Methysergide/methergine
• Neurotoxins
• Botulinum
• Angiotensin system
• ACE inhibitors
• Antagonists
• Other
• Riboflavin, Feverfew, Petasites
• Neuroleptics?

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Setting Treatment Priorities

• Comorbid and coexistent disease
• Therapeutic opportunity to treat two disorders
  with single drug
• Hypertension or angina ?-blocker
• Depression TCA or SSRI
• Epilepsy or mania divalproex or topiramate
• Therapeutic limitations
• Depression avoid ?-blocker

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Use Drug Best for Patient

• Take advantage of drugs side effects
• Underweight patient Use flunarizine
• Overweight Use topiramate
• Insomniac Use TCAs
• Elderly or cardiac patient Use divalproex or
  topiramate
• Athlete Avoid ?-blockers

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Cost of Medications Used for Migraine Prophylaxis

• Trade Name Dose (mg) Baht (tablet)
  Unit (month) Baht (month)
• Amitriptyline 10 0.50 30
  15
• 25 1 30
  30
• Flunarizine 1.50 30 45
• 1.50 60 90
• Propranolol 10 0.50 60
  30
• 40 1.50 30 45
• Depakine 200 7 90
  630
• 500 14 60 840
  
• Neurontin 300 33 90
  2970
• Topamax 100 45 30 1350
  

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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 41
• 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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cluster ????????????????????

• Cluster headache ??????
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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 gt 15 days/month, gt 6 months/year
• B. At least 2 of following
• 1. Pressing, tightening quality
• 2. Mild or moderately severity
• 3. Bilateral
• 4. No aggravation by routine activity
• C. No vomiting, no photophobia, phonophobia

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??????????????????? TTH

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2. ????????????????????????
3. ??????????????????????????????????????
4. ??????????????????????????
5. ????????????????????????/????????????

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Acute medication for TTH

• Drugs Efficacy Side effects
• ASA 2 2
• Paracetamol 2 1
• Indomethacin 3 2
• Ibuprofen 2 2
• Naproxen 3 2
• ASA Para Caffeine 3 2
• DZP ? 3

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Sinus headache criteria

• Headache location
• 1. Frontal, over the sinus, radiate to vertex,
  behind eyes
• 2. Maxillary, over antral area, radiate to upper
  teeth, forehead
• 3. Ethmoiditis, behind eyes, radiate to temporal
  area
• 4. 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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Treatment

• Carbamazepine, 75 responsive
• Initial dose 50-100 mg ? 600-1200 mg
• Vertigo, dizziness, ataxia are most common side
  effect
• Phenytoin, baclofen, valproate, gabapentin,
  topiramate, oxcarbazepine, clonazepam

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Post-traumatic headache

• Acute and chronic form
• TTH pattern 85
• Generalized, persistent, bilateral, mild to
  moderately pain
• Occipital, frontal, and generalized
• Non-headache symptoms
• Dizziness, hearing loss
• Vertigo
• Tinnitus, blurred vision

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Risk factors

• Women 1.9
• Age
• Severity
• Post-traumatic amnesia
• Skull fracture

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Treatment

• TCA
• Valproate

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Subdural hematoma
104

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  ??????????????????????
• CC ???????????????? 1 ???????
• PI ????????????????? 24.00 ?.
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  ????????
• PH Peripheral vertigo ???????? ENT ?????????
• PE A late middle-aged patient with fully of
  consciousness
• Neurological and general
  examination were normal

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Diagnosis Post-coital headache
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  ????????????? HN GB 0217
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• PH ????????????????? ???????????????

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Case demonstrationNomenclatureSyndromic
approach

• Common neuropsychiatric problems

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Common feature

• Psychic symptoms
• Organic pathology
• migraine, seizure , tumor
• Cortical function
• Treatment
• Psychotropic drug
• Etiological treatment
• Counseling

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Symptom

• Conscious delirium ,apathy
• Movement psychomotor
• Special sensation
• agnosia ,visuospatial
• Memory
• Phasia
• Emotion
• Behavior executive function

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Case discussion

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• CC ??????????? 3 ???
• PI 2 ??????????? ??. ???????????????????????
  ???????????
• ?? ??. ?? BP 212/100
• Dx HT
• ???????? HCTZ ½ x 1
• Dramamine 1 X 3
• Adalat 10 mg stat
• Atenolol (50 mg) 1 X OD
  

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• ????? ?? F/U BP 150/80
• Dx HT with vertigo
• 1 ????? ??????????????? ???????? ??????? ?
  ???????????????? ?????? ??????????????????
  ???????? ???????????? ??????????????????????????
  ?????? ?????????????????
• 3 ??? ????????????????? ?????????? ?????????
• ??????????????????????????????????????????
  ???????????????????

116
Physical examination

• Elderly man ,good looking ,not distress , mild
  agitation
• BP 163/64 Repeat 130/60
• Heart lung abdomen- WNL
• Neuro examinaiton
• good consciousness
• Motor - Grade V all ,DTR 2
• Palmomental bilat
• Finger agnosia
• Lt-Rt disorientation
• No definite weakness
• Sensory - intact
• Double simultaneous test NA

117
Discussion
118
Discussion

• Deterioration of cognitive function
• Episodic alteration of consciousness
• Urinary incontinence
• HT
• Localization at fronto-parietal area
• Nature tumor,chronic infection, NPH

119
Discussion
120
Investigation

• CBC Hct 34 NCNC,
• WBC 8400 ,PMN 70 EO 3
• FBS 89 mg
• Na 140,K 3.8,HCO3 25,Cl 108
• Ca,PO4,Mg - WNL
• CXR ---
• EKG ---

121
Any investigation

• CT
• EEG No
• X-ray

122
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123
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124
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125
Diagnosis

• Cysticercosis with secondary epilepsy
• Treatment
• Albendazole
• Dexamethazone
• Phenytoin
• B1-2-12

126
???????????? 2

• ??????????? 37 ??
• CC ?????????? 1 ???????
• PI ?????????????? 30 ?? ??????????????????????
  ????? 6 7 ?? ???????????????????
  ???????????????????? ? ????????????????
  ???????????? 10 23 ?????/??? ??????? 2 ???
• ?????? 1 ????????????????? ?????????
  
• ?????? 2 ???????????????????????
  ??????????????
• 1 ??????? ??????????????????????????????
  ???????? ??. ?????????????????????????? 1
  ????? ???????????????????????????

127
???????????? 2

• PEObesity ,gum hypertrophy ,hirsutism
• No skin stigmata
• Inducible positive both abdominal seizure
  ,GTC

128
Discussion
129
Discussion
Hiccup
130
Non-epileptic seizure
131
Complex partial seizure
132
Patient with chronic and active epilepsy

• 1. Review diagnosis and etiology
• history
• EEG
• neuroimaging
• other investigation
• 2. Classify epilepsy
• 3. Review compliance

133
Discussion
134
Investigation

• CBC WNL
• DTX ,electrolyte , BUN,Cr,Mg,Ca,PO4
• UA
• Thyroid function
• Psychological test IQ

135
Further investigation

• CT WNL
• EEG normal tracing
• MRI not available

136
Diagnosis

• Epilepsy
• Mental retardation ?
• Non epileptic seizure

137
Treatment

• Carbamazepine 1x 3
• counseling

138
Thank you for your interest