ติวสอบ ศรว.

August 11, 2017 | Author: Surat Tanprawate | Category: Migraine, Meningitis, Stroke, Dementia, Headache
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ติวสอบ ศรว. วิชาประสาทวิทยา นพ.สุรัตน์ ตันประเวช หน่วยประสาทวิทยา ภาควิชาอายุรศาสตร์ มหาวิทยาลัยเชียงใหม่

แนวข้อสอบ •

เป็นอาการวิทยา ถามหาตำแหน่งของรอยโรค

ถาม knowledge ของโรคนั้น ๆ

ให้เป็น case scenario แล้วถาม investigation, diagnosis and treatment

โรคต่าง ๆ •


Neuro-infectious disease

Stroke: ischemic infarct, hemorrhagic

Headache: migraine

Degenerative disease: Parkinson, Dementia


ข้อสอบ ให้โจทย์มาว่า ผู้ป่วยเป็น alteration of conscious แล้วถามว่า เป็นอะไร ระหว่าง seizure syncope TIA

ให้โจทย์มาเป็นอาการของโรคลมชัก ชนิดต่าง ๆ แล้ว ให้เลือกยา

ให้โจทย์มาเป็นชักต่อเนื่องแล้ว ถามว่าจะทำอะไรต่อ

ชัก(seizure) และ โรคลมชัก (epilepsy) •

ชัก (seizure) อาการที่เกิดจากสมองมีการสร้างคลื่นไฟฟ้า ผิดปกติ (epileptiform discharge) โดยอาการเกิดขึ้นกับ ตำแหน่งที่สร้างคลื่นชัก

โรคลมชัก (epilepsy) โรคที่ทำให้เกิดภาวะเสี่ยงให้เกิด อาการชักซ้ำ

วินิจฉัยแยกโรค: syncope

Seizure vs Syncope

Bhidayasiri R. et al. Neurological differential diagnosis 2005

อาการชักชนิดต่าง ๆ และการเลือก ยากันชัก •

Partial seizure (คลื่นชักสร้างออกจากส่วนเฉพาะที่) •

simple partial seizure ไม่หมดสติ

complex partial seizure หมดสติ แบบเหม่อ มักมีคลื่นชัก ออกจากสมองส่วน frontal หรือ temporal

Generalize seizure (คลื่นชักสร้างทั่วสมอง) •

tonic clonic, tonic, clonic, atonic, absence, myoclonic

70 years of AED development

20 years of new AED development

Antiepileptic drug classification Old generation

• • • • • •

1800’s Bromide Solution 1912 Phenobarbital 1938 Phenytoin 1960 Ethosuximide 1973 Carbamazepine 1978 Valproate

New generation

• • • • • • • • • •

1993 Felbamate 1993 Gabapentin 1994 Lamotrigine 1996 Fosphenytoin 1996 Topiramate 1997 Tiagabine 1999 Vigabatrin 2000 Oxcarbazepine 2000 Levetiracetam 2005 Pregabalin

Epilepsy Management

* Brodie MJ and Kwan P. CNS Drugs 2001;18:1-12

ห้ามให้ phenytoin

Status epilepticus

definition of SE • Lowenstein DH (1999) • SE > 5 minutes

Key • treat early as possible • step up AED is depended on stage of SE

• add on therapy is needed • monitor EEG regularly, even if no obvious seizure

Define stage of the status epilepticus

• Pre-monitory status(0-5 min) • Early status(5-30 min) • Established status(30-60 min) • Refractory status(>60 min)

Drug used • diazepam, phenytoin(Dilantin), valproic acid(Depakine), levetirazetam(Keppra)

• Phenobarbital, propofol, midazolam, thiopental

• Topiramate(feed)

drug use depend on stage of status stage of status

AED treatment

Premonitory (0-5 min)

Diazepam (i.v. bolus)

Early (5-30 min)

Diazepam (i.v. bolus) followed by phenytoin (iv load) or sodium valproate (i.v. loading) or levetiracetam (i.v.)

Established (30-60 min)

half dose i.v. load of previous drug, if seizure don’t stop, load another drug

Refractory ( > 60 min)

Propofol (i.v.), or midazolam (i.v.), or thiopental (i.v.) or phenobarbital (i.v.) or topiramate (feed)

Neuro-infectious disease

Meningitis •

Meningitis is a disease caused by the inflammation of the protective membranes covering the brain and spinal cord known as the meninges.

Clinical symptoms: fever, headache, stiffness of neck, sign of IICP, photophobia, alteration of conscious

Diagnosis: Lumbar puncture shows pleocytosis

Cause: infection (viral, bacteria, parasite), inflammation (autoimmune), cancer

CT or not CT in meningitis

Aseptic meningitis •

Lymphocytic pleocytosis, normalm CSF sugar, normal/slightly high protein

Causes: •

Viral: enterovirus(Coxsackie, echo, polio), HZV, VZV, arbovirus, EBV, etc.

Bacteria: partially treated bacterial meningitis, parameningeal infection, mycoplasma pneumoniae, Treponema pallidum

Fungal: crypto, histoplasma,

Parasitic: Toplasma, cysticercosis,

Drug: NSAIDs, Bactrium, amoxicillin)

Cancer: carcinomatous meningitis, lymphomatous meningitis

Vasculitis: CNS vasculitis, Behcet disease, SLE

Eosinophilic meningitis •

CSF presents eosinophilia of at least 10% of the total CSF leukocyte count.

Cause: •

Parasitic: angiostrongyliasis, gnathostomiasis

Non-parasitic infection: Tuberculous meningitis, Cryptococcal meningitis, syphilitic meningitis

Hematologic: Hodgkin’s disease, non-Hodgkin’s lymphoma, and eosinophilic leukemia

Non-Hematologic: carcinomatous meningitis

HIV infection

Viral Encephalitis •


clinical: fever, alter mental status, seizure, focal neurological deficit

CSF: aseptic profile

MRI, CT brain: brain lesion (fronto temporal involvement suggest Herpes simplex encephalitis)


EEG: periodic sharp wave

Treatment: acyclovir 10 mg/kg/dose q 8 hrs


Neurological disorder in HIV

Primary HIV-induced neurologic syndromes


Brain mass in HIV •

The concomitance of negative toxoplasmosis serology + a single lesion on radiographic imaging -> sufficient to warrant the performance of a stereotactic biopsy

Median time to response of Toxoplasmosis •

74% 7 days -> 91% 14 days

Lymphoma vs Toxoplasmosis Favors Lymphoma

Favors Toxoplasma

Large lesion size (>4 cm)

Large number of lesions

Extensive white matter involvement

Involvement of basal ganglia

Hemorrhagic lesions

Responses to anti-toxo drugs, usually within 7-14 days

Periventricular location/ subependymal spread

Contrast enhancement along ventricular surface

Extension across or involvement of corpus callosum

A HIV patient with alteration of consciousness for 3 days

Neuromuscular disorder

Neuromuscular disorder •

Neuropathy: polyneuropathy, cranial neuropathy

NMJ disorder: Myasthenia gravis

Muscle disease

Differential diagnosis of neuropathies by clinical course

Nerve conduction study: reveals demyelination of nerve (or axonal degeneration in axonal type)

Treatment of GBS •

ABCD support

IVIG or plasma exchange: effective

Combination treatment: no additive effect

Corticosteroid: not effective

NMJ disorder •

Myasthenia gravis


Lambert Eton Myasthenic Syndrome (LEMS)

Cause of MG •

caused by autoantibodies specific for the human nicotinic acetylcholine receptor (AChR)

Ach released per impulse normally decline on repeated activity= presynaptic rundawn

Autoimmune cause: The most important known cause is thymic tumour

30–60% of thymomas : associated with MG

10% of MG: have a thymoma

Diagnosis should be based on positive results from at least two of the main diagnostic tests •

AChR antibody assay (+ 75% in Generalize MG)

Edrophonium (Tensilon) test or Neostigmine test

repetitive nerve stimulation

single-fibre electromyography

• Associated disorder

– Disorder of thymus • Thymoma • Hyperplasia

– Other autoimmune disorder • • • •

Hashimoto thyroiditis Grave’s disease RA SLE

• Disorder or circumstance that may exacerbate MG

– Hyperthyroidism – Occult infection – Medical Rx of other condition (aminoglycoside, quinidine, antiarrhythmic drug)

• Disorder that may interfere therapy

– TB,DM,PU,GI bleed ,Asthma, osteoporosis

Treatment base therapy • Symptomatic therapy

– Short acting cholinesterase inhibitor • Pyridostigmine bromide (mestinon)

– Long acting cholinesterase inhibitor • Neostigmine(prostigmin ) • Mestinon timespan

• Immunosuppressive therapy – Long term immunosupression • Medical

– Corticosteroid – Immunosupressive drug

• Surgical

– thymectomy

– Short term immunosupression • Plasma exchange • IVIG

Myasthenic crisis •

MG with •

Respiratory failure

Bulbar involvement

Treatment •

Respiratory support

Plasma exchange or IVIG

No role of steroid / no role of anti-AChE in MG crisis


Stroke Subtypes Hemorrhagic Stroke (17%) Intracerebral Hemorrhage (59%)

Ischemic Stroke (83%) Atherothrombotic Cerebrovascular Disease (20%)

Cryptogenic and Other Known
 Cause (30%)

Subarachnoid Hemorrhage (41%) Lacunar (25%) Small vessel disease

Albers GW, et al. Chest. 1998;114:683S-698S. Rosamond WD, et al. Stroke. 1999;30:736-743.

Embolism (20%)

Condition that mimic stroke miscellaneous SAH TGA vertigo MS syncope/presyncope


dementia psychogenic migraine confusional state


SDH tumour PN palsy toxic/metabolic


seizures 0.0%





% of all stroke mimics (n=670)



What Is the Cause of Ischemic Stroke? ■ ■

Atherothrombosis Embolus: ■ ■

■ ■ ■

Material: Red (fibrin rich) or White (platelet rich) Source: Cardiac? Aortic? Carotid Artery?

Small artery disease Hypoperfusion: Hemodynamic Others: arterial dissection, arteritis, etc.

Lacunar Syndromes

Strategies for Preventing Stroke and Reducing Stroke Disability blood pressure glucose smoking lipids

stroke mortality mass popl. strategy

acute treatment

First stroke

Secondary prevention

recurrent stroke

high risk strategy

hypertension TIA Atrial fibrillation other vascular disease


Stroke related disability

Stroke: Well-Documented and
 Modifiable Risk Factors ■ ■


Asymptomatic carotid stenosis


Sickle cell disease

Postmenopausal hormone therapy


Atrial fibrillation

Diet and nutrition

Other cardiac conditions

Physical Inactivity

Cigarette smoke

Obesity and body fat distribution

Since 1995

rt-PA era

Thrombolysis • IV rtPA (recombinant tissue plasminogen activator ) – 31 – 51 % พิการเล็กน้อยหรือหายปกติที่ 3 เดือนหลังมี อาการ เทียบกับกลุ่มไม่ได้ยา 20 – 30% – Death rate at 3 months and 1 years is equal both group – Intracranial hemorrhage 6.4%


อาการเข้าได้กับโรคหลอดเลือดสมองขาด เลือด

• •


สามารถให้การรักษาได้ทันภายในเวลา 3-4.5 ชั่วโมง

อาการทางระบบประสาทไม่น้อยเกินไปเช่น มีอาการชาอย่างเดียว

ข้อบ่งชี้อื่นๆ Need check list

Additional exclusion criteria for rtPA within 3-4.5 hours 1. age > 80 years 2. NIHSS > 25 3. Previous stroke with diabetes 4. Receiving anti-coagulant

Stroke Treatment Stroke onset

Full recovery

Thrombolysis Drugs



Secondary prevention


Call emergency services Activated

A+E stroke team

Brain scan

Activate fast track when clinical stroke occur within 2-3.5 hours

CT brain, non-contrast • สามารถทำได้รวดเร็ว ใช้เวลาน้อย • วินิจฉัยภาวะเลือดออกในสมองเฉียบพลันได้โดย มี sensitivity เกือบ 100%

• Minor or subtle signs : loss of lentiform nucleus, loss of insular ribbon, loss of graywhite differentiation and sulcal effacement

Major complication of cerebral infarction • • • • •

Subfalcine (A) Uncal (B) Central (C) Extradural (D) Tonsillar (E)

Herniation syndrome

Treatment IICP • •

ให้นอนยกศีรษะและส่วนบนของร่างกายสูง 20-30 องศา

พิจารณาให้ osmotherapy:

จัดท่าผู้ป่วยให้หลีกเลี่ยงการกดทับของหลอดเลือดดำที่คอ (Jugular vein)

Mannitol* 0.25-0.5 g/kg ทางหลอดเลือดดำใน 20 นาที 4-6 ครั้งต่อวัน

หรือ 10% Glycerol 250 ml ทางหลอดเลือดดำใน 30-60 นาที วันละ 4 ครั้ง

• •

หรือ 50% Glycerol 50 ml ทางปากวันละ 4 ครั้ง และ/หรือ Furosemide 1 mg/Kg ทางหลอดเลือดดำ

Treatment IICP • •

หลีกเลี่ยงการให้ hypotonic solution

Hyperventilation เพื่อให้ Pco2 30-35 mmHg มีประโยชน์ในการลดความดันในสมองในช่วง สั้น ๆ ก่อนผ่าตัด

ไม่ควรให้ steroid

หลีกเลี่ยงภาวะขาดออกซิเจน พิจารณาใส่ท่อ ช่วยหายใจในกรณีที่มีการหายใจผิดปกติ

Hemicraniectomy in malignant middle cerebral artery infarction •

Malignant MCA infarction : การขาดเลือดของสมองบริเวณที่ เลี้ยงด้วย MCA เป็นบริเวณกว้าง (> 50% of MCA territory) จน อาจทำให้เกิดการกดเบียดต่อเนื้อสมอง ทำให้มีbrain herniation ตามมา


• • • • •

Contralateral weakness Eye deviate to ipsilateral lesion Global aphasia in dominant hemisphere Hemispatial neglect in nondominant hemisphere Signs of IICP, brain herniation


Amnestic and dementia syndrome Amnestic syndrome Profound loss of the episodic memory • Dementia Acquired and persistent compromise in multiple cognitive, domains that are severe enough to interfere with every day functioning • Delirium or acute confusional state(ACS) Prominent deficits or fluctuations in attention processing •

Dementia diagnosis: DSM IV criteria •

The development of multiple cognitive deficit that include memory impairment and at least one of the following •

Aphasia, Apraxia, Agnosia, Disturbance of executive function

The cognition deficit must meet the following criteria •

Be sufficiently severe to cause impairment in occupational or social functioning

Represent a decline from a previous from a previous higher level of functioning

Diagnosis should not be diagnosed if the cognitive deficit occur exclusively during the course of delirium. However, a dementia and a delirium both may be diagnosed if the dementia is present at times when the delirium is not present

Dementia may be related etiologically to a general medical condition, to the persisting effects of substance abuse(including toxin exposure), or to a combine of these factor

Dementia approach

Dementia Reversibel dementia

Irreversible dementia

- Drug - Syphilis - Hypothyroid - Vitamin deficiency - Organ failure


Stable - Vascular - Post traumatic - Post encephalitis - etc

Non-neurodegenerative - CJD - ADC - Vascular


Non-Alzheimer’s disease - Parkinson’s disease dementia - DLB - Parkinson plus syndrome - Genetic (Wilson, Huntington)

Alzheimer’s disease

Alzheimer’s disease Clinical manifestation •

Progressive, degenerative CNS disorder

Characterized by memory impairment plus one or more additional cognitive disturbances

Gradual decline in three key symptom domains •

Activities of daily living (ADL), Behavior and personality and Cognition

Most common cause of dementia in people 
 aged 65 and over

Clinical manifestation

Cognitive dysfunction

Neuropsychiatric symptoms

memory loss

affect or mood disturbance

language disturbance

psychosis (delusion/ hallucination)

visuospatial disturbance

personality change

behavioural (agitation/wondering)

Diagnostic studies •

MRI/CT brain •

generalized brain atrophy

medial temporal lobes reveals a disproportionate atrophy of the hippocampi



Patient presents with complaint of a headache

Critical first step: Hx taking, physical exam

Red flag signs (+)


Red flag signs or alarming signs Meets criteria for primary headache disorder?

Migraine headache Cluster headache and other TACs



Other (rare) headache disorder

Secondary headache disorder

Tension-type headache

Alarming signs and symptoms

• “Alarming s/s suggest the possibility of secondary headache

• The studies • Headache sample (specific or nonspecific)

• Pool analyzed data => guideline

ไมเกรนคลาสสิก, ไมเกรนที่มีอาการนํา (Migraine with aura)! ไมเกรนที่พบบ่อย (Common migraine)


Migraine without aura


• Life style modification • Acute treatment • Prophylactic treatment

 (trigger factors)"




 (trigger factors)"


รอบเดือน! แสงจ้า เสียง กลิ่น!

Pharmacotherapy of acute migraine attack Non-specific

• • • • •

Acetaminophen, NSAIDs caffeine opioids neuroleptic

DHE injection form


• • •

Dihydroergotamine Ergotamine Triptan

Ergotamine tartrate+ Caffeine

Analgesics with evidence of efficacy EFNS migraine treatment guideline 2009

Evers, S et al. European Journal of Neurology 2009, 16: 968–981


Evers, S et al. European Journal of Neurology 2009, 16: 968–981

Preventive Medication Aim

Reduce attack frequency, severity, and duration

Improve responsiveness to acute headache therapies

• •

Improve function and reduce disability Reduce overall cost associated with migraine treatment

Indication for preventive treatment in migraine

Recurring migraine that significantly interferes with quality of life

• • •

Frequency of migraine attacks > 1/weeks

Uncommon migraine: hemiplegic migraine, basilar migraine, prolonged, disabling or frequent aura, or migrainous cerebral infarction

Frequency of acute medication use>2/week Failure of, contraindication to, or trouble AE from acute medication

Pract Neurol 2007; 7: 383–393

Concept Right drug

Preventive medication that was proven the efficacy

Right person

Consider patient profiles, and co-morbidities

Right dose

Titrate into the appropriated dose

Right duration

On the preventive therapy long enough

Recommended medication for migraine prevention “EFNS guideline 2009”

Evers, S et al. European Journal of Neurology 2009, 16: 968–981

Indications, contraindications, and adverse effects of conventional migraine preventive drugs


Relative indications

Relative contraindication

Adverse effect

Amytriptiline (TCA)

Other pain disorders, depression, anxiety, insomnia

Mania, urinary Drowsiness, dry mouth, retention, heart blocks, increase appetite, glaucoma weight gain

Propranolol (B-blocker)

Hypertension, angina

Asthma, depression, Fatique, lethargy, nausea, CHF, Raynaud’s disease depression, dizziness

Flunarizine (CCB) Valproic acid (AED)

Topiramate (AED)

Hypertension, vertigo Epilepsy, mania, anxiety

Epilepsy, mania, anxiety

Obesity, depression, PD

Drowsiness, weight gain, depression, PD

Liver disease, bleeding disorder

Nausea dyspepsia, sedation, increase appetite, weight gain

Renal calculosis, liver disease

Paresthesia, weight loss, alter taste, language disturbance

F. Galletti et al. Progress in Neurobiology 89 (2009) 176–192

Continue preventive medication for 4-6 months

“Thunderclap Headache” (TCH) The sudden severe headache

DDx thunderclap headache •

Subarachnoid hemorrhage (SAH)

• •

Reversible cerebral vasoconstriction syndrome

Sentinel headache

• • •

Retroclival hematoma

• •

Primary thunderclap headache

• • • •

Cerebral venous sinus thrombosis (CVST) Cervical artery dissection Acute hypertensive crisis Ischemic stroke Pituitary apoplexy

Third ventricular colloid cyst Intracranial infection

Primary cough, sexual, exertional headache Dodick DW. JNNP 2002;72;6-11

Schwedt TS et al. Lancet Neurol 2006;5: 621-31

Subarachnoid hemorrhage (SAH)

• SAH is the most common cause of TCH • 11-25% of TCH may have SAH • associated symptoms... • loss of consciousness (1/3), seizure

(6-9%), delirium (16%), stroke, visual disturbance, N/V, dizziness, neck stiffness and photophobia

70% of patients presented with headache alone Linn FH et al. Lancet 1994. 344: 590-93

Diagnostic tool • CT brain: • within 12 hours: near 100% sensitivity • within 1 weeks: about 20% sensitivity • Lumbar puncture: look for Xanthochromia • Conventional angiography: to identify aneurysm

Edlow JA. et al. N Eng J Med 2000;342:29-36

Diagnostic approach in TCH

CT Negative

Positive Subarachnoid hemorrhage Stroke CVST Pituitary apoplexy Retrochival hematoma PRES

Lumbar puncture Positive


Subarachnoid hemorrhage




Stroke SIH Pituitary apoplexy Retrochival hematoma PRES

MR angiography or magnetic resonance venography

Schwedt TS et al. Thunderclap headache. Lancet Neurol 2006;5: 621-31

Positive Aneurysm CVST Dissection RCVS

Negative Primary TCH

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