Professional Documents
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Modul I
Group 5
MemBerS
Elvi Rahmi
Fenny Rahayu Feri Idham L Fitriana H Lucky Miftah S Widya Nursantari
1st scenario
A woman 22 years old brought by her college friend to hospital Emergency Unit because her sudden quadriparesis initially felt only cramps. Unclear existance story trauma in spine. Only known that he hasn't come previous few days lecture because experienced heavy influenzas. Defecate and urinate was normal. This experience is her first time.
Difficult Word
Tetraparesis Muscle weakness that hit all four extremity. (Medical Dictionary Dorland)
Key Word
1. 2. 3. 4. 5. 6. 7. 8. A woman 22 years old. Sudden tetraparesis, followed with cramps. Unclear existance story in trauma Heavy influenza in previous history. No cough story. Normal body temperature. Normal defecate and urinate. First time experienced.
Anatomy
Fisiology
Organization of nerves
Brain CNS Spinal Cords
Afferent
PNS
Efferent
Sensoric Stimulate
Muscle contruction
1. 2. 3.
Histology
Neuroglia is contributor neural. Neuroglia consists of : 1.Astrocyte 2.Oligodendrocyte 3.Mikroglia cell on CNS which Non-
1. 2. 3. 4. 5. 6.
Continue
ganglion cell consists of 3 part : 1.Endoneurium 2.Perineurium 3.Epineurium Ganglion has a body cell, axon, dendrite, and capsule cell or satellite cell.
Medulla Spinalis consist of 2 part : 1.White Substance (Alba) 2.Gray Substance (Grisea)
Medulla Spinalis mid-torakal area has cornu posterior grisea and cornu anterior grisea. Toracal area contain motorik nerve. Cornu lateral grisea grow greatly in toracal area.
Difference
Characteristics UMN Lesion at brain : piramidalis distribution, part of distal especially hand muscles; exstensor arm and flexsor feebler leg. LMN Depend that is radix segment, or which nerve that have a lesion.
Reflex
Fasiculation Klonus
Differential Diagnose
Guillain Barre Syndrome Definition Disease marked by paralysis ascendant that espoused subacute weakness and decrease tendon reflex. Myasthenia Gravis Condition marked by weakness or muscle stupefaction. Failure transmission neuromuscular and can become normal after few minutes. Paralisis Periodic Hereditary muscle weakness disease, Autosomal dominant fenotipe
Etiology
Vaccination infection, Damage AcH surgery, systematic receptor disease. neuromuscular junction disease consequence Autoimmune
Pathology
Virus that step into body is caught by T cell and makrofag assault myelin, besides T cell induction cell b to produce antibody that assault myelin so that disturb impulse conduction in nerve perifer.
Increasing of muscle weakness that caused by total decrease ACH receptor in neuromuscular junction
Muscle weakness happens because enter it ion potassium into muscle cell, finally membrane be hyperpolarisation so that happen pulse transmission obstacle neuromuscular.
Paralisis total fourth Symptoms movement member, takikardia, aritmia heart, disturbance vasomotor.
Diplopia, face muscle weakness, disfagia, neck muscle weakness and extremitas.
Muscle pain, very thirsty before happen weakness, weak taste is begun at extremitas under and followed with member on body and neck, fisiology reflex decreased or lost, but normal permanent skin sensation.
Epidemiology
Average incident per year 0,4-1,7 per 100.000 population. woman: man (2: 1) and many happen in young .
Prevalention 14 per 100.000 population with 36 thousands case happens at axis. In children, adult and parents. in 40 year age, woman more many while on 40 year man more many.
Incident number around 1 between 100.000 person, more many found in man usually aged 10-25 year. age the happening of first attack varies from 1-20 year, attack frequency more at age 15-35 year and then decreased with age enhanced Acetazolamide, Triamterene or Spironolactone if Acetazolamide there is no response.
Therapy
2. Guillain-Barre Syndrome
Sensation change that cause contracture Diplopia
3. Paralysis Periodic
No nuisance found
Anamnesis
Examinations: - Physical - Neurological Mental status Level of consciousness Cranial nerve function Motoric function Reflex Coordination Sensoric function
Laboratory examination:
Increasing of protein in LCS: > 0,5 mg % MMN< 10 cell/mm3 Electrophysioogy examination (EMG) Transmission of motoric nerve and sensoric nerve velocity become slow
Therapy
Medicamentosa: Plasma exchange Immunoglobulin IV: 0,4 mg/kgBB Corticosteroid Nonmedicamentosa:
Respiratory cure Physiotherapy
PRVENTION OF GBS
1. Varicella Vaccination (preventing varicella complication in Central Nerve System /CNS) 2. Mononucleosis 3. AIDS, Herpes simplex, Chalamydia trachomatis infection (STD) 4. Campylobacter jejuni infection 5. Hepatitis B 6. Mycoplasma pneumoniae (infecting CNS)
Miastenia Gravis
Diagnostic test:
Acetylcholine anti-receptor antibody Antibody anti-sceletal muscle(anti-striated muscle antibody) Tensilon test Wartenberg test Prostigmine test
Radiology:
AP & lateral position: looking for thymoma
Therapy
Medicamentosa: 1.Antikolinesterase: Piridostigmin 30-120 mg po every 3 hours Neostigmin bromide 15-45 mg po every 3 hours 2.) Steroid : 5-10 mg/week 3.) Azatioprin: 2,5 mg/kgBB (8 weeks early) 4.) Timectomy 5.) Plasmaferesis: 3-8 times 50mL/kgBB
Nonmedicamentosa:
Take a rest careful to sedative drugs: can cause respiratory depression
PREVENTION OF MG
Avoid unnecessary drugs such as: 1. D-Penicillamine 2. Interferon Alpha Avoid allogenic & Xenogenic Bone Marrow Transplantation
1. D-Penicillamine The mechanism was unclear Some theory says D-Penicillamine modifies the equilibrium of AcH binding properties of both purified receptor and receptor rich membrane fragments. Test in normal rat with normal dose no abnormalities Test in guinea pig with high dose Mild Degree Neuromuscular Block
2. Interferon Alpha
Stimulating over-expression of Interferon gamma at motor end plate, this test was taken in mice Results: generalized weakness, abnormal NMJ function, and improvement of cholinesterase inhibitor.
Periodic Paralysis
muscle atrophy, muscle contracture Examination: looking for indications such as trauma, poisoned, infection, and headache Neurological examination: strength test, reflex, and sensation Laboratory examination: CT Scan, MRI, EMG & nerve transmission velocity test (muscle function & peripheral nerve)
Therapy
Medicamentosa: K+ given po/parenteral Aldakton 100 mg po/day Thiamine HCl 50 mg/day Hipertiroidism therapy Nonmedicamentosa: High Calium diet, low carbohydrate, low Na, physical therapy, occupational therapy, Acupuncture ,speaking therapy , Constain Induce Treatment Therapy, Functional Electrical Stimulation, electrotherapy
References
Sobbota Neuro Anatomy Anatomi Dasar Klinis Patofisiologi Konsep Dasar Penyakit Neurologi Klinis Dasar Histologi fiore
www.medicineonline.com www.medlineplus.com
Group 5