Tetraparesis

Modul I

Group 5

Ade Tri Arlini

Amrullah Adji Dita Putri

MemBerS

Elvi Rahmi
Fenny Rahayu Feri Idham L Fitriana H Lucky Miftah S Widya Nursantari

1st scenario

Yan Floresta Yusrani R

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

System of nerve somatic

System of otonom nerve

Sensoric Stimulate

Viceral Stimulate Motoric Nerve

Simpatic nerve system

Parasimpatic nerve system

Muscle contruction

1. 2. 3.

Artless muscle Heart muscle Gland

Efector organ (consisted of muscle network and gland

Upper motor neuron

Lower motor neuron

Histology
Neuroglia is contributor neural. Neuroglia consists of : 1.Astrocyte 2.Oligodendrocyte 3.Mikroglia cell on CNS which Non-

Preparation of peripheral nerve

1. 2. 3. 4. 5. 6.

Endoneurium Myelin veil Akson Perineurium Epineurium Schwann cell

Preparation of Radix Ganglion Dorsales

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.

Preparation of Medulla Spinalis

Medulla Spinalis consist of 2 part : 1.White Substance (Alba) 2.Gray Substance (Grisea)

Medulla Spinalis Mid-torakal area

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.

Kind and weakness distribution

Lesion at medulla spinalis: vary to depend on the location of lesion.

Tonus Mass Muscle Spastisity: real in fleksor arm and ekstensor leg. Only a little experience disuse atrophy muscle. Increase; Babinski (+) No Oftentimes Flaccid Atrophy can be very clear Decrease or no; Babinski (-) Yes No

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

High carbohydrate food or Na, rest after activity.

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

Corticosteroid, complication prevention, Plasmaferesis, vital capacity monitoring, NGT

Anticolinesterase (piridostigmin), Corticosteroid, Imunosupresi, Timektomi, Plasmafaresis.

OTHER NEUROLOGY NUISANCE

1. Miasthenia Gravis
Diplopia (double vision)

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

Guillain Barre Syndrome

Paralyzed: LMN type symmetrical hyporeflex Sensorical deficit N.IV or N.III: diplopia N.IX and N.X: disphagia, disphonia Autonomic disorder Respiratory failure Papiledema

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.

3. Allogenic & Xenogenic Bone Marrow Transplatation

Results from manifestation of Graft Versus Host Disease (GVHD)

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

PREVENTION OF PARALYSIS PERIODIC

No prevention because of an hereditary disease.

References
Sobbota Neuro Anatomy Anatomi Dasar Klinis Patofisiologi Konsep Dasar Penyakit Neurologi Klinis Dasar Histologi fiore

www.medicineonline.com www.medlineplus.com

Group 5