Tetraparesis

Modul IGroup 5

MemBerS

Ade Tri Arlini

Fenny Rahayu

Yan Floresta

Widya Nursantari

Fitriana H

Lucky Miftah S

Dita Putri

Feri Idham L

Yusrani R

Amrullah Adji

Elvi Rahmi

Group 5

1st scenario

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. A woman 22 years old.

2. Sudden tetraparesis, followed with cramps.

3. Unclear existance story in trauma

4. Heavy influenza in previous history.

5. No cough story.

6. Normal body temperature.

7. Normal defecate and urinate.

8. First time experienced.

Anatomy

Organization of nerves

BrainBrain CNSCNS Spinal CordsSpinal Cords

AfferentAfferent

Sensoric

Stimulate

Sensoric

Stimulate

Viceral

Stimulate

Viceral

Stimulate

EfferentEfferent

System of nerve somatic

System of nerve somatic

System of otonom nerve

System of otonom nerve

Motoric NerveMotoric Nerve

Simpatic nerve system

Simpatic nerve system

Parasimpatic nerve systemParasimpatic nerve system

Muscle contruction

1. Artless muscle

2. Heart muscle

3. Gland

Efector organ (consisted of muscle network and gland

PNSPNS

Fisiology

Lower motor neuron

Upper motor neuron

HistologyNeuroglia is contributor cell on CNS which Non-neural.Neuroglia consists of :1.Astrocyte 2.Oligodendrocyte3.Mikroglia

Preparation of peripheral nerve

1. Endoneurium2. Myelin veil3. Akson4. Perineurium5. Epineurium6. 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.

Characteristics UMN LMN

Kind and weakness distribution

Lesion at brain :“piramidalis distribution”, part of distal especially hand muscles; exstensor arm and flexsor feebler leg.

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

Depend that is radix segment, or which nerve that have a lesion.

TonusSpastisity: real in fleksor arm and ekstensor leg.

Flaccid

Mass MuscleOnly a little experience disuse atrophy muscle.

Atrophy can be very clear

Reflex Increase; Babinski (+) Decrease or no; Babinski (-)

Fasiculation No Yes

Klonus Oftentimes No

Difference

Differential DiagnoseGuillain Barre

SyndromeMyasthenia Gravis Paralisis Periodic

Definition Disease marked by paralysis ascendant that espoused subacute weakness and decrease tendon reflex.

Condition marked by weakness or muscle stupefaction.

Failure transmission neuromuscular and can become normal after few minutes.

Hereditary muscle weakness disease, Autosomal dominant fenotipe

Etiology Vaccination infection, surgery, systematic disease.

Damage AcH receptor 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.

Symptoms

Paralisis total fourth 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

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

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

Acetazolamide, Triamterene or Spironolactone if Acetazolamide there is no response.

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

AnamnesisExaminations: - 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 GBS1. 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 GravisDiagnostic 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

TherapyMedicamentosa:1.Antikolinesterase:

– Piridostigmin 30-120 mg po every 3 hours– Neostigmin bromide 15-45 mg po every 3

hours2.) Steroid : 5-10 mg/week3.) 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)

TherapyMedicamentosa:• K+ given po/parenteral • Aldakton 100 mg po/day• Thiamine HCl 50 mg/day• Hipertiroidism therapyNonmedicamentosa: 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.

ReferencesSobbota

Neuro Anatomy

Anatomi Dasar Klinis

Patofisiologi Konsep Dasar Penyakit

Neurologi Klinis Dasar

Histologi fiore

www.medicineonline.com

www.medlineplus.com

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Group 5