Journal Reading:

Recurrent Guillain Barre

Syndrome
Barbara Aymee Hernandez*, Fermin Morera Mendez and Ibis Maria Elosegui

Cuban Neuroscience Center, Havana, Cuba

Annida Adityaningrum 30101206590

Pembimbing : dr. H. Muktasim Billah, Sp. S
Pengantar

 Guillain Barre Syndrome (GBS) adalah penyakit

neuropati autoimun akut, inflamasi, dan demielinasi dari
jalur monofasik yang menyebabkan kelumpuhan
flaksid.
 GBS sering muncul sebagai penyakit pasca infeksi
Campylobacter jejuni, Cytomegalovirus, virus Ebstein-
Bar dan Mycoplasma pneumonia; atau kondisi lain yaitu
kehamilan, melahirkan, operasi, pasca tindakan
anestesi.
 GBS merupakan penyakit neuropati akut yang paling
banyak terjadi, progresif dan fatal.
Epidemiologi

 Angka kejadian GBS dilaporkan sebanyak 1.8-2/100.000

penduduk per tahun.
 Angka mortalitas sebesar 3-15% dan sebesar 20%
pasien mengalami kecacatan.
Karakteristik

 Kelemahan otot simetris dan menyebar ke otot

respiratory.
 Refleks tendon menurun
 Abnormalitas pada fungsi otonom
 Nyeri, kram, mati rasa.
 Puncak deficit klinis terjadi pada minggu ke 2-4 setelah
terjadinya stimulasi kekebalan tubuh
 Terdapat protein di cairan serebrospinal
Diagnosis

GBS didiagnosis berdasarkan krireria Asbury, yaitu:

 Tanda-tanda klinis
 Cairan serebrospinal
 Study neurophysiology
Laporan Kasus

 a case of GBS with recurrent appearance that started 17

years after the first episode. It is the only case with
recurrent appearance of 50 cases of GBS that we have
followed for 18 years.
 Riwayat pasien: kulit putih, usia 48 tahun. Tahun 2001
(usia 32 tahun) pasien mengalami GBS setelah
melahirkan. Rawat inap selama 20 hari, diberi
immunoglobulin 0.4 g/kg BB IV selama 4 hari, tidak ada
kecacatan setelah menderita GBS sampai saat ini.
 Hasil

 Cairan serebrospinal pada tahun 2001: protein 1g/I dan

sel 0
 Awal Desember 2017 pasien mulai mengalami
kelemahan di kedua tangannya, kemudian hari
berikutnya mengalami nyeri pada bagian lumbar dan
kelemahan di kedua ekstremitas bawah. Tidak ada
gejala kelainan respirasi maupun digestif sebelum
muncul gejala neurologi.
Figure 1 Latencies value of proximal and distal motor
responses in different evaluated nerves, Notice the
enlargement of the latencies in both studies, with
predominance of the second study
Physical examination:

 Conscience level: Patient was aware and oriented.

 Muscular tone and trophism: Normal.
 Muscular force: Distal weakness in both upper limbs
(4/5). She was disabled to do abduction of first and fifth
finger of the hands. She showed proximal and distal
weakness in both lower limbs (2/5). She was disabled
to do ankle dorsiflexion. She was disabled to walk,
she was at wheelchair.
 Deep reflex: Generalized hyporreflexia.
 Superficial reflex: Normal.
Physical examination:

 Superficial sensory: Normal

 Deep sensory: Distal hypopalesthesia in upper and lower
limb.
 Cranial nerves without abnormalities.
 Static and dynamic coordination: Normal.
 No clonus or Babinski sign.
 No sensory level.
Laboratory tests:

 Cerebrospinal fluid test: It was clear, transparent,

proteins=1.4 g/l (increased), glucose=3.4 mmol/l, cells=0.
 Hematology: Normal
 Blood Chemistry: Normal
 Ionogram:
Sodium-124.2 meq/l (decreased)
 Other ions: Normal
 Gasometry
 pH-7.5 (increased) pO2-123.9 torr pCO2-25.5 torr
 Urine: Normal
Latencies values of sensory responses in different
evaluated nerves. Notice light enlargement of the
latencies in the second study.
Motor nerve conduction study of Median nerve (A and B) and Posterior Tibial (C
and D). Notice marked enlargement of the latencies slowing of conduction
velocities, abnormal morphology of the responses, partial conduction block. The
abnormalities are marked during second episode.
Sensory nerve conduction study of Median (A and B) and Sural nerves (C and
D). Notice light enlargement of the latencies, slowing of conduction velocities.
The abnormalities are marked during second episode.
 Diskusi
parameter Episode pertama Episode aktual
Tanda klinis sama Sama
Durasi progesitas > 10 hari < 6 hari
Faktor resiko Melahirkan 13 hari Tidak signifikan
sebelumnya sebelum muncul
gejala
Cairan Peningkatan protein Peningkatan protein
serebrospinal (1 g/l) (1.4 g/l)
Studi abnormal Abnormal (lebih
neurophysiologi tinggi dari episode
pertama)
Kesimpulan

 Rekuren GBS jarang terjadi, lama episode fase plateau

bervariasi bias tahunan hingga decade.
 Defisit neurologi pada Rekuren GBS lebih intense
disbanding pada episode pertama.
TERIMAKASIH