kuliah neurologi nk, vertigo
DESCRIPTION
Kuliah neurologiTRANSCRIPT
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dr. Biati, Sp.S
EPILEPSI
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BANGKITAN EPILEPSI Manifestasi klinis dr bangkitan serupa (stereotipik) yg berlebihan & abN, berlangs. sec. mendadak & sementara, dg atau tanpa perubahan kesadaran, disb-kan o/ hiperaktifitas listrik sekelompok sel saraf di otak yg bukan disb-kan o/ suatu peny. otak akut
DEFINISI
Seizure epilepsi min. 2x
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KLASIFIKASI EPILEPSI(ILAE 1981)
1. Serangan Parsial1.1. Serangan Parsial Sederhana
-Motorik-Sensorik-Otonom-Psikis
1.2. Serangan Parsial Kompleks-Serangan parsial sederhana+ggn
kesadaran-Ggn kesadaran saat awal serangan
1.3. Serangan Umum Sekunder-Parsial sederhana tonik klonik-Parsial kompleks tonik klonik-Parsial sederhana parsial
kompleks tonik klonik
2. Serangan UmumAbsans (Petit
Mal)MioklonikKlonikTonikTonik klonikAtonik
3. Tak tergolongkan
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Myoclonic seizures
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ETIOLOGI EPILEPSI• Idiopatik-- genetik• Kriptogenik• Simtomatik
TraumaInfeksiKelainan kongenitalLesi desak ruangGgn peredaran drh otakToksikMetabolik
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DIAGNOSIS EPILEPSI
• Anamnesa **• Pemeriksaan Fisis
UmumNeurologis
• Pemeriksaan PenunjangEEGNeuroimagingLaboratorium
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GEJALA KLINISSerangan Parsial Sederhanamis: motorik
- Klonik/ tonik/sadar- Jacksonian March mulut/jari tangan ke seluruh anggota gerak sisi yg sama- gerakan versif kepala menoleh/mata melirik ke sisi yg berlawanan dg fokus kejang di otak
Serangan Parsial Kompleks- Aura- Perubahan kesadaran- Automatisme
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GEJALA KLINIS
Seizure (tidak kejang) :- Absence : kejang -, hilang sadar +, tonus +
, jatuh –- Atonik : tonus postural - , jatuh +
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PATOFISIOLOGI EPILEPSI
• Eksitasi (berlebihan)– Ion : msk Na+, Ca++ – Neurotransmiter : glutamat, aspartat
• Inhibisi (berkurangnya)– Ion : msk Cl¯, keluar K+– Neurotransmiter : GABA
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GAMBARAN KLINIS
• Ggn kesadaran mendadak berlangsung bbrp detik
• Selama serangan kegiatan motorik terhenti
• Pasien diam tanpa reaksi• Pemulihan kesadaran segera
tanpa perasaan bingung
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3 Hz spike and wave
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BANGKITAN UMUM TONIK KLONIK
• Dpt didahului prodromal (spt jeritan, sentakan, mioklonik)
• Hilang kesadaran • Fase tonik (10 - 30 det)• Fase klonik (30 – 60 det) disertai mulut
berbusa• Fase flaksid : pasien lemas tampak
bingung• Pasien tidur setelah bangkitan
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BANGKITAN UMUM TONIK KLONIK
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FAKTOR PENCETUS
• Kurang tidur• Stress • Infeksi demam (t.u pd anak)• Obat-obat ttn (mis: sedatif)• Alkohol• Terlalu lelah• Fotosensitif
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PRINSIP TERAPI• Minim 2x bangkitan dalam 1 tahun• Diagnosa ditegakkan• Pemilihan jenis obat sesuai jenis bangkitan• Monoterapi • Dimulai OAE lini pertama
Penghentian OAE :• Minimal 2 tahun bebas bangkitan• Gb EEG : Normal
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OBAT ANTI EPILEPSI
JENIS BANGITAN
OAE LINI I OAE LINI II OAE yg dpt dipertimbangkan
Bangkitan Umum Tonik Klonik
• Sodium Valproat• Lamotrigine• Topiramate• Carbamazepine
• Clobazam• Levetiracetam• Oxcarbazepine
• Clonazepam• Phenobarbital• Phenytoin• Acetazolamide
Petit Mal (Absans)
• Sodium Valproat• Lamotrigine
• Clobazam• Topiramate
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PROGNOSIS
Tergantung:• Jenis epilepsi• Faktor penyebab• Ketaatan minum obat• Saat pengobatan dimulai
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DEFINISI
Suatu kondisi dimana bangkitan epilepsi berlangsung terus-menerus,
atau bangkitan berulang dg tanpa pemulihan kesadaran, selama periode ≥ 30menit
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Patofisiologi Status Epileptikus
Pd tingkat neurokimiaEksitasi yg berlebihan dari glutamat dan aspartat dan berkurangnya inhibisi dari neurotrasmiter GABA
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PRINSIP PENANGANAN STATUS EPILEPTIKUS
• Stabilkan pasien dengan prinsip kegawatan umum
• Menghentikan bangkitan dan mencari etiologi secara simultan
• Mencegah bangkitan ulang / mengatasi penyulit
• Mengatasi faktor pencetus• Bila stlh 60 menit blm teratasi
sebaiknya perawatan dilakukan di ICU
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PENATALAKSANAAN SE 0-10 men : perbaiki f/ kardio respirasi
perbaiki jln nafas 1-60 men : Diazepam 10-20mg
iv(kecep pemberian < 2-5 mg/men / rektal dpt diulang 15 men kmd
Bila kejang berlangsung terus selama 30 men stlh pemberian diazepam pertama, beri phenytoin iv 15-18 mg/kg dg kecepatan 50 mg/men
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Bila kejang tdk teratasi selama 30-60 men, transfer ke ICU
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CEPHALGIA
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Cephalgia ???
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Keluhan neurologik dengan berbagai
macam penyebab Intrakranial Ekstrakranial
PENDAHULUAN
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• Nyeri kepala dpt disebabkan :– inflamasi atau – traksi/tarikan– vasodilatasi– kontraksi otot
pada struktur peka nyeri
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BANGUNAN PEKA NYERI
Intrakranial
Ekstrakranial
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KLASIFIKASI(berdasarkan etiologi)
Nyeri kepala primer- Migren- Tension type headache- Nyeri kepala klaster (Cluster headache)- Nyeri kepala primer lainnya
Nyeri kepala sekunder Neuralgia kranial
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DIAGNOSIS Anamnesis Pemeriksaan Fisis Pemeriksaan Penunjang
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ANAMNESIS CEPHALGIA
LOKASI NYERI JENIS NYERI (berdenyut, terikat,dll) ONSET NYERI (akut, subakut & kronis) FREKUENSI kronik > 15 hr/bl, > 3 bl WAKTU TERJADINYA NYERI GEJALA PENYERTA FAKTOR PRESIPITASI FAKTOR YANG MEMBERATKAN & PEREDA
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MIGREN
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KLASIFIKASI MIGREN• Migren tanpa aura• Migren dg aura
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PATOFISIOLOGI MIGREN (Spierings 1988)
Faktor pencetusintrinsik & ekstrinsik
gxotonom
m↑-kan aktivitas
SS Simpatis
NK
• Vasodilatasi•m’↓ nilai ambang nyeri
Sistem trigeminovaskular
Spreedingdepression
p.d. melebar &berdenyut
•Vasodilatasi p.d. di luar otak•Vasokontriksi p.d. di dlm otak
inti-2 sarafdi batang otak
(reseptor serotonin& NA)
gx aura
MIGREN tanpa auraMIGREN dg aura
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MIGREN tanpa AURA= Common migren= Hemikrania simpleks
MIGREN dengan AURA
= Migren klasik
Terdapat gejala prodromal -Merasa sedih, senang, mudah marah- menguap-menguap
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KRITERIA DIAGNOSTIK Unilateral Berdenyut Intensitas sdg / berat Ber + berat
o/ aktivitas fisis Nausea + &/muntah + Fotofobia & fonofobia
Gb NK menyerupai migren tanpa aura
b/ timbul sesudah gej aura (5-20 menit)
Aura, berupa : Ggn visual (bintik2,
hilang penglihatan) Ggn sensorik (hilang
rasa) Ggn bicara (disfasia)
MIGREN tanpa AURAMIGREN dengan AURA
Diagnosa banding ????
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AURA
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T’ jd pd dekade 2 Stlh pubertas
wanita > Pd anak-anak (sblm
pubertas) wanita = laki-laki
Riwayat keluarga +
MIGREN
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FAKTOR PENCETUS MIGREN
Makanan Perubahan cuaca Perubahan pola tidur Hormonal (?)
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PENATALAKSANAAN MIGREN
Menghindari faktor pencetus Akut / abortif ( analgetik obat
spesifik) Preventif bila serangan berulang
mengganggu aktivitas
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Tension-type headache (TTH)= Nyeri kepala tegang otot= Muscle contraction headache= Psychomyogenic headache= Stress headache
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KLASIFIKASI Tension-type
headache 1. Nyeri kepala tegang episodik
a. Berhubungan dg ggn otot perikraniib. Tak berhubungan dg ggn otot perikranii
2. Nyeri kepala tegang otot kronisa. Berhubungan dg ggn otot perikraniib. Tak berhubungan dg ggn otot perikranii
3. Probable Nyeri kepala tegang otot
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PATOGENESIS Tension-type headache
Kontraksi otot-otot perikranial yg berkepanjangan
Hipersensitif dari neuron di nukleus kaudatus
Stress psikologi menyebabkan sejumlah perubahan aktivitas neurotransmiter di otak (menurunnya aktivitas GABA, menurunnya aktivitas serotonin, norepinefrin & sist. opioid endogen)
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KRITERIA DIAGNOSTIK Tension-type
headache Min. 10x serangan Bilateral Menekan/mengikat Intensitasnya ringan / sedang Tdk diperberat o/ aktivitas rutin Mual +/- atau muntah =/- Fotofobia + / fonofobia +
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Pd semua umur
Tension-type headache
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PENATALAKSANAAN Tension-type
headache Analgetik Anti depresan Anti ansietas Muscle relaxants Non-pharmakologis
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Cluster headache= Neuralgia siliaris= Erythromelalgia dari kepala= Bing’s erythroprosopalgia= Hemikrania angioparalitika= Hemikrania neuragiformis kronika= Neuralgia migrenous= Horton’s headache= Penyakit Harris-Horton
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PATOFISIOLOGI Cluster headache
Inflamasi yg mengganggu sinyal dari N.trigeminus
Kelainan pd hipotalamus
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KRITERIA DIAGNOSTIKCluster headache
Nyeri hebat / sangat hebat sekali Orbita / supraorbita & / temporal Unilateral Injeksi konjungtiva & / lakrimasi
ipsilateral Kongesti nasal & / rhinorrhoea ipsilateral Odem palpebra ipsilateral Dahi & wajah berkeringat ipsilateral Miosis & / ptosis ipsilateral
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Laki- laki > Onset pd dekade 3
Cluster headache
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PENATALAKSANAAN Cluster headache
Akut Sumatriptan s.c Dihydroergotamine
Profilaksis Kortikosteroid Derivat ergotamine Ca-chanel bloker
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VERTIGO
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DEFINISI VERTIGO
Ilusi dimana seseorang merasa tubuhnya bergerak terhadap lingkungannya / lingkungannya bergerak terhadap dirinya
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KLASIFIKASI VERTIGO
VERTIGO
fisiologik Mabuk gerak, dll
periferVestibuler
(true vertigo)
Non vestibuler(pseudo vertigo)
disquilibrium
syncopepatologik
sentral
psikogenik
BPPVMeniere’s, dll
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PERBEDAAN KLINIS VERTIGO TIPE PERIFER dan SENTRAL
tipe perifer tipe sentralOnset mendadak lambatKualitas rotasi k’tdk seimbang’Intensitas vertigo berat ringanKejadian episodik konstanDurasi det.,menit,jam/hr mingguPengaruh gerakan kpl sdg-berat ringanGej.otonom ++ ringanKetidakseimbangan ringan beratGej.pendengaran sering jarangTanda fokal otak jarang sering
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PATOFISIOLOGI VERTIGO
• Teori neural mismatch otak mempunyai memori/ingatan tentang pola gerakan tertentu; sehingga jika pada suatu saat dirasakan gerakan yang aneh/tidak sesuai dengan pola gerakan yang telah tersimpan, timbul reaksi dari susunan saraf otonom
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• Jika pola gerakan yg baru tsb dilakukan berulang-ulang akan terjadi mekanisme adaptasi shg berangsur - angsur tdk lagi timbul gejala.
Neural store
Comparator Unit
Sensory input(rangsangan gerakan)
Mismatch sign
Vestibular input
Somatosensory input
Visual input
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DIAGNOSISAnamnesis• Memastikan vertigo/bukan• Menentukan jenis vertigo• Kead. yg memprovokasi
timbulnya vertigo• profil wkt: akut/perlahan2• Ggn pendengaran/tinitus ?• Penggunaan obat• Adanya peny. sistemik :
anemia, peny. Jant., hipertensi, hipotensi
Pemeriksaan Fisis PF umum : nadi, tensi, dll PF neurologi:
- pemeriksaan nystagmus- test fungsi vestibular- test fungsi pendengaran
Pem. Penunjang
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TERAPI
• Kausal• Simtomatik• Rehabilitasi
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BPPV
= Benign Paroxysmal Positional Vertigo= Vertigo postural = Kupulolitiasis
•Wanita > pria•Usia pertengahan
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DIAGNOSA
Anamnesa• perasaan berputar
timb. mendadak pd perubahan posisi
• lamanya < 30 det (singkat)
• mual +, muntah (kd)
Pem. Fisik• kel. neurologi fokal +/-• Tes dix hallpike ada
masa laten nistagmus vertigo
• Pem. penunjang
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PENATALAKSANAAN
• Obat anti vertigo• Latihan posisional
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PENYAKIT MENIERE
= Endolymphatic hydrops= Hidrops labirin idiopatik
• Mulai pd usia 20 – 50th• Pria > wanita• Penyebab pasti – blm
diketahui
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Patofisiologi Penyakit Meniere• Endolymphatic hydrops leads to distortion of membranous
labyrinth
• Reisner’s membrane can be seen bulging into the scala vestibuli in some histologic studies
• Microruptures may lead to episodic attacks which resolve when the tears heal
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Patofisiologi Penyakit Meniere
• Edem labirin endolimfatik Mengganggu peredaran darahVasokonstriksiGgn permeabilitas kapiler setempat
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DIAGNOSIS PENYAKIT MENIERE
Gej. klinis (Anamnesa)• Vertigo episodik• Rasa tertekan / rasa
penuh di telinga• Tinitus• Ggn pendengaran
berfluktuasi
Pem. Fisik tes kalori Nistagmus + Pem. Penunjang
– Pem. Audiogram– BERA(Brain Evoked
Respon Audiometry)– Lab– Radiologi
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PENATALAKSANAAN PENYAKIT MENIERE
Konservatif– Diet rendah garam – Diuretik– Kortikosteroid– antihistamin
operatif
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