Download - Movement-Disorder Guty Ppt
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MOVEMENT DISORDER GUTY PUTRI
Kepaniteraan Klinik NeurologiFKK UMJ-RSIJ Cemput 2016
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OUTLINE Anatomi sistem ekstra pyramidal Gangguan gerak Terapi Prognosis
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Sistem extrapiramidal : Basal ganglia
Fungsi : inisiasi dan fasilitasi gerakan
volunter
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Basal Ganglia
Connection
Jaras aferen Jaras eferen
Input dari area broadmann 4,6 Sifat glutaminergik
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SKEMA SIRKIT GB
(+) = Kuning (-) = merah
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Pengaruh basal ganglia dalam sistem motorik
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Gangguan Gerak Gerak
› Interaksi sistem pyramidalis dengan ekstrapiramidalis serta serebelum
› Inisiasi gerak sistem piramidalis proses fasilitasi dan inhibisi sistem ekstrapiramidalis dan dikoordinasi serebelum
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Klasifikasi Gerak Jenis Deskripsi
Gerak otomatis Gerak yang sudah terbiasa yang dilakukan tanpa sadar
Gerak voluntar Gerak yang direncanakan dan diinisiasi sesuai keinginan
Gerak involuntar Gerak yang tidak dapat ditahan misal tremor
Gerak semivoluntar
Gerakan yang dicetuskan oleh rangsang sensori internal untuk menekan rasa tidak menyenangkan misal tics, RLS
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Klasifikasi gangguan gerak
Hipokinesia
Gg fungsi fasilitasi gerak
- Akinesia- Rigititas
- Respon postural - Freezing
Hiperkinesia
Gg supresi gerak
- Distonia- Tremor
- Chorea dll
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Hipokinesia Jenis Ciri-ciri Rigiditas Tonus otot meningkat
fleksor > kaku ekstensor fenomena lide pipe/cogwheel
Bradikinesia/akinesia Gerakan melambat Freezing Aksi motorik yang
terhenti sebentar
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Hiperkinesia Jenis Deskripsi Tremor Ritmis, selang-seling otot agonis antagonis Chorea Cepat, bertenaga dan setengah bertujuan Ballism Gerakan choreic beramplitudo besar pada proximal
anggota gerakAtetosis Lambat, melintir pada bagian distal anggota gerakDistonia Involuntar, kontraksi otot yang tertahan gerak melintir
berulang dan postur abnormalMioklonus Gerak involuntar mendadak, singkat, shock-like kontraksi
ototTics Gerak abnormal (motor tics) atau bunyi abnormal (phonic
tics) Akathisia Rasa tak tenang didalam (inner restlessness) yang
menimbulkan gerak stereotipi yang akan mengurangi rasa tersebut
Stereotipi Gerakan terkoordinasi berulang dan identik
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Lokasi kelainan anatomi Lokasi Deskripsi Basal ganglia Substansi nigra bradikinesia, rest tremor
Nukleus subthalamikus ballism Nc Caudatus chorea putamen distonia
Non basal ganglia
serebelum ataksia, dismetria, intention tremor batang otak palatal myoclonus, occular myoclonus kortek serebri cortical reflek myoclonus limbik dan basal ganglia tics
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Parkinsonism Suatu sindroma yang gejala utamanya
tremor istirahat, rigiditas, bradikinesia/akinesia dan instabilitas postural
Klasifikasi › Primer /idiopathic parkinson disease › Sekunder akibat infeksi, obat, toksin
dll
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Parkinson Disease (PD)
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Pendahuluan Dikenal sejak 2 abad yang lalu Penurunan dopamin Gejala motorik dan non motorik NMS (Non Motoric symptoms)
› Gangguan penciuman› Gangguan obstipasi › Gangguan tidur› Gangguan kognisi › Gangguan tingkah laku
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Epidemiologi Gangguan degeneratif >>> pada usia
lanjut dan jarang < 30 tahun Awitan usia 40-70 tahun, puncak dekade
6 Parkinson pada usia < 20 tahun
juvenile parkinsonism Pria > wanita (3 : 2) Di AS 160 per 100 rb , usia > 70 tahun
55 per 100 rb penduduk
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Definisi Bagian dari parkinsonism dimana
secara patologi adanya degenerasi basal ganglia terutama substansia nigra pars kompakta (SNC) disertai
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Kriteria diagnosis Kriteria hughes
Possible • Salah satu
gejala :• Resting tremor• Rigiditas• Bradikinesia• Postural
instability
Probable • Kombinasi 2
gejala utama • Alternatif -
resting tremor asimetris, rigiditas asimetris
Definite • 3 dari 4
gejala utama atau 2 gejala utama dengan satu gejala lain tidak simetris
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Kriteria UKPD society bank Step Kelainan I Bradikinesia + salah satu dibawah ini :
rigiditas4-6 Hz tremor saat istirahatPostural instability
II Kriteria ekslusi PD III Minimal 3 kriteria
unilateral onset resting tremorProgresif Gejala asimetri kadang menetapBerespon baik dengan levodopaPerjalanan klinis 10 tahun
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Patofisiologi Berkurangnya dopamin pada
substansia nigra ke striatum Hilangnya neuron di substansia nigra
pars kompakta yang memberikan inervasi dopaminergik ke striatum
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Patogenesis Penyakit Parkinson
Degen SNc degen jalur nigrostriatum DA.
Mekanisme :› Disfungsi
mitokondria.› Oxid. Stress.› Excitotox.› Inflamasi.
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Proses Kematian SN
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Pada PP hiperaktifitas jalur indirect &/ hipoaktifitas jalur direct.
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Klinis Trias
› Tremor , rigiditas dan akinesia, postural instability (TRAP)
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Stadium PP
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Diagnosis banding
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PENGOBATAN PP
Farmakologik Non Farmakologik
1. DA-ergik 1. Perawatan2. Kolinergik 2. Pembedahan3. Glutamatergik 3. Deep-Brain-Stimul4. Pelindung neuron 4. Transplantasi5. Lain-lain
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PENGOBATAN PP
Farmakologik1. DA-ergik : * l-dopa2. Kolinergik * l-dopa + DDCI3. Glutamatergik * l-dopa + DDCI +
COMTI4. Pelindung neuron * MAOI5. Lain-lain * Agonis DA
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AGONIS DAAgonist D1 D2 5-HT1/2
Derivat ergot :BromocriptineCabergolineLisuridePergolideDerivat non-ergot :PramipexoleRopiniroleTalipexole
-0++
000
+++++++
+++
++++++
++00
++
000
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Antagonis Kolinergik Artane (Trihexyl phenidyl) Congentin (Benztropin) Akineton (Biperidin) Disipal (Orphenadrin)
Tremor memori
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Antagonis Glu-ergik
Amantadine Remacemide Memantine L 235959
Jalur NST = GPi indirect .
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Pelindung Neuron
1. Neurotrophic factor2. Anti-excitotoxin : antagonis NMDA.3. Anti-Oksidan : selegiline.4. Bionergic Suppl : CoQ10.5. Immunosupressant : cyclo Sporine A.6. Bahan lain : estrogen, nicotin, kopi.
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Pengobatan Non Farmakologik
1. Perawatan :› Pendidikan› Rehabilitasi› Diet
2. Pembedahan :› Pollidotomi GPi.› Thalamotomi STN.
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Pengobatan Non Farmakologik
3. Deep Brain Stimulation :› Rangs. > 130 Hz – pulsa 60 – 90 s.› Implant pd GPi atau STN.
4. Transplantasi :› Graft pd. striatum/Put.› Graft : medula adrenal, ventral
mesensefalon, fibroblast, astrocyte, sertoli testis, dll.
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PARKINSONISME Kelainan neurologis dengan gejala
seperti PP Etio bisa idiopatik, simptomatik,
degeneratif, atau herediter.
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KLASIFIKASI PARKINSONISMEI. Primary (idiopathic) Parkinsonism • Parkinson disease• Juvenile parkinsonisms
II. Multisystem degenrations (Parkinsonsm-Plus)• Progressive supranuclear palsy (PSP), steele-Richardson-Olszewski
disease (SRO).• Multiple system atrophy (MSA)• Striatronigral degeneration (SND or MSA-P).• Olivopontocerebellar atrophy (OPCA or MSA-C).• Shy-Drager syndrome (SDS).• Lytico-Bodih or parkinsonism-dementia-ALS somplex of Guam
(PDACG).• Cortical-basal ganglionic degeneration (CBGD).• Progressive pallidal atrophy.• Parkinsonism-dementia complex• Pallidopyramidal disease.
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III. Heredodegenerative Parkinsonism• Hereditary juvenile dystonia-parkinsonsm• Autosomal dominant Lewy body disease.• Huntington disease• Wilson disease• Hereditary ceruloplasmin deficiency• Hallervorden-spatz disease• Olivapontacerebellar and spinocerebellar degenerations.• Machado-Josph disease.• Familial amyyoytophy-dementia-parkinsonism.• Disinhibition-dementia-parkinsonism-amyotrophy-
complex• Gerstmann-Strausler-Scheinker disease
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III. Heredodegenerative Parkinsonism• Familial progressive subcortical gliosis• Lubog (-linked dystonia-perkinsonism)• Familial basal ganglia calcification• Mitochondrial cytopathies with striatal necrosis.• Ceroid lipofuscinosis.• Familial parkinsonism with peripheral
neuropathy.• Parkinsonian-pyramidal syndrome• Neuroacanthacytosis.• Hereditary hemochromomatosis.
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IV. Secondary (aquired, Symptomatic) Parkinsonism • Infectious : postencephalitic, AIDS, SSPE, creuzfeldt-Jakob disease,
prion diseases.• Drugs : dopamine receptor-blocking drugs (antipsychotic, antiemetic
drugs), reserpine, tetrabenazine, alpha-methyl-dopa, lithium, flunarizine, cinnarizine.
• Toxins : 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine CO, Mn, Hg, CS, cyanide, methanol, ethanol.
• Vascular : multi-infarct, Binswanger disease• Trauma : pugilistic encephalopathy.• Other : parathyroid abnormalities, hypothyroidism, hepatocerebral
degeneration, brain tumor, paraneoplastic, normal pressure hydrocephalus, noncommunicating hydrocephalus, syringomesencephalia, hemiatrophy-hemiparkinsonism, peripherally induced tremor and parkinsonism, and psychogenic.
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PARKINS0NISME SEKUNDER / SIMPTOMATIK
Def : Sindroma Parkinson yg etiologinya jelas, meski disebabkan oleh berbagai mekanisme namun final common-pathway nya kelainan dopamin ( DA ) di GB.
Hanya dibahas sebagian sebagai contoh.
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PP ssd INFEKSI
Pasca infeksi virus Von Economo ( th. 1917 sd 1928 : pandemic encephalitis lethargica : 40 % mati, 5 th pasca infeksi 50% PP, bila sd 10 th : 80%. Gejala penyerta: oculogyric crises, hiperkinesia dan palilalia.Terapi l-dopa hasilnya baik.
Dx. histopatologi: inflamasi di midbrain dan paraventrikel. Tidak terbukti ada infeksi virus, namun diduga Vi influenza A.
Virus lainnya: Japanese encephalitis: lesi di Substansia Nigra, dan West Nile encephalitis dgn lesi sama dan gejala PP jelas.
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PP AKIBAT OBAT Penyebab parkinsonisme paling utama &
sulit dibedakan dr PP primer. Pengguna neuroleptika singkat ( 3 bulan )
atau lama ( saat dosis naik ) Prevalensi pemakai neuroleptika
menderita PP: 10-60 %, dipengaruhi : Usia (lanjut), sex (wanita), ada predisposisi genetik (tremor)
2/3 kasus sembuh ssd stop obat 7 minggu, tp dpt persisten sd 18 bulan.
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TOKSIN Ok. toksin MPTP yg merusak striatum,
patofisiol PP kian jelas. CO ( karbon monooksida ), manganese
( Mn ), Hg, cyanida dll merupakan etil. PP sekunder.
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VASCULAR PARKINSONISM : Terutama ok infark multipel yg sering kurang
responsif dgn gol. DA Leuco encephalopathy ok iskemia hipoksik
lebih responsif thd gol DA.
TRAUMA KEPALA : Jarang ok trauma tunggal, kecuali trauma
berat ssd masuk veg.stete Terutama ok trauma kepala berulang ( punch-
drunk ) atau pugilistic demensia pd petinju.
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NORMAL PRESSURE HYDROCEPHALUS (NPH)
Ok tidak selalu TIK normal, mk dsbt. Hidrosefalus kronik
Gejala : Gg. jalan ( magnetic gait ), bradykinesia, postural instability, inkontinensia dan demensia. Shunting salah satu pilihan terapi.
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TREMORA. Definisi : Gerak, ritmik, invol dan oscilasi dr bag.
tubuh dengan freq & amplitudo yang relatif tetap, terjadi dalam waktu lama.
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B. Patofisiologi 1. Oscilator Sentral
• Intrinsik membran thalamus & nucl olivary inferior menentukan terjadinya tremor
• Membran keluarkan oscilasi spontan.• Freq neuron thalamo cortical 3 – 6 Hz.• Freq neuron olivo cerebellar 8 – 10 Hz.• PET : glucose pd inferior olivary, aliran
darah otak ke cerebellum me .
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2. Disfungsi Feed Forward Loop• Pd. Cerebellum.• Normal : gerak Ballistic kontraksi
agonist – antagonist – agonist, dikontrol cerebellum.
• Ggn. Cerebellum : keterlambatan onset kontraksi antagonist – agonist ke berikutnya, koreksi melampaui target (hypermetria).
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3. Mekanisme Perifer • Negative feed back loop.
Resonansi dr muscle spindle dan mempengaruhi aktifitas otot terjadi tremor.
• Tremor fisiologis pd pengaruh feed back loop freq tremor ditentukan : panjangnya reflex arc freq reflex fisiologis distal > proximal.
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Etiologi Tremor1. Penyakit Neurodegeneratif
• Parkinson disease• Atypical/secondary parkinsonism• Huntington’s disease.
2. Penyakit Inflamasi• Infeksi central nervus system.• Multiple sclerosis
3. Cerebro Vascular Disease4. Tumor Otak5. Trauma Otak
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6. Penyebab Endokrin/metabolic• Hyperthyroidism• Hypoglycemia
7. Polyneuropathy• Hereditary motor and sensory neuropathy
(HMSN).• Chronic Inflamatory Demyelinating
Polyneuropathy (CIDP).8. Obat-obatan :
• Neuroleptic, sympathicomimetics.• Tricyclic antidepressants.
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9. Penyalah gunaan zat• Keracunan• Withdrawal.
10.Lain-lain • Kelelahan • Psikogenik.
11.Idiopathic :• Essential tremor (termasuk tremor
orthostatic dan pekerjaan spesifik.• Dystonic tremor.• Essential palatal tremor
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C. Diagnostik Ax : onset, perjalanan penyakit, bag tubuh
yg kena riwayat sakit dahulu, riwayat kelg, efek alkohol/obat-2an terhadap tremor.
Pemeriksaan :› Neurologi : uni/multi arah tremor.› Freq :
< 4 Hz : low 4 – 7 Hz : medium > 7 Hz : high.
› Tanda extrapyramidal : Regiditas. Cofwheel. Dystonia.
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Pemeriksaan :› Tanda cerebellar.› Gx. Neuropathic.› Gx. Gangguan thyroid.› Berdiri jalan (palp otot pd px
orthostatic tremor).
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D. Klinis1. Tremor Fisiologi :
• Oscilasi dg amplitudo kecil.terjadi seluruh tubuh, dalam keadaan abn (stress atau lelah).
• Termasuk action tremor dg freq 8 – 12 Hz pd tangan.
• Tremor : Stim. Reseptor adrenergic perifer, oleh
adrenalin endogen (ketakutan). Obat agonis (salbutamol).
• Tremor : blocker (propanolol).
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2. Tremor Essential (TE) :• Terserang pada dewasa.• Bentuk klasik TE :
Bilat postural tremor pd tangan & lengan bawah.
Sering diturunkan : autosomal dominant.
Onset kasus familial 65 th.• TE : asimetrik : kepala.• Freq TE : 4 – 12 Hz.• 60 – 70% Px. Baik dg alkohol
diagnostik.
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2. Terapi• Propanolol 80 – 32 mg/hr.• Primidone 25 – 1000 mg/hr. Kontra Indikasi Propanolol : COPD, gagal
jantung, AV block, DM. Px. COPD dg TE : Tx : Propanolol &
Metoprolol dosis rendah.• GABA-ergik : gabapentin 900 – 3600
mg/hr.• Alprazolam : 0,75 – 2,75 mg/hr.• Topiramat : 200 – 400 mg/hr.• Clozapine : 12,5 – 50 mg/hr.
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• Botulinum Toxin (Btx) : Efektif untuk TE, tetapi otot tangan
menjadi lemah. Tremor kepala, tremor suara.
• Surgical : Gagal dg Tx. Medical. Deep brain stimulation thalamus.
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3. Primary Orthostatic Tremor (POT) :• Termasuk TE.• Adalah tremor tungkai & badan saat
berdiri, sensasi subyek bukan pada tremor tetapi pada ketidak stabilnya saat berdiri.
• POT pd : berjalan, duduk, membungkuk. Kasus berat : jalan tidak stabil.
• Freq POT : 14 – 18 Hz. Sinkronisasi tinggi lengan & tungkai. POT : otot yg terkena dpt diraba,dg
stetoscop : gemuruh.
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• Diagnostik : EMG.• Terapi :
Paling efektif : clonazepam. Primidon, phenobarbital, valproic acid,
gabapentin. Levodopa bbrp Px. Dopaagonis membaik Propanolol, alkohol tidak efektif.
• Px. Disarankan dg tripod dan hindari berdiri lama.
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4. Task and Position Specific Tremor (TPT) :• Pada penulis, pemain musik.• Tremor fokal, asimetrik.• Freq writing tremor 5 – 6 Hz.• TPT termasuk varian dystonia;
diklasifikasikan subklas TE.• Etiologi & pathofisiologi TPT tidak
diketahui.• Terapi : propanolol, primidone,
anticholinergic, Btx.
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5. Dystonic Tremor (DT) :• Tremor fokal, iregular, freq < 7 Hz.• Hilang dg istirahat.• Tremor jerky bersama dg kontraksi otot,
sampai beberapa detik.• DT.terbanyak : spasmodic torticollis.• Amplitudo DT tergantung posis
extremitas.• True dystonic tremor :
Dystonia dan tremor pd extremitas beda. Disebut : dystonia – associated tremor. Termasuk tremor essential atau tremor
fisiologis yg .
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• Etiologi dan pathofisiologi dystonic tremor dan dystonia associated tremor tidak diketahui.
• Terapi : Menghilangkan dystonia dg inj. Btx. Btx gagal :
• Anticholinegic.• Benzodiazepin.• Alternatif : propanolol, primidone, levodopa.
Neuroleptic, carbamazepin, tetrabenzine.• Neuro surgical : selective dorsal rhizo tomy dan
deep brain stimulation pd globus pallidus.
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6. Tremor Parkinson :• Parkinson disease (PD) berhubungan
dengan resting tremor (RT) .• 30% px. PD : dg akinetic rigid murni,
tremor (-).• Freq 4 – 5 Hz, bag distal extremitas
atas, asimetri.• RT / (-) saat mulai bergerak.• RT bisa pd bibir, lidah, dagu, kepala
(jarang).
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7. Cerebellar Tremor• 2 bentuk CT : Postural tremor & kinetic
tremor.• Cerebellar postural tremor :
Freq 2 – 4 Hz. Terutama kepala & badan titubasi. Asal : sistem spino cerebellar.
• Cerebellar kinetic tremor = intention tremor Terjadi saat gerakan involunter extremitas. Freq 3 – 5 Hz dan me saat mencapai
target (gerakan jerky dan saat mau capai target kombinasi dg oscilasi).
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• CT terjadi : Lesi luas :
• cerebellum dan/atau Dismetri • Cerebular conection.
Multiple sclerosis Heriditary degenerative disorder Wilson disease Trauma cerebri.
• Terapi : Clonazepam, carbamazepin, bermanfaat. Ondansetron (Serotonin antagonis) me CT. Thalamic deep brain stimulation Obat-2/Tx. Tidak mempengaruhi ataxia, hanya Tx.
Tremor.
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8. Holmes Tremor (HT)• Tremor kasar, irregular, freq < 5 Hz, freq
bila berpose atau bergerak.• Otot prox lebih sering dr distal.• Simptomatik tremor :
Sering disebabkan lesi vascular atau traumatik pd mesencephalon.
Sedikit karena tremor, absesm demyelinating.
• Jarak terjadi lesi sp onset > 2 th.• HT mungkin sembuh spontan.
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• Terapi : HT sulit Tx. Utama : dopaminergic agent, efek
tidak dramatis. Alternatif : benzodiazepin,
anticholinergic propanolol, clozapin. Gagal : neuro surgical.
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9. Palatal Tremor • Freq 1 – 3 Hz, gerakan ritmik
dipalatum dan larynx, mungkin diikuti gerakan mulut, wajah, mata, lidah.
• 2 macam PT : Simptomatik PT. Essential PT.
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• Simptomatik PT : Berhubungan dg fibrilasi gliosis dan
hipertropi dr inferior olive akibat dari karusakan brainstem atau cerebellum.
Gerakan ritmik soft palate terutama levator velipalatiniolam mungkin berhubungan dg gerakan ritmik otot bulbar atau extremitas.
• Essential PT : Khas ear click ok ritmik kontraksi
m.tensor velipalatim, ear clik bisa didengar pemeriksa.
Tidak pd otot lain.• Terapi :
Dicoba : medical sp surgical Btx : dalam pertimbangan.
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10. Drug Induce Tremor • Terapi : stop obat/toxin.
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11. Neuropathic Tretmor (NT)• Terjadi pd : polineuropati terutama
HMSN, (Hereditary Motor ans Sensory Neuropathy), CIDP (Chronic Demyelinating Poly Neuropathy berhubungan dg tgM paraproteinemia).
• NT jarang : GBS fase penyembuhan, poluneuropati DM, uremia, posphyria pd porphyria tremor paroxysmal.
• Freq NT : 4 – 12 Hz.
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• Korelasi freq NT dg kecepatan hantar saraf NT berasal dr perifer.
• NT dpt terjadi tanpa ggn. Sensorik dan motorik.
• Terapi : Propanolol : efektif untuk tremor pd CIDP,
HMSN, GBS. Clonazepam IgM paraproteinemia berhubungan dg NT,
terapi penyakitnya.
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12. Psychogenic Tremor (PT)• Freq 4 – 5 Hz.• Onset mendadak, riwayat somatisasi (+)
sebelumnya.• Perubahan freq, amplitudo dan presentasi
PT tidak konsisten. Manisfestasi bisa seperti tremor fisiologi yg.
• Terapi : Psychoterapi : karena PT meruakan bagian
dr ggn. Somatoform (konversi, somatisasi, factitous disorder, malingering).
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CHOREA
a. Definisi Gerakan yg tdk dikehendaki dan
tidak dapat ditekan. Gerakan cepat, dalam waktu singkat,
pd seluruh otot volunter tubuh dg berbagai intensitas dan kekuatan.
b. Etiologi Obat-obatan Non obat-obatan.
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Obat-2 Penyebab Chorea : Neuroleptic. Obat Parkinson : levodopa, dopamin agonist,
amantadine, anti corticholinergic. Anti convulsant : phenytoin, carbamazepin,
gabapentin. Obat kontrasepsi : Stimulant : amphetamine, methyl phenidate,
aminophillin. Steroid. Opiate. Obat lain : tricyclic, antidepressant, lithium
digoxin, metoclopramide, methyldopa, isoniazide.
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Etiologi Chorea non Obat : Infeksi : bakterial, viral, mycoplasma,
sarcoidosis. Metabolik :
› Hypo/hypernatremi, renal insuficiency.› Hypo/hyper glycemia, defisiensi vitamin.
Hamil. Intoxikasi : alkohol, carbon monoxide Cerebrovascular disorder. Trauma cerebri.
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Chorea Sydenham (CS) Bentuk chorea yg sering terjadi pd remaja. Khas : chorea, emosi yg labil dan hypotonia. CS terjadi bbrp bulan setelah infeksi
streptococcus beta haemotytic group A. Terapi prophylaxis antibiotika 2 – 3 minggu. Chorea berat : valproat atau carbamazepin. Chorea sangat berat : dopamin reseptor
blocking agent (Tiapride, pimozide, haloperidl) atau corticosteroid.
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HUNTINGTON DISEASE
a. Definisi Gerakan choreatik. Penyakit pd otak. Gejala gangguan motorik, psikiatrik
dan cognitive.
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b. Etiologi HD autosomal dominant inherited
disease. Patologi :
› General atropi dan berkurangnya berat otak sp 30%.
› Khas atropi nucleus caudatus dan putamen, globus pallidus dilatasi vertricle lateralis.
› Jaringan neuronal didapatkan intracytoplasmic dan nuclear inclusion bodies.
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c. Klinik Onset usia 40 th, rata-2 usia 30 – 50 th, px.
Termuda 2 th dan tertua 45 th. 5% HD gejala timbul pd usia < 20 th.
Disebut : Juvenile HD, dimana 75% ayah Px. Menderita HD (diturunkan melalui laki-2).
25% HD onset usia > 50 th. Lama sakit 17 – 20 th, maksimal 45 th, 25%
px. hidup 25 th lebih. Penyebab kematian :
› Utama : pneumoni akibat aspirasi/tersedak.› Bunuh diri.› Jatuh.
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Gejala spesifik : gangguan motorik, gerakan choreatic yg tdk dikehendaki, emosi yg meningkat dan situasi yg membuat stress.
Sebagian pasien kehilangan berat badan, karena banyak energi untuk gangguan gerak, kesulitan makan dan menelan. Untuk kondisi tetap stabil makan 4000 calori/hari.
Gejala pertama :› Problem pengetahuan di sekolah atau problem
perilaku.› Meningkatnya ketegangan otot.› Gejala pyramidal dan epilepsi.
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Gejala & tanda motorik :› Pola motorik HD kombinasi hyper/dan hypo
kinesia.› Gerakan HD pd otot volunter, tidak pada
otot polos.› Gerakan utama terjadi pd otot wajah atau
badan, lengan, tungkai.› Keadaan biasa, ada gerakan lambat dan
dystonia, dg tubuh pd posis tertentu, kadang-2 gerakan myoclonic, ini membuat px. Cemas.
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› HD berat : Gerakan mengganggu aktifitas harian. Gangguan berjalan. Gangguan koordinasi Gerakan kaku, lambat. Articulasi bicara sulit. Menelan lebih sering tersedak atau
bersendawa bila menelan udara. Automatisasi motorik Awal gerak melambat (akinesia).
› Fase lanjut HD : beberapa penderita torticolis.
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Setiap kambuh gejala motorik memberat.
Gejala dan tanda psikiatrik :› Depresi, cemas, paranoid, compulsi,
schizophrenia, adiksi, gangguan kepribadian akan me di semua fase HD.
› Bisa terjadi : hipochondria dan phobia.› Depresi sering menimbulkan bunuh diri.› Sering penderita tampak agresif, mudah
tersinggung, mendadak berkurang dan lemas.
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Dementia :› Gejala awal kelambatan berpikir.› Gejala cognitive fungsi executive yaitu
kemampuan membuat rencana, mengorganisasi, mengambil keputusan.
› Gejala lanjut penurunan/hilangnya ketrampilan, kontrol emosi dan perilaku sosial, hilang inisiatif.
› Jarang aphasia murni atau apraxia murnia.› Penderita impulsif.
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Diagnostik Dasar diagnosis :
› Riwayat sakit penderita.› Riwayat sakit keluarga.› Konfirmasi dg CAG repeat (untuk mencari
bagian glutamat pd Huntington protein). Jumlah CAG repeat meningkat lebih tinggi pd onset muda.
› MRI, CT.› Pemeriksaan cognitive berkala.
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DYSTONIAa. Definisi
› Abnormal kontrol motorik.› Khas mempertahankan posisi tubuh
abnormal atau gerakan memutar.› Berulang.
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b. Etiologi Primary (idiopathic) dystonia. Secondary :
› Inherited dystonia plus.› Degenerasi disease.› Penyebab tidak diketahui : parkinson
disease dan parkinsonism› Penyebab exogen atau lingkungan.
Dystonia fenomena pd movement disorder.
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c. Klinis Dystonia dipicu gerakan volunter. Dystonia memburuk ok : kelelahan, stres
emosi. Dystonia berat & lama kontraktur sendi Usia onset prognosis :
› Onset anak-2/remaja general/multi focal dystonia.
› Terutama dystonia yg awal dr kaki. Cervical dystonia :
› Paling sering.› Otot-2 leher berkontraksi :
Torsicolis : posis kepala torsi horizontal.
Tilting : latero collis Flexi : antero collis. Retro collis : kepala extensi.
› 75% Px mengeluh nyeri leher.
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Blepharo spasme› Jarang dibandingkan cervical dystonia.› Adalah kontraksi orbicularis oculi› Kasus ringan : kedipan mata , lebih berat
mata terpejam. › Penyebab :
Gangguan visus Erosi cornea
Spasmodic dysphonia :› Dystonia pita suara› Abnormal adduksi suara tercekik. Lebih
sering dr abduksi pita suara suara nafas dan bisikan.
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Oromandibular : Dromandibular Dystonia
› Aktifitas abn pd wajah bag. Bawah, lidah, rahang otot pharyngeal gangguan bicara & menelan.
Brachial dystonia :› Primary focal dystonia.› Penulis writer cramp.› 15% tangan dominan (kanan) ke kontra lateral
bibrachial dystonia. Dystonia otot cranial
› Pd Meige syndrome› Kombinasi dg otot leher : cranio-cervical
dystonia.
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d. Terapi Sekunder dystonia ok peny. Lain tx.
Peny. Dasar. Acut dystonia, Tx. :
› Dopamin receptor blocking agent.› Stop obat penyebab.
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Dopa responsive dystonia Tx. Levodopa + carbidopa dosis rendah.
Primary dystonia Tx. (-). Trihexyphenidil :
› Banyak digunakan› Efek samping : mata kabur, mulut kering,
retensi urine, sedasi, bingung. Baclofen. Benzodiazepin Muscle relaxan. Topiramat, leviteracetam.
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HEMIFACIAL SPASME
a. Definisi Unilateral gerakan clonic jerk dan tonic spasme dari seluruh otot wajah, bisa berkembang menjadi dua sisi, spasme tidak sinkron.
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b. Etiologi 95% primer, ok. Vascular. 5% sekunder :
› Bell Palsy› Cerebello pontine angle tumor.› Lesi brain stem :
Multiple Sclerosis Tonic spasme Facial myokimia.
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c. Patofisiologi1. Hipotesis berasal dari saraf :
• Kompresi n.VII di brain stem tertekan demyelinisasi discharge abn spasme.
2. Hipotesis Nucleus Facialis• Lesi nucleus facialis discharge
abn kedipan mata me.
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d. Gambaran Klinis Spasme tiba-2, irregular, tidak terprediksi. Spasme dirangsang gerakan otot wajah. Spasme mulai sekitar mata mulut
platysma. Akibat spasme :
› Alis terangkat.› Otot wajah lemah dg para doxal synkinesis.
Sebag px. Juga menderita : regional neuropathi › Perubahan pendengaran.› Fungsi trigeminal .
Wanita : pria = 3 : 2.
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e. Diagnosis› MRI : cari kompresi vascular, cari tumor.
f. Terapi Carbamazepin, gabapentin, baclofen, anti
cholinergic, haloperidol, clonazepam. Botulimun toxin inj. Daerah periorbital.
Perbaikan 100%. Diulang tiap 3 – 6 bulan, injeksi ini efektif sampai 10 th.
Operasi : decompresi can. Facialis. Thermoregulasi n. facialis. Intracranial microvascular decompresi n.
facialis 90% hemifacialis spasme hilang + 15% kerusakan n. facialis & hilangnya pendengaran.
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TERIMA KASIH