pemeriksaan neurologi

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KESADARAN

• Kuantitatif ------GCS

• Kualitatif :

Tingkah laku: hipo, normo, hiperaktif aktif

Perasaan hati: euforia, hipertimik, dll

Orientasi : OWTS

Jalan pikiran: logorhea,remming, flight, dll

Kecerdasan : normal, RM

Daya ingat kejadian : baik, amnesia

Penurunan kesadaran - GCS• Membuka Mata (Eye opening)

Spontan

Jika dipanggil

Harus dengan rangsang sakit (dicubit)

Tidak ada respon• Respon verbal (Verbal response)

Orientasi penuh

Bicaranya setengah sadar

Kata-kata sulit dimengerti

Suara tidak jelas

Tidak ada sama sekali• Respon motorik (Motor response)

Mengikuti perintah

Dengan rangsang nyeri setempat

Fleksi normal (Withdrawl)

Fleksi abnormal (decorticate)

Ekstensi (decerebrate)

Tidak ada

4

3

2

1

5

4

3

2

1

6

5

4

3

2

1

Fungsi Sensorik

• Sensasi taktil

• Sensasi nyeri : superfisial/dalam

• Sensasi suhu

• Sensasi gerak & posisi

• Sensasi getar/fibrasi

• Sensasi tekan

• Sensasi diskriminasi : diskriminasi 2 titik, stereognosis, gramestesia

Pemeriksaan sensibilitas kulit :

– waktu yang lama – kesabaran dan ketelitian yang tinggi – kerja sama yang baik dengan pasien– sangat subyektif dan sulit dipertanggung

jawabkan.

Pemeriksaan sensibilitas yang ideal :

– obyektif– sederhana– mudah dikerjakan– repeatable – konsisten– murah biayanya – dapat dipertanggung-jawabkan hasilnya– belum ada yang memenuhi semua sifat tsb

– Ada macam-macam cara pemeriksaan sensibilitas

– sulit diperbandingkan hasilnya– membingungkan – perbedaan pendapat dalam menilai hasilnya.– diperlukan yang bersifat lebih obyektif

Pemeriksaan sensibilitas rutin:

– kapas– rambut kuda– jarum pentul

• --->- sangat kasar dan subyektif

• - sulit dipertanggung jawabkan

• - test penyaring saja

• curiga ada gangguan : test lebih teliti

SARAF KRANIAL

Classification of cranial nerves• Sensory cranial nerves: contain only afferent (sensory) fibers

– ⅠOlfactory nerve – ⅡOptic nerve– Ⅷ Vestibulocochlear nerve

• Motor cranial nerves: contain only efferent (motor) fibers– Ⅲ Oculomotor nerve – Ⅳ Trochlear nerve – ⅥAbducent nerve – Ⅺ Accessory nerve– Ⅻ Hypoglossal nerve

• Mixed nerves: contain both sensory and motor fibers--- – ⅤTrigeminal nerve, – Ⅶ Facial nerve,– ⅨGlossopharyngeal nerve– ⅩVagus nerve

Nervus I (Olfactorius)

• Fungsi pembauan/penciuman

Nervus II (Opticus)

• Daya penglihatan

Medan penglihatan

Pengenalan warna

Fundus okuli :

papil

retina

arteri /vena

perdarahan

•  

Nervus II (Opticus)

Nervus II (Opticus)

Nervus III (Oculomotorius)

• Ptosis• Gerak mata (atas,

bawah, medial)• Reflek cahaya

langsung & konsensuil• Reflek akomodatif • Ukuran pupil• Strabismus divergen• Diplopia• Bentuk pupil

Nervus IV (Trochlearis)

• Gerak mata ke lateral bawah

• Strabismus konvergen

• Diplopia

Nervus V (Trigeminus)

• Menggigit• Membuka mulut • Trismus• Reflek : kornea,

bersin, maseter, zigomatikus

• Sensibilitas muka (tengah, atas, bawah)

Nervus V (Trigeminus)

Nervus VI (Abducens)

• Gerak mata ke lateral

• Strabismus konvergen

• Diplopia

Nervus VI (Abducens)

Nervus VII (Facialis)

• Mengerutkan dahi & kerutan kulit dahi

• Menutup mata & kedipan mata

• Meringis, lipatan naso-labial, sudut mulut

• Mengembungkan pipi, bersiul

• Tiks fasial

• Lakrimasi

Nervus VII (Facialis)

• Daya kecap lidah 2/3 depan

• Reflek : visuo-palpebral, glabella, aurikulo-palpebral

• Tanda Myerson

• Tanda Chovstek

Nervus VII (Facialis)

Nervus VIII (Acusticus)

• Mendengar suara berbisik

• Mendengar detik arloji

• Tes Rinne • Tes Schwabach• Tes Weber

Nervus IX (Glosopharingeus)

• Arkus farings sengau

• Daya kecap lidah 1/3 belakang

• Reflek muntah -- tersedak

Nervus X (Vagus)

• Arkus farings

• Menelan

• Bersuara

• Nadi

Nervus X (Vagus)

Nervus XI (Acesorius)

• Memalingkan kepala

• Mengangkat bahu

• Sikap bahu

• Trofi otot bahu

Nervus XII (Hipoglosus)

• Sikap lidah • Menjulurkan

lidah • Kekuatan lidah• Artikulasi• Trofi otot lidah • Tremor lidah• Fasikulasi lidah

Variabel UMN/SPASTIC LMN/FLACCID

Kekuatan 0 0

Gerakan Terbatas 0 Terbatas 0

Trofi Normal Hipo atrofi

Tonus Normal Hiper Hipo

Klonus (+) (-) (-)

Refleks Fisiologis (+) hiper Hipo (-)

Refleks Patologis (+) (-)

KEKUATAN ARTI KLINIS

0 Tidak ada kontraksi, tidak ada gerakan

1 Ada kontraksi, tidak ada gerakan

2 Ada kontraksi, ada gerakan tanpa melawan gravitasi (geser)

3 Ada gerakan melawan gravitasi tanpa beban/tahanan

4 Ada gerakan melawan gravitasi dengan beban atau tahanan terbatas

5 Normal

ATROFI: Hilangnya atau mengecilnya bentuk otot disebabkan musnahnya serabut otot

ATROFI: • Neurogenic : lemah mengecil• Miogenic : mengecil lemah• Inaktifitas : (disuse atrofi)

hilangnya Sarcoplasma

TONUS :Tahanan otot sehat, normal pada waktu sehat

Syarat :Pasien tenang, periksa dengan tenang, tangan tidak dingin1. Tes kepala jatuh2. Tes lenggang lengan3. Tes goyang tangan4. Tes lengan jatuh5. Tes goyang tungkai6. Tes tungkai jatuh

REFLEKS :JAWABAN SPONTAN TERHADAP SUATU RANGSANGAN

TEKNIK PENGETUKAN:• Gerakan tangan bukan lengan• Tepat pada tendon, direct-indirect• Simetris• Intensitas• Santai tidak tegang

Refleks Superfisial adalah gerakan reflektorik yang timbul sebagai respon atas stimulasi terhadap kulit atau mukosa. Berbeda dengan refleks dalam, refleks superfisial tidak saja mempunyai busur refleks yang segmental melainkan mempunyai komponen supraspinal juga.

REFLEKS PATOLOGIS :

Refleks-refleks yang tidak dapat dibangkitkan pada orang sehat kecuali

bayi

Bentuk vertebra

Bentuk vertebra

Bentuk vertebra

Test Provokasi Nyeri

• Valsava test

• Naffziger test

• Lhermitte’s test

• Laseque test

• O’Connel test

• Patrick test

• Kontra Patrick test

• Gaenselen test

Test Meningeal sign

• Kernig sign

• Brudzinski I

• Brudzinski II

• Brudzinski III

• Brudzinski IV

 

Bell Palsy

Background

• Bell's palsy is a unilateral, peripheral facial paresis or paralysis that has an abrupt onset & no detectable cause.

• One of the most common neurologic disorders affecting the cranial nerves

• First described in 1821, by the Scottish anatomist & surgeon Sir Charles Bell, much controversy still surrounds its etiology & management.

Pathophysiology

• Actual pathophysiology is unknown; this is an area of interminable debate. A popular theory champions inflammation of the facial nerve. During this process, the nerve increases in diameter and becomes compressed as it courses through the temporal bone.

Anatomy

• The facial nerve (seventh cranial nerve) has 2 components. The larger portion comprises efferent fibers that stimulate the muscles of facial expression. The smaller afferent portion contains taste fibers to the anterior two thirds of the tongue, secretomotor fibers to the lacrimal and salivary glands, and some pain fibers.

Anatomy

Anatomy

Anatomy

Causes

• Remains unclear, although vascular, infectious, genetic, & immunologic causes have all been proposed. Patients with other diseases or conditions sometimes develop a peripheral facial nerve palsy, but these are not classified as Bell palsy.

Causes

• Viral infections: Herpes simplex :HSV-1; HSV-2; Human herpes virus (HHV); varicella zoster virus (VZV); Mycoplasma pneumoniae; Borrelia burgdorferi; influenza B; adenovirus; coxsackievirus; Ebstein-Barr virus; hepatitis A, B, and C; cytomegalovirus (CMV); and rubella virus.

Causes

• Pregnancy: Bell palsy is uncommon in pregnancy; however, the prognosis is significantly worse in pregnant women with Bell palsy than among nonpregnant women with palsy.

• Genetics: Recurrence rates (4.5-15%) and familial incidence (4.1%) have been addressed in various studies. Genetics may have a role in Bell palsy, but which factors are inherited is unclear.

Lab Studies

• No specific laboratory tests exist.

• Complete blood count, Erythrocyte sedimentation rate, Thyroid function, glucose level, Rapid plasma reagin (RPR) or Venereal Disease Research Laboratory (VDRL) test, Human immunodeficiency virus (HIV), CSF analysis, IgM, IgG, IgA titers for CMV, rubella, HSV, hepatitis A, hepatitis B, hepatitis C, Dll

Imaging Studies

• Bell palsy remains a clinical diagnosis.

• Imaging studies are not indicated in the ED. Excluding other causes of facial palsy may require one of the following imaging studies depending on clinical setting.

Other Tests

• Electrodiagnosis of the facial nerve: These studies assess the function of the facial nerve. These tests are rarely performed on an emergent basis.

• Electromyography (EMG)

• Electroneurography (ENoG) compares evoked potentials on the paretic side versus the healthy side.

Treatment

• Steroids : remains controversial. Numerous research articles have been written on the benefit or uselessness of steroids to treat patients with Bell palsy.

• Antiviral agents: Although there is insufficient research evaluating the efficacy of antiviral medicines in Bell palsy, most experts believe in a viral etiology.

• Eye care

Treatment

Treatment

Prognosis

• Group 1 regains complete recovery of facial motor function without sequelae.

• Group 2 experiences incomplete recovery of facial motor function, but no cosmetic defects are apparent to the untrained eye.

• Group 3 experiences permanent neurologic sequelae that are cosmetically and clinically apparent.

Prognosis

• Most patients develop an incomplete facial paralysis during the acute phase. This group has an excellent prognosis for full recovery. Patients demonstrating complete paralysis are at higher risk for severe sequelae.

• Of patients with Bell palsy, 85% achieve complete recovery. Ten percent are bothered by some asymmetry of facial muscles, while 5% experience severe sequelae.