mata dan neuro

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ILMU PENYAKIT MATA


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53. Vitamin A Deficiency

myorganicchemistry.wikispaces.com

Retinolelaboration of

rhodopsin by the rods the sensory receptors of the

retina responsible for visionunder low levels of

illumination Vitamin A deficiency

interfere with rhodopsinproduction

impair rod function

Night blindness

VITAMIN A DEFICIENCY AND ITS CONSEQUENCES A field guide to detectionand control.Alfred Sommer. World Health Organization. Geneva:1995


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Conjunctival Xerosis

The epithelium of the conjunctiva transformed to the stratified squamous typeLoss of gobletcells, formation of a granular cell layer and keratinization of the surfaceNcolumnar cell

appears in the temporal quadrantTherapyo resolve within 25 days, most will disappear within 2 weeks

Night blindness

Responds rapidly, usually within 2448 hours to vitamin A therapy

Corneal Xerosis

responds within 25 days with the cornea regaining its normal appearance in 12 weeks

Xerophthalmia Fundus

disappear within 2

4 months in response to vitamin A therapy


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VITAMIN A DEFICIENCY AND

ITS CONSEQUENCES A field

guide to detection and control.

Alfred Sommer. World Health

Organization. Geneva:1995


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http://www.moondrag

on.org/health/disorders/xerophthalmia.html


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54. REFRACTIVE DISORDER


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Refractive Disorder

Myopia Concave lens. The smallestDioptri to corret the visualaquity to 6/6Minus lenses to be used to

correct myopia should be nostronger than abso-lutely necessary.Accommodative asthenopia(rapid ocular fatigue) resultsfrom the excessive stresscaused by chronic con-traction of the atrophicciliary muscle.


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55. Cataract Any opacity of the lens or loss of transparency of the lens that causes

diminution or impairment of vision Classification : based on etiological, morphological, stage of maturity

Etiological classification :

Senile

Traumatic (penetrating, concussion, infrared irradiation, electrocution)

Metabolic (diabetes, hypoglicemia, galactosemia, galactokinase deficiency,hypocalcemia)

Toxic (corticosteroids, chlorpromazine, miotics, gold, amiodarone)

Complicated (anterior uveitis, hereditary retinal and vitreoretinal disorder, high

myopia, intraocular neoplasia

Maternal infections (rubella, toxoplasmosis, CMV)

Maternal drug ingestion (thalidomide, corticosteroids)

Presenile cataract (myotonic dystrophy, atopic dermatitis)

Syndromes with cataract (downs syndrome, werners syndrome, lowes

syndrome)

Hereditary

Secondary cataracthttp://sdhawan.com/ophthalmology/lens&cataract.pdf E-mail: [email protected]


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CataractSign & symptoms:

Near-sightedness (myopia shift)Early in the development of age-relatedcataract, the power of the lens may beincreasedReduce the perception of bluecolorsgradual yellowing andopacification of the lensGradual vision lossAlmost always one eye is affectedearlier than the otherShadow test +

Morphological classification : Capsular Subcapsular Nuclear Cortical Lamellar Sutural

Stage of maturity classification: Immature Mature Intumescent Hypermature

Morgagnian Chronological classification: Congenital (since birth) Infantile ( first year of life) Juvenile (1-13years) Presenile (13-35 years)

Senile


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Katarak Traumatik

Paling sering disebabkan oleh cedera benda asing di lensa atautrauma tumpul bola mata

Sering mengenai pekerja industri

Gejala dan Tanda:

Penglihatan kabur mendadak

Mata merah

Lensa opak

Perdarahan intraokular

gambaran bintangpada lensa posterior yang dapat dilihat

melalui pupil yang dilatasi maksimal

Komplikasi : infeksi, uveitis, ablasio retina, glaukoma

Tatalaksana : antibiotik sistemik dan topikal, kortikosteroid topikal,

katarak dikelurakan pada saat pengeluaran benda asing atau

setelah peradangan mereda

f


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Inflammatory diseases

Ocular toxocariasis

Congenital toxoplasmosis

Congenital cytomegalovirus retinitis

Herpes simplex retinitis

Other types of fetal iridochoroiditis

Pseudo-uveitis Endophthalmitis

Tumors

Retinoblastoma

Medulloepithelioma

Naevoxanthome juvenile

Glioneuroma

Leukemia

Choroidal hemangiomaCombined retinal hamartoma

Congenital malformations

Persistent Hyperplastic Fetal Vasculature (PHFV)

Posterior coloboma

Retinal fold

Myelinated nerve fibres

Morning Glory Syndrome

X-linked retinoschisis

Retinal dysplasia

Norries disease

Incontinentia pigmenti

Phakomatoses

Astrocytic hamartoma (Bournevilles tuberous

sclerosis)

Retinal capillary hemangioma (von Hippel-

Lindau)

Encephalotrigeminal syndrome (Sturge-

Weber)

Neurofibromatosis (von Recklinhausen) (NF1

Divers

Vitreous hemorrhageRetinal detachment

Strabismus (Brckners phenomenon)

Stickler syndrome

Trauma

Contusion of the globeIntraocular foreign body

Shaken baby syndrome

Vascular diseases

Retinopathy of prematurity

Coats

disease

Familial exudative vitreoretinopathy

56. Differential Diagnosis

in Pediatric Leukocoriahttp://www.ncbi.nlm.n

ih.gov/pmc

/articles/PMC2704541/


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Retinoblastoma Retinoblastoma(Rb) is a rapidly

developing cancer that develops inthe cells of retina, the light-detectingtissue of the eye.

Caused by a mutation in a genecontrolling cell division, causing cellsto grow out of control and becomecancerous.

Signs and Symptoms : The pupil of the eye appears white instead

of red when light shines into it (known as"cat's eye reflex" or "white eye"). This maybe seen in flash photographs of the patient.

The eyes appear to be looking in differentdirections (crossed eyes).

Pain or redness in the eye.

An enlarged or dilated pupil

Blurred vision or poor vision

Different colored irises

Treatment : The priority is to

preserve the life of the child, then topreserve vision, and then tominimize complications or sideeffects of treatment.

Treatment options :chemotherapy,cryotherapy, radioactive plaques,laser therapy, external beamradiotherapy and surgical removal ofthe eyeball (enucleation)


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Retinoblastoma


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Katarak sejenis kerusakan mata yang menyebabkan lensa mata berselaput

dan rabun. Lensa mata menjadi keruh dan cahaya tidak dapat

menembus

Ablasio retina Lepasnya retina sensorik dari RPE akibat adanya robekan, tarikan

atau terkumpulnya cairan pada retina. Gejala:vitreous floaters,

fotopsia, terhalang pandangan tepi seperti ada tirai

Displasia retina an eye disease affecting the retina of animals and, less commonly,humans. It is usually a nonprogressive disease and can be caused

by viral infections, drugs, vitamin A deficiency, or genetic defects.

Retinal dysplasia is characterized by folds or rosettes (round

clumps) of the retinal tissue.

Fibroplasia retrolental a disease of the eye affecting prematurely-born babies generally

having received intensive neonatal care. It is thought to be caused

by disorganized growth of retinal blood vessels which may result

in scarring and retinal detachment. Risk factor: prematurity,

oxygen toxicity

Inflammatory diseases Tumors


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Inflammatory diseases

Ocular toxocariasis

Congenital toxoplasmosis

Congenital cytomegalovirus retinitis

Congenital cataract

Herpes simplex retinitis

Other types of fetal iridochoroiditis

Pseudo-uveitis

Endophthalmitis

Tumors

Retinoblastoma

Medulloepithelioma

Naevoxanthome juvenile

Glioneuroma

Leukemia

Choroidal hemangioma

Combined retinal hamartoma

Congenital malformations

Persistent Hyperplastic Fetal Vasculature (PHFV)

Posterior coloboma

Retinal fold

Myelinated nerve fibresMorning Glory Syndrome

X-linked retinoschisis

Retinal dysplasia

Norries disease

Incontinentia pigmenti

Phakomatoses

Astrocytic hamartoma (Bournevilles

tuberous sclerosis)

Retinal capillary hemangioma (von Hippel-

Lindau)Encephalotrigeminal syndrome (Sturge-

Weber)

Neurofibromatosis (von Recklinhausen) (NF

1

DiversVitreous hemorrhage

Retinal detachment

Strabismus (Brckners phenomenon)

Stickler syndrome

TraumaContusion of the globe

Intraocular foreign body

Shaken baby syndrome

Vascular diseases

Retinopathy of prematurity

Coatsdisease

Familial exudative vitreoretino ath

57. Differential Diagnosis

in Pediatric Leukocoriahttp://www.ncbi.nlm.n

ih.gov/pmc/articles/PMC2704541/


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Katarak Kongenital Perubahan pada kebeningan struktur lensa mata yang muncul pada

saat kelahiran bayi atau segera setelah bayi lahir dengan usia < 1 tahun

Unilateral/Bilateral

Keruh/buram di lensa terlihat sebagai bintik/bercak putih dan dapatdilihat dengan mata telanjang

Faktor resiko :kelainan kromosom, atau gangguan penyakit maternalselama masa kehamilan seperti penyakit metabolis (galaktosemia),infeksi intraurin (rubella pada trimester pertama), pemakaian obatselama kehamilan, toksoplasmosis, DM, hipoparatiroidism

Penyulit : makula lutea tidak cukup mendapat rangsangan

tidakberkembang sempurnaambliopia sensoris; nistagmus; strabismus

Pengobatan : operasi.

Ilmu Penyakit Mata, Sidarta Ilyas, 2005


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Retinoblastoma Keganasan pada sel retina. Tampak seperti mata kucing/mata

memantulkan cahaya putih, pupil tampak membesar

Ablasio retina Lepasnya retina sensorik dari RPE akibat adanya robekan, tarikan

atau terkumpulnya cairan pada retina. Gejala:vitreous floaters,

fotopsia, terhalang pandangan tepi seperti ada tirai

Displasia retina an eye disease affecting the retina of animals and, less commonly,humans. It is usually a nonprogressive disease and can be caused

by viral infections, drugs, vitamin A deficiency, or genetic defects.

Retinal dysplasia is characterized by folds or rosettes (round

clumps) of the retinal tissue.

Fibroplasia retrolental a disease of the eye affecting prematurely-born babies generally

having received intensive neonatal care. It is thought to be caused

by disorganized growth of retinal blood vessels which may result

in scarring and retinal detachment. Risk factor: prematurity,

oxygen toxicity


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58. KORNEA

uveitis posterior

perdarahan vitreous Ablasio retina oklusi arteri atau

vena retinal neuritis optik

neuropati optik akutkarena obat(misalnyaetambutol), migrain,tumor otak

MATA TENANGVISUS TURUN

PERLAHAN

MATA TENANGVISUS TURUNMENDADAK

MATA MERAH

VISUS NORMALMATA MERAHVISUS TURUN

Keratitis Keratokonjungt

ivitis Ulkus Kornea Uveitis glaukoma akut Endoftalmitis

panoftalmitis

Katarak

Glaukoma retinopati

penyakitsistemik

retinitispigmentosa

kelainanrefraksi

konjungtivitismurni

Trakoma mata kering,

xeroftalmia Pterigium Pinguekula

Episkleritis skleritis

ANAMNESIS

mengenai mediarefraksi (kornea,uvea, atauseluruh mata)

struktur yangbervaskulersklerakonjungtiva

tidakmenghalangimedia refraksi

http://emedicine medscape com/article/798100


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Corneal Ulcer An inflammatory or more seriously, infective condition of the cornea

involving disruption of its epithelial layer with involvement of thecorneal stroma (Fluoresens test (+))

Causative Agent Feature Treatment

Fungal Fusarium & candida species, conjungtivalinjection, satellite lesion, stromal infiltration,hypopion, anterior chamber reaction

Natamycin,amphotericin B,Azole derivatives,

Flucytosine 1%Protozoa infection(Acanthamoeba)

associated with contact lens users swimming inpools

Viral HSV is the most common cause, Dendriticlesion,decrease visual accuity

Acyclovir

Staphylococcus(marginal ulcer)

Rapid corneal destruction; 24-48 hour, stromalabscess formation, corneal edema, anteriorsegment inflammation. Centered corneal ulcers.Traumatic events, contact lens, structuralmalposition

Tobramycin/cefazolin eye drops,quinolones(moxifloxacin)Pseudomonas

Streptococcus

connective tissuedisease

RA, Sjgren syndrome, Mooren ulcer, or asystemic vasculitic disorder (SLE)

http://emedicine.medscape.com/article/798100


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59. RETINOPATI

uveitis posterior

perdarahan vitreous Ablasio retina oklusi arteri atau

vena retinal neuritis optik

neuropati optik akutkarena obat(misalnyaetambutol), migrain,tumor otak

MATA TENANGVISUS TURUN

PERLAHAN

MATA TENANGVISUS TURUNMENDADAK

MATA MERAH

VISUS NORMALMATA MERAHVISUS TURUN

Keratitis Keratokonjungt

ivitis Ulkus Kornea Uveitis glaukoma akut Endoftalmitis

panoftalmitis

Katarak Glaukoma retinopati

penyakitsistemik

retinitis

pigmentosa kelainan

refraksi

konjungtivitismurni

Trakoma mata kering,

xeroftalmia Pterigium Pinguekula

Episkleritis skleritis

ANAMNESIS

mengenai mediarefraksi (kornea,uvea, atauseluruh mata)

struktur yangbervaskulersklerakonjungtiva

tidakmenghalangimedia refraksi


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RETINOPATI HIPERTENSI Kelainan retina dan pembuluh darah retina akibat tekanan

darah tinggiarteri besarnya tidak teratur, eksudat padaretina, edema retina, perdarahan retina

Kelainan pembuluh darah dapat berupa : penyempitan

umum/setempat, percabangan yang tajam, fenomena crossing,sklerose

Pada retina tampak : akibat sklerose (refleks copper wire/silverwire, lumen pembuluh irreguler, fenomena crossing);perdarahan atau eksudat retina (gambaran seperti bintang,cotton wool patches); perdarahan vena (flame shaped)

Ilmu Penyakit Mata, Sidarta Ilyas, 2005


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CLASSIFICATION SYMPTOMS FEATURE

Mild non-proliferative (mild

pre-proliferative)

None Microaneurysms only, reflects structural

changes in the retina

Proliferative retinopathy Floaters, sudden

visual loss

New vessel formation either at the disc

(NVD) or elsewhere (NVE), vitreous or

preretinal haemorrhage

Central and branch retinal

artery occlusion

Penurunanpenglihatanhebat yang tidak

nyeri yang terjadidalam periodebeberapa detik.

Funduskopi : retina superfisialis mengalamipengeruhan kecuali di foveolacherry redspot

Central and branch retinal vein

occlusion

penurunan

penglihatan

mendadak yangtidak nyeri

perdarahan retina kecil-kecil tersebar dan

bercak cotton-wool, dapat juga gambaran

perdarahan hebat dengan perdarahan retinasuperfisialis dan dalam, vena melebar dan

berkelok-kelok, edema makula dan retina

http://bestpractice.bmj.com/best-practice/monograph/532/basics/classification.html http://medweb.bham.ac.uk/easdec/gradingretinopathy.htm


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60-61. KONJUNGTIVITIS

Pathology Etiology Feature Treatment

Bacterial staphylococcistreptococci,

gonocciCorynebacteriumstrains

Acute onset of redness, grittiness,burning sensation, usually bilateral

eyelids difficult to open on waking,diffuse conjungtival injection,mucopurulent discharge, Papillae +

topical antibioticsArtificial tears

Viral Adenovirusherpes

simplex virusor varicella-zoster virus

Unilateral watery eye, redness,discomfort, photophobia, eyelid

edema & pre-auricularlymphadenopathy, follicularconjungtivitis, pseudomembrane(+/-)

Days 3-5 ofworst, clear upin 714 days without

treatmentArtificial tearsrelievedryness and inflammation(swelling)Antiviralherpes simplexvirus or varicella-zoster virus

http://www.cdc.gov/conjunctivitis/about/treatment.html

Conjunctivitis is swelling (inflammation) or infection

of the membrane lining the eyelids (conjunctiva)



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Fungal Candida spp. cancauseconjunctivitisBlastomyces

dermatitidisSporothrixschenckii

Not common, mostly occur inimmunocompromised patient,after topical corticosteroid andantibacterial therapy to an

inflamed eye

Topical antifungal

Vernal Allergy Chronic conjungtival bilateralinflammation, associated atopicfamily history, itching,photophobia, foreign bodysensation, blepharospasm,cobblestone pappilae, Horner-trantas dots

Removal allergenTopical antihistamineVasoconstrictors

Inclusion Chlamydia

trachomatis

several weeks/months of red,

irritable eye with mucopurulentsticky discharge, acute orsubacute onset, ocular irritation,foreign body sensation,watering, unilateral ,swollenlids,chemosis ,Follicles

Doxycycline 100 mg

PO bid for 21 days ORErythromycin 250 mgPO qid for 21 daysTopical antibiotics


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62. Cataract

Any opacity of the lens or loss of transparency of the lens that causes

diminution or impairment of vision Classification : based on etiological, morphological, stage of maturity Etiological classification : Senile Traumatic (penetrating, concussion, infrared irradiation, electrocution)

Metabolic (diabetes, hypoglicemia, galactosemia, galactokinasedeficiency, hypocalcemia) Toxic (corticosteroids, chlorpromazine, miotics, gold, amiodarone) Complicated (anterior uveitis, hereditary retinal and vitreoretinal

disorder, high myopia, intraocular neoplasia Maternal infections (rubella, toxoplasmosis, CMV)

Maternal drug ingestion (thalidomide, corticosteroids) Presenile cataract (myotonic dystrophy, atopic dermatitis) Syndromes with cataract (downs syndrome, werners syndrome,

lowes syndrome) Hereditary Secondary cataract

http://sdhawan.com/ophthalmology/lens&cataract.pdf E-mail: [email protected]


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Sign & symptoms: Near-sightedness (myopia

shift)Early in the developmentof age-related cataract, thepower of the lens may beincreased

Reduce the perception of blue

colors

gradual yellowing andopacification of the lens

Gradual vision loss

Almost always one eye isaffected earlier than the other

Shadow test +

Morphological classification : Capsular

Subcapsular Nuclear Cortical Lamellar Sutural

Stage of maturity classification:

Immature Mature Intumescent Hypermature Morgagnian

Chronological classification: Congenital (since birth) Infantile ( first year of life) Juvenile (1-13years) Presenile (13-35 years) Senile


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Cataract Treatment : Surgery

Cataract surgery is the removal of the natural lens of the eye that hasdeveloped an opacification then an artificial intraocular lens implant isinserted

Pirenoxine(Catalin) is a medication used in the possible treatment andprevention of cataracts.

A report in the journal of Inorganic Chemistryshowed that in liquid solutionsPirenoxine could cause decreased cloudiness of a crystallin solution producedto mimic the environment of the eye.

Abstract of a research on how pirenoxine (PRX) interacts with selenite orcalcium ions that have been proven as factors leading to the formation of

lens cataract is available athttp://pubs.acs.org/stoken/presspac/presspac/full/10.1021/ic102151p

Researchers found that pirenoxine reduced the cloudiness of the lenssolution containing calcium by 38 percent and reduced the cloudiness of theselenite solution by 11 per cent.

http://en.wikipedia.org/wiki/Pirenoxin
http://pubs.acs.org/stoken/presspac/presspac/full/10.1021/ic102151phttp://pubs.acs.org/stoken/presspac/presspac/full/10.1021/ic102151p


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Quinolone A family of synthetic broad-spectrum antibacterial drugs

Pilokarpine A parasympathomimetic alkaloid, used to treat chronic open-angle glaucoma, acute angle-closure glaucoma

Betamethasone Corticosteroid for eye inflammation. Contraindicated in fungal

infections and hypersensitivity

Hidroksietilselulosa Eye lubricants, for dry and irritated eye


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63. TRAUMA

Trauma tumpul menyebabkan peningkatan tekanan dalam

orbita dan intraokular disertai deformitas bola mata.

Tanda: nyeri ringan, kekaburan penglihatan, kemosis

hemoragik, laserasi konjungtiva, kamera anterior dangkaldengan atau tanpa dilatasi pupil yang eksentrik, ablasi retina,

hifema, atau perdarahan korpus vitreosus


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Ablasio Retina Ablasio retina adalah suatu keadaan terpisahnya sel kerucut dan batang

retina (retina sensorik) dari sel epitel pigmen retina

Mengakibatkan gangguan nutrisi retina pembuluh darah yang bila

berlangsung lama akan mengakibatkan gangguan fungsi penglihatan Terdapat tiga jenis utama/penyebab ablasio retina yaitu : ablasi retina

regmategenosa, ablasi retina traksi (tarikan) dan ablasi retina eksudatif

Gejala : vitreous floaters, fotopsia, terhalangnya pandangan tepi seperti ada

tirai, metamor-fopsia, dan penurunan visus, Ada semacam tirai tipisberbentuk parabola yang naik perlahan-lahan dari mulai bagian bawah bolamata dan akhirnya menutup pandangan

Funduskopi : adanya robekan retina, retina yang terangkat berwarna keabu-

abuan, biasanya ada fibrosis vitreous atau fibrosis preretinal bila ada traksi.Bila tidak ditemukan robekan kemungkinan suatu ablasio nonregmatogen

Pengobatan: konservatif(untuk nonregmatogen), pneumatic retinopexy,bakel sklera, vitrektomi tertutup

Vaughn DG, Oftalmologi Umum, ed.14


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Hifema Blood in the front (anterior) chamber of the eyea reddish tinge,or a small pool of blood at the bottom of the iris or in the cornea

Luksasio lensa Dislokasi lensa dapat pada anterior atau posterior. Anterior :penglihatan turun mendadak, sakit yang sangat, muntah, matamerah dengan blefarospasme, injeksi siliar, edema kornea.Posterior : skotoma pada lapang pandang dan gejala afakia

Iridosiklitis Radang uvea anterior. Gejala : mata merah, pupil kecil, nyeri,

fotofobia, penglihatan turun ringan dan berair

Perdarahan vitreum Sering timbul pada penderita DM, hipertensi, dan anemia sabit.Gejala :penglihatan buram tiba-tiba, peningkatan floater/kilatancahaya


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64. Eyelids DisordersPathology Feature

Chalazion(meibomian glandlipogranuloma)

Chronic inflamation of Zeis/Meibom gland; when acutely inflammedPainful,warm, swollen, and firm eyelids, granulomatous reaction, lipogranuloma, usuallyon the upper eyelid and inside the lid, painless nodules, Increased tearing,Sensitivity to light

Hordeolum Localized infection or inflammation of the eyelid margin involving hair follicles ofthe eyelashes (external hordeolum) or meibomian glands (internal

hordeolum),Staphylococcal infection; painful, warm, swollen, and tender eyelids,focal collection of PMN cells and necrotic tissue. erythematous, andlocalized,Purulent material exudates

http://en.w

ikipedia.org/wiki/

http://www.ncbi.nlm.n

ih.gov/pub

medhealth/


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http://www.healblog.net/wp-content/uploads/Hordeolum-and-Chalazion.jpg

Chalazion The result of obstruction of the duct of a meibomian gland, which is usually

idiopathic, with secondary lipogranulomatous inflammation

Epidemiology : higher incidence in seborrheoc dermatitis, rosacea, and DM Clinical features : a pale, round, firm lesion of the lid.

Diagnosis : made clinically Treatment : incision of the cyst and removed by curetting. Steroid injection

can initiate remission Prognosis : ocaasionally recurrent


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NEUROLOGI


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65. CAUDA EQUINA SYNDROME Cauda equina syndrome (CES) is a rare syndrome that has been described as a complex of

symptoms and signs

low back pain, unilateral or bilateral sciatica, motor weakness oflower extremities, sensory disturbance in saddle area, and loss of visceral functionresulting from compression of the cauda equina.

CES occurs in approximately 2% of cases of herniated lumbar discs and is one of the fewspinal surgical emergencies.

Etiology : tumors, trauma, spinal stenosis, inflammatory conditions

Signs : include weakness of the muscles of the lower extremeties innervated by thecompressed lumbar roots (often paraplegia), detrusor weaknesses causing urinaryretention and post-void residual incontinence, decreased anal tone and consequent fecalincontinence; sexual dysfunction; saddle anesthesia; bilateral (or unilateral) sciatic leg painand weakness; and absence of ankle reflex. Pain may, however, be wholly absent; thepatient may complain only of lack of bladder control and of saddle-anaesthesia, and maywalk into the consulting-room.

Red Flag Symptoms:(requiring urgent hospitalisation) include sciatic leg pain and/or severeback pain, with altered sensation over saddle area (genitals, uretha, anus, inner thighs),urine retention or incontinence

Diagnosis : CT or MRI

Treatment : Surgical decompression

http://en.wikipedia.org/wiki/Cauda_equina_syndrome


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66-67. HEAD INJURY

Brain hematoma : a collection of blood within brain tissue.

Hematoma inside the cranium is named according to itslocation:

Subdural hematoma: blood collection between brain and dura

Epidural hematoma: blood collection between dura and theskull

Subarachnoid Hemorrhage: beneath the arachnoid membrane

Intracerebral hematoma: blood collection within the brain


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Subdural Hematoma A collection of blood below the inner layer of the dura but external to the brain

and arachnoid membrane.

Subdural hematoma is the most common type of traumatic intracranial mass

lesion. Usually resulting from tears in bridging veins which cross the subdural space

May cause an increase in intracranial pressure (ICP) compression of anddamage to delicate brain tissue

Characterized on the basis of their size and location and the amount of timeelapsed since the inciting event age (ie, whether they are acute, subacute, or

chronic) : Acute subdural hematomas: less than 72 hours old and are hyperdense compared with

the brain on computed tomography scans.

Subacute phase: begins 3-7 days after acute injury; the surgical literature favors 3 days,whereas the radiological literature favors 7. Subacute subdural hematomas are isodenseor hypodense compared with the brain.

Chronic subdural hematomas are 21 days (3 wk) or older and are hypodense comparedwith the brain. However, may be mixed in nature, such as when acute bleeding hasoccurred into a chronic subdural hematoma.

Symptoms: gradually increasing headache and confusion.

CT Appearance : crescent shape

Treatment: depends on the size and rate of growth. Careful monitoring, insertionof small cathehersuck the blood, craniotomy removal of hematoma

http://emedicine.medscape.com/article/1137207


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Epidural Hematomas

70%-80% located intemporoparietal region whereskull fractures cross the path of

middle meningeal artery or itsdural branches

May present with lucid periodimmediately after trauma and adelay before symptoms evident

on CT : Lens shaped (biconvexlens) hematomas that do notcross suture lines

Subdural hematomas : crescent shaped density


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Crescent shaped density that may run length of skull

Subdural hematomas : crescent shaped density

that may run length of the skull

Subarachnoid

Hemorrhage

Intracranial Hemorrhage


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Menurut Penyebab Stroke dibagi:

1. Stroke Hemoragik

a. Intra cerebral hemoragik (ICH)

OK : Hypertensi, Aneurysma dan arterioveneus Malformasi (AVM)

b. Sub Arachnoid Hemoragik (SAH)

diagnosis medis : CT brain scan

2. Stroke Non Hemoragik (Iskemik)

OK : Arteriosklerosis & sering dikaitkan dengan : DM,

Hypercolesterolemia, Asam urat, hyperagregasi trombosit

3. Emboli Sumber dari tronkus di arteria carotis communis di jantung Lepas trombus embolus otak.

68. STROKE


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Stroke

Manifestasi Klinis : Kelumpuhan wajah atau anggota

badan (biasanya hemiparese),timbul mendadak

Gangguan hemisensorik

Perubahan mendadak statusmental

Afasia; disartria

Gangguan penglihatan atau

diplopia Ataksia

Vertigo, mual, muntah, nyerikepala

Faktor Resiko : Usia

Riw. TIA atau stroke

Peny. Jantung koroner

Hipertensi DM

Merokok

Dislipidemia


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Intracerebral Hemorrhage

Bleeding into brain tissue

Usually caused by chronichypertension

Non-hypertension cause more

likely if: No past history of

hypertension

Lobar (i.e., peripheral, notsubcortical)

May require emergency surgery

Accounts for 10% of strokes

Hemorrhage:Symptoms only suggestive ofhemorrhage.CT or LP needed for definitivediagnosis

Headache Neck stiffness

Neck pain

Light intolerance

Nausea, vomiting

Decreased consciousness

Pada kasus ini tidak didapatkan tanda-

tanda kemungkinan stroke hemoragik

jadi kemungkinan yang terjadi adalah

stroke iskemik


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6 HEADACHE


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69. HEADACHE

MIGRAINE


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MIGRAINE


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70. MENINGITIS

Meningitis: radang pada selaput otak yang melapisi otak dansumsum tulang belakang

Manifestasi klinis : nyeri kepala, dapat menjalar ke tengkuk dan

punggung, kaku kuduk, kernig (+), brudzinsky (+)

Klasifikasi (berdasarkan perubahan pada cairan otak) : Meningitis serosa : cairan otak jernih, paling sering disebabkan oleh

Mycobacterium tuberculosa, penyebab lain: virus, toxoplasma gondhii,

ricketsia

Meningitis purulenta : cairan mengandung pus, penyebabnya antara

lain diplococcus pneumoniae, neisseria meningitidis, streptococcushaemolyticus, staphylococcus aureus, haemophilus influenza,

pseudomonas aeruginosa

Kapita Selekta


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Meningitis TB


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Meningitis TB-Diagnosis Tuberculous meningitis (TBM) is an inflammation of the meninges covering the

brain and spinal cord caused by infection with mycobacteria, most usually

Mycobacterium tuberculosis.

The condition usually presents with headache, fever, and convulsions and is

diagnosed clinically, with confirmation by microscopy and culture of

cerebrospinal fluid.

CSF Examination Usually lymphocytic pleocytosis

Paradoxic change from lymphocytic to neutrophilic predominance over

48 hr pathognomonic for TB meningitis

Elevated protein with severely depressed glucose

Repeated specimens for AFB culture necessary Other Studies

Brain imaging demonstrates hydrocephalus, basilar exudates and

inflammation, tuberculoma, cerebral edema, cerebral infarction

CXR

Abnormal, sometimes miliary pattern


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Treatment


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CSF Findings in Meningitis


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71. EPILEPSI

A seizure is defined by release of excessive and

uncontrolled electrical activity in the brain. Seizures

themselves are not a disease, they are an event.

Epilepsy (seizure disorder) is a neurological condition,

that in different times produce brief disturbances in the

electrical functions of the brain. Seizures are a symptom

of epilepsy.


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Epilepsy - Classification

Focal seizures account for 80%of adult epilepsies

- Simple partial seizures

- Complex partial seizures

- Partial seizures secondarilly

generalised

Generalised seizures

Unclassified seizures


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Partial Seizure

Simple Seizure activity in the brain causing:

Rhythmic movements -

isolated twitching of arms, face, legs

Sensory symptoms -

tingling, weakness, sounds, smells,

tastes, feeling of upset stomach,

visual distortions

Psychic symptoms -

dj vu, hallucinations, feelings offear or anxiety

Usually last less than one minute

May precede a generalized seizure

Complex Characterized by altered

awareness Confusion, inability to respond Automatic, purposeless behaviors

such as picking at clothes,chewing or mumbling.

Emotional outbursts May be confused with:

Drunkenness or drug useWillful belligerence,

aggressiveness


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GENERALIZED SEIZURES

INVOLVE WIDE AREAS OF THE BRAIN AND LOSS OFCONSCIOUSNESS

PETIT MAL : CONSCIOUSNESS IS TRANSIENTLY LOST ANDTHE EEG DISPLAYS SPIKE AND WAVE ACTIVITY

GRAND MAL : CONSCIOUSNESS LOST FOR A LONGERPERIOD AND THE INDIVIDUAL WILL FALL IF STANDINGWHEN SEIZURE STARTS.

TONIC PHASE: GENERALIZED INCREASED MUSCLE

TONE. CLONIC PHASE: SERIES OF JERKY MOVEMENTS.

BOWEL AND BLADDER MAY EVACUATE.


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Epilepsi-Klasifikasi (etiologi)

Idiopatik epilepsi : biasanya berupa epilepsi dengan serangan kejangumum, penyebabnya tidak diketahui. Pasien dengan idiopatik epilepsi

mempunyai inteligensi normal dan hasil pemeriksaan juga normal dan

umumnya predisposisi genetik.

Kriptogenik epilepsi : Dianggap simptomatik tapi penyebabnya belum

diketahui. Kebanyakan lokasi yang berhubungan dengan epilepsi tanpadisertai lesi yang mendasari atau lesi di otak tidak diketahui. Termasuk

disini adalah sindroma West, Sindroma Lennox Gastaut dan epilepsi

mioklonik. Gambaran klinis berupa ensefalopati difus.

Simptomatik epilepsi : Pada simptomatik terdapat lesi struktural di otakyang mendasari, contohnya oleh karena sekunder dari trauma kepala,

infeksi susunan saraf pusat, kelainan kongenital, proses desak ruang di

otak, gangguan pembuluh darah diotak, toksik (alkohol, obat),

gangguan metabolik dan kelainan neurodegeneratif.Diagnosis Epilepsi Lengkap-Perdossi

PARESE N VII


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72. PARESE N. VII


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Menurut Penyebab Stroke dibagi:1. Stroke Hemoragik

a. Intra cerebral hemoragik (ICH)

OK : Hypertensi, Aneurysma dan arterioveneus Malformasi (AVM)

b. Sub Arachnoid Hemoragik (SAH)

diagnosis medis : CT brain scan

2. Stroke Non Hemoragik (Iskemik)

OK : Arteriosklerosis & sering dikaitkan dengan : DM,

Hypercolesterolemia, Asam urat, hyperagregasi trombosit

3. EmboliSumber dari tronkus di arteria carotis communis di jantungLepastrombus embolusotak.

73. STROKE


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Tatalaksana Khusus


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Tatalaksana KhususStroke Hemoragik :

Perawatan di ICU jika didapatkan volume hematoma lebih dari 30 cc,perdarahan intraventrikuler dengan hidrosefalus dan klinis cenderungmemburuk,

Tekanan darah diturunkan sampai tekanan darah premorbid atausebanyak 15-20% bila tekanan sistolik >180, diastolik >120, MAP >130, dan

volume hematoma bertambah. Bila terdapat gagal jantung maka tekanan darah segera diturunkan

dengan labetolol intravena dengan dosis 10 mg (pemberian dalam 2menit) sampai 20 mg (pemberian dalam 10 menit) maksimum 300 mg;enelapril intravena 0,625-1.25 mg per 6 jam; Captopril 3 kali 6,25-25 mg

peroral, Jika didapatkan tanda-tanda tekanan intra kranial meningkat, maka posisi

kepala dinaikkan 30 derajat, dengan posisi kepala dan dada pada satubidang, bisa dilakukan pemberian manitol (lihat stroke iskemik), danhiperventilasi (PCO2 20-35 mmHg),

Kapita Selekta Kedokteran


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74. CRANIAL NERVES


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75 VERTIGO


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75. VERTIGO

the illusion that the environment isspinning

a subtype of dizziness, where there is afeeling of motion when one isstationery

Classification :

Peripheral

Central

Common Causes:

1.Peripheral

Physiological (motion sickness)

Benign paroxysmal positional vertigo

(BPPV)most common

Vestibular neuronitis

Labyrinthitis

Menire disease

Perilymph fistula

2.Central

Brainstem TIA/infarct

Posterior fossa tumors

Multiple sclerosis Syringobulbia

Arnold - Chiari deformity

Temporal lobe epilepsy

Basilar migraine

3.OtherCardiac, GI, psycogen, toxins, medications,

anemia, hypotension


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Vertigo

Peripheral vertigo : caused byproblems within the innerear/vestibular system; alsocalled otologic or vestibularvertigo.

The most common cause :BPPV (32%)

Central vertigo : arises frominjury to the balance centersof the CNS; less prominentmovement illusion andnausea.

Has accompanying neurologic

deficits (e.g. slurred speechand double vision), andpathologic nystagmus (pure

vertical/ torsional)


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BPPV A clinical syndrome characterized by brief recurrentepisodes of vertigo triggered by changes in head position

with respect to gravity.

Meniere disease An inner ear disorder that causes one to experienceperiods of vertigo, dizziness, nausea, ear pressure,sensitivity to light and tinnitus

Migraine with aura Suatu kondisi kronis dengan karakteristik sakit kepala

episodik unilateral yang didahului dengan gejala aura

(gangguan visual, sensasi abnormal pada kulit, mual,

muntah, dll)

6 PARKINSON


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76. PARKINSONDISEASE

Parkinson Disease : a degenerative disorder of the central

nervous system.

The motor symptoms of Parkinson's disease result from

the death of dopamine-generating cells in the substantia

nigra, a region of the midbrain; the cause of this cell death

is unknown.

3 main symptoms:

Tremors

Rigidity

Slowed motion (Bradykinesia)

Other symptoms include:

Dementia, sleep disturbances,depression, etc.


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Parkinson Disease

No definitive tests for PD. PET scans can aid to determine levels ofdopamine.

Medical history and neurological tests are conducted to diagnose.

Usually, if two of the cardinal symptoms are present

Treatment can be divided into two stages.

Early and Later stages Early stage

Onset of symptoms, treated with physical therapy and medications(Levodopa, dopamine agonists, etc)

Later stage

Usually after having received 5+ years of levodopa treatment. Wearing-offand On/Offeffect develops, other medication in

conjunction levodopa is commenced.

MAO-B and COMT inhibitors.

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Treatment Physical Therapy

Regular exercise Recommended throughout the life of disorder.

Helps maintain and improve mobility and strength.

Physical exercise aids in rigidity relief, muscle strength and

flexibility, balance, etc. Caution is advised to avoid sudden movements or strenuous

activities fall could result in serious injury.

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