Neuro Emergency pada Stroke

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Dr. Eddy Ario Koentjoro Sp S

Penanganan Stroke Akut harus Penanganan Stroke Akut harus Cepat Tepat dan EfisienCepat Tepat dan Efisien

Mengurangi mortalitas, disabilitas, stroke Mengurangi mortalitas, disabilitas, stroke ulangulang

Mencegah Komplikasi Mencegah Komplikasi Komplikasi Serebral -------Minggu Pertama Komplikasi Serebral -------Minggu Pertama

Edema Serebri Edema SerebriKomplikasi Non Serebral ----Minggu 2-4Komplikasi Non Serebral ----Minggu 2-4

Medical Complication of StrokeMedical Complication of Stroke

I.I. NeurologicNeurologica.a. SeizuresSeizuresb.b. Vascular dementiaVascular dementia

II.II. InfectionInfectiona.a. Urinary tract infection, urosepsisUrinary tract infection, urosepsisb.b. Dysphagia, aspiratio pneumoniaDysphagia, aspiratio pneumonia

III.III. Complication of immobilityComplication of immobilitya.a. FallsFallsb.b. Hemiosteoporosis, fracturesHemiosteoporosis, fracturesc.c. Pressure ulcerPressure ulcer

IV.IV. ThromboembolismThromboembolisma.a. Deep vein thrombosisDeep vein thrombosisb.b. Pulmonary embolismPulmonary embolism

V.V. PainPaina.a. Shoulder painShoulder painb.b. Central poststroke painCentral poststroke pain

VI.VI. Psychological Psychological a.a. DepressionDepressionb.b. Anxiety Anxiety c.c. ConfusionConfusiond.d. Emotional incontinenceEmotional incontinence

Medical Complication of StrokeMedical Complication of Stroke

VII.VII. MiscellaneousMiscellaneousa.a. Gastrointestinal hemorrhageGastrointestinal hemorrhage

b.b. ConstipationConstipation

c.c. Cardiac failure, arrythmiasCardiac failure, arrythmias

d.d. ArthritisArthritis

e.e. Sleep apneaSleep apnea

f.f. Nutritional deficienciesNutritional deficiencies

(Langome et al 2000)(Langome et al 2000)

Medical Complication of StrokeMedical Complication of Stroke

1)1) Disorders of immobilityDisorders of immobilitya)a) Deep-vein thrombosis and pulmonary embolusDeep-vein thrombosis and pulmonary embolus

b)b) Hemiosteoporosis and hip fracturesHemiosteoporosis and hip fractures

c)c) FallsFalls

d)d) Pressure sore, skin ulcersPressure sore, skin ulcers

e)e) Peripheral nerve injuryPeripheral nerve injury

2)2) Pain Pain a)a) Shoulder painShoulder pain

b)b) Central poststroke painCentral poststroke pain

3)3) Incontinence Incontinence

Komplikasi NeurologikKomplikasi Neurologik

Timbulnya edema serebral : memperburuk Timbulnya edema serebral : memperburuk daerah penumbra dan menaikan TIK daerah penumbra dan menaikan TIK keadaan darurat/kritiskeadaan darurat/kritis

Proses stroke akut dapat menimbulkan Proses stroke akut dapat menimbulkan komplikasi darurat medik : komplikasi darurat medik : Perdarahan gastrointestinal neurologikPerdarahan gastrointestinal neurologikEdema pulmoner neurologikEdema pulmoner neurologikHyponatremiaHyponatremiaKomplikasi cardiac neurologikKomplikasi cardiac neurologik

EDEMA CEREBRAL PADA STROKEEDEMA CEREBRAL PADA STROKE

1.1. Sering timbul pada infark cerebri yang Sering timbul pada infark cerebri yang luasluas

2.2. Maximum pada hari ke 7-10 dan Maximum pada hari ke 7-10 dan kemudian berkurangkemudian berkurang

3.3. Korelasi dengan effect massa, Korelasi dengan effect massa, pergeseran garis tengah, keadaan klinik pergeseran garis tengah, keadaan klinik dan outcomedan outcome

4.4. Penyebab kematian utama pada stroke Penyebab kematian utama pada stroke minggu pertamaminggu pertama

Pengobatan Cerebral EdemaPengobatan Cerebral Edema

1.1. Pengobatan pharmakologik cerebral Pengobatan pharmakologik cerebral edema dengan pengobatan zat-zat edema dengan pengobatan zat-zat osmolarosmolar

2.2. Pengobatan dengan diuretikaPengobatan dengan diuretika

3.3. Pengobatan dengan intubasi dan Pengobatan dengan intubasi dan hyperventilasihyperventilasi

Zat-zat Hyper Osmolar Pada Cerebral Zat-zat Hyper Osmolar Pada Cerebral EdemaEdema

A.A. Glycerol mengurangi dengan efektif cerebral edema Glycerol mengurangi dengan efektif cerebral edema (Rogvi-Hansen & Boysen,1995)(Rogvi-Hansen & Boysen,1995)

B.B. Mengurangi “odds of early death” sebanyak 42% dan Mengurangi “odds of early death” sebanyak 42% dan pada final meta analisis terjadi penurunan 18% sajapada final meta analisis terjadi penurunan 18% saja

C.C. Diberikan dalam bentuk larutan 10% glycerol dalam Diberikan dalam bentuk larutan 10% glycerol dalam isotonic saline, 500 cc per 4-6jam, rebound jarangisotonic saline, 500 cc per 4-6jam, rebound jarang

D.D. Mannitol 1-2 gr/bb secara iv yang diberikan selama 30 Mannitol 1-2 gr/bb secara iv yang diberikan selama 30 menit merupakan dosis initial dan jika diperlukan dapat menit merupakan dosis initial dan jika diperlukan dapat ditambah 0,25-0,5 gr diberikan selama 30-60 menit ditambah 0,25-0,5 gr diberikan selama 30-60 menit dan dapat di ulang tiap 4-6 jamdan dapat di ulang tiap 4-6 jam

E.E. Akhir-akhir ini larutan hypertonic saline diberikan Akhir-akhir ini larutan hypertonic saline diberikan secara bolus dapat mengurangi edema cerebralsecara bolus dapat mengurangi edema cerebral

F.F. Furosemide diberikan tersendiri atau denga kombinasi Furosemide diberikan tersendiri atau denga kombinasi manitol. Dapat digunakan sebagai alternatif lainmanitol. Dapat digunakan sebagai alternatif lain

Zat-Zat Hyper Osmolar pada Cerebral Zat-Zat Hyper Osmolar pada Cerebral EdemaEdema

G.G. Upaya terakhir adalah pasien dimasukkan ke ICU Upaya terakhir adalah pasien dimasukkan ke ICU kemudian di Intubasi, dan dilakukan hyperventilasi kemudian di Intubasi, dan dilakukan hyperventilasi terkontrol dengan sasaran PACO2 dipertahankan 25-terkontrol dengan sasaran PACO2 dipertahankan 25-30 mmHg30 mmHg

H.H. Dekompresi dengan kraniotomi dengan segala Dekompresi dengan kraniotomi dengan segala resikonyaresikonya

Intracranial ContentIntracranial Content

Brain Brain 1400 cc1400 cc 80% 80% BloodBlood 150 cc150 cc 10% 10% CSFCSF 150 cc150 cc 10% 10% Total Total 1700 cc 1700 cc 100%100%

Intracranial Decompressive SurgeryIntracranial Decompressive Surgery

1)1) Age less than 40 Age less than 40 2)2) Glasgow coma scale score greater than 3 on Glasgow coma scale score greater than 3 on

initial examination initial examination 3)3) No extra or intracerebral mass lesion or No extra or intracerebral mass lesion or

infarction on CTinfarction on CT4)4) Objective evidence of neurologic deterioration Objective evidence of neurologic deterioration

(change in Glasgow, coma scale score, pupils, (change in Glasgow, coma scale score, pupils, EEG or CBF)EEG or CBF)

5)5) Absence of irreversible neurologic damageAbsence of irreversible neurologic damage6)6) Failure of medical therapies for elevated Failure of medical therapies for elevated

intracranial pressure (Gaab et al 1990)intracranial pressure (Gaab et al 1990)

Perdarahan Gastro-Intestinal pada StrokePerdarahan Gastro-Intestinal pada Stroke Sering terjadi pada akut stroke Sering terjadi pada akut stroke Akibat stimulasi central simpatetik, pada infark cerebri Akibat stimulasi central simpatetik, pada infark cerebri

lebih sering terjadi hyperasiditas lambunglebih sering terjadi hyperasiditas lambung Pada perdarahan intracerebral lebih sering terjadi Pada perdarahan intracerebral lebih sering terjadi

perdarahan lambung perdarahan lambung Pada keadaan koma/kesadaran menurun, Pada keadaan koma/kesadaran menurun,

pemasangan tube nasogastrik diharuskan untuk pemasangan tube nasogastrik diharuskan untuk mengeluarkan cairan lambung dan mencegah mengeluarkan cairan lambung dan mencegah aspirasi cairan aspirasi cairan

Pengobatan Pengobatan Pada keadaan hyper asiditas dilakukan spooling Pada keadaan hyper asiditas dilakukan spooling cairan lambung yang periodic dan ditambahkan cairan lambung yang periodic dan ditambahkan cairan yang bersifat basa untuk mengikat asam cairan yang bersifat basa untuk mengikat asam lambunglambung

Perdarahan lambung diatasi dengan puasa dengan Perdarahan lambung diatasi dengan puasa dengan pemberian obat-obatan yang memblokade sekresi pemberian obat-obatan yang memblokade sekresi asam ( H receptor Antagonis)asam ( H receptor Antagonis)

Neurogenic Pulmonary EdemaNeurogenic Pulmonary Edema Akibat stimulasi sympatetik sentralAkibat stimulasi sympatetik sentral Lesi di Hypotalamus, Nukleus Tractus Lesi di Hypotalamus, Nukleus Tractus

Solitarius dan Medulla OblongataSolitarius dan Medulla Oblongata

Bentuk Klinik :Bentuk Klinik :A.A. Bentuk Klasik timbul Menit - Jam setelah Bentuk Klasik timbul Menit - Jam setelah

InsultInsult

B.B. ““Delayed Form” timbul 12-72 Jam Post Delayed Form” timbul 12-72 Jam Post InsultInsult

Gambaran Klinik Neurogenic Pulmonary Gambaran Klinik Neurogenic Pulmonary Edema Edema

1.1. Berupa dyspnea, nyeri dada, dan Berupa dyspnea, nyeri dada, dan hemoptisis ringanhemoptisis ringan

2.2. Pemeriksaan menunjukkan tachypnea, Pemeriksaan menunjukkan tachypnea, tachycardia dan rhonchi Basah difustachycardia dan rhonchi Basah difus

3.3. Thoraks foto : Gambaran Edema paruThoraks foto : Gambaran Edema paru

4.4. Umumnya menghilang spontan atau Umumnya menghilang spontan atau dicegah dengan ganglion blocker (misal : dicegah dengan ganglion blocker (misal : Dobutamin)Dobutamin)

HyponatremiaHyponatremia

1.1. Syndrome of inapropriate secretion of Syndrome of inapropriate secretion of antidiuretic hormone (SADH): antidiuretic hormone (SADH): Hyponatermia urine, Hypernatremia dan Hyponatermia urine, Hypernatremia dan Hypervolumia Hypervolumia Restriksi cairan Restriksi cairan (Scwartz, 1957) (Scwartz, 1957)

2.2. Cerebral Salt Wasting Syndrome Cerebral Salt Wasting Syndrome (CSW) : Hypernatremia, urine (CSW) : Hypernatremia, urine hypernatermia, dan Hypovolumia -----hypernatermia, dan Hypovolumia -----Salt & fluid Replacement (Peters, 1950)Salt & fluid Replacement (Peters, 1950)

Komplikasi Cardiak Pada StrokeKomplikasi Cardiak Pada Stroke1.1. Berupa aritmia dan gangguan repolarisasi Berupa aritmia dan gangguan repolarisasi

transient :transient :• AV Block AV Block • Supra ventrikular tachycardiSupra ventrikular tachycardi• Sinus bradicardiSinus bradicardi• Paroksisma ventricular tachycardiParoksisma ventricular tachycardi• AV disosiasiAV disosiasi• Ritme nodalRitme nodal

2.2. Penyebab: Penyebab: • Degenerasi miofibriler otot jantungDegenerasi miofibriler otot jantung• Di duga karena stress myocard akibat stimulasi Di duga karena stress myocard akibat stimulasi

symphatetic centralsymphatetic central

Kejang dan StrokeKejang dan Stroke

1.1. Frekuensi 5-10% dalam 2 minggu Frekuensi 5-10% dalam 2 minggu pertama. Resiko paling tinggi pada pertama. Resiko paling tinggi pada perdarahan intracerebral lobar/kortikalperdarahan intracerebral lobar/kortikal

2.2. Daerah lainnya:Daerah lainnya:• Stroke di daerah teritori karotisStroke di daerah teritori karotis• Stroke yang luas dengan defisit neurologik Stroke yang luas dengan defisit neurologik

yang menetapyang menetap(Olsen et al 1987, Giroud et al 1994, Killpatrick et al 1990)(Olsen et al 1987, Giroud et al 1994, Killpatrick et al 1990)

Neurological PathologyNeurological Pathology NeurovascularNeurovascular

Thrombo - emboli ischemic StrokeThrombo - emboli ischemic StrokeVascular malformationsVascular malformationsHemorrhagic states resulting from the aboveHemorrhagic states resulting from the above

TumorTumorPrimaryPrimaryMetastaticMetastatic

CTN infectionCTN infectionAbscesAbscesMeningitisMeningitisEncephalitisEncephalitis

Inflammtory diseaseInflammtory diseaseVasculitisVasculitis

Acute disseminated encephalomyelitisAcute disseminated encephalomyelitis TraumaTrauma

ContusionContusionHemorragheHemorraghe

Primary epilepsyPrimary epilepsy Primary inherited CNS metabolic disturbancePrimary inherited CNS metabolic disturbance

Risk factor for recurrenceRisk factor for recurrence after an initial seizure after an initial seizure

GreaterGreater LessLess

ChildrenChildren AdultAdult

Abnormal EEG, esp.epileptiform Abnormal EEG, esp.epileptiform featuresfeatures

Normal EEGNormal EEG

Symptomatic causeSymptomatic cause Cryptogenic seizuresCryptogenic seizures

Focal onset with secondary Focal onset with secondary generalizationgeneralization

Seizure occuring during sleepSeizure occuring during sleep

COMMON PRESENTATION OF SEIZURES IN COMMON PRESENTATION OF SEIZURES IN THE ICUTHE ICU

SEIZURE TYPESEIZURE TYPE CLINICAL EXPRESSIONCLINICAL EXPRESSION

Fokal motorFokal motor Face or limb motor seizure, may propagate Face or limb motor seizure, may propagate from distal to proximal, no alteration of from distal to proximal, no alteration of sensoriumsensorium

Generalized Tonic ClonicGeneralized Tonic Clonic Loss of consciouness, generalized Loss of consciouness, generalized convulsions with tonic phase followed by convulsions with tonic phase followed by clonic phase and post-ictal altered sensor clonic phase and post-ictal altered sensor sensoriumsensorium

Complex PartialComplex Partial Disturbed sensorium (aura), can br followed Disturbed sensorium (aura), can br followed by generalized tonic-clonic seizureby generalized tonic-clonic seizure

Non-Consultive StatusNon-Consultive Status Disturbed sensorium or loss of Disturbed sensorium or loss of consciousness, minimal face or distal limb consciousness, minimal face or distal limb twitchestwitches

Proposed Duration of Status EpilepticusProposed Duration of Status Epilepticus

19831983 30 minutes - EFA Working Group on 30 minutes - EFA Working Group on SESE

19911991 20 minutes - Bleck20 minutes - Bleck

10 minutes - Treiman et al10 minutes - Treiman et al

1998 5 minutes - Lowenstein1998 5 minutes - Lowenstein

1.1. Brief single seizures (<60 scc)Brief single seizures (<60 scc) Observer Ensure adequate O2 saturation and vital signs. Eliminate Observer Ensure adequate O2 saturation and vital signs. Eliminate

etiology.etiology. Consider chronic therapy : phenytoin 15-20mg / kg or Consider chronic therapy : phenytoin 15-20mg / kg or

fosphenytoin15-20 mg/kg phenytoin equivalents (PE) loading dose fosphenytoin15-20 mg/kg phenytoin equivalents (PE) loading dose and 300-400 mg/day. Goal serum level 10-20 mcg/ml or free level 1-2 and 300-400 mg/day. Goal serum level 10-20 mcg/ml or free level 1-2 mcg/ml.mcg/ml.

Phenytoin intolerant patients: IV/PO valproic acid, 15-20 mg/kg load, Phenytoin intolerant patients: IV/PO valproic acid, 15-20 mg/kg load, maintenance 600-3000 mg/day or PO carbamezapine 600-1200 maintenance 600-3000 mg/day or PO carbamezapine 600-1200 mg/day.mg/day.

Seizure precautions - padding bed rails, increased observation.Seizure precautions - padding bed rails, increased observation.2.2. Prolonged or > 1 seizureProlonged or > 1 seizure

Ensure adequate oxygen saturation, vital signsEnsure adequate oxygen saturation, vital signs IV benzodiazepine - lorazepam 1-2 mg, diazepam 10-20 mg or IV benzodiazepine - lorazepam 1-2 mg, diazepam 10-20 mg or

midazolam 2-5 mg with concurrent loading dose phenytoin or midazolam 2-5 mg with concurrent loading dose phenytoin or fosphenytoin (PE) 15-20 mg/kg and maintenance as above.fosphenytoin (PE) 15-20 mg/kg and maintenance as above.

Phenytoin intolerant : Valproic acid 15-20 mg/kg, maintenance 400-Phenytoin intolerant : Valproic acid 15-20 mg/kg, maintenance 400-600 mg q6hr600 mg q6hr

Similar seizure precautions.Similar seizure precautions.

TREATMENT OF ICU SEIZURESTREATMENT OF ICU SEIZURES

TREATMENT OF ICU SEIZURESTREATMENT OF ICU SEIZURES3.3. Recurrent or refractory seizures > 5 min 0r > 2 discrete seizures Recurrent or refractory seizures > 5 min 0r > 2 discrete seizures

without recovery of coenynsciousnesswithout recovery of coenynsciousness

Consider as status epilepticusConsider as status epilepticus Maintain airway, preserve ventilation and oxygenation, endotracheal Maintain airway, preserve ventilation and oxygenation, endotracheal

intubation if indicated to protect airway.intubation if indicated to protect airway. Measure blood glucose. IV glucose only if less 10-60 mg/100 dl.Measure blood glucose. IV glucose only if less 10-60 mg/100 dl. Immediate benzodiazepines-IV, lorazepam 5-10mg, diazepam 20-40 mg, or Immediate benzodiazepines-IV, lorazepam 5-10mg, diazepam 20-40 mg, or

midazolam 5-20 mg over 5 min.midazolam 5-20 mg over 5 min. Phenytoin loading dose 20 mg/kg at 50 mg/min or fosphenytoin 20 mg/kg Phenytoin loading dose 20 mg/kg at 50 mg/min or fosphenytoin 20 mg/kg

PE at 150 mg/min.PE at 150 mg/min. Continuous EEG, if available.Continuous EEG, if available. If Seizures continue phenytoin or fosphenytoin (additional 5-10mg/Kg or 5-If Seizures continue phenytoin or fosphenytoin (additional 5-10mg/Kg or 5-

10mg/Kg PE)10mg/Kg PE) If seizures continue : pharmacological EEG seizures supression, burst If seizures continue : pharmacological EEG seizures supression, burst

supression if necessary- profapol 2 mg/Kg and 150-200mcg/Kg/min supression if necessary- profapol 2 mg/Kg and 150-200mcg/Kg/min infusion or thiopental 4 mg/Kg and 0,3-0,4 mg/Kg/mininfusion or thiopental 4 mg/Kg and 0,3-0,4 mg/Kg/min

Hemodynamic support : fluids, pressors, inotropesHemodynamic support : fluids, pressors, inotropes Once EEG supressed, complete loading of anticonvulsant, add aditional Once EEG supressed, complete loading of anticonvulsant, add aditional

benzodiazepine if necessary, and consider wearing infusion agent several benzodiazepine if necessary, and consider wearing infusion agent several hrs after optimal anticonvulsant levels obtained through serum levels hrs after optimal anticonvulsant levels obtained through serum levels measurementmeasurement

If seizures persist, consider prolonged barbiturate or anesthetic coma with If seizures persist, consider prolonged barbiturate or anesthetic coma with pentobarbital 12 mg/Kg at 0,2-0,1 mg/Kg/min followed by an infusion of pentobarbital 12 mg/Kg at 0,2-0,1 mg/Kg/min followed by an infusion of 0,25-2,0 mg/Kg/hr for continued EEG supression 0,25-2,0 mg/Kg/hr for continued EEG supression

THROMBOE STRMBOLISME PADA STROKETHROMBOE STRMBOLISME PADA STROKE

Bentuk Klinik :Bentuk Klinik :A.A. Thrombosis vena dalamThrombosis vena dalamB.B. Emboli pulmunalEmboli pulmunal Frekuensi terjadi pada 10-20% kasus stroke akut, penyebab 5-Frekuensi terjadi pada 10-20% kasus stroke akut, penyebab 5-

10% kematian (kelly, 2001)10% kematian (kelly, 2001) Faktor penting lain : Hypertensi, Obesitas, dan merokokFaktor penting lain : Hypertensi, Obesitas, dan merokok Resiko tinggi pada stroke dengan imobilitas berat.Resiko tinggi pada stroke dengan imobilitas berat. Diagnosa dengan :Diagnosa dengan :

1. CT Scan paru dengan spiral CT1. CT Scan paru dengan spiral CT2. Pemeriksaan baku emas : Angiografi pulmoner2. Pemeriksaan baku emas : Angiografi pulmoner

Pengobatan dengan Pengobatan dengan 1. Heparin 5000 unit 2x sehari selama 1-2 minggu1. Heparin 5000 unit 2x sehari selama 1-2 minggu

Dilanjutkan dengan oral anti kuagulan selama 6 bulan.Dilanjutkan dengan oral anti kuagulan selama 6 bulan.2. Low moleculer weight heparin diberikan beberapa minggu 2. Low moleculer weight heparin diberikan beberapa minggu kemudian di teruskan dengan oral anti kuagulan selam 6 bulan.kemudian di teruskan dengan oral anti kuagulan selam 6 bulan.

Medical Treatment for CentralMedical Treatment for Central Poststroke Pain Poststroke Pain

First-lineFirst-line AmitriptylineAmitriptyline LamotrigineLamotrigine

Alternative and adjunctive optionsAlternative and adjunctive options Lidocaine, intravenousLidocaine, intravenous Other tricyclic antidepressants : nortriptyline, desipramine, Other tricyclic antidepressants : nortriptyline, desipramine,

maprotilinemaprotiline Other anticonvulsants valproate, Other anticonvulsants valproate, carbamazepinecarbamazepine, , phenytoinphenytoin MexiletineMexiletine NaloxoneNaloxone BaclofenBaclofenSupported by controlled clinical trials dataSupported by controlled clinical trials data

Factors Contributing to Poststroke Factors Contributing to Poststroke Urinary IncontinenceUrinary Incontinence

Premorbid conditionsPremorbid conditionsa)a) Peripheral neuropathy (eg, diabetic Peripheral neuropathy (eg, diabetic

dysautonomia)dysautonomia)

b)b) Changes in the urinary tract (eg, prostatic Changes in the urinary tract (eg, prostatic hypertrophy)hypertrophy)

c)c) Medications : anticholinergic drugs Medications : anticholinergic drugs (precipitate retention), alpha-adrenergic (precipitate retention), alpha-adrenergic blockers (worsen urethral sphincter blockers (worsen urethral sphincter weakness), diuretics (detrusor contraction weakness), diuretics (detrusor contraction by causing rapid bladder filling)by causing rapid bladder filling)

Acute Stroke-related dificitsAcute Stroke-related dificits

a)a) Impairment of neurologic micturition Impairment of neurologic micturition control mechanism, causing a control mechanism, causing a hyperreflexic bladderhyperreflexic bladder

b)b) Acute bladder hypotonia at the time of Acute bladder hypotonia at the time of strokestroke

c)c) Lapse in diabetic control, leading to Lapse in diabetic control, leading to glycosuriaglycosuria

Depression After StrokeDepression After Stroke Symptoms :Symptoms :

Sadness, anxiety, tension, less of interest, sleep disturbance Sadness, anxiety, tension, less of interest, sleep disturbance with early morning awakening , apetite and weight loss, difficulty with early morning awakening , apetite and weight loss, difficulty in concentrating and thingking, and thoughts of death (at least 5 in concentrating and thingking, and thoughts of death (at least 5 symptoms should be present)symptoms should be present)

Frequency :Frequency : 40-50% acute stroke patients sufferd from major depression 40-50% acute stroke patients sufferd from major depression

(burville et al, 1995)(burville et al, 1995) Major post stroke depression is asociated with left cortical lesion Major post stroke depression is asociated with left cortical lesion

(mainly frontal) and sub cortical lesion (mainly basal ganglia)(mainly frontal) and sub cortical lesion (mainly basal ganglia) Management : Management :

Treatment with anti depression :Treatment with anti depression : Nortrityline (Lipse et al, 1984)Nortrityline (Lipse et al, 1984) Fluoexetine (Robinson et al 2000)Fluoexetine (Robinson et al 2000) Trazodon (Reading et al, 1986)Trazodon (Reading et al, 1986)

Peripheral Neuropathies in Stroke Peripheral Neuropathies in Stroke PatientsPatients

Peroneal neuropathyPeroneal neuropathyUlnar neuropathyUlnar neuropathyMedian neuropathyMedian neuropathyFemoral neuropathyFemoral neuropathyConcomitant Concomitant diabetic neuropathydiabetic neuropathy