داکتر محمد صمیم سردار M.Samim sardar

داکتر محمد صمیم سردار M.Samim sardar Dr.Mohammad Samim Sardar
Neurosurgical specialist
جراح مغز و اعصاب و استاد پوهنتون

Brief information about chiari malformation...
30/12/2025

Brief information about chiari malformation...

Low back pain Radiating to left and right legs L4/5 and L5/S1 disc prolapse L4/L5 right side fenestraion and discectomy ...
29/12/2025

Low back pain
Radiating to left and right legs
L4/5 and L5/S1 disc prolapse
L4/L5 right side fenestraion and discectomy
L5/S1 left side fenestration and discectomy

Dr. Mohammad Samim Sardar
MD
Neurosurgeon

قشر دماغ با هستولوژی،وظایف و ارتباطات آن.....
28/12/2025

قشر دماغ با هستولوژی،وظایف و ارتباطات آن.....

انواع شخصیتی ....
25/12/2025

انواع شخصیتی ....

Radiculopathy Myelopathy Myopathy
22/12/2025

Radiculopathy
Myelopathy
Myopathy

موژ په یوه داسی تولنه کی ژوند کوو چی دیر زیات مشکلات پکی ده خصوصا تعلیمی سویه کشته ده. که ناروغ ته ووایو چی شکری ناروغی ...
17/12/2025

موژ په یوه داسی تولنه کی ژوند کوو چی دیر زیات مشکلات پکی ده خصوصا تعلیمی سویه کشته ده.
که ناروغ ته ووایو چی شکری ناروغی لری نو بیا د مرچو په خوراک پیل کوی داسی فکر کوی چی مرچکی شکر ختموی او که ورته وویل شی چی ستا پر ملا فشار راغلی او هدوکی د سره نژدی شوی بیا د پخو او لاسو حان کشوی.
نو پخپل فکر زان تداوی کوی .
پرته له دی چی مشوره وکری یا د مربوط بخش متخصص ته مراجعه وکری پخپل سر علاج شروع کوی چی کله کله دا پخپل سری کارونه سره له دی چی فایده نلری د ناروغ مشکلات نور هم ور زیاتوی
هیله مو داده چی اول باید داکتر ته مراجعه وکری د هر بخش لپاره خپل متخصص وی بیا د هغی د مشوری سره سم خپل تداوی پیل کری آن شاالله چی شه پایله به ولری .

Intraventricular Hemorrhage in the NeuroICU: VI. Medical ManagementAcute Stabilization (First Hour)Airway Protection: GC...
11/12/2025

Intraventricular Hemorrhage in the NeuroICU:

VI. Medical Management
Acute Stabilization (First Hour)

Airway Protection: GCS ≤8 → intubation with neuroprotective agents (etomidate, fentanyl)
Blood Pressure Management:
ICH Guidelines: Target SBP 140-160 mmHg
IVH Specific: More aggressive control may be needed (SBP 120-140) to prevent expansion
Agents: Nicardipine drip (first-line), labetalol, clevidipine
Avoid precipitous drops >25% in first 24 hours
Coagulation Reversal (Immediate):
Warfarin: 4-factor PCC (25-50 IU/kg) + IV vitamin K
DOACs: Andexanet alfa (apixaban/rivaroxaban) or PCC
Heparin: Protamine sulfate
Platelets: Maintain >100,000 for procedural safety

ICP and Hydrocephalus Management
EVD Strategy:
Early Placement: Modified Graeb ≥5 or any IVH with hydrocephalus
Drainage Protocol: Intermittent vs continuous drainage
Weaning: Begin when CT shows resolving blood, CSF clears (5-7 days)
Intraventricular Thrombolytics (see Section VII)
Medical Adjuncts:
Acetazolamide: 500 mg IV q8h for communicating hydrocephalus
Mannitol/Hypertonic Saline: For transtentorial herniation
CSF Production Suppression: Omeprazole, furosemide

Neuroprotection and Secondary Prevention
Temperature Control: Strict normothermia (36-37.5°C), avoid fever
Glycemic Control: Target 140-180 mg/dL

Seizure Prophylaxis:
Levetiracetam: 20 mg/kg load, then 500-1000 mg BID
Duration: 7 days for lobar hemorrhage, 30 days if cortical involvement

Venous Thromboembolism Prevention:
SCDs immediately, chemical prophylaxis at 24-48 hours if stable
Nutrition: Early enteral feeding, avoid overfeeding (target 25 kcal/kg)

VII. Intraventricular Thrombolysis (IVT)
Evidence Base
CLEAR III Trial: Largest RCT (n=500)
Protocol: 1 mg alteplase q8h via EVD until clot clearance

Result: No mortality benefit but improved functional outcomes in moderate IVH
Subgroup benefit if clot reduction >80%
Modified Protocols:
Accelerated lysis: 1-2 mg tPA q6-8h
Low-dose: 0.3-0.5 mg tPA for milder IVH
Combined with lumbar drainage: For communicating hydrocephalus
Current Indications
Primary IVH with Graeb score ≥6
Obstructive hydrocephalus not resolving with EVD alone
Fourth ventricular casts with obstructive hydrocephalus
Young patients with large IVH burden

Contraindications
Absolute: Unsecured aneurysm/AVM, coagulopathy, platelets 30 mL), brainstem compression

Technique
"Clot Lysis Irrigation" Protocol:
Clamp EVD, instill 1 mg tPA in 3 mL saline
Clamp 60 minutes
Unclamp to drain, repeat q8h
Monitor: Daily CT, fibrinogen levels, neurological exam
"Dose-to-Clear" Approach:
Continue lysis until third/fourth ventricle cleared
Average: 4-8 doses over 2-3 days

VIII. Surgical Interventions
Endoscopic Evacuation
Techniques:
Neuroendoscopic Washout: Rigid scope, irrigation/suction
Endoscopic Third Ventriculostomy: For obstructive hydrocephalus
Combined Approaches: Evacuation + ETV
Evidence: Multiple small series show faster clot clearance, reduced EVD duration

Timing: Early (24-72 hours) for maximal benefit
Candidates: Young patients, primary IVH, failed IVT
Minimally Invasive Surgery
Stereotactic Aspiration: For localized clots (occipital horn)
IR-guided Aspiration: Combined with thrombolytics
Neuroendoscopic-Assisted Evacuation: Real-time visualization
Decompressive Craniectomy
Indications: Massive IVH with parenchymal component >60 mL, refractory ICP
Timing: Early (1000, glucose 1 month)
Chronic Hydrocephalus: NPH syndrome (gait, cognition, incontinence)
Post-Hemorrhagic Ventricular Slit: Decreased compliance
Cognitive Impairment: Executive dysfunction, memory deficits
Endocrine Dysfunction: Hypothalamic-pituitary injury
X. Prognostication and Outcomes
Predictors of Poor Outcome
Clinical:
Age >75 years
GCS ≤8 on admission
Absent pupillary reflexes
Medical comorbidities (CAD, CKD, diabetes)

Radiographic:
Modified Graeb score ≥8
Fourth ventricular involvement
Concurrent parenchymal hemorrhage >30 mL
Midline shift >5 mm
Physiologic:
Refractory ICP >25 mmHg
PbtO₂ 2 hours
Malignant EEG patterns (burst suppression, periodic discharges)
Functional Outcomes
Mortality: 30-50% overall, 80% if Graeb ≥10
Good Recovery (mRS 0-2): 15-25% with aggressive management
Severe Disability (mRS 4-5): 30-40%
Long-Term Shunt Dependence: 30-50%
Prognostic Scales
IVH Score (0-3): Simple bedside tool
FUNC Score: Predicts functional independence
ICH Score Modified for IVH: Adds ventricular extension
XI. Special Populations
Neonatal IVH
Grading (Papile): I-IV based on location and severity
Unique Considerations: Germinal matrix hemorrhage in preterm infants
Management: Serial LPs, ventricular reservoir, eventual shunt
Traumatic IVH
Usually from shearing forces or extension
Correlates with diffuse axonal injury
Monitor for evolving contusions
Anticoagulant-Associated IVH
Higher expansion rates
Aggressive reversal critical
Consider delayed angiography if etiology unclear

XII. Neurorehabilitation and Recovery
Acute Rehabilitation
Begin in ICU: Physical/occupational therapy, speech evaluation
Screen for dysphagia: 40-60% incidence
Early mobilization protocols
Cognitive Rehabilitation
Frontal/Executive Dysfunction: Common with frontal horn involvement
Memory Impairment: Fornix/hippocampal circuit disruption
Behavioral Changes: Disinhibition, apathy
Ventriculoperitoneal Shunt Management
Shunt Malfunction Signs: Headache, nausea, decreased consciousness
Shunt Infection: Usually within 6 months
Overdrainage: Slit ventricle syndrome, hygromas

XIII. Future Directions and Research
Emerging Therapies
Intraventricular Neuroprotective Agents:
Erythropoietin, N-acetylcysteine
Iron chelators (deferoxamine)
Advanced Clearance Techniques:
Automated irrigation systems
Ultrasound-enhanced thrombolysis
Biomarker-Guided Therapy:
CSF inflammatory markers (IL-6, MMP-9)
Microdialysis-guided management
Clinical Trials Needed
Optimal thrombolytic dose and timing
Endoscopic vs medical management trials
Neuroprotective agent trials
Shunt vs no shunt in chronic hydrocephalus

XIV. Summary and Key Practice Points
IVH is treatable: Aggressive modern management improves outcomes
EVD is first-line: Place early for hydrocephalus or Graeb ≥5
Consider thrombolytics: For significant IVH burden, especially in younger patients
Search for etiology: All non-hypertensive IVH needs vascular imaging
Multimodality monitoring: Guides therapy in severe cases
Anticipate complications: Hydrocephalus, infection, delayed deterioration
Rehabilitation is crucial: Begin early, address cognitive deficits....

Dr Mohammad Samim Sardar
Neurosurgeon

Neurodynamic test for brachial plexus injury
10/12/2025

Neurodynamic test for brachial plexus injury

01/12/2025
clear comparison of *Spinal Shock*, *Neurogenic Shock*, and *Autonomic Dysreflexia*:---*1. Spinal Shock*- *Definition:* ...
23/11/2025

clear comparison of *Spinal Shock*, *Neurogenic Shock*, and *Autonomic Dysreflexia*:

---

*1. Spinal Shock*
- *Definition:* Temporary loss of all spinal cord functions (motor, sensory, reflexes, autonomic) below the level of injury.
- *Cause:* Acute spinal cord injury (usually traumatic).
- *Duration:* Hours to weeks (until reflexes return).
- *Symptoms:*
- Flaccid paralysis
- Areflexia (absent reflexes)
- Loss of sensation
- Hypotension and bradycardia (if high level)
- *Key point:* It's a *physiological response* to cord injury, not true shock.

---

*2. Neurogenic Shock*
- *Definition:* A type of distributive shock due to *disruption of sympathetic pathways* in high spinal cord injuries (above T6).
- *Cause:* High spinal cord injury or spinal anesthesia.
- *Symptoms:*
- *Hypotension* (due to vasodilation)
- *Bradycardia* (due to unopposed vagal tone)
- Warm, dry skin
- *Key point:* True shock with hemodynamic compromise due to loss of sympathetic tone.

---

*3. Autonomic Dysreflexia*
- *Definition:* A potentially life-threatening condition of *uncontrolled sympathetic discharge* in response to stimuli below the injury level in patients with spinal cord injury *above T6*.
- *Trigger:* Bladder distension, f***l impaction, skin irritation, etc.

- *Symptoms:*
- Severe *hypertension*
- *Bradycardia*
- Sweating, flushing above lesion
- Headache, blurred vision
- *Management:* Remove stimulus immediately, lower BP.

داکتر محمد صمیم سردار M.Samim sardar
متخصص جراحی اعصاب و ستون فقرات

سو اشکال ولادی (نقایص مادرزادی)  سیستم عصبی شامل اختلالاتی است که در دوران جنینی در نتیجه مشکلات رشد لوله عصبی یا سایر  ...
17/11/2025

سو اشکال ولادی (نقایص مادرزادی) سیستم عصبی شامل اختلالاتی است که در دوران جنینی در نتیجه مشکلات رشد لوله عصبی یا سایر ساختارهای مغز و نخاع به‌وجود می‌آیند. مهم‌ترین آن‌ها عبارتند از

1. *آننسفالی (Anencephaly)*
- فقدان قسمت‌های بزرگ مغز، جمجمه و پوست سر
- ناسازگار با حیات

2. *اسپینا بیفیدا (Spina Bifida)*
- نقص در بسته شدن لوله عصبی در ناحیه خلفی
- انواع:
- *Spina bifida occulta* (خفیف‌ترین، بدون علامت)
- *Meningocele* (بیرون‌زدگی مننژ)
- *Myelomeningocele* (بیرون‌زدگی نخاع + مننژ، شدیدترین)

3. *انسفالوسیل(Encephalocele)*
- بیرون‌زدگی بافت مغز و مننژها از طریق نقص در جمجمه

4. *هولونسفالی (Holoprosencephaly)*
- نقص در تقسیم نیم‌کره‌های مغزی
- مرتبط با ناهنجاری‌های صورت (مانند سیکلوپیا)

5. *Hydranencephaly*
- جایگزینی مغز با مایع مغزی‌نخاعی

6. *میکروسفالی (Microcephaly)*
- کوچکی غیر طبیعی جمجمه و مغز

7. *ماکروسفالی (Macrocephaly)*
- بزرگی غیر طبیعی سر (مثلاً در هیدروسفالی)

8. *Chiari Malformation*
- نزول ساختارهای مغزی به داخل فورامن مگنوم

9. *Dandy-Walker Malformation*
- ناهنجاری مخچه و چهارمین بطن مغزی

این اختلالات می‌توانند خفیف تا بسیار شدید و تهدیدکننده حیات باشند. تشخیص بیشتر آن‌ها از طریق *سونوگرافی دوران بارداری*، *MRI یا CT* پس از تولد انجام می‌شود

داکتر محمد صمیم سردار M.Samim sardar
متخصص جراحی اعصاب و ستون فقرات

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Kabul

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+93783147774

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