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1. Phantom Limb Pain – Pathophysiological Mechanism
- Peripheral: Neuroma formation at nerve endings causes ectopic discharges.
- Spinal: Central sensitization in the dorsal horn leads to heightened pain response.
- Supraspinal: Cortical reorganization in the somatosensory cortex misinterprets signals.
- Sympathetic: Abnormal sympathetic-somatic coupling contributes to pain.
2. Phantom Limb Pain – Symptoms, Approach, Management and Evaluation
- Symptoms: Burning, tingling, stabbing sensations in the missing limb; worse at night or during stress.
- Approach: Detailed history, pain assessment, exclude other causes.
- Management: Multidisciplinary – includes medication, physiotherapy, psychological support.
- Evaluation: Pain scales (e.g., VAS), response to interventions, functional assessments.
3. Phantom Limb Pain – Treatment and Differential Diagnosis
- Treatment:
• Medications: Antidepressants (amitriptyline), anticonvulsants (gabapentin), opioids.
• Non-drug: Mirror therapy, CBT, TENS.
• Interventional: Nerve blocks, spinal cord stimulation.
- Differential Diagnosis: Residual limb pain, neuroma, infection, CRPS.
4. Migraine – Classification, Etiology, and Triggers
- Classification: Migraine without aura, with aura, chronic migraine, hemiplegic migraine.
- Etiology: Genetic predisposition, abnormal brainstem activation, cortical spreading depression.
- Triggers: Stress, hormonal fluctuations, sleep changes, alcohol, aged cheese.
5. Migraine – Pathophysiological Mechanism
- Initiated by cortical spreading depression (CSD).
- Activation of trigeminovascular system → neuropeptides (CGRP, substance P) → inflammation.
- Sensitization of central pain pathways.
- Hypothalamic dysfunction may initiate attack.
6. Migraine – Positive Diagnosis (including Signs and Symptoms)
- Diagnosis: Based on ICHD-3 criteria.
- Signs and Symptoms:
• Headache: Pulsating, unilateral, aggravated by movement.
• Associated: Nausea, photophobia, phonophobia.
• Aura (if present): Visual, sensory, or language disturbances.
7. Migraine – Treatment
- Acute:
• NSAIDs, triptans, antiemetics.
- Preventive:
• Beta-blockers (propranolol), antiepileptics (topiramate), antidepressants, CGRP inhibitors.
8. Stroke – Etiology
- Ischemic: Thromboembolism, atherosclerosis, atrial fibrillation.
- Hemorrhagic: Hypertension, aneurysm rupture, trauma.
- Less common: Vasculitis, hypercoagulability, dissection.
9. Stroke – Main Types of Stroke and General Signs and Symptoms
- Types: Ischemic, hemorrhagic, transient ischemic attack (TIA).
- Signs/Symptoms: Sudden weakness, speech disturbance, facial droop, vision loss, headache.
10. Ischemic Stroke – Pathophysiology
- Vascular occlusion → reduced cerebral perfusion.
- Energy failure → Na+/K+ pump dysfunction → excitotoxicity.
- Inflammation, oxidative stress, apoptosis follow.
- Ischemic core and penumbra form.
11. Ischemic Stroke – Signs and Symptoms
- Hemiparesis, facial asymmetry, dysarthria, aphasia.
- Visual field deficits, ataxia, neglect (depends on area affected).
- Symptoms are sudden in onset.
12. Ischemic Stroke – Treatment
- Acute:
• IV thrombolysis (tPA) within 4.5 hours.
• Mechanical thrombectomy up to 24 hours (selected cases).
- Secondary prevention: Antiplatelets, statins, anticoagulants (if cardioembolic), risk factor control.
13. IHS – Definition and Classification
- Definition: Syndrome of elevated intracranial pressure without mass lesion or hydrocephalus.
- Classification:
• Acute
• Chronic
• Benign (idiopathic intracranial hypertension)
14. IHS – Pathophysiology
- CSF overproduction or reduced absorption.
- Obstruction of venous outflow.
- Intracranial pressure exceeds brain compliance → symptoms.
15. IHS – Causes, Signs and Symptoms
- Causes: Brain tumor, trauma, venous sinus thrombosis, idiopathic (especially in obese women).
- Symptoms: Headache, vomiting, visual disturbances, papilledema.
- Signs: Sixth nerve palsy, altered consciousness (late).
16. GBS – Definition and Subtypes
- Definition: Acute autoimmune polyneuropathy targeting peripheral nerves.
- Subtypes:
• AIDP (most common in West)
• AMAN, AMSAN (motor/sensory axonal variants)
• Miller Fisher syndrome (ophthalmoplegia, ataxia, areflexia)
17. GBS – Pathophysiology
- Molecular mimicry (often post-infectious) → autoimmune attack on myelin or axons.
- Demyelination and/or axonal degeneration → slowed/blocked conduction.
18. GBS – Risk Factors, Signs and Symptoms
- Risk factors: Recent infection (Campylobacter jejuni, CMV), vaccination, surgery.
- Symptoms: Ascending weakness, paresthesia, areflexia, cranial nerve involvement, respiratory failure.
19. GBS – Positive Diagnosis, Differential Diagnosis and Treatment
- Diagnosis: Clinical + CSF (albuminocytologic dissociation), EMG/NCS.
- Differential: Myasthenia gravis, transverse myelitis, botulism, poliomyelitis.
- Treatment: IVIG or plasmapheresis; supportive care essential.
20. Myasthenia Gravis – Definition, Generalities and Incidence
- Definition: Autoimmune disorder causing fluctuating weakness of voluntary muscles.
- Generalities: Due to antibodies against ACh receptors or MuSK.
- Incidence: ~20/100,000; more common in women under 40 and men over 60.
21. Myasthenia Gravis – Pathophysiology
- Autoantibodies block/destroy acetylcholine receptors at the neuromuscular junction.
- Reduced transmission → muscle weakness and fatigue.
22. Myasthenia Gravis – Positive Diagnosis
- Diagnosis:
• Clinical: Fatigable weakness.
• Antibody testing: Anti-AChR, anti-MuSK.
• EMG: Decremental response.
• Edrophonium (Tensilon) test (historical).
23. The Myasthenic Crisis
- Definition: Acute exacerbation with respiratory muscle weakness → respiratory failure.
- Triggers: Infection, surgery, certain medications (e.g., aminoglycosides).
- Requires ICU care, mechanical ventilation, IVIG or plasmapheresis.
24. Myasthenia Gravis – Treatment
- Symptomatic: Acetylcholinesterase inhibitors (pyridostigmine).
- Immunosuppressive: Corticosteroids, azathioprine.
- Rapid: IVIG or plasmapheresis.
- Surgical: Thymectomy (especially in younger patients).