MSC Neuro 25 p2

Brachial plexopathy causes paralysis and sensory loss in the shoulder and arm depending on which part of the plexus is affected. Early diagnosis and supportive treatment with physical therapy and vitamins is essential. Surgery is considered for severe or persistent cases to restore nerve function.

This condition is common after trauma or surgery around the shoulder and requires a careful multidisciplinary approach.

28. Vertebrogenic radiculopathy S1 and L5. Pathogenesis, clinic, treatment.

Vertebrogenic Radiculopathy S1 and L5: Summary for Medical Students

Pathogenesis

Radiculopathy is caused by irritation or compression of spinal nerve roots, often due to degenerative spine changes (osteochondrosis).

The gelatinous nucleus of the intervertebral disc loses water and becomes brittle.

Fibrous ring weakens, cracks, and herniation occurs as disc material protrudes posteriorly.

Herniated discs or bone spurs compress nerve roots at lumbar levels, mainly L4-5 (affecting L5 root) and L5-S1 (affecting S1 root).

Autoimmune factors contribute to osteochondrosis progression.

Clinical Features

L5 Radiculopathy (5th lumbar nerve root):

Sharp, shooting pain from upper buttock, lateral thigh, outer lower leg to dorsum of foot.

Numbness and tingling (paresthesia) in the same area.

Weakness and atrophy of toe extensor muscles, difficulty lifting big toe.

Decreased sensation on back of foot and lateral lower leg.

Achilles reflex is preserved.

S1 Radiculopathy (1st sacral nerve root):

Pain in posterior buttock, back of thigh and calf, outer foot edge, heel, and little toe.

Weakness and atrophy of calf muscles; difficulty plantar flexing foot/toes.

Reduced or absentAchilles reflex.

Antalgic posture: patient lies with leg bent outward and half-flexed when walking, walking on toes.

Physical Signs

Painful valgus scoliosis (spinal curvature away from pain).

Tenderness over spinous processes of L4, L5, S1.

Positive nerve tension signs (Lasegue's straight leg raise positive, Neri's sign, Dejerine's triad).

Tenderness at specific Valle points along sciatic nerve.

Treatment

Acute Phase

Rest, analgesics, and anti-inflammatory drugs.

Bed rest on a firm board.

Antihistamines and diuretics to reduce swelling.

Vitamins (B and C), nicotinic acid, and antioxidants (thioctic acid).

Topical treatments (snake or bee venom ointments, Fastum-gel, Finalgon).

Physiotherapy: diadynamic therapy, electrophoresis with analgesics, UV radiation.

Nerve blocks (epidural, intramuscular) with hydrocortisone or novocaine to relieve pain.

Chronic Phase

Manual therapy and spinal traction.

Exercise therapy to strengthen muscles.

Spa therapy and rehabilitation.

Psychotropic drugs such as antidepressants for persistent pain.

Surgical decompression if conservative treatment fails or if there is disc prolapse with pelvic dysfunction.

29.Lumbar osteochondrosis. Reflex and compression syndromes.

Lumbar Osteochondrosis: Reflex and Compression Syndromes

Lumbar osteochondrosis is a degenerative condition affecting the lower back, characterized by wear and tear of the intervertebral discs.

Pathogenesis

Degenerative disorder of intervertebral discs and adjacent vertebrae.

Gelatinous nucleus in discs loses water content, becomes brittle.

Fibrous ring of disc develops cracks, tears, and loses elasticity.

Intervertebral disc height decreases, increasing load on vertebral joints.

Fragments of nucleus pulposus may herniate and compress nerve roots.

Autoimmune processes contribute to degeneration and inflammation.

Compression or inflammation of nerve roots causes radicular symptoms.

Clinical Presentation

Lumbago (Lumbar Backache)

Acute sharp pain due to fissures in fibrous ring.

Antalgic posture with forward bending.

Local lumbar pain worsened by sitting, standing, twisting.

Muscle spasm or myotonic defense around spine.

Lumbago attacks resolve in days; chronic pain called lumbalgia. Radicular Syndrome (Radiatic Syndrome)

Radicular pain radiating in narrow band along affected nerve root.

L4 nerve root: pain inner thigh and leg.

L5 nerve root: pain outer thigh and leg, dorsum of foot.

S1 nerve root: pain posterior leg and lateral foot.

Sensory disturbances like hypoesthesia in root distribution.

Peripheral paresis of associated muscles:

L4: weakness in anterior tibial group, foot drop, "cock's gait".

S1: weakness in calf muscles, difficulty walking on toes, decreasedAchilles reflex.

Autonomic symptoms: decreased skin temperature, dry skin, reduced sweat, altered skin resistance.

Spinal Syndrome

Deviation of body away from pain to widen vertebral spacing.

Loss of lumbar lordosis.

Muscle guarding.

Pain worsened by spinal flexion and sitting; eased by lying on unaffected side.

Positive tension signs: Neri's (neck flexion causing lumbar pain), Lasègue's test (straight leg raise pain), Dejerine's signs (increased pain on coughing, sneezing).

Medial Disc Herniation

Disc herniates medially affecting cauda equina.

Severe low back pain radiating to both legs.

Numbness in legs and perineum.

Peripheral paralysis of leg muscles and pelvic dysfunction causing incontinence.

Requires urgent surgery within hours to days.

Treatment

Acute Stage:

Bed rest on firm surface, limited activity.

Analgesics and anti-inflammatory drugs.

Antihistamines, diuretics to reduce edema.

Vitamins B and C, nicotinic acid, thioctic acid for nerve support.

Physiotherapy: diadynamic currents, analgesic electrophoresis, UV therapy.

Nerve root blocks with hydrocortisone or novocaine for pain control. Chronic Stage:

Manual therapy and spinal traction.

Therapeutic exercises to strengthen and improve flexibility.

Spa and rehabilitation treatments.

Psychotropic drugs like antidepressants for chronic pain.

Surgery if no improvement or worsening neurological symptoms appear, especially with disc prolapse and pelvic dysfunction.

Lumbar osteochondrosis causes back pain and nerve root compression symptoms (radiculopathy). Treatment is usually conservative but surgery is indicated for severe complications.

30. Principles of conservative treatment of osteochondrosis of the spine. Indications for surgical treatment of osteochondrosis of the spine.

Conservative Treatment Principles for Spinal Osteochondrosis

Orthopedic Treatment

Skeletal traction: Helps decompress the spine and reduce nerve root irritation.

Underwater traction: Patient lies on a board in a warm bath with traction applied to the legs.

Corsets and belts: Provide external support and limit excessive movement, stabilizing the spine.

Manual therapy: Includes spinal manipulation and mobilization to relieve muscle spasm and improve mobility.

Medical Therapy

1.Fight swelling: Use diuretics and anti-inflammatory agents to reduce edema around nerve roots.

2.Antispasmodics: To relieve muscle spasms and myotonia.

3.Analgesics: For pain relief.

4.Non-steroidal anti-inflammatory drugs (NSAIDs): To reduce inflammation and pain.

5.Muscle relaxants: To ease muscle tension.

6.Chondroprotectors: Supplements thought to help cartilage repair and regeneration.

7.Vitamins and biostimulants: Especially B vitamins and antioxidants to promote nerve health and recovery.

Physical Methods of Treatment

Iontophoresis, diadynamophoresis, amplipulse therapy: Electrical stimulation techniques to reduce pain and inflammation.

Galvanic mud applications: For anti-inflammatory and reparative effects.

Phonophoresis with hydrocortisone: Ultrasound therapy to deliver corticosteroids locally.

Thermal procedures: Paraffin and ozocerite applications for muscle relaxation and pain relief.

Acupuncture and electrical muscle stimulation: To manage pain and improve muscle function.

Indications for Surgical Treatment

Chronic compression of the spinal nerve roots (cauda equina syndrome) lasting 3-6 months without improvement.

Persistent and severe pain syndrome despite conservative care.

Large intervertebral disc herniation (≥15 mm), causing nerve root or spinal cord compression.

Acute compression of radicular-spinal artery causing neurological deficits.

Development of urinary or fecal incontinence indicating severe nerve involvement.

Surgery typically involves decompression of nerve roots by removing herniated disc fragments to relieve pressure and prevent permanent neurological damage.

31. Classification of headaches. The pathogenesis of headache. Examination of patients with headache. Tension headache.

Headache Definition:

Pain or unpleasant sensation located from the eyebrows up to the neck and occipital region. Pain arises from irritation of pain receptors in skin, scalp, periosteum, meninges near vessels, cranial vessels, and sensory cranial nerves.

Pathogenetic Types of Headache

1.Vascular Headache:

Caused by craniocerebral arterial and venous tone abnormalities (arteriodilation, arterial spasm, venous insufficiency).

Arterial dilation causes throbbing pain; arterial spasm results in dull aching and ischemic symptoms.

Venous type causes dull, heavy headaches often worse when lying down.

Examples: migraine, headache with vegetovascular dystonia, hypertensive headaches.

Diagnosed by rheoencephalography (REG) and fundoscopy.

2.Muscle Tension Headache:

Results from tension or spasms in scalp and neck muscles.

Feels like tight band or pressure around the head.

Exacerbated by stress, systemic illnesses, or local conditions (eye or ear disease).

Accompanied by muscle tenderness, irritability, and sensitivity to light/noise.

3.Liquorodynamic Headache:

Caused by abnormal cerebrospinal fluid (CSF) pressure or flow.

High CSF pressure: bursting headache, worse with straining, coughing.

Low CSF pressure: dull headache worsened when upright (“drainage headache” after lumbar puncture).

Diagnosed by imaging and lumbar puncture.

4.Neuralgic Headache:

Paroxysmal, sharp, shooting pains in nerve distribution areas.

Characterized by trigger zones provoking attacks.

Often due to central nociceptive system hyperactivity or nerve compression.

Common in trigeminal neuralgia and occipital neuralgia.

Treated with antiepileptic drugs and local therapies.

5.Psychalgic (Hallucinatory) Headache:

Related to pathological excitation in brain areas processing pain perception.

Often linked to latent depression and psychiatric disorders.

No consistent physical findings; treated with antidepressants and psychiatric care.

6.Mixed Origin Headache:

Combination of different pathogenetic factors, as in migraine or severe brain diseases.

Requires both symptomatic and disease-specific treatment.

Clinical Examination of Headache

Assess headache pattern, duration, location, intensity, and associated symptoms.

Identify trigger factors and neurological signs.

Perform neuroimaging when indicated to rule out secondary causes.

Use diagnostic criteria (e.g., ICHD-3) for accurate classification.

Classification (ICHD-3)

Primary Headaches: Migraine, tension-type headache, cluster headaches, trigeminal autonomic cephalalgias, others.

Secondary Headaches: Due to trauma, vascular disorders, infections, substance use, metabolic or psychiatric causes.

Cranial Neuralgias and Facial Pain: Trigeminal neuralgia, occipital neuralgia, glossopharyngeal neuralgia.

Unclassified Headaches

32.Migraine, cluster headache: pathogenesis, diagnosis, treatment.

Migraine:

Classification

Classical (10%): With aura (warning signs like visual disturbances, hemianopsia, and sensory symptoms before headache)

Atypical (85%): Without aura, more common, longer lasting headaches often starting during sleep or upon awakening; may lead to migraine status

Associated (5%): Migraine with neurological deficits like hemiparesis, cranial nerve palsies, cerebellar symptoms; linked to vascular malformations

Also classified as:

Simple migraine (without aura)

Migraine with aura or complicated forms (may progress to status migrainosus or stroke)

Pathogenesis

Constitutional (often hereditary) predisposition.

Migraine attack has four phases related to vascular and neurological changes:

1.Prodrome: Triggers (stress, hormonal changes, hypoxia) cause vasospasm in cerebral arteries causing aura symptoms.

2.Vasodilation:Arteries and veins dilate, vessel walls stretch causing throbbing pain.

3.Vascular permeability and edema: Biochemical mediators (serotonin, histamine) released causing inflammation and more pain.

4.Resolution: Pain subsides, fatigue and weakness follow.

Complex neurovascular mechanisms with serotonin deficiency and release of vasoactive peptides contribute.