MSC Neuro 25 p2
.pdf
Physiotherapy and massage to preserve muscle and joint function.
Exercise therapy adapted for nerve pain and muscle weakness.
Additional Therapies
Antioxidants (vitaminsA, E), angioprotectors (pentoxifylline, sulodexide), and membrane protectors (oxymethylethylpyridine succinate as used regionally).
Advanced wound care includes semi-permeable dressings and moist wound healing strategies.
Monitoring and Prevention
Annual neurological assessment.
Education about foot care, risk factors, and the importance of glycemic control.
Early surgical intervention for moderate to severe foot infections or gangrene.
22.Alcoholic neuropathy. Mechanisms of development, Syndromology, course, prognosis, treatment.
Alcoholic neuropathy is a chronic polyneuropathy predominantly seen in patients with longterm alcohol abuse. It involves nerve damage mainly due to direct neurotoxic effects of alcohol and its metabolites, coupled with nutritional deficiencies (especially vitamin B1/thiamine).
Mechanisms of Development
Direct Toxicity: Ethanol and its toxic metabolite acetaldehyde damage peripheral nerves by inducing oxidative stress, mitochondrial dysfunction, and apoptosis in neurons.Acetaldehyde forms harmful protein adducts leading to neuronal injury.
Nutritional Deficiency: Chronic alcoholism impairs absorption and metabolism of thiamine (vitamin B1) and other B vitamins, essential for nerve function and myelin maintenance, causing demyelination and axonal degeneration.
Metabolic and Inflammatory Pathways: Alcohol induces pro-inflammatory cytokines, activates protein kinase C, and stress-related neuroendocrine axes contributing to neuropathic pain and nerve injury.
Dying-backAxonopathy: The neuropathy typically shows distal axonal degeneration ("dying-back") affecting long sensory and motor fibers, starting in feet and hands.
Syndromology (Clinical Features)
Gradual onset of burning pain, numbness, paresthesias predominantly in distal legs.
Muscle cramps, painful spasms especially in lower legs.
Distal sensory loss in a "glove and stocking" distribution.
Tendon reflexes, especiallyAchilles, are diminished or absent.
Muscle wasting and weakness in distal limbs, later proximal involvement possible.
Pain on palpation of muscles and nerve trunks; heightened skin sensitivity to touch.
Autonomic symptoms: pupillary abnormalities, hyperhidrosis of palms and feet, skin color changes, nail dystrophy, peripheral edema, impotence.
Cranial nerve involvement is less common but may occur.
Course and Prognosis
Symptoms often progress slowly but may stabilize.
Nutritional supplementation and alcohol cessation early may halt progression.
Recovery is slow and often incomplete; chronic disability can result.
Severe motor involvement can cause significant disability.
Relapses may worsen symptoms after renewed alcohol intake.
Treatment
Absolute cessation of alcohol intake is crucial.
Nutritional support with high doses of thiamine (vitamin B1) initially parenteral (e.g., 100 mg intramuscularly 2-3 times daily), later oral supplements, along with other B vitamins and folic acid as multivitamins.
Supportive therapies: vitamins C and others, metabolic agents (amyridine, dibazol).
Physiotherapy and rehabilitation to maintain muscle function.
Address complications like muscle cramps with analgesics and muscle relaxants.
For acute alcoholic myopathy (painful muscle weakness and necrosis), emergency management including fluid-electrolyte correction and monitoring for renal failure is needed.
Smoking cessation is also advised to reduce neurological complications related to tobacco use.
23.Trigeminal neuralgia, clinic, treatment.
What is Trigeminal Neuralgia?
Trigeminal neuralgia is a condition causing sudden, very intense, and brief episodes of sharp, electric shock-like facial pain. The pain usually affects one side of the face in the area served by the trigeminal nerve, commonly the middle (maxillary) or lower (mandibular) branches.
Who gets it?
Mostly people over 50 years old
More common in women
Can occur in younger patients, especially with multiple sclerosis
What causes it?
Usually caused by a blood vessel pressing on the trigeminal nerve near its origin in the brainstem.
Sometimes caused by tumors or nerve damage from multiple sclerosis.
This pressure irritates the nerve causing pain signals.
Symptoms
Brief attacks lasting seconds to 2 minutes of very sharp, shooting pain.
Pain is one-sided and does not cross to the other side.
Attacks can be triggered by everyday activities like talking, chewing, brushing teeth, washing face, or even wind.
Patients might stop moving or freeze during a pain attack to avoid worsening pain.
There may be twitching or spasms of facial muscles on the painful side (called "tic douloureux").
No pain between attacks.
Diagnosis
Mostly clinical based on characteristic pain history.
Neurological exam to localize affected branches and exclude other causes.
MRI/MRAto identify neurovascular compression, MS plaques, or tumors.
Rule out other facial pain syndromes like cluster headaches, postherpetic neuralgia, TMJ disorders.
Treatment
Medical
First-line treatment: carbamazepine, effective in ~90%, dose individualized (400-1200 mg/day). Side effects include dizziness, drowsiness, nausea, blood dyscrasias.
Alternatives: oxcarbazepine (similar efficacy, better tolerated), lamotrigine, baclofen, gabapentin, phenytoin, topiramate.
Muscle relaxants like baclofen can be adjunctive.
Botulinum toxin (Botox) injections may reduce pain in refractory cases (more research needed).
Surgical (for medically refractory cases)
Microvascular decompression: relieves nerve compression by vascular loop; highly effective.
Other procedures include radiofrequency ablation, gamma knife radiosurgery, glycerol rhizotomy.
Trigeminal neuralgia presents with very characteristic brief, intense facial pain episodes mostly triggered by minor stimuli, with medical treatment mainly involving antiepileptic drugs and surgery reserved for refractory cases.
24.Acute facial neuropathy. Etiology, pathogenesis, clinic, course, care.
Acute Facial Neuropathy (Bell's palsy)
What is it?
Acute inflammation of the facial nerve (7th cranial nerve) causing sudden weakness or paralysis of one side of the face.
Also called Bell’s palsy, named after the scientist who first described it.
Can affect one nerve (mononeuritis) or multiple facial nerves (polyneuritis).
Causes (Etiology)
Most common causes include:
Ear infections (otitis) due to proximity of nerve
Dental infections or injuries
Pregnancy and childbirth stress
Emotional stress, exhaustion, hypothermia
Diabetes and tumors
Immune system weakening, intoxications
Facial injuries and ischemic diseases
Viral infections (herpes simplex virus often implicated)
How it develops (Pathogenesis)
Inflammation causes swelling and compression of the facial nerve in its bony canal.
This leads to disrupted nerve signal transmission, causing muscle weakness and paralysis.
Sometimes autoimmune processes and vascular changes contribute.
Symptoms (Clinical Features)
Sudden sharp pain and headaches near the ear or face initially.
Drooping of one side of the face – inability to close eyelid, mouth corner droops, nasal fold flattens.
Dry or watery eye on the affected side.
Loss of facial movement or expression on the affected side.
Excessive drooling and sometimes loss of taste sensation.
Increased sensitivity to loud sounds (hyperacusis).
Disease Course
Symptoms come on quickly and are often severe early on.
Without treatment, recovery may be slow and incomplete.
Severe pain can cause some patients to lose consciousness (rare).
Treatment
1.Medications:
Corticosteroids (like prednisolone) to reduce nerve inflammation.
Antiviral drugs (acyclovir) if viral cause suspected.
Vascular agents and antispasmodics.
Multivitamins including B-complex and nicotinic acid for nerve health.
2.Physical therapy and procedures:
Warming treatments (mud packs, paraffin).
UHF therapy, electrophoresis.
Acupressure, acupuncture, laser therapy.
Facial muscle exercises and speech therapy.
3.Eye care:
Eye drops and ointments to prevent dryness and injury.
Taping eyelids closed during sleep if necessary.
4.Surgery:
Rarely needed, includes nerve repair or plastic surgery if nerve is severely damaged.
Goal of Treatment
Decrease inflammation.
Promote nerve recovery.
Restore facial muscle function.
Prevent complications, especially eye damage.
Prevention
Avoid hypothermia and facial injuries.
Early treatment improves chances of recovery.
Bell’s palsy is a treatable yet serious condition with good recovery potential if managed early with medications and supportive therapies
25. Radial, median and ulnar neuropathies. Carpal tunnel syndrome.
Radial Nerve Neuropathy
Causes:
Sleeping with the arm under the head or torso (sometimes called “Saturday night palsy”)
Fracture of the humerus, crutch use (“crutch palsy”)
Compression by tourniquets or improper injections
Less commonly infections, toxins (alcohol, lead)
Clinical Features:
Wrist drop (“hanging hand”) due to inability to extend wrist and fingers
Inability to abduct thumb, finger clustering abnormalities
Sensory loss on the back of the hand, especially over the anatomical triangle (first and second fingers)
Ulnar Nerve Neuropathy
Causes:
Compression at the elbow (cubital tunnel syndrome), work-related pressure on elbow
Fracture of medial epicondyle or supracondylar humerus fracture
Sometimes associated with infections (typhus, typhoid)
Clinical Features:
Numbness and paresthesia in the ring (fourth) and little finger
“Claw hand” deformity due to weakness of finger adductors and abductors
Hypesthesia on the ulnar side of the hand and half of third finger
Atrophy of interosseous and hypothenar muscles
Median Nerve Neuropathy
Causes:
Injuries during intravenous injections, fractures near wrist (palmar side)
Repetitive hand use (carpal tunnel syndrome common in typists, musicians, carpenters)
Associated with rheumatoid arthritis, hypothyroidism, diabetes
Clinical Features:
Pain and numbness in thumb, index, middle, and half of ring finger
Weakened wrist flexion and pronation
Atrophy of thenar eminence muscles (thumb abduction weak)
“Ape hand” deformity due to thumb muscle weakness
Positive Tinel’s sign (tingling on tapping median nerve at wrist)
Positive Phalen’s test (wrist flexion reproduces symptoms)
Diagnosis & Treatment
Diagnosis: Clinical exam, electromyography (EMG), nerve conduction studies.
Treatment:
Non-surgical: B vitamins, anticholinesterase drugs, vascular agents (dibazol, pentoxifylline, nicotinic acid), physiotherapy, massage, exercise therapy.
Carbamazepine may be used for severe paresthesia.
Avoid prolonged pressure and repetitive strain.
For carpal tunnel syndrome, treat underlying diseases and consider wrist splints.
Surgery if no improvement after 1-2 months or severe nerve damage (e.g., decompression or nerve release surgery).
What is Carpal Tunnel Syndrome?
Carpal tunnel syndrome is a common nerve compression disorder where the median nerve gets squeezed as it passes through the carpal tunnel in the wrist. The carpal tunnel is a narrow passage made of bones and ligaments at the wrist.
Causes and Risk Factors
Repetitive hand and wrist movements (typing, playing instruments, assembly line work)
Prolonged wrist flexion or extension
Fluid retention (pregnancy)
Metabolic or systemic diseases like diabetes, rheumatoid arthritis, hypothyroidism, amyloidosis
Women are more commonly affected due to naturally narrower carpal tunnels
Symptoms
Numbness, tingling, and burning sensation in the thumb, index, middle, and half of the ring finger
Symptoms usually start intermittently and worsen over time
Nighttime pain or numbness that may wake patients up
Pain may radiate from wrist up the forearm, sometimes to the elbow
Weakness in hand grip and difficulty with fine hand movements
Wasting of the muscles at the base of the thumb (thenar eminence) in severe cases
Clinical Signs
Positive Tinel's sign: tingling on lightly tapping the median nerve at the wrist
Positive Phalen's test: flexing the wrist for 1-2 minutes causes symptoms
Reduced sensation to pain and temperature in the first three fingers
Weakness or atrophy of muscles opposing the thumb (abductor pollicis brevis)
Diagnosis
Primarily clinical based on history and physical examination
Electrodiagnostic tests (nerve conduction studies, electromyography) confirm diagnosis and severity
Imaging (ultrasound) can show swelling of the median nerve
Rule out other causes like arthritis or cervical radiculopathy
Treatment
Early treatment improves outcome and may include:
Wrist splinting, especially at night to keep wrist in neutral position
Activity modification and ergonomic changes to reduce repetitive strain
Nonsteroidal anti-inflammatory drugs (NSAIDs) for pain relief
Corticosteroid injections to reduce inflammation and nerve compression
Surgery (carpal tunnel release) is considered if conservative therapy fails or symptoms are severe.
It involves cutting the transverse carpal ligament to relieve pressure on the nerve
This is usually an outpatient procedure with gradual recovery of function
Carpal tunnel syndrome causes characteristic sensory and motor symptoms in the median nerve distribution due to nerve compression in the wrist. Early diagnosis and management prevent permanent nerve damage and disability.
26. Fibular and tibial neuropathies. Tunnel syndromes, conservative therapy and indications for surgical treatment.
Peroneal and Tibial Neuropathy - Summary for Medical Students
Anatomy and Function
Tibial Nerve:
Branch of the sciatic nerve (roots L4-S3).
Motor: Innervates muscles in the posterior leg that flex (plantar flex) the foot and toes and invert (turn inward) the foot.
Sensory: Supplies the back of the lower leg, sole, and plantar surface of the foot and toes.
Runs through the popliteal fossa, posterior leg, and into the foot via the tarsal tunnel. Peroneal (Fibular) Nerve:
Another branch of the sciatic nerve (roots L4-S2).
Motor: Innervates muscles in the anterior and lateral leg compartments that dorsiflex (lift) and evert (turn outward) the foot, and extend the toes.
Sensory: Supplies the anterolateral lower leg and dorsum of the foot.
Wraps around the neck of the fibula, dividing into deep and superficial branches.
Symptoms and Clinical Features
Tibial Neuropathy:
Weakness/paralysis of foot and toe plantar flexion.
Loss of foot inversion.
Achilles tendon reflex loss.
Sensory loss on the posterior leg and sole.
Foot deformities such as deep arch and clawing due to muscle atrophy.
Difficulty walking, especially walking on toes.
Peroneal Neuropathy:
Foot drop ("hanging foot") — inability to dorsiflex and evert the foot.
Toes slightly flexed.
Muscle wasting on anterolateral lower leg.
Sensory loss on the front and outer leg and the top of the foot.
"Steppage gait" — lifting the foot high to avoid dragging.
Tunnel Syndromes
Nerve compression occurs at anatomical narrow points (e.g., fibular neck for peroneal nerve, tarsal tunnel for tibial nerve).
Causes include trauma, prolonged positioning, fractures, metabolic diseases like diabetes, vascular disease, infections.
Symptoms worsen with nerve compression.
Diagnosis
Clinical exam: muscle strength, reflexes, sensory testing.