Nerves are covered by what 3 connective tissue layers
Endoneurium - innermost; surrounds each individual axon
Perineurium - middle layer; covers groups (fascicles) of axons; responsible for the blood-brain barrier
Epineurium - outermost; covers entire nerve and provides cushion
Clinical manifestations of Thoracic Outlet Syndrome (TOS)
Clinical Manifestations
Neurological Symptoms:
Paresthesias (tingling) and pain in the arm.
Nocturnal pain that disrupts sleep.
Pain in the neck, face, ear, anterior chest, and scapula.
Vascular Symptoms:
Coldness and edema in the hand or arm.
Fatigue in the hand or arm due to compromised blood flow.
Electrical insulation - for rapid saltatory conduction of the axon potentials; sodium channels to reinforce efficient saltatory conduction
Myelin
The Causes, Associated Conditions, Risk Factors and structures involved with Carpal Tunnel Syndrome
Causes: Increased volume of carpal tunnel contents or decreased tunnel volume can raise pressure on the median nerve.
Associated Conditions: rheumatoid arthritis (RA), edema, congestive heart failure (CHF), pregnancy, tumors, callus formation, and obesity increase the risk.
Risk Factors: Occupational activities involving force, repetition, or poor posture, and ergonomic issues.
Anatomy: The carpal tunnel contains 10 structures and normally has a pressure of 7-8 mmHg. Wrist flexion or extension raises pressure, causing blood flow restriction (ischemia).
Diagnosis and treatment of Thoracic Outlet Syndrome (TOS)
Diagnosis
Provocative Tests: Often yield false positives; these tests assess for changes in symptoms or vascular response.
Adson’s Maneuver: Involves placing the arm in slight abduction while palpating the radial pulse; the patient holds their breath and extends and rotates their neck toward the affected side. A positive test results in paresthesias or a decrease in pulse quality.
Monitoring: Observation of pulse quality and any symptom changes during maneuvers.
Management/Treatment
Conservative Treatment:
Postural Adjustments: Improving posture to relieve pressure on the thoracic outlet.
Breathing Techniques: Exercises to enhance breathing and reduce tension.
Gentle Stretching and Strengthening: Focused on the shoulder girdle to improve muscle function and reduce symptoms.
Further Interventions: If conservative measures fail, additional treatments may include physical therapy, pain management strategies, and, in severe cases, surgical intervention to relieve compression.
hereditary motor and sensory neuropathy; peroneal muscular atrophy
Involves peroneal nerve (muscles of foot) and progresses to forearms and hands
Characterized by symmetrical distal muscle weakness, skeletal deformities, abnormalities of DTRs
Charcot-Marie-Tooth disease
Clinical manifestations of Carpal Tunnel Syndrome
Sensory Symptoms: Numbness, tingling, or burning in the thumb, index, and middle fingers.
Pain: Pain can occur in the wrist, thumb, index and middle fingers, forearm, shoulder, arm, or neck.
Nocturnal Pain: Characterized by painful numbness that commonly occurs at night.
Thenar Weakness: Weakness in thumb muscles (thenar eminence), leading to reduced grip strength, pinching ability, and difficulties with fine motor tasks.
Clinical manifestations and treatment Saturday night palsy/sleep palsy
Varies based on level of lesion
More proximal = more extensive paralysis
Axilla - weakness occurs in elbow flexion, extension, supination
Upper arm - no weakness in tricep
Both instances: paralysis of wrist extensors and extensors of the fingers and thumb, diminishing grip strength
Treatment: cockup splint to maintain wrist in extended position until return of function
Condition caused by compression of the median nerve within the carpal tunnel at the wrist, leading to sensory and motor symptoms. It is the most common type of neuropathy.
Carpal Tunnel Syndrome (CTS)
How to diagnosis Carpal Tunnel Syndrome (CTS)
Provocation Tests: Used to reproduce symptoms of CTS.
Phalen’s Test: Wrist is flexed to 90 degrees for 1 minute to check for symptoms.
Tinel’s Test: Tapping over the carpal tunnel area to check for tingling or pain.
Carpal Compression Test: Applying pressure over the flexor retinaculum to assess discomfort.
Positive Findings: Pain, numbness, or tingling reproduction confirms suspicion of CTS.
Nerve Conduction Velocity (NCV) Test: Measures sensory conduction speed across the wrist; the most sensitive indicator for CTS.
A- Phalen’s test
B- Tinel’s test
Causes, symptoms, diagnosis, and treatment of Morton’s neuroma
Caused by: diminished intermetatarsal head distance, poor foot mechanics (excessive pronation), high heels
Causes: thickening of endoneurium and perineurium, hyalinization of endoneurial vessels, demyelination of nerve fibers
Symptoms: burning, tingling, sharp lancing pain - especially while walking
Diagnosis
Plantar palpation
Mulder’s sign: compression to metatarsal heads
Laseague’s sign: compression to heads with dorsiflexion of the toe involved
Treatment: pressure relief, soft orthosis, metatarsal pad
Type of radiculopathy involving compression or irritation of the sciatic nerve roots, which can cause pain and neurological symptoms in the lower back and legs.
Sciatica
Management/Treatment of Carpal Tunnel Syndrome
Conservative Treatments:
Steroid Injections: Injected into the carpal tunnel to reduce inflammation and relieve pressure on the nerve.
Ergonomic Modifications: Changes to workstations or activities to reduce wrist strain.
Wrist Splints: Keeps the wrist in a neutral position to lower carpal tunnel pressure.
Surgical Treatment:
Carpal Tunnel Release Surgery: Involves cutting the transverse carpal ligament to reduce pressure on the median nerve.
Post-Surgical Care: Early movement is advised to prevent scarring and adhesions.
The etiology and pathophysiology of Guillain-Barre Syndrome (GBS)
Etiology: GBS is an immune-mediated disorder often triggered by an acute infection. About two-thirds of patients report an infection within two months preceding the onset of symptoms, with 90% experiencing an illness in the 30 days prior.
Pathophysiology: The syndrome involves lesions throughout the peripheral nervous system (PNS), affecting spinal nerve roots and both motor and sensory fibers.
A condition characterized by sudden, unilateral paralysis of the facial nerve, resulting in weakness or paralysis on one side of the face.
Bell’s Palsy (Idiopathic Facial Paralysis)
What is the pathophysiology and anatomy involved with sciatica
Pathophysiology: Sciatica results from nerve root compression, often caused by disc herniation, spinal stenosis, or other structural changes affecting the nerve pathways.
Anatomy of Innervation:
Epidural Space: Innervated by the meningeal branch of the spinal nerve (recurrent sinuvertebral nerve).
Dorsal Root Ganglia: Located within the intervertebral foramen, with branches dividing into ascending and descending segments to distribute nerve signals.
What are the clinical manifestations of Guillain-Barré Syndrome
Weakness: Rapidly ascending, symmetric motor weakness, often starting in the lower extremities and progressing to the trunk, arms, and facial muscles.
Sensory Impairment: Distal sensory deficits may occur, including numbness and tingling.
Onset: Symptoms may begin with paralysis of the toes and weakness in the legs, gradually spreading to involve other muscle groups.
A delayed onset neuropathy involving the ulnar nerve, which results in weakness and deformity in the hand due to prolonged or recurrent compression or injury.
Tardy Ulnar Palsy (Retroepicondylar Palsy)
The clinical manifestations of sciatica
Pain: Typically starts as low back pain and radiates into one or both legs, often following the path of the sciatic nerve.
Aggravating Factors: Pain often worsens with activities that increase intra-abdominal pressure, such as coughing, sneezing, or sitting.
How to diagnosis Guillain-Barre Syndrome (GBS)
Clinical Evaluation: Diagnosis is primarily based on clinical symptoms, including the pattern and progression of weakness.
Electrophysiological Studies: Nerve conduction studies may show demyelination.
Lumbar Puncture: Analysis of cerebrospinal fluid (CSF) often reveals albuminocytologic dissociation (elevated protein levels with normal white cell counts).
A entrapment syndrome caused by pressure from structures in the thoracic outlet on the brachial plexus, typically occurring between the interscalene triangle and the inferior border of the axilla.
Thoracic Outlet Syndrome (TOS)
How to diagnosis and treat sciatica
Diagnosis
Magnetic Resonance Imaging (MRI): Used to visualize nerve compression or structural abnormalities (e.g., bulging discs). It is noted, however, that up to 60% of asymptomatic individuals may show a bulging disc on MRI.
Physical Examination: May include tests such as the straight-leg raise, where raising the leg in a supine position can reproduce sciatica symptoms.
Management/Treatment
Conservative Treatments:
NSAIDs (Non-Steroidal Anti-Inflammatory Drugs): Used to reduce pain and inflammation associated with sciatica.
Selective Epidural Steroid Injection: Corticosteroids may be injected into the epidural space to reduce inflammation around the compressed nerve root.
Surgical Treatment:
Discectomy: Removal of a herniated disc portion to relieve nerve compression in cases where conservative treatments fail.
Management and treatment of Guillain-Barré Syndrome (GBS)
Plasmapheresis: A procedure that removes plasma from circulation, filtering it to dilute circulating antibodies, which may help improve symptoms and shorten recovery time.
High-Dose Immunoglobulin Therapy: Administration of immunoglobulin, a protein that the immune system uses to attack foreign organisms, to modulate the immune response.
Prognosis
The prognosis for Guillain-Barré Syndrome varies, with most patients reaching maximal weakness within 2-3 weeks and experiencing a recovery period that can take weeks to
radial nerve compression from direct pressure against a firm object
Saturday night palsy/sleep palsy
Sleeping on arm with compression of radial nerve in spiral groove of the humerus
Crutch palsy - when radial nerve is compressed in the axilla
What is the pathophysiology of Bell’s Palsy
Onset: Rapid onset, usually within hours to days.
Pathophysiology: Inflammation of the facial nerve (VII) leads to compression, which initially causes demyelination of the nerve. In some cases, latent herpes virus may play a role, causing pain near the mastoid area or a sensation of fullness in the ear.
What is some basic information and pathophysiology in regards to Postpolio Syndrome (PPS)
Historical Context: Polio was eradicated in the United States with the widespread use of vaccines, with the last polio epidemic occurring in the 1950s.
Initial Polio Infection: Polio is associated with unique neuropathies that lead to focal and asymmetric motor impairments, contrasting with other neuropathies that typically exhibit distal and symmetric motor and sensory losses.
Pathophysiology: The condition is related to the original disorder of the motor neuron cell body affected by the poliovirus. Recovery of muscle strength after polio was due to the reinnervation of denervated muscle fibers by collateral sprouts from surviving nearby axons. However, this compensatory mechanism is not sustainable over time, leading to a decline in function.
A entrapment neuropathy of the forefoot - most often 3rd toe interspace
Morton’s neuroma
What are the clinical manifestations of Bell’s Palsy
Facial Paralysis: Drooping of the corner of the mouth, flattening of the nasolabial fold, and difficulty with facial expressions on the affected side.
Eye Symptoms: Inability to close the eyelid on the affected side, leading to dry eyes and risk of corneal damage.
Oral Symptoms: Thicker saliva production and potential difficulty with eating and drinking.
Associated Pain: Some cases may have severe pain near the mastoid bone or fullness in the ear, especially if associated with herpes virus reactivation.
Clinical manifestations of Post polio Syndrome
Muscle Weakness: Decline in muscle strength in previously affected muscles, often leading to increased disability.
Pain and Myalgias: Muscle pain and discomfort are common complaints.
Bulbar Symptoms: Issues with respiration and swallowing may arise due to involvement of bulbar motor neurons.
Fatigue: Patients often experience excessive fatigue with minimal physical activity, significantly impacting daily functioning.
occurs after total loss of axon and connective tissue; toe is severed
Gunshot wound, stab wound, avulsion injury
Surgical management: suture connective tissue bundles together - guide regeneration
Neurotmesis
How to diagnosis and treat Bells Palsy
Diagnosis
Clinical Examination: Based on physical examination and symptom presentation (e.g., unilateral facial droop, inability to close the eye, drooping mouth).
Additional Tests: Imaging or laboratory tests are not typically needed unless there is suspicion of other neurological conditions.
Management/Treatment
Medications:
Corticosteroids: High-dose corticosteroids administered for 5 days, followed by a tapered dose, to reduce inflammation and improve recovery.
Acyclovir (Antiviral): Used if herpes virus reactivation is suspected as a contributing factor.
Protective Measures:
Eye Protection: Covering the eye on the affected side to prevent dryness and protect the cornea from damage, especially when blinking is compromised.
Prognosis
Bell's Palsy generally has a favorable prognosis, with most people recovering fully within weeks to months. Early corticosteroid treatment can improve outcomes, though a small percentage of cases may experience residual facial weakness.
How to diagnose manage and treat polio
Diagnosis
Clinical Evaluation: Diagnosis is based on the history of prior polio infection and the emergence of new symptoms, typically in individuals who had recovered from acute polio.
Exclusion of Other Causes: It is important to rule out other potential causes of muscle weakness and fatigue through clinical examination and, if necessary, additional testing.
Management/Treatment
Symptomatic Treatment: Focuses on managing pain and improving quality of life through medication and physical therapy.
Activity Modification: Patients are advised to adjust their activities to conserve energy and reduce fatigue, incorporating pacing strategies and ergonomic adaptations.
Prognosis
The prognosis for Postpolio Syndrome varies; while some individuals may experience significant functional decline, others maintain a relatively stable condition with appropriate management. Early recognition and treatment of symptoms can help improve quality of life and maintain functional abilities.
chronic metabolic disturbances affecting nerve and schwann cells
Diabetic neuropathy
What is the anatomy, common causes, aggrevating factors of Retroepicondylar Palsy
Anatomy: The ulnar nerve originates from the lower trunk of the brachial plexus (C8-T1) and travels behind the medial epicondyle of the elbow, then passes between the two heads of the flexor carpi ulnaris through the forearm to the wrist.
Common Causes: Often arises as a complication of elbow fractures, callus formation, or repeated trauma to a shallow ulnar groove.
Aggravating Factors: Elbow flexion can worsen symptoms due to increased compression on the ulnar nerve.
An elevated levels of sorbitol and fructose → deficiencies of sodium-potassium and ATP = alter function of peripheral nerves
Hyperglycemia
What are the clinical manifestations of Tardy Ulnar Palsy
Claw Hand Deformity: Characterized by hyperextension at the metacarpophalangeal (MCP) joints and flexion at the interphalangeal (IP) joints of the 4th and 5th fingers, resulting from unopposed action of the extensor muscles and paralysis of the 3rd and 4th lumbrical muscles.
Flattening of the Hypothenar Eminence: Muscle atrophy in the hypothenar region of the hand.
Sensory and Motor Symptoms: Weakness in grip strength, tingling, or numbness in the ring and little fingers.
An abnormalities in microcirculation - endothelial capillary changes and local ischemia to the affected nerve
Excess sorbitol damages schwann cells
Chronic hyperglycemia
How to diagnosis and treat Tardy Ulnar Palsy
Diagnosis
Clinical Examination: Identification of characteristic claw hand deformity and sensory deficits in the ulnar nerve distribution.
Imaging: X-rays or MRI may be used to identify any structural abnormalities around the elbow that could be causing nerve compression.
Management/Treatment
Surgical Options:
Nerve Decompression: Relieves pressure on the ulnar nerve to improve function and reduce symptoms.
Transposition Surgery: Moves the ulnar nerve to the anterior aspect of the elbow to protect it from further compression.
Splinting:
Anti-Claw Splint: Blocks hyperextension of the MCP joints to prevent claw hand deformity.
An acute autoimmune disorder characterized by flaccid paralysis and areflexia (loss of reflexes). It typically presents as rapidly progressing weakness affecting the peripheral nervous system.
Guillain-Barré Syndrome (GBS)
Anatomy, complex diagnosis, vascular symptoms and risk factors of Thoracic Outlet Syndrome (TOS)
Anatomy: The brachial plexus interacts with surrounding anatomical structures, including ribs, muscles, tendons, and vascular supply, leading to a combination of neurological and vascular symptoms.
Complex Diagnosis: Symptoms are often vague and vary widely among individuals, making the diagnosis controversial.
Vascular Symptoms: Compression can also affect the subclavian artery, leading to additional symptoms.
Risk Factors:
Postural changes
Trauma to the shoulder girdle
Body composition and anatomy
Gravity can increase tension on the shoulder girdle.
A condition characterized by new muscular symptoms that occur decades after recovery from the initial acute paralytic episode of poliomyelitis (polio).
Postpolio Syndrome (PPS)