Mononeuropathies, gait, and dizziness

Question 1

Types of Neurons

Answer 1

1. Sensory neurons - brings information to the CNS. They are structurally very simple, not a lot of branching
2. Interneurons - associate sensory and motor activity with the CNS (i.e., information is processed).
3. Motor neurons - send signals from the brain and spinal cord to muscles. Structurally has complex dendrites, long axons that connect to the muscles located in lower brainstem ans spinal cord.

Question 2

Structure of a Nerve

Answer 2

• A nerve is a bundle axon in the peripheral nervous system. It supports the transmission of electical impluses down axons. Within a nerve, each axon is surrounded by connective tissue, known as endoneurim. The axons are then further bundled together into groups known as fascicles, and each fascicle is wrapped in another layer of connective tissue known as the perineurium.
• Within the endoneurium, individual nerve fivers are also surrounded by endoneural fluid, which prevents certain molecules from passing through the blood.
• Finally, the entire nerve is wrapped is a layer of connective tissue known as the epineurium.

Question 3

Types of Peripheral Nerves

Answer 3

Peripheral nerves are grouped based on diameter, signal conduction velocity, and myelination state of axons.

• Fibers of A group: Large diameter, high conduction velocity, myelinated.
• Fibers of B group: Small diameter, low conduction velocty, myelinated. Main role is to transmit autonomic information.
• Fivers of C group: Small diameter, low conduction velocited, unmyelinated.
• A-delta and C fibers both contribute to detection of diverse painful stimuli. Due to higher conduction velocity, A-delta fibers are responsible for sensation of sharp, initial pain, and respond to a weaker intensity of stimulus and make up the afferent portion of the reflex arc. C fibers, on the other hand, carry slow, longer-lasting pain sensation.

Question 4

Action potential propagation

Answer 4

• Axon hillock receives summation of signals from dendrites and initiates action potential.
• Increase in positive charge inside the cell where the stimulus occured will cause an increase in positive charge in adjacent regions along the membrane, resulting in Na⁺ channels opening in adjacent area. This continues until the action potential has moved along the entire length of the axon.
• Remember, the action potential does not propagate backward because of the absolute refractory period

Question 5

Postsynaptic Potentials

Answer 5

• Changes in membrane potential of the postsynaptic terminal of chemical synapse.
• They graded potentials.
• Caused by presynaptic neurons releasing neurotransmitters into the synaptic cleft. Neurotransmitters can bind to ion-channel and cause conformational change, resulting in influx or efflux of ions.

Question 6

Graded Potentials

Answer 6

• Changes in membrane potential due to summation of individual action of ligand-gated ion channels. Not all or nothing.
• Excitatory postsynaptic potentials (EPSP) - make membrane potential more positive (increase chance of action potential). Due to influx of Na⁺ or Ca²⁺ into cell.
• Inhibitory postsynaptic potentials (IPSP) - make membrane potential more negative. Due to influx of Cl^- if efflux of K⁺
• Summation of EPSPs and IPSPs will determine if there will be an action potential
  
  • Temporal summation - occur so rapidly together that they build on each other before the other fades.
  • Spatial summation - potentials that occur at different spots add together.

Question 7

Traumatic Mononeuropathies

Etiologies

Answer 7

• Etiology - traumatic nerve injury is due to application of kinetic energy to the nerve - compressive and tensile forces applied to nerve.
  
  • Traction/stretch - nerves can accomodate 10-20% of stretch before trauma occurs. However, once this amount is exceeded, internal and external nerve damage occurs. Furthermore, vasa nervorum may rupture and cause bleeding into nerve sheath, resulting in compressive hematoma and ischemia.
  • Contusion/compression - can occur either through continuous pressure applied over hours (i..e, staturday night palsy) or repeatedly applied with cumulative effect (i..e, habitual leaning on elbow). Can also occur through chronic compression by abnormal neighbouring structures.
  • Nerve laceration - transected nerve, either partial or complete.
  • Combined injuries - any of the above combined.

Question 8

Classification of peripheral nerve injury

Answer 8

• Neurapraxia - demyelination and conduction block. This is a mild grade lesion with an excellent prognosis. Caused by mild injury (ischmia, mechanical compression, metabolic or toxic factors) that results in axonal demyelination. However, the axon is still intact, and there is nerve continuity across the site of injury. Patients experience weakness and sensory loss due to conduction block.
• Axonotmesis - demyelination and axon loss. Surrounding stroma (endoneurium, perineurium) remains intact. Partial recovery is suspected. Proximal to lesion, cells body undergoes swelling and chromatolysis; distal to lesion axon degenerates and myelin sheath involutes (Wallerian degeneration). Caused by crush, nerve stretch or percussion injuries.
• Neurotmesis -axon, myelin sheath, and surrounding stroma are all irreversibly damaged. No significant regeneration occurs. Caused by sharp injuries, percussion, or exposure to neurotoxic substances.

Question 9

Carpal Tunnel Syndrome (CTS)

Answer 9

• Complex of symptoms brought on by compression of median nerve as it travels through the carpal tunnel

Question 10

Etiology Carpal Tunnel

Answer 10

• Carpal tunnel is formed by the flexor retinaculum superiorly and the carpal bones inferiorly. The median nerve passes through the tunnel along with the nine flexor muscles tendons. Thus, inflammation and compression of the medium nerve occurs most commonly in the carpal tunnel.
• In upper portion of forearm the median nerve innverates the pronator teres, flexor carpi radialis, palmaris longus, and flexor digitorum superficialis before giving rise to various peripheral nerve branches:
  
  • Anterior interosseous nerve - supplies deep muscles in anterior foremar
  • Palmar cutaneous nerve - innervates the skinof the lateral palm (passes over tunnel - not affected).
• Median nerve then enters the hand via the carpal tunnel - where it terminates by dividing into 2 branches:
  
  • Recurrent branch
  • Palmar digital branch
  • These innverates sensation of lateral 3.5 fingers and some intrinsic muscles of the hand - abductor pollicus brevis, flexor pollicis brevis, opponens pollicis, lateral 2 lumbricals. These muscles can be affected in severe CTS.

Question 11

Clinical Features Carpal Tunnel Syndrome

Answer 11

• Pain and parestehmia involving lateral 3.5 fingers; weakness, or clumsiness of hand.
• Symptoms tend to be worse at night and often awaken patients from sleep.
• Not uncommon to radiate proximally into forearm.
• Symptoms can be provoked by activities that involve flexing or extending the wrist.
• Bilateral CTS involvement is common

Question 12

Causes of Weakness in Gait

Answer 12

• Upper motor neuron dysfunction - dysfunction of cord and/or high central motor pathways
  
  • Tends to involve hip flexion, foot and dorsiflexion, leg flexion at the knees, and thigh abduction.
  • Presentation - toes scuff floor with each step.
• Lower motor neuron dysfunction - pathology in spinal motor neurons or peripheral nervous system
  
  • May affect any particular muscle group if a root is involved. Predominant quadricep weakness is always LHN in origin. Toe flexion and foot plantar flexion weakness if usually LMN.
  • Presentation - With goot drop you will see high stepping gait as hip flexors compenstate for weakness to allow foot clearance.
• Mypothatic process - secondary to muscle disease.
  
  • Proximal muscles are typically involved and Trendelenburg test is positive (due to weakness in gluteaus medius).
  • Presentation - waddling gait

Question 13

Spasticity

Answer 13

• Spasticity in lower limbs is a component of upper motor neuron syndrome. May occur without weakness and suggest a myelopathy.
• In spactic gait the toes turn in and scrape the floor with each step.

Question 14

Deafferentation and gait

Answer 14

• Results in loss of proprioception of feet. Pathology is usually in posterior colume of the spinal cord. Causes include cervical spondylotic myelopathy, low B₁₂, syphilis, and spinal cord compression.
• Gait is described as high stepping and stamping. Stamping is thought to be an attempt to increase sensory feedback. Gait deteriorates markedly in the dark.

Question 15

Extrapyramidal disorders and gait

Answer 15

• Movement disorders in basal gangli can be hyperkinetic or hypokinetic (parkinsosim). Hyperkinetic tend to not interfere with gait unless very advanced. PD, on the other hand, causes significnt dysfunction in gait, posture, and balance problems.
  
  • PD gait - reduced straid length, stooped posutre, poor or no arm swing, festinating steps, difficulty initiating gait, freezing while turning.

Question 16

Cerebellar Ataxia and gait

Answer 16

• Cerebellum is the information processing centre of learned and programmed movement and for control of balance by feedback meachanisms. Due to cerebellar lesion or metabolic abnormalities, Vit E deficiency, CVD, demyelination, etc.
• Gait- stumblig, lurching, staggering, slow, reduced step lenth, wide base, reeling, and “drunken”. Often coupled with other signs of ataxia (scanning, low speech, finger-nose and heel-shin dysmetria and dyssyngeria).

Question 17

Vestibular Dysfunction and gait

Answer 17

• Vestibular organ senses body’s position.
• Bilateral - loss of vestibulo-occular reflex. Leads to oscillopsia with head movement and unsteadiness when visual and somatosensory input is reduced (i.e., walking in dark or on uneven ground).
• Unilateral - rotary vertigo and feeling of body tilt. Nystagmus is prominant and there is a subjective sense of self-motion.
• Gait - deviation on walking on side of affected ear. Gait varies from occasional stumble to frank veering.

Question 18

Frontol Lobe dysfunction and Gait

Answer 18

• In higher-level gait disorders, basic motor and sensory functions are intract and problem is due to failure of motor programming. Cognitive screen may be abnormal and demonstrate loss of executive skills.
• Gait - patients walk cautiously with shortened stride length on a normal or slightly wide base.

Question 19

1. Orthostatic myoclonus and gait
2. Functional gait disorder (Psycogenic)

Answer 19

1. Myoclonus (twitches, jerks, or seizures) that occur when upright. Appears to be a symptom associated with multiple neurodengerative and systemic conditions.
   
   • Gait - observable leg jerking when upright. May see gait initiation difficulty.
2. Clinical syndromes defined by occurence of abnormal involuntary movements that are incongruent with known neurologic cause and are significantly improved on neurologic examination with distraction or nonphysiologic maneuvers.

Question 20

Non-neurologic Causes of giat abnormalities

Answer 20

• Visual loss, orthopedic disorders, rheumatologic disorders, pain, side effects of drugs, cardiorespiratory problems.

Question 21

Guillain Barre

Answer 21

• Acute immune mediated polyneuropathies usually provoked by preceeding illness - heterogenous group of disorders, but acute inflammatory demyelinating polyradiculoneuropathy is the most common.

Question 22

Etiology Guillain Barre

Answer 22

• Antecedent infection evokes immune response that cross reacts with peripheral nerve components because of molecular mimicry. Immune response can be directed towards myelin or axon of peripheral nerve, causing demyelinating and axonal forms of Guillain Barre.
• Antecedent events
  
  • Camplyobacter jejuni infection is most common
  • HIV
  • Influenze-like illness
  • Cytomegalovirus
  • Epstein-Barr
  • Possible very low risk with certain vaccinations

Question 23

Presentation Guillain Barre

Answer 23

• Progressive, symmetric, muscle weakness (anywhere from mild difficulty walking to nearly complete paralysis.
• Severe respiratory muscle weakness necessitiating ventilatory support may develop
• Facial nerve palsies
• Oropharyngeal weakness
• Oculomotor weakness
• Absent or depressed reflexes
• Distal and symmetric paresthesias, loss of proprioception and vibration sense
• Neuropathic pain
• Autonomic dysfunction - BP dysregulation, arrhythmias, bladder dysfunction

Question 24

Laboratory Features Guillain Barre

Answer 24

• Lumbar puncture - elevated CSF protein with normal WBC
• EMG and nerve conduction studies - feature will differ depending on the type
  
  • Acute inflammatory demyelinating polyradiculoneuropathy - predominatly demyelinating features. See decreased motor nerve conduction velocity, prolonged distal motor latency, conduction blocks, and temporal dispersion.
  • Acute motor (and sensory) axonal neuropathy - predominatly axonal features. See decreased distal motor and/or sensory amplitudes
• MRI may show thickening and enhancement of intrathecal spinal nerve roots and cauda equina.

Question 25

Diagnosis Guillain Barre

Answer 25

• Required features:
  
  • Progressive weakness of legs and arms (may start with only legs)
  • Absent or decreased reflexes in weak limbs
• Supportive features:
  
  • Symptom progression over days to 4 weeks
  • Relative symmetry
  • Mild sensory symptoms or signs
  • Cranial nerve involvement, especially bilateral facial nerve weakness
  • Recovery starting 2-4 weeks after progression stops
  • Autonomic dysfunction
  • Pain
  • No fever at onset
  • Elevated protein in CSF
  • EMG abnormalities

Question 26

Treatment Guillain Barre

Answer 26

• IVIg
• Plasmapheresis (filters blood and removes harmful antibodies)
• Pain managment
• Monitor vitals and vital capacity

Question 27

Vertigo

Answer 27

A symptom that arises from an acute asymmetry of the vestibular system.

• Vestibular system - vestibular apparatus in inner ear, vestibular nerve, and nucleaus within medullla that connects to and from vestibular portions of cerebellum.
• Vertgio is experienced as an illusion of motion either of self or the environment. Patients may use words like “spinning”, “whirling”, “tiliting”, or “moving”.
• Vertigo is due to asymmetry in vestibular system due to damage or dysfunction of labyrinth, vestibular nerve, or central vestibular stracutures in brainstem.
• However, sensation of spinning, or lack thereof, is not sufficient to rule in/out vertigo. Time course, provoking factors, and aggravating factors are more useful to establish cause of dizziness.
  
  • Time course - true nystagmus and vertigo caused by a peripheral lesion will never last longer than a few weeks, due to compensation from cerebellum. Central lesions do not compensate, so nystagmus and vertgio will persist.
  • Provoking factors - certain types of vertigo occur spontaneously, while others are precpitated by maneuvers that change head position or middle ear pressure.
  • Aggravating factors - all vertigo is made worse by moving the head. If head movement does not worsen dizziness, it is not vertigo.
  • Associated signs and symptoms - nystagmus and postural instability. May also see hearing loss and brainstem signs (ataxia gait, vomiting, headache, double vision, visiual loss, slurred speech, numbness of face and body, weakness, clumsiness, or incoordination.

Question 28

Presyncope

Answer 28

• “Near fainting”
• usually lasts for seconds to minuets and is often described as “nearly blacking out” or “nearly fainting”.
• Patients may also report lightheadness, feeling of warmth, diaphoresis, nausea, and blurred vision
• Tends to occur when patient is standing or seated. Supine (suggests cardiac arrhytmias rather than hypotension).
• Common causes - orthostatic hypotension, cardiacarrhy thmias, and vasovagal attacks.

Question 29

Disequilibrium/unsteadiness

Answer 29

• Sense of imbalance that occurs mainly when walking
• May be caused by peripheral neuropathy, MSK disorder interfering with gait, vestibular disorders, cerebellular disorders, or cervical spondylosis.

Question 30

Peripheral vs. Central Vertigo

Answer 30

Question 31

Benign Paroxysmal Positional Vertigo (BPPV)

Answer 31

• Define - acute attacks of rotatory vertigo (peripheral) lasting seconds-minuets, initiated by certain head position, accompanied by rotatory nystagmus
• Etiology - due to canalithiasis (calcium debris within semicircular canal)
• Diagnosis - history (time course, provoking factors, associative symptoms) + positive Dix-Hallpike maneuver
• Treatment - reassure that process process resolves spontaneousl; particle repositioning maneuvers; surgery for refractory cases; anti-emetics for N/V

Question 32

Meniere Disease

Answer 32

• Define - peripheral vestibular disorder characterized by episodic attacks of tinnitus, hearing loss, aural fullness, and vertigo lasting minutes to hours.
• Etiology - inadequate absorption of endolymph leading to endolymphatic hydrops that distorts membranous labyrinth
• Presentation - episodic vertigo, fluctuating low frequency sensorineural hearing loss, and aural fulness, +/- drop attacls, +/- N/V.
  
  • Vertigo disappears with time, but hearing loss remains.
• Treatment
  
  • Acute - bed rest, antiemetics, antivertiginous drugs, and anticholinergic
  • Long-term - low salt diet, serc (antivertigo med), intratympanic gentamincin to destroy vestibular end organ (results in complete SNHL), intratympanic glucocorticoids may improve vertigo symptoms, surgical options.

Question 33

Vestibular Neuritis

Answer 33

• Define - A viral or postviral inflammatory disorder, affecting the vestibular portion of the eighth cranial nerve. It is an acute oneset vertigo, often accompanied by N/V and imbalance without hearing loss that resolves over days. However, imbalance can last weeks.
• Treatment
  
  • Acute phase - bed rest; antivertiginous drugs; corticosteriods +/- antivirals; if bacterial infection treat with IV antiboitics, drain midle ear +/- mastiodectomy.
  • Convalescent phase - progressive ambulation, vestibular exercises.

Question 34

Acoustic Neuroma/ vestibular schwannoma

Answer 34

• Define - schwannoma of vestibular portionof CN 8.
• Etiology - starts in auditory canal and expans into cerebellopontine angle, compressing cerebellum and brainstem.
• Presentation - unilateral SNHL or tinnitus; dizziness and unsteadiness may be present, but true vertigo is rare as tumour grows slowly allowing for compensation; facial nerve palsy an trigeminal sensory deficit are late complications.
• Treatment: expectant management if tumour is very small; surfucal excision or gamma knife radiation if larger.

Question 35

Vestigbular migraine

Answer 35

• Define - a cause of recurrent vertigo. Can have central and peripherial manifestations with variations in severity and duration.
• Mechanism is not understood.
• For diagnosis, some episodes of vertigo need to be associated with migraine or other migraine phenomenon

Question 36

Brainstem Ischemia and vertigo

Answer 36

• Central vertigo may be a dominating clincial presentaiton, but it is rarely sole manifestation. It is important to rule out, especially if patient has vascular risk factors