Pain, Motor Control & Neurological Disorders: OT Study Guide

Somatosensory Pathway:

Relays sensory info via three order neurons: First-order (peripheral input), Second-order (thalamus), and Third-order (cerebral cortex).

Nociceptive pain

stems from tissue injury activating nociceptors (typically acute).

Neuropathic pain

arises from nerve damage persisting after the injury is addressed (typically chronic).

Mechanisms of Neuropathic Pain:

Driven by cortical reorganization, increased/abnormal connections on nociceptive pathways, elevated excitatory transmitters, increased density of somatosensory fields, and central sensitization (excessive responsiveness of central neurons, likely with epigenetic components).

The Pain Matrix:

The subjective experience of pain alters how an individual feels, thinks, and behaves.

Counterirritant Theory:

Nociceptive and mechanoreceptive signals travel on the same nerve pathways; the brain registers whichever signal is strongest (e.g., rubbing a bumped elbow).

Gate Control Theory:

Pain "gates" can be modulated:

Open (Worsens pain):

Stress, tension, focusing heavily on pain, inactivity.

Close (Lessens pain):

Relaxation, stress management, distraction, being active, counter-stimulation (heat, cold, massage, vibration).

Acute & Nociceptive Pain Management:

Use Physical Agent Modalities (PAMs) to manage pain, reduce inflammation, and promote movement.

Acute & Nociceptive Pain.

Conservative use of the impacted area, progressing slowly back to prior level of function (PLOF).

Acute & Nociceptive Pain Modify

occupations, roles, and routines; practice energy conservation and "respect the pain".

Chronic & Neuropathic Pain Management Warning:

Conservative rehabilitation will worsen neuropathic or chronic pain. Focus on managing and reducing pain rather than eliminating it.

Chronic & Neuropathic Pain Client education.

regarding pain theories (e.g., "A Car with Four Flat Tires" analogy).

Chronic & Neuropathic Pain Pushing through.

pain using distraction, identifying what opens/closes pain gates, increasing cardiovascular strength/endurance, increasing meaningful occupations, and target-area desensitization.

Amplified Musculoskeletal Pain Syndrome (AMPS):

Characterized by severe pain and skin sensitivity, typically following an injury or medical intervention and complicated by psychological stressors. 70-80% of cases occur in prepubescent/adolescent girls. Therapy is more effective than medication/medical intervention.

Complex Regional Pain Syndrome (CRPS):

(Referenced via clinical presentation/slides) Marked by severe autonomic and inflammatory changes, extreme localized pain, and skin/color temperature shifts.

Fibromyalgia:

Features components of nociceptive and neurogenic pain with amplification of pain signals. Symptoms include muscle tenderness, soft-tissue stiffness, aching pain, generalized weakness, and a strong genetic component.

Migraines:

Amplified nociceptive signals in the trigemino-thalamo-cortical pathway. Diagnosed by at least two unilateral, pulsating features that interfere with/are aggravated by routine activities; can include nausea, vomiting, dizziness, light/noise sensitivity, and scalp/neck tenderness.

Phantom Pain vs. Limb Sensation:

Phantom limb sensation is a persistent sensation of a missing limb despite absent peripheral nerves. Phantom pain is extremely painful/debilitating perception in a missing limb (distinct from residual limb pain). Managed via approaches like virtual reality.

Mechanisms for Movement Co-contraction:

Simultaneous contraction of opposing muscles to stabilize joints (prevents movement). Dysfunction: Abnormal co-contraction restricts range of movement and causes stiffness during tasks like standing to sit.

Mechanisms for Movement Muscle Synergy:

Activation of multiple muscles together to execute a movement, utilizing prime movers, synergists, and fixators. Dysfunction: Abnormal muscle synergy forces alternative muscle patterns (e.g., abnormal upper-extremity synergy patterns during reaching).

Reciprocal Inhibition:

Inhibition of antagonist muscles during agonist contraction to prevent unwanted antagonist activation.

Recurrent Inhibition:

Neurons within a muscle group fire excitatory and inhibitory signals simultaneously via Renshaw cells to refine and adjust movement to task demands.

Feedforward:

Anticipatory use of sensory information to prepare for movement (e.g., postural adjustments before throwing a ball).

Feedback:

Use of sensory information during or after movement to make corrections for future actions.

Muscle Tone vs. Strength:

Muscle tone is the resting resistance to passive stretch (has a wide normal bell-curve spectrum) and is distinct from muscle strength (the force-generating capacity of a muscle).

Hypertonia (High Tone):

Rigid or stuck in shortened positions; stiff, jerky, abnormal movements; difficulty isolating muscles.

Spasticity:

Velocity-dependent resistance to passive movement; worsens with fast input. Associated with cerebral or spinal damage (CVA, TBI, spastic CP).

Rigidity:

Velocity-independent resistance; resistance remains identical regardless of input speed. Associated with basal ganglia/thalamus damage (Parkinson's, Huntington's). Subtypes include lead-pipe (constant), cogwheel (start-stop jerky), and clasp-knife (resistance drops off at the end of range).

Postural Rigidities:

Decerebrate rigidity (brainstem damage below red nucleus: extension/internal rotation of arms, leg extension) vs. Decorticate rigidity (damage above red nucleus: flexed arms, extended legs).

Contractures:

Permanent shortening of muscle fibers and loss of ROM due to disuse and prolonged spasticity.

Hypertonia Interventions:

Bacolofen (oral or intrathecal pump), Botox (paralyzes muscle), serial casting, and tendon release surgery.

Hypotonia (Low Tone):

Muscles feel loose, floppy ("low muscle tone"), requiring more active effort to apply force; common in Down syndrome and genetic disorders.

Flaccidity:

Extreme low tone/absence of tone caused by lower motor neuron or nerve degeneration (ALS, spinal muscular atrophy).

Tone Assessment:

Observation at rest, active range of motion (AROM), passive range of motion (PROM), and the Modified Ashworth Scale.

Spinal Reflexes:

Involuntary reactions to sensory stimuli bypassing direct brain input.

Phasic stretch reflex / Deep tendon reflexes (DTR):

Muscle contraction responding to a quick tendon tap.

Cutaneous withdrawal reflex:

Motor withdrawal from a noxious stimulus.

Hyperreflexia / Abnormal Reflexes:

Clonus (rhythmic oscillations following quick stretch), positive Babinski sign (toe extension/fan on sole stimulation), and Hoffman's sign (finger flexion response when flicking the 3rd middle finger).

Dysmetria:

Inability to control the distance, scale, or force of a movement.

Dyssynergia:

Inability to coordinate multi-joint muscle groups for smooth, controlled movement.

Dysdiadochokinesia:

Inability to perform rapid alternating movements.

Cerebellum:

Processes vestibular/sensory input to adjust posture against gravity, integrates frontal lobe motor plans with sensory feedback, and ensures smooth gross/fine motor execution. Damage leads to ataxia, unsteadiness, and intention tremors.

Basal Ganglia:

Works alongside cerebellar circuits to refine movement, regulate muscle force, manage multi-joint sequences, and govern movement scaling. Damage causes hypo- or hyperkinetic movement disorders.

UMN Lesions (Brain/Spinal Cord):

Cause paresis/paralysis, hyperreflexia, hypertonia (spasticity), clonus, and positive Babinski. Examples: CVA, TBI, CP, Huntington's disease (cortical degeneration).

LMN Lesions (Anterior horn/spinal nerves/peripheral nerves):

Cause paresis/paralysis, hyporeflexia/areflexia, hypotonia/flaccidity, severe muscle atrophy, and fasciculations. Examples: Spinal muscular atrophy, ALS, Acute Flaccid Myelitis.

Hyperkinetic (Excessive/Involuntary Movement) Huntington's Disease (HD):

Autosomal dominant neurodegenerative disorder causing cortex/basal ganglia degeneration. Features chorea, dystonia, cognitive decline (executive dysfunction), and psychiatric shifts.

Tourette Syndrome:

Childhood-onset neurodegenerative/developmental disorder marked by abrupt, repetitive involuntary vocal and motor tics, exacerbated by stress.

Hypokinetic (Slow or Missing Movement) Parkinson's Disease (PD):

Caused by basal ganglia dysfunction (dopamine depletion). Features bradykinesia, resting tremor, cogwheel rigidity, postural instability, shuffling gait, freezing, and masked facies. Managed via L-DOPA, deep brain stimulation (DBS), and high-intensity resistance training.

Parkinson-Plus Syndromes:

Rapidly progressive neurodegenerative conditions mimicking PD symptoms alongside severe autonomic and early cognitive decline (e.g., Dementia with Lewy Bodies).

Resting tremor:

Present at rest, diminishes during movement (hallmark of Parkinson's; hyperkinetic feature).

Intention tremor:

Appears during targeted movement, diminishes at rest (hallmark of cerebellar pathology; slow/hypokinetic-associated rule-breaker).

Dystonia:

Involuntary sustained or intermittent muscle contractions causing twisting, repetitive movements and abnormal postures; worsens with attempted movement.

Chorea

Rapid jerky movements (chorea)

Athetosis.

slow writhing movements

Ballismus.

large-amplitude flinging limb movements

Fast Symptom Progression / Fatal Disorders:

ALS (amyotrophic lateral sclerosis, destroying upper/lower motor neurons with average 3-5 year life expectancy) and rapid Parkinson-Plus / Lewy Body variants.

Section 4: Cranial Nerves

Cranial Nerve Overview Table

CN I

Olfactory, Sensory ,Sense of smell, Anosmia (loss of smell)

CN II

Optic, Sensory, Vision, pupillary light reflex, Ipsilateral blindness, visual field cuts

CN III

Oculomotor, Motor, Eye movement (4 extraocular muscles), pupil constriction, eyelid elevation, Ptosis, diplopia, blown pupil, eye pulled down and out

CN IV

Trochlear, Motor, Superior oblique muscle (down/in eye movement) , Vertical diplopia, difficulty looking down and out

CN V

Trigeminal, Both, Facial sensation (V1-V3) & muscles of mastication, Jaw deviation to weak side, jaw jerk reflex, Trigeminal Neuralgia (severe stabbing facial pain)

CN VI

Abducens, Motor, Lateral rectus muscle (abducts eye), Estropia / inability to look laterally, horizontal diplopia

CN VII

Facial, Both, Muscles of facial expression, taste (anterior 2/3 tongue),Bell's Palsy (ipsilateral facial droop, inability to close eye, dry mouth)

CN VIII

Vestibulocochlear, Sensory, Hearing (cochlear) and balance/equilibrium (vestibular),Vertigo, nystagmus, sensorineural hearing loss, tinnitus, Ménière's disease

CN IX

Glossopharyngeal, Both, Taste/sensation (posterior tongue), pharyngeal muscles, salivation, gag reflex, Loss of gag reflex, dysphagia, reduced salivation

CN X

Vagus, Both,Pharynx/larynx motor/sensory, autonomic control of visceral organs (heart, lungs, GI),Hoarseness, dysphagia, autonomic disruption (vasovagal syncope / fainting)

CN XI

Accessory, Motor, Innervates sternocleidomastoid and trapezius muscles,Weakness turning head or shrugging shoulders, scapular winging

CN XII

Hypoglossal, Motor, Intrinsic and extrinsic muscles of the tongue, Tongue deviates toward the lesion side when protruded, ipsilateral atrophy

Specialized CN Bell's Palsy:

Idiopathic facial nerve (CN VII) inflammation causing acute unilateral facial paralysis (drooling, inability to close eye).

Specialized CN Trigeminal Neuralgia:

Severe, sharp, stabbing electric-shock facial pain along CN V branches caused by neurovascular compression.

Specialized CNMénière's Disease:

Inner ear disorder (CN VIII involvement) causing vertigo, fluctuating hearing loss, tinnitus, and aural fullness due to endolymphatic fluid buildup.

Gray Matter (Interior): Divided into horns:

Dorsal horn (Sensory processing), Ventral horn (Motor output), and Lateral horn (Autonomic system).

White Matter (Exterior):

Ascending sensory and descending motor tracts.

Spinal Nerves & Vertebrae Relationship:

Cervical nerves exit above their corresponding vertebrae (with C8 exiting below C7 vertebra); thoracic, lumbar, and sacral nerves exit below their corresponding vertebrae.

Dermatomes & Myotomes Reference

Dermatomes (Sensory Maps):

Used to locate sensory levels of spinal lesions.

C3:

Neck/collar area

C5:

Lateral arm/shoulder

C6:

Thumb and radial forearm

C7:

Middle finger

C8:

Ring and little finger

T4:

Nipple line

T10:

Umbilicus

L1-L3:

Anterior and inner thigh

L4:

Medial lower leg and medial foot

L5:

Lateral leg and dorsum of foot

S1:

Lateral/posterior foot and sole

Myotomes (Motor Maps):

C2-C3:

Head and neck movement

C3-C5:

Diaphragm / Breathing

C4:

Scapular elevation and retraction (Trapezius/Levator Scapulae)

C5: Shoulder abduction and elbow flexion (Deltoid/Biceps)

C6:

Wrist extension (Wrist extensors)

C7:

Elbow extension and wrist flexion (Triceps)

C8:

Finger flexion

T1:

Finger abduction/adduction (Hand intrinsics)