Week 3

Apraxia, SCI, MS, Physical Activity, Vestibular system, Parkinsons

Apraxia

A disorder of the execution of learned movement which cannot be accounted for by weakness, incoordination, sensory loss, or by incomprehension of or inattention to command. It involves impaired planning & sequencing of movement.

Ideational Apraxia

A failure in the construction stage. The patient has no idea of what to do.

Ideomotor Apraxia

A failure in the production stage.

Limb Apraxia / Motor Apraxia

Affects skilled movement. Most neurological patients have a dysfunction in both praxis systems

Other Common Apraxias

Dressing apraxia, Constructional apraxia (disorder of drawing), Ocular apraxia (disordered eye movement), and Speech apraxia.

Functional Impact of Apraxia

Challenges independent functioning, has an adverse effect on ADLs and return to work abilities

Apraxia Incidence in Stroke

30-60% of stroke patients. Higher in left hemisphere strokes. Often coexists with aphasia (80%).

What is a key characteristic of apraxia’s impact on motor control?

Affects movement patterns on both sides of the body.

Lateralization of Praxis Systems

Praxis systems are lateralized to the left cerebral hemisphere in most right handers.

Lesion Location, Apraxia

Inferior parietal lobe in the left hemisphere (primary). Inferior frontal gyrus and Lateral occipito-temporal cortex.

Role of the Right Hemisphere in Apraxia

Placement of the limb within 3D space. Errors may include location & amplitude of the limb relative to objects.

Deficits/errors in Praxis Construction System

Misuse errors (inappropriate use of objects/tools), Omission errors (skipping steps), and Tool selection errors

Deficits in Praxis Production System

Spatial errors (upside down/angle), Temporal errors (rhythm), Perseveration (repeating movement after completion), Body part as object errors, Gesture fragmentation (failing to complete gesture), and Gesture addition (adding unnecessary movements)

Apraxia Assessment

Largely relies on the therapist's clinical reasoning and personal experience. Formal testing is done by an Occupational Therapist (OT). Assessments use neuropsychological tests in a standardized environment.

Specific Assessment Components Apraxia

Assessing movements to verbal command, movements to imitation, and movements with real objects.

General Management Principles for Apraxia

Use functional activities within usual environment. gesture/demonstration. Keep instructions simple & process automatic. Maual guidance where required

Strategy Training for Apraxia

OT's teach compensation strategies, either internal or external

External Compensation (Strategy Training in Apraxia)

Using aids, such as a picture demonstrating distinct steps in an activity.

Internal Compensation (Strategy Training in Apraxia)

Utilizing cognitive functions like visual & verbal functions. Example: Asking a patient to verbalize the sequence of steps required whilst performing the task.

What is gesture training in Apraxia?

A rehabilitation approach where patients practice producing gestures (with or without objects) to improve motor planning and execution

Which stroke patients should be screened for Apraxia

Those with suspected difficulties executing tasks but have adequate limb movement & sensation

Multiple Sclerosis (MS) Definition

A chronic progressive demyelinating disease of the CNS where the immune system mistakenly attacks the brain, spinal cord, and optic nerves. interfering with nerve impulses

Aetiology/Proposed Causes of MS

Genetic predisposition + risk factors: low Vitamin D, childhood obesity (< girls), smoking, Epstein Barr Virus (EBV), chemical solvents, and ethnicity/climate/sun exposure (colder climates > hot).

Types of MS

Relapsing-remitting, secondary progressive, primary progressive, progressive-relapsing, Clinically isolated syndrome

Common Clinical Presentations at Onset of MS

Reduced vision in one eye + painful eye movement; double vision; ascending sensory disturbance/weakness; progressive balance & gait difficulties, altered sensation/pain traveling in back/limbs when bending the neck forwards (electric shock vibes).

Relapsing-Remitting MS (RRMS)

Caused by flare-ups or exacerbations of neurological symptoms, followed by periods of recovery or remission. Characterised by periods of partial recovery due to remyelinated nerves, though potentially not to the extent they used to be. Initially diagnosed with CIS. 70-75% of cases.

Secondary Progressive MS (SPMS)

A secondary phase of remitting MS that can develop years to decades following initial onset of symptoms. Characterized by a reduction in relapses and a progressive worsening of symptoms over time, with no obvious signs of remission.

Primary Progressive MS (PPMS)

Characterized by progressive worsening of symptoms and disability right from the beginning, with no periods of recovery or remission. Relapses are possible but not common. More common in males. May have periods of plateau when progression can stabilize.

Progressive-Relapsing MS

Rarest form, characterized by a constant worsening of the condition from the beginning, with clear attacks or relapses occurring in between

Clinical Isolated Syndrome (CIS)

The first presentation of MS (first relapse). A diagnosis of MS cannot be made until a second episode occurs or new lesions develop in the CNS. Not everyone who experiences CIS will develop MS.

MS Pathophysiology (Immune Cells)

An autoimmune disorder where the immune system mistakenly attacks the myelin sheath. T cells cross the blood-brain barrier into the CNS, release inflammatory cytokines, and activate other immune cells. B cells produce antibodies that target CNS components, amplifying damage.

Consequences of Immune Attack MS

Leads to demyelination, axonal injury, and formation of plaques in the CNS.

Demyelination Effects in MS

Results in reduced insulation of nerves. The action potential is not transmitted at normal speed along the nerve, despite the axon remaining intact.

Remyelination Potential MS

Partial remyelination can occur in early stages of the disease, but the regenerated myelin sheath has reduced quality and density.

Formation and Location of Plaques/Lesions MS

Randomly throughout the CNS (hemispheres, SC, cerebellum, brainstem). Predominantly white-matter (periventricular), specifically around the anterior and posterior horns of the lateral ventricles. Also affects the optic nerves and chiasm and long tracts of the spinal cords.

Acute vs. Older Lesions in MS

Acute lesions show marked inflammation around the plaques. Older lesions show scarring or fibrotic acellular tissue, which has no potential for remyelination or recovery.

Neurological Symptom Presentation in MS

Are a result of the location and size of these plaques (and inflammation in the acute period).

Characteristics of Axonal Damage in MS

Primarily occurs later in the disease and in progressive forms of the disease. Low grade atrophy can occur throughout the disease course independent of lesions.

MRI Findings in MS

Atrophy of white matter, degeneration of ascending and descending tracts of the brain and spinal cord, and ventricular dilation.

Prognosis / Progression of MS

Patients live approximately 6-7 years less than the general population. MS is not the primary cause of death, but having MS can increase the risk of certain diseases/conditions that may ultimately cause death.

Clinical Progression of MS

Related to the accumulation of neuro-axonal loss and the relative imbalance between damage, repair, and brain functional reserve.

3 Biological Processes Involved in MS Progression

Neurodegeneration, Inflammation, and Breakdown of CNS tolerance/repair mechanisms.

Progression of Untreated RRMS

half progress to SPMS in 10 years. 90% progress to SPMS in 25 years.

Progression of Treated RRMS

If treated with MDT, approximately 10% convert to SPMS over a median of 32 years.

Predictors of PPMS Development

Male sex and spinal cord lesions.

Factors Affecting Progression of MS

Vitamin D, smoking, genetics, lifestyle, and treatment with Disease Modifying Treatments (DMT).

Which clinical features suggest a higher risk of MS progression?

Early spinal cord lesions (within 3 years), initial balance/walking problems, cerebellar and pyramidal signs, and multifocal onset. Overall progression remains hard to predict

Diagnosis of MS (McDonald's Criteria)

Uses clinical symptoms, presence of lesions in the CNS on MRI scan, and episodes are inflammatory in nature. Other neurological pathologies must be excluded.

Diagnosis of PPMS (Specifics)

May use CSF analysis. Must have a history of one year progression. No distinction between symptomatic and asymptomatic lesions is required.

Diagnosis of RRMS (Specifics)

Requires 2 clinical attacks and 2 lesions in different locations OR 1 clinical attack with 1 lesion (possible MS).

MS Differential Diagnosis’

Migraines, neurotoxicity, and stroke.

MS Disease Modifying Drugs (DMD/DMT)

Reduce the frequency of exacerbations and slow disability progression.

Disease modifying therapy/drug Classifications

Immunomodulating (reduce activity of immune system or make it 'more normal') or Immunosuppressive (suppress immune reactions; broader reduction of immune system).

Ocrevus Uses & requirements & side effects (Immunosuppressive Example in MS)

Used for active RRMS, very active RRMS, and early PPMS. IV infusion. Can reduce relapse or slow disease progression. Must be <15 years post-diagnosis and able to mobilise >20m. Side effects/risks: infusion-related and infection risk

Corticosteroid use in MS

Used to reduce inflammation and speeds up recovery from acute relapses

Autologous Hematopoietic Stem Cell Transplantation (AHSCT) in MS

Uses immune-suppressing chemotherapy plus reinfusion of the patient's own stem cells to rebuild the immune system to reduce/stabilise MS activity/disability. Highly selective, not suitable for everyone, aggressive treatment

MS Disease Steps (0-1)

0 = Normal: No functional limitations; minor signs only. 1 = Mild disability: Mild sensory/bladder issues, fatigue, weakness; gait normal; may use symptomatic meds

MS Disease Steps (2-3)

2 = Moderate disability: abnormal gait; NIL aids; RR or progressive pattern. 3 = Early cane: Intermittent unilateral support for long distances; can walk ≥25 ft unaided.

MS Disease Steps (4-5)

4 = Late cane: Dependent on unilateral support; cannot walk 25 ft without it; may use scooter for distance. 5 = Bilateral support: Needs two canes/crutches or walker for 25 ft; scooter for longer distances.

MS Disease Steps (6-U)

6 = Wheelchair bound progressive decline in hand function. U = Unclassifiable: Disability not fitting above (e.g., severe cognitive/visual impairment, fatigue, bowel/bladder issues).

Expanded Disability Status Scale (EDSS)

Quantifies disability of MS. Monitors changes in the level of disability over time. Scoring is based on examination by a neurologist. Measures impairments in 8 function systems (steps 0-4.5) and impairment in walking (steps 5-9.5).

MS Specific Outcome Measures

MS Impact scale (MSIS-29) (20 physical, 9 psychological items), 12 item MS walking scale (MSWS-12), and MS QoL.

Fatigue Specific Outcome Measure

Modified Fatigue Impact Scale (21 items).

Impairment Specific Outcome Measures for MS

9 hole peg test, 2 min walk test, 6 min walk test (endurance), and 5 x STS (sit-to-stand).

Early Phase Management of MS

Assessment to establish baseline. Encourage PA and exercise. Management of any impairments, posture, and fatigue. Education, referral to MDT, and lifestyle mods

Early Phase Physiotherapy Targets in MS

Falls prevention, postural stability, coordination, agility, and dual tasking.

Agility Modalities for MS

Balance training, Pilates, hippotherapy, dance, Virtual Reality, and yoga.

Healthy Brain Lifestyle

Keep as active as possible, keep mind active, keep weight under control, avoid smoking, avoid stress, reorganize life/priorities, find a support team, and take medications for comorbidities.

MS Annual Assessment Components

MDT approach. Review MS symptoms, disease course, general health, levels of fatigue, social activity/participation, and care/carers

Common Impairments in MS

Weakness, spasticity, fatigue, tremor, pain, ataxia & incoordination, heat intolerance, oculomotor & vestibular dysfunction, bladder & bowel dysfunction, sexual dysfunction, cognitive decline, and depression.

Fatigue Impact in MS

Often one of the most disabling symptoms, occurs in most people. Can temporarily worsen other symptoms. More likely to interfere with daily activities than normal fatigue.

Causes of Fatigue in MS

Immune dysregulation, CNS mechanisms, endocrine abnormalities, and neurotransmitter dysregulation. deconditioning, sleep dysfunction, pain, psychological factors, depression, and medication side effects.

Non-MS Causes of Tiredness to Exclude

Infection, anaemia, iron deficiency, and thyroid dysfunction.

Factors that may exacerbate fatigue in MS populations

Heat, overexertion, stress, or time of day

Impaired Thermoregulation (Uhthoff's Phenomenon)

Temporary worsening of neurological symptoms, most commonly associated with multiple sclerosis, that occurs when a person's body temperature rises

Cause of Uhthoff's Phenomenon

Occurs when increased body temperature further slows or blocks action potential conduction in demyelinated axons. MS lesions also impair autonomic and endocrine regulation, contributing to heat intolerance

Heat Management During Exercise in MS

Minimize core body temperature elevation. 30 minutes of rest after. Use of cooling vests/ice vests, wet towels, or spray bottles during exercise. HIIT may help reduce risk of heat sensitivity.

Pain Management via Temperature (MS)

Heat can be used to slow conduction and reduce pain symptoms. Panadol or aspirin can reduce body temperature during exercise in adults.

Resting Tremor

Present in a body part that is completely supported against gravity and is not voluntarily activated (e.g., in hand, full muscle relaxation).

Action Tremor

Occurs when there is voluntary movement of a muscle or whilst maintaining a position against gravity. Includes postural tremor and intention tremor.

Intention Tremor (Kinetic Tremor)

Present during target-directed movement. Tremor amplitude increases as the limb approaches the target. Assessed using the finger-to-finger test.

Tremor Characteristics & cause in MS

Most tremors in MS are action tremors. Predominantly arises as a consequence of cerebellar or thalamic disease.

Physical Therapy for Tremor in MS

Using weights during activity may dampen intention tremors. This decreases muscle activity. Can be effective for improving ADLs while weight is worn/used. Caution: heavy weights may worsen tremor frequency. More effective for tremor than ataxia.

Oculomotor & Vestibular Dysfunction in MS

Dizziness & difficulty with vision reported in about 50%. Patients can report oscillopsia (jumping of the environment). Most symptoms are associated with brainstem and cerebellar lesions and increased disability.

Oculomotor Management in MS

Oculomotor retraining (smooth pursuit, ocular ranging, saccades, VOR cancellation). Functional integration training (challenging oculomotor and vestibular system during functional task training).

Vestibular Management in MS

Vestibular rehabilitation (VOR adaptation, desensitisation).

Frequent Cognitive Problems in MS

Memory, attention, processing speed, visuospatial abilities, and executive function.

Benefits of Exercise in MS

Evidence shows exercise improves cardiorespiratory fitness, strength, fatigue, balance, and quality of life.

Mobility Management for MS

Gait retraining (including dual tasking), balance retraining & falls assessment, and assistive devices & orthoses as required.

Evidence for Physical Therapy in MS

improve functional outcomes, reduce fatigue, and improve QoL. Inpatient or outpatient MDT (multidisciplinary team) care leads to longer-term gains. Information is good for improved knowledge

Parkinson's Disease (PD)

A slowly progressive neurodegenerative disorder that begins years before diagnosis can be made, implicates multiple neuroanatomical areas, results from a combination of genetic & environmental factors, and manifests with a broad range of symptoms.

PD Pathophysiology

Degeneration of dopaminergic neurons in the substantia nigra reduces dopamine in basal ganglia circuits. This disrupts the balance between direct (facilitatory) and indirect (inhibitory) pathways, increasing thalamic inhibition and reducing cortical excitation—leading to bradykinesia and poverty of movement

Core Pathological Features of PD

Loss of dopaminergic neurons in the substantia nigra compacta. Accumulation of Lewy bodies. Neuronal loss in multiple other areas of the brain.

Lewy Bodies

Clumps of misfolded protein seen in cell bodies of the nervous system.

Locations of Lewy Bodies in PD

Peripheral nervous system, spinal cord, and brain.

Braak Staging Model for PD

A model for the progression of Lewy body pathology in PD that seems to explain the clinical course of the disease.

Braak Stage 1 (PD)

Involves the PNS, olfactory system & medulla (starting in the GI system, moving up to olfactory/medulla).

Braak Stage 2 (PD)

Involves the pons, spinal cord grey matters.

Braak Stage 3 (PD)

Involves the pons, midbrain, basal forebrain, limbic system. This is typically where motor systems start to emerge.

Braak Stage 4 (PD)

Involves the limbic system, thalamus, temporal cortex.