Other Neurological Disorders

Parkinson’s Disease(PD)

group of disorders

Most common movement disorder in the US

Pathophysiology

• Chronic progressive disorder

• Lack of dopamine-producing neurons

• Disorder of the substantia nigra located in the basal ganglia

Clinical features of PD

Bradykinesia

Rigidity

Resting tremor

Postural instability

Festinating gait

Bradykinesia

Slow movement affects ADLs

Oral movement

• unintelligible speech, soft monotone voice, swallowing difficulties

Akinesia

• trouble initiated movement

Rigidity

Not dependent on movement velocity

Lead pipe and cogwheel

Restricted chest wall that affects breathing and phonation

Tremors

Often 1st sign

Resting tremors

“Pill rolling”

Postural Instability

Loss of postural extension

Flexed posture

• COG is forward

• Loss of extension, rotation, arm swing

Inability to respond to postural disturbances

Increased fall risk

Decrease proprioception

Relies on vision for movement cues

Other features of PD

Masked face

Dysphagia

Festinating gait

• Shuffling feet with progressive increase in speed

Freezing episodes

• Triggered by changing surfaces like doorways or flooring

Fatigue - worsens as the day progresses

Gait

Falls

Cognition

• ½ have dementia and cognitive changes

• Slow thought processes, decreased attention and concentration, depression

Stages of PD

Hoehn and Yahr classification of disability for Parkinson’s

Average person has a life expectancy slightly less than a person without Parkinson’s

Stage 0 to Stage 5

• Stage 0 = no signs of disease

• Stage 5 = needing a wheelchair or is bedridden unless assisted

Surgical management of PD

Deep brain stimulation (DBS)

Electrodes in the sub-thalamic nucleus with a stimulation box placed under the skin by the clavicle

• Pt can turn on/off

• Blocks nerve signals that produce symptoms

Physical therapy management of PD

Gait interventions, p. 466

Postural interventions, p. 466-468

Lee Silverman voice treatment (LSVT) BIG

• Certification

• Motor training principle

• Big movement and big stretches with voice commands

Exercise strategy and results, p. 469, Table 13-3

Multiple Sclerosis (MS) Pathophysiology

Demyelination of white matter in the brain and spinal cord

Axon is unprotected and sclerotic plaques form in the brain and spinal cord

Usually ages 20-40 with females being more prevalent

Areas that are usually affected with MS

Optic nerve

• Decreased acuity, diplopia, nystagmus,

Periventricular white matter

Corticospinal tract

• Weakness in one or both legs

Posterior columns

• Sensory disturbances are the 1st sign

• “Pins and needles” or “burning/aching”

Cerebellar peduncles

• Clumsiness with reaching (overshooting)

• Impaired coordination of movement

• Poor balance

• Ataxia

Clinical features of MS

Fatigue

• Most common complaint

• Worsens with heat

Cognitive impairment

• ½ will have some kind of impairment (problem solving, short-term memory, visual-spatial perception)

Autonomic dysfunction

• Bowel and bladder problems (urinary frequency, constipation, inadequate emptying)

Disease course

• Variable

• Exacerbations and remissions

Diagnosis of MS

Based on clinical evidence of multiple lesions in the CNS white matter, distinct time intervals, and age of occurrence (10-50 yrs old)

Cerebrospinal fluid examination

• Higher amounts of myelin protein

Magnetic resonance imaging (MRI)

• Best way to diagnosis

Medical management of MS

Purpose is to reduce the frequency and severity of the attacks. All are injectables.

• Avonex

• Betaseron

• Copaxone

New medications (IV):

• Tysabri

• Novantrone

Most common neurologic symptoms of MS

Weakness

• Lesions in corticospinal tract or cerebellum, inactivity

• Deconditioning

• Needs low to moderate intensity exercises

• Frequent repetitions and rest periods

• Avoid overexertion and overheating

Spasticity

• UMN damage

• Slow stretching or self stretching

• Slow rhythmical rotation

• Most often spastic plantar flexors, adductors, and quadriceps

Ataxia

• PNF techniques

• Balance activities

• Frenkel exercises (coordination ex), p. 477 Table 13-5

Additional concerns

• Mood swings

• Continuous nystagmus

• Vertigo

Clinical presentation of ALS

A progressive neurodegenerative disease that affects nerve cells in the brain and the spinal cord

Usually patients are 40-70 years old

Muscle weakness – cardinal sign

Distal symptoms occur before proximal

Most have asymmetrical muscle weakness in an arm or leg

Early signs: muscle cramps, weakness, atrophy, and fatigue

May lose the ability to speak, eat, move and breathe

Diagnosis based on S&S, EMG, imaging, nerve and muscle biopsies

No involvement of eye muscle or sensory

½ of the patients will have cognitive impairment

Death is usually from respiratory complications as muscles weaken

Medical management of ALS

No cure

Symptom management

There is one FDA-approved drug, riluzole, that slows the progression of ALS in some people

Physical therapy management of ALS

General initial guidelines:

• Avoid heavy eccentric exercise

• Moderate resistance can increase strength

• Needs to rest in between exercises

Pulmonary care at late stages for aspiration and airway clearance

Later on, need support of weak muscles by using orthosis (neck)

Pressure reducing devices

Pathophysiology of GBS

Autoimmune reaction

Schwann cells destroyed in peripheral nervous system but the axons are intact so after 2-3 weeks, the cells begin to proliferate, inflammation dissipates, and remyelination begins

Clinical features of GBS

Symmetrical ascending progressive disorder

Weakness begins distally and progresses proximally

• Burning and tingling of toes or hyperesthesia distally

• Motor involvement more than sensory

• If progresses to diaphragm, mechanical ventilation is needed

• ½ will have ANS changes (BP and HR)

• ½ oral-motor involvement (dysarthria and dysphagia)

Myalgia

• Throughout the process

DTRs absent due to areflexia (demyelination) of peripheral nerves

Medical management of GBS

Plasmapheresis (PE)

Infusion of IV immunoglobulins

Phases of GBS

Acute phase

• Up to 4 wks

• Symptoms continue to worsen

Plateau phase

• Up to 4 wks

• Stabilzation of symptoms

Recovery phase

• From a few months to a couple of years

• Improvement

• 80% recover in a year but may still have some deficits

Physical therapy management of GBS

Acute phase

• Usually in ICU on a ventilator

• Treat symptoms as they occur

Plateau phase

• Upright positions (slowly)

• Gradually increase ROM and movements as tolerated

Recovery phase

• Muscle strength returns in reverse order (descending)

• Tilt table—>standing—>transfers—>gait training

Chronic Inflammatory Demyelinating Polyradiculoneuropathy (CIDP)

is a slowly developing autoimmune disorder of the peripheral nervous system in which the body's immune system attacks the myelin sheath

Unknown etiology

It’s most common in older adults, and more in men than women.

No specific test to determine diagnosis but weakness must be present for at least 2 months

There are periods of remission and relapse

Common symptoms are gradual weakness or sensation changes in the arms or legs

Symmetrical motor and sensory involvement

Stocking glove distribution of numbness and tingling

Hypo or areflexia

Postural tremor of the hands

Papilledema, vision loss

Facial weakness

CIDP vs GBS

CIDP

• Nerve involvement

• Weakness

• Numbness

• Not linked to illness

• Tends to be a long-term recovery

• Chronic

GBS

• Nerve involvement

• Weakness

• Numbness

• Begins after an illness

• Most recover fairly quickly

• Acute

• May develop into CIDP if it reoccurs

Medical Management of CIDP

Corticosteroids

Plasmaphoresis

Intravenous immunoglobin (IVIG)

Physical Therapy Management of CIDP

ROM

Balance

Aerobic conditioning

Strengthening

Gait training

Avoid overexertion

Post-Polio Syndrome (PPS) Etiology

Most believe that it is caused by increased metabolic demand made on the body by giant motor units that were formed during the recovery process from the original viral infections

Clinical features of Post-Polio Syndrome

Fatigue

• Overwhelming tiredness

• Can occur at the same time of day and have autonomic distress( HA or sweating)

New weakness

• Hallmark sign

• Occurs in muscle already involved and in muscles that did not show any effects of the original infection

• Asymmetrical proximal weakness and progressive

• Permanent damage now

• Precaution of overuse

Pain

• Muscle and joint pain

Cold intolerance

Decreased function

• Due to fatigue, pain, and weakness cycle

• SOB

• Interrupted sleep due to apnea or pain

• Increased fall risk and decreased bone density

• Compensatory movement for gait

Medical management of Post-Polio Syndrome

No specific medication

Healthy diet

Sleep apnea treatment

Increase activity

Staying warm

Good pulmonary ventilation

Physical therapy management of Post-Polio Syndrome

Exercise

• General guidelines: avoid overuse and disuse, modify activity level to decrease pain, monitor vitals

• Customize exercise programs with rests periods

Stretching – caution due to joint instability

Pain management

• Cramping, musculoskeletal, and biomechanical

Lifestyle modification

• Must change and slow down

Energy conservation

• Helps to manage fatigue