Treatment approaches, outcome measures, and medications
Neurodevelopmental treatment (NDT)
The treatment approach follows the principles below.
- Developmental stages
- Each individual with neurological deficits has varied functional deficits
- The developmental stage aims to assess the individual’s current functional status and then aid in progressing to the next stage
- Example: A stroke patient who can sit independently would progress next to working on standing before gait
- Sensory integration
- Individuals with neurological deficits require sensory input to understand their environment and how to respond to it
- Postural control
- Emphasizing the need for appropriate postural alignment and stability to aid in improving movement patterns
- Hands-on approach
- Therapists provide tactile feedback to build the individual’s understanding of correct movement patterns
Frenkel exercises
Description
- Frenkel exercises are slow, repetitive, and precise movements performed in supine, sitting, and standing positions.
- They emphasize visual control to compensate for loss of proprioception.
- Movements are performed actively, and the patient is instructed to watch their limbs while moving.
- Exercises are progressed from simple to complex, and from unilateral to bilateral movements.
- Rhythm, speed, and range are gradually increased as control improves.
- Can be done with or without verbal cues and metronome guidance to aid timing.
- Sensory ataxia worsens with the eyes closed (a positive Romberg sign), which is why visual compensation works especially well. Frenkel exercises are also a standard coordination intervention for cerebellar ataxia, where the slow, precise repetition does most of the work.
Role in neurological rehabilitation
- Improves coordination in sensory (proprioceptive) ataxia and in cerebellar ataxia.
- Promotes motor control and timing through visual compensation and repetition.
- Enhances concentration and motor planning through attention to precise limb movement.
Example exercises
- Supine: Heel slides along a straight line to the knee or shin of the opposite leg.
- Sitting: Touch heel to a series of marked points on the floor in a set sequence.
- Standing: Step to and from targets marked on the floor without losing balance.
Treatment strategies for individuals with pusher syndrome
Pusher syndrome can be caused by lesions to the right or left side of the thalamus. It can be associated with neglect and aphasia. Pusher syndrome typically does not last longer than 6 months, but in the short term impairs functional mobility and movement.
Treatment strategies
- Do not push/pull to correct posture
- Utilize visual cues in the environment to assist with achieving an upright position, such as door frames or windows
- This gives the individual with pusher syndrome a cue as to what is vertical
- Stand/sit with non-paretic side against the wall to provide support for vertical alignment
- Encourage weight shifting toward the non-paretic side to achieve midline orientation
- Place tape on the floor to assist with giving a visualization of vertical
- Distract the patient’s attention from the non-paretic side to reduce pushing with that extremity
Cueing strategies for Parkinson’s disease
External cues help many people with Parkinson’s disease start walking and keep walking, because they shift gait from automatic control, which the basal ganglia impairment disrupts, to conscious control:
- Auditory cues: a metronome, music, or rhythmic counting sets the stepping rhythm and lengthens the steps
- Visual cues: lines or tape on the floor to step over, especially at doorways and turns, where freezing of gait is most common
- Turn in wide arcs rather than rapid pivots, and hold off on complex dual-task walking, which worsens freezing, until single-task walking is safe
When to stop and report during neurological interventions
These signs apply to every neurological diagnosis, not only Parkinson’s disease.
Outcome measures
The PTA administers these outcome measures and reports the results and any changes to the supervising PT, who interprets the findings and determines whether the plan of care needs to change.
| Outcome measure | Purpose | Setting | Key cutoffs/notes |
|---|---|---|---|
| Berg balance scale | Predicts fall risk and the need for an assistive device; assesses static and dynamic balance in sitting and standing | Inpatient rehab, outpatient | Score of 45 or less indicates increased fall risk |
| Functional gait assessment (FGA) | Evaluates balance and postural stability during gait; a modification of the DGI with improved reliability and less ceiling effect | Inpatient rehab, outpatient | Score of 22 or less indicates increased fall risk; a change of 4 or more is a significant change |
| Dynamic gait index (DGI) | Measures the ability to respond to changing demands during gait beyond steady-state walking, especially for balance and vestibular deficits; includes head turns and obstacle navigation | Inpatient rehab, outpatient | Score of 19 or less predicts falls |
| Tinetti (POMA) | Performance-based test of balance (sitting, standing, turning) and gait to determine fall risk; maximum score 28 | Inpatient rehab, outpatient | Score of 19-23 = moderate fall risk; 18 or less = high fall risk |
| Functional reach | Measures balance and stability related to fall risk, especially for stepping and reaching deficits | Acute care, inpatient rehab, outpatient | More than 10 inches indicates low fall risk; 6-10 inches, about twice the risk; 6 inches or less, about four times the risk |
| Fugl-Meyer | Quantifies motor recovery, balance, and sensory status post-stroke | Inpatient rehab | Max score of 226; no normal score - goal is increased independence, typically compared from evaluation to discharge |
| Activities-specific balance confidence scale (ABC scale) | Self-reported confidence performing activities without losing balance | Outpatient | 80% or higher = high functioning; 50-80% = moderate; 50% or less = low functioning |
| 5-time sit-to-stand | Assesses lower limb strength, balance, and functional mobility | Acute care, inpatient rehab | Age-based norms: 11.4 sec (60-69), 12.6 sec (70-79), 14.8 sec (80-89) |
| Timed up and go (TUG) | Assesses mobility, balance, and walking while estimating fall risk | Inpatient rehab, outpatient | 10 seconds or less is considered normal |
| Modified Ashworth scale (MAS) | Grades spasticity by resistance to passive stretch | Inpatient rehab, outpatient | Graded 0, 1, 1+, 2, 3, 4; 0 = no increase in tone, 4 = rigid in flexion/extension |
| 10-meter walk test | Measures gait speed to classify ambulation status | Inpatient rehab, outpatient | Less than 0.4 m/s = household ambulator; 0.4-0.8 m/s = limited community ambulator; more than 0.8 m/s = community ambulator |
| Functional independence measure (FIM) | Evaluates level of disability and assistance needed for mobility and ADLs across 18 items | Inpatient rehab | No normal score - goal is increased independence over the course of therapy |
| Mini-Mental State Examination (MMSE) | 30-point pen-and-paper screening tool that gives an overall measure of cognitive impairment, evaluating attention and orientation, memory, registration, recall, calculation, and language | Varies | Cognitive screening |
Medical tests and procedures
The physician orders and interprets these tests; the PTA reads the results and follows the precautions they create.
| Test | What it shows | What it means for the PTA |
|---|---|---|
| Noncontrast head CT | First study in a suspected stroke; quickly shows bleeding | Bleeding is ruled out before tPA; glucose is checked too, since hypoglycemia mimics stroke |
| MRI | More sensitive than CT for early or small ischemic strokes and diffuse axonal injury | Implants are screened first (see DBS below) |
| Nerve conduction studies (NCS) and electromyography (EMG) | Slowed conduction points to demyelination (e.g., GBS), low amplitudes to axonal loss; fibrillation potentials on EMG show denervation; a decremental response to repetitive stimulation points to myasthenia gravis | Localizes a peripheral lesion |
| Lumbar puncture | Samples CSF from the lumbar subarachnoid space; high protein with a normal cell count supports GBS; also used for meningitis, subarachnoid hemorrhage, and MS | A headache afterward that worsens upright and eases lying down is a post-dural puncture headache: have the patient lie down and report it |
| Electroencephalogram (EEG) | Records the brain’s electrical activity to classify seizures and locate their onset | Background for seizure precautions |
Deep brain stimulation (DBS) treats Parkinson’s disease with electrodes in a deep brain target (usually the subthalamic nucleus or globus pallidus interna) wired to a pulse generator in the chest wall; it can improve tremor, bradykinesia, and gait. Any diathermy (shortwave, microwave, or therapeutic ultrasound) is contraindicated with DBS, and MRI is done only under the device maker’s conditions; check the chart for implants before any modality.
Common neuromuscular medications
- Levodopa
- Mechanism of action: replaces dopamine in the basal ganglia; used for Parkinson’s disease
- System interactions:
- Cardiovascular: orthostatic hypotension - check blood pressure with position changes
- Motor: dyskinesias at peak dose; wearing-off and on-off fluctuations - schedule therapy during the “on” period, about 1 hour after a dose
- Gastrointestinal: nausea
- Neuro: confusion, hallucinations, delusions, psychosis, agitation
- Baclofen
- Mechanism of action: a GABA-B receptor agonist that inhibits spinal reflexes to reduce spasticity
- System interactions:
- Neuro: drowsiness, dizziness, fatigue, generalized muscle weakness - weakness can reduce function in patients who rely on their tone to stand or transfer
- Abrupt discontinuation (including an intrathecal pump malfunction) can cause withdrawal: rebound spasticity, high fever, altered mental status, hallucinations, seizures. This is a medical emergency, so report it immediately.
- Tizanidine
- Mechanism of action: a skeletal muscle relaxant used to relieve muscle spasms, cramping, and tightness caused by conditions such as multiple sclerosis and spinal injury
- Donepezil
- Mechanism of action: an acetylcholinesterase inhibitor used in the treatment of Alzheimer’s disease to slow the progression of memory loss and confusion
- System interactions:
- Cardiac: bradycardia, syncope - monitor heart rate and fall risk
- Musculoskeletal: muscle cramps, weakness, tremors
- Gastrointestinal: nausea, vomiting, diarrhea, weight loss
- Neuro: headache, seizures, dizziness
- tPA (tissue plasminogen activator)
- Mechanism of action: dissolves blood clots, specifically for the treatment of ischemic stroke
- System interactions:
- Bleeding risk, including intracranial hemorrhage: watch for bleeding (gums, IV sites, urine, stool) and any sudden neurological decline (worsening weakness, severe headache, change in level of consciousness); stop the session and notify the nurse or PT immediately. Mobility is usually held or restricted for about 24 hours after tPA, per facility protocol.
- Neuro: headache, dizziness, blurred vision
- Gastrointestinal: nausea, vomiting
- Pulmonary: cough
- Keppra (levetiracetam)
- Mechanism of action: an antiepileptic used to treat seizures
- System interactions:
- Neuro: drowsiness, dizziness, mood swings, headache
- Neuromuscular: weakness (asthenia) and fatigue - monitor fall risk during mobility
- Behavioral: irritability, aggression, or depression - report new or worsening behavior changes