Neuro Final Exam

What is a Traumatic Brain Injury (TBI)?

A brain injury caused by an external physical force. TBI is technically a type of acquired brain injury (ABI). Common causes include falls, motor vehicle accidents, sports injuries, shaken baby syndrome, gunshot wounds, domestic violence, and military combat injuries.

What is an Acquired Brain Injury (ABI)?

Any brain injury acquired after birth. Includes TBI, CVA (stroke), brain infections, tumors, metabolic disorders, seizures, and anoxic injuries. Treatment interventions are the same regardless of cause.

High-risk populations for TBI

• Males (2:1 ratio compared to females)

• Children under 4 years

• Adolescents ages 15–19

• Adults over 75

• Individuals with previous TBI

• Military personnel

• Individuals with history of alcohol or drug abuse
  
  

Mild TBI

Loss of consciousness and/or confusion lasting less than 30 minutes. Often referred to as a concussion.

Moderate TBI

 Loss of consciousness lasting 30 minutes to 24 hours. May include skull fracture.

Severe TBI

Loss of consciousness longer than 24 hours and/or post-traumatic amnesia longer than 24 hours.

Open Head Injury (OHI)

 Skull is penetrated (e.g., gunshot wound). Often results in focal brain damage.

Closed Head Injury (CHI)

Skull remains intact. Causes focal and diffuse brain damage. May lead to cerebral edema and increased intracranial pressure (ICP).

Coup–Contrecoup injury

Injury occurs at the site of impact (coup) and the opposite side of the brain (contrecoup) due to rapid acceleration and deceleration.

Diffuse Axonal Injury (DAI)

Widespread damage caused by shearing forces from acceleration/deceleration. Axons are stretched or torn, disrupting signal transmission and leading to severe cognitive deficits.

What is secondary brain injury?

Damage that occurs minutes to days after the initial injury due to chemical and physiological responses in the brain. It is the leading cause of death following TBI.

 Examples of secondary injury effects

Intracranial hematoma, cerebral edema, increased ICP, hydrocephalus, infection, and seizures.

 What is an anoxic brain injury?

 Brain injury caused by lack of oxygen (hypoxia/anoxia). Brain cells begin to die after ~4 minutes; permanent damage may occur after ~5 minutes.

Causes of anoxic brain injury

Near drowning, choking, cardiac arrest, respiratory failure, carbon monoxide poisoning.

Physical symptoms of brain injury

Weakness/paralysis, dysphagia, balance and vestibular deficits, visual impairments, coordination problems.

Cognitive & perceptual symptoms of brain injury

Cognitive deficits, apraxia, aphasia, memory impairment, perceptual deficits, impaired problem-solving.

Behavioral & emotional symptoms of brain injury

Personality changes, impulsivity, agitation, poor insight, impaired safety awareness.

Glasgow Coma Scale (GCS) purpose

 Assesses severity of brain injury based on eye opening, verbal response, and motor response.

GCS score classifications

• Severe: ≤ 8

• Moderate: 9–12

• Mild: 13–15
  
  

Purpose of Rancho Levels

Describes patterns of cognitive and behavioral recovery after brain injury and guides OT intervention planning

Rancho Level I(1) – No Response ( Total Assistance)

• At this stage, clients do not responding to external stimulation, do not open their eyes and do not respond to painful stimuli

• Treatment: PROM and Positioning

Rancho Level II (2)– Generalized Response ( Total Assistance)

• At this stage, clients react to stimulation inconsistently in a non-specific, non-purposeful manner and it is considered to be in a vegetative stage

• Treatment: Positioning, PROM, Orthoses, Sensory stimulation, Visual, auditory, vestibular, olfactory, Family education and training

• May begin working on head control and balance at EOB or in w/c (as appropriate)

Rancho Level III (3)– Localized Response ( Total Assistance)

• At this stage, client responds in a specific manner to stimulation , but response may be delayed or inconsistent

• Treatment:

Sensory Stimulation

• Family education

• Positioning and orthoses (Due to tone)

• PROM and AAROM

Olfactory stimulation in TBI

Uses familiar scents to increase arousal and emotional engagement due to limbic system involvement.

Gustatory stimulation in TBI

Lemon swabs, cold swabs, flavored oral swabs (toothettes) to stimulate oral awareness when not eating by mouth.

Vestibular stimulation considerations

Upright positions increase alertness. Monitor vital signs closely. Risk of orthostatic hypotension—use slow transitions or tilt table.

Rancho Level IV(4) – Confused, Agitated ( Maximal Assistance)

Severe confusion, impulsivity, agitation, poor safety awareness. OT focuses on behavior management, attention, safety, ADLs, mobility, and low-stimulation environments.

Rancho Level V(5) – Confused, Inappropriate (Non-Agitated) ( Maximal Assistance)

Inappropriate responses, memory deficits, poor insight. OT emphasizes familiar functional tasks, cognition, ADLs/IADLs, balance, and mobility.

Rancho Level VI(6) – Confused, Appropriate (Moderate Assistance)

Appropriate responses with memory deficits. Uses external cues. OT focuses on structured routines, safety awareness, adaptive equipment, dual-task activities.

Rancho Level VII (7)– Automatic, Appropriate (Minimal Assistance)

Performs daily routines with impaired judgment. OT emphasizes IADLs, community reintegration, cognitive strategies, and group therapy.

 Rancho Level VIII (8) – Purposeful, Appropriate

Oriented with impaired abstract reasoning. OT focuses on independence, vocational rehab, driving rehab, and advanced cognitive skills.

Rancho Level IX (9) – Purposeful, Appropriate (SBA)

 Aware of limitations and asks for help. OT focuses on compensatory strategies and vocational transition.

Rancho Level X (10) – Purposeful, Appropriate (Mod I)

 Independent with compensatory strategies. OT acts as consultant/resource.

OT role on the interdisciplinary team for TBI

Focuses on function, integrates PT mobility, SLP swallowing/cognition, neuropsych behavioral insights, and family education.

 OT family & caregiver education topics

Safety, behavior management, physical and cognitive adaptations, home modifications, social awareness, and body mechanics.

What is lower motor neuron (LMN) dysfunction?

 Damage to the motor neuron from the anterior horn cell to the muscle fiber, resulting in flaccid paralysis, muscle weakness, atrophy, decreased tone, and absent or diminished reflexes.

Common causes of LMN dysfunction

Nerve root compression, trauma, toxins, infections, neoplasms, vascular disorders, degenerative CNS diseases, and congenital malformations

Diseases covered under motor unit & myopathic disorders

 Guillain-Barré Syndrome (GBS), Myasthenia Gravis (MG), Post-Polio Syndrome (PPS), Duchenne & Becker Muscular Dystrophy, Charcot-Marie-Tooth (CMT), Myotonic Muscular Dystrophy (MMD), Limb-Girdle MD (LGMD), Facioscapulohumeral MD (FSHD), Spinal Muscular Atrophy (SMA).

What is Guillain-Barré Syndrome?

 A rapidly progressing, life-threatening autoimmune disorder that damages the myelin sheath of peripheral nerves, often following viral infection, immunization, or surgery.

Hallmark pattern of weakness in GBS

Ascending weakness (distal → proximal), starting in the legs and moving upward.

Key signs and symptoms of GBS

 Tingling in extremities, progressive weakness, unsteady gait, difficulty breathing, facial weakness, dysphagia, bowel/bladder dysfunction, abnormal heart rate and BP.

GBS subtypes

• AIDP (most common)

• Miller Fisher syndrome (eye muscles first)

• Acute motor axonal neuropathy

• Acute motor sensory axonal neuropathy

• Acute panautonomic neuropathy

• Bickerstaff brainstem encephalitis
  

Diagnosis and prognosis of GBS

Diagnosed via lumbar puncture, EMG, and clinical presentation. Recovery averages 3–6 months but may be longer. Secondary complications greatly affect rehab outcomes.

Medical treatment for GBS

Plasmapheresis and high-dose immunoglobulin therapy; mechanical ventilation if respiratory muscles are involved.

 OT treatment priorities for GBS

ROM, orthoses, bed/wheelchair positioning, BADLs/IADLs, caregiver education, energy conservation, and submaximal exercise only (especially first 6–12 months).

What is Myasthenia Gravis?

A progressive autoimmune disorder where antibodies block acetylcholine receptors at the neuromuscular junction, preventing effective muscle contraction

Hallmark symptom of MG

Muscle weakness that worsens with activity and improves with rest

Common muscles affected in MG

Eye muscles (ptosis, diplopia), facial muscles, muscles of swallowing and speech.

Factors that exacerbate MG symptoms

Fatigue, emotional stress, lack of sleep, anxiety, overexertion, extreme temperatures, hot foods/drinks, and certain medications.

Diagnosis and medical management of MG

Blood antibody testing, Tensilon (Edrophonium) test, EMG; treated with immunosuppressants, thymectomy, plasmapheresis, and fatigue management.

OT interventions for MG

Energy conservation, work simplification, adaptive equipment, NO fatigue, gentle exercise, home evaluation, and patient education on avoiding triggers.

 What is poliomyelitis?

A contagious viral disease affecting anterior horn cells of the spinal cord, causing flaccid paralysis with intact sensation

Classic symptoms of polio

Flaccid paralysis, LE involvement with atrophy, possible UE involvement, swallowing difficulties, contractures, intact sensation.

What is Post-Polio Syndrome (PPS)?

New onset muscle weakness, pain, or fatigue occurring 15–30 years after recovery from acute polio infection.

Symptoms of PPS

Progressive weakness, muscle atrophy, joint pain, fatigue, breathing/swallowing issues, sleep apnea, cold intolerance.

OT management for PPS

Energy conservation, ADL training, pacing strategies, psychosocial support, and counseling.

What are muscular dystrophies?

A group of genetic disorders causing progressive muscle weakness due to defects in muscle proteins.

Key difference between Duchenne and Becker MD

DMD is more severe with earlier onset and shorter life expectancy; BMD has slower progression and longer ambulation.

Role of dystrophin in muscle

Strengthens muscle fibers and protects them from damage during contraction and relaxation.

Common complications of DMD

 Scoliosis, respiratory failure, need for power wheelchair, BiPAP or ventilator, pain, anxiety, depression, social withdrawal.

OT role in DMD

Maintain strength, prevent obesity and osteoporosis, pain management, wheelchair positioning, pressure relief, contracture management, adaptive equipment.

Exercise guidelines for DMD

Submaximal aerobic activity (walking, cycling, swimming); no high-resistance strengthening.

What is Charcot-Marie-Tooth disease?

A hereditary peripheral neuropathy affecting axons or myelin, causing distal muscle weakness and sensory loss.

Common clinical features of CMT

High-arched feet, foot drop, muscle wasting, numbness in hands/feet, balance deficits.

OT and exercise considerations for CMT

Symptom management, gentle aerobic exercise, core strengthening, avoidance of overuse and pain.

What is myotonia?

Inability of a muscle to relax voluntarily after contraction.

Difference between MMD1 and MMD2

MMD1 affects distal muscles first and includes vision and facial weakness; MMD2 affects proximal muscles and walking earlier but is less severe

 OT treatment for MMD

Symptom management, ROM, strengthening, aerobic exercise under cardiology supervision.

Key features of LGMD

Weakness of shoulder and hip girdles, scapular winging, abnormal gait, progression to walker or wheelchair use.

Treatment considerations for LGMD

Emerging therapies (antisense, stem cell), ROM, contracture prevention, adaptive mobility strategies.

Primary muscles affected in FSHD

Face, shoulder girdle, upper arms, trunk, hips, and legs.

 OT management for FSHD

Symptomatic treatment, submaximal exercise, pain management, avoidance of overuse, posture and positioning strategies.

What is Spinal Muscular Atrophy?

A motor neuron disease characterized by loss of anterior horn cells leading to symmetrical proximal weakness.

Key features of SMA

Proximal > distal weakness, legs > arms, preserved sensation, decreased reflexes, bulbar weakness, scoliosis, contractures.

OT focus for SMA

Positioning, contracture management, respiratory support strategies, adaptive equipment, caregiver education.

What are degenerative diseases of the CNS?

Progressive neurological conditions characterized by gradual deterioration of neurons in the brain and/or spinal cord, leading to declining motor, sensory, cognitive, and functional abilities.

Primary role of OT/OTA with progressive neurological diseases

• Manage symptoms

• Maintain function as long as possible

• Optimize quality of life

• Compensate for declining abilities

• Promote client-centered, respectful care

• Support both client and caregivers
  
  

Key factors OT must consider in degenerative CNS diseases

• Progressive decline in occupational performance

• Fluctuating performance during the day

• Increased caregiver burden

• Limited medical cure

• Psychosocial and end-of-life concerns

General OT treatment goals for degenerative CNS diseases

• Maximize participation in meaningful occupations
  
  

• Prevent secondary complications
  
  

• Teach self-management strategies
  
  

• Educate caregivers on safe assistance
  
  

• Preserve dignity and autonomy
  
  

What is Multiple Sclerosis (MS)?

An autoimmune disease of the CNS in which the immune system attacks myelin, causing demyelination and plaque formation in the brain and spinal cord.

Typical MS population and risk factors

• Women ages 20–50
  
  

• Caucasians of Northern European ancestry
  
  

• Low vitamin D levels
  
  

• Higher latitudes
  
  

Smoking increases risk

Diagnostic criteria for MS

• Evidence of CNS damage in at least two locations
  
  

• Damage occurred at least one month apart
  
  

• Other diagnoses ruled out
  
  

• Confirmed via MRI, blood tests, and clinical findings
  
  

Common symptoms of MS

• Fatigue
  
  

• Spasticity and weakness
  
  

• Visual disturbances
  
  

• Cognitive impairment
  
  

• Heat intolerance
  
  

• Bowel/bladder dysfunction
  
  

• Sensory changes
  
  

• Tremor and dizziness

MS precautions for OT intervention

Avoid overfatigue

Keep environment cool

Use heat cautiously

Expect fluctuating performance

Monitor safety closely

OT focus areas for MS

• ADL/IADL adaptation
  
  

• Energy conservation
  
  

• Adaptive equipment
  
  

• Cognitive and visual strategies
  
  

• Client and family education
  
  

What is Parkinson’s Disease?

A slow, chronic, progressive neurological disease caused by degeneration of dopamine-producing neurons in the substantia nigra.

Four cardinal signs of Parkinson’s Disease

1. Resting tremor (pill-rolling)
   
   

2. Rigidity (cogwheel rigidity)
   
   

3. Bradykinesia
   
   

Postural instability

Functional symptoms of PD affecting occupations

• Shuffling gait and freezing
  
  

• Micrographia
  
  

• Masked facial expression
  
  

• Dysphagia and drooling
  
  

• Orthostatic hypotension
  
  

Fatigue and depression

Stages of Parkinson’s Disease

• Stage 1: One side affected
  
  

• Stage 2: Both sides affected, balance intact
  
  

• Stage 3: Balance impaired, independent
  
  

• Stage 4: Severe disability, can stand/walk
  
  

• Stage 5: Wheelchair or bed-bound
  
  

OT interventions for Parkinson’s Disease

• Adaptive equipment for tremors
  
  

• Task simplification
  
  

• Fall prevention strategies
  
  

• Balance and mobility training
  
  

• Caregiver education
  
  

Exercise considerations for PD

• Improves balance, flexibility, strength
  
  

• Reduces depression and anxiety
  
  

• Dancing, walking, swimming beneficial
  
  

Must account for fall risk

What is ALS?

A rapidly progressive, fatal motor neuron disease affecting voluntary muscle control, including breathing and swallowing.

Diagnostic criteria for ALS

• Upper motor neuron signs: increased tone, hyperreflexia
  
  

• Lower motor neuron signs: weakness, atrophy, decreased reflexes
  
  

Typical progression of ALS

• Progressive muscle weakness
  
  

• Loss of functional mobility
  
  

• Eventual paralysis
  
  

• Cognition often intact
  
  

• Leads to “locked-in” state

OT role in ALS management

• Adaptive equipment and technology
  
  

• ROM to prevent contractures
  
  

• Positioning and pressure relief
  
  

• Caregiver training
  
  

Energy conservation

Exercise considerations for ALS

• No aggressive strengthening
  
  

• Gentle ROM and stretching
  
  

Focus on safety and comfort

What is Huntington’s Disease?

A genetic, neurodegenerative disease causing progressive motor, cognitive, and psychiatric impairments.

Hallmark motor symptoms of HD

• Chorea (involuntary movements)
  
  

• Poor voluntary motor control
  
  

• Ataxia
  
  

Difficulty with self-feeding

Cognitive and psychiatric symptoms of HD

• Depression
  
  

• Irritability
  
  

• Apathy
  
  

• Anxiety
  
  

Impaired judgment and decision-making

OT interventions for early-stage HD

• Structured routines
  
  

• Visual schedules and reminders
  
  

• Adaptive equipment
  
  

• Proximal stability for self-feeding
  
  

• Fatigue management