Physical Medicine Rehab · Supplementary · from Physical Medicine Rehab

Case 3: Traumatic Brain Injury Cognitive Rehabilitation

Patient Presentation

Demographics: 34-year-old male software engineer

Chief Complaint: "I can't concentrate, I forget everything, and I can't do my job anymore"

History of Present Illness: This 34-year-old male software engineer presents to the outpatient brain injury rehabilitation clinic 4 months after a severe traumatic brain injury (TBI) sustained in a cycling accident. He was not wearing a helmet when he was struck by a motor vehicle at an intersection. He was found unconscious at the scene with a GCS of 6 (E1V2M3). He was intubated in the field and transported to a Level I trauma center.

CT head revealed bifrontal contusions, a small right temporal epidural hematoma (managed conservatively), and diffuse axonal injury with punctate hemorrhages in the corpus callosum and brainstem. He remained in a coma for 12 days (post-traumatic amnesia lasted 35 days). He underwent tracheostomy and PEG tube placement during the acute hospital stay. He spent 4 weeks in acute inpatient rehabilitation where he was decannulated, transitioned to oral diet, and regained independent ambulation.

He was discharged home 2 months ago and has been attending outpatient therapies. His wife reports persistent cognitive deficits that significantly impact his daily life. He has difficulty sustaining attention for more than 10-15 minutes, cannot multitask, frequently loses track of conversations, and forgets appointments and recent events. He becomes easily frustrated and has had several episodes of verbal outbursts toward his wife and children. He attempted to return to work part-time 3 weeks ago but was unable to perform his programming tasks and became overwhelmed. His employer has placed him on medical leave.

Past Medical History:

• Severe TBI (GCS 6, PTA 35 days) 4 months ago
• Bifrontal contusions and diffuse axonal injury
• Right temporal epidural hematoma (managed conservatively)
• Post-traumatic seizure (one episode during acute hospitalization, on levetiracetam)
• No prior medical or psychiatric history

Medications:

• Levetiracetam 500 mg twice daily (seizure prophylaxis)
• Amantadine 100 mg twice daily (cognitive enhancement)
• Methylphenidate 10 mg every morning (attention)
• Melatonin 5 mg at bedtime (sleep-wake cycle regulation)
• Sertraline 50 mg daily (mood/irritability)

Social History:

• Software engineer at a tech company (10 years of experience)
• Married with two children (ages 4 and 7)
• Master's degree in computer science
• Premorbid high functioning, no learning disabilities
• Non-smoker, occasional craft beer enthusiast (abstinent since injury)
• Previously active: cycling, hiking, rock climbing
• Currently unable to drive (visual processing and reaction time concerns)
• Wife has reduced work hours to part-time to provide supervision and support

Family History:

• No family history of neurologic or psychiatric disease
• Father with hypertension
• Mother healthy

Physical Examination

• Vital Signs: BP 122/76 mmHg, HR 72 bpm, RR 14/min, Temp 36.8°C, SpO2 99% on room air, BMI 25.4
• General: Well-appearing male, ambulatory without assistive device. Appears restless, frequently shifts in chair. Oriented to person, place, date, and situation
• Neurologic — Motor: 5/5 strength in all extremities bilaterally. Normal muscle tone. No pronator drift
• Neurologic — Coordination: Mildly impaired finger-to-nose on left (intention tremor). Tandem gait mildly unsteady
• Cranial Nerves: Intact except for mild left CN VII upper motor neuron weakness (subtle flattening of left nasolabial fold with emotional expression). Visual fields full to confrontation. PERRLA
• Speech/Language: Fluent speech. Mild word-finding pauses under time pressure. No aphasia. Mildly dysarthric with rapid speech
• Cognition (bedside assessment):
• Attention: Digit span forward 5 (normal 7+), backward 3 (normal 5+). Unable to sustain serial 7s beyond 3 subtractions
• Memory: Recalls 2/5 words at 5 minutes (with cuing, recalls 4/5). Unable to recall what he had for breakfast
• Executive Function: Impaired verbal fluency (8 animals in 60 seconds, normal >14). Unable to perform Trail Making Test B (loses set after 4 alternations)
• Processing Speed: Markedly slowed on timed tasks
• Behavioral Observations: Becomes visibly frustrated when struggling with cognitive tasks. Interrupts examiner. Distractible — looks away from examiner toward door sounds. Impaired self-awareness (states "I'm mostly fine, just a little slow")
• Gait: Independent, mildly wide-based. Normal arm swing. No assistive device needed

Workup and Results

Laboratory Studies:

Imaging/Additional Studies:

• MRI Brain (3 months post-injury): Encephalomalacia in bilateral frontal lobes (right > left) with ex vacuo ventriculomegaly. Hemosiderin deposits in the corpus callosum (splenium) and right dorsolateral midbrain consistent with prior diffuse axonal injury. Resolved right temporal epidural hematoma with minimal residual gliosis
• EEG: No epileptiform activity. Mild generalized background slowing
• Neuropsychological Testing (formal, 3 months post-injury):
• Attention/Concentration: Impaired (1st-5th percentile on CPT-3, PASAT)
• Processing Speed: Severely impaired (1st percentile on WAIS-IV PSI)
• Working Memory: Impaired (5th percentile on WAIS-IV WMI)
• Verbal Memory: Impaired (5th-10th percentile on CVLT-3)
• Visual Memory: Impaired (3rd percentile on BVMT-R)
• Executive Function: Severely impaired (1st percentile on WCST, D-KEFS Tower)
• Language: Low average (20th percentile on BNT)
• Visuospatial: Average (40th percentile on JOLO)
• Emotional: Elevated irritability and depression scales; impaired self-awareness on PCRS
• Driving Assessment: Failed simulated driving evaluation due to impaired divided attention and reaction time
• PHQ-9: Score 12 (moderate depression)
• Neuro-QOL: Significant impairment in cognitive function, social participation, and emotional well-being domains

Clinical Image

Diagram illustrating areas of brain injury in diffuse axonal injury, the Rancho Los Amigos Scale for cognitive functioning, and components of a cognitive rehabilitation program. Source: Educational illustration.

Diagnosis

Severe Traumatic Brain Injury with Post-Traumatic Cognitive Impairment (Attention, Memory, Executive Function, and Processing Speed Deficits), Behavioral Dysregulation, and Impaired Self-Awareness — Rancho Los Amigos Level VII (Automatic-Appropriate)

Key Diagnostic Criteria:

• Severe TBI by criteria: GCS 6, PTA >7 days (35 days)
• Neuropsychological testing confirming severe impairments in attention, processing speed, memory, and executive function
• MRI evidence of bifrontal contusions and diffuse axonal injury
• Functional limitations in work, driving, and complex ADLs
• Impaired self-awareness consistent with frontal lobe injury

Treatment Plan

1. Comprehensive cognitive rehabilitation program (3-5 days/week for 12-16 weeks):

• Attention training: Direct attention training using APT (Attention Process Training) program targeting sustained, selective, alternating, and divided attention. Graded computer-based exercises with progressive difficulty. Environmental modification to reduce distractions
• Memory rehabilitation: External compensatory strategy training (smartphone reminders, written checklists, calendar system, voice recorder). Spaced retrieval training. Errorless learning techniques for new procedures. Memory notebook/planner system with structured training
• Executive function training: Goal management training (GMT), metacognitive strategy instruction, problem-solving training, self-monitoring techniques. Use of structured routines and checklists for complex tasks
• Processing speed: Timed practice activities with progressive demands. Computer-assisted cognitive training

1. Speech-language pathology: Pragmatic communication skills training (turn-taking, topic maintenance, emotional regulation during conversation). Cognitive-communication therapy
2. Behavioral management: Positive behavioral support plan. Anger management training. Structured behavioral feedback. Family education on TBI-related behavioral changes
3. Self-awareness intervention: Structured experiential feedback during therapy tasks. Video self-modeling. Discrepancy-based feedback comparing self-ratings to therapist ratings. Gradual development of metacognitive skills
4. Medication management: Continue amantadine 100 mg BID (evidence-based for TBI cognitive recovery). Consider titrating methylphenidate to 20 mg AM if tolerated. Monitor testosterone level (borderline low, may contribute to fatigue and mood; recheck in 3 months, consider endocrinology referral if persistently low). Continue levetiracetam (reassess at 12 months for discontinuation if seizure-free)
5. Vocational rehabilitation: Neuropsychological re-evaluation at 6 months. Gradual return-to-work program with workplace accommodations (reduced hours, quiet workspace, written instructions, frequent breaks, simplified tasks initially). Collaboration with employer and vocational counselor
6. Family support: Caregiver education and training. Family therapy. Referral to Brain Injury Association support group. Respite care resources
7. Driving rehabilitation: Repeat driving evaluation in 6 months after cognitive rehabilitation. Adaptive driving program if appropriate

Key Learning Points

• Post-traumatic amnesia (PTA) duration is the best predictor of long-term cognitive outcome after TBI: PTA >4 weeks is associated with severe disability and prolonged recovery, though meaningful improvement can continue for 1-2 years or longer
• Cognitive rehabilitation should use a combined approach of restorative training (directly exercising impaired functions) and compensatory strategies (teaching alternative methods to bypass deficits); compensatory strategies are particularly important for memory rehabilitation
• Impaired self-awareness (anosognosia) is common after frontal lobe injury and is one of the greatest barriers to rehabilitation participation and outcome; it requires specific therapeutic interventions
• Amantadine is the best-studied pharmacologic agent for cognitive recovery after TBI, with Level I evidence from the IMPACT trial showing acceleration of recovery during the subacute phase
• Post-TBI endocrinopathy (particularly hypogonadism and growth hormone deficiency) occurs in 25-50% of moderate-severe TBI patients and should be screened for, as it can contribute to fatigue, depression, and impaired recovery

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