BCS 242 Pathology

MILD TBI LOC

0-30 min

mild TBI PTA

0-24 hrs

Mild TBI GCS

12-15

Mild TBI imaging

usually normal

mild TBI clinical presentation

Headache, dizziness,

slowed processing,

attention deficits;

recovery in weeks–3

monthsHeadache, dizziness,

slowed processing,

attention deficits;

recovery in weeks–3

months

Moderate TBI LOC

30 min to 24 hrs

Moderate TBI Post-traumatic Amnesia

1-7 days

Moderate TBi imaging

may show contusions/bleeds

Moderate TBI Clinical Presentation

memory deficits, slowed cognition, agitation, major gains first 6 months

Severe TBI LOC

>24 hrs

Severe TBI PTA

>7 days

Severe TBI imaging

often abnormal (contusion, subdural hematona, diffuse axonal injury)

Severe TBI clinical presentation

persistent cognitive/motor/language deficits, long recovery trajectory

Diffuse Axonal Injury (DAI) affected brain regions

white matter tracts, corpus callosum, brainstem

DAI underlying pathophysiology

shearing from acceleration-deceleration

DAI clinical features

severe attention deficits, slowed processing, impaired awareness

Focal Contusion (Frontal/Temporal) affected Brain Regions

frontal poles, OFC, anterior temporal

Focal Contusion (Frontal/Temporal) underlying psychphysiology

coup-contrecoup bruising

Focal Contusion (Frontal/Temporal) clinical features

impulsivity, emotional dysregulation, word-finding difficulty

Subdural Hematoma (SDH) affected regions/systems

cortical surface

Subdural Hematoma (SDH) underlying pathophysiology

venous bleed —> Intercranial pressure

subdural hematoma clinical features

headache, confusion, focal deficits based on region

epidural Hematoma (EDH) affect brain regions/systems

temporal region

epidural Hematoma (EDH) underlying pathophysiology

arterial bleed —> rapid expansion

epidural Hematoma (EDH) Clinical Features

‘lucid interval’ then rapid decline; neurosurgical emergency

penetrating/open TBI brain region affected

region specific

penetrating/open TBI underlying pathophysiology

skull + tissue breach

penetrating/open TBI Clinical Features

highly focal deficits; motor/sensory/language loss

Secondary Injury Processes affected brain regions

global brain systems

Secondary Injury Processes underlying pathophysiology

edema, intercranial pressure, ischemia, inflammation

Secondary Injury Processes Clinical Features

worsening deficits hours-days after injury

TBI domain

typical pattern

TBI attention

distractibility, difficulty sustaining focus

TBI processing speed

universally slowed in moderate-severe TBI

memory

poor encoding, poor free recall, recognition more preserved

executive function TBI

poor planning, organization, inhibition

language TBI

word-finding problems, slowed fluency

motor TBI

weaknesses, coordination issues depending on injury

Hypoxic/Anoxic Brain Injury Vulnerable Brain Regions

Hippocampus, watershed cortex, basal ganglia, cerebellum

why is the hippocampus at risk in hypoxic/anoxic brain injury?

high metabolic demand

why is the watershed cortex at risk in hypoxic/anoxic brain injury?

border-zone perfusion sensitivity

why is the basal ganglia at risk in hypoxic/anoxic brain injury?

metabolic sensitivity

why is the cerebellum at risk in hypoxic/anoxic brain injury?

purkinje cell vulnerability

clinical presentation of hippocampus in hypoxic/anoxic brain injury

severe anterograde memory impairment, poor free recall but intact recognition

clinical presentation of watershed cortex in hypoxic/anoxic brain injury

executive dysfunction; attention deficits

clinical presentation of basal ganglia in hypoxic/anoxic brain injury

motor slowing; apathy

clinical presentation of cerebellum in hypoxic/anoxic brain injury

ataxia, coordination problems

Music Therapy: Brain Regions it uses

auditory cortex, language areas, hippocampus, NAcc, Cerebellum

Mechanism of Music Therapy

rhythmic entrainment; dopamine activation; cross-network engagement

clinical benefits of music therapy

improved attention, sequencing, language output, motor planning, emotional regulation

Pediatric TBI Growing Into Deficit

injury disrupts circuits not yet matured

Pediatric TBI Growing Into Deficit clinical implications

deficits emerge later as demands increase (reading, executive Function)

Pediatric TBI Early Injury Worse

child must recover + develop simultaneously

Pediatric TBI Growing Into Deficit Clinical Implications

later academic and social difficulties

Pediatric TBI Affected Domains

processing speed, attention, phonological skills, executive function

Pediatric TBI Clinical Implications of Affected Domains

reading disorders, impulsivity, poor planning

Adrenoleukodystrophy (ALD) affected region

parietal-occipital white matter

Adrenoleukodystrophy (ALD) affected mechanism

VLCFA accumlation —> inflammatory demyelinaton

Adrenoleukodystrophy (ALD) Clinical Profile

regression, sensory/motor decline, seizures, BMT best early with mild MRI findings

Dyslexia affected Regions

left temporoparietal, Inferior Frontal Gyrus, Visual Word Form Area, angular gyrus

Dyslexia deficits

phonemic Processing + sound-letter mapping

dyslexia presentation

slow decoding; comprehension difficulties, highly heritable