TBI and spinal cord injury

mechanisms of TBI injuries

-blunt trauma-dura remains intact, brain tissues not exposed to environment, causes focal or diffuse brain injuries, more common than open

-open-injury breaks dura, exposes cranial contents to environment, primarily focal injuries

glasgow coma scale

-mild-13-15, mild concussion

-moderate-9-12, structural injury(hemorrhage or contusion)

-severe-3-8, cognitive/physical disability or death

what's a hallmark of severe brain injury

-loss of consciousness for 6+ hrs

essentials of mild TBI dx

-loss of consciousness <30 mins

-post trauma amnesia <1 hr

-GCS 13-15

essentials of moderate TBI dx

-LOC <24 hrs

-PTA 1-7 days

-GCS 9-12

essentials of severe TBI dx

-LOC >24 hrs

-PTA >7 d

-GCS <8

what is the initial modality of choice for TBI

CT

primary phase of TBI

-caused by the impact

-involves neural injury, primary glial injury, vascular responses, shearing, and rotational forces

secondary phase of TBI

-indirect consequence of primary injury

-cascade of cellular and molecular brain events

tertiary phase of TBI

-can develop days or months later

-pneumonia, fever, infection, immobility, contributes to further brain injury or delays repair

classifications of TBI

-focal-affects 1 area of brain, more common

-diffuse-more than 1 area, causes severe disability

coup/contrecoup injuries

coup-injury is directly below point of impact

-contrecoup- injury is on pole opposite site of impact

focal brain injury

-produces contusions-blood leak from injured vessel

-loss of consciousness(<5 mins)

-control ICP, possible surgery

-smaller area of impact=grater severity of injury

what does a traumatic cerebral contusion look like on CT

hyperdense hemorrhagic region in anterior temporal lobe

what can contusions cause

-epidural hematoma(bleeding between dura mater and skull, usually arterial w/ skull fx)

-subdural hematoma(blood between dura mater and arachnoid membrane, usually venous)

-intracerebral hematoma/hemorrhage

epidural hematoma

-most common cause MVA, also falls or sports

-most common site is temporal fossa-injury to middle meningeal artery

manifestations of epidural hematoma

-loss of consciousness at time of injury, followed by lucid period that lasts from few hrs to few days

-increasingly severe HA

-needs surgery

acute epidural hematoma on CT

-lenticular shaped hemorrhage

subdural hematoma

-MVA most common cause, due to tearing of bridging veins, assoc w/ skull fractures

-chronic-falls, causes reversible dementia

when should a subdural hematoma be considered

-any comatose pt w/ suspected supratentorial mass lesion

-more common older pt-cerebral atrophy stretches bridging cortical veins, renders them more susceptible to laceration or spontaneous rupture

acute subdural hematoma

-develops within 48 hrs, often at top of skull

-expanding clots compress brain

-begins w/ HA, drowsiness, restlessness, agitation, slowed cognition, confusion

-burr hole to remove clot

acute subdural hematoma on non contrast CT

-hyperdense clot that has irregular border with the brain and causes more horizontal displacement

subacute subdural hematoma

-develops 48 hrs-2 wks

chronic subdural hematoma

-develops week-months

-subdural space slowly fills w/ blood

-chronic HA, tenderness at site of injury

-craniotomy to evacuate gelatinous blood

-percutaneous drainage

chronic bilateral subdural hematoma on CT

-collections begin as acute hematomas and become hypodense in comparison to adjacent brain after period during which they were isodense and difficult to see

intracerebral hematoma

-associated w/ MVA and falls

-hematoma acts as expanding mass-increased ICP and compression of brain tissues w/ edema and ischemia

-delayed appearance 3-10 d after injury

-decreased level of consciousness

-reduce ICP, allow hematoma to reabsorb, surgery

open brain trauma

-produces focal and diffuse injuries

-compound skull fx-cranial contents in contact w/ environment

-complications-infection

mechanisms of injury with open brain trauma

-crush injury- laceration or crushing

-stretch injury-blood vessels and nerves damaged without direct contact

manifestations of open brain trauma

-most lose consciousness

-depth of coma and length of unresponsive state depend on location of injury, extent of damage, and amount of bleeding

open brain trauma tx

-debridement

-cranioplasty with insertion of bone or artificial graft

-abx

-manage ICP

-bedrest

what drugs are used to manage ICP

-steroids

-dehydrating agents

- osmotic diuretics

diffuse brain injury

-widespread areas, rotational/twisting movements, acceleration/deceleration forces

-axonal damage

-mild concussion, classic concussion, mild DAI, moderate DAI, severe DAI

what is a concussion

damage to axonal fibers and white matter tracts that project to cerebral cortex

-immediate but transitory effects

-temporary axonal disturbances, causing attention and memory deficits but no loss of consciousness in grade I/II

grade I concussion

confusion, disorientation, momentary amnesia, resolving within 15 mins

grade II concussion

momentary confusion and retrograde amnesia

grade III concussion

confusion w/ retrograde and anterograde amnesia upon and after impact, loss of consciousness for seconds or minutes

grade IV concussion

physiologic and neuro dysfunction without substantial anatomic disruption

-loss of consciousness <6 hrs

-anterograde and retrograde amnesia

-uncomplicated( no focal injury)

-complicated(focal injury)

signs of concussion

-can't recall events prior to or after a hit/fall

-appears dazed or stunned

-forgets an instruction, is confused about an assignment or position

-moves clumsily

-answers questions slowly

-loses consciousness

-mood, behavior, personality changes

concussion symptoms

-headache/pressure in head

-nausea or vomiting

-balance problems or dizziness, double/blurred vision

-bothered by light/noise

-feeling sluggish, hazy, foggy, groggy

-confusion, concentration, memory problems

manifestations of post concussive syndrome

-headache

-nervousness or anxiety

-irritability

-insomnia

-depression

-inability to concentrate, forgetfulness

-fatigability

post concussive syndrome tx

-symptomatic relief

-observation for 24 hrs

exam for concussion

-neuro-consciousness, coordination, memory

-neck-tenderness, ROM, limb sensation/strength

-balance

-coordination

-orientation

-immediate and delayed memory

-concentration

patterns of CTE

-dysarthria, pyramidal problems, cognitive deficits(memory, insight, orientation, processing speed)

-second pattern-pyramidal problems, dysarthria, spared cognitive abilities

other CTE symptoms

agitation, depression, aggression, poor judgement, social withdrawal, paranoia

diffuse axonal injury

-produces prolonged traumatic coma lasting longer than 6 hrs from axonal disruption

mild DAI

-posttraumatic coma lasts 6-24 hrs

-death uncommon but residual cognitive, psychologic, sensorimotor deficits persist

moderate DAI

-most common type

-widespread physiologic impairment throughout cerebral cortex and diencephalon

-actual tearing of axons occurs in both hemispheres

-posttraumatic coma lasts >24 hrs

severe DAI

-severe mechanical disruption of many axons in both hemispheres, extend to diencephalon and brainstem

-brainstem signs that disappear in few wks

-moderate-sev disability

what does DAI look like on non contrast CT

multiple small areas of hemorrhage and tissue disruption in white matter

DAI tx

-maintain cerebral perfusion and oxygenation

-hypertonic saline/mannitol to manage ICP

-antiepileptics

-fluid and nutrition management

brown sequard syndrome

deficits are referable to a lesion of the lateral half of the cord

-loss of ipsilateral motor, touch, proprioception, vibration sensation

-contralateral loss of pain and temp sensation

central cord syndrome

-bilateral loss of motor function involving upper extremities but sparing lower

-"man in barrel syndrome"

-proximal weakness greater than distal

-pain and temp sensation reduced

-proprioception and vibration spared

anterior cord syndrome

-deficits referrable to bilateral anterior and lateral spinal cord columns or funiculi

-loss of touch, pain, temp sensation, motor function below level of lesion

-posterior column functions of proprioception and vibratory sensation remain intact

posterior cord syndrome

-loss of dorsal column function, including light touch, proprioception, deep pressure sensation

-preservation of pain, temp, light touch, varying degrees of motor function

-Lhermitte's sign

-assoc w/ metabolic and infectious diseases(syphilis, B12 deficiency)

epiconus syndrome

-involves segment above conus medullaris, consisting of L4-S1 cord segments

-spares reflex function of sacral segments

-manifests as UMN lesion of L4-S1

conus medullaris syndrome

-involves terminal end of spinal cord between L1/L2

-symmetric LMN lesion of S2-4 nerve roots

-may have low back pain

-flaccid bladder and rectum

-lower limb strength may be preserved or flaccid w/ findings of LMN lesion

primary spinal cord injury

-mechanical trauma and immediate tissue destruction-hyperextension/flexion, vertical compression or rotation

-most common cervical(1, 2, 4-7) and thoracic lumbar (T1-L2)

secondary spinal cord injury

-cascade of vascular, cellular, biochemical events

-begins few mins after injury, continues for wks

mechanisms of secondary spinal cord injury

-microscopic hemorrhages

-edema

-ischemia

-excitotoxicity

-inflammation

-oxidative damage

-activation of necrotic and apoptotic cell death

-cord swelling makes it hard to determine which changes are permanent

manifestations of secondary spinal cord injury

-activity of spinal cord cells cease at/below level of injury

-spinal shock

what is spinal shock

-loss of continuous tonic discharge from brain or brainstem and inhibition of suprasegmental impulses

-complete loss of reflex function in all segments below the level of the lesion

-may persist for few days-3 m

manifestations of spinal shock

-complete loss of reflex function, flaccid paralysis, sensory deficit, loss of bladder and rectal control

-transient drop in BP, poor venous circulation

-loss of thermal control, causing body to assume air temp

neurogenic shock

-loss of sympathetic outflow, occurs w/ cervical or upper thoracic cord injury

-vasodilation

-hypotension

-bradycardia

-hypothermia

autonomic hyperreflexia

-syndrome of sudden massive reflex sympathetic discharge assoc w/ spinal cord injury at thoracic level of T5-T6 or above

-supraspinal control of sympathetic nervous system disrupted

-involves stimulation of sensory receptors below level of lesion

-results in uncompensated CV response

manifestations of autonomic hyperreflexia

-hypertension

-bradycardia

-pounding headache

-blurred vision

-sweating above the lesion with flushing of skin

-piloerection

autonomic hyperreflexia tx

-elevate head of bed

-stimulus should be found and removed (empty bowel or bladder)

-topical nitroglycerin paste above level of lesion, CCB(nefedipine) or B adrenergic receptor blocker

neuro exam for spinal cord injuries

-sensory test to pinprick and light touch

-rectal exam for voluntary anal contraction and sensation to deep anal pressure

-motor strength reflects corticospinal tract

-sensation to pinprick and light touch are functions of spinothalamic tract and dorsal columns

-

imaging for spinal cord injury

-plain films and CT to quickly evaluate bony spinal column and localize injury

-MRI is ideal for viewing spinal cord and edema but CT better to scan vertebral fractures

spinal cord injury tx

-spine immobilization and bracing

-decompression and surgical fixation

-corticosteroids

-therapeutic hypothermia

-manage nutrition, lung function, skin integrity, bladder and bowels

-rehab