Abrupt Lesions Pitt Stuff

False (opposite)

True or False? total TBIs have decreases in recent years while the number of TBI related deaths has increased.

elderly

what age group has the highest incidence of hospitalization for
TBIs

child abuse

common cause of TBI-related deaths among those ages 0-4

MVAs

common cause of TBI-related deaths among young children and young adults

self-inflicted TBIs

common cause of TBI-related deaths among middle and late adulthood

falls

common cause of TBI-related deaths among the elderly

falls

account for the majority of TBI-related emergency department visits, hospitalizations, and deaths

reduced mobility, impaired senses

why are the elderly particularly vulnerable to TBIs

elderly 65+

have the highest rate and greatest number of TBI-related deaths

age 15-24

account for the majority of TBI-related emergency department visits

5.4 per 100,000

incidence of SCIs

43 (used to be 29)

avg age of SCIs

incomplete quadriplegia

most common neurological level of SCIs

20

% of incomplete paraplegia cases

20

% of complete paraplegia

10

% of complete quadriplegia

1. MVAs

2. falls

3. violence

4. sports injuries

5. medical/surgical

most common causes of SCIs from greatest to least

males (80%), black americans

Risk factors or vulnerable groups for SCIs

ischemic stroke

stroke occurring from disruption of blood flow and leading to infarction

penumbra

area of damaged tissue around an infarct

hemorrhagic stroke

stroke caused by a rupturing of blood vessels within the cerebrum, subarachnoid space, subdural space, or epidural space that leads to infarction downstream from the rupture

240/100,000

incidence of strokes

first strokes (75%)

are first strokes or recurrent strokes more common?

ischemic (85%)

are ischemic strokes or hemorrhagic strokes more common?

65+ (risk doubles after age 55 every 10 years)

age that most commonly has strokes

• gene mutations causing malformation of vascular smooth muscle

• sickle cell disease

genetic risk factors for stroke

hypertension, cardiac disease (forming emboli), athersclerosis

cardiovascular risk factors for stroke

high LDL, low HDL, obesity

dietary risk factors for stroke

statins, dietary fiber & phytosterol consumption

ways to reduce LDLs

smoking, heavy alcohol consumption, cocaine and amphetamine usage

drug risk factors for stroke

increasing HDL levels, thinning blood

why would lower levels of alcohol consumption result in a 20% lower stroke risk?

leukemia, diabetes mellitus

systematic risk factors for stroke

open injury

primary injury in which the skull in penetrated

closed injury

primary injury in which the skull remained in tact

diffuse axonal injury

brain injuries that occur in the absence of physical contact with the skull, caused by rotational forces

Wallerian degeneration

in diffuse axonal injury, axons are rip apart by shearing forces,, resulting in what type of degeneration?

wallerian degeneration

degeneration of the distal portion of the axon and myelin sheath

PNS; allows axon regrowth
CNS; does not allow axon regrowth

What part of the NS are axons able to regrow?

oligodendrocytes, astrocytes

what specific aspects of the CNS inhibit axon regrowth

Schwann cells

what specific aspects of the PNS facilitate axon regrowth

secondary inflammation

injuries that occur over the course of days to months as a result of swelling and
inflammation

MAP-ICP

Equation for CPP

reduces CPP

how can hypotension, or increased ICP affect CPP

increased ICP

how do swelling/inflammation from a primary injury affect ICP?

neurovascular coupling

Changes in neural activity produce changes in blood flow and brain metabolism

dilate

Following TBI, neurovascular coupling is disrupted and cerebral blood vessels vaso________.

nitric oxide

a gas released by the endothelial cells to promote blood flow via vasodilation, which is not release following TBI

vasoconstriction

If NO is not released following TBIs, what happens to peripheral blood vessels?

BBB

this structure becomes more permeable following a TBI, due to vascular damage or inflammation

1. mechanical stimulation via TBI or swelling

2. reactive gliosis (↓ glutamate and K⁺ uptake)

3. ATP depletion due to hypoxia/ischemia

How can a TBI induce excitotoxicity?

1. oxidative damage

2. osmotic necrosis

3. glutamate/calcium toxicity

specific mechanisms of neurodegeneration as a result of elevated neuronal activity after a TBI

anticonvulsants

how can we control excessive neuronal activity

subfalcine herniation

herniation in which the cingulate gyrus crosses the midline, passing under the falx cerebri to compress the contralateral cerebral hemisphere

transtentorial herniation

herniation in which brain matter is pushed past the tentorial membrane, which separates the cerebrum from the brainstem (1)

central herniation

transtentorial herniation where the diencephalon and midbrain are pushed downward onto the brainstem

uncal herniation

transtentorial herniation where the uncus of the temporal lobes is pushed downward onto the brainstem

upward herniation

transtentorial herniation where the midbrain is push upward into the cerebrum (5)

tonsillar herniation

the cerebellum herniates downward, pushing caudal portions of the brainstem through the foramen magnum. This has a high chance of compressing the medulla. (4)

transcalvarial herniation

brain matter squeezes through a fracture or opening in the skull. This only occurs in the case of open injuries or craniotomy (4)

medulla

Herniation that compresses the brainstem, particularly the ______________, can cause paralysis or death due to respiratory failure

respiratory function controlled in the medulla

why would herniation onto medulla increase risk of respiratory failure?

chronic traumatic encephalopathy

progressive neurodegenerative disorder marked by cortical degeneration and the accumulation of tau neurofibrillary tangles (often from repeated injuries)

cognitive impairments, behavioral changes, dementia

cortical degeneration from CTEs can lead to:

axonal transport

neurofibrillary tangles impair what function of a neuron?

Aβ

plaques often found in those with TBI

ApoE

gene product that is used to clear Aβ

ApoE4

gene product that is associated with poor outcomes following TBI dues to decreased ability to clear Aβ

alzheimer's disease

what condition associated with Abeta and tau tangles is also commonly associated with TBIs

hyperextension/flexion

accounts for 50% of SCIs

hangman's fracture

Unstable, serious fracture of posterior elements of C2 usually with C2 anterolisthesis on C3. Caused by hyperextension and distraction (head against dashboard). Possibly compresses the spinal cord

1. compress SC and kill nervous tissue

2. compress vertebral arteries and disrupt blood flow, killing nervous tissue

how can any type of enlargement or shifting of the vertebra affect the nervous system?

neurapraxia

a temporary loss of motor and sensory function caused by narrowing of the vertebral canal and aggravated by any bending

False (both deal with primary and secondary)

TBIs can involve primary and secondary injuries, but SCIs only deal with primary injuries. True or False

structural damage

common causes primary injury

1. impaired synaptic communication (neutroptrophic support)

2. altered blood flow

3. inflammation (reactive gliosis, toxicity from macrophages)

common causes of secondary injury

syringomyelia

a tube-shaped cystic lesion (called a syrinx) forms over multiple spinal levels, often in the cervical and thoracic regions; typically develop from SCIs

CSF

what are syrinx's filled with in a syringomyelia

sharp neck pain, decreased pain and temp sense in cape-like distribution, muscle atrophy and weakness, autonomic dysfunction

common signals of a syringomyelia

posterior column/dorsal columns

tract of the spinal cord which contains ipsilateral somatosensory fibers that convey fine touch

anterolateral tract / spinothalamic tract

tract of the spinal cord which contains contralateral nonconscious tactile sensation as well as conscious nociceptive and temperature information

lateral corticospinal tract

tract of the spinal cord which runs on the lateral portion of the spinal cord and controls ipsilateral limbs

anterior corticospinal tract

tract of the spinal cord which runs on the anterior portion of the spinal cord and controls the trunk and contains a mix of crossed and uncrossed fibers

hypothalamospinal tract, reticulospinal tracts

tracts of the spinal cord which innervate the preganglionic neurons of the autonomic nervous system. Damage to these tracts
affects autonomic function

Brown-Séquard syndrome (BSS)

caused by damage to one side of the spinal cord; typically the result of gunshot or stab wounds.

ipsilateral sensory loss

in Brown-Séquard syndrome (BSS), damage to the posterior columns creates:

contralateral temperature and pain loss

in Brown-Séquard syndrome (BSS) damage to the anterolateral tract creates

ipsilateral motor weakness/paralysis

in Brown-Séquard syndrome (BSS) damage to the CST creates:

LMN weakness

in Brown-Séquard syndrome (BSS) damage to the anterior horn at the level injury creates:

anterior cord syndrome

caused by bilateral damage to the anterolateral
tract and CST

loss of blood supply by anterior spinal artery

typical cause of anterior cord syndrome, orbilateral damage to the anterolateral
tract and CST

posterior cord syndrome

SCI caused by damage to the posterior columns

• preserved motor function, pain, and temperature sensation

• sensory ataxia/uncoordinated walking

symptoms of posterior cord syndrome

central cord syndrome

caused by damage to the central aspect of the spinal cord, usually by syringomyelia or intramedullary tumors

sacral

what part of the spine is commonly spared from central cord syndrome?

Conus medullaris syndrome, cauda equina syndrome

caused by damage at the base of the spinal cord. These cause flaccid paralysis of the lower limbs and pelvic floor

first 6 months, in muscles with some level of strength after injury

when does most motor recovery occur after a SCI?

limited axonal regrowth in CNS

What contributes to the inability to restore function after an SCI?

true

True or false? Neurons in the spinal cord adapt over time following SCI

spinal shock leading to flaccid paralysis below levl eof lesion

immediately following a SCI, what symptoms occur

sensory feedback

over time, neurons in the spinal cord can adapt to loss of descending input and become more excitable via what input?