Neuropsychology -- Closed Head Injury

Front 1

Two main categories of brain disorders?

Back 1

(1) Specific Disorders (focial region of the brain damaged) -- e.g., gun shout wound where the damage is localized, stroke where a specific area is deprived of oxygen, or a lesion to a specific brain region with specific deficits.

(2) Generalized Disorders (distributed/diffuse brain damage) -- Includes closed head injuries, dementing disorders (like AD), demlyinating disorders (multiple sclerosis), exposure to toxins, etc.

Front 2

What is important to note about generalized brain disorders?

Back 2

The damage can be diffuse, and different from person to person, affecting multiple cognitive and brain systems, thus the emphasis is on making subtle, but important inferences/observations on their neuro-psychological manifestations.

Front 3

Closed head injury -- what is it, and what are its rates, causes, etc.

Back 3

Results from the brain coming into contact with another object, without that object penetrating the brain. e.g., head against windshield.

**Accounts for apprx. 1 million new cases a year in US, higher than the rates of AD, PD, and MS.

**Accident related.. not dealt with in the same way as the disease model. Therefore it's not represented in the literature as much as the disease ones, because there is implicit fault at work.

Front 4

Rates and facts for young and old?

Back 4

Most common in adolescents/young adults 15-24, attributed mainly to (1) motorized vehicle accidents, (2) SRI (sports related), and it also seems that alcohol is often involved.

In the elderly (65+), it occurs most often in falls.

Front 5

Main mechanism of damage?

Back 5

Acceleration-deceleration.
- Energy imparted to the brain causes it move within the skull, which leads to twisting and shearing of the neurons and their projections/connections.
- The focal damage occurs due to the brain hitting the hard inner surface of skull.
- **Also note that the neurons that comprise the white matter tracts are the most vulnerable to twisting and shearing , and they have long connections to distant parts of the brain.

Front 6

Acute stage?

Back 6

CHI damage is often not revealed right away by anatomical imaging. The only thing that can be detected early is usually cerebral edema.

Front 7

After acute?

Back 7

As the swelling (edema) goes down, imagining often reveals the damage -- enlargement of the ventricles, loss of volume in mylineated tracts, CHANGES IN THE CORPUS CALLOSUM.
**These anatomical changes are correlated with the degree of the damage.

Front 8

Focal damage? Coup/countercoup?

Back 8

Orbito-frontal and temporal regions often suffer the worst acute damage due to the bones protruding out at these points.

- Coup = focal damage at the sight of injury.

Countercoup = focal damage at the opposite side of the impact site.

Front 9

Clinical CHI and Brain Stem?

Back 9

Presents with significant alternations in consciousness
- Basic aspects of wakefulness and consciousness are controlled by the brain stem'
- the deficits in these brain stem areas is an indication of the severity of the overall brain damage incurred.

Front 10

Three subscales on the Glasgow Coma Scale, and the three general categories of scores?

Back 10

(1) Visual responsiveness (4 points) -- eye opening
(2) Motor responsiveness (6 points) -- pain response
(3) Verbal responsiveness (5 points) -- Speech

Three categories of scores:
Severe injury (8 or<)
Moderate (9-12)
Mild (13-15)

Front 11

Though CHI deficits vary, and their associated damage vary, what are the two most common deficits? Describe each:

Back 11

Memory and attention

Memory -- posttraumatic amnesia: can't form memories after the event. Initial presentation of memory issues tends to be indicative of the general trend of the severity of the injury e.g., PTA >3 weeks is associated with poor subsequent cognitive functioning.
Neurologically, the cholinergic system seems to be the most comprised by CHI, which may account for the memory problems.

Attention -- Unable to maintain vigilance and alertness.
- Particular problems with divided or selective attention (similar to frontal lobe injury).
Poor control of behavior -- appear compulsive, impatient.
Ability to plan and follow through on goals is compromised.
Deficits also in abstract thought and conceptualization.

Front 12

Mild Head Injury (concussion). Happens when?

Back 12

(1) A chance in consciousness (not necessarily unconsciousness) for 2-30 minutes. Could just be feeling groggy, not your self, etc.
(2) exhibits no other gross signs of neurological damage (no lesions, white matter degradation, etc.)

Front 13

Some frequently observed behaviors in mild head injury?

Back 13

Vacant stare, delayed responses, inability to focus, disorientation, atypical speech, gross incoordination, hyperemotionality, memory deficits, and loss of consciousness.

Front 14

What is mild head injury often associated with?

Back 14

Depression, especially with concussions in childhood.

Front 15

Three main areas of deficits in MHI?

Back 15

(1) Cognitive -- Concentration, memory, etc.

(2) Somatic -- Dizziness, blurred vision, sesitivity to noise and lights, headaches, sleep problems, etc.

(3) Emotional changes -- fear, depression, anxiety, loss of patience, increased temper, etc.

Front 16

Problem with the rule of thumb approach in coaches and MHI? Australia study?

Back 16

Symptoms often disipate quick enough to let the player return to playing, but the long term implications are still there.

Study: Studied those football players with MHI and those without. 2 weeks after the MHI, their cognitive performance and reaction time was slower. After a year it was better, but there were lingering defictis in directing visual attention compared to their age matched controls.

Front 17

Bimanual sequencing task and concussion?

Back 17

Neurologically intact people (NIC) were age matched iwth post-concussion people. Bimanual task where they had to press buttons with each hand when prompted. Results: the NIC are using their preSMA, and not much else. The post concussions people are using A LOT of their brain, similar to the aging brain, showing that the deficits are still lingering.

Front 18

Debeaumont et al. study?

Back 18

Compared former football players that had at least one concussion with those who did not. Found that those who had the concussion, had problems in their cognition on the oddball p300 task. They report that they feel fine, but clearly they are having issues efficiently processing.

** Decificts also correlated with decrease in memory test performance and response inhibition on the go/nogo task.

Front 19

Debeaumont and TMS?

Back 19

They also found in their stiudy that the amount of TMS is took to make their hands move was significantly larger in the concussed people, than the NIC... they require more stimulation to move their hands !

Front 20

Segalowitz et al., ? (MHI to NIC comparisons)

Back 20

Showed that on a variety of tasks, the MHI people response time was slower than NIC.

Also, p3a and p3b is lower across the boards for MHI than NIC.
The p3b was decreased across the board in MHI, but it was higher in older people that had concussions back in the day, than younger people.

Front 21

So, how to treat a MHI?

Back 21

Rest until asymptomatic. Light exercise, and if symptoms return, go back to 1. Then do some sport specific activity, then without body contact, then with contact, then game play.

Other things, acupuncture (right into the bones), antidepressants, helmets, seat belts, etc., Follow up cognitive and imaging tests.