Hypoxic and Ischemic Brain Injury

Question 1

What does anoxic and hypoxic damage stem from?

Answer 1

Conditions that affect the cardiac and/or respiratory systems. Deficient oxygen supply to the brain can result from reduced oxygen in the blood or deficient perfusion of blood to the brain.

Question 2

Why are terms hypoxia and ischemia often co-related?

Answer 2

Because both processes are usually involved in the injury - reduced oxygen and reduced blood flow (ischemia = insufficient blood flow to an organ)

Question 3

What are medical conditions that may cause hypoxic-ischemic damage?

Answer 3

Acute conditions: Cardiac arrest, carbon monoxide poisoning, suffocation, drowning, hanging, massive blood loss due to trauma, prolonged seizures, anesthesia accidents during surgical procedures, prolonged coma.
Chronic conditions: COPD, sleep apnea, asthma, conditions that paralyze the respiratory system including ALS and myasthenia gravis.

Question 4

Which brain regions are most vulnerable to hypoxic-ischemic insult?

Answer 4

Brain regions with high metabolic demands and those at the distal end of cerebral arteries (in particular the watershed areas - where multiple vascular territories meet, PCA, MCA, etc).
Brain regions that show high vulnerability to such insults are:
Neocortex
Hippocampus
Basal ganglia
Cerebellar regions
Visual cortex
Thalamus

Question 5

How do brain changes evolve after hypoxic-ischemic insult?

Answer 5

Lesions may evolve over weeks or months and recovery can be quite variable.
Basal ganglia and neocortex regions may show damage on neuroimaging first
Hippocampal damage may show days or weeks later

Question 6

Why does damage to the brain occur?

Answer 6

The brain has almost no inherent energy stores and is critically dependent on uninterrupted flow of oxygen and glucose. A sudden loss of blood flow or reduced oxygen in blood causes a critical shortage of oxygen and glucose supply, and processes that occur that result in neuronal death. Further, additional toxic processes occur, as sodium and calcium pumps fail, resulting in depolarization of neuronal membrane and glutamate is released in excess to toxic levels.

Question 7

How does carbon monoxide poisoning occur?

Answer 7

Carbon monoxide has a very high affinity for binding with hemoglobin, forming carboxyhemoglobin. The effect is to displace oxygen binding sites on red blood cells, resulting in hypoxia and acidosis. Effects are similar to what is seen with cardiac arrest.

Question 8

What happens with carbon monoxide poisoning in the brain?

Answer 8

Carbon monoxide poisoning often results in delayed neurologic deterioration, which may occur 1-3 weeks after severe exposure. Basal ganglia damage is common contributing to EPS. Hippocampal atrophy and generalized brain atrophy may be seen months afterward.

Question 9

What is the neuropsychological pattern of deficits with carbon monoxide poisoning?

Answer 9

Deficits in attention, processing speed, executive functioning, anterograde memory/verbal and nonverbal memory. Memory is the most commonly affected cognitive domain. With severe injury, recovery outlook is grim/flat and return to independent living is rarely achieved.

Question 10

What is the primary determinant of CNS damage?

Answer 10

If hypoxia is not severe enough to disrupt consciousness, then CNS damage is unlikely.

More favorable outcomes are generally seen in patients who had shorter period of impaired consciousness, regain purposeful motor movements, and have preserved memory within a few hours following resuscitation.

Question 11

How do individuals with hypoxia/anoxia compare to individuals with TBI?

Answer 11

May have similar lengths of inpatient stay but those with hypoxia/anoxia may show slower progress and poorer outcomes, functionally (need residential care)

Question 12

Discuss neuroimaging results following hypoxic/ischemic insult.

Answer 12

Initial head CT or brain MRi often does not reveal significant changes. Follow up studies at a later date might reveal white matter changes, corpus callosum atrophy, cortical edema, cerebellar lesions, basal ganglia lesions, thalamic lesions, and/or hippocampal atrophy. These abnormalities may take weeks or months before they can be visualized on traditional scans.

Question 13

How is npsych assessment helpful for these patients?

Answer 13

Characterize strengths and weaknesses and associate to daily functions
Help identify target goals for rehab
Identify factors such as mood that could affect recovery and rehab
Determine decisional capacity and need for supervision
Identify areas for which accommodations will be needed in return to school and employment

Question 14

What kind of treatment will be needed for these patients?

Answer 14

Cog rehab

PT and OT often indicated for motor impairment due to damage to cerebellar and basal ganglia structures.

Question 15

Discuss lasting outcomes for these patients, cognitively.

Answer 15

The worst outcome is brain death/persistent minimally responsive state.
Less severe cases may show variable confusion/periods of coma and lasting cog problems later on.
A high number of patients show general cognitive impairment. Even more have focal deficits in memory, attention, or processing speed.
Personality changes are reported in a third of these patients.

Question 16

Describe the nature of the memory problems for these patients.

Answer 16

Problems with storage, capacity, and retrieval. In severe cases with bilateral hippocampal damage, a marked amnestic state may be present.

Question 17

How does hypoxic/ischemic injury affect motor functions?

Answer 17

Due to effects on basal ganglia and cerebellum - these areas are at high risk for injury. Severe insult can lead to spastic quadriparesis, ataxia, parkinsonism, etc.

Question 18

How does hypoxic/ischemic injury affect emotion and personality?

Answer 18

Some patients sustain orbitofrontal damage as this is a watershed region.
Anosognosia is common early after injury and may persist.
Depression is common.
Changes in self-regulation of emotions may occur due to medial temporal and frontal system injury. Behavioral problems may be chronic.

Question 19

What are considerations for treating hypoxic/ischemic patients (recommendations)?

Answer 19

1) May need high level of supervision due to memory and motor impairment. Will need to develop routines and compensatory strategies to allow them to live semi-independently as long as they adhere to a rigid daily structure with some external monitoring.
2) May not be able to return to driving.
3) May not be able to return to work. Some may benefit from alternative vocational or volunteer placements.
4) Capacity may be limited due to memory impairment and executive dysfunction.
5) Medications on improving attention and memory may be administered (like Ritalin) or acetylcholinesterase inhibitors (Aricept), may be helpful, but there is not much evidence to support use.
6) SSRIs might be helpful for mood
7) Compensatory strategy training is critical. Patients who display progressive cognitive improvement within the 1st moth post injury might benefit more relative to those who make limited cognitive gains. Emphasis should be made on errorless learning, procedural learning, attention process training, etc.

Question 20

What are some geriatric considerations?

Answer 20

Older brains are less able to recover from anoxic injury and will likely suffer more permanent and severe cognitive deficits due to reduced cerebral reserve. Questions regarding functional independence post injury may be more pertinent for them.

Question 21

What is sleep apnea?

Answer 21

A disorder that involves recurrent episodes of blood oxygen desaturation and also disrupts normal sleep architecture. During episodes of total breathing cessation (apnea) or partial (hypopnea), blood oxygen saturation can fall to harmfully low levels, resulting in repeated hypoxic periods.