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CNS Flashcards

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1
Q

Hallmark of severe brain injury

A

Loss of sonsciousness for six or more hours

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2
Q

Causes of focal brain injury

A

Lesions, edema, coup and contrecoup injury (contusions)

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3
Q

EDH

A 
85% arterial (middle meningeal artery)
15% venous / dural sinus
90% due to skull fracture
Temporal fossa is the most common location
Earliest symptom is HA
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4
Q

SDH

A

50% due to skull gractures. Mostly due to bridging veins from torque to the brain

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5
Q

Types of SDH

A

Acute- Develops within 48 hours of injury and is often located at the top of skull (near bridging veins)

Chronic- develops over weeks to months. Causes chronic HA and tenderness at site. Common in alcoholics.

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6
Q

ICH

A

Associated with MVA and falls

The hemorrhage acts as an expanding mass. Causes compression of brain tissue with edema

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7
Q

Causes of DAI

A

AXONAL DAMAGE due to shearing, stretching, or tearing of nerve fibers from shaking, acceleration / deceleration injury, inertial injury

Severity depends on the amount of shearing force applied to brain and brainstem

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8
Q

Grades of Concussion

A

Grade I- confusion, disorientation, and momentary amnesia

Grade II- momentary confusion and retrograde amnesia

Grade III- confusion with anterograde and retrograde amnesia

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9
Q

Classic Cerebral Concussion

A

Grade IV
Disconnection of the cerebrum from the brainstem and RAS, causing unconsciousness (<6 hours), anterograde and retrograde amnesia, physiologic and neurologic dysfunction (but ANS still intact).

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10
Q

Types of classic concussion

A

Complicated (focal injury)

Uncomplicated (no focal injury)

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11
Q

Where is our memory forming system located?

A

The hippocampus

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12
Q

Postconcussive syndrome symptoms and treatment

A

HA, cognitive impairments, psychologic and somatic complaints, cranial nerve deficits

Treatment- Reassurance and relief of symptoms. Close monitoring for 24 hours to watch for worsening of symptoms.

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13
Q

Location of most spinal cord trauma

A

Cervical (1,2,4-7)
Thoracic (T1-L2)

These are the most mobile locations of the vertebral column AND where the cord takes up most of the spinal canal. The area is mobile and the cord doesn’t have much space.

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14
Q

Spinal stenosis

A

Narrowing at the area where the spinal nerve leaves the vertebra. Can cause numbness, pain, or both, similar to hitting your funny bone. The pain is way out of proportion to the injury actually occurring. Difficult to detect by CT and MRI.

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15
Q

Spinal Shock Affects

A

Lost normal function below level of injury.
Loss of reflexive function (skeletal, bladder, bowerl, sexual, thermal control, and autonomics).

Remember, if you damage the cord, you will lose your sympathetics because they come from T1-L2. PSNS will be unaffected because that is craniosacral outflow.

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16
Q

Neurogenic Shock

A

LOSS OF SNS
What would happen if you didn’t have any SNS outflow?
- Vasodilation
- Hypotension
- Bradycardia
- Hypothermia
Think about Garmin’s finger story, and how low your BP could go if actual sympathetics were severed.

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17
Q

Autonomic hyperreflexia

A

Think about the name. Massive, uncompensated cardio response from SNS outflow due to stimulation of sensory receptors below the level of the cord lesion.

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18
Q

Classic Cerebral Concussion

A

Grade IV
Disconnection of the cerebrum from the brainstem and RAS, causing unconsciousness (<6 hours), anterograde and retrograde amnesia, physiologic and neurologic dysfunction (but ANS still intact).

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19
Q

Types of classic concussion

A

Complicated (focal injury)

Uncomplicated (no focal injury)

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20
Q

Where is our memory forming system located?

A

The hippocampus

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21
Q

Postconcussive syndrome symptoms and treatment

A

HA, cognitive impairments, psychologic and somatic complaints, cranial nerve deficits

Treatment- Reassurance and relief of symptoms. Close monitoring for 24 hours to watch for worsening of symptoms.

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22
Q

Location of most spinal cord trauma

A

Cervical (1,2,4-7)
Thoracic (T1-L2)

These are the most mobile locations of the vertebral column AND where the cord takes up most of the spinal canal. The area is mobile and the cord doesn’t have much space.

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23
Q

Spinal stenosis

A

Narrowing at the area where the spinal nerve leaves the vertebra. Can cause numbness, pain, or both, similar to hitting your funny bone. The pain is way out of proportion to the injury actually occurring. Difficult to detect by CT and MRI.

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24
Q

Spinal Shock Affects

A

Lost normal function below level of injury.
Loss of reflexive function (skeletal, bladder, bowerl, sexual, thermal control, and autonomics).

Remember, if you damage the cord, you will lose your sympathetics because they come from T1-L2. PSNS will be unaffected because that is craniosacral outflow.

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25
Neurogenic Shock
LOSS OF SNS What would happen if you didn't have any SNS outflow? - Vasodilation - Hypotension - Bradycardia - Hypothermia Think about Garmin's finger story, and how low your BP could go if actual sympathetics were severed.
26
Autonomic hyperreflexia
Think about the name. Massive, uncompensated cardio response from SNS outflow due to stimulation of sensory receptors below the level of the cord lesion.
27
Why do neurons take forever to re-grow?
Because they are often feet in length and products for repair are only made in the cell body. Products travel at a rate of about 4mm/day.
28
Why don't injured axons in the spinal cord regrow?
Because scar tissue develops before the axons can grow. To avoid this, we can induce hyperthermia to suppress the immune system from entering the site and causing scar-tissue to form.
29
Where may cord swelling be life threatening?
Cervical spine
30
Where do we get many clots that embolize to the brain?
DVT, carotid artery, or left atrium
31
What is papilledema?
Edema of the retina
32
These proteins are associated with higher risk of stroke
Lipoprotein A and homocystein
33
What is a mycotic aneurysm?
An aneurysm resulting from a bacterial infection of the arterial wall
34
Examples of vascular malformations
Cavernous angioma Venous angioma Capillary telangiectasis AVM
35
Do we get cancers of the neurons?
No, because neurons are not mitotic
36
Brain cells that are responsible for most brain cancers
Glial cells (except the microglia, because these are macrophages, and macrophages do not divide)
37
Primary intracerebral tumors (gliomas of the CNS)
Astrocytomas (lead to GBM) Oligodendroglioma Ependymomas
38
Primary extracerebral tumors (in the PNS)
Meningioma Nerve sheath tumors Metastatic carcinoma
39
Symptoms of brain tumors/ IICP
Decreased cognition, HA, vomiting, seizures, balance issues, papilledema, loss of sphincter control Problems with speech and walking are very sensitive to brain problems because they are complicated acts
40
What is papilledema?
Edema of the retina
41
What is syringomyelic syndrome?
Inflammation of the spinal cord
42
Most brain tumors (are/are not) metastatic
Are not
43
Types of meningitis
Bacteria Aseptic (viral) Fungal TB
44
Neurologic complications of AIDS
Neuropathy, cognitive dysfunction, opportunistic meningitis infections, neoplasms, myelopathy (spinal cord pathology), and neuropathy
45
Conditions cause by brain degeneration
``` Alzheimers Parkinson's Huntington's ALS MS Guillain-Barre MG Poliomyelitis ```
46
Classifications of dementia
``` Cortical - Alzheimer's and Pick's disease Subcortical - Parkinson and huntington Cortical and subcortical - Infection and CJD ```
47
Parkinson Dementia
50% have depression 50% excessive daytime sleepiness Disorientation, confusion, punding, memory loss, distractibility, and difficulty with concept formation, abstraction, calculations, thinking, and judgement Symptoms will fluctuate, but progressively worsen
48
What is punding?
Intense fascination with repetitive handling and examining of mechanical objects
49
Cause of Huntington's
Hereditary (Autosomal dominant) | Severe degeneration of the basal ganglia (caudate and putamen) and frontal cortex. Depletion of GABA.
50
Symptoms of Huntington's
Choreiform movements and disturbed thought processes
51
Consequences of seizures
250% increase in brain ATP consumption 250% increase in CBF 60% increase in brain O2 consumption Available glucose and oxygen are depleted. Lactate accumulates in brain tissue. May result in progressive brain tissue injury due to cellular exhaustion and destruction.
52
ALS
Causes progressive weakness leading to resp failure and death. Normal cognition until death. Think of Stephen Hawking.
53
Guillain Barre Syndrome
Ascending motor paralysis. Inflammatory disease caused by demyelination of peripheral nerves. Often triggered by a stomach flu *****
54
MG Cause
IgG produced against ACh receptors. Hallmark is weakness that progresses with use
55
What happens during a myasthenic crisis?
Can't breath
56
What causes coma?
Damage to bilateral hemispheres | Damage to the RAS
57
Why are pupils diagnostic?
Because contracting pupils is a complex process. Depending on what happens to the pupils will hint where the damage is located.
58
Cerebral death causes
Persistant vegetative state. Can also progress into a minimal conscious state such as akinetic mutism or locked-in syndrome
59
What is status epilepticus?
Sustained seizure for more than 30 minutes. Also can be a second seizure that begins before a person regains consciousness from their first one.
60
Consequences of seizures
250% increase in brain ATP consumption 250% increase in CBF 60% increase in brain O2 consumption
61
Types of cerebral edema
Vasogenic Cytotoxic Ischemic Interstitial
62
Causes of hydrocephalus
``` Decreased reabsorption (damage to arachnoid granulations) Increased fluid production (tumor of choroid plexus) Obstruction within ventricular system ```
63
Normal hydrocephalus
Hydro without IICP. May be caused in conditions such as Huntington's, where you are losing brain material and i is replaced by CSF. Here you have more CSF than normal, but it is not causing pressure
64
Biggest risk factors of having a CVA
Smoking, age, and HTN
65
Cause of MG
IgG produced against ACh receptors

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