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CM- Neurosurgery Flashcards

1
Q

What are the 3 main categories for the Glasgow Coma Score?

A
  1. Best eye opening [1-4]
  2. best verbal [1-5]
  3. best motor [1-6]
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2
Q

What correlates with 1, 2, 3, 4 for best eye opening on the Glasgow Coma Score?

A 
1 = none
2 = to pain
3= to speech
4= spontaneous
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3
Q

What correlates to 1, 2, 3, 4, 5 for best verbal on the Glasgow coma score?

A 
1 = none
2= incomprehensible
3= inappropriate
4 = confused 
5 = oriented
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4
Q

What correlates with 1, 2, 3, 4,5, 6 for best motor of the Glasgow coma score?

A 
1= none
2= extensor [decerebrate]
3 = flexion [decorticate]
4 = withdraw to pain
5 = localizes pain
6 = obeys
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5
Q

What is the maximum score that can be achieved on the Glasgow Coma Score? What does this mean for each category?
What is the minimum score on GCS?
What does this mean for each category?

A

Max score on glasgow is 15
eyes = 4 = spontaneously open
verbal = 5 = oriented
motor = 6 = obeys

Min score is 3
eyes = 1= don’t open
verbal = 1= none
motor =1=none

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6
Q

What GCS scores correlate with:

  1. severe head injury/coma
  2. moderate head injury
  3. mild head injury
A
  1. 3 to 8
  2. 9 to 12
  3. over 13
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7
Q

Severe head injury on the GCS is 3-8. What is the percent recovery for a person that has a 3? 8?

A 
3 = 4% recovery 
8= 50% recovery
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8
Q

What is the difference in treatment for an open skull fracture and a closed skull fracture?

A

Open - requires operative treatment to prevent infection

Closed - may be elevated if depressed by more than the thickness of the bone. If it is just a linear fracture, it should heal on its own.

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9
Q

What are the 5 major signs associated with a skull base fracture?

A
  1. CSF leak through skull base [rhinorrhea, otorrhea] due to dural lacerations
  2. 7th nerve palsy [facial]
  3. Battle’s sign - ecchymoses over the mastoid [just behind the ear]
  4. “racoon eyes” - periorbital ecchymosis
  5. hemotympanum - blood in the ear
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10
Q

What is the most frequent cause of an epidural hematoma [EDH]?
What is the classic scenario for a person getting an EDH?
What signs will be present on PE?

A

EDH is caused by skull fracture/trauma that lacerates the middle meningeal artery [or middle meningeal vein, sinus veins]

Presentation:

  1. hit in the temporal area with brief loss of consciousness
  2. “lucid interval” where they feel fine
  3. rapid neurologic deterioration

Physical exam:

  1. dilated pupil ipsilaterally
  2. hemiparesis contralaterally
  3. possible ipsilateral hemiparesis [Kernohan’s phenomenon] if the opposite cerebral peduncle gets compressed onto the tentorial notch
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11
Q

What is treatment for EDH?

A

Surgical evacuation –> must be done quickly

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12
Q

Describe the appearance of EDH on CT.

A
  1. Unilateral bright while elliptoid shape
  2. attached to bone
  3. does not cross suture lines
  4. mass effect pushes brain matter contralaterally
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13
Q

Who is predisposed to a chronic subdural hematoma [SDH]?
Why?
How are CSDH usually formed and what vessels tend to be involved?

A

Elderly and alcoholics have a predisposition for subdural hematomas because they have atrophic brains.

SDH is caused by tearing of bridging veins due to acceleration/deceleration resulting in bleeding into the subdural space.
“trauma” is often minor and not remembered.

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14
Q

Describe the appearance of chronic SDH on CT.

A

Because SDH are caused by the tearing of bridging veins, the blood will fill the subdural space slowly
[artery=fast, vein =slow]

  1. slow filling allows membrane formation on the inner and outer surface of the clot which liquifies [black on the CT].
  2. outer membrane is vascularized and repeat bleeds occur [brighter white]
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15
Q

What leads to the formation of an acute subdural hematoma [SDH]?

What differentiates it from a chronic subdural hematoma on CT ? What differentiates it from epidural hematoma on CT?

A

Tearing of bridging veins as the brain moves within the skull due to acceleration/deceleration OR from laceration of a cortical vein/artery.

It is is associated with significant parenchymal damage and has worse outcome. Treatment is surgical.

On CT you see bright white filling the brain cavity [different from the dark and light spaces of chronic]. It is able to cross sutures likes [different from epidural hematoma]

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16
Q

What is a contusion/intracerebral hematoma?
What are the 2 main types?
What causes each type and where are they commonly seen?

A

Direct trauma to the brain parenchyma:

  1. Coup - injury occurs at the point of impact [where the brain hit the skull]. It is usually caused by direct impact applied to a non-moving skull [hammer, bat, etc]
  2. Contre-coup is injury that occurs opposite the site of impact and is usually due to a motile skull striking a fixed surface [falling backward and hitting your head on a table]. For this reason, most contre coup are on the frontal and temporal lobes because of an occipital blow
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17
Q

What is diffuse axonal injury?
How does this occur?
What would you see on microscopy?

A

Diffuse axonal injury is shearing injury to white matter tracts due to acceleration/deceleration.

  • lateral/coronal acceleration is most important with saggital movement producing less damage.

On microscopy, you would see spheroids which are bundles of the sheared axons.

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18
Q

What is the Monroe-Kellie doctrine of closed head injury managment?

A

ICP is related to:
1. the volume of the brain
2, blood in the intracranial space
3. CSF

The skull is a fixed box so an increase in any of the 3 volumes will lead to increased pressure and compensatory decrease in the other compartments

Cerebral perfusion pressure = mean arterial pressure- intracranial pressure

19
Q

What are treatments for head injury centered around?

A
  1. surgical removal of mass lesions
  2. ICU supportive care to decrease ICP
    - drain CSF via ventriculostomy
    - maintain normal pCO2
    - osmotic diuresis
    - venous outflow [elevate the head of the bed]
  3. Dilantin to prevent seizures
20
Q

A 35 year old man is hit on one side of the head with a baseball. He has brief loss of consciousness but returns to the dugout where he gets progressively lethargic.
What is it likely that he has?

A

EDH

21
Q

A 78 year old woman on Coumadin for A. Fib has an increasing history of falls at her assisted living center. She has a history of headaches that last 2 wks. She has has one episode of slurred speech.
What is it likely that she has?

A

chronic SDH [elderly atrophic brain, frequent falls/trauma]

22
Q

A 22 year old male is in a car accident. Extensor posturing on arrival but no eye opening or verbalization. What is his GCS?
What is the likely cause of the problem?

A

Extensor = 2
None = 1
None =1

GCS 4 = SEVERE head trauma

Diffuse axonal injury due to acceleration/deceleration

23
Q

A patient presents with “the worst headache of her life”. It came on suddenly.
She is nauseas and has vomited 2x since getting to the hospital.
She have photophobia and meningismus with positive Kernig and Brudazinski signs.
She is showing acute 3rd nerve palsy [manifesting with pupil involvment]
Lumbar puncture shows RBCs that do not clear with successive tubes, elevated opening pressure and xanthochromia [yellow from RBC breakdown].

What is the likely problem?
Where did the issue probably originate?
What does the CT show?
What is diagnosis?

A

Problem: subarachnoid hemorrhage
Origination: aneurysm at branch point in cerebral circulation. B/c of 3rd nerve involvement it is most likely a posterior communicating artery aneurysm

CT:
1. subarachnoid blood filling the dark areas where cisterns should be
2. hydrocephalus
3. intraventricular blood or a parenchymal clot
[it looks like a star!!]

Angiography is the gold standard for diagnosis

24
Q

A patient is asymptomatic with a mild headache and slight nuchal rigidity. What is the Hunter Hess score?

A

1

25
Q

A patient is in a stupor with moderate to severe hemiparesis. They have early decerebrate [extensor] rigidity. What is the Hunter Hess score?

A

4

26
Q

A patient presents with CNIII and CNIV palsy, moderate/severe headache, and nuchal rigidity. What is the hunter hess score?

A

2

27
Q

A patient presents in a deep coma with decerebrate rigidity, and a moribund appearance. What hunter hess stage are they?

A

5

28
Q

A patient has mild focal neurological deficits, lethary and confusion. What is the hunter hess score?

A

3

29
Q

What conditions would you add one to the Hunter Hess score?

A

Add 1 for:

  1. serious systemic disease [DM, HTN, atherosclerosis, COPD]
  2. Severe vasospasm on arteriography
30
Q

On the Hunter Hess scale for grading cerebral aneurysms, what modified classification adds:
0?
1a?

A 
0 = unruptured aneurysm
1a = no acute meningeal reaction but with neuro deficit
31
Q

What is the pathogenesis of a berry aneurysm?

Where do 85-95% of them form?

A

Saccular [berry] aneurysms form at branch points of vessels due to hemodynamic factors causing degeneration of the vessel wall which breaks down:

  • elastic internal membrane
  • media

85-95% occur in the anterior circulation

32
Q

Where are fusiform aneurysms most likely to occur?

What is the underlying cause?

A

They form in posterior circulation and are related to atherosclerotic processes

33
Q

Where are infectious [mycotic] aneurysms most likely to occur?

A

distal branches of cerebral circulation

34
Q

What are 4 modifiable risk factors for subarachnoid hemorrhage?

A
  1. smoking
  2. OCPs
  3. HTN
  4. cocaine
35
Q

What are the conditions associated with aneurysms?

A
  1. polycystic kidney disease
  2. fibromuscular dysplasia
  3. Marfan, EDS
  4. AV malformations
36
Q

What are the 2 treatment options for saccular aneurysms?

A
  1. surgical clipping - tried and true method

2. endovascular coiling- currently used to cause thrombosis of aneurysm [reducing the chance of rupture]

37
Q

What is a sequelae/vascular complication associated with blood in the subarachnoid space?
What is treatment for this?

A

irritation and spasm of cerebral arteries

Vasospasm occurs in 30-70% of cases [20-30 are symptomatic]

Treatment is:

  1. Ca channel blockers
  2. Hypervolemia, hemodilution, hypertension HHH therapy
  3. Catheter treatment
  4. mechanical balloon dilation
38
Q

What is a classic symptoms of increased ICP and potential brain tumor?
What are signs seen on PE that support increased ICP?

A

Morning headache

PE:

  • papilledema
  • seizures
  • headache
39
Q

A patient presents with morning headaches. She has also had 2 seizures. On PE, you note papilledema. You do a CT and see hydrocephalus and a mass.
Where in the brain is the mass likely to be?

A

Mass will be by the ventricles because it is causing hydrocephalus and increased ICP

40
Q

How does the overall presentation of a brain tumor differ from that of a vascular insult?

A 
Tumor = gradual and progressive onset
Vascular = rapid/sudden
41
Q

What is the most common type of brain tumor?

A

Mets:

  • breast, lung melanoma
  • 15-30% of patients with cancer develop cerebral mets
  • mets can be parenchymal or meningeal [carcinomatous]
42
Q

What mass effects are expected with macroadenomas [>1cm] of the pituitary?

A
  1. headache
  2. bitemporal hemianopsia due to compression of optic chiasm
  3. hypopituitarism [hypo everything, hyperprolactinemia]
43
Q

How will a patient present if they have ACTH secreting adenoma?
GH secreting?
Prolactinoma?

A

ACTH- cushings [supraclavicular fat pads, moon face, hypertension, stria, hyperglycemia, hyperpigmentation, etc]

GH - acromegaly or gigantism

Prolactinoma - amenorrhea/galactorrhea, decreased libido, impontence, infertility

Nervous System (32 decks)

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