Neuro Mod 6 Flashcards

1
Q

Ventricle System

A
  1. 2 lateral ventricles
  2. the 3rd ventricle
  3. R/L foramen of Monro
    a. interventricular foramen that connect the R/L lateral ventricles with the third ventricle.
  4. the cerebral aqueduct (aqueduct of Sylvius)
  5. the fourth ventricle
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2
Q

CSF from the 4th ventricle goes where?

A

a. CSF from fourth ventricle exits to the subarachnoid space of the spinal cord through
• R/L lateral foramen of Luschka (singular: foramen of Luschka)
• midline foramen of Magendie

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3
Q

The choroid plexuses located in the ventricles

A
  1. produce CSF

2. CSF fills the ventricles and flows into subarachnoid space

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4
Q

Cerebrospinal Fluid

A

A. produced in the ventricles and flows into the subarachnoid space
B. surrounds the CNS (brain and spinal cord)
1. CSF fills the ventricles and the subarachnoid space of both the brain and spinal cord
C. contained by the meningeal layers
D. “sponge” for the brain
1. Brain weighs approximately 3 lbs (1,400 gms) bathed in fluid
a. Estimated net “dry” wt = 1-2 ounces (50 gms)

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5
Q

CSF Function

A

A. cushions and insulates the brain to protect from “interial forces”
B. exchange of gases (O2, CO2), nutrients and metabolic waste
C. provide equilibrium or stable ECF environment for the brain

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6
Q

CSF Volume

A

A. Total quantity of CSF = 150 ml
B. Rate of formation = 20-25 ml/hr
C. Total formation per day = 550 ml
1. CSF turns over about 3.7x’s times per day

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7
Q

CSF Formation

A

A. produced in two locations

  1. choroid plexus (approx. 50-70% produced from choroid plexus)
  2. ventricle walls (CSF flow across ependymal cells from the brain to the ventricles)
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8
Q

CSF Pathway

A

A. Lateral ventricle → foramen of Monro → third ventricle → cerebral aquaduct → 4th ventricle → foramens of Magendie & Luschka into the subarachnoid space of the brain and spinal cord

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9
Q

Distribution of CSF

A
  1. Brain (70 ml)
    a. 30-40 ml within the ventricles
    b. 25-30 ml in the subarachnoid of the brain
  2. Spinal cord (80 ml)
    a. 75-80 ml in subarachnoid space of spinal cord
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10
Q

CSF absorption back into blood stream

A

A. absorbed into the arachnoid villi → dural sinus → jugular system
1. arachnoid villi (90%)
2. directly into cerebral venules (10%)
B. absorption into arachnoid villi is directly related to CSF pressure

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11
Q

Hydrostatic pressure in subarachnoid space > pressure in dural sinuses

A
  1. subarachnoid space: CSF = 5-11 mmHg

2. dural sinuses = 5 mmHg

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12
Q

Arachnoid villi are one-way valves CSF pressure

A
  1. open when subarachnoid space pressure is 1.5 mmHg ≥ the pressure in the venous sinuses
  2. absorption of CSF increases linearly as pressure rises above 5 mmHg pressure
    C. The rate of formation of CSF is constant and is not affected by intracranial pressure
    D. At a pressure of about 8 mmHg the rate of secretion & absorption are equal
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13
Q

CSF composition

A

A. identical to brain ECF
B. different from plasma.
1. pCO2 is higher (50 mmHg)
2. pH is slightly lower in CSF
a. CSF pH (7.3) vs plasma pH (7.3-7.4)
3. potassium, protein, glucose and cholesterol lower in CSF
4. chloride and sodium concentration higher in CSF
a. Na/Cl transport critical in CSF production

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14
Q

Function of the blood brain barrier

A

A. The blood-brain barrier (BBB) separates the brain from the circulatory system and

  1. protects CNS from harmful chemicals/substances
  2. allows/regulates transport of essential molecules for maintaining a stable environment.
  3. formed by specialized endothelial cells that line brain capillaries
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15
Q

CSF is separated from blood by the blood-brain barrier

A
  1. Empendymal capillaries – extremely tight junction

2. Choroidal capillaries - fenestrated junction

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16
Q

Primary vs secondary injury in an acute phase spinal cord injury

A

a. Primary injury: immediate necrosis/damage associated with impact of injury
b. Secondary injury: occurs as cascades of inflammation spread to surrounding area resulting in additional cell death

17
Q

Spinal Shock

A

a. First 2-3 weeks of injury (rarely permanent)

b. total disruption of spinal function below level of injury

18
Q

Signs/Symptoms of Spinal Shock

A

• flaccid paralysis below level of injury
• absence of reflexes (areflexia)
• bowel/bladder dysfunction
• complete anesthesia below level of injury
• respiratory dysfunction (if high cervical level)
• sympathetic impairment if upper spinal levels
(i) hypotension (without associated tachycardia)
(ii) Horner’s syndrome (ptosis, anhydrosis and miosis)

19
Q

Subacute phase of spinal cord injury

A

a. occurs after 2-3 weeks of injury

b. hyper-reflexia and hyper-tonicity signal end of spinal shock

20
Q

Signs/Symptoms of subacute phase

A

• flaccid paralysis transitions into spastic paralysis
(i) loss of inhibition from upper CNS facilitates excessive muscle tone
• absence of reflexes replaced by hyper-reflexia
(i) loss of inhibition at spinal cord level allows spinal reflex loops to be excessive
• hypotension resolves however orthostatic hypotension will persist and reflects autonomic dysfunction
• autonomic dysreflexia

21
Q

Autonomic dysreflexia (aka….autonomic hyper-reflexia)

A
  • Simplistic description: Imbalance of blood pressure feedback is “out of sync” due to spinal cord injury causing hyper-responsiveness of ANS.
  • SCI above T-5 are most susceptible to the condition
22
Q

Irritating Stimulus that occurs below the level of injury

autonomic dysreflexia

A
  1. bladder/bowel – distention or stimulation

2. cutaneous – painful or cold stimulation

23
Q

Injury stimulates excessive sympathetic discharge

autonomic dysreflexia

A
  1. results in extreme hypertension (as high as 300 mmHg)
    a. consequence may lead to cerebral hemorrhage, cognitive confusion and potential death
  2. HTN feedback to brainstem signals inhibition of sympathetic discharge but descending pathways can’t reach lower sympathetic levels due to spinal cord injury
    a. Result: Sympathetics continue to fire excessively – elevating BP
  3. Feedback to vagus nerve in brainstem does inhibit heart rate
    a. “Extreme HTN with bradycardia”
24
Q

Treatment of autonomic dysreflexia

A

• IMMEDIATE treatment of autonomic dysreflexia

(i) Sit up to decrease BP
1. DO NOT lay the patient down – this will EXACERBATE the symptoms
(ii) Remove irritating stimulus ASAP
1. Bladder:
a. full bladder is the most common cause – evaluate catheter system
2. Bowel:
a. constipation/impacted bowels
b. CAUTIOUS: digital stimulus performed bowel programs can also trigger autonomic dysreflexia
3. Skin:
a. clothes, sores, etc…