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Phase 1 > Ch. 26, 28, 29 Neurosurgery > Flashcards

Ch. 26, 28, 29 Neurosurgery Flashcards

1
Q

what are the six parts of the neurologic exam

A
  1. sensorium and behavior
  2. posture and gait
  3. postural reactions
  4. spinal reflexes, muscle mass, muscle tone
  5. cranial nerves
  6. cutaneous sensation
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2
Q

what is decerebrate rigidity

A

severe intracranial lesion can lead to decerebrate rigidity which is opisthotonus with rigid extension of the neck and all four limbs and is usually associated with midbrain or rostral cerebellar lesions
Lesions that result in decerebrate rigidity will always have a severe impact on mentation and the menace response

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3
Q

what is decerebellate rigidity

A

severe cerebellar lesions that have opisthotonus and extensor rigidity of the limbs but the hips are flexed!
may or may not affect mentation

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4
Q

what is pleurothotonus

A

deviation of the head and neck to one side and may be present with mid to rostral brainstem or cerebral lesions

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5
Q

what is the typical gait associated with general proprioceptive ataxia

A

elements of both incoordination typified by hypermetria and upper motor neuron spasticity/rigidity

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6
Q

why are paw placing (checking CP deficits) not totally reliable for checking conscious proprioception

A
  1. the patient may not be able to replace the paw because of a pure lower motor neuron disease - like it is too weak to replace the paw
  2. proprioceptive placing does not isolate the conscious proprioceptive pathway from other afferent sensory pathways- there could be a problem in a different sensory pathway and you would still get a CP deficit
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7
Q

what nerve mediates the patellar tendon reflex

A

the femoral nerve, which comes through spinal cord segments L4-L6
hyperreflexive - upper motor neuron disease
hypo or absent - occurs with a disease in the reflex arc so LMN or sensory

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8
Q

what nerve mediates the biceps tendon reflex

A

musculocutaneous nerve from C6-8

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9
Q

what nerve mediates the triceps reflex

A

radial nerve from C7-T2

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10
Q

where do the nerves for the thoracic limb reflex originate from?

A

C6-T2

dorsal thoracic, axillary, musculocutaneous, median, ulnar, radial nerves

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11
Q

Where do the nerves for the withdrawal reflex of the pelvic limb arise

A

all from the sciatic nerve from L6-S1

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12
Q

how does a positive crossed extensor reflex occur

A

normally, a patient in lateral recumbency will not have extension of the contralateral limb because of UMN inhibition
With lesions that are cranial to the spinal cord segments containing the LMN of the limb, however, the crossed extensor reflex may be shown

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13
Q

what nerve mediates the perineal reflex

A

pudendal nerve

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14
Q

what must be intact for the menace response to be present

A

requires a functional retina, optic nerve, optic tract, lateral geniculate nucleus of the thalamus (diencephalon) and optic radiation and occipital lobe of the cerebrum as well as the efferent pathway (facial neurons, nerves, muscles)
also requires a functional cerebellum

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15
Q

How does schiff sherrington syndrome occur

A

peracute T3-L3 spinal cord lesions produce the markedly increased extensor tone in the thoracic limbs because of disruption of ascending inhibitory axons from interneurons (border cells) located in the dorsolateral border of the ventral gray column of spinal cord segments L1-L4
These ascending interneurons normally have some inhibition on the LMN of the cervical intumescence

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16
Q

what do you see in spinal shock

A

lesions in T3-L3 which normally would show as UMN lesions in the hind limbs actually are flaccid and act like LMN lesions
usually accompanied by schiff sherrington posture

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17
Q

what are the parts of a lower motor neuron unit

A 
alpha motor neuron (nerve cell in the ventral gray matter of spinal cord)
ventral nerve root
spinal nerve
nerve plexus
named nerves of the limb
neuromuscular junction
muscle
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18
Q

why is the spatial resolution of MRI generally superior to CT

A

MRI images are obtained with separate acquisitions whereas CT is reformatted from the transverse images

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19
Q

what is back projection

A

computer generated images of each slice of scanned CT anatomy are constructed to an image we can use - back projection

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20
Q

what is the hounsfield unit of water

A

0

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21
Q

what is the hounsfield unit of air

A

-1000

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22
Q

what is the hounsfield unit of fat

A

-100

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23
Q

what is the hounsfield unit of brain

A

30-40

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24
Q

what is the hounsfield unit of acute to subacute clotted blood

A

60 to 100

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25
Q

what is the hounsfield unit of mineral and bone

A

variable but 100 to >1000

26
Q

what is the hounsfield unit of metal

A

variable but 100 to >3000 (includes iodine)

27
Q

How will an MRI be weighted if the operator selects a short repetition time?

A

the differences between tissues that differ in T1 relaxation times will be accentuated and the image will be T1 weighted

28
Q

How will an MRI be weighted with a long echo time?

A

It will be T2 weighted

29
Q

How does gadolinium work as a contrast agent to increase the intensity on T1 weighted images

A

Gadolinum is paramagnetic and strengthens the field
It will shorten the relaxation times of neighboring hydrogen protons and then will make tissue appear hyperintense on T1 (T1 shows substance with short T1 recovery time)

30
Q

what are the layers of the meninges? what is the leptomeninges? what is the pachymeninges?

A

pia mater
arachnoid mater
dura mater

Pia and arachnoid make up the leptomeninges
Arachnoid and dura make up the pachymeninges

31
Q

What is the subarachnoid space

A

the space between the arachnoid and the pia mater and contains CSF

32
Q

what is the subdural space

A

a potential space, this is between the dura and the arachnoid where blood vessels pass

33
Q

what is the epidural space

A

a fat-filled space surrounding the dura in the vertebral column
*in the cranial cavity, the dura is already fused with the periosteum of the skull

34
Q

what is the falx cerebri

A

this is the separation of the two cerebral hemispheres

35
Q

what is the tentorium cerebelli

A

the separation between the cerebellum and cerebrum

36
Q

what cells produce myelin

A

oligodendrocytes

37
Q

What change in PaCO2 results in a 5% change in cerebral perfusion?

A

a 1 mmHg change in PaCO2 results in a 5% change in cerebral perfusion - perfusion is extremely sensitive to changes in the partial pressure of CO2

38
Q

what is the normal intracranial pressure for dogs and cats

A

8-15 mmHg

39
Q

what compensatory mechanisms will manage increased intracranial pressure

A

move CSF to the subarachnoid space
reduce CSF production
decrease cerebral blood flow

40
Q

How much will a durotomy decrease intracranial pressure?

A

a durotomy will decrease ICP by 65%

a craniotomy alone decreases it by 15%

41
Q

what are the components of the blood brain barrier

A

tight junctions between endothelial cells and foot processes of astrocytes
basal lamina
pericytes
perivascular miroglia

42
Q

what antibiotics have good BBB penetration

A 
third generation cephalosporins
fluoroquinolones
metronidazole
sulfonamides
chloramphenicol
trimethoprim
43
Q

what antibiotics have moderate penetration of BBB with a meningitis

A

tetracyclines (especially doxy and minocycline)
erythromycin
penicillins
rifampin

44
Q

what antibiotics have poor BBB penetration

A

first and second generation cephalosporins
aminoglycosides
clindamycin
vancomycin

45
Q

What are the Trp genes?

A

transient membrane potential monovalent cation channels
Trpm4 and Trpm5 are two genes that, if knocked out, will have less hemorrhage, reduced lesion volume and improved outcome
They play a role in the secondary injury changes with a contusion of the brain

46
Q

what does increased intracellular calcium lead to?

A
  1. activates intracellular proteases such as calpains and caspase, which destroys the cytoskeleton and chromosomes and initiates cell death
  2. activates phospholipase A2 –> produces eicosanoids and initiates an inflammatory response
  3. binds intracellular phosphates, further depleting the cell of energy
47
Q

what is the role of peptidase matrix metalloproteinase 9 in spinal cord injury?

A

may be an important early trigger to the inflammatory response

48
Q

what is CIDS in relation to spinal cord injury

A

central nervous system injury-induced immunodepression
a syndrome of immunodeficiency that is associated with central nervous system injury
elevation of ACTH and catecholamines –> increased cortisol… is this why steroids are contraindicated in spinal injury patients

49
Q

what is cytotoxic edema

A

cellular swelling that is secondary to intracellular increases in Na, Cl, and Ca that will increase the osmotic pressure and cause swelling

50
Q

what is excitotoxicity

A

neuron and oligodendrocyte death from increased glutamate levels

51
Q

which is more affected by vascular obstruction, white or gray matter?

A

gray matter is more severely affected

52
Q

Hemorrhage affects spinal cord tissue in a similar way to contusion. What is a unique feature that also causes damage

A

iron and copper complexes will oxidize and hemoglobin is released into the parenchyma. the hemoglobin release produces free radicals

53
Q

how can malformations of the CNS lead to dysfunction?

A

either by compression, like an obstructive hydrocephalus, or by disruption of normal patterns of central nervous system circuitry

54
Q

what are some mechanisms by which metabolic/toxic diseases like hypoglycemia, hepatic encephalopathy, uremic encephalopathy may occur

A
  • an interruption in the energy supply like hypoglycemia or thiamine deficiency
  • imbalance of excitatory and inhibitory neurotransmitters (like hepatic encephalopathy)
  • presence of neurotoxins like ammonia, urea, phosphates
  • ionic imbalances (uremic encephalopathy)
  • blood pressure changes (uremic encephalopathy)
55
Q

what are the three most common neoplasms to metastasize to the CNS

A

hemangiosarcoma
melanoma
carcinomas

56
Q

what is vasogenic edema

A

results from increased vascular permeability and causes accumulation of extracellular fluid, particularly within white matter tracts
commonly associated with contusion, inflammatory disease, vascular disease, and compressive diseases such as neoplasia

*corticosteroids are ususally effective with this type of edema

57
Q

what is the etiology of Hansen type 1 degenerative disc

A
  • nucleus undergoes progressive decrease in proteoglycan content with consequant dehydration and accumulation of mineral (aka chondroid degeneration)
  • this degeneration leads to loss of its ability to withstand pressure equally and causes secondary degeneration and tearing in the annulus fibrosus
  • annulus will tear and the nucleus will be expelled
  • injury is some contusion and some compression
58
Q

what is the etiology of Hansen type II disc degeneration

A
  • nucleus is progressively dehydrated and replaced by fibrinoid tissue with a consequent increase in stress transfer to the annulus
  • annulus undergoes wear and tear degeneration that leads to rupture of fibers over months to years –> nucleus will cause protrusions of the dorsal aspect of the annulus
  • injury is compressive
59
Q

what are the two main theories for why we cannot regrow axons?

A
  1. reactive astrocytes produce a large number of inhibitory molecules in the extracellular space, including chondroitin sulfate proteoglycan
  2. CNS myelin is known to contain several ligands that activate receptors (like the nogo receptor) to mediate growth cone collapse
60
Q

what is syringomyelia

A

accumulation of CSF within the parenchyma of the spinal cord

Phase 1 (35 decks)

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