0:00

Now when a nerve is injured, uh, we look for direct signs

0:05

of neuropathy.

0:07

So this is an example of someone

0:09

who fell asleep on a bar stool for several hours

0:12

and woke up with severe pain in the

0:15

sciatic nerve distribution.

0:17

So on, Mr. We look for an increase in the tissue,

0:21

single intensity of the nerve that becomes close

0:24

to the adjacent vessels.

0:26

But remember that this is very sensitive,

0:29

but not very specific

0:31

because we have to remember that, um,

0:34

the magic angle effect can affect the, uh, nerves

0:38

if even at at high TE, uh, sequences

0:42

and non stir, uh, imaging.

0:44

So to be more specific, we also look for an increase in size

0:48

of the nerve or a change in caliber.

0:50

We look for a loss of the vesicular pattern

0:53

and surrounding edema.

0:55

Of course, these changes are better appreciated

0:58

in larger nerves.

1:00

If a motor nerve is uh, compressed,

1:04

then we can also find secondary signs, uh,

1:07

of denervation in the muscles innervated by that nerve.

1:11

Uh, the changes in the muscle are usually distal

1:15

to the compression, so if it, it may be, uh,

1:20

not in the field of view at the site

1:22

of compression on the IMA images you're looking at,

1:25

but uh, may be more distal in the acute phase.

1:30

If the compression is severe, the,

1:31

the increased T two signal with will appear within days.

1:36

Uh, but if the compression is mild

1:38

or intermittent, it might take weeks for the, uh,

1:41

increased tissue tissue signal of the nerve to appear.

1:45

Now in the subacute phase,

1:46

we'll start seeing muscle atrophy developing in the muscles

1:50

in the, in a nerve territory, uh,

1:54

and that atrophy will coexist

1:55

with the increased T two single.

1:58

And then finally, uh, in the chronic phase,

2:01

we will have just severe atrophy of the muscle.

2:05

Now, of course, if a sensory nerve is compressed,

2:07

then we will have no secondary signs.

2:10

And this is an example here of a patient

2:14

with femoral neuropathy

2:15

and he has, uh,

2:17

severe denervation changes in the quadriceps muscle, uh,

2:21

and notice the normal subcutaneous fat

2:23

and fascia that helps distinguish this from other causes

2:27

of muscle edema, such as, um, a muscle, uh,

2:30

injury or an infection.

2:33

So muscle edema is a non-specific response to, uh,

2:37

a muscle insult and there is a broad differential diagnosis.

2:42

So if the muscle edema does not correspond

2:45

to a nerve territory, then we can think of other causes

2:48

of muscle edema such as polymyositis and dermatomyositis.

2:52

Uh, remember that up to 24% of these patients have

2:56

or will develop a malignancy

2:58

Within one or two years of the polymyositis.

3:02

We can also think of a drug toxicity

3:06

that can cause muscle edema, such as patients taking statins

3:10

for dyslipidemia.

3:12

HIV patients taking a ZT

3:15

and illicit drugs such as cocaine, which can cause, uh,

3:18

ischemic changes in the muscles.

3:21

Pulse radiation, uh, changes

3:23

in the muscles are usually recognized by a sharp demarcation

3:27

between the normal and abnormal muscle.

3:31

And this is usually appears months after the radiation and,

3:35

and can persist for years.

3:38

Diabetic rhabdomyolysis is a uncommon

3:41

complication of diabetes.

3:44

Usually patients who are poorly controlled

3:46

and they can have severe pain

3:48

and swelling in the muscles, in the thighs

3:51

and legs that can mimic infection.

3:54

Uh, finally we can think about graft versus host disease,

3:58

infections, trauma and compartment syndrome.