Need info about reflexes

[rdmc]

I should have asked the neuro NP this when I was in for my six month check, but "oops" slipped my mind. And I got to thinking about it this morning and figured maybe one of you experts would know.

Early on in my MS journey I had hyperactive reflexes, especially in my legs. I do have a baclofen pump now so my spasticity in my legs is manageable and I'm still mobile.

But now I have no reflexes during a neuro exam, none, nada, zilch at any of the places they test. She mentioned it out loud this time, and said "Well, guess you have no reflexes now." It seemed as though in recent years they've been waning, but this time arms, and legs, every place she "hammered" nothing. In my mind, I formed the question to ask her why, but then got carried away with the rest of the neuro exam, "Do this, touch here, walk this way...etc."

What causes reflexes to eventually quit responding, anybody know?

[22cyclist]

Making Clinical Sense of Reflexes:

Normal reflexes require that every aspect of the system function normally. Breakdowns cause specific patterns of dysfunction. These are interpreted as follows:

Disorders in the sensory limb will prevent or delay the transmission of the impulse to the spinal cord. This causes the resulting reflex to be diminished or completely absent. Diabetes induced peripheral neuropathy (the most common sensory neuropathy seen in developed countries), for example, is a relatively common reason for loss of reflexes.

Abnormal lower motor neuron (LMN) function will result in decreased or absent reflexes. If, for example, a peripheral motor neuron is transected as a result of trauma, the reflex dependent on this nerve will be absent.(Or a baclofen pump in your case).

If the upper motor neuron (UMN)is completely transected, as might occur in traumatic spinal cord injury, the arc receiving input from this nerve becomes disinhibited, resulting in hyperactive reflexes. Of note, immediately following such an injury, the reflexes are actually diminished, with hyper-reflexia developing several weeks later. A similar pattern is seen with the death of the cell body of the UMN (located in the brain), as occurs with a stroke affecting the motor cortex of the brain.
Primary disease of the neuro-muscular junction or the muscle itself will result in a loss of reflexes, as disease at the target organ (i.e. the muscle) precludes movement.
A number of systemic disease states can affect reflexes. Some have their impact through direct toxicity to a specific limb of the system. Poorly controlled diabetes, as described above, can result in a peripheral sensory neuropathy. Extremes of thyroid disorder can also affect reflexes, though the precise mechanisms through which this occurs are not clear. Hyperthyroidisim is associated with hyperreflexia, and hypothyroidism with hyporeflexia.
Detection of abnormal reflexes (either increased or decreased) does not necessarily tell you which limb of the system is broken, nor what might be causing the dysfunction. Decreased reflexes could be due to impaired sensory input or abnormal motor nerve function. Only by considering all of the findings, together with their rate of progression, pattern of distribution (bilateral v unilateral, etc.) and other medical conditions can the clinician make educated diagnostic inferences about the results generated during reflex testing.

Trouble Shooting
If you are unable to elicit a reflex, stop and consider the following:

Are you striking in the correct place? Confirm the location of the tendon by observing and palpating the appropriate region while asking the patient to perform an activity that causes the muscle to shorten, making the attached tendon more apparent.

Make sure that your hammer strike is falling directly on the appropriate tendon. If there is a lot of surrounding soft tissue that could dampen the force of the strike, place a finger firmly on the correct tendon and use that as your target.

Make sure that the muscle is uncovered so that you can see any contraction (occasionally the force of the reflex will not be sufficient to cause the limb to move).

Sometimes the patient is unable to relax, which can inhibit the reflex even when all is neurologically intact. If this occurs during your assessment of lower extremity reflexes, ask the patient to interlock their hands and direct them to pull, while you simultaneously strike the tendon. This sometimes provides enough distraction so that the reflex arc is no longer inhibited.

Occasionally, it will not be possible to elicit reflexes, even when no neurological disease exists. This is most commonly due to a patient's inability to relax. In these settings, the absence of reflexes are of no clinical consequence. This assumes that you were otherwise thorough in your history taking, used appropriate examination techniques, and otherwise identified no evidence of disease.

[rdmc]

Thanks 22, I sort of understood most of that..UMN and LMN always confuse me I know MS is usually UMN, but I have a medulla lesion and that can cause LMN symptoms. Beyond that I'm stumped, it's a good thing I'm not a doctor, because I'd never get that. I'm one of those folks who says the pledge to the flag in my mind in order to visualize which hand I put over my heart, in order to follow directions that say "right side" or "right hand."
So the Upper and Lower really confuses me.

I wondered if the pump could cause it. That doesn't explain no reflexes in my arms though because my pump catheter is at T9. When I was going through diagnosis phase, and for about 10 years after my legs were really spastic, it was "doctor beware" if you tap my knee.

But in the last couple of years, I've noticed less response during those neuro exams every 6 months, and slowly but surely I seem to have lost all response to the hammer.

I also don't have a gag reflex on one side, and I have a positive Babinski, but only on what I would consider my good leg...go figure...screwy disease.

P.S. Glad you're out of the hospital (worst thing about hospitals to me is the noise), so I know you'll rest much better at home.