Impaired Motor Function Caused by Pain – Reversible Following Analgesia

Dear Pain Matters blog readers,

In some pain patients, the source of pain may emanate from a finger, hand, arm, toe, foot, ankle or leg.  This pain may be sooooo painful that physiotherapy is simply not possible.

In the following case, physiotherapy was finally rendered possible following a novel pharmaceutical block.

SUCCESSFUL CASE STUDY:

A 54-year old man suffered intense pain and an inability to flex his index finger following an operation for a proximal phalangeal fracture.

Dr Maxwell and his colleagues were able to perform an ultrasound-guided continuous median nerve block in the proximal forearm of the pain patient.  This led to a temporary and successful block of all sensation including elimination of intense pain in the median nerve distribution for 11 consecutive days.

Importantly, motor function remained unaffected by this ultrasound-guided block of a selected terminal nerve branch.  This enabled the patient to fully participate in hand physical therapy that resulted in successful rehabilitation to restore flex function to his index finger.

Oral opioid medication was also discontinued (Maxwell et al, 2013).

(Conventional blocks often block both sensory and motor pathways, the latter preventing physical therapy to be undertaken due to block-induced temporary loss of motor function.)

SUMMARY:

Intense pain can hinder and even sabotage rehabilitation including motor re-training efforts.

Take away the pain temporarily (via a pharmaceutical block) … et voilà … physiotherapy is finally possible!  Thus, treatment should be aimed at blocking the pain first before commencing physical therapy.

In other words, ultrasound-guided perineurial catheters may be useful for targeting terminal branches of nerves and blocking pain without affecting motor function.  This may enable physical therapy to finally proceed in the absence of pain.

The absence of pain may also lead to plasticity in the brain.  Pain relief via block may also enable the autonomic nervous system to ‘recalibrate itself’ leading to improved parasympathetic activity.

Wishing less pain to more people,

Sabina Walker,

Blogger, Pain Matters (in WordPress)

FOR PAIN ACADEMICS:

Certain chronic pain conditions (eg complex regional pain syndrome, CRPS) may also involve impaired motor function.  This results in reduced muscle (grip) strength, decreased skeletal muscle activity and muscle loss/wastage due to inactivity of the painful limb.

When intense pain affects motor function including skeletal muscle weakness, this is called ‘nociception/motor interaction‘.

Inhibited visceromotor function including inhibition of cutaneous sympathetic vasoconstriction was observed in the CRPS-affected limb.  This can cause shunting of blood away from the capillaries, impaired capillary blood circulation and hypoxia in the CRPS limb, followed by intense pain (Wasner et al, 2001).

Question:

Does inhibition of muscle sympathetic nerve activity (MSNA) also occur in CRPS?  If yes, does inhibited MSNA contribute to weakened skeletal muscle strength in CRPS?  After all (as noted above), inhibition of cutaneous sympathetic vasoconstriction occurs in CRPS.  Research is warranted.

Reduced efferent vagal outflow may also contribute to localized inflammation and a prolonged and repetitive pain/inflammation cycle.

Other neural circuits including afferent pathways may also be impaired.

REFERENCES:

(1) Maxwell et al. Ultrasound-guided Continuous Median Nerve Block to Facilitate Intensive Hand Rehabilitation. Clinical Journal of Pain (January 2013); 29(1): 86–88.

doi: 10.1097/AJP.0b013e318246d1ca

http://www.ncbi.nlm.nih.gov/pubmed/22751029

(2) Nijs et al. Nociception Affects Motor Output: A Review on Sensory-Motor Interaction With Focus on Clinical Implications. Clinical Journal of Pain (February 2012); 28(2): 175–181.

doi: 10.1097/AJP.0b013e318225daf3

http://www.ncbi.nlm.nih.gov/pubmed/21712714

(3) Wasner G, Schattschneider J, Heckmann K, Maier C, Baron R. Vascular Abnormalities In Reflex Sympathetic Dystrophy (CRPS I): Mechanisms And Diagnostic Value. Brain (2001); 124: 587–599.

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