4 Interpretation

Serious pathology does occur. It is appropriate for the patients suffering from a pelvic pain to have undergone an evaluation by their medical doctor to rule out the presence of disease, ailment, and structural injury. Once overall health has been confirmed, the following interpretation is helpful in assisting the patient who is suffering.

Unlike the evaluation of the axial spine or peripheral joints, the clinician evaluating the patient with pelvic pain must often make functional assessments based on the series of findings that indicate where and why the patient is suffering. The findings may be parallel in nature indicating a relationship. An example of this would be the patient presenting with the following history:

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  Initial diagnosis of irritable bowel disease

  
  
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  Secondary diagnosis of “interstitial cystitis”

  
  
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  Third diagnosis of pudendal neuralgia

  
  
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  History:

  
  
  
  
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    Six months ago the patient had a forceful bowel movement, after becoming dehydrated after a night of alcohol consumption.

    
    
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    This lead to persistent malaise throughout the gastrointestinal tract.

    
    
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    She states that she was told that her pelvic pain is due to damage of the pudendal nerve and it is a life-long condition and that she should “get used to it.”

    
    
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    She continues by stating that she feels abandoned by the medical community and spends wakeful nights “researching” pelvic pain on her smartphone.

    
    
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    The more she “learns” the more fearful she becomes. She senses that her symptoms are worsening monthly.

  
  
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  Current symptoms:

  
  
  
  
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    Abdominal malaise

    
    
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    Pain with bowel movements

    
    
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    Dyspareunia

    
    
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    Discomfort, with palpable spasms throughout the abdominal musculature below the umbilicus

    
    
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    Burning sensation throughout “urethra” and “bladder”

    
    
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    Sensation of sitting on a golf ball

  
  
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  Current presentation:

  
  
  
  
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    Patient sits in hyperkyphotic fashion

    
    
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    Angle of declination is 45 degrees

    
    
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    Apical respiration pattern

    
    
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    Constant, low-grade writhing in waiting room and evaluation room

    
    
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    Active range of motion (AROM) of spine is grossly limited from T10 to L3 with side flexion; flexion is appropriate and extension is limited to 10%

  
  
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  Tests:

  
  
  
  
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    Positive prone knee flexion with palpable fasciculation

    
    
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    Positive hypomobility of central posterior-to-anterior (CPA) at T10 to L3

    
    
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    Increased tone of bilateral iliopsoas

    
    
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    Palpable muscle “tender points” throughout abdominal musculature below umbilicus

    
    
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    Provision of CPA at T11 to L2, grade II

    
    
    
    
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      90% reduction of patient’s symptoms at abdomen and saddle region

      
      
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      Elimination of muscle “tender points” throughout the abdominal musculature

      
      
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      75% reduction of iliopsoas tone

  
  
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  Commonalities:

  
  
  
  
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    Positive prone knee flexion (L1–3)

    
    
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    Iliopsoas tenderness

    
    
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    Bladder, colon, vagina, uterus, ureter, and ovaries have same embryologic derivation

  
  
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  Diagnosis:

  
  
  
  
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    Central sensitization of T11 to L2, with convergence and symptom propagation to segmentally common viscus and secondary muscle tender points

  
  
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  Explanation:

  
  
  
  
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    The distal colon and vagina have a common embryological derivation.

    
    
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    The segmental distribution of muscle spasm/malaise from T12 to L2 is the lower abdominal region.

    
    
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    Anxiety regarding the rapid onset of a pelvic pain, loss of comfortable intimacy, and perseveration over a “life-long injury,” coupled with gross fatigue due to poor sleep, led to a hyperkyphotic posture.

    
    
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    Patient’s history did not indicate an internal pelvic examination as appropriate at this time.

  
  
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  Treatment:

  
  
  
  
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    Postural education

    
    
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    Postural re-conditioning exercises

    
    
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    Education of the patient regarding the interaction of the nervous system, referred pain, and resultant tenderness, and of the interaction her actions and postures will have in perpetuating or eliminating her pain.

As noted above, there were no glaring findings that led the clinician to the diagnosis. What occurred was the summarization of commonalities during the course of the evaluation, followed by the application of a segmental mobilization at a grade II to these segments in an attempt to address the patient’s pain. Following the application of the mobilizations, the findings of abdominal tender points, increased iliopsoas tone, and subjective symptoms were reassessed. Any reduction of symptoms strongly indicates the involvement of that/those spinal segment(s), and a phenomenon of central sensitization.

What were the patient’s primary complaints during the history taking component of the evaluation? Did they indicate a region of the body that was involved? Urological? Bowel? Gynecologic? Or did the symptoms represent allodynia or hyperalgesia? If so, was the pain local or regional and are the symptoms progressing from one system to another? If the symptoms appear to be “progressing” from one system to another, are those structures related embryologically?

If the symptoms were isolated to a single aspect of the urological, bowel, or gynecologic system, was there any aspect of the history or the clinical testing that indicated a reason for this pain? Were there any segmental losses of motion during the active lumbar screening that reflect the viscus’ embryological derivation? If so, did a manipulation/mobilization locally positively influence these symptoms? If so, then the patient is likely suffering from a facilitated segment and is an appropriate patient for physical therapy care. If not, then further testing may be indicated, a referral to a gynecologist, urologist, or colo-rectal specialist, or the patient may possibly be insincere.

Did the history and clinical findings indicate a local nerve entrapment? If so, were these symptoms alterable with manipulations/mobilizations to the spine, or local transverse friction massage to the pelvic musculotendinous structures?

Were there any scars that impede motion, entrap peripheral nerves, perpetuate pain, limit or prevent complete closure during internal manual muscle testing (MMT)? If addressing the scar(s), were the patient’s symptoms eliminated? If so, then the clinician can deduce that the scarring was a considerable factor in pain initiation and propagation. Addressing the appropriate spinal segment may further alleviate the patient’s pain, as the segment will likely have become sensitized due to the persistent noxious stimulation from the scar.

Were any of the special tests positive? If so, do they implicate a region that requires additional testing? Or does local treatment to the region alleviate the patient’s symptoms?

Discerning findings of the evaluation:

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  Were there active motions of the spine that reproduce symptoms that indicate a closer evaluation of that region of the spine?

  
  
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  Was there local, segmental hypomobility of the spine that reflects the patient’s symptoms, a somatic representation of embryogenesis?

  
  
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  Segmental weaknesses suggest a closer inspection of the suspected spinal level. Is there a correlation of segmental weakness to neuroanatomy with presenting symptoms?

  
  
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  Neural tension testing is reflective of the overall mobility of the nervous system. Are there any restrictions that relate to the level of spinal integration?

  
  
  
  
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    Are there any fasciculations with prone knee flexion (PKF)?

  
  
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  Does the hip have any restrictions? Does passive movement reproduce the patient’s pain?

  
  
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  CPAs and unilateral posterior-to-anterior (UPA)s: do they move appropriately? Do they reproduce pain along the suspected segment? Do they eliminate pain, spasm, or neurological symptoms?

  
  
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  During the course of the pelvic evaluation, was there any pain while assessing the “pelvic map”?

  
  
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  Were there any asymmetries in strength right versus left, and between the layers one, two, and three?

  
  
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  Was there any scarring within the birth canal?

  
  
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  Was there a lack of muscle bulk, indicating breach of musculature along any of the pelvic floor muscles?

  
  
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  Was there a positive Tinel test of any of the sacral nerves, or the pudendal nerves?

  
  
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  Was the bulbospongiosus symmetrical, latent or hyper-reflexive?

  
  
  
  
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    Does this correlate with any of the SIJ findings?

  
  
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  Was there the presence of the distal rectum, bladder, or uterus within the vaginal canal?

  
  
  
  
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    Did the mobilization of this structure improve contraction grade of the PFM?

  
  
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  Was the anterior SIJ ligament painful and/or noted to have crepitus along its length?